Take-Home Points

• Use fluoroscopy, isometry, or both to double-check the femoral attachment point. Failure to do so can lead to an overtensioned or undertensioned graft caused by anisometric graft placement.
• To minimize the risk of fracture, avoid drilling transverse tunnels across the patella.
• Do not “pre-tension” the medial patellofemoral ligament graft. There should be little or no tension in the graft when the patella is centered in the groove, regardless of the angle of knee flexion.
• The angle of knee flexion during securing of the graft may be important for inaccurate femoral tunnel placement. Before final fixation of the graft, always range the knee fully to make sure full passive motion will be possible once the graft is secured.
• Understanding the anatomy of the MPFL is key before considering reconstructing: That is, fluoroscopy only suggests a “cloud” to begin assessment of the femoral attachment site and is secondary to anatomic references and check of length changes between the attachment point through range of motion. New studies demonstrate the patellar attachment is broad and extends proximally from the historical patellar attachment site to an equal distance along the distal quadriceps.

The medial patellofemoral ligament (MPFL), which is essential in preventing lateral patellar instability, becomes torn in almost 100% of dislocation events.¹ Therefore, in cases of failed nonoperative management, this important constraint should be reconstructed. Reconstruction is technically challenging, precision is needed to avoid postoperative complications, and a thorough understanding of the native MPFL anatomy is paramount.

As a thickening of the medial patellar retinaculum, the MPFL connects the medial patella to the medial femur. The femoral insertion has been described a few ways. In a cadaveric study, LaPrade and colleagues² noted that it inserts 1.9 mm anterior and 3.2 mm distal to the adductor tubercle. Radiographically, the attachment has been described by Schöttle and colleagues³ and Stephen and colleagues.⁴ These techniques are discussed in more detail later.

The MPFL is a static restraint to lateral patellar translation—it acts only as a checkrein. It functions mainly in 0° to 30° of knee flexion because once the patella engages the trochlear groove, the bony articulation guides the patella during the rest of knee flexion.⁵ Most authors agree that the native MPFL is mostly isometric, and the re-created ligament should replicate it.^6,7 Using cadaveric specimens, Steensen and colleagues⁶ found that, from 0° to 90° of knee flexion, the distance from the inferior patellar attachment to the superior femoral attachment changed only 1.1 mm.

Biomechanical studies have shown that a MPFL graft with excessive tension predisposes to postoperative abnormal patellofemoral contact pressures, which cause anterior knee pain, loss of knee flexion, and patellofemoral chondrosis.^8-10 Furthermore, an overtensioned graft can cause iatrogenic medial patellar subluxation, and an undertensioned graft may still allow for pathologic lateral patellar translation.

Anatomical Bony Insertions

Femoral Insertion

Precise localization of the proper anatomical femoral attachment of the MPFL is a crucial step in reconstruction.¹¹ Small errors in femoral location have resulted in significant loss of graft isometry, increased patellofemoral contact pressures in cadaveric models,^4,7 and increased rates of failure after both MPFL repair¹² and reconstruction.¹³ Several methods for confirming proper femoral location during surgery have been described; these methods help obviate the need for large formal dissection of the medial knee.

In a cadaveric study, Schöttle and colleagues³ described a reproducible radiographic point that precisely identifies the appropriate femoral location for MPFL graft placement. The point is located on a standard true lateral radiograph of the distal femur. First, a line is drawn extending the posterior cortex of the femur distally. Next, 2 lines are drawn perpendicular to the first: one intersecting the posterior point of the Blumensaat line, the other intersecting the transition between the posterior femoral condyle and the posterior femoral cortex³ (Figure 1).

Patellar Insertion

The patellar attachment of the MPFL has received considerably less attention than the femoral attachment.¹¹ Anatomical studies have shown that the MPFL inserts on the superomedial half to third of the patella, in addition to a portion inserting on the undersurface of the vastus medialis.¹⁷

Troubleshooting

It is essential to check graft tension through full knee ROM and observe how the graft behaves in order to prevent iatrogenic complications¹¹ (Figures 6A, 6B).

If the graft is secured in high degrees of knee flexion, and the femoral location is not anatomical, a different phenomenon occurs when the knee is brought back into extension. For proximal femoral tunnels, the graft loosens in knee extension and may lead to continued lateral patellar instability. On the other hand, a distal femoral tunnel may result in iatrogenic medial patellar subluxation as the graft becomes too tight in extension.

Correct Amount of Graft Tension

Overtightening the MPFL during fixation is an easy but avoidable mistake. Unlike the anterior cruciate ligament, the MPFL should not be secured while applying maximum tension. Stephen and colleagues⁷ and Beck and colleagues⁸ found that tension of only 2 N (~0.5 lb) is needed to accurately re-create the biomechanics of the native graft.

The amount of tension may inadvertently be increased by an interference screw, which tends to pull the graft into the femoral tunnel during insertion. Attention should be given to watching and palpating the graft as the screw is inserted, especially during the last few turns. Turning the screw half a turn backwards after full insertion can release this increased tension and help avoid overtensioning.

Correct Amount of Knee Flexion

This is probably the least studied aspect of MPFL reconstruction. Recommendations range from 0° to 90° of knee flexion during fixation.^7,25-30 Most recommendations are surgeon preference, or are based on a sound rationale that lacks supporting research. Tensioning in full extension has been advocated for assessing for the appropriate amount of lateral patellar translation.²⁷ Authors who endorse deeper knee flexion (60°-90°) think that, because the patella engages a deeper trochlear groove in increased flexion, the bony articulation can be used to establish graft length.^30,31

Our cadaveric study showed that lower degrees of knee flexion are safest for minimizing the effect of a malpositioned femoral tunnel.²⁶ If femoral tunnel location is not exactly anatomical, any errors are magnified (with even worse graft mechanics) the deeper in flexion the graft is fixed. Once the patella engages the trochlear groove, at about 30° of knee flexion, this can assist in establishing correct graft length. Therefore, we recommend fixation of the graft in 30° to 45° of knee flexion. Our study results also showed that, if femoral tunnel location is anatomical, the graft will be mostly isometric through knee ROM, and, therefore, amount of initial knee flexion does not affect graft behavior.

Regardless of knee flexion chosen, it is imperative to take the knee through full ROM after fixation to ensure the graft does not excessively loosen or tighten in flexion or extension.

Conclusion

MPFL reconstruction is fraught with errors and technical nuances that may be underappreciated. Accurately locating the femoral insertion is crucial to a biomechanically sound graft, and this location should be scrutinized during surgery with accurate radiographs or bony landmarks and verified with knee ROM. Although there is no clear gold standard for fixation and graft options, the graft should be secured while pulling very little tension (2 N) and with the knee in 30° to 45° of flexion to minimize the effect of any inaccuracies in femoral location. Overall, most patients do well after MPFL reconstruction, and attention to surgical technical detail helps maximize the chances of a satisfactory outcome.

Am J Orthop. 2017;46(2):76-81. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Use fluoroscopy, isometry, or both to double-check the femoral attachment point. Failure to do so can lead to an overtensioned or undertensioned graft caused by anisometric graft placement.
• To minimize the risk of fracture, avoid drilling transverse tunnels across the patella.
• Do not “pre-tension” the medial patellofemoral ligament graft. There should be little or no tension in the graft when the patella is centered in the groove, regardless of the angle of knee flexion.
• The angle of knee flexion during securing of the graft may be important for inaccurate femoral tunnel placement. Before final fixation of the graft, always range the knee fully to make sure full passive motion will be possible once the graft is secured.
• Understanding the anatomy of the MPFL is key before considering reconstructing: That is, fluoroscopy only suggests a “cloud” to begin assessment of the femoral attachment site and is secondary to anatomic references and check of length changes between the attachment point through range of motion. New studies demonstrate the patellar attachment is broad and extends proximally from the historical patellar attachment site to an equal distance along the distal quadriceps.

The medial patellofemoral ligament (MPFL), which is essential in preventing lateral patellar instability, becomes torn in almost 100% of dislocation events.¹ Therefore, in cases of failed nonoperative management, this important constraint should be reconstructed. Reconstruction is technically challenging, precision is needed to avoid postoperative complications, and a thorough understanding of the native MPFL anatomy is paramount.

As a thickening of the medial patellar retinaculum, the MPFL connects the medial patella to the medial femur. The femoral insertion has been described a few ways. In a cadaveric study, LaPrade and colleagues² noted that it inserts 1.9 mm anterior and 3.2 mm distal to the adductor tubercle. Radiographically, the attachment has been described by Schöttle and colleagues³ and Stephen and colleagues.⁴ These techniques are discussed in more detail later.

The MPFL is a static restraint to lateral patellar translation—it acts only as a checkrein. It functions mainly in 0° to 30° of knee flexion because once the patella engages the trochlear groove, the bony articulation guides the patella during the rest of knee flexion.⁵ Most authors agree that the native MPFL is mostly isometric, and the re-created ligament should replicate it.^6,7 Using cadaveric specimens, Steensen and colleagues⁶ found that, from 0° to 90° of knee flexion, the distance from the inferior patellar attachment to the superior femoral attachment changed only 1.1 mm.

Biomechanical studies have shown that a MPFL graft with excessive tension predisposes to postoperative abnormal patellofemoral contact pressures, which cause anterior knee pain, loss of knee flexion, and patellofemoral chondrosis.^8-10 Furthermore, an overtensioned graft can cause iatrogenic medial patellar subluxation, and an undertensioned graft may still allow for pathologic lateral patellar translation.

Anatomical Bony Insertions

Femoral Insertion

Precise localization of the proper anatomical femoral attachment of the MPFL is a crucial step in reconstruction.¹¹ Small errors in femoral location have resulted in significant loss of graft isometry, increased patellofemoral contact pressures in cadaveric models,^4,7 and increased rates of failure after both MPFL repair¹² and reconstruction.¹³ Several methods for confirming proper femoral location during surgery have been described; these methods help obviate the need for large formal dissection of the medial knee.

In a cadaveric study, Schöttle and colleagues³ described a reproducible radiographic point that precisely identifies the appropriate femoral location for MPFL graft placement. The point is located on a standard true lateral radiograph of the distal femur. First, a line is drawn extending the posterior cortex of the femur distally. Next, 2 lines are drawn perpendicular to the first: one intersecting the posterior point of the Blumensaat line, the other intersecting the transition between the posterior femoral condyle and the posterior femoral cortex³ (Figure 1).

Patellar Insertion

The patellar attachment of the MPFL has received considerably less attention than the femoral attachment.¹¹ Anatomical studies have shown that the MPFL inserts on the superomedial half to third of the patella, in addition to a portion inserting on the undersurface of the vastus medialis.¹⁷

Troubleshooting

It is essential to check graft tension through full knee ROM and observe how the graft behaves in order to prevent iatrogenic complications¹¹ (Figures 6A, 6B).

If the graft is secured in high degrees of knee flexion, and the femoral location is not anatomical, a different phenomenon occurs when the knee is brought back into extension. For proximal femoral tunnels, the graft loosens in knee extension and may lead to continued lateral patellar instability. On the other hand, a distal femoral tunnel may result in iatrogenic medial patellar subluxation as the graft becomes too tight in extension.

Correct Amount of Graft Tension

Overtightening the MPFL during fixation is an easy but avoidable mistake. Unlike the anterior cruciate ligament, the MPFL should not be secured while applying maximum tension. Stephen and colleagues⁷ and Beck and colleagues⁸ found that tension of only 2 N (~0.5 lb) is needed to accurately re-create the biomechanics of the native graft.

The amount of tension may inadvertently be increased by an interference screw, which tends to pull the graft into the femoral tunnel during insertion. Attention should be given to watching and palpating the graft as the screw is inserted, especially during the last few turns. Turning the screw half a turn backwards after full insertion can release this increased tension and help avoid overtensioning.

Correct Amount of Knee Flexion

This is probably the least studied aspect of MPFL reconstruction. Recommendations range from 0° to 90° of knee flexion during fixation.^7,25-30 Most recommendations are surgeon preference, or are based on a sound rationale that lacks supporting research. Tensioning in full extension has been advocated for assessing for the appropriate amount of lateral patellar translation.²⁷ Authors who endorse deeper knee flexion (60°-90°) think that, because the patella engages a deeper trochlear groove in increased flexion, the bony articulation can be used to establish graft length.^30,31

Our cadaveric study showed that lower degrees of knee flexion are safest for minimizing the effect of a malpositioned femoral tunnel.²⁶ If femoral tunnel location is not exactly anatomical, any errors are magnified (with even worse graft mechanics) the deeper in flexion the graft is fixed. Once the patella engages the trochlear groove, at about 30° of knee flexion, this can assist in establishing correct graft length. Therefore, we recommend fixation of the graft in 30° to 45° of knee flexion. Our study results also showed that, if femoral tunnel location is anatomical, the graft will be mostly isometric through knee ROM, and, therefore, amount of initial knee flexion does not affect graft behavior.

Regardless of knee flexion chosen, it is imperative to take the knee through full ROM after fixation to ensure the graft does not excessively loosen or tighten in flexion or extension.

Conclusion

MPFL reconstruction is fraught with errors and technical nuances that may be underappreciated. Accurately locating the femoral insertion is crucial to a biomechanically sound graft, and this location should be scrutinized during surgery with accurate radiographs or bony landmarks and verified with knee ROM. Although there is no clear gold standard for fixation and graft options, the graft should be secured while pulling very little tension (2 N) and with the knee in 30° to 45° of flexion to minimize the effect of any inaccuracies in femoral location. Overall, most patients do well after MPFL reconstruction, and attention to surgical technical detail helps maximize the chances of a satisfactory outcome.

Am J Orthop. 2017;46(2):76-81. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Use fluoroscopy, isometry, or both to double-check the femoral attachment point. Failure to do so can lead to an overtensioned or undertensioned graft caused by anisometric graft placement.
• To minimize the risk of fracture, avoid drilling transverse tunnels across the patella.
• Do not “pre-tension” the medial patellofemoral ligament graft. There should be little or no tension in the graft when the patella is centered in the groove, regardless of the angle of knee flexion.
• The angle of knee flexion during securing of the graft may be important for inaccurate femoral tunnel placement. Before final fixation of the graft, always range the knee fully to make sure full passive motion will be possible once the graft is secured.
• Understanding the anatomy of the MPFL is key before considering reconstructing: That is, fluoroscopy only suggests a “cloud” to begin assessment of the femoral attachment site and is secondary to anatomic references and check of length changes between the attachment point through range of motion. New studies demonstrate the patellar attachment is broad and extends proximally from the historical patellar attachment site to an equal distance along the distal quadriceps.

The medial patellofemoral ligament (MPFL), which is essential in preventing lateral patellar instability, becomes torn in almost 100% of dislocation events.¹ Therefore, in cases of failed nonoperative management, this important constraint should be reconstructed. Reconstruction is technically challenging, precision is needed to avoid postoperative complications, and a thorough understanding of the native MPFL anatomy is paramount.

As a thickening of the medial patellar retinaculum, the MPFL connects the medial patella to the medial femur. The femoral insertion has been described a few ways. In a cadaveric study, LaPrade and colleagues² noted that it inserts 1.9 mm anterior and 3.2 mm distal to the adductor tubercle. Radiographically, the attachment has been described by Schöttle and colleagues³ and Stephen and colleagues.⁴ These techniques are discussed in more detail later.

The MPFL is a static restraint to lateral patellar translation—it acts only as a checkrein. It functions mainly in 0° to 30° of knee flexion because once the patella engages the trochlear groove, the bony articulation guides the patella during the rest of knee flexion.⁵ Most authors agree that the native MPFL is mostly isometric, and the re-created ligament should replicate it.^6,7 Using cadaveric specimens, Steensen and colleagues⁶ found that, from 0° to 90° of knee flexion, the distance from the inferior patellar attachment to the superior femoral attachment changed only 1.1 mm.

Biomechanical studies have shown that a MPFL graft with excessive tension predisposes to postoperative abnormal patellofemoral contact pressures, which cause anterior knee pain, loss of knee flexion, and patellofemoral chondrosis.^8-10 Furthermore, an overtensioned graft can cause iatrogenic medial patellar subluxation, and an undertensioned graft may still allow for pathologic lateral patellar translation.

Anatomical Bony Insertions

Femoral Insertion

Precise localization of the proper anatomical femoral attachment of the MPFL is a crucial step in reconstruction.¹¹ Small errors in femoral location have resulted in significant loss of graft isometry, increased patellofemoral contact pressures in cadaveric models,^4,7 and increased rates of failure after both MPFL repair¹² and reconstruction.¹³ Several methods for confirming proper femoral location during surgery have been described; these methods help obviate the need for large formal dissection of the medial knee.

In a cadaveric study, Schöttle and colleagues³ described a reproducible radiographic point that precisely identifies the appropriate femoral location for MPFL graft placement. The point is located on a standard true lateral radiograph of the distal femur. First, a line is drawn extending the posterior cortex of the femur distally. Next, 2 lines are drawn perpendicular to the first: one intersecting the posterior point of the Blumensaat line, the other intersecting the transition between the posterior femoral condyle and the posterior femoral cortex³ (Figure 1).

Patellar Insertion

The patellar attachment of the MPFL has received considerably less attention than the femoral attachment.¹¹ Anatomical studies have shown that the MPFL inserts on the superomedial half to third of the patella, in addition to a portion inserting on the undersurface of the vastus medialis.¹⁷

Troubleshooting

It is essential to check graft tension through full knee ROM and observe how the graft behaves in order to prevent iatrogenic complications¹¹ (Figures 6A, 6B).

If the graft is secured in high degrees of knee flexion, and the femoral location is not anatomical, a different phenomenon occurs when the knee is brought back into extension. For proximal femoral tunnels, the graft loosens in knee extension and may lead to continued lateral patellar instability. On the other hand, a distal femoral tunnel may result in iatrogenic medial patellar subluxation as the graft becomes too tight in extension.

Correct Amount of Graft Tension

Overtightening the MPFL during fixation is an easy but avoidable mistake. Unlike the anterior cruciate ligament, the MPFL should not be secured while applying maximum tension. Stephen and colleagues⁷ and Beck and colleagues⁸ found that tension of only 2 N (~0.5 lb) is needed to accurately re-create the biomechanics of the native graft.

The amount of tension may inadvertently be increased by an interference screw, which tends to pull the graft into the femoral tunnel during insertion. Attention should be given to watching and palpating the graft as the screw is inserted, especially during the last few turns. Turning the screw half a turn backwards after full insertion can release this increased tension and help avoid overtensioning.

Correct Amount of Knee Flexion

This is probably the least studied aspect of MPFL reconstruction. Recommendations range from 0° to 90° of knee flexion during fixation.^7,25-30 Most recommendations are surgeon preference, or are based on a sound rationale that lacks supporting research. Tensioning in full extension has been advocated for assessing for the appropriate amount of lateral patellar translation.²⁷ Authors who endorse deeper knee flexion (60°-90°) think that, because the patella engages a deeper trochlear groove in increased flexion, the bony articulation can be used to establish graft length.^30,31

Our cadaveric study showed that lower degrees of knee flexion are safest for minimizing the effect of a malpositioned femoral tunnel.²⁶ If femoral tunnel location is not exactly anatomical, any errors are magnified (with even worse graft mechanics) the deeper in flexion the graft is fixed. Once the patella engages the trochlear groove, at about 30° of knee flexion, this can assist in establishing correct graft length. Therefore, we recommend fixation of the graft in 30° to 45° of knee flexion. Our study results also showed that, if femoral tunnel location is anatomical, the graft will be mostly isometric through knee ROM, and, therefore, amount of initial knee flexion does not affect graft behavior.

Regardless of knee flexion chosen, it is imperative to take the knee through full ROM after fixation to ensure the graft does not excessively loosen or tighten in flexion or extension.

Conclusion

MPFL reconstruction is fraught with errors and technical nuances that may be underappreciated. Accurately locating the femoral insertion is crucial to a biomechanically sound graft, and this location should be scrutinized during surgery with accurate radiographs or bony landmarks and verified with knee ROM. Although there is no clear gold standard for fixation and graft options, the graft should be secured while pulling very little tension (2 N) and with the knee in 30° to 45° of flexion to minimize the effect of any inaccuracies in femoral location. Overall, most patients do well after MPFL reconstruction, and attention to surgical technical detail helps maximize the chances of a satisfactory outcome.

Am J Orthop. 2017;46(2):76-81. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Ensure that relative rest and activity modification allow the knee to stay within the available “envelope of function” of the joint.
• Careful physical examination is imperative to assess strength, flexibility, and altered movement patterns, which in many cases are all part of the etiology of AKP.
• Patience and perseverance are paramount. Patients need to clearly understand the goals of rehabilitation as well as the concepts related to “envelope of function” so they can continue to keep themselves within this envelope. This education is crucial to their success.
• Only once a patient has been brought into the pain-free functional envelope can rehabilitation be redirected to expanding the envelope toward the patient’s particular goals.

• Quantity does not equal quality. To create an appropriate care plan, the physician must assess the adequacy of the patient’s rehabilitation thus far—ask specific questions about the types of exercises the patient is doing in physical therapy and quickly assess strength with a few simple in-office tests.

Anterior knee pain (AKP) is a common presentation. Although the exact etiology and nature of AKP continue to be poorly understood, overuse principles can be useful in directing treatment. In overuse injury, repetitive submaximal or subclinical trauma results in macroscopic trauma, microscopic trauma, or both. The structural tissue unit is damaged or its clinical responsiveness is exceeded, which can lead to pain or movement dysfunction. Overuse injuries commonly have an endogenous source, mechanical circumstances in which the musculoskeletal tissue is subjected to more tensile force or stress than the tissue can tolerate. The approach to treatment and rehabilitation of AKP is best facilitated with a thorough understanding of the concept of tissue homeostasis and the “envelope of function.”

Although the cause of AKP is multifactorial, the contributions of muscle strength deficits, diminished neuromuscular control, and altered muscle firing patterns to the development and severity of AKP are well established.^1-5 The hallmark of nonoperative management of AKP is physiotherapy that re-establishes strength, neuromuscular control, muscle activation, and optimal biomechanics during daily activities, advancing to graded levels of sporting activities.

The purpose of this paper is to discuss the factors associated with the diminished neuromuscular control observed in AKP and to review appropriate rehabilitation concepts for patients with AKP. Practical tools are provided to aid the surgeon to identify neuromuscular deficits in the clinic setting, along with assessing the adequacy of prior therapy and the need for further rehabilitation.

Common Neuromuscular Deficits in AKP

Weakness of the knee extensor muscles has long been implicated as the main issue in AKP, and therefore the focus of rehabilitation has been on muscle strengthening, especially of the vastus medialis obliquus. Research has found that knee extensor weakness is not only a characteristic of patients with AKP but a risk factor for developing AKP.⁴ Restoration of knee extensor strength and function is essential for recovery.⁶ Another issue in AKP may be incorrect firing of the knee extensor muscles. Altered vastus medialis obliquus response time and a motor control deficit of the quadriceps musculature have been demonstrated.^7,8 Restoration of knee extensor strength, though important, is too often the sole focus of some rehabilitation programs.

Hip muscle weakness has also been implicated as an important component of AKP.^9-12 Impaired gluteal muscle function can lead to increased hip joint adduction and internal rotation during activities such as stair climbing, squatting, and sports.^9,10,13 In a systematic review, Meira and Brumitt¹² concluded that hip strength and position are linked to AKP and that patients with AKP present with a common deficit once symptomatic. The dysfunction in neuromuscular control in AKP may also stem from disordered firing sequences in the muscles. A systematic review of hip electromyographic studies found moderate to strong evidence that gluteus medius muscle activity is delayed and of shorter duration during stair ascent and descent in patients with AKP.¹¹ The study also found some evidence that this activity is delayed and of shorter duration during running and that gluteus maximus muscle activity is increased during stair descent. The authors recommended that interventions focused on correcting these deficits—such as hip strengthening, biofeedback, and gait retraining—should be included in AKP treatment and research.

