Orthopedics

Function and Outcomes Research for Comparative Effectiveness in Total Joint Replacement and Quality Improvement (FORCE-TJR), the most comprehensive national registry for total hip and knee joint replacement patients and their outcomes, is now certified as a Qualified Clinical Data Registry (QCDR).

In meeting QCDR requirements, FORCE-TJR has successfully collected and tracked more than 30,000 patients with total joint replacements across the US, in more than 150 provider institutions. The FORCE-TJR registry continues to expand, providing patient and disease tracking, implant performance, patient-reported outcomes, and quality monitoring of total joint replacements.

With QCDR certification, FORCE-TJR is able to complete the collection and submission of Physician Quality Reporting System (PQRS) quality measures on behalf of member hospitals and physicians, allowing FORCE-TJR members to avoid the 2016 payment adjustment of 2.0%.

“The value of being involved in a registry such as FORCE-TJR is that I can concentrate on my patient and my practice,” said Courtland Lewis, MD, Orthopedic Surgery Chief, Department of Orthopedics, at Hartford Hospital and core member of FORCE-TJR. “FORCE-TJR makes it easy to capture and report this data to QCDR and PQRS for incentive payments, internal quality monitoring, and improving the value of the care we provide to patients and insurance plans.”

As part of this certification, FORCE-TJR has developed new non-PQRS measures, which include:

• Pain and functional status assessment for hip and knee replacements

• Improvement in pain and function after hip and knee replacements

• Assessment and improvement on patients with osteoarthritis in the hip or knee

• Mental health assessment for patients who undergo hip and knee replacements

“The new QCDR designation allows FORCE-TJR to define new quality measures, including patient-reported outcomes, and to submit these data to Centers for Medicare and Medicaid Services (CMS) on behalf of our members—without any additional data collection. The data serve both their internal quality monitoring and meet the CMS mandate,” said Patricia Franklin, MD, FORCE-TJR’s registry director.

FORCE-TJR, originally a 4-year, national research project funded by the Agency for Healthcare Research and Quality (AHRQ), is the first registry for total joint replacement to identify risk-adjusted national benchmarks, including patient risk factors, and other clinical measures, to guide surgeon and patient decisions regarding timing of surgery and optimal patient selection.

FORCE-TJR is now serving as a comprehensive orthopedic registry, expanding to enroll surgeons and hospitals beyond the original Agency for Healthcare Research and Quality-funded cohort.

In addition to assisting with reporting requirements and securing quality incentive payments, the FORCE-TJR registry provides access to national TJR benchmarks, real-time patient-reported outcome scoring, comprehensive, comparative arthroplasty practice feedback and data to improve patient care, and compare performance to peer surgeons and institutions.

Function and Outcomes Research for Comparative Effectiveness in Total Joint Replacement and Quality Improvement (FORCE-TJR), the most comprehensive national registry for total hip and knee joint replacement patients and their outcomes, is now certified as a Qualified Clinical Data Registry (QCDR).

In meeting QCDR requirements, FORCE-TJR has successfully collected and tracked more than 30,000 patients with total joint replacements across the US, in more than 150 provider institutions. The FORCE-TJR registry continues to expand, providing patient and disease tracking, implant performance, patient-reported outcomes, and quality monitoring of total joint replacements.

With QCDR certification, FORCE-TJR is able to complete the collection and submission of Physician Quality Reporting System (PQRS) quality measures on behalf of member hospitals and physicians, allowing FORCE-TJR members to avoid the 2016 payment adjustment of 2.0%.

“The value of being involved in a registry such as FORCE-TJR is that I can concentrate on my patient and my practice,” said Courtland Lewis, MD, Orthopedic Surgery Chief, Department of Orthopedics, at Hartford Hospital and core member of FORCE-TJR. “FORCE-TJR makes it easy to capture and report this data to QCDR and PQRS for incentive payments, internal quality monitoring, and improving the value of the care we provide to patients and insurance plans.”

As part of this certification, FORCE-TJR has developed new non-PQRS measures, which include:

• Pain and functional status assessment for hip and knee replacements

• Improvement in pain and function after hip and knee replacements

• Assessment and improvement on patients with osteoarthritis in the hip or knee

• Mental health assessment for patients who undergo hip and knee replacements

“The new QCDR designation allows FORCE-TJR to define new quality measures, including patient-reported outcomes, and to submit these data to Centers for Medicare and Medicaid Services (CMS) on behalf of our members—without any additional data collection. The data serve both their internal quality monitoring and meet the CMS mandate,” said Patricia Franklin, MD, FORCE-TJR’s registry director.

FORCE-TJR, originally a 4-year, national research project funded by the Agency for Healthcare Research and Quality (AHRQ), is the first registry for total joint replacement to identify risk-adjusted national benchmarks, including patient risk factors, and other clinical measures, to guide surgeon and patient decisions regarding timing of surgery and optimal patient selection.

FORCE-TJR is now serving as a comprehensive orthopedic registry, expanding to enroll surgeons and hospitals beyond the original Agency for Healthcare Research and Quality-funded cohort.

In addition to assisting with reporting requirements and securing quality incentive payments, the FORCE-TJR registry provides access to national TJR benchmarks, real-time patient-reported outcome scoring, comprehensive, comparative arthroplasty practice feedback and data to improve patient care, and compare performance to peer surgeons and institutions.

Function and Outcomes Research for Comparative Effectiveness in Total Joint Replacement and Quality Improvement (FORCE-TJR), the most comprehensive national registry for total hip and knee joint replacement patients and their outcomes, is now certified as a Qualified Clinical Data Registry (QCDR).

In meeting QCDR requirements, FORCE-TJR has successfully collected and tracked more than 30,000 patients with total joint replacements across the US, in more than 150 provider institutions. The FORCE-TJR registry continues to expand, providing patient and disease tracking, implant performance, patient-reported outcomes, and quality monitoring of total joint replacements.

With QCDR certification, FORCE-TJR is able to complete the collection and submission of Physician Quality Reporting System (PQRS) quality measures on behalf of member hospitals and physicians, allowing FORCE-TJR members to avoid the 2016 payment adjustment of 2.0%.

“The value of being involved in a registry such as FORCE-TJR is that I can concentrate on my patient and my practice,” said Courtland Lewis, MD, Orthopedic Surgery Chief, Department of Orthopedics, at Hartford Hospital and core member of FORCE-TJR. “FORCE-TJR makes it easy to capture and report this data to QCDR and PQRS for incentive payments, internal quality monitoring, and improving the value of the care we provide to patients and insurance plans.”

As part of this certification, FORCE-TJR has developed new non-PQRS measures, which include:

• Pain and functional status assessment for hip and knee replacements

• Improvement in pain and function after hip and knee replacements

• Assessment and improvement on patients with osteoarthritis in the hip or knee

• Mental health assessment for patients who undergo hip and knee replacements

“The new QCDR designation allows FORCE-TJR to define new quality measures, including patient-reported outcomes, and to submit these data to Centers for Medicare and Medicaid Services (CMS) on behalf of our members—without any additional data collection. The data serve both their internal quality monitoring and meet the CMS mandate,” said Patricia Franklin, MD, FORCE-TJR’s registry director.

FORCE-TJR, originally a 4-year, national research project funded by the Agency for Healthcare Research and Quality (AHRQ), is the first registry for total joint replacement to identify risk-adjusted national benchmarks, including patient risk factors, and other clinical measures, to guide surgeon and patient decisions regarding timing of surgery and optimal patient selection.

FORCE-TJR is now serving as a comprehensive orthopedic registry, expanding to enroll surgeons and hospitals beyond the original Agency for Healthcare Research and Quality-funded cohort.

In addition to assisting with reporting requirements and securing quality incentive payments, the FORCE-TJR registry provides access to national TJR benchmarks, real-time patient-reported outcome scoring, comprehensive, comparative arthroplasty practice feedback and data to improve patient care, and compare performance to peer surgeons and institutions.

Primary rotator cuff repair is a common procedure that consistently yields favorable clinical results.¹ Revision rotator cuff repair and reconstruction yield less consistent clinical results and are associated with a significant incidence of recurrent cuff tearing.² Possible factors contributing to the loss of tissue continuity have included poor quality or frank loss of rotator cuff tissue, diminished biological potential of the rotator cuff tendon, and excessive mechanical stress on or strain of the reconstructive surgical construct.³

I conducted a pilot study involving a technique that addresses these potential factors, amalgamating several contemporary surgical methods with the addition of a novel step: an autogenous tendon graft incubated in autologous bone marrow concentrate.

Materials and Methods

Ten consecutive patients (7 men, 3 women) enrolled in this retrospective case series. Mean age at time of surgery was 58 years (range, 47-65 years). Mean follow-up was 24 months (range, 12-44 months), and no patients were lost to follow-up. Mean time between original primary repair and current reconstruction was 36 months (range, 6-120 months). Criteria for enrollment included unremitting shoulder pain, radiographs showing no significant degenerative joint disease, magnetic resonance imaging confirming a large (3-5 cm) full-thickness rotator cuff tear with retraction, and history of prior rotator cuff repair on the affected shoulder without associated biceps tenodesis. The intraoperative inclusion criterion was direct visualization of a 3- to 5-cm full-thickness rotator cuff tear with retraction of at least 3 cm. Validated Constant, American Shoulder and Elbow Surgeons (ASES), and University of California Los Angeles (UCLA) shoulder scoring systems were used to collect range-of-motion, pain, strength, daily function, and patient satisfaction data before and after surgery. Standard error was calculated. Two-sample t test was used for preoperative–postoperative comparisons. Postoperative integrity of the rotator cuff reconstruction was evaluated by an independent full-time academic musculoskeletal radiologist using dynamic diagnostic ultrasound (iU22 xMatrix Ultrasound System [Philips Healthcare] at L 9-3 MHz). Informed consent was obtained from each patient. The study was approved by institutional review board.

After induction of general anesthesia, each patient was placed in the lateral decubitus position. Bone marrow (60 mL) was aspirated through a 14-gauge needle from a dorsal iliac table, just inferior to the iliac crest (Figure 1). The patient was then placed into the beach-chair position on a surgical shoulder table. The aspirated marrow was centrifuged at 2800 and 3800 rpm for 14 to 17 minutes (Magellan Autologous Platelet Separator; Arteriocyte Medical Systems) to yield 10 mL of a concentrated (4- to 5-fold) mixture of platelet-rich plasma (PRP) and mesenchymal stem cells. Surgery was performed through a 3-cm oblique anterior mini-open incision between the anterior corner of the acromion and the coracoid process, as I previously described.⁴ The deltoid muscle was split, not detached. Acromioplasty and release of the coracoacromial ligament were performed. The rotator cuff was inspected under ×4.5 optical magnification. The cuff tissue was mobilized and débrided back to a healthy-appearing margin. The size and shape of the rotator cuff defect were then estimated. The long head of the biceps was harvested from its origin just distal to the superior glenoid labrum unto the intertubercular sulcus on the proximal humerus. The remainder of the biceps tendon was tenodesed to the surgical neck of the humerus. The biceps tendon graft was then manipulated and fashioned (by longitudinal partial-thickness incision and expansion) to fit the cuff defect (Figures 2, 3). The expanded graft was incubated in the concentrated marrow (10 mL) for 60 minutes (Figure 4). Débridement at the base of the greater tuberosity down to bleeding cancellous bone was followed by insertion of multiple bone anchors bearing several strands of No. 2 synthetic suture. These strands were then passed through the biceps tendon graft for secure fixation (Figure 5). The débrided end of the rotator cuff was then sewn to the biceps tendon graft using locking stitches under zero tissue tension with the arm in full adduction. The free end of the graft was sewn to the subscapularis tendon (Figure 6). The remaining marrow concentrate was injected both deep and superficial to the rotator cuff construct. No additional wound irrigation fluid was injected or suction drain inserted. After surgery, the patient was placed into an abduction pillow for 1 month and then engaged in passive motion for 1 month. Active-assisted motion began 3 months after surgery.

Results

Clinically, all patients improved with respect to pain, motion, strength, function, and satisfaction by virtue of the reconstructive surgery. After surgery, mean Constant score was increased, from 13 to 71 (P < .001). Mean ASES score increased from 18 to 75 (P < .001). Mean UCLA score increased from 4 to 28 (P < .001) (Table). Ultrasound showed 0% incidence of full-thickness retearing. Dynamic scanning during abduction showed maintained reduction of the humeral head within the glenoid socket; superior subluxation of the humeral head was not detected. The biceps tendon graft was continuous with the rotator cuff tendon, indicative of graft integration: tissue healing at the graft–bone and graft–tendon interfaces (Figures 7, 8). There were no intraoperative or postoperative patient-related complications.