In recent AKP research, the core, including hip and abdominal muscles, demonstrated decreased strength and altered recruitment patterns during functional movement.^14,15 The authors recommended including core strengthening and core stability exercises in AKP management. In combination, these knee extensor, hip, and core strength deficits in patients with AKP lead to altered movement patterns during functional activities and may in turn exacerbate symptoms. Addressing both the strength deficits and the recruitment patterns of these core and lower extremity muscles is essential for optimizing rehabilitation and limiting recurrence of AKP symptoms.

Stretching to improve muscle tendon length is another component of AKP treatment. Reduced quadriceps muscle length has been implicated as a cause of AKP and is a common finding in symptomatic patients.¹⁶ In addition, a recent randomized controlled trial found decreased hip flexibility in patients with AKP.¹⁷ It is important to assess the flexibility of the gastrocnemius, soleus, quadriceps, and hamstrings muscles and the iliotibial band, as well as the hip flexors, extensors, and rotators, so that rehabilitation can be designed to address any specific deficits in range of motion (ROM).^16-23 In patients with AKP, it is also important to address muscle tendon length deficits and strengthening simultaneously to avoid exceeding the available envelope of function. Gaining full ROM at joints can facilitate increasing strength gains²⁴ and potentially improve the synergy of muscle contractions during functional activities.

Appropriate Rehabilitation in AKP

Appropriate rehabilitation addresses all identified strength and flexibility deficits in order to improve functional biomechanics and normalize altered body movement patterns during daily activities (eg, walking, squatting, stair climbing). Often, if part of the kinetic chain is weak or injured, the body engages in an activity by “working around” the injured body part. This change often results in faulty body mechanics or altered movement patterns. In AKP, these modified biomechanics can result in pain centered on the patella and associated soft-tissue structures. In developing ways to compensate for strength and ROM deficits, patients with AKP exacerbate their symptoms. In long-standing AKP, these compensatory strategies are most often unintentional and ingrained.

The main role of physical therapists is to identify any faulty movement patterns, dissect the underlying neuromuscular causes of these deficits, and build an individualized rehabilitation program. Physical therapy should be customized to the patient’s level of strength and fitness and whenever possible should be made challenging (and fun!) for the patient. The exercises should be increased in intensity and duration as the patient improves strength, endurance, and control in the activities. The patient’s response to each intervention will help guide exercise progression and define the need for further treatments.

Patients should be assessed for overuse patterns. Overuse can occur with repetitive exercise activity, such as running, or with repetitive work activity that involves lifting, squatting, or stair climbing. It is important to modify or reduce such activity to ensure that a patient with AKP remains within an envelope of pain-free function. Once the patient is functioning in this envelope, rehabilitation can be redirected to expand it, while improving strength, coordination, balance, and overall dynamic control of the core and lower limbs.

The purpose of any rehabilitation program is to build strength through the entire kinetic chain, focusing on hip and core strength initially, and then adding concentric and eccentric lower limb strength. Having a strong base from which to initiate lower limb movements makes correct lower limb form more likely to follow. Corrected muscle firing patterns allow for appropriate sequencing of the muscle activation needed for proper movements. Corrected muscle tendon lengths allow for optimal firing of the muscles controlling the lower limb, and for the flexibility needed for everyday ROM and biomechanics. Patients with AKP require re-education of movements that occur during daily functional activities, including gait. Once correct movement patterns are established in daily activities, it is important to address sporting or work-related activities. This is one important reason to ensure that physiotherapy visits are distributed over time and that patient-centered goals are addressed during each visit. In addition, during therapy, it is essential to reexamine body movement patterns to identify any relapse to prior dysfunction as the intensity or frequency of activity increases.

In AKP management, the dosage and duration of exercise prescriptions are challenging, and patience and perseverance are paramount. The initial goal of therapy is to increase strength and ROM to enable practice of correct motion in daily activities (eg, stair climbing, sitting, and walking). The physical therapist’s challenge is to teach correct motion within the envelope of function, as described by Dye.²⁵ Pain is not gain, and all exercises must be performed without pain to avoid flaring symptoms. The patient and the therapist must collaborate to complete a pain free rehabilitation program, and must operate within that zone. Providing prescriptions with specific goals may be helpful. Example goals are, “Increase core and lower extremity strength to achieve squatting without medial collapse of knee,” “Hip and core strengthening and endurance,” “Equal quadriceps strength and girth,” and “Functional movement retraining.”

Assessing Adequacy of Rehabilitation in AKP

When a patient presents with a diagnosis of AKP, it can be difficult to establish whether a prior rehabilitation program was appropriate. The fact that a patient attended physiotherapy says nothing about the quality of the therapy provided. Neither does the number of sessions attended. To assess the quality of the rehabilitation and determine if there are any major deficits in neuromuscular function, the physician can perform a simple battery of screening tests (Figure 1).²⁶

More advanced tests can be used to better understand the neuromuscular function of the patient with AKP and tease out specific deficits. Figure 2²⁶ describes some of these tests and the typical compensatory motions seen in patients with altered movement patterns.

Am J Orthop. 2017;46(2):82-86. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Ensure that relative rest and activity modification allow the knee to stay within the available “envelope of function” of the joint.
• Careful physical examination is imperative to assess strength, flexibility, and altered movement patterns, which in many cases are all part of the etiology of AKP.
• Patience and perseverance are paramount. Patients need to clearly understand the goals of rehabilitation as well as the concepts related to “envelope of function” so they can continue to keep themselves within this envelope. This education is crucial to their success.
• Only once a patient has been brought into the pain-free functional envelope can rehabilitation be redirected to expanding the envelope toward the patient’s particular goals.

• Quantity does not equal quality. To create an appropriate care plan, the physician must assess the adequacy of the patient’s rehabilitation thus far—ask specific questions about the types of exercises the patient is doing in physical therapy and quickly assess strength with a few simple in-office tests.

Anterior knee pain (AKP) is a common presentation. Although the exact etiology and nature of AKP continue to be poorly understood, overuse principles can be useful in directing treatment. In overuse injury, repetitive submaximal or subclinical trauma results in macroscopic trauma, microscopic trauma, or both. The structural tissue unit is damaged or its clinical responsiveness is exceeded, which can lead to pain or movement dysfunction. Overuse injuries commonly have an endogenous source, mechanical circumstances in which the musculoskeletal tissue is subjected to more tensile force or stress than the tissue can tolerate. The approach to treatment and rehabilitation of AKP is best facilitated with a thorough understanding of the concept of tissue homeostasis and the “envelope of function.”

Although the cause of AKP is multifactorial, the contributions of muscle strength deficits, diminished neuromuscular control, and altered muscle firing patterns to the development and severity of AKP are well established.^1-5 The hallmark of nonoperative management of AKP is physiotherapy that re-establishes strength, neuromuscular control, muscle activation, and optimal biomechanics during daily activities, advancing to graded levels of sporting activities.

The purpose of this paper is to discuss the factors associated with the diminished neuromuscular control observed in AKP and to review appropriate rehabilitation concepts for patients with AKP. Practical tools are provided to aid the surgeon to identify neuromuscular deficits in the clinic setting, along with assessing the adequacy of prior therapy and the need for further rehabilitation.

Common Neuromuscular Deficits in AKP

Weakness of the knee extensor muscles has long been implicated as the main issue in AKP, and therefore the focus of rehabilitation has been on muscle strengthening, especially of the vastus medialis obliquus. Research has found that knee extensor weakness is not only a characteristic of patients with AKP but a risk factor for developing AKP.⁴ Restoration of knee extensor strength and function is essential for recovery.⁶ Another issue in AKP may be incorrect firing of the knee extensor muscles. Altered vastus medialis obliquus response time and a motor control deficit of the quadriceps musculature have been demonstrated.^7,8 Restoration of knee extensor strength, though important, is too often the sole focus of some rehabilitation programs.

Hip muscle weakness has also been implicated as an important component of AKP.^9-12 Impaired gluteal muscle function can lead to increased hip joint adduction and internal rotation during activities such as stair climbing, squatting, and sports.^9,10,13 In a systematic review, Meira and Brumitt¹² concluded that hip strength and position are linked to AKP and that patients with AKP present with a common deficit once symptomatic. The dysfunction in neuromuscular control in AKP may also stem from disordered firing sequences in the muscles. A systematic review of hip electromyographic studies found moderate to strong evidence that gluteus medius muscle activity is delayed and of shorter duration during stair ascent and descent in patients with AKP.¹¹ The study also found some evidence that this activity is delayed and of shorter duration during running and that gluteus maximus muscle activity is increased during stair descent. The authors recommended that interventions focused on correcting these deficits—such as hip strengthening, biofeedback, and gait retraining—should be included in AKP treatment and research.

In recent AKP research, the core, including hip and abdominal muscles, demonstrated decreased strength and altered recruitment patterns during functional movement.^14,15 The authors recommended including core strengthening and core stability exercises in AKP management. In combination, these knee extensor, hip, and core strength deficits in patients with AKP lead to altered movement patterns during functional activities and may in turn exacerbate symptoms. Addressing both the strength deficits and the recruitment patterns of these core and lower extremity muscles is essential for optimizing rehabilitation and limiting recurrence of AKP symptoms.

Stretching to improve muscle tendon length is another component of AKP treatment. Reduced quadriceps muscle length has been implicated as a cause of AKP and is a common finding in symptomatic patients.¹⁶ In addition, a recent randomized controlled trial found decreased hip flexibility in patients with AKP.¹⁷ It is important to assess the flexibility of the gastrocnemius, soleus, quadriceps, and hamstrings muscles and the iliotibial band, as well as the hip flexors, extensors, and rotators, so that rehabilitation can be designed to address any specific deficits in range of motion (ROM).^16-23 In patients with AKP, it is also important to address muscle tendon length deficits and strengthening simultaneously to avoid exceeding the available envelope of function. Gaining full ROM at joints can facilitate increasing strength gains²⁴ and potentially improve the synergy of muscle contractions during functional activities.

Appropriate Rehabilitation in AKP

Appropriate rehabilitation addresses all identified strength and flexibility deficits in order to improve functional biomechanics and normalize altered body movement patterns during daily activities (eg, walking, squatting, stair climbing). Often, if part of the kinetic chain is weak or injured, the body engages in an activity by “working around” the injured body part. This change often results in faulty body mechanics or altered movement patterns. In AKP, these modified biomechanics can result in pain centered on the patella and associated soft-tissue structures. In developing ways to compensate for strength and ROM deficits, patients with AKP exacerbate their symptoms. In long-standing AKP, these compensatory strategies are most often unintentional and ingrained.

The main role of physical therapists is to identify any faulty movement patterns, dissect the underlying neuromuscular causes of these deficits, and build an individualized rehabilitation program. Physical therapy should be customized to the patient’s level of strength and fitness and whenever possible should be made challenging (and fun!) for the patient. The exercises should be increased in intensity and duration as the patient improves strength, endurance, and control in the activities. The patient’s response to each intervention will help guide exercise progression and define the need for further treatments.

Patients should be assessed for overuse patterns. Overuse can occur with repetitive exercise activity, such as running, or with repetitive work activity that involves lifting, squatting, or stair climbing. It is important to modify or reduce such activity to ensure that a patient with AKP remains within an envelope of pain-free function. Once the patient is functioning in this envelope, rehabilitation can be redirected to expand it, while improving strength, coordination, balance, and overall dynamic control of the core and lower limbs.

The purpose of any rehabilitation program is to build strength through the entire kinetic chain, focusing on hip and core strength initially, and then adding concentric and eccentric lower limb strength. Having a strong base from which to initiate lower limb movements makes correct lower limb form more likely to follow. Corrected muscle firing patterns allow for appropriate sequencing of the muscle activation needed for proper movements. Corrected muscle tendon lengths allow for optimal firing of the muscles controlling the lower limb, and for the flexibility needed for everyday ROM and biomechanics. Patients with AKP require re-education of movements that occur during daily functional activities, including gait. Once correct movement patterns are established in daily activities, it is important to address sporting or work-related activities. This is one important reason to ensure that physiotherapy visits are distributed over time and that patient-centered goals are addressed during each visit. In addition, during therapy, it is essential to reexamine body movement patterns to identify any relapse to prior dysfunction as the intensity or frequency of activity increases.

In AKP management, the dosage and duration of exercise prescriptions are challenging, and patience and perseverance are paramount. The initial goal of therapy is to increase strength and ROM to enable practice of correct motion in daily activities (eg, stair climbing, sitting, and walking). The physical therapist’s challenge is to teach correct motion within the envelope of function, as described by Dye.²⁵ Pain is not gain, and all exercises must be performed without pain to avoid flaring symptoms. The patient and the therapist must collaborate to complete a pain free rehabilitation program, and must operate within that zone. Providing prescriptions with specific goals may be helpful. Example goals are, “Increase core and lower extremity strength to achieve squatting without medial collapse of knee,” “Hip and core strengthening and endurance,” “Equal quadriceps strength and girth,” and “Functional movement retraining.”

Assessing Adequacy of Rehabilitation in AKP

When a patient presents with a diagnosis of AKP, it can be difficult to establish whether a prior rehabilitation program was appropriate. The fact that a patient attended physiotherapy says nothing about the quality of the therapy provided. Neither does the number of sessions attended. To assess the quality of the rehabilitation and determine if there are any major deficits in neuromuscular function, the physician can perform a simple battery of screening tests (Figure 1).²⁶

More advanced tests can be used to better understand the neuromuscular function of the patient with AKP and tease out specific deficits. Figure 2²⁶ describes some of these tests and the typical compensatory motions seen in patients with altered movement patterns.

Am J Orthop. 2017;46(2):82-86. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Ensure that relative rest and activity modification allow the knee to stay within the available “envelope of function” of the joint.
• Careful physical examination is imperative to assess strength, flexibility, and altered movement patterns, which in many cases are all part of the etiology of AKP.
• Patience and perseverance are paramount. Patients need to clearly understand the goals of rehabilitation as well as the concepts related to “envelope of function” so they can continue to keep themselves within this envelope. This education is crucial to their success.
• Only once a patient has been brought into the pain-free functional envelope can rehabilitation be redirected to expanding the envelope toward the patient’s particular goals.

• Quantity does not equal quality. To create an appropriate care plan, the physician must assess the adequacy of the patient’s rehabilitation thus far—ask specific questions about the types of exercises the patient is doing in physical therapy and quickly assess strength with a few simple in-office tests.

Anterior knee pain (AKP) is a common presentation. Although the exact etiology and nature of AKP continue to be poorly understood, overuse principles can be useful in directing treatment. In overuse injury, repetitive submaximal or subclinical trauma results in macroscopic trauma, microscopic trauma, or both. The structural tissue unit is damaged or its clinical responsiveness is exceeded, which can lead to pain or movement dysfunction. Overuse injuries commonly have an endogenous source, mechanical circumstances in which the musculoskeletal tissue is subjected to more tensile force or stress than the tissue can tolerate. The approach to treatment and rehabilitation of AKP is best facilitated with a thorough understanding of the concept of tissue homeostasis and the “envelope of function.”

Although the cause of AKP is multifactorial, the contributions of muscle strength deficits, diminished neuromuscular control, and altered muscle firing patterns to the development and severity of AKP are well established.^1-5 The hallmark of nonoperative management of AKP is physiotherapy that re-establishes strength, neuromuscular control, muscle activation, and optimal biomechanics during daily activities, advancing to graded levels of sporting activities.

The purpose of this paper is to discuss the factors associated with the diminished neuromuscular control observed in AKP and to review appropriate rehabilitation concepts for patients with AKP. Practical tools are provided to aid the surgeon to identify neuromuscular deficits in the clinic setting, along with assessing the adequacy of prior therapy and the need for further rehabilitation.

Common Neuromuscular Deficits in AKP

Weakness of the knee extensor muscles has long been implicated as the main issue in AKP, and therefore the focus of rehabilitation has been on muscle strengthening, especially of the vastus medialis obliquus. Research has found that knee extensor weakness is not only a characteristic of patients with AKP but a risk factor for developing AKP.⁴ Restoration of knee extensor strength and function is essential for recovery.⁶ Another issue in AKP may be incorrect firing of the knee extensor muscles. Altered vastus medialis obliquus response time and a motor control deficit of the quadriceps musculature have been demonstrated.^7,8 Restoration of knee extensor strength, though important, is too often the sole focus of some rehabilitation programs.

Hip muscle weakness has also been implicated as an important component of AKP.^9-12 Impaired gluteal muscle function can lead to increased hip joint adduction and internal rotation during activities such as stair climbing, squatting, and sports.^9,10,13 In a systematic review, Meira and Brumitt¹² concluded that hip strength and position are linked to AKP and that patients with AKP present with a common deficit once symptomatic. The dysfunction in neuromuscular control in AKP may also stem from disordered firing sequences in the muscles. A systematic review of hip electromyographic studies found moderate to strong evidence that gluteus medius muscle activity is delayed and of shorter duration during stair ascent and descent in patients with AKP.¹¹ The study also found some evidence that this activity is delayed and of shorter duration during running and that gluteus maximus muscle activity is increased during stair descent. The authors recommended that interventions focused on correcting these deficits—such as hip strengthening, biofeedback, and gait retraining—should be included in AKP treatment and research.

In recent AKP research, the core, including hip and abdominal muscles, demonstrated decreased strength and altered recruitment patterns during functional movement.^14,15 The authors recommended including core strengthening and core stability exercises in AKP management. In combination, these knee extensor, hip, and core strength deficits in patients with AKP lead to altered movement patterns during functional activities and may in turn exacerbate symptoms. Addressing both the strength deficits and the recruitment patterns of these core and lower extremity muscles is essential for optimizing rehabilitation and limiting recurrence of AKP symptoms.

Stretching to improve muscle tendon length is another component of AKP treatment. Reduced quadriceps muscle length has been implicated as a cause of AKP and is a common finding in symptomatic patients.¹⁶ In addition, a recent randomized controlled trial found decreased hip flexibility in patients with AKP.¹⁷ It is important to assess the flexibility of the gastrocnemius, soleus, quadriceps, and hamstrings muscles and the iliotibial band, as well as the hip flexors, extensors, and rotators, so that rehabilitation can be designed to address any specific deficits in range of motion (ROM).^16-23 In patients with AKP, it is also important to address muscle tendon length deficits and strengthening simultaneously to avoid exceeding the available envelope of function. Gaining full ROM at joints can facilitate increasing strength gains²⁴ and potentially improve the synergy of muscle contractions during functional activities.

Appropriate Rehabilitation in AKP

Appropriate rehabilitation addresses all identified strength and flexibility deficits in order to improve functional biomechanics and normalize altered body movement patterns during daily activities (eg, walking, squatting, stair climbing). Often, if part of the kinetic chain is weak or injured, the body engages in an activity by “working around” the injured body part. This change often results in faulty body mechanics or altered movement patterns. In AKP, these modified biomechanics can result in pain centered on the patella and associated soft-tissue structures. In developing ways to compensate for strength and ROM deficits, patients with AKP exacerbate their symptoms. In long-standing AKP, these compensatory strategies are most often unintentional and ingrained.

The main role of physical therapists is to identify any faulty movement patterns, dissect the underlying neuromuscular causes of these deficits, and build an individualized rehabilitation program. Physical therapy should be customized to the patient’s level of strength and fitness and whenever possible should be made challenging (and fun!) for the patient. The exercises should be increased in intensity and duration as the patient improves strength, endurance, and control in the activities. The patient’s response to each intervention will help guide exercise progression and define the need for further treatments.

Patients should be assessed for overuse patterns. Overuse can occur with repetitive exercise activity, such as running, or with repetitive work activity that involves lifting, squatting, or stair climbing. It is important to modify or reduce such activity to ensure that a patient with AKP remains within an envelope of pain-free function. Once the patient is functioning in this envelope, rehabilitation can be redirected to expand it, while improving strength, coordination, balance, and overall dynamic control of the core and lower limbs.

The purpose of any rehabilitation program is to build strength through the entire kinetic chain, focusing on hip and core strength initially, and then adding concentric and eccentric lower limb strength. Having a strong base from which to initiate lower limb movements makes correct lower limb form more likely to follow. Corrected muscle firing patterns allow for appropriate sequencing of the muscle activation needed for proper movements. Corrected muscle tendon lengths allow for optimal firing of the muscles controlling the lower limb, and for the flexibility needed for everyday ROM and biomechanics. Patients with AKP require re-education of movements that occur during daily functional activities, including gait. Once correct movement patterns are established in daily activities, it is important to address sporting or work-related activities. This is one important reason to ensure that physiotherapy visits are distributed over time and that patient-centered goals are addressed during each visit. In addition, during therapy, it is essential to reexamine body movement patterns to identify any relapse to prior dysfunction as the intensity or frequency of activity increases.

In AKP management, the dosage and duration of exercise prescriptions are challenging, and patience and perseverance are paramount. The initial goal of therapy is to increase strength and ROM to enable practice of correct motion in daily activities (eg, stair climbing, sitting, and walking). The physical therapist’s challenge is to teach correct motion within the envelope of function, as described by Dye.²⁵ Pain is not gain, and all exercises must be performed without pain to avoid flaring symptoms. The patient and the therapist must collaborate to complete a pain free rehabilitation program, and must operate within that zone. Providing prescriptions with specific goals may be helpful. Example goals are, “Increase core and lower extremity strength to achieve squatting without medial collapse of knee,” “Hip and core strengthening and endurance,” “Equal quadriceps strength and girth,” and “Functional movement retraining.”

Assessing Adequacy of Rehabilitation in AKP

When a patient presents with a diagnosis of AKP, it can be difficult to establish whether a prior rehabilitation program was appropriate. The fact that a patient attended physiotherapy says nothing about the quality of the therapy provided. Neither does the number of sessions attended. To assess the quality of the rehabilitation and determine if there are any major deficits in neuromuscular function, the physician can perform a simple battery of screening tests (Figure 1).²⁶

More advanced tests can be used to better understand the neuromuscular function of the patient with AKP and tease out specific deficits. Figure 2²⁶ describes some of these tests and the typical compensatory motions seen in patients with altered movement patterns.

Am J Orthop. 2017;46(2):82-86. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

NEW ORLEANS – While many Americans have been dithering over the relative health benefits of high- versus low-carbohydrate diets, various pop-culture weight loss programs, vegetarianism, gluten-free living, and other nutritional matters, a quiet revolution in mainstream scientific thinking has occurred regarding the role of full-fat dairy products.

Saturated fatty acid–rich dairy products, formerly viewed as the enemy of cardiovascular health, have gone from foe to friend, according to Arne Astrup, MD, professor and head of the department of nutrition, exercise and sports at the University of Copenhagen.

Ingram Publishing/Thinkstock

The classic lipid hypothesis of cardiovascular disease holds that dietary saturated fat raises blood cholesterol, in turn accelerating atherosclerosis and resultant coronary heart disease. But the published literature of the past few years indicates it’s not that simple. All saturated fats are not equally harmful. They have very different biologic effects, and the food matrix in which they occur seems to be important. The saturated fatty acids found in red meat are clearly damaging. Ditto trans fats.

In contrast, the saturated fats present in milk, hard cheeses, and fermented dairy products such as yogurt have been shown in a variety of study formats to be cardioprotective. They also appear to protect against other chronic diseases as well, according to the researcher.

“If we look at all the different meta-analyses addressing the various cardiovascular risk factors, it really looks like cheese, despite its high content of sodium and saturated fat, seems to exert some beneficial effects. So I think we need to address the food matrix much more. We’ve done controlled feeding trials in humans and found that if we give subjects the same amount of saturated fat from either butter or cheese, you see following the cheese [that] the subjects do not increase their total or LDL-cholesterol as you would expect based upon their intake of saturated fat. So there’s something going on with cheese,” Dr. Astrup said.

What’s going on, he continued, is the saturated fats in cheese benefit from the company they keep. Fermented dairy products contain an arm-long list of potentially beneficial nutrients, including protein, calcium, short-chain fatty acids, bioactive peptides, and phospholipids.

Take, for example, calcium: “We’ve found the calcium content of cheese completely modifies the metabolism of the saturated fat. The calcium seems to bind the bile acids and fatty acids, resulting in increased fecal fat secretion,” according to Dr. Astrup.

Although at the AHA meeting he focused mainly on the effects of cheese and other dairy products on cardiovascular health, in a recent review article he expanded upon the scientific evidence regarding the impact of these foods on the risks of obesity, type 2 diabetes, cancer, and osteoporosis (Food Nutr Res. 2016 Nov 22;60:32527).

There is solid evidence that a diet high in dairy products reduces the risk of childhood obesity and enhances body composition in adults. It aids in weight loss by promoting satiety during periods of energy restriction. A recent meta-analysis of observational studies found an inverse relationship between consumption of fermented dairy products – yogurt and cheese – and risk of type 2 diabetes (Am J Clin Nutr. 2016 Apr;103[4]:1111-24).

Regarding cancer, the World Cancer Research Fund has issued a series of evidence reviews concluding that dairy products probably protect against colorectal, breast, gastric, and bladder cancer. The jury is still out regarding prostate cancer risk.

A wealth of evidence indicates dairy consumption has a beneficial effect on bone health in children and adolescents. However, meta-analyses haven’t shown a protective effect against osteoporosis and fractures in adults. This is consistent with the adage that osteoporosis is a pediatric disease with geriatric consequences, Dr. Astrup noted.

He reported receiving research grants from the Danish Dairy Research Foundation, the Global Dairy Platform, the Danish Agriculture and Food Council, and the European Milk Forum. He serves on advisory boards for the Dutch Beer Knowledge Institute, Suntory, Weight Watchers, and several food companies.
 

[email protected]

NEW ORLEANS – While many Americans have been dithering over the relative health benefits of high- versus low-carbohydrate diets, various pop-culture weight loss programs, vegetarianism, gluten-free living, and other nutritional matters, a quiet revolution in mainstream scientific thinking has occurred regarding the role of full-fat dairy products.

Saturated fatty acid–rich dairy products, formerly viewed as the enemy of cardiovascular health, have gone from foe to friend, according to Arne Astrup, MD, professor and head of the department of nutrition, exercise and sports at the University of Copenhagen.

Ingram Publishing/Thinkstock

The classic lipid hypothesis of cardiovascular disease holds that dietary saturated fat raises blood cholesterol, in turn accelerating atherosclerosis and resultant coronary heart disease. But the published literature of the past few years indicates it’s not that simple. All saturated fats are not equally harmful. They have very different biologic effects, and the food matrix in which they occur seems to be important. The saturated fatty acids found in red meat are clearly damaging. Ditto trans fats.

In contrast, the saturated fats present in milk, hard cheeses, and fermented dairy products such as yogurt have been shown in a variety of study formats to be cardioprotective. They also appear to protect against other chronic diseases as well, according to the researcher.

“If we look at all the different meta-analyses addressing the various cardiovascular risk factors, it really looks like cheese, despite its high content of sodium and saturated fat, seems to exert some beneficial effects. So I think we need to address the food matrix much more. We’ve done controlled feeding trials in humans and found that if we give subjects the same amount of saturated fat from either butter or cheese, you see following the cheese [that] the subjects do not increase their total or LDL-cholesterol as you would expect based upon their intake of saturated fat. So there’s something going on with cheese,” Dr. Astrup said.

What’s going on, he continued, is the saturated fats in cheese benefit from the company they keep. Fermented dairy products contain an arm-long list of potentially beneficial nutrients, including protein, calcium, short-chain fatty acids, bioactive peptides, and phospholipids.

Take, for example, calcium: “We’ve found the calcium content of cheese completely modifies the metabolism of the saturated fat. The calcium seems to bind the bile acids and fatty acids, resulting in increased fecal fat secretion,” according to Dr. Astrup.

Although at the AHA meeting he focused mainly on the effects of cheese and other dairy products on cardiovascular health, in a recent review article he expanded upon the scientific evidence regarding the impact of these foods on the risks of obesity, type 2 diabetes, cancer, and osteoporosis (Food Nutr Res. 2016 Nov 22;60:32527).

There is solid evidence that a diet high in dairy products reduces the risk of childhood obesity and enhances body composition in adults. It aids in weight loss by promoting satiety during periods of energy restriction. A recent meta-analysis of observational studies found an inverse relationship between consumption of fermented dairy products – yogurt and cheese – and risk of type 2 diabetes (Am J Clin Nutr. 2016 Apr;103[4]:1111-24).

Regarding cancer, the World Cancer Research Fund has issued a series of evidence reviews concluding that dairy products probably protect against colorectal, breast, gastric, and bladder cancer. The jury is still out regarding prostate cancer risk.

A wealth of evidence indicates dairy consumption has a beneficial effect on bone health in children and adolescents. However, meta-analyses haven’t shown a protective effect against osteoporosis and fractures in adults. This is consistent with the adage that osteoporosis is a pediatric disease with geriatric consequences, Dr. Astrup noted.

He reported receiving research grants from the Danish Dairy Research Foundation, the Global Dairy Platform, the Danish Agriculture and Food Council, and the European Milk Forum. He serves on advisory boards for the Dutch Beer Knowledge Institute, Suntory, Weight Watchers, and several food companies.
 

[email protected]

NEW ORLEANS – While many Americans have been dithering over the relative health benefits of high- versus low-carbohydrate diets, various pop-culture weight loss programs, vegetarianism, gluten-free living, and other nutritional matters, a quiet revolution in mainstream scientific thinking has occurred regarding the role of full-fat dairy products.

Saturated fatty acid–rich dairy products, formerly viewed as the enemy of cardiovascular health, have gone from foe to friend, according to Arne Astrup, MD, professor and head of the department of nutrition, exercise and sports at the University of Copenhagen.

Ingram Publishing/Thinkstock

The classic lipid hypothesis of cardiovascular disease holds that dietary saturated fat raises blood cholesterol, in turn accelerating atherosclerosis and resultant coronary heart disease. But the published literature of the past few years indicates it’s not that simple. All saturated fats are not equally harmful. They have very different biologic effects, and the food matrix in which they occur seems to be important. The saturated fatty acids found in red meat are clearly damaging. Ditto trans fats.

In contrast, the saturated fats present in milk, hard cheeses, and fermented dairy products such as yogurt have been shown in a variety of study formats to be cardioprotective. They also appear to protect against other chronic diseases as well, according to the researcher.

“If we look at all the different meta-analyses addressing the various cardiovascular risk factors, it really looks like cheese, despite its high content of sodium and saturated fat, seems to exert some beneficial effects. So I think we need to address the food matrix much more. We’ve done controlled feeding trials in humans and found that if we give subjects the same amount of saturated fat from either butter or cheese, you see following the cheese [that] the subjects do not increase their total or LDL-cholesterol as you would expect based upon their intake of saturated fat. So there’s something going on with cheese,” Dr. Astrup said.

What’s going on, he continued, is the saturated fats in cheese benefit from the company they keep. Fermented dairy products contain an arm-long list of potentially beneficial nutrients, including protein, calcium, short-chain fatty acids, bioactive peptides, and phospholipids.

Take, for example, calcium: “We’ve found the calcium content of cheese completely modifies the metabolism of the saturated fat. The calcium seems to bind the bile acids and fatty acids, resulting in increased fecal fat secretion,” according to Dr. Astrup.

Although at the AHA meeting he focused mainly on the effects of cheese and other dairy products on cardiovascular health, in a recent review article he expanded upon the scientific evidence regarding the impact of these foods on the risks of obesity, type 2 diabetes, cancer, and osteoporosis (Food Nutr Res. 2016 Nov 22;60:32527).

There is solid evidence that a diet high in dairy products reduces the risk of childhood obesity and enhances body composition in adults. It aids in weight loss by promoting satiety during periods of energy restriction. A recent meta-analysis of observational studies found an inverse relationship between consumption of fermented dairy products – yogurt and cheese – and risk of type 2 diabetes (Am J Clin Nutr. 2016 Apr;103[4]:1111-24).

Regarding cancer, the World Cancer Research Fund has issued a series of evidence reviews concluding that dairy products probably protect against colorectal, breast, gastric, and bladder cancer. The jury is still out regarding prostate cancer risk.

A wealth of evidence indicates dairy consumption has a beneficial effect on bone health in children and adolescents. However, meta-analyses haven’t shown a protective effect against osteoporosis and fractures in adults. This is consistent with the adage that osteoporosis is a pediatric disease with geriatric consequences, Dr. Astrup noted.

He reported receiving research grants from the Danish Dairy Research Foundation, the Global Dairy Platform, the Danish Agriculture and Food Council, and the European Milk Forum. He serves on advisory boards for the Dutch Beer Knowledge Institute, Suntory, Weight Watchers, and several food companies.
 

[email protected]

Take-Home Points

• MPFL repair has the best results with isolated ligament avulsions in first-time dislocations. This can be demonstrated on MRI and verified at the time of arthroscopy.
• Recurrent dislocations, even if acute, have a higher failure rate with MPFL repair. In this setting, MPFL reconstruction provides more consistent outcomes.
• In cases of chronic lateral patellar dislocation, imbrication may be enough when other associated procedures have sufficiently stabilized the patella without the need for a strong soft-tissue checkrein.
• Femoral-sided repairs are more challenging due to the need to optimize the insertion point on the femur, as small changes in positioning can cause increased stress on the repaired tissue and lead to failure.
• If a repair is to have a chance to work, it must be performed at the site of the tear. Thus, preoperative planning and intraoperative inspection is important to precisely identify the site, which can involve intrasubstance and multifocal injuries as well as the femoral and patellar complex attachments.

The medial patellofemoral ligament (MPFL) is the primary soft-tissue restraint to lateral patellar translation.¹ In cases of first-time acute lateral patellar dislocation, injury to the MPFL is described as the essential lesion, occurring in almost 100% of cases.^2-4 Because of the relatively high frequency of recurrent instability after first-time acute lateral patellar dislocation,^5-7 much research has been focused on MPFL repair and reconstruction.^8-11 Although the clinical results of isolated MPFL repair are highly variable, this variability is likely secondary to relatively inconsistent clinical indications for repair, with repair described for patients with acute as well as chronic or recurrent instability.^10-13 From these early successes and failures, much has been learned about the appropriate indications for MPFL repair as well as medial retinacular “reefing” or imbrication in the chronic setting.

Relevant Anatomy

The MPFL is an extracapsular thickening of the medial retinacular structures and can be most consistently identified just distal to the vastus medialis obliquus, running within layer 2 of the medial side of the knee (using the often-referenced layer system popularized by Warren and Marshall¹⁴). The MPFL origin on the medial aspect of the femur falls within a well-defined saddle between the adductor tubercle and the medial epicondyle.¹⁵ From this relatively narrow origin, the MPFL broadens before attaching to the proximal one-third of the medial aspect of the patella.

Over the past 2 decades, the osseous anatomy surrounding the femoral origin of the MPFL has been of much interest in large part because of the increasing popularity of MPFL reconstruction. Although useful for MPFL reconstruction, the vast amount of literature and our improved understanding of this anatomical region can be extrapolated to MPFL repair. The radiographic landmarks described by Schöttle and colleagues¹⁶ have advanced our knowledge of the femoral origin of the MPFL, with fluoroscopic guidance allowing for more limited dissection and increased accuracy of repair for femoral-sided MPFL injuries.

Location of MPFL Injury

Understanding and appreciating the specific location of the MPFL injury are paramount to successful MPFL repair. Unfortunately, the location and pattern of MPFL injury cannot be consistently predicted. Although early surgical dissections described femoral-sided injuries as the most common injury site,⁴ more recent studies using magnetic resonance imaging (MRI) have described a more even distribution of MPFL injury patterns, which include patella-based ruptures, femoral-based ruptures, intrasubstance ruptures, and multifocal injuries.¹⁷ In addition, age and skeletal maturity likely play a role in the MPFL injury location, as skeletally immature patients more often have patella-based ruptures.^2,18,19 In acute MPFL repair, MRI appears to be the most accurate imaging modality for determining the patella- or femoral-based injuries most amenable to repair and for identifying clinically significant osteochondral lesions, which are not uncommon after first-time patellar dislocation.^20,21

Medial Reefing, Imbrication, and Advancement

Medial reefing, imbrication, and advancement, collectively referred to as proximal realignment procedures, describe a variety of techniques that essentially shorten or tighten the medial retinacular structures.^22-24 Although the terms cover a variety of similar surgical techniques and are often used interchangeably in the literature, imbrication, or overlapping of adjacent edges, is the single most accurate term used to define this spectrum of procedures. These procedures historically were performed in the setting of chronic or recurrent patellar instability, with the primary goal being to imbricate the attenuated medial retinaculum, which includes the MPFL. However, the procedure has had good clinical outcomes when performed in isolation for patients with normal bony anatomy.²⁵ Such anatomy is rare in chronic or recurrent dislocators, and these proximal soft-tissue procedures are often combined with other osseous realignment procedures, including distal realignment, trochleoplasty, and distal femoral osteotomy.²⁶

Discussion

MPFL Repair: Indications and Surgical Technique

Although optimal management of first-time patellar dislocation continues to be a topic for debate, the frequency of recurrent instability,^7,27 particularly in young patients, has led some to advocate early surgical management.^9,28 A clear indication for early operative intervention is the presence of a large osteochondral lesion that can undergo fixation or is causing persistent mechanical symptoms with recurrent effusion (Figures 1A, 1B).

Numerous open and arthroscopic MPFL repair techniques have been described.^10,30-33 Nevertheless, comparative studies are limited, and the greatest debate about MPFL repair continues to be appropriate indications. Arthroscopic MPFL repair can be technically demanding and can fully visualize only patella-based injuries. In addition, all-arthroscopic repair techniques may place suture material in the joint, which causes concern regarding suture irritation. As a result, the majority of MPFL repair techniques described in the literature use an open approach, which typically includes a 4-cm to 5-cm longitudinal incision along the medial aspect of the patella. Sharp dissection is carried down through the medial retinaculum to the underlying joint capsule. The plane between the medial retinaculum and the underlying joint capsule is bluntly developed posteriorly until the medial epicondyle and the adductor tubercle are palpated. For a patella-based rupture, the MPFL is defined within layer 2, and 2 suture anchors are placed within the superior third of the patella. Although there are other patellar fixation methods, suture anchors provide adequate fixation with minimal risk of iatrogenic patellar fracture. With anchors in place, horizontal mattress sutures are placed in the stump of the MPFL. For femoral-based ruptures, the same surgical exposure is used to identify the MPFL. However, depending on the size of the incision and the mobility of the tissue, a second incision can be made posterior and parallel to the first—best achieved using a spinal needle to fluoroscopically localize Schöttle’s point.¹⁶ An incision is made in line with the spinal needle, and dissection is continued down to the previously developed extracapsular plane. Under fluoroscopic guidance (Figure 3), 1 or 2 suture anchors are placed at Schöttle point, and horizontal mattress sutures are placed through the avulsed MPFL femoral origin.

MPFL Imbrication: Indications and Surgical Technique

MPFL reconstruction is the technique of choice in recurrent patellofemoral instability when no other procedures are required. When combined with distal realignment procedures, distal femoral osteotomy, open patellofemoral cartilage resurfacing procedures, or trochleoplasty, MPFL imbrication can be considered in place of MPFL reconstruction. Recurrent patellofemoral instability is influenced by various factors, including static soft-tissue restraints, dynamic muscle action, and bony anatomy, only one of which is directly addressed with MPFL imbrication. Relying on native tissues without a graft increases the risk for recurrent instability because of concern that the already attenuated native tissues will stretch out further, particularly in the presence of hyperlaxity. Although the significance of trochlear dysplasia in patellofemoral instability was first noted by Dejour and colleagues,³⁴ the presence of trochlear dysplasia has been shown to negatively influence outcomes of isolated MPFL imbrication.³⁵ Because of the relative frequency of trochlear dysplasia and axial or coronal plane malalignment in patients with chronic or recurrent patellar instability, MPFL imbrication typically is not performed on its own, and it is best used in conjunction with a distal realignment procedure or distal femoral osteotomy. MPFL reconstruction should be performed instead of MPFL imbrication in patients with severe trochlear dysplasia, in patients with hyperlaxity signs, and in young patients who participate in cutting or pivoting sports.

When distal realignment procedures are performed for axial alignment, or distal femoral osteotomy is performed for severe genu valgum, patellofemoral laxity is tested after the bony correction is completed. If the patella is still dislocatable, MPFL reconstruction provides the most predictable outcome. If laxity is increased, but the patella remains in the trochlea, typically MPFL imbrication is adequate.

Similar to MPFL repair, both open and arthroscopic techniques have been described in the literature.^36-38 As MPFL imbrication is most commonly performed in conjunction with large open procedures, this procedure can often be incorporated with other open incisions. In addition, open MPFL imbrication allows for precise control and tensioning of the medial retinacular structures, which is not always easily achieved by arthroscopic methods.

If a separate incision is required, a 4-cm to 5-cm longitudinal incision is made along the medial border of the patella, just as described for MPFL repair. The medial retinacular tissue, including the MPFL, is identified and isolated extracapsularly. Imbrication can be performed with sutures only (using a cuff of tissue along the medial border of the patella and placing pants-over-vest sutures in the adjacent tissue) or with sutures and anchors (more similar to MPFL repair described earlier). In either scenario, adequately tensioning the MPFL and associated medial retinaculum is essential in order to restore the checkrein function of the attenuated MPFL. Although typically described in the setting of MPFL reconstruction, the MPFL can easily be overtensioned during MPFL imbrication. This potential pitfall can be avoided by recognizing that forces over 2 N will overtension medial structures and thereby increase contact pressures at the medial patellar facet.³⁹ The complication can easily be prevented simply by placing the knee in 30° flexion and centering the patella in the trochlear groove while performing the MPFL imbrication.

Conclusion

Careful patient selection is the most important element for successful MPFL repair or imbrication. MPFL repair is most reliably used in patients with clear patella- or femoral-sided avulsions and in patients with a first-time patellar dislocation and a clear surgical indication, such as a large osteochondral fragment. Proximal realignment procedures, which include MPFL reefing, imbrication, and advancement, typically are not performed in isolation, as other osseous procedures are often needed concomitantly in order to preserve the checkrein effect provided by proximal realignment procedures. As is the case with MPFL reconstruction, understanding the relevant anatomy and avoiding overtensioning of the medial structures during MPFL repair or proximal realignment procedures are crucial.

Am J Orthop. 2017;46(2):87-91. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• MPFL repair has the best results with isolated ligament avulsions in first-time dislocations. This can be demonstrated on MRI and verified at the time of arthroscopy.
• Recurrent dislocations, even if acute, have a higher failure rate with MPFL repair. In this setting, MPFL reconstruction provides more consistent outcomes.
• In cases of chronic lateral patellar dislocation, imbrication may be enough when other associated procedures have sufficiently stabilized the patella without the need for a strong soft-tissue checkrein.
• Femoral-sided repairs are more challenging due to the need to optimize the insertion point on the femur, as small changes in positioning can cause increased stress on the repaired tissue and lead to failure.
• If a repair is to have a chance to work, it must be performed at the site of the tear. Thus, preoperative planning and intraoperative inspection is important to precisely identify the site, which can involve intrasubstance and multifocal injuries as well as the femoral and patellar complex attachments.

The medial patellofemoral ligament (MPFL) is the primary soft-tissue restraint to lateral patellar translation.¹ In cases of first-time acute lateral patellar dislocation, injury to the MPFL is described as the essential lesion, occurring in almost 100% of cases.^2-4 Because of the relatively high frequency of recurrent instability after first-time acute lateral patellar dislocation,^5-7 much research has been focused on MPFL repair and reconstruction.^8-11 Although the clinical results of isolated MPFL repair are highly variable, this variability is likely secondary to relatively inconsistent clinical indications for repair, with repair described for patients with acute as well as chronic or recurrent instability.^10-13 From these early successes and failures, much has been learned about the appropriate indications for MPFL repair as well as medial retinacular “reefing” or imbrication in the chronic setting.

Relevant Anatomy

The MPFL is an extracapsular thickening of the medial retinacular structures and can be most consistently identified just distal to the vastus medialis obliquus, running within layer 2 of the medial side of the knee (using the often-referenced layer system popularized by Warren and Marshall¹⁴). The MPFL origin on the medial aspect of the femur falls within a well-defined saddle between the adductor tubercle and the medial epicondyle.¹⁵ From this relatively narrow origin, the MPFL broadens before attaching to the proximal one-third of the medial aspect of the patella.

Over the past 2 decades, the osseous anatomy surrounding the femoral origin of the MPFL has been of much interest in large part because of the increasing popularity of MPFL reconstruction. Although useful for MPFL reconstruction, the vast amount of literature and our improved understanding of this anatomical region can be extrapolated to MPFL repair. The radiographic landmarks described by Schöttle and colleagues¹⁶ have advanced our knowledge of the femoral origin of the MPFL, with fluoroscopic guidance allowing for more limited dissection and increased accuracy of repair for femoral-sided MPFL injuries.

Location of MPFL Injury

Understanding and appreciating the specific location of the MPFL injury are paramount to successful MPFL repair. Unfortunately, the location and pattern of MPFL injury cannot be consistently predicted. Although early surgical dissections described femoral-sided injuries as the most common injury site,⁴ more recent studies using magnetic resonance imaging (MRI) have described a more even distribution of MPFL injury patterns, which include patella-based ruptures, femoral-based ruptures, intrasubstance ruptures, and multifocal injuries.¹⁷ In addition, age and skeletal maturity likely play a role in the MPFL injury location, as skeletally immature patients more often have patella-based ruptures.^2,18,19 In acute MPFL repair, MRI appears to be the most accurate imaging modality for determining the patella- or femoral-based injuries most amenable to repair and for identifying clinically significant osteochondral lesions, which are not uncommon after first-time patellar dislocation.^20,21

Medial Reefing, Imbrication, and Advancement

Medial reefing, imbrication, and advancement, collectively referred to as proximal realignment procedures, describe a variety of techniques that essentially shorten or tighten the medial retinacular structures.^22-24 Although the terms cover a variety of similar surgical techniques and are often used interchangeably in the literature, imbrication, or overlapping of adjacent edges, is the single most accurate term used to define this spectrum of procedures. These procedures historically were performed in the setting of chronic or recurrent patellar instability, with the primary goal being to imbricate the attenuated medial retinaculum, which includes the MPFL. However, the procedure has had good clinical outcomes when performed in isolation for patients with normal bony anatomy.²⁵ Such anatomy is rare in chronic or recurrent dislocators, and these proximal soft-tissue procedures are often combined with other osseous realignment procedures, including distal realignment, trochleoplasty, and distal femoral osteotomy.²⁶

Discussion

MPFL Repair: Indications and Surgical Technique

Although optimal management of first-time patellar dislocation continues to be a topic for debate, the frequency of recurrent instability,^7,27 particularly in young patients, has led some to advocate early surgical management.^9,28 A clear indication for early operative intervention is the presence of a large osteochondral lesion that can undergo fixation or is causing persistent mechanical symptoms with recurrent effusion (Figures 1A, 1B).