Discussion

Primary rotator cuff surgery is beneficial.⁵ Irrespective of technique, open versus arthroscopic,⁶ single- versus double-row repair,⁷ the clinical results have been satisfactory.⁸ Nevertheless, the “tissue failure” rate of rotator cuff surgery (full-thickness discontinuity of rotator cuff) has been as high as 31% in primary repairs.⁹ In revision rotator cuff repair and reconstruction, the radiographic tissue failure rate has been even higher, particularly in the setting of chronic large tears with retraction, with tissue failure rates up to 91%.¹⁰ Although small to medium full-thickness tears and retears are well tolerated by patients with reduced activity levels,¹¹ and pain symptoms do not necessarily correlate with rotator cuff tear size,¹² large retracted full-thickness tears in active patients seldom result in optimal clinical outcomes or patient satisfaction.^13,14 In addition, although recurrent tearing does not preclude a satisfactory clinical result, maintenance of cuff tissue integrity tends to produce a better objective clinical score and a more desirable clinical outcome.²

Few evidence-based restorative solutions exist for large recurrent rotator cuff tears with retraction in active non­geriatric patients.¹⁵ The no-treatment option in this context may result in gradual enlargement of the tear, chronic pain, weakness, and progressive degeneration of the glenohumeral joint and acromiohumeral confluence—so-called rotator cuff arthropathy, for which reverse total shoulder arthroplasty is required.^16,17 Partial repair of a large rotator cuff tear by margin convergence, interval slide, split deltoid flap, or nonanatomical reinsertion may improve clinical outcome scores but may not alter or prevent the progressive degenerative changes associated with rotator cuff arthropathy.^18,19 Synthetic scaffolds with and without biological enhancement have been used with varying degrees of success, particularly pain improvement and tissue integration.²⁰ Nevertheless, the failure rate has been reported to be 17% to 51%,²¹ and no evidence exists that allograft augmentation improves functional outcomes.²² Tendon transfer using the latissimus dorsi has also proved to be a surgical alternative in younger, active patients.²³ However, dissection in this procedure is a major undertaking for both surgeon and patient—compared with the minimally invasive technique used in the present study.²⁴

I selected a cohort of active, symptomatic patients for application of a synthesis of accepted surgical techniques through a mini-open incision in order to improve the reliability of the surgical construct while minimizing surgical morbidity. Débridement of marginal tissue, safe mobilization of remaining cuff, and tension-free suture line using locking sutures maximized the mechanical strength of the construct.^25,26 Biological enhancement with autogenous tissue (the patient’s own biceps tendon) as graft material (scaffolding), as well as autologous concentrated marrow delivering viable responding cells and chemokine/cytokine biofactors, increased the probability of reparative activity at the graft site.²⁷ The net effect was consistent tissue healing at a biologically challenging locus. Nonenhanced biceps tendon grafting in the setting of “irreparable” primary rotator cuff repair has had a 40-year history of orthopedic utility and an excellent record of clinical success.²⁸ Nevertheless, the retear rate has been 7% to 30%.²⁹ There are no previous reports of biologically enhanced autogenous biceps tendon grafting for reconstruction of a torn rotator cuff, either primary or in the setting of chronic revision surgery.

Previous well-designed PRP enhancement studies in the context of primary rotator cuff repair failed to demonstrate a consistent benefit with concentrated platelet-only augmentation.^30,31 The shared experimental design of these published studies used intra-articular injection as the sole delivery method without guarantee that the injected platelets would migrate, adhere to, and persist at the intended destination, the healing edge of the rotator cuff. In the present study, extended exposure of the splayed tendon graft by incubation in concentrated marrow was specifically designed to increase the probability that biologically active components would settle at the desired location by cellular seeding and plasmatic imbibition.³² Furthermore, use of PRP for growth factor (platelet-derived, PDGF; basic fibroblast, bFGF; transforming, TGF-β; epidermal, EGF; vascular endothelial, VEGF; connective tissue, CTGF) therapy, in addition to pluripotential mesenchymal cells for marrow-derived stem cell therapy, is in theory biologically superior to use of PRP alone.^33,34

The recent expansion of information about biologics has generated much interest in augmentation of soft-tissue healing. Unfortunately, the optimal technique of using cellular processing to upregulate stem-cell capacity at the graft interface is yet to be defined.³⁵ Clinical studies using PRP and related products to promote tendon healing have been both inconsistent and contradictory with respect to benefit of outcome. As we have been unable to harness the biological potential of this medium, application of biologics in contemporary clinical orthopedics remains narrow, random, and infrequent. The technique presented in this clinical series appears to be a small advancement in a positive direction. The described construct provides a starting point for study, combining mechanical as well as biological steps to promote rotator cuff healing. The consistency of the outcome in a clinical model in which retearing is an expectation rather than an exception is noteworthy. The zero tissue failure rate at 1 to 4 years, compared with the literature values in similar patient cohorts, is very promising.³⁶ The clinical outcome as measured by validated shoulder scores is also comparable to literature outcome values.¹⁹ Also noteworthy is the dynamic stability the construct gives to the glenohumeral joint. Ideally, the reconstructed rotator cuff provides active force coupling with the deltoid, simulating normal shoulder biomechanics. At a minimum, the reconstructed cuff provides a viable passive barrier to superior migration of the humeral head—thus supporting the mechanical efficiency of the deltoid and preventing rotator cuff arthropathy.

This study’s small sample (10 patients) puts its conclusions at risk for type I statistical error, in that too few patients were examined over a long enough period to demonstrate failure. Nevertheless, retears typically occur within 6 months of repair.^37,38 Therefore, minimum follow-up of 1 year was deemed sufficient. None of the 10 patients had diabetes or another chronic comorbidity. Nine of the 10 had either no or only mild preoperative fatty atrophy of the rotator cuff muscles. Eight of the 10 were nonsmokers. These factors, which suggest optimal surgical candidates, may prove to be significant as the clinical series expands over time. Incubation of the autogenous biceps graft in concentrated marrow for 60 minutes was arbitrarily chosen. In future in vitro examination, marrow cell viability as a function of incubation time will be assessed.

Conclusion

In active, middle-aged patients with chronic recurrent large retracted rotator cuff tears, the technique presented here, using autogenous biceps tendon and autologous concentrated marrow containing PRP and mesenchymal cells, consistently yielded satisfactory clinical results and promoted rotator cuff tissue healing without full-thickness retearing.

Primary rotator cuff repair is a common procedure that consistently yields favorable clinical results.¹ Revision rotator cuff repair and reconstruction yield less consistent clinical results and are associated with a significant incidence of recurrent cuff tearing.² Possible factors contributing to the loss of tissue continuity have included poor quality or frank loss of rotator cuff tissue, diminished biological potential of the rotator cuff tendon, and excessive mechanical stress on or strain of the reconstructive surgical construct.³

I conducted a pilot study involving a technique that addresses these potential factors, amalgamating several contemporary surgical methods with the addition of a novel step: an autogenous tendon graft incubated in autologous bone marrow concentrate.

Materials and Methods

Ten consecutive patients (7 men, 3 women) enrolled in this retrospective case series. Mean age at time of surgery was 58 years (range, 47-65 years). Mean follow-up was 24 months (range, 12-44 months), and no patients were lost to follow-up. Mean time between original primary repair and current reconstruction was 36 months (range, 6-120 months). Criteria for enrollment included unremitting shoulder pain, radiographs showing no significant degenerative joint disease, magnetic resonance imaging confirming a large (3-5 cm) full-thickness rotator cuff tear with retraction, and history of prior rotator cuff repair on the affected shoulder without associated biceps tenodesis. The intraoperative inclusion criterion was direct visualization of a 3- to 5-cm full-thickness rotator cuff tear with retraction of at least 3 cm. Validated Constant, American Shoulder and Elbow Surgeons (ASES), and University of California Los Angeles (UCLA) shoulder scoring systems were used to collect range-of-motion, pain, strength, daily function, and patient satisfaction data before and after surgery. Standard error was calculated. Two-sample t test was used for preoperative–postoperative comparisons. Postoperative integrity of the rotator cuff reconstruction was evaluated by an independent full-time academic musculoskeletal radiologist using dynamic diagnostic ultrasound (iU22 xMatrix Ultrasound System [Philips Healthcare] at L 9-3 MHz). Informed consent was obtained from each patient. The study was approved by institutional review board.

After induction of general anesthesia, each patient was placed in the lateral decubitus position. Bone marrow (60 mL) was aspirated through a 14-gauge needle from a dorsal iliac table, just inferior to the iliac crest (Figure 1). The patient was then placed into the beach-chair position on a surgical shoulder table. The aspirated marrow was centrifuged at 2800 and 3800 rpm for 14 to 17 minutes (Magellan Autologous Platelet Separator; Arteriocyte Medical Systems) to yield 10 mL of a concentrated (4- to 5-fold) mixture of platelet-rich plasma (PRP) and mesenchymal stem cells. Surgery was performed through a 3-cm oblique anterior mini-open incision between the anterior corner of the acromion and the coracoid process, as I previously described.⁴ The deltoid muscle was split, not detached. Acromioplasty and release of the coracoacromial ligament were performed. The rotator cuff was inspected under ×4.5 optical magnification. The cuff tissue was mobilized and débrided back to a healthy-appearing margin. The size and shape of the rotator cuff defect were then estimated. The long head of the biceps was harvested from its origin just distal to the superior glenoid labrum unto the intertubercular sulcus on the proximal humerus. The remainder of the biceps tendon was tenodesed to the surgical neck of the humerus. The biceps tendon graft was then manipulated and fashioned (by longitudinal partial-thickness incision and expansion) to fit the cuff defect (Figures 2, 3). The expanded graft was incubated in the concentrated marrow (10 mL) for 60 minutes (Figure 4). Débridement at the base of the greater tuberosity down to bleeding cancellous bone was followed by insertion of multiple bone anchors bearing several strands of No. 2 synthetic suture. These strands were then passed through the biceps tendon graft for secure fixation (Figure 5). The débrided end of the rotator cuff was then sewn to the biceps tendon graft using locking stitches under zero tissue tension with the arm in full adduction. The free end of the graft was sewn to the subscapularis tendon (Figure 6). The remaining marrow concentrate was injected both deep and superficial to the rotator cuff construct. No additional wound irrigation fluid was injected or suction drain inserted. After surgery, the patient was placed into an abduction pillow for 1 month and then engaged in passive motion for 1 month. Active-assisted motion began 3 months after surgery.

Results

Clinically, all patients improved with respect to pain, motion, strength, function, and satisfaction by virtue of the reconstructive surgery. After surgery, mean Constant score was increased, from 13 to 71 (P < .001). Mean ASES score increased from 18 to 75 (P < .001). Mean UCLA score increased from 4 to 28 (P < .001) (Table). Ultrasound showed 0% incidence of full-thickness retearing. Dynamic scanning during abduction showed maintained reduction of the humeral head within the glenoid socket; superior subluxation of the humeral head was not detected. The biceps tendon graft was continuous with the rotator cuff tendon, indicative of graft integration: tissue healing at the graft–bone and graft–tendon interfaces (Figures 7, 8). There were no intraoperative or postoperative patient-related complications.

Discussion

Primary rotator cuff surgery is beneficial.⁵ Irrespective of technique, open versus arthroscopic,⁶ single- versus double-row repair,⁷ the clinical results have been satisfactory.⁸ Nevertheless, the “tissue failure” rate of rotator cuff surgery (full-thickness discontinuity of rotator cuff) has been as high as 31% in primary repairs.⁹ In revision rotator cuff repair and reconstruction, the radiographic tissue failure rate has been even higher, particularly in the setting of chronic large tears with retraction, with tissue failure rates up to 91%.¹⁰ Although small to medium full-thickness tears and retears are well tolerated by patients with reduced activity levels,¹¹ and pain symptoms do not necessarily correlate with rotator cuff tear size,¹² large retracted full-thickness tears in active patients seldom result in optimal clinical outcomes or patient satisfaction.^13,14 In addition, although recurrent tearing does not preclude a satisfactory clinical result, maintenance of cuff tissue integrity tends to produce a better objective clinical score and a more desirable clinical outcome.²

Few evidence-based restorative solutions exist for large recurrent rotator cuff tears with retraction in active non­geriatric patients.¹⁵ The no-treatment option in this context may result in gradual enlargement of the tear, chronic pain, weakness, and progressive degeneration of the glenohumeral joint and acromiohumeral confluence—so-called rotator cuff arthropathy, for which reverse total shoulder arthroplasty is required.^16,17 Partial repair of a large rotator cuff tear by margin convergence, interval slide, split deltoid flap, or nonanatomical reinsertion may improve clinical outcome scores but may not alter or prevent the progressive degenerative changes associated with rotator cuff arthropathy.^18,19 Synthetic scaffolds with and without biological enhancement have been used with varying degrees of success, particularly pain improvement and tissue integration.²⁰ Nevertheless, the failure rate has been reported to be 17% to 51%,²¹ and no evidence exists that allograft augmentation improves functional outcomes.²² Tendon transfer using the latissimus dorsi has also proved to be a surgical alternative in younger, active patients.²³ However, dissection in this procedure is a major undertaking for both surgeon and patient—compared with the minimally invasive technique used in the present study.²⁴

I selected a cohort of active, symptomatic patients for application of a synthesis of accepted surgical techniques through a mini-open incision in order to improve the reliability of the surgical construct while minimizing surgical morbidity. Débridement of marginal tissue, safe mobilization of remaining cuff, and tension-free suture line using locking sutures maximized the mechanical strength of the construct.^25,26 Biological enhancement with autogenous tissue (the patient’s own biceps tendon) as graft material (scaffolding), as well as autologous concentrated marrow delivering viable responding cells and chemokine/cytokine biofactors, increased the probability of reparative activity at the graft site.²⁷ The net effect was consistent tissue healing at a biologically challenging locus. Nonenhanced biceps tendon grafting in the setting of “irreparable” primary rotator cuff repair has had a 40-year history of orthopedic utility and an excellent record of clinical success.²⁸ Nevertheless, the retear rate has been 7% to 30%.²⁹ There are no previous reports of biologically enhanced autogenous biceps tendon grafting for reconstruction of a torn rotator cuff, either primary or in the setting of chronic revision surgery.

Previous well-designed PRP enhancement studies in the context of primary rotator cuff repair failed to demonstrate a consistent benefit with concentrated platelet-only augmentation.^30,31 The shared experimental design of these published studies used intra-articular injection as the sole delivery method without guarantee that the injected platelets would migrate, adhere to, and persist at the intended destination, the healing edge of the rotator cuff. In the present study, extended exposure of the splayed tendon graft by incubation in concentrated marrow was specifically designed to increase the probability that biologically active components would settle at the desired location by cellular seeding and plasmatic imbibition.³² Furthermore, use of PRP for growth factor (platelet-derived, PDGF; basic fibroblast, bFGF; transforming, TGF-β; epidermal, EGF; vascular endothelial, VEGF; connective tissue, CTGF) therapy, in addition to pluripotential mesenchymal cells for marrow-derived stem cell therapy, is in theory biologically superior to use of PRP alone.^33,34

The recent expansion of information about biologics has generated much interest in augmentation of soft-tissue healing. Unfortunately, the optimal technique of using cellular processing to upregulate stem-cell capacity at the graft interface is yet to be defined.³⁵ Clinical studies using PRP and related products to promote tendon healing have been both inconsistent and contradictory with respect to benefit of outcome. As we have been unable to harness the biological potential of this medium, application of biologics in contemporary clinical orthopedics remains narrow, random, and infrequent. The technique presented in this clinical series appears to be a small advancement in a positive direction. The described construct provides a starting point for study, combining mechanical as well as biological steps to promote rotator cuff healing. The consistency of the outcome in a clinical model in which retearing is an expectation rather than an exception is noteworthy. The zero tissue failure rate at 1 to 4 years, compared with the literature values in similar patient cohorts, is very promising.³⁶ The clinical outcome as measured by validated shoulder scores is also comparable to literature outcome values.¹⁹ Also noteworthy is the dynamic stability the construct gives to the glenohumeral joint. Ideally, the reconstructed rotator cuff provides active force coupling with the deltoid, simulating normal shoulder biomechanics. At a minimum, the reconstructed cuff provides a viable passive barrier to superior migration of the humeral head—thus supporting the mechanical efficiency of the deltoid and preventing rotator cuff arthropathy.

This study’s small sample (10 patients) puts its conclusions at risk for type I statistical error, in that too few patients were examined over a long enough period to demonstrate failure. Nevertheless, retears typically occur within 6 months of repair.^37,38 Therefore, minimum follow-up of 1 year was deemed sufficient. None of the 10 patients had diabetes or another chronic comorbidity. Nine of the 10 had either no or only mild preoperative fatty atrophy of the rotator cuff muscles. Eight of the 10 were nonsmokers. These factors, which suggest optimal surgical candidates, may prove to be significant as the clinical series expands over time. Incubation of the autogenous biceps graft in concentrated marrow for 60 minutes was arbitrarily chosen. In future in vitro examination, marrow cell viability as a function of incubation time will be assessed.

Conclusion

In active, middle-aged patients with chronic recurrent large retracted rotator cuff tears, the technique presented here, using autogenous biceps tendon and autologous concentrated marrow containing PRP and mesenchymal cells, consistently yielded satisfactory clinical results and promoted rotator cuff tissue healing without full-thickness retearing.

Primary rotator cuff repair is a common procedure that consistently yields favorable clinical results.¹ Revision rotator cuff repair and reconstruction yield less consistent clinical results and are associated with a significant incidence of recurrent cuff tearing.² Possible factors contributing to the loss of tissue continuity have included poor quality or frank loss of rotator cuff tissue, diminished biological potential of the rotator cuff tendon, and excessive mechanical stress on or strain of the reconstructive surgical construct.³

I conducted a pilot study involving a technique that addresses these potential factors, amalgamating several contemporary surgical methods with the addition of a novel step: an autogenous tendon graft incubated in autologous bone marrow concentrate.

Materials and Methods

Ten consecutive patients (7 men, 3 women) enrolled in this retrospective case series. Mean age at time of surgery was 58 years (range, 47-65 years). Mean follow-up was 24 months (range, 12-44 months), and no patients were lost to follow-up. Mean time between original primary repair and current reconstruction was 36 months (range, 6-120 months). Criteria for enrollment included unremitting shoulder pain, radiographs showing no significant degenerative joint disease, magnetic resonance imaging confirming a large (3-5 cm) full-thickness rotator cuff tear with retraction, and history of prior rotator cuff repair on the affected shoulder without associated biceps tenodesis. The intraoperative inclusion criterion was direct visualization of a 3- to 5-cm full-thickness rotator cuff tear with retraction of at least 3 cm. Validated Constant, American Shoulder and Elbow Surgeons (ASES), and University of California Los Angeles (UCLA) shoulder scoring systems were used to collect range-of-motion, pain, strength, daily function, and patient satisfaction data before and after surgery. Standard error was calculated. Two-sample t test was used for preoperative–postoperative comparisons. Postoperative integrity of the rotator cuff reconstruction was evaluated by an independent full-time academic musculoskeletal radiologist using dynamic diagnostic ultrasound (iU22 xMatrix Ultrasound System [Philips Healthcare] at L 9-3 MHz). Informed consent was obtained from each patient. The study was approved by institutional review board.

After induction of general anesthesia, each patient was placed in the lateral decubitus position. Bone marrow (60 mL) was aspirated through a 14-gauge needle from a dorsal iliac table, just inferior to the iliac crest (Figure 1). The patient was then placed into the beach-chair position on a surgical shoulder table. The aspirated marrow was centrifuged at 2800 and 3800 rpm for 14 to 17 minutes (Magellan Autologous Platelet Separator; Arteriocyte Medical Systems) to yield 10 mL of a concentrated (4- to 5-fold) mixture of platelet-rich plasma (PRP) and mesenchymal stem cells. Surgery was performed through a 3-cm oblique anterior mini-open incision between the anterior corner of the acromion and the coracoid process, as I previously described.⁴ The deltoid muscle was split, not detached. Acromioplasty and release of the coracoacromial ligament were performed. The rotator cuff was inspected under ×4.5 optical magnification. The cuff tissue was mobilized and débrided back to a healthy-appearing margin. The size and shape of the rotator cuff defect were then estimated. The long head of the biceps was harvested from its origin just distal to the superior glenoid labrum unto the intertubercular sulcus on the proximal humerus. The remainder of the biceps tendon was tenodesed to the surgical neck of the humerus. The biceps tendon graft was then manipulated and fashioned (by longitudinal partial-thickness incision and expansion) to fit the cuff defect (Figures 2, 3). The expanded graft was incubated in the concentrated marrow (10 mL) for 60 minutes (Figure 4). Débridement at the base of the greater tuberosity down to bleeding cancellous bone was followed by insertion of multiple bone anchors bearing several strands of No. 2 synthetic suture. These strands were then passed through the biceps tendon graft for secure fixation (Figure 5). The débrided end of the rotator cuff was then sewn to the biceps tendon graft using locking stitches under zero tissue tension with the arm in full adduction. The free end of the graft was sewn to the subscapularis tendon (Figure 6). The remaining marrow concentrate was injected both deep and superficial to the rotator cuff construct. No additional wound irrigation fluid was injected or suction drain inserted. After surgery, the patient was placed into an abduction pillow for 1 month and then engaged in passive motion for 1 month. Active-assisted motion began 3 months after surgery.

Results

Clinically, all patients improved with respect to pain, motion, strength, function, and satisfaction by virtue of the reconstructive surgery. After surgery, mean Constant score was increased, from 13 to 71 (P < .001). Mean ASES score increased from 18 to 75 (P < .001). Mean UCLA score increased from 4 to 28 (P < .001) (Table). Ultrasound showed 0% incidence of full-thickness retearing. Dynamic scanning during abduction showed maintained reduction of the humeral head within the glenoid socket; superior subluxation of the humeral head was not detected. The biceps tendon graft was continuous with the rotator cuff tendon, indicative of graft integration: tissue healing at the graft–bone and graft–tendon interfaces (Figures 7, 8). There were no intraoperative or postoperative patient-related complications.

Discussion

Primary rotator cuff surgery is beneficial.⁵ Irrespective of technique, open versus arthroscopic,⁶ single- versus double-row repair,⁷ the clinical results have been satisfactory.⁸ Nevertheless, the “tissue failure” rate of rotator cuff surgery (full-thickness discontinuity of rotator cuff) has been as high as 31% in primary repairs.⁹ In revision rotator cuff repair and reconstruction, the radiographic tissue failure rate has been even higher, particularly in the setting of chronic large tears with retraction, with tissue failure rates up to 91%.¹⁰ Although small to medium full-thickness tears and retears are well tolerated by patients with reduced activity levels,¹¹ and pain symptoms do not necessarily correlate with rotator cuff tear size,¹² large retracted full-thickness tears in active patients seldom result in optimal clinical outcomes or patient satisfaction.^13,14 In addition, although recurrent tearing does not preclude a satisfactory clinical result, maintenance of cuff tissue integrity tends to produce a better objective clinical score and a more desirable clinical outcome.²

Few evidence-based restorative solutions exist for large recurrent rotator cuff tears with retraction in active non­geriatric patients.¹⁵ The no-treatment option in this context may result in gradual enlargement of the tear, chronic pain, weakness, and progressive degeneration of the glenohumeral joint and acromiohumeral confluence—so-called rotator cuff arthropathy, for which reverse total shoulder arthroplasty is required.^16,17 Partial repair of a large rotator cuff tear by margin convergence, interval slide, split deltoid flap, or nonanatomical reinsertion may improve clinical outcome scores but may not alter or prevent the progressive degenerative changes associated with rotator cuff arthropathy.^18,19 Synthetic scaffolds with and without biological enhancement have been used with varying degrees of success, particularly pain improvement and tissue integration.²⁰ Nevertheless, the failure rate has been reported to be 17% to 51%,²¹ and no evidence exists that allograft augmentation improves functional outcomes.²² Tendon transfer using the latissimus dorsi has also proved to be a surgical alternative in younger, active patients.²³ However, dissection in this procedure is a major undertaking for both surgeon and patient—compared with the minimally invasive technique used in the present study.²⁴

I selected a cohort of active, symptomatic patients for application of a synthesis of accepted surgical techniques through a mini-open incision in order to improve the reliability of the surgical construct while minimizing surgical morbidity. Débridement of marginal tissue, safe mobilization of remaining cuff, and tension-free suture line using locking sutures maximized the mechanical strength of the construct.^25,26 Biological enhancement with autogenous tissue (the patient’s own biceps tendon) as graft material (scaffolding), as well as autologous concentrated marrow delivering viable responding cells and chemokine/cytokine biofactors, increased the probability of reparative activity at the graft site.²⁷ The net effect was consistent tissue healing at a biologically challenging locus. Nonenhanced biceps tendon grafting in the setting of “irreparable” primary rotator cuff repair has had a 40-year history of orthopedic utility and an excellent record of clinical success.²⁸ Nevertheless, the retear rate has been 7% to 30%.²⁹ There are no previous reports of biologically enhanced autogenous biceps tendon grafting for reconstruction of a torn rotator cuff, either primary or in the setting of chronic revision surgery.