Numerous open and arthroscopic MPFL repair techniques have been described.^10,30-33 Nevertheless, comparative studies are limited, and the greatest debate about MPFL repair continues to be appropriate indications. Arthroscopic MPFL repair can be technically demanding and can fully visualize only patella-based injuries. In addition, all-arthroscopic repair techniques may place suture material in the joint, which causes concern regarding suture irritation. As a result, the majority of MPFL repair techniques described in the literature use an open approach, which typically includes a 4-cm to 5-cm longitudinal incision along the medial aspect of the patella. Sharp dissection is carried down through the medial retinaculum to the underlying joint capsule. The plane between the medial retinaculum and the underlying joint capsule is bluntly developed posteriorly until the medial epicondyle and the adductor tubercle are palpated. For a patella-based rupture, the MPFL is defined within layer 2, and 2 suture anchors are placed within the superior third of the patella. Although there are other patellar fixation methods, suture anchors provide adequate fixation with minimal risk of iatrogenic patellar fracture. With anchors in place, horizontal mattress sutures are placed in the stump of the MPFL. For femoral-based ruptures, the same surgical exposure is used to identify the MPFL. However, depending on the size of the incision and the mobility of the tissue, a second incision can be made posterior and parallel to the first—best achieved using a spinal needle to fluoroscopically localize Schöttle’s point.¹⁶ An incision is made in line with the spinal needle, and dissection is continued down to the previously developed extracapsular plane. Under fluoroscopic guidance (Figure 3), 1 or 2 suture anchors are placed at Schöttle point, and horizontal mattress sutures are placed through the avulsed MPFL femoral origin.

MPFL Imbrication: Indications and Surgical Technique

MPFL reconstruction is the technique of choice in recurrent patellofemoral instability when no other procedures are required. When combined with distal realignment procedures, distal femoral osteotomy, open patellofemoral cartilage resurfacing procedures, or trochleoplasty, MPFL imbrication can be considered in place of MPFL reconstruction. Recurrent patellofemoral instability is influenced by various factors, including static soft-tissue restraints, dynamic muscle action, and bony anatomy, only one of which is directly addressed with MPFL imbrication. Relying on native tissues without a graft increases the risk for recurrent instability because of concern that the already attenuated native tissues will stretch out further, particularly in the presence of hyperlaxity. Although the significance of trochlear dysplasia in patellofemoral instability was first noted by Dejour and colleagues,³⁴ the presence of trochlear dysplasia has been shown to negatively influence outcomes of isolated MPFL imbrication.³⁵ Because of the relative frequency of trochlear dysplasia and axial or coronal plane malalignment in patients with chronic or recurrent patellar instability, MPFL imbrication typically is not performed on its own, and it is best used in conjunction with a distal realignment procedure or distal femoral osteotomy. MPFL reconstruction should be performed instead of MPFL imbrication in patients with severe trochlear dysplasia, in patients with hyperlaxity signs, and in young patients who participate in cutting or pivoting sports.

When distal realignment procedures are performed for axial alignment, or distal femoral osteotomy is performed for severe genu valgum, patellofemoral laxity is tested after the bony correction is completed. If the patella is still dislocatable, MPFL reconstruction provides the most predictable outcome. If laxity is increased, but the patella remains in the trochlea, typically MPFL imbrication is adequate.

Similar to MPFL repair, both open and arthroscopic techniques have been described in the literature.^36-38 As MPFL imbrication is most commonly performed in conjunction with large open procedures, this procedure can often be incorporated with other open incisions. In addition, open MPFL imbrication allows for precise control and tensioning of the medial retinacular structures, which is not always easily achieved by arthroscopic methods.

If a separate incision is required, a 4-cm to 5-cm longitudinal incision is made along the medial border of the patella, just as described for MPFL repair. The medial retinacular tissue, including the MPFL, is identified and isolated extracapsularly. Imbrication can be performed with sutures only (using a cuff of tissue along the medial border of the patella and placing pants-over-vest sutures in the adjacent tissue) or with sutures and anchors (more similar to MPFL repair described earlier). In either scenario, adequately tensioning the MPFL and associated medial retinaculum is essential in order to restore the checkrein function of the attenuated MPFL. Although typically described in the setting of MPFL reconstruction, the MPFL can easily be overtensioned during MPFL imbrication. This potential pitfall can be avoided by recognizing that forces over 2 N will overtension medial structures and thereby increase contact pressures at the medial patellar facet.³⁹ The complication can easily be prevented simply by placing the knee in 30° flexion and centering the patella in the trochlear groove while performing the MPFL imbrication.

Conclusion

Careful patient selection is the most important element for successful MPFL repair or imbrication. MPFL repair is most reliably used in patients with clear patella- or femoral-sided avulsions and in patients with a first-time patellar dislocation and a clear surgical indication, such as a large osteochondral fragment. Proximal realignment procedures, which include MPFL reefing, imbrication, and advancement, typically are not performed in isolation, as other osseous procedures are often needed concomitantly in order to preserve the checkrein effect provided by proximal realignment procedures. As is the case with MPFL reconstruction, understanding the relevant anatomy and avoiding overtensioning of the medial structures during MPFL repair or proximal realignment procedures are crucial.

Am J Orthop. 2017;46(2):87-91. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• MPFL repair has the best results with isolated ligament avulsions in first-time dislocations. This can be demonstrated on MRI and verified at the time of arthroscopy.
• Recurrent dislocations, even if acute, have a higher failure rate with MPFL repair. In this setting, MPFL reconstruction provides more consistent outcomes.
• In cases of chronic lateral patellar dislocation, imbrication may be enough when other associated procedures have sufficiently stabilized the patella without the need for a strong soft-tissue checkrein.
• Femoral-sided repairs are more challenging due to the need to optimize the insertion point on the femur, as small changes in positioning can cause increased stress on the repaired tissue and lead to failure.
• If a repair is to have a chance to work, it must be performed at the site of the tear. Thus, preoperative planning and intraoperative inspection is important to precisely identify the site, which can involve intrasubstance and multifocal injuries as well as the femoral and patellar complex attachments.

The medial patellofemoral ligament (MPFL) is the primary soft-tissue restraint to lateral patellar translation.¹ In cases of first-time acute lateral patellar dislocation, injury to the MPFL is described as the essential lesion, occurring in almost 100% of cases.^2-4 Because of the relatively high frequency of recurrent instability after first-time acute lateral patellar dislocation,^5-7 much research has been focused on MPFL repair and reconstruction.^8-11 Although the clinical results of isolated MPFL repair are highly variable, this variability is likely secondary to relatively inconsistent clinical indications for repair, with repair described for patients with acute as well as chronic or recurrent instability.^10-13 From these early successes and failures, much has been learned about the appropriate indications for MPFL repair as well as medial retinacular “reefing” or imbrication in the chronic setting.

Relevant Anatomy

The MPFL is an extracapsular thickening of the medial retinacular structures and can be most consistently identified just distal to the vastus medialis obliquus, running within layer 2 of the medial side of the knee (using the often-referenced layer system popularized by Warren and Marshall¹⁴). The MPFL origin on the medial aspect of the femur falls within a well-defined saddle between the adductor tubercle and the medial epicondyle.¹⁵ From this relatively narrow origin, the MPFL broadens before attaching to the proximal one-third of the medial aspect of the patella.

Over the past 2 decades, the osseous anatomy surrounding the femoral origin of the MPFL has been of much interest in large part because of the increasing popularity of MPFL reconstruction. Although useful for MPFL reconstruction, the vast amount of literature and our improved understanding of this anatomical region can be extrapolated to MPFL repair. The radiographic landmarks described by Schöttle and colleagues¹⁶ have advanced our knowledge of the femoral origin of the MPFL, with fluoroscopic guidance allowing for more limited dissection and increased accuracy of repair for femoral-sided MPFL injuries.

Location of MPFL Injury

Understanding and appreciating the specific location of the MPFL injury are paramount to successful MPFL repair. Unfortunately, the location and pattern of MPFL injury cannot be consistently predicted. Although early surgical dissections described femoral-sided injuries as the most common injury site,⁴ more recent studies using magnetic resonance imaging (MRI) have described a more even distribution of MPFL injury patterns, which include patella-based ruptures, femoral-based ruptures, intrasubstance ruptures, and multifocal injuries.¹⁷ In addition, age and skeletal maturity likely play a role in the MPFL injury location, as skeletally immature patients more often have patella-based ruptures.^2,18,19 In acute MPFL repair, MRI appears to be the most accurate imaging modality for determining the patella- or femoral-based injuries most amenable to repair and for identifying clinically significant osteochondral lesions, which are not uncommon after first-time patellar dislocation.^20,21

Medial Reefing, Imbrication, and Advancement

Medial reefing, imbrication, and advancement, collectively referred to as proximal realignment procedures, describe a variety of techniques that essentially shorten or tighten the medial retinacular structures.^22-24 Although the terms cover a variety of similar surgical techniques and are often used interchangeably in the literature, imbrication, or overlapping of adjacent edges, is the single most accurate term used to define this spectrum of procedures. These procedures historically were performed in the setting of chronic or recurrent patellar instability, with the primary goal being to imbricate the attenuated medial retinaculum, which includes the MPFL. However, the procedure has had good clinical outcomes when performed in isolation for patients with normal bony anatomy.²⁵ Such anatomy is rare in chronic or recurrent dislocators, and these proximal soft-tissue procedures are often combined with other osseous realignment procedures, including distal realignment, trochleoplasty, and distal femoral osteotomy.²⁶

Discussion

MPFL Repair: Indications and Surgical Technique

Although optimal management of first-time patellar dislocation continues to be a topic for debate, the frequency of recurrent instability,^7,27 particularly in young patients, has led some to advocate early surgical management.^9,28 A clear indication for early operative intervention is the presence of a large osteochondral lesion that can undergo fixation or is causing persistent mechanical symptoms with recurrent effusion (Figures 1A, 1B).

Numerous open and arthroscopic MPFL repair techniques have been described.^10,30-33 Nevertheless, comparative studies are limited, and the greatest debate about MPFL repair continues to be appropriate indications. Arthroscopic MPFL repair can be technically demanding and can fully visualize only patella-based injuries. In addition, all-arthroscopic repair techniques may place suture material in the joint, which causes concern regarding suture irritation. As a result, the majority of MPFL repair techniques described in the literature use an open approach, which typically includes a 4-cm to 5-cm longitudinal incision along the medial aspect of the patella. Sharp dissection is carried down through the medial retinaculum to the underlying joint capsule. The plane between the medial retinaculum and the underlying joint capsule is bluntly developed posteriorly until the medial epicondyle and the adductor tubercle are palpated. For a patella-based rupture, the MPFL is defined within layer 2, and 2 suture anchors are placed within the superior third of the patella. Although there are other patellar fixation methods, suture anchors provide adequate fixation with minimal risk of iatrogenic patellar fracture. With anchors in place, horizontal mattress sutures are placed in the stump of the MPFL. For femoral-based ruptures, the same surgical exposure is used to identify the MPFL. However, depending on the size of the incision and the mobility of the tissue, a second incision can be made posterior and parallel to the first—best achieved using a spinal needle to fluoroscopically localize Schöttle’s point.¹⁶ An incision is made in line with the spinal needle, and dissection is continued down to the previously developed extracapsular plane. Under fluoroscopic guidance (Figure 3), 1 or 2 suture anchors are placed at Schöttle point, and horizontal mattress sutures are placed through the avulsed MPFL femoral origin.

MPFL Imbrication: Indications and Surgical Technique

MPFL reconstruction is the technique of choice in recurrent patellofemoral instability when no other procedures are required. When combined with distal realignment procedures, distal femoral osteotomy, open patellofemoral cartilage resurfacing procedures, or trochleoplasty, MPFL imbrication can be considered in place of MPFL reconstruction. Recurrent patellofemoral instability is influenced by various factors, including static soft-tissue restraints, dynamic muscle action, and bony anatomy, only one of which is directly addressed with MPFL imbrication. Relying on native tissues without a graft increases the risk for recurrent instability because of concern that the already attenuated native tissues will stretch out further, particularly in the presence of hyperlaxity. Although the significance of trochlear dysplasia in patellofemoral instability was first noted by Dejour and colleagues,³⁴ the presence of trochlear dysplasia has been shown to negatively influence outcomes of isolated MPFL imbrication.³⁵ Because of the relative frequency of trochlear dysplasia and axial or coronal plane malalignment in patients with chronic or recurrent patellar instability, MPFL imbrication typically is not performed on its own, and it is best used in conjunction with a distal realignment procedure or distal femoral osteotomy. MPFL reconstruction should be performed instead of MPFL imbrication in patients with severe trochlear dysplasia, in patients with hyperlaxity signs, and in young patients who participate in cutting or pivoting sports.

When distal realignment procedures are performed for axial alignment, or distal femoral osteotomy is performed for severe genu valgum, patellofemoral laxity is tested after the bony correction is completed. If the patella is still dislocatable, MPFL reconstruction provides the most predictable outcome. If laxity is increased, but the patella remains in the trochlea, typically MPFL imbrication is adequate.

Similar to MPFL repair, both open and arthroscopic techniques have been described in the literature.^36-38 As MPFL imbrication is most commonly performed in conjunction with large open procedures, this procedure can often be incorporated with other open incisions. In addition, open MPFL imbrication allows for precise control and tensioning of the medial retinacular structures, which is not always easily achieved by arthroscopic methods.

If a separate incision is required, a 4-cm to 5-cm longitudinal incision is made along the medial border of the patella, just as described for MPFL repair. The medial retinacular tissue, including the MPFL, is identified and isolated extracapsularly. Imbrication can be performed with sutures only (using a cuff of tissue along the medial border of the patella and placing pants-over-vest sutures in the adjacent tissue) or with sutures and anchors (more similar to MPFL repair described earlier). In either scenario, adequately tensioning the MPFL and associated medial retinaculum is essential in order to restore the checkrein function of the attenuated MPFL. Although typically described in the setting of MPFL reconstruction, the MPFL can easily be overtensioned during MPFL imbrication. This potential pitfall can be avoided by recognizing that forces over 2 N will overtension medial structures and thereby increase contact pressures at the medial patellar facet.³⁹ The complication can easily be prevented simply by placing the knee in 30° flexion and centering the patella in the trochlear groove while performing the MPFL imbrication.

Conclusion

Careful patient selection is the most important element for successful MPFL repair or imbrication. MPFL repair is most reliably used in patients with clear patella- or femoral-sided avulsions and in patients with a first-time patellar dislocation and a clear surgical indication, such as a large osteochondral fragment. Proximal realignment procedures, which include MPFL reefing, imbrication, and advancement, typically are not performed in isolation, as other osseous procedures are often needed concomitantly in order to preserve the checkrein effect provided by proximal realignment procedures. As is the case with MPFL reconstruction, understanding the relevant anatomy and avoiding overtensioning of the medial structures during MPFL repair or proximal realignment procedures are crucial.

Am J Orthop. 2017;46(2):87-91. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Loss of tissue homeostasis from overuse or injury produces pain.
• In patients with AKP, treatment should begin with activity modification with the envelope of function; pain-free rehabilitation; an anti-inflammatory program of cold, nonsteroidal anti-inflammatory drugs, and sometimes steroid injection.
• Physical therapy should be done without painful exercise, otherwise it could be counter-productive.
• Patellofemoral syndrome and chondromalacia are not valid clinical diagnoses. A more specific diagnosis based on careful clinical evaluation to determine anatomic origin of pain will better direct treatment.
• Even when lateral retinacular tightness is identified as the probable source of pain, surgery is seldom required.

Symptoms of patellofemoral pain (PFP) without a readily identifiable cause are perhaps the most common yet vexing clinical complaint heard by orthopedic surgeons worldwide. PFP typically occurs over the anterior knee, is often diffuse, and worsens with prolonged knee flexion and the use of stairs. Some prefer the term anterior knee pain (AKP) because we do not always know the pain is patellofemoral in anatomical origin; we know only that it is felt in the anterior knee. Pain is inherently and irreducibly a subjective phenomenon, a function of very discrete central nervous system activity within the sensory area of the contralateral cerebral cortex to the symptomatic knee. Pain is purely subjective and therefore by definition not objectively and consistently measurable between patients. Emotions play a role in pain as well, and somatization resulting in knee pain is a well-known phenomenon, particularly in adolescent women related to stress or even abuse. There is no imaging study that can be used to guide the rational treatment of pain. The best we can do is to ask patients to draw pain diagrams, which provide useful information proven to correlate with areas of tenderness.¹

Although many have referred to patients with PFP as having patellofemoral pain syndrome, we reject that term, as it implies a clearly defined syndrome—a consistent set of symptoms, signs, and test results—that does not exist. More complex AKP cases, such as those involving major trauma, complex regional pain syndrome, or multiple operative procedures, are beyond the scope of this article, though many of the principles discussed are applicable. Surprisingly, despite decades of research and clinical experience with a vast number of patients, there still is controversy regarding the underlying etiology of the symptoms and the best, safest treatment.

Primum non nocere. First, do no harm. Let us understand how to reach that noble goal.

Our Hypothesis: Loss of Homeostasis Causes Pain

Homeostasis is a natural process of maintaining relatively stable and asymptomatic physiologic conditions in all organ systems under fluctuating environmental conditions. We hypothesize that pain is the result when load applied to musculoskeletal tissues exceeds the ability to maintain homeostasis. As in other organ systems, in musculoskeletal tissues homeostasis is restored and maintained with appropriate treatment. To illustrate this hypothesis, Dr. Dye coined the term envelope of function (EOF). A combination of magnitude and frequency of load causes loss of homeostasis; with respect to the knee, activity or injury pushes it out of its acceptable EOF in which homeostasis is maintained (Figure 1).²

The therapeutic recommendations that follow from this new biocentric paradigm of joint function are quite different from those associated with hypotheses attributing AKP to chondromalacia and malalignment. This new “common sense” approach, which never encourages treatment that makes symptoms worse, recognizes healing as a complex, rate-limited biological phenomenon that can take time to achieve, especially within a harsh and unforgiving biomechanical environment such as the human patellofemoral joint.

Traditional Explanations and Treatment Strategies

In traditional teaching, 2 causes of AKP have been prominent: chondromalacia patella (CMP) (softening of the articular surface of the patella) and malalignment of the extensor mechanism. Ironically, many of the worst AKP cases are iatrogenic, resulting from surgery to “correct” CMP and/or patellofemoral malalignment or maltracking. Even exercises encouraged by ill-informed physical therapists—such as excessive squats and lunges—can easily worsen AKP symptoms. We think the clinical failure of these traditional methods reflects a profound misunderstanding of the most common cause of AKP.

Chondromalacia Patella—Not the Problem

If chondromalacia is the source of AKP, what is it about conservative treatment that “cures” or even improves structurally softened articular cartilage? How can mere activity modification and exercise result in symptom resolution secondary to improvement in cartilage structure? There is no evidence of this occurring. Nevertheless, patients with this “diagnosis” commonly respond to nonoperative treatment.

Dr. Dye has had personal experience in the possible genesis of AKP in CMP. When he was 46 years old, he allowed his asymptomatic knees to be arthroscopically inspected, without intra-articular anesthesia, so that a neurosensory map of their internal components could be drawn (Figure 2).³

Malalignment—Not Often the Problem

That brings us to the historically popular concept of patellofemoral “malalignment/maltracking” as a primary cause for AKP. Although this etiology appeals to many in the orthopedic and physical therapy community,^5,6 we and others^7-10 reject the notion that it is common. What objective malalignment changes occur when a patient becomes asymptomatic without operative treatment? Imaging measures of malalignment do not change significantly after effective treatment. In studying patients with AKP in the mid 1980’s, Dr. Dye found no difference between 104 adults with PFP and 79 age- and activity-matched controls with respect to 9 objective indicators of malalignment, including quadriceps (Q) angle, congruence angle, sulcus angle, and subchondral sclerosis of the lateral patellar facet.

The clinical success of McConnell taping, which often produces instant pain relief by using tape to apply loads to the patella and peripatellar soft tissues, is sometimes cited as evidence that maltracking or malalignment is the cause of the pain. We disagree with that conclusion. This pain relief more likely results from relieving pressure and tension on sensitive soft tissues, including synovial, fat-pad, and retinacular tissues—equivalent to, say, using a finger to pull inflamed and swollen bitten cheek tissues away from the teeth, which might repetitively traumatize them. In both cases, healing is not spontaneous; but relieving the sensitive tissue of the exacerbating load is the common principle. We think subtle changes in the tension and impingement of synovial and fat-pad tissues can have profound effects on AKP. Pain relief with McConnell taping no more proves that the source of the pain is malalignment or maltracking than a finger pulling away inflamed and swollen cheek tissues proves that cheek pain is caused by malocclusion.

Patellar Bone Overload—Part of the Problem

Patellar bone has been long assumed to be a source of AKP. To understand this better, Dr. Dye had one of his residents push a 15-gauge needle into the medial facet of his asymptomatic right patella to obtain real-time intraosseous pressure measurements as a control. This was done under local anesthesia, so no pain was felt as the needle entered the patella. However, when an arterial line was connected and flushed prior to pressure measurements, Dr. Dye experienced sharp lancinating pain. Patellar bone is richly innervated, and even mildly increased intraosseous pressure can produce severe symptoms. Dr. Dye’s patella was sore for about 7 months afterward.

Loss and restoration of osseous homeostasis occur often in AKP patients whose positive patellar bone scans (focal or diffuse) show resolution to normal (homeostasis) after symptom dissipation (Figures 9A, 9B).

The Mosaic of Anterior Knee Pain

The densely innervated synovial, fat-pad, and patellar bone tissues are nociceptive sources of AKP in the absence of homeostasis.

Clinical Applications of Homeostasis and Common Sense

Essential points to be covered in the history include overuse, injury, weight gain, systemic illness (which may produce weakness and deconditioning), prior treatment (especially physical therapy) and response to medications or injections. In the case of prior surgery, preoperative and postoperative identification of the patient’s exact symptoms can shed light on the underlying diagnosis and on any symptom changes resulting from treatment.

Sudden pain in the anterior knee can result in pain-mediated reflex quadriceps inhibition and the sensation that the knee is “giving way.” Typically, patients describe the knee collapsing into flexion and when asked if their knee is “unstable” after experiencing such episodes they will readily say yes. However, such a knee is not “unstable” in the sense that there is patholaxity that might require surgery. This is a critical distinction to avoid tragic-ally unnecessary surgery.

Careful evaluation for areas of tenderness may direct treatment to focal pathology, such as patellar or quadriceps tendinitis or tendinosis, pathologic medial parapatellar plica, or postoperative neuroma. Palpation and Tinel testing can uncover a neuroma or neuropathy of the infrapatellar branch of the saphenous nerve (Figure 11) that no other diagnostic tools can.

Treatment Options

Activity Modification

Avoid aggravating the problem. Consider this like a fire. If you are trying to put out a fire (AKP), would you throw sticks (increased activity/aggressive exercise) on it? Of course not. You would turn a hose on it (nonsteroidal anti-inflammatory drug [NSAID] regularly) or perhaps throw a bucket of water (steroid injection) on it. You would not throw gasoline (excessive exercise or activity) on it. Explaining to patients how to remain within their envelope by avoiding any activity that increases symptoms is crucial. No pain no gain is a lie from hell for patients with AKP. Don’t throw sticks on the fire.