Previous well-designed PRP enhancement studies in the context of primary rotator cuff repair failed to demonstrate a consistent benefit with concentrated platelet-only augmentation.^30,31 The shared experimental design of these published studies used intra-articular injection as the sole delivery method without guarantee that the injected platelets would migrate, adhere to, and persist at the intended destination, the healing edge of the rotator cuff. In the present study, extended exposure of the splayed tendon graft by incubation in concentrated marrow was specifically designed to increase the probability that biologically active components would settle at the desired location by cellular seeding and plasmatic imbibition.³² Furthermore, use of PRP for growth factor (platelet-derived, PDGF; basic fibroblast, bFGF; transforming, TGF-β; epidermal, EGF; vascular endothelial, VEGF; connective tissue, CTGF) therapy, in addition to pluripotential mesenchymal cells for marrow-derived stem cell therapy, is in theory biologically superior to use of PRP alone.^33,34

The recent expansion of information about biologics has generated much interest in augmentation of soft-tissue healing. Unfortunately, the optimal technique of using cellular processing to upregulate stem-cell capacity at the graft interface is yet to be defined.³⁵ Clinical studies using PRP and related products to promote tendon healing have been both inconsistent and contradictory with respect to benefit of outcome. As we have been unable to harness the biological potential of this medium, application of biologics in contemporary clinical orthopedics remains narrow, random, and infrequent. The technique presented in this clinical series appears to be a small advancement in a positive direction. The described construct provides a starting point for study, combining mechanical as well as biological steps to promote rotator cuff healing. The consistency of the outcome in a clinical model in which retearing is an expectation rather than an exception is noteworthy. The zero tissue failure rate at 1 to 4 years, compared with the literature values in similar patient cohorts, is very promising.³⁶ The clinical outcome as measured by validated shoulder scores is also comparable to literature outcome values.¹⁹ Also noteworthy is the dynamic stability the construct gives to the glenohumeral joint. Ideally, the reconstructed rotator cuff provides active force coupling with the deltoid, simulating normal shoulder biomechanics. At a minimum, the reconstructed cuff provides a viable passive barrier to superior migration of the humeral head—thus supporting the mechanical efficiency of the deltoid and preventing rotator cuff arthropathy.

This study’s small sample (10 patients) puts its conclusions at risk for type I statistical error, in that too few patients were examined over a long enough period to demonstrate failure. Nevertheless, retears typically occur within 6 months of repair.^37,38 Therefore, minimum follow-up of 1 year was deemed sufficient. None of the 10 patients had diabetes or another chronic comorbidity. Nine of the 10 had either no or only mild preoperative fatty atrophy of the rotator cuff muscles. Eight of the 10 were nonsmokers. These factors, which suggest optimal surgical candidates, may prove to be significant as the clinical series expands over time. Incubation of the autogenous biceps graft in concentrated marrow for 60 minutes was arbitrarily chosen. In future in vitro examination, marrow cell viability as a function of incubation time will be assessed.

Conclusion

In active, middle-aged patients with chronic recurrent large retracted rotator cuff tears, the technique presented here, using autogenous biceps tendon and autologous concentrated marrow containing PRP and mesenchymal cells, consistently yielded satisfactory clinical results and promoted rotator cuff tissue healing without full-thickness retearing.

Proximal humerus fractures account for 4% to 5% of all fractures.¹ These fractures occur most frequently in the elderly—patients older than 60 years sustain 71% of these injuries²—and in females.^1,3 Given an aging population, this incidence is predicted to increase 3-fold over the next 30 years.⁴ There is much debate regarding management of acute, displaced proximal humerus fractures. A recent Cochrane Review of published outcomes of operative and nonoperative treatment of displaced proximal humerus fractures found insufficient evidence supporting either modality, though surgery was associated with additional procedures.⁵ A review of 1000 proximal humerus fractures found that 49% had less than 1 cm of displacement of the major fragments or angulation of less than 45°.³ Other authors have reported similar findings.^6,7 Although the incidence of proximal humerus fractures has remained stable over the past decade, from 1999 to 2005 there was a 25% relative increase in surgical management, including a relative increase of 29% in open reduction and internal fixation (ORIF) versus a 20% increase in arthroplasty.¹

Locking plates have consistently demonstrated biomechanical superiority over other forms of fixation in osteoporotic bone.^8-11 Egol and colleagues⁸ found that osteoporotic bone limited the torque of fixation to values less than what is required for adequate frictional force between the plate and the bone. This problem can be overcome with fixed-angle devices, such as locked plates.⁹ Compared with locked nail constructs, proximal humerus locking plates have demonstrated superiority in torsion, loading, and varus bending.^10,11 Compared with blade plates, proximal humerus locking plates exhibited increased stiffness and torsional fatigue resistance.¹² In a randomized clinical trial, Olerud and colleagues¹³ reported superior functional results with locking plate fixation compared with nonoperative treatment of displaced 3-part fractures in elderly patients with 2-year follow-up, though these clinical results were not supported by others.¹⁴ Two recent case–control studies comparing functional outcomes for 3- and 4-part fractures with follow-up of more than 2 years revealed higher Constant scores after locked plating compared with hemiarthroplasty, though complications were higher with locked plates.^15,16 Adoption of locked proximal humerus plating has been correlated with good clinical outcomes and union rates, though this has been accompanied by a higher rate of reoperation.⁷ Reoperation rates from 1999 to 2005 increased both in the immediate postoperative period (odds ratio, 3.36) and at 1 year (odds ratio, 3.90).¹

Complications of Locked Plating

Regardless of fixation type, reduced humeral head bone mass and quality may lead to implant loosening, fracture redisplacement, and, ultimately, poor outcomes. Baseline osteoporosis may predict likelihood of fixation failure.¹⁷ Multiple studies have reported on the implant-related complications associated with locking plate fixation—most commonly, intra-articular screw penetration, postoperative fracture displacement, and avascular necrosis (AVN)^18-24 (Figure 1). A meta-analysis of 12 studies with a total of 514 proximal humerus fractures treated with locking plate fixation showed an overall complication rate of 49% and a 13.8% reoperation rate.²⁵ The most common indication for reoperation involved intra-articular screw perforation. The most common complications were varus malunion (16%), osteonecrosis (10%), intra-articular screw penetration (8%), subacromial impingement (6%), and infection (4%).

Suboptimal intraoperative fracture reduction, specifically with residual varus, has been correlated with loss of fracture fixation. In a series of 153 fractures, loss of fixation occurred in 13.7% of cases, with the leading risk factor being varus malreduction.¹⁹ Failure rates were 30.4% and 11% when the head shaft angle was less than 120° and when it was 120° or more, respectively. Solberg and colleagues¹⁶ found that initial postoperative varus angulation of more than 20° resulted in universal loss of fixation. Conversion of these cases to hemiarthroplasty resulted in poor outcomes. Preoperative fracture alignment may also predict fixation failure.²² In one series, initial varus angulation healed with a mean 16° varus and a Constant score of 63, whereas initial valgus alignment healed with 6° varus and a Constant score of 71.²² Complications occurred in fractures that were initially in varus 79% of the time and initially in valgus 19% of the time. Screw perforation has been associated with loss of reduction 44% of the time.²⁰

In an analysis of locking plate constructs revised after early (<4 weeks) failure in 8 patients with osteoporosis, Micic and colleagues²¹ found implant pullout leading to varus malalignment. All cases lacked medial support and subchondral screw purchase; 3 were initially malreduced. Owsley and Gorczyca²³ retrospectively reviewed 53 cases of displaced proximal humerus fractures treated with locked plating. Despite the high rate of radiographic union, 36% developed complications, including screw cutout (23%), varus displacement of more than 10° (25%), and AVN (4%); 13% required revision. These complications disproportionately affected patients older than 60 years (57%) and negatively affected functional outcomes.

Augmentation Techniques

Despite its reported complications, proximal humerus locked plating remains the most widely used type of fixation.¹ Advancements in locking plate design, improved understanding of fixation principles, and adoption of techniques augmenting proximal humerus locking plate fixation, particularly in osteoporotic bone, have reduced postoperative complications (Table 1).

Rotator Cuff Sutures

A widely adopted technique for neutralizing rotator cuff–deforming forces, which theoretically can cause fracture displacement, is incorporation of heavy nonabsorbable sutures. These sutures are placed through the rotator cuff–tuberosity junction and tied down after being passed through the plate. Obtaining and maintaining tuberosity reduction are essential in achieving good functional outcomes after fixation. In addition, tension band sutures may be particularly useful in the setting of initial varus deformity.²⁶

Although clinical use of these sutures is common, biomechanical studies of their adjunctive contribution to fracture stability are lacking.²⁷ The rotator cuff musculature has a maximal contractile force of 3.5 kg/cm².²⁸ Ricchetti and colleagues²⁹ described a technique that involves using a locked plate and tagging the rotator cuff with heavy nonabsorbable sutures. Selective traction on the sutures can help obtain and maintain fracture reduction. Multiple studies have reported on suture use with locked plating for proximal humerus fractures.^29-34 Badman and colleagues³⁰ retrospectively reviewed 81 cases of metaphyseal defects or medial comminution treated with locked plating, rotator cuff sutures, and structural allograft. All cases healed within 6 months after surgery. The incidence of screw cutout was 3.7%, the incidence of AVN was 6.2%, and the incidence of varus collapse was 6%. A cadaveric study that used specimens (mean age, 77 years) with a simulated 3-part proximal humerus fracture treated with a locked plate both with and without cerclage sutures found no difference in interfragmentary motion between the groups.²⁷ The authors concluded that additive sutures are not required for anatomically reduced fractures. Multiple sutures may counteract the deforming forces that act on bony segments that cannot be adequately maintained with screws, such as an osteoporotic greater tuberosity.

Medial Column Restoration

The importance of reducing and maintaining the medial calcar to provide biomechanical support for a laterally placed plate has been recognized.^26,34-37 Gardner and colleagues²⁶ suggested that medial support was achieved if the medial cortex was anatomically reduced, if the proximal fragment was impacted laterally onto the shaft, or if 1 or more inferomedial screws were placed. Cases that did not achieve medial support developed significantly more humeral head subsidence (5.8 mm vs 1.2 mm) and screw penetration. Krappinger and colleagues³⁶ found that factors leading to fixation failure included age, local bone mineral density, anatomical reduction, and restoration of the medial cortical support. The authors concluded that anatomical reduction and restoration of the medial cortex were important in minimizing mechanical loads at the bone–implant interface. Biomechanically, Lescheid and colleagues³⁷ found that the most stable construct was anatomical reduction with medial cortical contact. In the setting of comminution, however, it may be preferable to intentionally perform varus malreduction to achieve medial contact than to achieve anatomical reduction with a fracture gap. Badman and colleagues³⁰ found that the incidence of screw penetration was 6% in patients with an intact medial calcar versus 29% in patients without medial support. In a retrospective analysis of patients treated with a locking plate and suture augmentation, Jung and colleagues³⁵ concluded that restoring medial support was the most reliable factor in the prevention of loss of reduction with or without screw perforation. Last, Solberg and colleagues¹⁶ reported better clinical outcomes when the length of the metaphyseal segment attached to the articular fragment was more than 2 mm. A length of less than 2 mm was predictive of developing AVN.

Use of Bone Void Fillers

Allograft. Allograft is cancellous or corticocancellous chips or tricortical graft used as osteoconductive filler for metaphyseal defects.³⁸ An increasingly popular technique involves using an endosteal fibular allograft strut to indirectly reduce the fracture and help support the medial calcar.^39-42 Hettrich and colleagues⁴⁰ reported on radiographic outcomes of displaced proximal humerus fractures with medial comminution treated with a locked plate and an endosteal fibular allograft or semitubular plate. The reduction was maintained in 96% of cases; there was 1 varus collapse. There were no cases of implant failure, screw perforation, or AVN. Other authors have also reported on successful use of fibular allograft in conjunction with a locked plate; the rate of reduction loss was low, and there were no cases of screw cutout or intra-articular screw penetration.^30,41,42 These clinical outcomes are supported by results of biomechanical studies of the added benefit of intramedullary fibular allograft.^43-46 Mathison and colleagues⁴³ reported that a construct with fibular allograft and a locking plate increased the failure load by 1.72 times and the stiffness by 3.84 times compared with a control group of locking plate only. Bae and colleagues⁴⁶ found significantly higher maximum failure load and construct stiffness with no varus collapse in specimens prepared with locked plate and fibular strut augmentation compared with a control group.