We are frustrated that patients with PFP are still often told by well-meaning therapists to perform exercises that end up substantially increasing symptoms. Patients are admonished to push forward with “quad strengthening” by any means necessary, including painful lunges and squats, which can exacerbate synovial and fat-pad impingement and put excessive tension on muscle and tendon tissue, which is ill equipped to absorb the loads. Damaged tissues can usually return to pain-free biological homeostasis if given the opportunity and a reasonable mechanical environment.

Pain-free loading means that each of the hundreds of millions of sensory nerve endings is unperturbed, and is reporting, in effect, “I’m fine in my sector.” Minor discomfort is inevitable, but real pain during activity, and exacerbations after activity, is activity outside the EOF. Strive for patients to have “clinically quiet” knees during activity. This common sense approach is often rewarded with dramatic recovery, over time, even in patients with severe AKP. In long-standing cases, patients may take months or even years to recover, but slow and steady progress should be expected. Later, these may be among your most grateful patients.

Cold Therapy

Cold therapy relieves pain, decreases swelling, slows the metabolic rate, is simple, and has few complications. Many AKP-related tissues are superficial, and the application of cold is logical and effective. However, we should not overdo it, either. Cold applied for 20 minutes once or twice daily is sufficient in most cases, at least initially. If it does not help resolve symptoms, it may be abandoned. Likewise, if a patient does not tolerate cryotherapy, it should not be demanded. Some patients respond better to the application of warmth, which is allowed within reason.

Anti-Inflammatory Medication

Inflammation clearly plays a role in the production of pain and swelling in the soft tissues of the anterior knee (synovium, fat pad, patella and quadriceps tendons/peritenon, and retinacular tissues). Consistent use of oral NSAIDs in the absence of medical contraindications can be valuable, and there are benefits to using mild oral NSAIDs (eg, solubilized ibuprofen 400 mg 2 times daily). Prescription NSAIDs should be used short-term, if possible, to avoid complications; long-term use requires medical supervision and laboratory testing. Oral steroids can be used in similar fashion.

Intra-articular steroids (eg, triamcinolone or methylprednisolone 40 mg with a few cubic centimeters of local anesthetic) can be very helpful in quickly reducing inflammation within synovial and fat-pad tissues. In addition, an intra-articular steroid injection is diagnostic when the pain goes away, even if only for the duration of the local anesthetic; this change indicates the pain must be coming from a structure that is bathed by the intra-articular medication. Longer-term relief provides strong circumstantial evidence of causation related to intra-articular soft-tissue inflammation (loss of homeostasis) and not to chondromalacia or malalignment.

Physical Therapy

Therapy must be performed within the EOF as much as possible. Muscle soreness after a therapeutic workout is acceptable. There can easily be a lag time of 24 hours or more in the production of an activity-induced inflammatory enzyme spike. Therefore, when exercises are being done every other day, the rest days should also be kept well within the EOF. The patient must be essentially pain-free all the time, on exercise days and on rest days. Gentle stretching of tight muscles (especially quadriceps but also hips, hamstrings, and gastrocsoleus) and strengthening of hips and core are encouraged. Gentle stretching on rest days is encouraged as well.

The physical therapist must teach the principles of moderating activities of daily living (ADLs) within the EOF (eg, safe use of stairs, safely getting in and out of chairs and vehicles), for it is in these ADLs that many symptomatic patients experience recurrent overload. Total load in ADLs and in therapy must remain within the EOF to maximize the chance of return to homeostasis. Exercise-induced substantial patellofemoral soreness, effusion, or increased temperature in the knee is not acceptable.

Imaging

Advanced imaging in AKP can be a contentious subject. It is too easy to assume images hold the answers. A finding of CMP or alignment abnormality must be viewed with caution, as usually it is not an indication for patellofemoral surgery. You are treating a patient, not a picture. You must be responsible to integrate all available data (history, physical examination, imaging, response to treatment, etc) to make an accurate diagnosis. Always inspect all the imaging data yourself. Do not “push in the mental clutch” but rather do the challenging work of putting all the clinical pieces of the puzzle together to reach the right answer. Do not let the radiologist make the diagnosis!

Radiographs

It is imperative to obtain good-quality radiographs, including axial radiographs of the patella in early flexion, to check for evidence of arthrosis and other joint pathology that may be producing pain. Dr. Post always obtains bilateral knee radiographs to help understand the degree of any arthrosis or malalignment in the contralateral asymptomatic knee. The information in bilateral radiographs is also instructive for patients. Knowing that the contralateral knee shows the same radiographic changes, or even more, helps them understand that the structural factors as imaged do not dictate symptoms. More advanced or extensive imaging is not needed unless appropriate and patient therapy reaches a stalemate.

Bone Scans

In recalcitrant patients with persistent pain, a bone scan provides sensitive imaging of osseous metabolic activity and thereby clarifies the etiology of the pain. A negative scan rules out the bone as a significant cause, freeing the clinician to concentrate solely on the soft tissues. In a way that MRI can miss, a positive bone scan identifies specific regions that have lost osseous homeostasis and are being overloaded. Microscopically, these regions’ changes are very similar to the abnormal bone remodeling that occurs in early-stage stress fractures. Whether focal or diffuse, a positive bone scan means symptoms likely will take longer to reverse than is the case with a negative scan. Often, the stark findings of a positive bone scan can grab the patient’s attention and improve understanding and compliance. Focal inferior pole uptake is the most difficult pattern to reverse, perhaps because it may represent the most extreme biomechanical environment of the patellofemoral joint. In Dr. Dye’s experience, patients with this pattern may often require drilling of the inferior pole to achieve restoration of tissue homeostasis.

Magnetic Resonance Imaging

MRI can be useful, though scans are commonly read as normal. In some cases, MRI evidence of tendinopathy and other intra-articular pathology can direct both operative and nonoperative treatment of AKP. Carefully look for evidence of soft-tissue impingement—such as mild synovial swelling, low-grade effusion, and neovascularization of the fat pad—as in many cases it exists, and has been missed by the radiologist (Figures 12A, 12B).

When Surgery Is Needed: General Principles

Although the majority of patients with AKP do not need surgery, some do. Think of surgery as a tool used to create an environment in which homeostasis may be restored. Arthroscopy and meticulous débridement may be used to treat recalcitrant focal synovitis or fat-pad hypertrophy—or focal chondral pathology (eg, unstable flap of articular cartilage) that has produced mechanical symptoms with secondary inflammation. A well-localized area of patellar tendinosis may respond to either arthroscopic or open débridement. A true mechanical alignment abnormality may produce focal overload to such a degree that the most complete nonoperative programs cannot overcome the loss of homeostasis. In such a case, imaging studies that precisely document overloaded areas and associated malalignment must make sense given the clinical picture, and then must be used in developing a rational surgical plan for unloading bone and soft-tissue pathology to create a mechanical and biological environment for healing and return to homeostasis. At times, the articular damage may be so severe that patellofemoral arthroplasty is the best choice. The exact indications for these procedures are well described elsewhere.¹³

Surgery for Patients With PFP Caused by Recalcitrant Synovitis

As this type of surgery is not often covered in the literature, we offer some treatment pearls here. Arthroscopy for persistent focal synovitis should not be approached lightly; though the mechanics of removing abnormal inflamed synovial tissue may be straightforward, perioperative management and long-term postoperative management are not. The patient must be mentally prepared for the process; blood-thinning agents, fish oil, and turmeric must be discontinued; and hemostasis must be meticulous (Figures 13A-13C).

Conclusion

The history of medicine has included many misunderstandings of cause and effect. Trephination was used for headaches, leeches for fever, and, more recently, antacids for Helicobacter pylori caused duodenal ulcers. Stimulated by the enigma of AKP, we think our common sense way of thinking about tissue homeostasis in the musculoskeletal system represents an emerging orthopedic biological paradigm that is applicable to the entire body. We should let the remarkable capacity of vertebrate biology do the “heavy lifting” of healing. The traditional orthopedic emphasis on structure and alignment has a role, but we see it as complementary and secondary to the biological paradigm and find that the evidence presented herein supports our contention. The answer is seen only when one looks beyond the viewbox.

Primum non nocere. Your patients will be most grateful.

Am J Orthop. 2017;46(2):92-100. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Loss of tissue homeostasis from overuse or injury produces pain.
• In patients with AKP, treatment should begin with activity modification with the envelope of function; pain-free rehabilitation; an anti-inflammatory program of cold, nonsteroidal anti-inflammatory drugs, and sometimes steroid injection.
• Physical therapy should be done without painful exercise, otherwise it could be counter-productive.
• Patellofemoral syndrome and chondromalacia are not valid clinical diagnoses. A more specific diagnosis based on careful clinical evaluation to determine anatomic origin of pain will better direct treatment.
• Even when lateral retinacular tightness is identified as the probable source of pain, surgery is seldom required.

Symptoms of patellofemoral pain (PFP) without a readily identifiable cause are perhaps the most common yet vexing clinical complaint heard by orthopedic surgeons worldwide. PFP typically occurs over the anterior knee, is often diffuse, and worsens with prolonged knee flexion and the use of stairs. Some prefer the term anterior knee pain (AKP) because we do not always know the pain is patellofemoral in anatomical origin; we know only that it is felt in the anterior knee. Pain is inherently and irreducibly a subjective phenomenon, a function of very discrete central nervous system activity within the sensory area of the contralateral cerebral cortex to the symptomatic knee. Pain is purely subjective and therefore by definition not objectively and consistently measurable between patients. Emotions play a role in pain as well, and somatization resulting in knee pain is a well-known phenomenon, particularly in adolescent women related to stress or even abuse. There is no imaging study that can be used to guide the rational treatment of pain. The best we can do is to ask patients to draw pain diagrams, which provide useful information proven to correlate with areas of tenderness.¹

Although many have referred to patients with PFP as having patellofemoral pain syndrome, we reject that term, as it implies a clearly defined syndrome—a consistent set of symptoms, signs, and test results—that does not exist. More complex AKP cases, such as those involving major trauma, complex regional pain syndrome, or multiple operative procedures, are beyond the scope of this article, though many of the principles discussed are applicable. Surprisingly, despite decades of research and clinical experience with a vast number of patients, there still is controversy regarding the underlying etiology of the symptoms and the best, safest treatment.

Primum non nocere. First, do no harm. Let us understand how to reach that noble goal.

Our Hypothesis: Loss of Homeostasis Causes Pain

Homeostasis is a natural process of maintaining relatively stable and asymptomatic physiologic conditions in all organ systems under fluctuating environmental conditions. We hypothesize that pain is the result when load applied to musculoskeletal tissues exceeds the ability to maintain homeostasis. As in other organ systems, in musculoskeletal tissues homeostasis is restored and maintained with appropriate treatment. To illustrate this hypothesis, Dr. Dye coined the term envelope of function (EOF). A combination of magnitude and frequency of load causes loss of homeostasis; with respect to the knee, activity or injury pushes it out of its acceptable EOF in which homeostasis is maintained (Figure 1).²

The therapeutic recommendations that follow from this new biocentric paradigm of joint function are quite different from those associated with hypotheses attributing AKP to chondromalacia and malalignment. This new “common sense” approach, which never encourages treatment that makes symptoms worse, recognizes healing as a complex, rate-limited biological phenomenon that can take time to achieve, especially within a harsh and unforgiving biomechanical environment such as the human patellofemoral joint.

Traditional Explanations and Treatment Strategies

In traditional teaching, 2 causes of AKP have been prominent: chondromalacia patella (CMP) (softening of the articular surface of the patella) and malalignment of the extensor mechanism. Ironically, many of the worst AKP cases are iatrogenic, resulting from surgery to “correct” CMP and/or patellofemoral malalignment or maltracking. Even exercises encouraged by ill-informed physical therapists—such as excessive squats and lunges—can easily worsen AKP symptoms. We think the clinical failure of these traditional methods reflects a profound misunderstanding of the most common cause of AKP.

Chondromalacia Patella—Not the Problem

If chondromalacia is the source of AKP, what is it about conservative treatment that “cures” or even improves structurally softened articular cartilage? How can mere activity modification and exercise result in symptom resolution secondary to improvement in cartilage structure? There is no evidence of this occurring. Nevertheless, patients with this “diagnosis” commonly respond to nonoperative treatment.

Dr. Dye has had personal experience in the possible genesis of AKP in CMP. When he was 46 years old, he allowed his asymptomatic knees to be arthroscopically inspected, without intra-articular anesthesia, so that a neurosensory map of their internal components could be drawn (Figure 2).³

Malalignment—Not Often the Problem

That brings us to the historically popular concept of patellofemoral “malalignment/maltracking” as a primary cause for AKP. Although this etiology appeals to many in the orthopedic and physical therapy community,^5,6 we and others^7-10 reject the notion that it is common. What objective malalignment changes occur when a patient becomes asymptomatic without operative treatment? Imaging measures of malalignment do not change significantly after effective treatment. In studying patients with AKP in the mid 1980’s, Dr. Dye found no difference between 104 adults with PFP and 79 age- and activity-matched controls with respect to 9 objective indicators of malalignment, including quadriceps (Q) angle, congruence angle, sulcus angle, and subchondral sclerosis of the lateral patellar facet.

The clinical success of McConnell taping, which often produces instant pain relief by using tape to apply loads to the patella and peripatellar soft tissues, is sometimes cited as evidence that maltracking or malalignment is the cause of the pain. We disagree with that conclusion. This pain relief more likely results from relieving pressure and tension on sensitive soft tissues, including synovial, fat-pad, and retinacular tissues—equivalent to, say, using a finger to pull inflamed and swollen bitten cheek tissues away from the teeth, which might repetitively traumatize them. In both cases, healing is not spontaneous; but relieving the sensitive tissue of the exacerbating load is the common principle. We think subtle changes in the tension and impingement of synovial and fat-pad tissues can have profound effects on AKP. Pain relief with McConnell taping no more proves that the source of the pain is malalignment or maltracking than a finger pulling away inflamed and swollen cheek tissues proves that cheek pain is caused by malocclusion.

Patellar Bone Overload—Part of the Problem

Patellar bone has been long assumed to be a source of AKP. To understand this better, Dr. Dye had one of his residents push a 15-gauge needle into the medial facet of his asymptomatic right patella to obtain real-time intraosseous pressure measurements as a control. This was done under local anesthesia, so no pain was felt as the needle entered the patella. However, when an arterial line was connected and flushed prior to pressure measurements, Dr. Dye experienced sharp lancinating pain. Patellar bone is richly innervated, and even mildly increased intraosseous pressure can produce severe symptoms. Dr. Dye’s patella was sore for about 7 months afterward.

Loss and restoration of osseous homeostasis occur often in AKP patients whose positive patellar bone scans (focal or diffuse) show resolution to normal (homeostasis) after symptom dissipation (Figures 9A, 9B).

The Mosaic of Anterior Knee Pain

The densely innervated synovial, fat-pad, and patellar bone tissues are nociceptive sources of AKP in the absence of homeostasis.

Clinical Applications of Homeostasis and Common Sense

Essential points to be covered in the history include overuse, injury, weight gain, systemic illness (which may produce weakness and deconditioning), prior treatment (especially physical therapy) and response to medications or injections. In the case of prior surgery, preoperative and postoperative identification of the patient’s exact symptoms can shed light on the underlying diagnosis and on any symptom changes resulting from treatment.

Sudden pain in the anterior knee can result in pain-mediated reflex quadriceps inhibition and the sensation that the knee is “giving way.” Typically, patients describe the knee collapsing into flexion and when asked if their knee is “unstable” after experiencing such episodes they will readily say yes. However, such a knee is not “unstable” in the sense that there is patholaxity that might require surgery. This is a critical distinction to avoid tragic-ally unnecessary surgery.

Careful evaluation for areas of tenderness may direct treatment to focal pathology, such as patellar or quadriceps tendinitis or tendinosis, pathologic medial parapatellar plica, or postoperative neuroma. Palpation and Tinel testing can uncover a neuroma or neuropathy of the infrapatellar branch of the saphenous nerve (Figure 11) that no other diagnostic tools can.

Treatment Options

Activity Modification

Avoid aggravating the problem. Consider this like a fire. If you are trying to put out a fire (AKP), would you throw sticks (increased activity/aggressive exercise) on it? Of course not. You would turn a hose on it (nonsteroidal anti-inflammatory drug [NSAID] regularly) or perhaps throw a bucket of water (steroid injection) on it. You would not throw gasoline (excessive exercise or activity) on it. Explaining to patients how to remain within their envelope by avoiding any activity that increases symptoms is crucial. No pain no gain is a lie from hell for patients with AKP. Don’t throw sticks on the fire.

We are frustrated that patients with PFP are still often told by well-meaning therapists to perform exercises that end up substantially increasing symptoms. Patients are admonished to push forward with “quad strengthening” by any means necessary, including painful lunges and squats, which can exacerbate synovial and fat-pad impingement and put excessive tension on muscle and tendon tissue, which is ill equipped to absorb the loads. Damaged tissues can usually return to pain-free biological homeostasis if given the opportunity and a reasonable mechanical environment.

Pain-free loading means that each of the hundreds of millions of sensory nerve endings is unperturbed, and is reporting, in effect, “I’m fine in my sector.” Minor discomfort is inevitable, but real pain during activity, and exacerbations after activity, is activity outside the EOF. Strive for patients to have “clinically quiet” knees during activity. This common sense approach is often rewarded with dramatic recovery, over time, even in patients with severe AKP. In long-standing cases, patients may take months or even years to recover, but slow and steady progress should be expected. Later, these may be among your most grateful patients.

Cold Therapy

Cold therapy relieves pain, decreases swelling, slows the metabolic rate, is simple, and has few complications. Many AKP-related tissues are superficial, and the application of cold is logical and effective. However, we should not overdo it, either. Cold applied for 20 minutes once or twice daily is sufficient in most cases, at least initially. If it does not help resolve symptoms, it may be abandoned. Likewise, if a patient does not tolerate cryotherapy, it should not be demanded. Some patients respond better to the application of warmth, which is allowed within reason.

Anti-Inflammatory Medication

Inflammation clearly plays a role in the production of pain and swelling in the soft tissues of the anterior knee (synovium, fat pad, patella and quadriceps tendons/peritenon, and retinacular tissues). Consistent use of oral NSAIDs in the absence of medical contraindications can be valuable, and there are benefits to using mild oral NSAIDs (eg, solubilized ibuprofen 400 mg 2 times daily). Prescription NSAIDs should be used short-term, if possible, to avoid complications; long-term use requires medical supervision and laboratory testing. Oral steroids can be used in similar fashion.

Intra-articular steroids (eg, triamcinolone or methylprednisolone 40 mg with a few cubic centimeters of local anesthetic) can be very helpful in quickly reducing inflammation within synovial and fat-pad tissues. In addition, an intra-articular steroid injection is diagnostic when the pain goes away, even if only for the duration of the local anesthetic; this change indicates the pain must be coming from a structure that is bathed by the intra-articular medication. Longer-term relief provides strong circumstantial evidence of causation related to intra-articular soft-tissue inflammation (loss of homeostasis) and not to chondromalacia or malalignment.

Physical Therapy

Therapy must be performed within the EOF as much as possible. Muscle soreness after a therapeutic workout is acceptable. There can easily be a lag time of 24 hours or more in the production of an activity-induced inflammatory enzyme spike. Therefore, when exercises are being done every other day, the rest days should also be kept well within the EOF. The patient must be essentially pain-free all the time, on exercise days and on rest days. Gentle stretching of tight muscles (especially quadriceps but also hips, hamstrings, and gastrocsoleus) and strengthening of hips and core are encouraged. Gentle stretching on rest days is encouraged as well.

The physical therapist must teach the principles of moderating activities of daily living (ADLs) within the EOF (eg, safe use of stairs, safely getting in and out of chairs and vehicles), for it is in these ADLs that many symptomatic patients experience recurrent overload. Total load in ADLs and in therapy must remain within the EOF to maximize the chance of return to homeostasis. Exercise-induced substantial patellofemoral soreness, effusion, or increased temperature in the knee is not acceptable.

Imaging

Advanced imaging in AKP can be a contentious subject. It is too easy to assume images hold the answers. A finding of CMP or alignment abnormality must be viewed with caution, as usually it is not an indication for patellofemoral surgery. You are treating a patient, not a picture. You must be responsible to integrate all available data (history, physical examination, imaging, response to treatment, etc) to make an accurate diagnosis. Always inspect all the imaging data yourself. Do not “push in the mental clutch” but rather do the challenging work of putting all the clinical pieces of the puzzle together to reach the right answer. Do not let the radiologist make the diagnosis!

Radiographs

It is imperative to obtain good-quality radiographs, including axial radiographs of the patella in early flexion, to check for evidence of arthrosis and other joint pathology that may be producing pain. Dr. Post always obtains bilateral knee radiographs to help understand the degree of any arthrosis or malalignment in the contralateral asymptomatic knee. The information in bilateral radiographs is also instructive for patients. Knowing that the contralateral knee shows the same radiographic changes, or even more, helps them understand that the structural factors as imaged do not dictate symptoms. More advanced or extensive imaging is not needed unless appropriate and patient therapy reaches a stalemate.

Bone Scans

In recalcitrant patients with persistent pain, a bone scan provides sensitive imaging of osseous metabolic activity and thereby clarifies the etiology of the pain. A negative scan rules out the bone as a significant cause, freeing the clinician to concentrate solely on the soft tissues. In a way that MRI can miss, a positive bone scan identifies specific regions that have lost osseous homeostasis and are being overloaded. Microscopically, these regions’ changes are very similar to the abnormal bone remodeling that occurs in early-stage stress fractures. Whether focal or diffuse, a positive bone scan means symptoms likely will take longer to reverse than is the case with a negative scan. Often, the stark findings of a positive bone scan can grab the patient’s attention and improve understanding and compliance. Focal inferior pole uptake is the most difficult pattern to reverse, perhaps because it may represent the most extreme biomechanical environment of the patellofemoral joint. In Dr. Dye’s experience, patients with this pattern may often require drilling of the inferior pole to achieve restoration of tissue homeostasis.

Magnetic Resonance Imaging

MRI can be useful, though scans are commonly read as normal. In some cases, MRI evidence of tendinopathy and other intra-articular pathology can direct both operative and nonoperative treatment of AKP. Carefully look for evidence of soft-tissue impingement—such as mild synovial swelling, low-grade effusion, and neovascularization of the fat pad—as in many cases it exists, and has been missed by the radiologist (Figures 12A, 12B).

When Surgery Is Needed: General Principles

Although the majority of patients with AKP do not need surgery, some do. Think of surgery as a tool used to create an environment in which homeostasis may be restored. Arthroscopy and meticulous débridement may be used to treat recalcitrant focal synovitis or fat-pad hypertrophy—or focal chondral pathology (eg, unstable flap of articular cartilage) that has produced mechanical symptoms with secondary inflammation. A well-localized area of patellar tendinosis may respond to either arthroscopic or open débridement. A true mechanical alignment abnormality may produce focal overload to such a degree that the most complete nonoperative programs cannot overcome the loss of homeostasis. In such a case, imaging studies that precisely document overloaded areas and associated malalignment must make sense given the clinical picture, and then must be used in developing a rational surgical plan for unloading bone and soft-tissue pathology to create a mechanical and biological environment for healing and return to homeostasis. At times, the articular damage may be so severe that patellofemoral arthroplasty is the best choice. The exact indications for these procedures are well described elsewhere.¹³

Surgery for Patients With PFP Caused by Recalcitrant Synovitis

As this type of surgery is not often covered in the literature, we offer some treatment pearls here. Arthroscopy for persistent focal synovitis should not be approached lightly; though the mechanics of removing abnormal inflamed synovial tissue may be straightforward, perioperative management and long-term postoperative management are not. The patient must be mentally prepared for the process; blood-thinning agents, fish oil, and turmeric must be discontinued; and hemostasis must be meticulous (Figures 13A-13C).