Others have successfully used cancellous allograft to fill humeral head bone defects.^29,32,47-49 Duralde and Leddy⁴⁷ reported 100% radiographic union and 81% good to excellent results in cases treated with a locking plate and morselized cancellous allograft to fill bone voids. Varus collapse and screw cutout did not occur, but there were 2 cases of AVN. Ricchetti and colleagues²⁹ reviewed 54 cases treated with a locking plate and rotator cuff suture construct. Allograft cancellous chips and demineralized bone matrix were used in 3- and 4-part fractures (70% of cases) along with shorter screws in the humeral head. Major complications included AVN (1), fixation failure (3), and varus malunion (5). Others investigators have had less favorable results with use of cancellous bone graft. Schliemann and colleagues¹⁹ reported on 27 patients who were older than 65 years when they underwent ORIF with rotator cuff sutures to stabilize the tuberosities and either cancellous graft or a synthetic bone substitute in patients with massive metaphyseal defects. Patient-reported outcomes were superior to Constant scores. Complications included screw penetration (22.2%), reduction loss (44.4%), implant failure (3.7%), and AVN (29.6%).

Autograft. Autograft has both osteoconductive and osteoinductive properties and has been successfully used for metaphyseal defects.^32,50 Kim and colleagues⁵⁰ reported on patients with 4-part proximal humerus fractures treated with a locking plate and autologous iliac graft. All cases achieved union and had good or excellent outcomes. There were no cases of AVN, varus collapse, or hardware-related complications.

Bone Cement. Calcium phosphate cement has osteoconductive properties and enhances screw purchase in cancellous bone (Figures 2A–2F). It can be injected or molded into bone voids to provide improved compressive strength. It is resorbed through cell-mediated processes resembling bone remodeling and does not disappear until new bone forms. (Calcium sulfate cement, on the other hand, resorbs through a chemical process independent of new bone formation.⁵¹) Egol and colleagues⁵² reviewed the cases of 92 patients (mean age, 61 years) with 2-, 3-, and 4-part proximal humerus fractures treated with locked plate fixation. Metaphyseal defects were treated with no augmentation, augmentation with cancellous chips, or augmentation with calcium phosphate cement. Adding calcium phosphate cement was associated with lower incidence of intra-articular screw penetration and humeral head settling. In a recent cadaveric biomechanical study using 2-part proximal humerus fractures with metaphyseal comminution, the group augmented with calcium phosphate cement had enhanced axial stiffness and load to failure with reduced screw penetration.⁵³ Other biomechanical studies have found increased screw pullout strength⁵⁴ and decreased interfragmentary motion when specimens were augmented with calcium phosphate cement.⁵⁵

Similar good clinical and radiographic outcomes have been observed with use of calcium sulfate cement.^56,57 Somasundaram and colleagues⁵⁶ reported good clinical outcomes in 82% of patients treated with locking plates and calcium sulfate cement used to fill metaphyseal voids. All fractures united without infection, fixation failure, subsequent malunion, tuberosity failure, or AVN. Lee and Shin⁵⁷ compared outcomes of 14 patients who received calcium sulfate augmentation with outcomes of patients who did not receive this augmentation. Overall, 89% of patients had good or excellent results. Calcium sulfate cement did not affect the reduction failure rate or clinical outcomes in cases in which medial cortical reduction was achieved. However, postoperative displacement caused by lack of medial support was associated with poor outcomes.

Screw Placement

Screws optimally should be placed in the posterior-medial-inferior aspect of the humeral head to provide medial support for the fracture and mechanical stability.⁵⁸ Cadaveric studies have shown the highest cancellous bone density in the proximal, posterior, and medial portions of the humeral head.^59-63 Similarly, in a cadaveric study, Liew and colleagues⁶¹ found greater screw purchase and higher pullout strength when the screw was placed in the center of the humeral head, within subchondral bone; fixation was poorest when the screw was placed in the anterosuperior region of the humeral head. Tingart and colleagues⁶² reported that humeral head trabecular density significantly affected pullout strength of cancellous screws. In addition, the most pullout strength was at the center of the head, and the least within the anterosuperior head. Trabecular density was higher in the inferior and posterior regions than in the superior and anterior regions.

Most locking plate designs allow screws to be placed at the level of the medial calcar—the goal being to provide medial column support (Table 2). Zhang and colleagues⁵⁸ treated 2-, 3-, and 4-part fractures with a locking plate and randomized them into receiving the plate with or without medial support screws. For 3- and 4-part fractures, the group with these screws had a significantly greater final neck-shaft angle and smaller angulation loss compared with the group without screws. No additional benefit was found for 2-part fractures. Erhardt and colleagues⁶³ simulated unstable proximal humerus fractures using cadavers and testing different fixation methods using a polyaxial locking plate. They found that 5 screws in the head fragment and an inferomedial support screw significantly reduced the risk of screw perforation. Other authors have concluded that placing 1 or more inferomedial screws is important in cases of medial comminution or medial column malreduction.²⁶ Interestingly, compared with use of a polyaxial implant, which allows for adjustment of screw direction, use of a monoaxial locking plate did not lead to a clinically different outcome or complication profile.⁶⁴

Techniques have been used to achieve subchondral purchase of locking screws while reducing iatrogenic articular perforation.⁶⁵ However, given the incidence of fracture settling and subsequent postoperative screw penetration, many authors currently recommend using shorter divergent screws combined with other augmentation techniques, described previously.^17,29,32

Physical Therapy

There is no standardized physiotherapy regimen for postoperative management of proximal humerus fractures treated with locking plates.²⁵ In older patients, immediate active range of motion (ROM) exercises should be delayed until early callus is noted, though there is a risk for stiffness. Lee and Shin⁵⁷ found that a delay in rehabilitation after ORIF was an independent risk for poor clinical outcome. Namdari and colleagues¹⁷ recommended sling use only for comfort and initiated non-load-bearing activities and pendulum exercises immediately after surgery. Patients with adequate reduction at 4 to 6 weeks were advanced to full weight-bearing. Badman and colleagues³⁰ initiated passive-assisted ROM exercises when the wound was healed at 2 weeks in 2-part fractures, whereas patients with 3- and 4-part fractures were immobilized until radiographic healing. Formal therapy was started after 6 weeks. Stiffness was reported in 5% of patients. For patients with stable fixation, Ricchetti and colleagues²⁹ recommended passive shoulder ROM exercises on postoperative day 1; at 4 to 6 weeks, patients should start active shoulder ROM exercises, and then resistance exercises at 10 to 12 weeks. Other authors are more conservative—only sling immobilization and pendulum exercises the first month.⁶⁶ Barlow and colleagues³² immobilized their patients (age, >75 years) for 6 weeks. No patient developed disabling stiffness. The authors suggested that patients older than 75 years may not be prone to stiffness.

Our Preferred Treatment Method

All proximal humerus fractures are approached anteriorly through the deltopectoral interval (Figure 3A). The long head biceps is identified and truncated for later tenodesis. Multiple No. 5 Ethibond sutures (Ethicon) are placed at the bone–tendon interface. The fracture is reduced with a Cobb elevator (Figure 3B), and provisional Kirschner wires are placed within the head (Figure 3C). The plate is affixed to the humeral head with its anterior border paralleling the posterior aspect of the bicipital groove. Multiple locking screws are placed within the superior and posterior humeral head. Nonlocking screws are then used to fix the plate to the shaft to reduce the specific deformity. Under fluoroscopy, any metaphyseal void is filled with calcium phosphate cement (Figure 3D). The remaining inferior screws are placed within the humeral head. Dr. Gruson uses screws 4 to 6 mm short of subchondral bone to reduce the risk for joint penetration. The rotator cuff sutures are tied down through the plate. Patients are started on progressive supine passive ROM exercises at 7 days, followed by supine active-assisted ROM exercises 6 weeks after fracture healing is confirmed radiographically.

Conclusion

Use of locked plating for proximal humerus fractures has increased, particularly in the elderly. Resulting complications include intra-articular screw penetration, postoperative fracture displacement, and AVN. Recognition of the importance of reducing and supporting the medial calcar, filling any metaphyseal defects, and selectively placing screws within the humeral head has lowered the incidence of these complications. Further comparative studies evaluating the efficacy of individual augmentation techniques are needed to determine their contribution to successful fracture healing and their cost-effectiveness. Results of such studies may help in the development of protocols for more standardized implementation of these techniques and in understanding which specific fracture patterns and patients would benefit from their use.

Proximal humerus fractures account for 4% to 5% of all fractures.¹ These fractures occur most frequently in the elderly—patients older than 60 years sustain 71% of these injuries²—and in females.^1,3 Given an aging population, this incidence is predicted to increase 3-fold over the next 30 years.⁴ There is much debate regarding management of acute, displaced proximal humerus fractures. A recent Cochrane Review of published outcomes of operative and nonoperative treatment of displaced proximal humerus fractures found insufficient evidence supporting either modality, though surgery was associated with additional procedures.⁵ A review of 1000 proximal humerus fractures found that 49% had less than 1 cm of displacement of the major fragments or angulation of less than 45°.³ Other authors have reported similar findings.^6,7 Although the incidence of proximal humerus fractures has remained stable over the past decade, from 1999 to 2005 there was a 25% relative increase in surgical management, including a relative increase of 29% in open reduction and internal fixation (ORIF) versus a 20% increase in arthroplasty.¹

Locking plates have consistently demonstrated biomechanical superiority over other forms of fixation in osteoporotic bone.^8-11 Egol and colleagues⁸ found that osteoporotic bone limited the torque of fixation to values less than what is required for adequate frictional force between the plate and the bone. This problem can be overcome with fixed-angle devices, such as locked plates.⁹ Compared with locked nail constructs, proximal humerus locking plates have demonstrated superiority in torsion, loading, and varus bending.^10,11 Compared with blade plates, proximal humerus locking plates exhibited increased stiffness and torsional fatigue resistance.¹² In a randomized clinical trial, Olerud and colleagues¹³ reported superior functional results with locking plate fixation compared with nonoperative treatment of displaced 3-part fractures in elderly patients with 2-year follow-up, though these clinical results were not supported by others.¹⁴ Two recent case–control studies comparing functional outcomes for 3- and 4-part fractures with follow-up of more than 2 years revealed higher Constant scores after locked plating compared with hemiarthroplasty, though complications were higher with locked plates.^15,16 Adoption of locked proximal humerus plating has been correlated with good clinical outcomes and union rates, though this has been accompanied by a higher rate of reoperation.⁷ Reoperation rates from 1999 to 2005 increased both in the immediate postoperative period (odds ratio, 3.36) and at 1 year (odds ratio, 3.90).¹

Complications of Locked Plating

Regardless of fixation type, reduced humeral head bone mass and quality may lead to implant loosening, fracture redisplacement, and, ultimately, poor outcomes. Baseline osteoporosis may predict likelihood of fixation failure.¹⁷ Multiple studies have reported on the implant-related complications associated with locking plate fixation—most commonly, intra-articular screw penetration, postoperative fracture displacement, and avascular necrosis (AVN)^18-24 (Figure 1). A meta-analysis of 12 studies with a total of 514 proximal humerus fractures treated with locking plate fixation showed an overall complication rate of 49% and a 13.8% reoperation rate.²⁵ The most common indication for reoperation involved intra-articular screw perforation. The most common complications were varus malunion (16%), osteonecrosis (10%), intra-articular screw penetration (8%), subacromial impingement (6%), and infection (4%).