Conclusion

The history of medicine has included many misunderstandings of cause and effect. Trephination was used for headaches, leeches for fever, and, more recently, antacids for Helicobacter pylori caused duodenal ulcers. Stimulated by the enigma of AKP, we think our common sense way of thinking about tissue homeostasis in the musculoskeletal system represents an emerging orthopedic biological paradigm that is applicable to the entire body. We should let the remarkable capacity of vertebrate biology do the “heavy lifting” of healing. The traditional orthopedic emphasis on structure and alignment has a role, but we see it as complementary and secondary to the biological paradigm and find that the evidence presented herein supports our contention. The answer is seen only when one looks beyond the viewbox.

Primum non nocere. Your patients will be most grateful.

Am J Orthop. 2017;46(2):92-100. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Loss of tissue homeostasis from overuse or injury produces pain.
• In patients with AKP, treatment should begin with activity modification with the envelope of function; pain-free rehabilitation; an anti-inflammatory program of cold, nonsteroidal anti-inflammatory drugs, and sometimes steroid injection.
• Physical therapy should be done without painful exercise, otherwise it could be counter-productive.
• Patellofemoral syndrome and chondromalacia are not valid clinical diagnoses. A more specific diagnosis based on careful clinical evaluation to determine anatomic origin of pain will better direct treatment.
• Even when lateral retinacular tightness is identified as the probable source of pain, surgery is seldom required.

Symptoms of patellofemoral pain (PFP) without a readily identifiable cause are perhaps the most common yet vexing clinical complaint heard by orthopedic surgeons worldwide. PFP typically occurs over the anterior knee, is often diffuse, and worsens with prolonged knee flexion and the use of stairs. Some prefer the term anterior knee pain (AKP) because we do not always know the pain is patellofemoral in anatomical origin; we know only that it is felt in the anterior knee. Pain is inherently and irreducibly a subjective phenomenon, a function of very discrete central nervous system activity within the sensory area of the contralateral cerebral cortex to the symptomatic knee. Pain is purely subjective and therefore by definition not objectively and consistently measurable between patients. Emotions play a role in pain as well, and somatization resulting in knee pain is a well-known phenomenon, particularly in adolescent women related to stress or even abuse. There is no imaging study that can be used to guide the rational treatment of pain. The best we can do is to ask patients to draw pain diagrams, which provide useful information proven to correlate with areas of tenderness.¹

Although many have referred to patients with PFP as having patellofemoral pain syndrome, we reject that term, as it implies a clearly defined syndrome—a consistent set of symptoms, signs, and test results—that does not exist. More complex AKP cases, such as those involving major trauma, complex regional pain syndrome, or multiple operative procedures, are beyond the scope of this article, though many of the principles discussed are applicable. Surprisingly, despite decades of research and clinical experience with a vast number of patients, there still is controversy regarding the underlying etiology of the symptoms and the best, safest treatment.

Primum non nocere. First, do no harm. Let us understand how to reach that noble goal.

Our Hypothesis: Loss of Homeostasis Causes Pain

Homeostasis is a natural process of maintaining relatively stable and asymptomatic physiologic conditions in all organ systems under fluctuating environmental conditions. We hypothesize that pain is the result when load applied to musculoskeletal tissues exceeds the ability to maintain homeostasis. As in other organ systems, in musculoskeletal tissues homeostasis is restored and maintained with appropriate treatment. To illustrate this hypothesis, Dr. Dye coined the term envelope of function (EOF). A combination of magnitude and frequency of load causes loss of homeostasis; with respect to the knee, activity or injury pushes it out of its acceptable EOF in which homeostasis is maintained (Figure 1).²

The therapeutic recommendations that follow from this new biocentric paradigm of joint function are quite different from those associated with hypotheses attributing AKP to chondromalacia and malalignment. This new “common sense” approach, which never encourages treatment that makes symptoms worse, recognizes healing as a complex, rate-limited biological phenomenon that can take time to achieve, especially within a harsh and unforgiving biomechanical environment such as the human patellofemoral joint.

Traditional Explanations and Treatment Strategies

In traditional teaching, 2 causes of AKP have been prominent: chondromalacia patella (CMP) (softening of the articular surface of the patella) and malalignment of the extensor mechanism. Ironically, many of the worst AKP cases are iatrogenic, resulting from surgery to “correct” CMP and/or patellofemoral malalignment or maltracking. Even exercises encouraged by ill-informed physical therapists—such as excessive squats and lunges—can easily worsen AKP symptoms. We think the clinical failure of these traditional methods reflects a profound misunderstanding of the most common cause of AKP.

Chondromalacia Patella—Not the Problem

If chondromalacia is the source of AKP, what is it about conservative treatment that “cures” or even improves structurally softened articular cartilage? How can mere activity modification and exercise result in symptom resolution secondary to improvement in cartilage structure? There is no evidence of this occurring. Nevertheless, patients with this “diagnosis” commonly respond to nonoperative treatment.

Dr. Dye has had personal experience in the possible genesis of AKP in CMP. When he was 46 years old, he allowed his asymptomatic knees to be arthroscopically inspected, without intra-articular anesthesia, so that a neurosensory map of their internal components could be drawn (Figure 2).³

Malalignment—Not Often the Problem

That brings us to the historically popular concept of patellofemoral “malalignment/maltracking” as a primary cause for AKP. Although this etiology appeals to many in the orthopedic and physical therapy community,^5,6 we and others^7-10 reject the notion that it is common. What objective malalignment changes occur when a patient becomes asymptomatic without operative treatment? Imaging measures of malalignment do not change significantly after effective treatment. In studying patients with AKP in the mid 1980’s, Dr. Dye found no difference between 104 adults with PFP and 79 age- and activity-matched controls with respect to 9 objective indicators of malalignment, including quadriceps (Q) angle, congruence angle, sulcus angle, and subchondral sclerosis of the lateral patellar facet.

The clinical success of McConnell taping, which often produces instant pain relief by using tape to apply loads to the patella and peripatellar soft tissues, is sometimes cited as evidence that maltracking or malalignment is the cause of the pain. We disagree with that conclusion. This pain relief more likely results from relieving pressure and tension on sensitive soft tissues, including synovial, fat-pad, and retinacular tissues—equivalent to, say, using a finger to pull inflamed and swollen bitten cheek tissues away from the teeth, which might repetitively traumatize them. In both cases, healing is not spontaneous; but relieving the sensitive tissue of the exacerbating load is the common principle. We think subtle changes in the tension and impingement of synovial and fat-pad tissues can have profound effects on AKP. Pain relief with McConnell taping no more proves that the source of the pain is malalignment or maltracking than a finger pulling away inflamed and swollen cheek tissues proves that cheek pain is caused by malocclusion.

Patellar Bone Overload—Part of the Problem

Patellar bone has been long assumed to be a source of AKP. To understand this better, Dr. Dye had one of his residents push a 15-gauge needle into the medial facet of his asymptomatic right patella to obtain real-time intraosseous pressure measurements as a control. This was done under local anesthesia, so no pain was felt as the needle entered the patella. However, when an arterial line was connected and flushed prior to pressure measurements, Dr. Dye experienced sharp lancinating pain. Patellar bone is richly innervated, and even mildly increased intraosseous pressure can produce severe symptoms. Dr. Dye’s patella was sore for about 7 months afterward.

Loss and restoration of osseous homeostasis occur often in AKP patients whose positive patellar bone scans (focal or diffuse) show resolution to normal (homeostasis) after symptom dissipation (Figures 9A, 9B).

The Mosaic of Anterior Knee Pain

The densely innervated synovial, fat-pad, and patellar bone tissues are nociceptive sources of AKP in the absence of homeostasis.

Clinical Applications of Homeostasis and Common Sense

Essential points to be covered in the history include overuse, injury, weight gain, systemic illness (which may produce weakness and deconditioning), prior treatment (especially physical therapy) and response to medications or injections. In the case of prior surgery, preoperative and postoperative identification of the patient’s exact symptoms can shed light on the underlying diagnosis and on any symptom changes resulting from treatment.

Sudden pain in the anterior knee can result in pain-mediated reflex quadriceps inhibition and the sensation that the knee is “giving way.” Typically, patients describe the knee collapsing into flexion and when asked if their knee is “unstable” after experiencing such episodes they will readily say yes. However, such a knee is not “unstable” in the sense that there is patholaxity that might require surgery. This is a critical distinction to avoid tragic-ally unnecessary surgery.

Careful evaluation for areas of tenderness may direct treatment to focal pathology, such as patellar or quadriceps tendinitis or tendinosis, pathologic medial parapatellar plica, or postoperative neuroma. Palpation and Tinel testing can uncover a neuroma or neuropathy of the infrapatellar branch of the saphenous nerve (Figure 11) that no other diagnostic tools can.

Treatment Options

Activity Modification

Avoid aggravating the problem. Consider this like a fire. If you are trying to put out a fire (AKP), would you throw sticks (increased activity/aggressive exercise) on it? Of course not. You would turn a hose on it (nonsteroidal anti-inflammatory drug [NSAID] regularly) or perhaps throw a bucket of water (steroid injection) on it. You would not throw gasoline (excessive exercise or activity) on it. Explaining to patients how to remain within their envelope by avoiding any activity that increases symptoms is crucial. No pain no gain is a lie from hell for patients with AKP. Don’t throw sticks on the fire.

We are frustrated that patients with PFP are still often told by well-meaning therapists to perform exercises that end up substantially increasing symptoms. Patients are admonished to push forward with “quad strengthening” by any means necessary, including painful lunges and squats, which can exacerbate synovial and fat-pad impingement and put excessive tension on muscle and tendon tissue, which is ill equipped to absorb the loads. Damaged tissues can usually return to pain-free biological homeostasis if given the opportunity and a reasonable mechanical environment.

Pain-free loading means that each of the hundreds of millions of sensory nerve endings is unperturbed, and is reporting, in effect, “I’m fine in my sector.” Minor discomfort is inevitable, but real pain during activity, and exacerbations after activity, is activity outside the EOF. Strive for patients to have “clinically quiet” knees during activity. This common sense approach is often rewarded with dramatic recovery, over time, even in patients with severe AKP. In long-standing cases, patients may take months or even years to recover, but slow and steady progress should be expected. Later, these may be among your most grateful patients.

Cold Therapy

Cold therapy relieves pain, decreases swelling, slows the metabolic rate, is simple, and has few complications. Many AKP-related tissues are superficial, and the application of cold is logical and effective. However, we should not overdo it, either. Cold applied for 20 minutes once or twice daily is sufficient in most cases, at least initially. If it does not help resolve symptoms, it may be abandoned. Likewise, if a patient does not tolerate cryotherapy, it should not be demanded. Some patients respond better to the application of warmth, which is allowed within reason.

Anti-Inflammatory Medication

Inflammation clearly plays a role in the production of pain and swelling in the soft tissues of the anterior knee (synovium, fat pad, patella and quadriceps tendons/peritenon, and retinacular tissues). Consistent use of oral NSAIDs in the absence of medical contraindications can be valuable, and there are benefits to using mild oral NSAIDs (eg, solubilized ibuprofen 400 mg 2 times daily). Prescription NSAIDs should be used short-term, if possible, to avoid complications; long-term use requires medical supervision and laboratory testing. Oral steroids can be used in similar fashion.

Intra-articular steroids (eg, triamcinolone or methylprednisolone 40 mg with a few cubic centimeters of local anesthetic) can be very helpful in quickly reducing inflammation within synovial and fat-pad tissues. In addition, an intra-articular steroid injection is diagnostic when the pain goes away, even if only for the duration of the local anesthetic; this change indicates the pain must be coming from a structure that is bathed by the intra-articular medication. Longer-term relief provides strong circumstantial evidence of causation related to intra-articular soft-tissue inflammation (loss of homeostasis) and not to chondromalacia or malalignment.

Physical Therapy

Therapy must be performed within the EOF as much as possible. Muscle soreness after a therapeutic workout is acceptable. There can easily be a lag time of 24 hours or more in the production of an activity-induced inflammatory enzyme spike. Therefore, when exercises are being done every other day, the rest days should also be kept well within the EOF. The patient must be essentially pain-free all the time, on exercise days and on rest days. Gentle stretching of tight muscles (especially quadriceps but also hips, hamstrings, and gastrocsoleus) and strengthening of hips and core are encouraged. Gentle stretching on rest days is encouraged as well.

The physical therapist must teach the principles of moderating activities of daily living (ADLs) within the EOF (eg, safe use of stairs, safely getting in and out of chairs and vehicles), for it is in these ADLs that many symptomatic patients experience recurrent overload. Total load in ADLs and in therapy must remain within the EOF to maximize the chance of return to homeostasis. Exercise-induced substantial patellofemoral soreness, effusion, or increased temperature in the knee is not acceptable.

Imaging

Advanced imaging in AKP can be a contentious subject. It is too easy to assume images hold the answers. A finding of CMP or alignment abnormality must be viewed with caution, as usually it is not an indication for patellofemoral surgery. You are treating a patient, not a picture. You must be responsible to integrate all available data (history, physical examination, imaging, response to treatment, etc) to make an accurate diagnosis. Always inspect all the imaging data yourself. Do not “push in the mental clutch” but rather do the challenging work of putting all the clinical pieces of the puzzle together to reach the right answer. Do not let the radiologist make the diagnosis!

Radiographs

It is imperative to obtain good-quality radiographs, including axial radiographs of the patella in early flexion, to check for evidence of arthrosis and other joint pathology that may be producing pain. Dr. Post always obtains bilateral knee radiographs to help understand the degree of any arthrosis or malalignment in the contralateral asymptomatic knee. The information in bilateral radiographs is also instructive for patients. Knowing that the contralateral knee shows the same radiographic changes, or even more, helps them understand that the structural factors as imaged do not dictate symptoms. More advanced or extensive imaging is not needed unless appropriate and patient therapy reaches a stalemate.

Bone Scans

In recalcitrant patients with persistent pain, a bone scan provides sensitive imaging of osseous metabolic activity and thereby clarifies the etiology of the pain. A negative scan rules out the bone as a significant cause, freeing the clinician to concentrate solely on the soft tissues. In a way that MRI can miss, a positive bone scan identifies specific regions that have lost osseous homeostasis and are being overloaded. Microscopically, these regions’ changes are very similar to the abnormal bone remodeling that occurs in early-stage stress fractures. Whether focal or diffuse, a positive bone scan means symptoms likely will take longer to reverse than is the case with a negative scan. Often, the stark findings of a positive bone scan can grab the patient’s attention and improve understanding and compliance. Focal inferior pole uptake is the most difficult pattern to reverse, perhaps because it may represent the most extreme biomechanical environment of the patellofemoral joint. In Dr. Dye’s experience, patients with this pattern may often require drilling of the inferior pole to achieve restoration of tissue homeostasis.

Magnetic Resonance Imaging

MRI can be useful, though scans are commonly read as normal. In some cases, MRI evidence of tendinopathy and other intra-articular pathology can direct both operative and nonoperative treatment of AKP. Carefully look for evidence of soft-tissue impingement—such as mild synovial swelling, low-grade effusion, and neovascularization of the fat pad—as in many cases it exists, and has been missed by the radiologist (Figures 12A, 12B).

When Surgery Is Needed: General Principles

Although the majority of patients with AKP do not need surgery, some do. Think of surgery as a tool used to create an environment in which homeostasis may be restored. Arthroscopy and meticulous débridement may be used to treat recalcitrant focal synovitis or fat-pad hypertrophy—or focal chondral pathology (eg, unstable flap of articular cartilage) that has produced mechanical symptoms with secondary inflammation. A well-localized area of patellar tendinosis may respond to either arthroscopic or open débridement. A true mechanical alignment abnormality may produce focal overload to such a degree that the most complete nonoperative programs cannot overcome the loss of homeostasis. In such a case, imaging studies that precisely document overloaded areas and associated malalignment must make sense given the clinical picture, and then must be used in developing a rational surgical plan for unloading bone and soft-tissue pathology to create a mechanical and biological environment for healing and return to homeostasis. At times, the articular damage may be so severe that patellofemoral arthroplasty is the best choice. The exact indications for these procedures are well described elsewhere.¹³

Surgery for Patients With PFP Caused by Recalcitrant Synovitis

As this type of surgery is not often covered in the literature, we offer some treatment pearls here. Arthroscopy for persistent focal synovitis should not be approached lightly; though the mechanics of removing abnormal inflamed synovial tissue may be straightforward, perioperative management and long-term postoperative management are not. The patient must be mentally prepared for the process; blood-thinning agents, fish oil, and turmeric must be discontinued; and hemostasis must be meticulous (Figures 13A-13C).

Conclusion

The history of medicine has included many misunderstandings of cause and effect. Trephination was used for headaches, leeches for fever, and, more recently, antacids for Helicobacter pylori caused duodenal ulcers. Stimulated by the enigma of AKP, we think our common sense way of thinking about tissue homeostasis in the musculoskeletal system represents an emerging orthopedic biological paradigm that is applicable to the entire body. We should let the remarkable capacity of vertebrate biology do the “heavy lifting” of healing. The traditional orthopedic emphasis on structure and alignment has a role, but we see it as complementary and secondary to the biological paradigm and find that the evidence presented herein supports our contention. The answer is seen only when one looks beyond the viewbox.

Primum non nocere. Your patients will be most grateful.

Am J Orthop. 2017;46(2):92-100. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Anterior knee pain is common, particularly in young females.
• For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
• In physical therapy, core stability, weight loss, and hip strengthening are essential.
• Surgery is required only in a very small subset of patients with anterior knee pain.
• Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.¹

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain² and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye³ has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.⁴ In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.⁵ Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,³ and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Anterior knee pain is common, particularly in young females.
• For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
• In physical therapy, core stability, weight loss, and hip strengthening are essential.
• Surgery is required only in a very small subset of patients with anterior knee pain.
• Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.¹

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain² and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye³ has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.⁴ In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.⁵ Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,³ and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Anterior knee pain is common, particularly in young females.
• For most patients, activity modification and rest will control the pain; continuing to engage in painful activity only prolongs symptoms.
• In physical therapy, core stability, weight loss, and hip strengthening are essential.
• Surgery is required only in a very small subset of patients with anterior knee pain.
• Traumatic and overload- related chondral defects that have resisted a reasonable amount of conservative (nonoperative) treatment may be arthroscopically assessed and treated when documented to cause persistent pain.

Anterior knee pain is common (AKP), particularly in young females. Understanding the biomechanics of a rapidly growing young female knee, whose pelvis is relatively wider than her male counterpart, helps greatly in understanding origins of AKP.¹

Compared with males of similar weight and size, females often walk and run with increased valgus at the knee and internal rotation of the hip on heel strike. The patella contacts the lateral edge of the trochlea with more focal load on the distal lateral patella for a longer time in a female than in a male of similar stature because of the increased lateral force vector. Add the rigors of athletics, excessive body weight, use of high heels, or a predisposing structural anomaly, and painful focal overload can develop—resulting in pain on stairs, inability to run, and a visit to your office. Some male patients also develop AKP, often related to patellofemoral dysplasia or activity-related overload leading to a similar pattern and need for care. Fortunately, most young patients improve when they reduce physical activity, attain stable musculoskeletal maturity, or both.

In addition to focal articular overload occurring, retinacular structures about the anterior knee can be stressed by the structural imbalance resulting from the excessive and sudden internal rotation of the hip that occurs even during normal gait and often is related to female lower extremity function. Small nerve damage in the stressed retinaculum is an important cause of peripatellar pain² and is best identified by clinical examination. Additionally, the infrapatellar fat pad may become pinched, causing synovial inflammation.

With these patients, reassurance can go a long way, and resting, taping, bracing, and anti-inflammatory medications are helpful. Dye³ has emphasized nonoperative treatmentand allowing patients to re-establish homeostatic balance of the patellofemoral joint. Establishing normal body weight plays a key role in the process, and focusing on lower extremity core stability, starting with increased strength in the hip external rotators, is important.⁴ In the majority of patients, these measures are all that is needed.

Traumatic Anterior Knee Pain

Direct trauma to the anterior knee causes an entirely different sort of pain. Knee pain may be retinacular, neuronal, synovial, bony, or articular. Nothing replaces careful, detailed clinical history taking and physical examination in determining the source of this pain. Much AKP, particularly in its early stages, is very focal. A specific injection of an anesthetic into a suspected retinacular pain location may solve the diagnostic dilemma. With many patients, paying attention to the specific degree of knee flexion in which the injury occurred helps in localizing the lesion. A flexed-knee impact injury (dashboard or fall directly onto anterior knee) is a common cause of articular damage on the mid or proximal patella and distal medial femoral condyle. Identifying this cause is particularly important in worker’s compensation cases, as the pattern is diagnostic of a direct blow to the knee and may confirm the patient’s history.

Treating painful patellofemoral lesions related to direct trauma can be difficult. Once they are identified and correlated with the physical examination and magnetic resonance imaging (MRI) findings, a treatment plan can be developed.

Examination, Testing, Imaging

Knowing how AKP started is important. Asking a patient to point to the origin of pain is essential. A pain diagram (having the patient draw a picture of the pain location) is also very helpful.⁵ Spontaneous onset suggests an underlying structural and/or functional problem rather than a traumatic event. Examination should include palpation of all structures and the retinaculum about the knee; careful appraisal of patella tracking, location of pain, and crepitus (angle of knee flexion), and evidence of possible pain referred from the back or hip; gait analysis for functional aberrations; assessment of patellar mobility; and standard radiographs, including a perfect lateral radiograph and a knee-flexion axial radiograph of no more than 30° to 45°. Computed tomography, radionuclide scintigraphy,³ and MRI can be very useful in select patients, but such imaging generally is not necessary in the management of routine AKP. However, these studies can be extremely helpful in patients with resistant pain.

Resistant Anterior Knee Pain

When nonoperative measures (rest, bracing, taping, physical therapy, activity modification) fail to relieve pain, more aggressive treatment may be warranted. The clinician must take extra time to listen to the patient, look for the precise source of the pain, and address it directly. Treatment depends on the specific source of pain. A chronically painful retinacular lesion or neuroma usually responds to release of the painful segment. After a retinacular source of pain has been identified and temporarily eliminated with injection of a local anesthetic, the pain source can be accurately resected and the patient quickly cured. When the chronically painful locus is an injured fat pad, resection provides complete relief.

For most orthopedic surgeons, the greatest dilemma is how to address a young person’s persistent pain in the setting of minimal objective evidence. In my experience with hundreds of arthroscopies, distinct distal lateral patella articular softening is common. In some cases, the degree of articular softening can be extreme, extending toward the central ridge or even across the center of the patella and involving 40% to 50% of the patella articular surface. This spongy, soft cartilage does not resist load normally, and in many cases pain is disabling. Most important is to acknowledge the problem, as many of these patients have been living with articular lesion pain for a year or more. As quality of life can be severely diminished by chronic patellofemoral pain, it behooves us to find answers and provide appropriate treatment. Although patients with this degree of articular softening and breakdown represent a small percentage of all patients with patellofemoral pain, identifying these cases is essential.

However benign-appearing, a resistant, painful patella articular lesion can be disabling. The key to treating a young person with a patella articular lesion objectively proved with imaging or arthroscopy is to inform the patient and family of the resistant nature of some lesions. In a referral patellofemoral practice, I see many patients who are disabled and depressed about the results of articular breakdown related to focal overload. Once the problem is identified, there is hope.