Suboptimal intraoperative fracture reduction, specifically with residual varus, has been correlated with loss of fracture fixation. In a series of 153 fractures, loss of fixation occurred in 13.7% of cases, with the leading risk factor being varus malreduction.¹⁹ Failure rates were 30.4% and 11% when the head shaft angle was less than 120° and when it was 120° or more, respectively. Solberg and colleagues¹⁶ found that initial postoperative varus angulation of more than 20° resulted in universal loss of fixation. Conversion of these cases to hemiarthroplasty resulted in poor outcomes. Preoperative fracture alignment may also predict fixation failure.²² In one series, initial varus angulation healed with a mean 16° varus and a Constant score of 63, whereas initial valgus alignment healed with 6° varus and a Constant score of 71.²² Complications occurred in fractures that were initially in varus 79% of the time and initially in valgus 19% of the time. Screw perforation has been associated with loss of reduction 44% of the time.²⁰

In an analysis of locking plate constructs revised after early (<4 weeks) failure in 8 patients with osteoporosis, Micic and colleagues²¹ found implant pullout leading to varus malalignment. All cases lacked medial support and subchondral screw purchase; 3 were initially malreduced. Owsley and Gorczyca²³ retrospectively reviewed 53 cases of displaced proximal humerus fractures treated with locked plating. Despite the high rate of radiographic union, 36% developed complications, including screw cutout (23%), varus displacement of more than 10° (25%), and AVN (4%); 13% required revision. These complications disproportionately affected patients older than 60 years (57%) and negatively affected functional outcomes.

Augmentation Techniques

Despite its reported complications, proximal humerus locked plating remains the most widely used type of fixation.¹ Advancements in locking plate design, improved understanding of fixation principles, and adoption of techniques augmenting proximal humerus locking plate fixation, particularly in osteoporotic bone, have reduced postoperative complications (Table 1).

Rotator Cuff Sutures

A widely adopted technique for neutralizing rotator cuff–deforming forces, which theoretically can cause fracture displacement, is incorporation of heavy nonabsorbable sutures. These sutures are placed through the rotator cuff–tuberosity junction and tied down after being passed through the plate. Obtaining and maintaining tuberosity reduction are essential in achieving good functional outcomes after fixation. In addition, tension band sutures may be particularly useful in the setting of initial varus deformity.²⁶

Although clinical use of these sutures is common, biomechanical studies of their adjunctive contribution to fracture stability are lacking.²⁷ The rotator cuff musculature has a maximal contractile force of 3.5 kg/cm².²⁸ Ricchetti and colleagues²⁹ described a technique that involves using a locked plate and tagging the rotator cuff with heavy nonabsorbable sutures. Selective traction on the sutures can help obtain and maintain fracture reduction. Multiple studies have reported on suture use with locked plating for proximal humerus fractures.^29-34 Badman and colleagues³⁰ retrospectively reviewed 81 cases of metaphyseal defects or medial comminution treated with locked plating, rotator cuff sutures, and structural allograft. All cases healed within 6 months after surgery. The incidence of screw cutout was 3.7%, the incidence of AVN was 6.2%, and the incidence of varus collapse was 6%. A cadaveric study that used specimens (mean age, 77 years) with a simulated 3-part proximal humerus fracture treated with a locked plate both with and without cerclage sutures found no difference in interfragmentary motion between the groups.²⁷ The authors concluded that additive sutures are not required for anatomically reduced fractures. Multiple sutures may counteract the deforming forces that act on bony segments that cannot be adequately maintained with screws, such as an osteoporotic greater tuberosity.

Medial Column Restoration

The importance of reducing and maintaining the medial calcar to provide biomechanical support for a laterally placed plate has been recognized.^26,34-37 Gardner and colleagues²⁶ suggested that medial support was achieved if the medial cortex was anatomically reduced, if the proximal fragment was impacted laterally onto the shaft, or if 1 or more inferomedial screws were placed. Cases that did not achieve medial support developed significantly more humeral head subsidence (5.8 mm vs 1.2 mm) and screw penetration. Krappinger and colleagues³⁶ found that factors leading to fixation failure included age, local bone mineral density, anatomical reduction, and restoration of the medial cortical support. The authors concluded that anatomical reduction and restoration of the medial cortex were important in minimizing mechanical loads at the bone–implant interface. Biomechanically, Lescheid and colleagues³⁷ found that the most stable construct was anatomical reduction with medial cortical contact. In the setting of comminution, however, it may be preferable to intentionally perform varus malreduction to achieve medial contact than to achieve anatomical reduction with a fracture gap. Badman and colleagues³⁰ found that the incidence of screw penetration was 6% in patients with an intact medial calcar versus 29% in patients without medial support. In a retrospective analysis of patients treated with a locking plate and suture augmentation, Jung and colleagues³⁵ concluded that restoring medial support was the most reliable factor in the prevention of loss of reduction with or without screw perforation. Last, Solberg and colleagues¹⁶ reported better clinical outcomes when the length of the metaphyseal segment attached to the articular fragment was more than 2 mm. A length of less than 2 mm was predictive of developing AVN.

Use of Bone Void Fillers

Allograft. Allograft is cancellous or corticocancellous chips or tricortical graft used as osteoconductive filler for metaphyseal defects.³⁸ An increasingly popular technique involves using an endosteal fibular allograft strut to indirectly reduce the fracture and help support the medial calcar.^39-42 Hettrich and colleagues⁴⁰ reported on radiographic outcomes of displaced proximal humerus fractures with medial comminution treated with a locked plate and an endosteal fibular allograft or semitubular plate. The reduction was maintained in 96% of cases; there was 1 varus collapse. There were no cases of implant failure, screw perforation, or AVN. Other authors have also reported on successful use of fibular allograft in conjunction with a locked plate; the rate of reduction loss was low, and there were no cases of screw cutout or intra-articular screw penetration.^30,41,42 These clinical outcomes are supported by results of biomechanical studies of the added benefit of intramedullary fibular allograft.^43-46 Mathison and colleagues⁴³ reported that a construct with fibular allograft and a locking plate increased the failure load by 1.72 times and the stiffness by 3.84 times compared with a control group of locking plate only. Bae and colleagues⁴⁶ found significantly higher maximum failure load and construct stiffness with no varus collapse in specimens prepared with locked plate and fibular strut augmentation compared with a control group.

Others have successfully used cancellous allograft to fill humeral head bone defects.^29,32,47-49 Duralde and Leddy⁴⁷ reported 100% radiographic union and 81% good to excellent results in cases treated with a locking plate and morselized cancellous allograft to fill bone voids. Varus collapse and screw cutout did not occur, but there were 2 cases of AVN. Ricchetti and colleagues²⁹ reviewed 54 cases treated with a locking plate and rotator cuff suture construct. Allograft cancellous chips and demineralized bone matrix were used in 3- and 4-part fractures (70% of cases) along with shorter screws in the humeral head. Major complications included AVN (1), fixation failure (3), and varus malunion (5). Others investigators have had less favorable results with use of cancellous bone graft. Schliemann and colleagues¹⁹ reported on 27 patients who were older than 65 years when they underwent ORIF with rotator cuff sutures to stabilize the tuberosities and either cancellous graft or a synthetic bone substitute in patients with massive metaphyseal defects. Patient-reported outcomes were superior to Constant scores. Complications included screw penetration (22.2%), reduction loss (44.4%), implant failure (3.7%), and AVN (29.6%).

Autograft. Autograft has both osteoconductive and osteoinductive properties and has been successfully used for metaphyseal defects.^32,50 Kim and colleagues⁵⁰ reported on patients with 4-part proximal humerus fractures treated with a locking plate and autologous iliac graft. All cases achieved union and had good or excellent outcomes. There were no cases of AVN, varus collapse, or hardware-related complications.

Bone Cement. Calcium phosphate cement has osteoconductive properties and enhances screw purchase in cancellous bone (Figures 2A–2F). It can be injected or molded into bone voids to provide improved compressive strength. It is resorbed through cell-mediated processes resembling bone remodeling and does not disappear until new bone forms. (Calcium sulfate cement, on the other hand, resorbs through a chemical process independent of new bone formation.⁵¹) Egol and colleagues⁵² reviewed the cases of 92 patients (mean age, 61 years) with 2-, 3-, and 4-part proximal humerus fractures treated with locked plate fixation. Metaphyseal defects were treated with no augmentation, augmentation with cancellous chips, or augmentation with calcium phosphate cement. Adding calcium phosphate cement was associated with lower incidence of intra-articular screw penetration and humeral head settling. In a recent cadaveric biomechanical study using 2-part proximal humerus fractures with metaphyseal comminution, the group augmented with calcium phosphate cement had enhanced axial stiffness and load to failure with reduced screw penetration.⁵³ Other biomechanical studies have found increased screw pullout strength⁵⁴ and decreased interfragmentary motion when specimens were augmented with calcium phosphate cement.⁵⁵

Similar good clinical and radiographic outcomes have been observed with use of calcium sulfate cement.^56,57 Somasundaram and colleagues⁵⁶ reported good clinical outcomes in 82% of patients treated with locking plates and calcium sulfate cement used to fill metaphyseal voids. All fractures united without infection, fixation failure, subsequent malunion, tuberosity failure, or AVN. Lee and Shin⁵⁷ compared outcomes of 14 patients who received calcium sulfate augmentation with outcomes of patients who did not receive this augmentation. Overall, 89% of patients had good or excellent results. Calcium sulfate cement did not affect the reduction failure rate or clinical outcomes in cases in which medial cortical reduction was achieved. However, postoperative displacement caused by lack of medial support was associated with poor outcomes.

Screw Placement

Screws optimally should be placed in the posterior-medial-inferior aspect of the humeral head to provide medial support for the fracture and mechanical stability.⁵⁸ Cadaveric studies have shown the highest cancellous bone density in the proximal, posterior, and medial portions of the humeral head.^59-63 Similarly, in a cadaveric study, Liew and colleagues⁶¹ found greater screw purchase and higher pullout strength when the screw was placed in the center of the humeral head, within subchondral bone; fixation was poorest when the screw was placed in the anterosuperior region of the humeral head. Tingart and colleagues⁶² reported that humeral head trabecular density significantly affected pullout strength of cancellous screws. In addition, the most pullout strength was at the center of the head, and the least within the anterosuperior head. Trabecular density was higher in the inferior and posterior regions than in the superior and anterior regions.

Most locking plate designs allow screws to be placed at the level of the medial calcar—the goal being to provide medial column support (Table 2). Zhang and colleagues⁵⁸ treated 2-, 3-, and 4-part fractures with a locking plate and randomized them into receiving the plate with or without medial support screws. For 3- and 4-part fractures, the group with these screws had a significantly greater final neck-shaft angle and smaller angulation loss compared with the group without screws. No additional benefit was found for 2-part fractures. Erhardt and colleagues⁶³ simulated unstable proximal humerus fractures using cadavers and testing different fixation methods using a polyaxial locking plate. They found that 5 screws in the head fragment and an inferomedial support screw significantly reduced the risk of screw perforation. Other authors have concluded that placing 1 or more inferomedial screws is important in cases of medial comminution or medial column malreduction.²⁶ Interestingly, compared with use of a polyaxial implant, which allows for adjustment of screw direction, use of a monoaxial locking plate did not lead to a clinically different outcome or complication profile.⁶⁴

Techniques have been used to achieve subchondral purchase of locking screws while reducing iatrogenic articular perforation.⁶⁵ However, given the incidence of fracture settling and subsequent postoperative screw penetration, many authors currently recommend using shorter divergent screws combined with other augmentation techniques, described previously.^17,29,32

Physical Therapy

There is no standardized physiotherapy regimen for postoperative management of proximal humerus fractures treated with locking plates.²⁵ In older patients, immediate active range of motion (ROM) exercises should be delayed until early callus is noted, though there is a risk for stiffness. Lee and Shin⁵⁷ found that a delay in rehabilitation after ORIF was an independent risk for poor clinical outcome. Namdari and colleagues¹⁷ recommended sling use only for comfort and initiated non-load-bearing activities and pendulum exercises immediately after surgery. Patients with adequate reduction at 4 to 6 weeks were advanced to full weight-bearing. Badman and colleagues³⁰ initiated passive-assisted ROM exercises when the wound was healed at 2 weeks in 2-part fractures, whereas patients with 3- and 4-part fractures were immobilized until radiographic healing. Formal therapy was started after 6 weeks. Stiffness was reported in 5% of patients. For patients with stable fixation, Ricchetti and colleagues²⁹ recommended passive shoulder ROM exercises on postoperative day 1; at 4 to 6 weeks, patients should start active shoulder ROM exercises, and then resistance exercises at 10 to 12 weeks. Other authors are more conservative—only sling immobilization and pendulum exercises the first month.⁶⁶ Barlow and colleagues³² immobilized their patients (age, >75 years) for 6 weeks. No patient developed disabling stiffness. The authors suggested that patients older than 75 years may not be prone to stiffness.

Our Preferred Treatment Method

All proximal humerus fractures are approached anteriorly through the deltopectoral interval (Figure 3A). The long head biceps is identified and truncated for later tenodesis. Multiple No. 5 Ethibond sutures (Ethicon) are placed at the bone–tendon interface. The fracture is reduced with a Cobb elevator (Figure 3B), and provisional Kirschner wires are placed within the head (Figure 3C). The plate is affixed to the humeral head with its anterior border paralleling the posterior aspect of the bicipital groove. Multiple locking screws are placed within the superior and posterior humeral head. Nonlocking screws are then used to fix the plate to the shaft to reduce the specific deformity. Under fluoroscopy, any metaphyseal void is filled with calcium phosphate cement (Figure 3D). The remaining inferior screws are placed within the humeral head. Dr. Gruson uses screws 4 to 6 mm short of subchondral bone to reduce the risk for joint penetration. The rotator cuff sutures are tied down through the plate. Patients are started on progressive supine passive ROM exercises at 7 days, followed by supine active-assisted ROM exercises 6 weeks after fracture healing is confirmed radiographically.

Conclusion

Use of locked plating for proximal humerus fractures has increased, particularly in the elderly. Resulting complications include intra-articular screw penetration, postoperative fracture displacement, and AVN. Recognition of the importance of reducing and supporting the medial calcar, filling any metaphyseal defects, and selectively placing screws within the humeral head has lowered the incidence of these complications. Further comparative studies evaluating the efficacy of individual augmentation techniques are needed to determine their contribution to successful fracture healing and their cost-effectiveness. Results of such studies may help in the development of protocols for more standardized implementation of these techniques and in understanding which specific fracture patterns and patients would benefit from their use.

Proximal humerus fractures account for 4% to 5% of all fractures.¹ These fractures occur most frequently in the elderly—patients older than 60 years sustain 71% of these injuries²—and in females.^1,3 Given an aging population, this incidence is predicted to increase 3-fold over the next 30 years.⁴ There is much debate regarding management of acute, displaced proximal humerus fractures. A recent Cochrane Review of published outcomes of operative and nonoperative treatment of displaced proximal humerus fractures found insufficient evidence supporting either modality, though surgery was associated with additional procedures.⁵ A review of 1000 proximal humerus fractures found that 49% had less than 1 cm of displacement of the major fragments or angulation of less than 45°.³ Other authors have reported similar findings.^6,7 Although the incidence of proximal humerus fractures has remained stable over the past decade, from 1999 to 2005 there was a 25% relative increase in surgical management, including a relative increase of 29% in open reduction and internal fixation (ORIF) versus a 20% increase in arthroplasty.¹

Locking plates have consistently demonstrated biomechanical superiority over other forms of fixation in osteoporotic bone.^8-11 Egol and colleagues⁸ found that osteoporotic bone limited the torque of fixation to values less than what is required for adequate frictional force between the plate and the bone. This problem can be overcome with fixed-angle devices, such as locked plates.⁹ Compared with locked nail constructs, proximal humerus locking plates have demonstrated superiority in torsion, loading, and varus bending.^10,11 Compared with blade plates, proximal humerus locking plates exhibited increased stiffness and torsional fatigue resistance.¹² In a randomized clinical trial, Olerud and colleagues¹³ reported superior functional results with locking plate fixation compared with nonoperative treatment of displaced 3-part fractures in elderly patients with 2-year follow-up, though these clinical results were not supported by others.¹⁴ Two recent case–control studies comparing functional outcomes for 3- and 4-part fractures with follow-up of more than 2 years revealed higher Constant scores after locked plating compared with hemiarthroplasty, though complications were higher with locked plates.^15,16 Adoption of locked proximal humerus plating has been correlated with good clinical outcomes and union rates, though this has been accompanied by a higher rate of reoperation.⁷ Reoperation rates from 1999 to 2005 increased both in the immediate postoperative period (odds ratio, 3.36) and at 1 year (odds ratio, 3.90).¹

Complications of Locked Plating

Regardless of fixation type, reduced humeral head bone mass and quality may lead to implant loosening, fracture redisplacement, and, ultimately, poor outcomes. Baseline osteoporosis may predict likelihood of fixation failure.¹⁷ Multiple studies have reported on the implant-related complications associated with locking plate fixation—most commonly, intra-articular screw penetration, postoperative fracture displacement, and avascular necrosis (AVN)^18-24 (Figure 1). A meta-analysis of 12 studies with a total of 514 proximal humerus fractures treated with locking plate fixation showed an overall complication rate of 49% and a 13.8% reoperation rate.²⁵ The most common indication for reoperation involved intra-articular screw perforation. The most common complications were varus malunion (16%), osteonecrosis (10%), intra-articular screw penetration (8%), subacromial impingement (6%), and infection (4%).

Suboptimal intraoperative fracture reduction, specifically with residual varus, has been correlated with loss of fracture fixation. In a series of 153 fractures, loss of fixation occurred in 13.7% of cases, with the leading risk factor being varus malreduction.¹⁹ Failure rates were 30.4% and 11% when the head shaft angle was less than 120° and when it was 120° or more, respectively. Solberg and colleagues¹⁶ found that initial postoperative varus angulation of more than 20° resulted in universal loss of fixation. Conversion of these cases to hemiarthroplasty resulted in poor outcomes. Preoperative fracture alignment may also predict fixation failure.²² In one series, initial varus angulation healed with a mean 16° varus and a Constant score of 63, whereas initial valgus alignment healed with 6° varus and a Constant score of 71.²² Complications occurred in fractures that were initially in varus 79% of the time and initially in valgus 19% of the time. Screw perforation has been associated with loss of reduction 44% of the time.²⁰

In an analysis of locking plate constructs revised after early (<4 weeks) failure in 8 patients with osteoporosis, Micic and colleagues²¹ found implant pullout leading to varus malalignment. All cases lacked medial support and subchondral screw purchase; 3 were initially malreduced. Owsley and Gorczyca²³ retrospectively reviewed 53 cases of displaced proximal humerus fractures treated with locked plating. Despite the high rate of radiographic union, 36% developed complications, including screw cutout (23%), varus displacement of more than 10° (25%), and AVN (4%); 13% required revision. These complications disproportionately affected patients older than 60 years (57%) and negatively affected functional outcomes.

Augmentation Techniques

Despite its reported complications, proximal humerus locked plating remains the most widely used type of fixation.¹ Advancements in locking plate design, improved understanding of fixation principles, and adoption of techniques augmenting proximal humerus locking plate fixation, particularly in osteoporotic bone, have reduced postoperative complications (Table 1).

Rotator Cuff Sutures

A widely adopted technique for neutralizing rotator cuff–deforming forces, which theoretically can cause fracture displacement, is incorporation of heavy nonabsorbable sutures. These sutures are placed through the rotator cuff–tuberosity junction and tied down after being passed through the plate. Obtaining and maintaining tuberosity reduction are essential in achieving good functional outcomes after fixation. In addition, tension band sutures may be particularly useful in the setting of initial varus deformity.²⁶

Although clinical use of these sutures is common, biomechanical studies of their adjunctive contribution to fracture stability are lacking.²⁷ The rotator cuff musculature has a maximal contractile force of 3.5 kg/cm².²⁸ Ricchetti and colleagues²⁹ described a technique that involves using a locked plate and tagging the rotator cuff with heavy nonabsorbable sutures. Selective traction on the sutures can help obtain and maintain fracture reduction. Multiple studies have reported on suture use with locked plating for proximal humerus fractures.^29-34 Badman and colleagues³⁰ retrospectively reviewed 81 cases of metaphyseal defects or medial comminution treated with locked plating, rotator cuff sutures, and structural allograft. All cases healed within 6 months after surgery. The incidence of screw cutout was 3.7%, the incidence of AVN was 6.2%, and the incidence of varus collapse was 6%. A cadaveric study that used specimens (mean age, 77 years) with a simulated 3-part proximal humerus fracture treated with a locked plate both with and without cerclage sutures found no difference in interfragmentary motion between the groups.²⁷ The authors concluded that additive sutures are not required for anatomically reduced fractures. Multiple sutures may counteract the deforming forces that act on bony segments that cannot be adequately maintained with screws, such as an osteoporotic greater tuberosity.

Medial Column Restoration

The importance of reducing and maintaining the medial calcar to provide biomechanical support for a laterally placed plate has been recognized.^26,34-37 Gardner and colleagues²⁶ suggested that medial support was achieved if the medial cortex was anatomically reduced, if the proximal fragment was impacted laterally onto the shaft, or if 1 or more inferomedial screws were placed. Cases that did not achieve medial support developed significantly more humeral head subsidence (5.8 mm vs 1.2 mm) and screw penetration. Krappinger and colleagues³⁶ found that factors leading to fixation failure included age, local bone mineral density, anatomical reduction, and restoration of the medial cortical support. The authors concluded that anatomical reduction and restoration of the medial cortex were important in minimizing mechanical loads at the bone–implant interface. Biomechanically, Lescheid and colleagues³⁷ found that the most stable construct was anatomical reduction with medial cortical contact. In the setting of comminution, however, it may be preferable to intentionally perform varus malreduction to achieve medial contact than to achieve anatomical reduction with a fracture gap. Badman and colleagues³⁰ found that the incidence of screw penetration was 6% in patients with an intact medial calcar versus 29% in patients without medial support. In a retrospective analysis of patients treated with a locking plate and suture augmentation, Jung and colleagues³⁵ concluded that restoring medial support was the most reliable factor in the prevention of loss of reduction with or without screw perforation. Last, Solberg and colleagues¹⁶ reported better clinical outcomes when the length of the metaphyseal segment attached to the articular fragment was more than 2 mm. A length of less than 2 mm was predictive of developing AVN.

Use of Bone Void Fillers

Allograft. Allograft is cancellous or corticocancellous chips or tricortical graft used as osteoconductive filler for metaphyseal defects.³⁸ An increasingly popular technique involves using an endosteal fibular allograft strut to indirectly reduce the fracture and help support the medial calcar.^39-42 Hettrich and colleagues⁴⁰ reported on radiographic outcomes of displaced proximal humerus fractures with medial comminution treated with a locked plate and an endosteal fibular allograft or semitubular plate. The reduction was maintained in 96% of cases; there was 1 varus collapse. There were no cases of implant failure, screw perforation, or AVN. Other authors have also reported on successful use of fibular allograft in conjunction with a locked plate; the rate of reduction loss was low, and there were no cases of screw cutout or intra-articular screw penetration.^30,41,42 These clinical outcomes are supported by results of biomechanical studies of the added benefit of intramedullary fibular allograft.^43-46 Mathison and colleagues⁴³ reported that a construct with fibular allograft and a locking plate increased the failure load by 1.72 times and the stiffness by 3.84 times compared with a control group of locking plate only. Bae and colleagues⁴⁶ found significantly higher maximum failure load and construct stiffness with no varus collapse in specimens prepared with locked plate and fibular strut augmentation compared with a control group.

Others have successfully used cancellous allograft to fill humeral head bone defects.^29,32,47-49 Duralde and Leddy⁴⁷ reported 100% radiographic union and 81% good to excellent results in cases treated with a locking plate and morselized cancellous allograft to fill bone voids. Varus collapse and screw cutout did not occur, but there were 2 cases of AVN. Ricchetti and colleagues²⁹ reviewed 54 cases treated with a locking plate and rotator cuff suture construct. Allograft cancellous chips and demineralized bone matrix were used in 3- and 4-part fractures (70% of cases) along with shorter screws in the humeral head. Major complications included AVN (1), fixation failure (3), and varus malunion (5). Others investigators have had less favorable results with use of cancellous bone graft. Schliemann and colleagues¹⁹ reported on 27 patients who were older than 65 years when they underwent ORIF with rotator cuff sutures to stabilize the tuberosities and either cancellous graft or a synthetic bone substitute in patients with massive metaphyseal defects. Patient-reported outcomes were superior to Constant scores. Complications included screw penetration (22.2%), reduction loss (44.4%), implant failure (3.7%), and AVN (29.6%).

Autograft. Autograft has both osteoconductive and osteoinductive properties and has been successfully used for metaphyseal defects.^32,50 Kim and colleagues⁵⁰ reported on patients with 4-part proximal humerus fractures treated with a locking plate and autologous iliac graft. All cases achieved union and had good or excellent outcomes. There were no cases of AVN, varus collapse, or hardware-related complications.