Prolonged rest and activity withdrawal usually help, but in some cases pain with stairs and daily activities continues. Running is usually impossible, which can be devastating for many young people.

My approach is to exhaust the nonoperative measures, which include focusing intensely on core stability training. The physical therapist must understand the importance of this treatment component; the patient must understand the importance of strengthening the hip external rotators and the vastus medialis oblique, modifying gait, avoiding pain-inducing activities, controlling weight, using proper footwear, and being patient. Applying heavy resistance to the quadriceps during rehabilitation will likely perpetuate or exacerbate the problem. The goals are to limit loading of the articular lesion and improve lower extremity function emphasizing reduction and balanced distribution of load.

Other Causes of Anterior Knee Pain

The possibility of an unusual source of pain should always be considered. Some causes (osteochondral lesion, bipartite patella, patella baja, radiographic evidence of focal overload) are apparent only on imaging. MRI may provide evidence of hypertrophic synovium, thickened fat pad, or patellar tendonitis. The physical examination is important in determining unusual sources of pain, such as those related to trauma or retinacular neuronal injury from direct impact. Pain referred from the hip or back can also cause AKP. As kinesiophobia may also play a role, it should be considered whenever an objective cause of the pain cannot be identified.

Surgery for Anterior Knee Pain

Surgery should be considered only after prolonged rest and healing have failed to resolve the pain caused by sustained direct trauma to the anterior knee. Physical therapy typically is not useful in direct trauma. If a painful traumatic articular lesion persists, then direct treatment—removing loose articular fragments and resurfacing or unloading a damaged articular surface—may be appropriate. In most cases, 6 to 12 months should be allowed before considering surgery. Meanwhile, rest, bracing, anti-inflammatory measures, reassurance, and work modification are the cornerstones of treatment.

After all conservative measures have failed in a patient with spontaneous-onset AKP related to repetitive focal overload, and disability caused by an objectively proven articular lesion related to mechanical dysfunction or dysplasia, diagnostic arthroscopy may be appropriate. Quantitation and characterization of the lesion with images and measurements are imperative in forming an optimal surgical plan. Remember that not all problems can be cured with surgery, and there is no patellofemoral problem that cannot potentially be made worse with improper surgery.

Am J Orthop. 2017;46(2):101-103. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
• Many of these revision cases will have profound glenoid bone loss.
• Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
• Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
• Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues¹ described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.^2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.^4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues⁶ and Seebauer and colleagues,⁷ often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.^8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.¹² In different form, this idea was reported by Chammaa and colleagues¹³ in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.

Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
• Many of these revision cases will have profound glenoid bone loss.
• Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
• Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
• Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues¹ described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.^2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.^4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues⁶ and Seebauer and colleagues,⁷ often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.^8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.¹² In different form, this idea was reported by Chammaa and colleagues¹³ in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.

Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• With more shoulder arthroplasties being performed on younger patients, we can expect more revisions in the future.
• Many of these revision cases will have profound glenoid bone loss.
• Bone grafting the glenoid defects in shoulder arthroplasty has been less successful especially with significant vault defects.
• Based on the CAD-CAM success in total hip and knee replacement surgery, a patient-specific glenoid vault reconstruction system has been developed by Zimmer Biomet to deal with profound glenoid bone loss and cuff insufficiency.
• Early results of this vault reconstruction system have been promising in these most difficult clinical situations.

Early results of this vault reconstruction system have been promising in these most difficult clinical situations. Complex glenoid deformities present the most difficult challenges in shoulder arthroplasty (SA). These deformities may be caused by severe degenerative or congenital deformity, posttraumatic anatomy, tumor, or, in most cases, bone loss after glenoid failure in anatomical total SA.

Walch and colleagues¹ described the pathologic glenoid lesions seen in progressive degenerative arthritis and some congenital defects. The most severe were initially characterized as Walch B2 and Walch C deformities. These lesions have been further classified to include Walch B3 posteroinferior glenoid deformities.^2,3 Each of these deformities can result in severe glenoid vault deficiency.

In some revision cases and in severe rheumatoid cases, these deformities can present as cavitary lesions with or without failure of the glenoid rim or wall resulting in significant compromise of glenoid vault lesions.^4,5 In these cases, the degree of “medialization” of the native glenohumeral joint line and the amount of peripheral bone loss can have profound effects on the amount of bone available for fixation and on the ability to allow component positioning for best surgical and biomechanical outcomes.

Other bone loss deformities, which have been described by Antuna and colleagues⁶ and Seebauer and colleagues,⁷ often accompany disease processes with severe cuff deficiency. These deformities historically have been treated with intercalary-type bone grafts in 1- or 2-stage revision of reverse SA or in salvage to hemiarthroplasty. Treatment of these pathologies with the technique described produced only fair results in short-term to midterm follow-up. The most commonly reported complications have been component loosening, bone graft failure, infection, and instability.^8-11Borrowing from hip and knee arthroplasty surgeons’ experience in using CAD/CAM (computer-aided design/computer-aided manufacturing) patient-specific implants to fill significant bony defects, Dr. D. M. Dines and Dr. Craig developed a patient-specific glenoid vault reconstruction system (VRS) in conjunction with the Comprehensive Shoulder Arthroplasty System (Zimmer Biomet). For a number of years, the Food and Drug Administration allowed this patient-specific glenoid VRS component to be made available only as a custom implant. Recently, however, full 510K clearance was granted to use the VRS in reverse SA patients with severe soft-tissue deficiency and significant glenoid bone loss.

In this article, we describe the implant and its indications, technical aspects of production, and surgical technique.

Vault Reconstruction System

Severe glenoid bone loss often requires an implant that specifically matches the patient’s anatomy. The patient-specific glenoid VRS (Figure 1) is made from a 3-dimensional reconstruction of a 2-dimensional computed tomography image.

In some cases in which the bone is sufficient to enhance fixation in the deficient glenoid vault, a custom boss may be added to the implant, as well as a custom guide matching the implant.

Glenoid Exposure

In most cases of severe glenoid bone loss, the associated soft-tissue deficiency allows for easier glenoid exposure. In this implant system, however, maximal peripheral en face exposure of the glenoid is required. In addition, it is mandatory to avoid disturbing the remaining glenoid bone surfaces, which often are thin or fragile, because the patient-specific implant is referenced to this anatomy. Bone that is not maintained changes the orientation of the patient-specific guide and ultimately the fixation of the component. Using the correct retractors and meticulously excising soft-tissue scar tissue are crucial for success.

Implant Positioning

With the glenoid surface properly exposed, the removable inserter handle and the built-in lip on the implant are used to position the patient-specific guide. Next, a central guide pin is placed through the inserter for temporary fixation and further instrumentation. If enough bone is present, a boss reamer can be used over the guide pin to prepare and increase the fixation surface.

The central 6.5-mm nonlocking compression screw is placed to provide strong initial compressive fixation in best bone.

Case Examples

A 49-year-old man underwent hemiarthroplasty for osteoarthritis. The procedure failed and, 3 years later, was revised to conventional total SA. Unfortunately, the cemented all-polyethylene glenoid loosened secondary to active Propionibacterium acnes infection, which required excisional arthroplasty with antibiotic spacer. Significant cavitary bone loss was found with anterior glenoid wall bone loss compromising the glenoid vault. Given the history of bone loss and infection, patient-specific glenoid vault reconstruction was performed after infection eradication. Within 4 years after this surgery, the patient had resumed all activities. At age 57 years, he had restricted active forward elevation and abduction to 120° but was satisfied with the outcome.

A 71-year-old man underwent reverse SA for rotator cuff-deficient osteoarthritis. After implant excision and spacer placement, he was left with severe soft-tissue deficiency and glenoid bone loss, which caused substantial disability. After treatment for infection, a work-up was performed for glenoid bone deficiency and insertion of a patient-specific glenoid VRS implant.

Discussion

Glenoid bone deformity and deficiency are among the most difficult challenges in SA—a particularly compelling fact given the increasing number of SAs being performed in younger, more active patients. SA surgeons can now expect to be performing even more revisions with concomitant bone defects, which may be severe in some cases.

In addition to these causes of extreme bone loss, recent awareness of the importance of recognizing and treating bone deficits in osteoarthritis, rheumatoid arthritis, trauma, and instability has led to the development of patient-specific guides, instrumentation, and implants. Concepts from the use of CAD/CAM acetabular implants in total hip arthroplasty for severe acetabular bony defects were applied to the use of patient-specific glenoid reconstruction implants without bone graft augmentation.¹² In different form, this idea was reported by Chammaa and colleagues¹³ in 30 cases, and clinical and durable results were very promising.

We have described use of this technique in 2 extreme cases of glenoid vault deficiency. In each case, short-term results were quite satisfactory. However, both patients were relatively young, and long-term clinical and radiographic follow-up is needed.

Many of the severe cases of glenoid bone loss require an implant that specifically matches the patient’s anatomy. The glenoid VRS implant described here may be of great benefit in these difficult reconstructions and is a valuable addition to the armamentarium of treatments for distorted glenoid anatomy. Eventually, the idea may become useful in treating other, less significant defects by re-creating more-normal biomechanics in SA without bone graft.

Am J Orthop. 2017;46(2):104-108. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Arthrex Synergy MSK Ultrasound by Clarius(http://www.synergy-ultrasound.com/)

Arthrex Synergy MSK Ultrasound by Clarius is a new wireless ultrasound scanner that can connect to any iOS or Android device through a secure WiFi Direct connection. The scanner sets up the connection to an app on the device. Ultrasound and wireless technology have been around for decades, but combinations thereof have produced poor results. The main challenge has been to create and wirelessly transmit high-quality images without latency to a display while maintaining a reasonably sized transducer. Handheld ultrasound transducers scan effectively and process the scanned information in compact form. Recent advances in image processing and proprietary imaging algorithms now allow creation of high-resolution images comparable to those produced by most midrange or high-range machines costing $30,000 to $50,000. This new unit costs about $12,000. Ultrasound use has increased over the past decade. Numerous studies have found improved accuracy, efficacy, and outcomes of injections, and reduced pain, with ultrasound-guided injections over blind injections, and cost savings over magnetic resonance imaging.^1-12

Three scanners are capable of targeting different tissue types and depths. We prefer the Synergy MSK Linear Ultrasound by Clarius, a linear transducer that can evaluate tissue to depths of 7 cm and use frequencies from 4 MHz to 13 MHz. Its battery holds a standby charge for 7 days and can be actively used for 45 minutes. The unit has a magnesium shell; with the battery removed, the unit can be completely immersed in liquid without being damaged, which allows for easy cleaning and, potentially, sterilization with a soak solution. Color Doppler (for blood-flow assessment) and proprietary advanced needle visualization technology will be available in June.

The app is simply controlled with typical smart-device gestures. Depth control requires a finger swipe, and zoom takes a pinch. Other controls, such as optimal gain and frequency settings, are automated. Images and videos can be stored on the device and uploaded either to the Clarius Cloud or to a PACS (picture archiving and communication system) device. New features will allow the device to use a Synergy arthroscopy tower (Arthrex) as its display for surgeons and anesthesiologists in the surgical suite.

This technology finally allows ultrasound to be used in the operating room without the hassles of cumbersome machines and the potential contamination by the sleeves covering the cord that connects the transducer and the base unit (Figure 1).

Stryker(http://www.stryker.com/en-us/products/Orthopaedics/MakoRobotic-ArmAssistedSurgery/index.htm)

Mako Robotic-Arm Assisted Surgery

The role of new technology in the treatment of knee arthritis is to enable accurate execution of the surgical plan for each individual’s arthritic presentation. A robotic-assisted approach allows a surgeon to perform a unicompartmental to a tricompartmental knee replacement in a consistent and reproducible manner.¹

The desire is to address the technical inaccuracies (malalignment, malrotation, and soft tissue imbalance) that lead to early revisions and patient dissatisfaction.

Preoperative planning utilizing a computed tomography- based approach enables the evaluation of the entire limb pathology, and aids the surgeon in“patient-matching” the implant position based on anatomic references 3-dimensionally.

Intraoperative tracking informs the surgeon on pre-resection alignment, and flexion-extension gaps. The surgeon can define a fixed vs correctable deformity, and then adjust the implant position prior to cutting, if required, while defining the desired implant and limb alignment.

Haptically guiding the saw allows the surgeon to perform accurate bony cuts in 3 planes while protecting the soft tissues (Figure 1).

Stryker(http://www.stryker.com/en-us/products/Orthopaedics/MakoRobotic-ArmAssistedSurgery/index.htm)

Mako Robotic-Arm Assisted Surgery

The role of new technology in the treatment of knee arthritis is to enable accurate execution of the surgical plan for each individual’s arthritic presentation. A robotic-assisted approach allows a surgeon to perform a unicompartmental to a tricompartmental knee replacement in a consistent and reproducible manner.¹

The desire is to address the technical inaccuracies (malalignment, malrotation, and soft tissue imbalance) that lead to early revisions and patient dissatisfaction.

Preoperative planning utilizing a computed tomography- based approach enables the evaluation of the entire limb pathology, and aids the surgeon in“patient-matching” the implant position based on anatomic references 3-dimensionally.

Intraoperative tracking informs the surgeon on pre-resection alignment, and flexion-extension gaps. The surgeon can define a fixed vs correctable deformity, and then adjust the implant position prior to cutting, if required, while defining the desired implant and limb alignment.

Haptically guiding the saw allows the surgeon to perform accurate bony cuts in 3 planes while protecting the soft tissues (Figure 1).

Stryker(http://www.stryker.com/en-us/products/Orthopaedics/MakoRobotic-ArmAssistedSurgery/index.htm)

Mako Robotic-Arm Assisted Surgery

The role of new technology in the treatment of knee arthritis is to enable accurate execution of the surgical plan for each individual’s arthritic presentation. A robotic-assisted approach allows a surgeon to perform a unicompartmental to a tricompartmental knee replacement in a consistent and reproducible manner.¹

The desire is to address the technical inaccuracies (malalignment, malrotation, and soft tissue imbalance) that lead to early revisions and patient dissatisfaction.

Preoperative planning utilizing a computed tomography- based approach enables the evaluation of the entire limb pathology, and aids the surgeon in“patient-matching” the implant position based on anatomic references 3-dimensionally.

Intraoperative tracking informs the surgeon on pre-resection alignment, and flexion-extension gaps. The surgeon can define a fixed vs correctable deformity, and then adjust the implant position prior to cutting, if required, while defining the desired implant and limb alignment.

Haptically guiding the saw allows the surgeon to perform accurate bony cuts in 3 planes while protecting the soft tissues (Figure 1).

Bedbugs have been unwelcome bedfellows for humans for thousands of years. An increase in pyrethroid resistance, a ban on the insecticide dichloro-diphenyl-trichloroethane (DDT), increased international travel, and increased population density in large cities have led to an exponential rise in the incidence of bedbug infestations. Physicians are often at the forefront of bedbug infestation diagnosis.

See related editorial

Once the diagnosis is suggested, symptomatic treatment of the patient and extermination of the pests are essential, though time-consuming, costly, and often problematic. Measures to eliminate infestation and to prevent spread include identification of the pest, early detection, patient education, and professional eradication.

BEDBUGS: A BRIEF HISTORY

The term bedbug refers to the obligate parasitic arthropod Cimex lectularius (the common bedbug) and, less commonly, its tropical cousin C hemipterus. Bedbugs have coexisted with humans for centuries, dating back to the ancient Egyptians 3,500 years ago.¹ Through the mid-20th century, about 30% of US households were infested with bedbugs.² The introduction of pesticides during World War II markedly decreased the incidence, but with increased international travel, pesticide resistance, and the banning of certain pesticides in the last decade, bedbugs have reemerged worldwide.³

BIOLOGY

Source: US Centers for Disease Control and Prevention.

Bedbugs are red-brown, wingless, oval-shaped insects measuring 4 to 5 mm in length (Figure 1). They are hematophagous ectoparasites that preferentially feed on human blood, although they feed on some animals as well.²

Cimex lectularius dwells in temperate climates and C hemipterus in more tropical climates, but overlap and interbreeding are common. The usual life cycle is about 6 months, but some bugs live 12 months or longer. The female bedbug lays 5 to 8 eggs per week, or approximately 500 eggs in her lifetime, and each egg hatches in 5 to 10 days.⁴

These photophobic parasites do not live on their human hosts but rather simply visit for a meal. They cohabitate in dark locations, attacking human hosts when they are inactive or sleeping for long periods of time. Common living areas include mattress seams, box springs, bed linens and clothes, wallpaper seams, electrical outlets, and furniture seams (Table 1).⁵ The female bedbug lays her eggs in these secluded crevices, ensuring their safety until hatching. The dense nests of adult bedbugs, their eggs, and accumulated fecal matter allow for easy visual identification of infestation.⁵

Bedbugs typically feed between 1:00 am and 5:00 am. Though wingless, they successfully navigate towards their human host, attracted by emitted heat and carbon dioxide.² Once attached to human skin, the bedbug bite releases enzymes and chemicals including nitrophorin and nitric oxide that facilitate bleeding; these substances are responsible for the resultant dermatitis. (Of note, bedbugs with experimentally excised salivary glands do not cause skin disease in humans.⁶) After feeding for 3 to 20 minutes, the length and weight of the arthropod can increase by 50% to 200%. A fully sated bedbug can survive for a year until its next meal.^2,7 Even if an establishment, home, room, or article of clothing infested with bedbugs has been abandoned for several months, without proper eradication the item still represents a possible nidus for recurrent disease if used, inhabited, or worn again.

EPIDEMIOLOGY

From the earliest documented cases of Cimex in ancient Egyptian tombs to the mid-1900s, the cohabitation of humans and bedbugs was seen as inevitable. With the introduction of DDT 60 years ago, the bedbug population significantly decreased.⁸ Since DDT’s prohibition, coupled with increased travel and heightened resistance to over-the-counter insecticides, the bedbug population has reemerged exponentially.^9,10

Infestations have been reported worldwide, on every continent, and in all 50 of the United States. In Australia, infestations have risen 4,500% in the last 10 to 15 years.¹¹ In the United States, infestation occurs exclusively with C lectularius and the incidence is rising. Philadelphia and New York City are among the most bedbug-infested US cities. New York City experienced a 2,000% increase in bedbug complaints between 2004 and 2009.⁸

Bedbugs can be transmitted either through active migration of colonies from one area to another adjacent living area through wall spaces or ventilation, or through passive transportation in luggage, clothing, furniture, used mattresses, bookbags, and other personal items.¹ Although infestation affects people of all socioeconomic classes and backgrounds, the likelihood increases in people who frequently travel and people who live in lower income neighborhoods with tightly packed apartments. Bedbug infestations are also common in refugee camps: 98% of the rooms in a refugee camp in Sierra Leone had bedbugs, and almost 90% of the residents had signs of bites.¹² Unlike scabies, direct person-to-person, skin-to-skin transfer is rare.

CLINICAL FINDINGS

Bedbug bites are analogous, almost identical, to other arthropod bites: bites begin as pink macules that progress to papules (Figure 2), large plaques, or wheals (hives).¹³ Bites can arise minutes or even days after the initial assault. Some papules and plaques may have a central crust or erosion suggesting a bite.

Bites are typically intensely pruritic, and occasionally, hypersensitive victims can develop bullae, necrotic plaques, or even vasculitis. New papules and plaques form as older ones heal. Some patients may have fever and malaise.¹³ About 30% of patients may not have skin disease from bedbugs, making diagnosis in those individuals impossible.

The nonspecific nature of this presentation and the subsequent difficulty in prompt diagnosis can lead to a prolonged period of morbidity for the patient, as well as increasing the window of opportunity for the bedbugs to affect other surrounding individuals.

THE DIFFERENTIAL DIAGNOSIS IS BROAD

Commonly, bedbug bites have been misdiagnosed as drug eruptions, food allergies, dermatitis herpetiformis, staphylococcal or varicella infection, and scabies, as well as other arthropod bites.¹¹ This broad differential diagnosis can often be narrowed by careful observation of the bite distribution. The clustering of bites in groups of 3, often in a linear pattern, sometimes overlying blood vessels, is known as the “breakfast, lunch, and dinner” sign (Figure 3), and this can help to guide the clinician toward the diagnosis of a bite as opposed to a diffuse urticarial response.²

If the characteristic clusters of bites are not present, distinguishing clinically between the various causes of pruritic urticarial lesions is difficult. Subtle clues that point towards bedbug bites can be that the rash appears to be most edematous in the morning and flattens throughout the day, as the bites occur typically during sleep.¹⁴ Likewise, the rash associated with bedbug bites has also been reported to last longer, to blanch less, and to be less responsive to steroid and antihistamine treatment than other urticarial rashes.¹⁴ If a skin biopsy specimen is available, histologic assessment can help to rule out similarly presenting conditions such as prodromal bullous pemphigoid, dermatitis herpetiformis, and urticarial dermatosis, even if it cannot provide a definitive answer as to the etiology.¹⁵

Bedbug bites vs other arthropod bites

Once a bite is suspected, differentiating between bedbug and other arthropod bites is the next challenge.

Once again, a detailed assessment of the location of the bites can yield valuable information. The waist, axillae, and uncovered parts of the body are the usual sites for bedbug bites.² Likewise, inflammatory papules along the eyelid (the “eyelid sign”) are highly suggestive of a bedbug bite.¹⁶

The scant involvement of covered body areas, the lack of shallow burrows in the skin, and the lack of scabetic elements on skin scrapings exclude scabies as a diagnosis.

Skin biopsy is not helpful in differentiating arthropod bites, as the histologic findings are nonspecific. The key to a definitive diagnosis in these cases is identification of the suspected bug in characteristic locations. Patients should be encouraged to carefully inspect mattresses, floorboards, and other crevices for the small ovaloid bugs or the reddish-brown specks of heme and feces they typically leave behind on bed linens.¹⁵ A positive reported sighting of the bugs can lend credence to the diagnosis, whereas capture and laboratory assessment of a specimen is ideal.

BEDBUGS AS DISEASE VECTORS

Extracutaneous manifestations of bedbug assault are rare. Anaphylaxis to proteins in Cimex saliva may occur, as well as significant blood loss, even anemia, from extensive feeding.¹⁷ Bedbug infestations can exacerbate asthma, preexisting mental illness, anxiety, and insomnia.¹⁸ Since bedbugs extract blood from hosts, they have a putative ability to act as vectors of disease. Some 45 known pathogens have been isolated from the Cimex species including hepatitis B, human immunodeficiency virus (HIV), Trypanosoma cruzi, and methicillin-resistant Staphylococcus aureus. To date, however, there is no evidence to demonstrate transmission of pathogens to humans.⁵

TREATMENT AND ERADICATION

Treatment is mainly symptomatic—systemic antihistamines and topical corticosteroids to reduce pruritus and alleviate the dermatitis.² Patients should be instructed to avoid scratching to prevent infection. Secondary bacterial infection can be treated with topical or systemic antibiotics. Rare cases of bite-induced asthma or anaphylaxis necessitate appropriate emergency treatment. Extermination of infestation is critical to therapy.

If bedbug infestation is suggested, mattresses, bedding, sleeping areas, and bed clothing should be inspected for insects, eggs, and fecal spotting. Adhesives or traps that emit heat or carbon dioxide can be used to capture the bedbugs. During widespread infestation, the arthropods release a pungent odor, which allows trained dogs to detect them with 95% to 98% accuracy.¹⁹

Eradication techniques

Once infestation is confirmed, patients should contact an exterminator who can confirm the presence of bedbugs. Typical eradication measures often require nonchemical control and chemical pesticides.

Professional exterminators have special equipment that can heat a room to 48 to 50°C (118–122°F). Heat sustained at this temperature for 90 minutes is sufficient to kill bedbugs.²⁰

The infested area should be vacuumed daily, and vacuum bags and unwanted items should be sealed in plastic before discarding. Clothing, linens, and infested fabrics should be washed and dried in heat at 60°C (140°F) or greater.

Mattresses and furniture should be sealed in a special plastic that allows treatment with heat, steaming, or pesticides. Most professional pesticides contain pyrethroids, but resistance to these products is common, necessitating the use of multiple formulations to overcome resistance.⁸

Over-the-counter pesticides, almost exclusively pyrethroids, are variably effective and potentially hazardous to consumers.⁸ Patients must be advised to follow label directions to avoid adverse effects and toxicity.

Alternative chemical eradication methods to circumvent the problem of resistance include piperonyl butoxide, S-methoprene, boric acid, silicates (diatomaceous earth dust), and sulfuryl fluoride. Recent research has also posited the use of antiparasitic agents such as ivermectin and moxidectin in cases of resistant bedbug infestation, with promising results.²¹

All extermination products and techniques have variable risks, efficacies, and costs,⁸ and repeat inspections and retreatment are often required.

Prevention strategies include visual inspection of possibly infested rooms, with particular attention to mattress seams and crevices, placing luggage on a luggage rack away from the floor and bed, and careful examination of acquired second-hand items.⁷

Educating patients is the key to success

While all of the above eradication techniques are important curative strategies, the success of any treatment is contingent on appropriate patient education about the nature of the problem.

Resolving a bedbug infestation is notoriously difficult and requires meticulous adherence to hygiene and cleansing instructions throughout the household or institution for a sustained period of time. Information from sources such as the US Environmental Protection Agency (www.epa.gov) can empower patients to perform the necessary eradication protocols, and clinicians should routinely recommended them as part of a holistic treatment strategy.

Bedbugs have been unwelcome bedfellows for humans for thousands of years. An increase in pyrethroid resistance, a ban on the insecticide dichloro-diphenyl-trichloroethane (DDT), increased international travel, and increased population density in large cities have led to an exponential rise in the incidence of bedbug infestations. Physicians are often at the forefront of bedbug infestation diagnosis.

See related editorial

Once the diagnosis is suggested, symptomatic treatment of the patient and extermination of the pests are essential, though time-consuming, costly, and often problematic. Measures to eliminate infestation and to prevent spread include identification of the pest, early detection, patient education, and professional eradication.

BEDBUGS: A BRIEF HISTORY

The term bedbug refers to the obligate parasitic arthropod Cimex lectularius (the common bedbug) and, less commonly, its tropical cousin C hemipterus. Bedbugs have coexisted with humans for centuries, dating back to the ancient Egyptians 3,500 years ago.¹ Through the mid-20th century, about 30% of US households were infested with bedbugs.² The introduction of pesticides during World War II markedly decreased the incidence, but with increased international travel, pesticide resistance, and the banning of certain pesticides in the last decade, bedbugs have reemerged worldwide.³

BIOLOGY

Source: US Centers for Disease Control and Prevention.

Bedbugs are red-brown, wingless, oval-shaped insects measuring 4 to 5 mm in length (Figure 1). They are hematophagous ectoparasites that preferentially feed on human blood, although they feed on some animals as well.²

Cimex lectularius dwells in temperate climates and C hemipterus in more tropical climates, but overlap and interbreeding are common. The usual life cycle is about 6 months, but some bugs live 12 months or longer. The female bedbug lays 5 to 8 eggs per week, or approximately 500 eggs in her lifetime, and each egg hatches in 5 to 10 days.⁴

These photophobic parasites do not live on their human hosts but rather simply visit for a meal. They cohabitate in dark locations, attacking human hosts when they are inactive or sleeping for long periods of time. Common living areas include mattress seams, box springs, bed linens and clothes, wallpaper seams, electrical outlets, and furniture seams (Table 1).⁵ The female bedbug lays her eggs in these secluded crevices, ensuring their safety until hatching. The dense nests of adult bedbugs, their eggs, and accumulated fecal matter allow for easy visual identification of infestation.⁵

Bedbugs typically feed between 1:00 am and 5:00 am. Though wingless, they successfully navigate towards their human host, attracted by emitted heat and carbon dioxide.² Once attached to human skin, the bedbug bite releases enzymes and chemicals including nitrophorin and nitric oxide that facilitate bleeding; these substances are responsible for the resultant dermatitis. (Of note, bedbugs with experimentally excised salivary glands do not cause skin disease in humans.⁶) After feeding for 3 to 20 minutes, the length and weight of the arthropod can increase by 50% to 200%. A fully sated bedbug can survive for a year until its next meal.^2,7 Even if an establishment, home, room, or article of clothing infested with bedbugs has been abandoned for several months, without proper eradication the item still represents a possible nidus for recurrent disease if used, inhabited, or worn again.

EPIDEMIOLOGY

From the earliest documented cases of Cimex in ancient Egyptian tombs to the mid-1900s, the cohabitation of humans and bedbugs was seen as inevitable. With the introduction of DDT 60 years ago, the bedbug population significantly decreased.⁸ Since DDT’s prohibition, coupled with increased travel and heightened resistance to over-the-counter insecticides, the bedbug population has reemerged exponentially.^9,10

Infestations have been reported worldwide, on every continent, and in all 50 of the United States. In Australia, infestations have risen 4,500% in the last 10 to 15 years.¹¹ In the United States, infestation occurs exclusively with C lectularius and the incidence is rising. Philadelphia and New York City are among the most bedbug-infested US cities. New York City experienced a 2,000% increase in bedbug complaints between 2004 and 2009.⁸

Bedbugs can be transmitted either through active migration of colonies from one area to another adjacent living area through wall spaces or ventilation, or through passive transportation in luggage, clothing, furniture, used mattresses, bookbags, and other personal items.¹ Although infestation affects people of all socioeconomic classes and backgrounds, the likelihood increases in people who frequently travel and people who live in lower income neighborhoods with tightly packed apartments. Bedbug infestations are also common in refugee camps: 98% of the rooms in a refugee camp in Sierra Leone had bedbugs, and almost 90% of the residents had signs of bites.¹² Unlike scabies, direct person-to-person, skin-to-skin transfer is rare.

CLINICAL FINDINGS

Bedbug bites are analogous, almost identical, to other arthropod bites: bites begin as pink macules that progress to papules (Figure 2), large plaques, or wheals (hives).¹³ Bites can arise minutes or even days after the initial assault. Some papules and plaques may have a central crust or erosion suggesting a bite.

Bites are typically intensely pruritic, and occasionally, hypersensitive victims can develop bullae, necrotic plaques, or even vasculitis. New papules and plaques form as older ones heal. Some patients may have fever and malaise.¹³ About 30% of patients may not have skin disease from bedbugs, making diagnosis in those individuals impossible.

The nonspecific nature of this presentation and the subsequent difficulty in prompt diagnosis can lead to a prolonged period of morbidity for the patient, as well as increasing the window of opportunity for the bedbugs to affect other surrounding individuals.

THE DIFFERENTIAL DIAGNOSIS IS BROAD

Commonly, bedbug bites have been misdiagnosed as drug eruptions, food allergies, dermatitis herpetiformis, staphylococcal or varicella infection, and scabies, as well as other arthropod bites.¹¹ This broad differential diagnosis can often be narrowed by careful observation of the bite distribution. The clustering of bites in groups of 3, often in a linear pattern, sometimes overlying blood vessels, is known as the “breakfast, lunch, and dinner” sign (Figure 3), and this can help to guide the clinician toward the diagnosis of a bite as opposed to a diffuse urticarial response.²

If the characteristic clusters of bites are not present, distinguishing clinically between the various causes of pruritic urticarial lesions is difficult. Subtle clues that point towards bedbug bites can be that the rash appears to be most edematous in the morning and flattens throughout the day, as the bites occur typically during sleep.¹⁴ Likewise, the rash associated with bedbug bites has also been reported to last longer, to blanch less, and to be less responsive to steroid and antihistamine treatment than other urticarial rashes.¹⁴ If a skin biopsy specimen is available, histologic assessment can help to rule out similarly presenting conditions such as prodromal bullous pemphigoid, dermatitis herpetiformis, and urticarial dermatosis, even if it cannot provide a definitive answer as to the etiology.¹⁵

Bedbug bites vs other arthropod bites

Once a bite is suspected, differentiating between bedbug and other arthropod bites is the next challenge.

Once again, a detailed assessment of the location of the bites can yield valuable information. The waist, axillae, and uncovered parts of the body are the usual sites for bedbug bites.² Likewise, inflammatory papules along the eyelid (the “eyelid sign”) are highly suggestive of a bedbug bite.¹⁶

The scant involvement of covered body areas, the lack of shallow burrows in the skin, and the lack of scabetic elements on skin scrapings exclude scabies as a diagnosis.

Skin biopsy is not helpful in differentiating arthropod bites, as the histologic findings are nonspecific. The key to a definitive diagnosis in these cases is identification of the suspected bug in characteristic locations. Patients should be encouraged to carefully inspect mattresses, floorboards, and other crevices for the small ovaloid bugs or the reddish-brown specks of heme and feces they typically leave behind on bed linens.¹⁵ A positive reported sighting of the bugs can lend credence to the diagnosis, whereas capture and laboratory assessment of a specimen is ideal.

BEDBUGS AS DISEASE VECTORS

Extracutaneous manifestations of bedbug assault are rare. Anaphylaxis to proteins in Cimex saliva may occur, as well as significant blood loss, even anemia, from extensive feeding.¹⁷ Bedbug infestations can exacerbate asthma, preexisting mental illness, anxiety, and insomnia.¹⁸ Since bedbugs extract blood from hosts, they have a putative ability to act as vectors of disease. Some 45 known pathogens have been isolated from the Cimex species including hepatitis B, human immunodeficiency virus (HIV), Trypanosoma cruzi, and methicillin-resistant Staphylococcus aureus. To date, however, there is no evidence to demonstrate transmission of pathogens to humans.⁵

TREATMENT AND ERADICATION

Treatment is mainly symptomatic—systemic antihistamines and topical corticosteroids to reduce pruritus and alleviate the dermatitis.² Patients should be instructed to avoid scratching to prevent infection. Secondary bacterial infection can be treated with topical or systemic antibiotics. Rare cases of bite-induced asthma or anaphylaxis necessitate appropriate emergency treatment. Extermination of infestation is critical to therapy.

If bedbug infestation is suggested, mattresses, bedding, sleeping areas, and bed clothing should be inspected for insects, eggs, and fecal spotting. Adhesives or traps that emit heat or carbon dioxide can be used to capture the bedbugs. During widespread infestation, the arthropods release a pungent odor, which allows trained dogs to detect them with 95% to 98% accuracy.¹⁹

Eradication techniques

Once infestation is confirmed, patients should contact an exterminator who can confirm the presence of bedbugs. Typical eradication measures often require nonchemical control and chemical pesticides.

Professional exterminators have special equipment that can heat a room to 48 to 50°C (118–122°F). Heat sustained at this temperature for 90 minutes is sufficient to kill bedbugs.²⁰

The infested area should be vacuumed daily, and vacuum bags and unwanted items should be sealed in plastic before discarding. Clothing, linens, and infested fabrics should be washed and dried in heat at 60°C (140°F) or greater.

Mattresses and furniture should be sealed in a special plastic that allows treatment with heat, steaming, or pesticides. Most professional pesticides contain pyrethroids, but resistance to these products is common, necessitating the use of multiple formulations to overcome resistance.⁸

Over-the-counter pesticides, almost exclusively pyrethroids, are variably effective and potentially hazardous to consumers.⁸ Patients must be advised to follow label directions to avoid adverse effects and toxicity.

Alternative chemical eradication methods to circumvent the problem of resistance include piperonyl butoxide, S-methoprene, boric acid, silicates (diatomaceous earth dust), and sulfuryl fluoride. Recent research has also posited the use of antiparasitic agents such as ivermectin and moxidectin in cases of resistant bedbug infestation, with promising results.²¹

All extermination products and techniques have variable risks, efficacies, and costs,⁸ and repeat inspections and retreatment are often required.

Prevention strategies include visual inspection of possibly infested rooms, with particular attention to mattress seams and crevices, placing luggage on a luggage rack away from the floor and bed, and careful examination of acquired second-hand items.⁷

Educating patients is the key to success

While all of the above eradication techniques are important curative strategies, the success of any treatment is contingent on appropriate patient education about the nature of the problem.

Resolving a bedbug infestation is notoriously difficult and requires meticulous adherence to hygiene and cleansing instructions throughout the household or institution for a sustained period of time. Information from sources such as the US Environmental Protection Agency (www.epa.gov) can empower patients to perform the necessary eradication protocols, and clinicians should routinely recommended them as part of a holistic treatment strategy.

Bedbugs have been unwelcome bedfellows for humans for thousands of years. An increase in pyrethroid resistance, a ban on the insecticide dichloro-diphenyl-trichloroethane (DDT), increased international travel, and increased population density in large cities have led to an exponential rise in the incidence of bedbug infestations. Physicians are often at the forefront of bedbug infestation diagnosis.

See related editorial

Once the diagnosis is suggested, symptomatic treatment of the patient and extermination of the pests are essential, though time-consuming, costly, and often problematic. Measures to eliminate infestation and to prevent spread include identification of the pest, early detection, patient education, and professional eradication.

BEDBUGS: A BRIEF HISTORY

The term bedbug refers to the obligate parasitic arthropod Cimex lectularius (the common bedbug) and, less commonly, its tropical cousin C hemipterus. Bedbugs have coexisted with humans for centuries, dating back to the ancient Egyptians 3,500 years ago.¹ Through the mid-20th century, about 30% of US households were infested with bedbugs.² The introduction of pesticides during World War II markedly decreased the incidence, but with increased international travel, pesticide resistance, and the banning of certain pesticides in the last decade, bedbugs have reemerged worldwide.³

BIOLOGY

Source: US Centers for Disease Control and Prevention.

Bedbugs are red-brown, wingless, oval-shaped insects measuring 4 to 5 mm in length (Figure 1). They are hematophagous ectoparasites that preferentially feed on human blood, although they feed on some animals as well.²

Cimex lectularius dwells in temperate climates and C hemipterus in more tropical climates, but overlap and interbreeding are common. The usual life cycle is about 6 months, but some bugs live 12 months or longer. The female bedbug lays 5 to 8 eggs per week, or approximately 500 eggs in her lifetime, and each egg hatches in 5 to 10 days.⁴

These photophobic parasites do not live on their human hosts but rather simply visit for a meal. They cohabitate in dark locations, attacking human hosts when they are inactive or sleeping for long periods of time. Common living areas include mattress seams, box springs, bed linens and clothes, wallpaper seams, electrical outlets, and furniture seams (Table 1).⁵ The female bedbug lays her eggs in these secluded crevices, ensuring their safety until hatching. The dense nests of adult bedbugs, their eggs, and accumulated fecal matter allow for easy visual identification of infestation.⁵

Bedbugs typically feed between 1:00 am and 5:00 am. Though wingless, they successfully navigate towards their human host, attracted by emitted heat and carbon dioxide.² Once attached to human skin, the bedbug bite releases enzymes and chemicals including nitrophorin and nitric oxide that facilitate bleeding; these substances are responsible for the resultant dermatitis. (Of note, bedbugs with experimentally excised salivary glands do not cause skin disease in humans.⁶) After feeding for 3 to 20 minutes, the length and weight of the arthropod can increase by 50% to 200%. A fully sated bedbug can survive for a year until its next meal.^2,7 Even if an establishment, home, room, or article of clothing infested with bedbugs has been abandoned for several months, without proper eradication the item still represents a possible nidus for recurrent disease if used, inhabited, or worn again.

EPIDEMIOLOGY

From the earliest documented cases of Cimex in ancient Egyptian tombs to the mid-1900s, the cohabitation of humans and bedbugs was seen as inevitable. With the introduction of DDT 60 years ago, the bedbug population significantly decreased.⁸ Since DDT’s prohibition, coupled with increased travel and heightened resistance to over-the-counter insecticides, the bedbug population has reemerged exponentially.^9,10

Infestations have been reported worldwide, on every continent, and in all 50 of the United States. In Australia, infestations have risen 4,500% in the last 10 to 15 years.¹¹ In the United States, infestation occurs exclusively with C lectularius and the incidence is rising. Philadelphia and New York City are among the most bedbug-infested US cities. New York City experienced a 2,000% increase in bedbug complaints between 2004 and 2009.⁸

Bedbugs can be transmitted either through active migration of colonies from one area to another adjacent living area through wall spaces or ventilation, or through passive transportation in luggage, clothing, furniture, used mattresses, bookbags, and other personal items.¹ Although infestation affects people of all socioeconomic classes and backgrounds, the likelihood increases in people who frequently travel and people who live in lower income neighborhoods with tightly packed apartments. Bedbug infestations are also common in refugee camps: 98% of the rooms in a refugee camp in Sierra Leone had bedbugs, and almost 90% of the residents had signs of bites.¹² Unlike scabies, direct person-to-person, skin-to-skin transfer is rare.

CLINICAL FINDINGS

Bedbug bites are analogous, almost identical, to other arthropod bites: bites begin as pink macules that progress to papules (Figure 2), large plaques, or wheals (hives).¹³ Bites can arise minutes or even days after the initial assault. Some papules and plaques may have a central crust or erosion suggesting a bite.

Bites are typically intensely pruritic, and occasionally, hypersensitive victims can develop bullae, necrotic plaques, or even vasculitis. New papules and plaques form as older ones heal. Some patients may have fever and malaise.¹³ About 30% of patients may not have skin disease from bedbugs, making diagnosis in those individuals impossible.

The nonspecific nature of this presentation and the subsequent difficulty in prompt diagnosis can lead to a prolonged period of morbidity for the patient, as well as increasing the window of opportunity for the bedbugs to affect other surrounding individuals.

THE DIFFERENTIAL DIAGNOSIS IS BROAD

Commonly, bedbug bites have been misdiagnosed as drug eruptions, food allergies, dermatitis herpetiformis, staphylococcal or varicella infection, and scabies, as well as other arthropod bites.¹¹ This broad differential diagnosis can often be narrowed by careful observation of the bite distribution. The clustering of bites in groups of 3, often in a linear pattern, sometimes overlying blood vessels, is known as the “breakfast, lunch, and dinner” sign (Figure 3), and this can help to guide the clinician toward the diagnosis of a bite as opposed to a diffuse urticarial response.²

If the characteristic clusters of bites are not present, distinguishing clinically between the various causes of pruritic urticarial lesions is difficult. Subtle clues that point towards bedbug bites can be that the rash appears to be most edematous in the morning and flattens throughout the day, as the bites occur typically during sleep.¹⁴ Likewise, the rash associated with bedbug bites has also been reported to last longer, to blanch less, and to be less responsive to steroid and antihistamine treatment than other urticarial rashes.¹⁴ If a skin biopsy specimen is available, histologic assessment can help to rule out similarly presenting conditions such as prodromal bullous pemphigoid, dermatitis herpetiformis, and urticarial dermatosis, even if it cannot provide a definitive answer as to the etiology.¹⁵

Bedbug bites vs other arthropod bites

Once a bite is suspected, differentiating between bedbug and other arthropod bites is the next challenge.

Once again, a detailed assessment of the location of the bites can yield valuable information. The waist, axillae, and uncovered parts of the body are the usual sites for bedbug bites.² Likewise, inflammatory papules along the eyelid (the “eyelid sign”) are highly suggestive of a bedbug bite.¹⁶

The scant involvement of covered body areas, the lack of shallow burrows in the skin, and the lack of scabetic elements on skin scrapings exclude scabies as a diagnosis.

Skin biopsy is not helpful in differentiating arthropod bites, as the histologic findings are nonspecific. The key to a definitive diagnosis in these cases is identification of the suspected bug in characteristic locations. Patients should be encouraged to carefully inspect mattresses, floorboards, and other crevices for the small ovaloid bugs or the reddish-brown specks of heme and feces they typically leave behind on bed linens.¹⁵ A positive reported sighting of the bugs can lend credence to the diagnosis, whereas capture and laboratory assessment of a specimen is ideal.

BEDBUGS AS DISEASE VECTORS

Extracutaneous manifestations of bedbug assault are rare. Anaphylaxis to proteins in Cimex saliva may occur, as well as significant blood loss, even anemia, from extensive feeding.¹⁷ Bedbug infestations can exacerbate asthma, preexisting mental illness, anxiety, and insomnia.¹⁸ Since bedbugs extract blood from hosts, they have a putative ability to act as vectors of disease. Some 45 known pathogens have been isolated from the Cimex species including hepatitis B, human immunodeficiency virus (HIV), Trypanosoma cruzi, and methicillin-resistant Staphylococcus aureus. To date, however, there is no evidence to demonstrate transmission of pathogens to humans.⁵

TREATMENT AND ERADICATION

Treatment is mainly symptomatic—systemic antihistamines and topical corticosteroids to reduce pruritus and alleviate the dermatitis.² Patients should be instructed to avoid scratching to prevent infection. Secondary bacterial infection can be treated with topical or systemic antibiotics. Rare cases of bite-induced asthma or anaphylaxis necessitate appropriate emergency treatment. Extermination of infestation is critical to therapy.

If bedbug infestation is suggested, mattresses, bedding, sleeping areas, and bed clothing should be inspected for insects, eggs, and fecal spotting. Adhesives or traps that emit heat or carbon dioxide can be used to capture the bedbugs. During widespread infestation, the arthropods release a pungent odor, which allows trained dogs to detect them with 95% to 98% accuracy.¹⁹

Eradication techniques

Once infestation is confirmed, patients should contact an exterminator who can confirm the presence of bedbugs. Typical eradication measures often require nonchemical control and chemical pesticides.

Professional exterminators have special equipment that can heat a room to 48 to 50°C (118–122°F). Heat sustained at this temperature for 90 minutes is sufficient to kill bedbugs.²⁰

The infested area should be vacuumed daily, and vacuum bags and unwanted items should be sealed in plastic before discarding. Clothing, linens, and infested fabrics should be washed and dried in heat at 60°C (140°F) or greater.

Mattresses and furniture should be sealed in a special plastic that allows treatment with heat, steaming, or pesticides. Most professional pesticides contain pyrethroids, but resistance to these products is common, necessitating the use of multiple formulations to overcome resistance.⁸

Over-the-counter pesticides, almost exclusively pyrethroids, are variably effective and potentially hazardous to consumers.⁸ Patients must be advised to follow label directions to avoid adverse effects and toxicity.

Alternative chemical eradication methods to circumvent the problem of resistance include piperonyl butoxide, S-methoprene, boric acid, silicates (diatomaceous earth dust), and sulfuryl fluoride. Recent research has also posited the use of antiparasitic agents such as ivermectin and moxidectin in cases of resistant bedbug infestation, with promising results.²¹

All extermination products and techniques have variable risks, efficacies, and costs,⁸ and repeat inspections and retreatment are often required.

Prevention strategies include visual inspection of possibly infested rooms, with particular attention to mattress seams and crevices, placing luggage on a luggage rack away from the floor and bed, and careful examination of acquired second-hand items.⁷

Educating patients is the key to success

While all of the above eradication techniques are important curative strategies, the success of any treatment is contingent on appropriate patient education about the nature of the problem.

Resolving a bedbug infestation is notoriously difficult and requires meticulous adherence to hygiene and cleansing instructions throughout the household or institution for a sustained period of time. Information from sources such as the US Environmental Protection Agency (www.epa.gov) can empower patients to perform the necessary eradication protocols, and clinicians should routinely recommended them as part of a holistic treatment strategy.