Bone Cement. Calcium phosphate cement has osteoconductive properties and enhances screw purchase in cancellous bone (Figures 2A–2F). It can be injected or molded into bone voids to provide improved compressive strength. It is resorbed through cell-mediated processes resembling bone remodeling and does not disappear until new bone forms. (Calcium sulfate cement, on the other hand, resorbs through a chemical process independent of new bone formation.⁵¹) Egol and colleagues⁵² reviewed the cases of 92 patients (mean age, 61 years) with 2-, 3-, and 4-part proximal humerus fractures treated with locked plate fixation. Metaphyseal defects were treated with no augmentation, augmentation with cancellous chips, or augmentation with calcium phosphate cement. Adding calcium phosphate cement was associated with lower incidence of intra-articular screw penetration and humeral head settling. In a recent cadaveric biomechanical study using 2-part proximal humerus fractures with metaphyseal comminution, the group augmented with calcium phosphate cement had enhanced axial stiffness and load to failure with reduced screw penetration.⁵³ Other biomechanical studies have found increased screw pullout strength⁵⁴ and decreased interfragmentary motion when specimens were augmented with calcium phosphate cement.⁵⁵

Similar good clinical and radiographic outcomes have been observed with use of calcium sulfate cement.^56,57 Somasundaram and colleagues⁵⁶ reported good clinical outcomes in 82% of patients treated with locking plates and calcium sulfate cement used to fill metaphyseal voids. All fractures united without infection, fixation failure, subsequent malunion, tuberosity failure, or AVN. Lee and Shin⁵⁷ compared outcomes of 14 patients who received calcium sulfate augmentation with outcomes of patients who did not receive this augmentation. Overall, 89% of patients had good or excellent results. Calcium sulfate cement did not affect the reduction failure rate or clinical outcomes in cases in which medial cortical reduction was achieved. However, postoperative displacement caused by lack of medial support was associated with poor outcomes.

Screw Placement

Screws optimally should be placed in the posterior-medial-inferior aspect of the humeral head to provide medial support for the fracture and mechanical stability.⁵⁸ Cadaveric studies have shown the highest cancellous bone density in the proximal, posterior, and medial portions of the humeral head.^59-63 Similarly, in a cadaveric study, Liew and colleagues⁶¹ found greater screw purchase and higher pullout strength when the screw was placed in the center of the humeral head, within subchondral bone; fixation was poorest when the screw was placed in the anterosuperior region of the humeral head. Tingart and colleagues⁶² reported that humeral head trabecular density significantly affected pullout strength of cancellous screws. In addition, the most pullout strength was at the center of the head, and the least within the anterosuperior head. Trabecular density was higher in the inferior and posterior regions than in the superior and anterior regions.

Most locking plate designs allow screws to be placed at the level of the medial calcar—the goal being to provide medial column support (Table 2). Zhang and colleagues⁵⁸ treated 2-, 3-, and 4-part fractures with a locking plate and randomized them into receiving the plate with or without medial support screws. For 3- and 4-part fractures, the group with these screws had a significantly greater final neck-shaft angle and smaller angulation loss compared with the group without screws. No additional benefit was found for 2-part fractures. Erhardt and colleagues⁶³ simulated unstable proximal humerus fractures using cadavers and testing different fixation methods using a polyaxial locking plate. They found that 5 screws in the head fragment and an inferomedial support screw significantly reduced the risk of screw perforation. Other authors have concluded that placing 1 or more inferomedial screws is important in cases of medial comminution or medial column malreduction.²⁶ Interestingly, compared with use of a polyaxial implant, which allows for adjustment of screw direction, use of a monoaxial locking plate did not lead to a clinically different outcome or complication profile.⁶⁴

Techniques have been used to achieve subchondral purchase of locking screws while reducing iatrogenic articular perforation.⁶⁵ However, given the incidence of fracture settling and subsequent postoperative screw penetration, many authors currently recommend using shorter divergent screws combined with other augmentation techniques, described previously.^17,29,32

Physical Therapy

There is no standardized physiotherapy regimen for postoperative management of proximal humerus fractures treated with locking plates.²⁵ In older patients, immediate active range of motion (ROM) exercises should be delayed until early callus is noted, though there is a risk for stiffness. Lee and Shin⁵⁷ found that a delay in rehabilitation after ORIF was an independent risk for poor clinical outcome. Namdari and colleagues¹⁷ recommended sling use only for comfort and initiated non-load-bearing activities and pendulum exercises immediately after surgery. Patients with adequate reduction at 4 to 6 weeks were advanced to full weight-bearing. Badman and colleagues³⁰ initiated passive-assisted ROM exercises when the wound was healed at 2 weeks in 2-part fractures, whereas patients with 3- and 4-part fractures were immobilized until radiographic healing. Formal therapy was started after 6 weeks. Stiffness was reported in 5% of patients. For patients with stable fixation, Ricchetti and colleagues²⁹ recommended passive shoulder ROM exercises on postoperative day 1; at 4 to 6 weeks, patients should start active shoulder ROM exercises, and then resistance exercises at 10 to 12 weeks. Other authors are more conservative—only sling immobilization and pendulum exercises the first month.⁶⁶ Barlow and colleagues³² immobilized their patients (age, >75 years) for 6 weeks. No patient developed disabling stiffness. The authors suggested that patients older than 75 years may not be prone to stiffness.

Our Preferred Treatment Method

All proximal humerus fractures are approached anteriorly through the deltopectoral interval (Figure 3A). The long head biceps is identified and truncated for later tenodesis. Multiple No. 5 Ethibond sutures (Ethicon) are placed at the bone–tendon interface. The fracture is reduced with a Cobb elevator (Figure 3B), and provisional Kirschner wires are placed within the head (Figure 3C). The plate is affixed to the humeral head with its anterior border paralleling the posterior aspect of the bicipital groove. Multiple locking screws are placed within the superior and posterior humeral head. Nonlocking screws are then used to fix the plate to the shaft to reduce the specific deformity. Under fluoroscopy, any metaphyseal void is filled with calcium phosphate cement (Figure 3D). The remaining inferior screws are placed within the humeral head. Dr. Gruson uses screws 4 to 6 mm short of subchondral bone to reduce the risk for joint penetration. The rotator cuff sutures are tied down through the plate. Patients are started on progressive supine passive ROM exercises at 7 days, followed by supine active-assisted ROM exercises 6 weeks after fracture healing is confirmed radiographically.

Conclusion

Use of locked plating for proximal humerus fractures has increased, particularly in the elderly. Resulting complications include intra-articular screw penetration, postoperative fracture displacement, and AVN. Recognition of the importance of reducing and supporting the medial calcar, filling any metaphyseal defects, and selectively placing screws within the humeral head has lowered the incidence of these complications. Further comparative studies evaluating the efficacy of individual augmentation techniques are needed to determine their contribution to successful fracture healing and their cost-effectiveness. Results of such studies may help in the development of protocols for more standardized implementation of these techniques and in understanding which specific fracture patterns and patients would benefit from their use.

For the past 9 years, I have interviewed the president of the American Academy of Orthopaedic Surgeons (AAOS) to better understand the roles the AAOS and its president play in our professional lives.

At the 2015 AAOS Annual Meeting in Las Vegas this past March, David D. Teuscher, MD, assumed leadership of the AAOS as its 83rd president. Dr. Teuscher is a partner and past president of the Beaumont Bone & Joint Institute in Beaumont, Texas, and has had a broad experience in leadership positions in both Texas medical professional societies and the AAOS. Dr. Teuscher obtained his undergraduate degree from the University of Illinois at Champaign/Urbana and his medical degree from the University of Texas Medical School at San Antonio. He completed his orthopedic residency at the Brooke Army Medical Center, in Fort Sam Houston, and, following 13 years of military service, he entered private practice in 1993.

He has led numerous AAOS committees over the years, most notably the team that in 2014 completed a revision of the AAOS Strategic Plan, “Vision 20/20,” which outlines the Academy’s goals over the next 6 years, including the following elements:

• AAOS Mission: Serving our profession to provide the highest-quality musculoskeletal care.
• AAOS Vision: Keeping the world in motion through the prevention and treatment of musculoskeletal conditions.
• Core Values: Excellence, Professionalism, Leadership, Collegiality, Lifelong Learning.
• Strategic Domains: Advocacy, Education, Membership, Organizational Excellence, Quality and Patient Value.

Read more at: http://www.aaos.org/about/strategicplan.asp.

Dr. Teuscher explained that his role as president for the coming year is really that of spokesperson for a leadership group that has developed a 4-year presidential line and governance structure to ensure a solid platform for continuity and to achieve the goals of the AAOS Strategic Plan year after year. While the Academy president does not set his or her own agenda for the year, David has several priority goals during his tenure, which include ensuring that the rules governing the repeal and replacement of the Medicare Sustainable Growth Rate (SGR) formula treat our patients fairly, opening of the new digital and modular Orthopaedic Learning Center (OLC), preventing the harmful effects of unnecessary and premature ICD-10 (International Classification of Diseases, Tenth Revision) implementation, leading a cultural change in surgical patient safety, and advances in AAOS technology offerings in education and online lifelong learning.

Dr. Teuscher stated that the repeal of the SGR formula this year was a major step forward for orthopedic surgeons. Averting a 21% reduction in physician reimbursement in 2015, the new legislation will increase physician payments by 0.5% annually through 2019, at which time the Centers for Medicare and Medicaid Services (CMS) will begin a new payment system, based not on the traditional fee-for-service model, but on a new incentive: the quality and value of care.¹ David firmly believes that the AAOS has a major role to assist the practicing orthopedic surgeon manage this new payment system by:

• establishing standards of performance and quality that will drive payment for medical services.
• helping the practicing orthopedic surgeon report useful quality outcomes in a simple and accessible format.
• linking these new reporting measures to satisfy Maintenance of Certification (MOC) requirements.

David is especially proud of the recently opened OLC. This cutting-edge facility, sponsored by the AAOS and its equity partners (Arthroscopy Association of North America, American Orthopaedic Society for Sports Medicine, American Association of Hip and Knee Surgeons, OLC), is clear evidence of the Academy’s commitment to the highest quality of musculoskeletal care and lifelong learning for its members.

Dr. Teuscher is concerned that CMS may not be fully prepared for implementation of the new ICD-10 codes on October 1, 2015. In the spirit of advocacy for its members, the AAOS is actively engaged to recommend delay of ICD-10 implementation until reliable operating systems to process this new system can be ensured.

David and orthopedic patient safety experts are working with national perioperative stakeholders to plan and implement a National Surgical Patient Safety Summit in 2016. This will cause a cultural change in how we lead treatment teams to deliver a highly reliable and safe surgical experience for all our patients.

Finally, Dr. Teuscher is extremely excited about improvements in technology offered to Academy members. Many of us enjoyed the new AAOS My Academy app available this year at the Las Vegas meeting that enabled review of the 2015 program on your smartphone. Dr. Teuscher anticipates that upgrades to the AAOS Access app will provide the most comprehensive mobile platform for continuing medical education and educational videos available to all Academy members. The AAOS website is undergoing a complete update and expansion of offerings by the end of this year.

Over the years of interviewing current presidents of the AAOS, I have been impressed by consistent characteristics of our leaders: enormously energetic, engaging, articulate, and tirelessly committed to the Academy and its members. David Teuscher processes all these qualities. We are very fortunate to have someone of David’s organizational and leadership skills navigate our course through the turbulent health care waters that lie ahead of us in the coming years.◾

For the past 9 years, I have interviewed the president of the American Academy of Orthopaedic Surgeons (AAOS) to better understand the roles the AAOS and its president play in our professional lives.

At the 2015 AAOS Annual Meeting in Las Vegas this past March, David D. Teuscher, MD, assumed leadership of the AAOS as its 83rd president. Dr. Teuscher is a partner and past president of the Beaumont Bone & Joint Institute in Beaumont, Texas, and has had a broad experience in leadership positions in both Texas medical professional societies and the AAOS. Dr. Teuscher obtained his undergraduate degree from the University of Illinois at Champaign/Urbana and his medical degree from the University of Texas Medical School at San Antonio. He completed his orthopedic residency at the Brooke Army Medical Center, in Fort Sam Houston, and, following 13 years of military service, he entered private practice in 1993.

He has led numerous AAOS committees over the years, most notably the team that in 2014 completed a revision of the AAOS Strategic Plan, “Vision 20/20,” which outlines the Academy’s goals over the next 6 years, including the following elements:

• AAOS Mission: Serving our profession to provide the highest-quality musculoskeletal care.
• AAOS Vision: Keeping the world in motion through the prevention and treatment of musculoskeletal conditions.
• Core Values: Excellence, Professionalism, Leadership, Collegiality, Lifelong Learning.
• Strategic Domains: Advocacy, Education, Membership, Organizational Excellence, Quality and Patient Value.

Read more at: http://www.aaos.org/about/strategicplan.asp.

Dr. Teuscher explained that his role as president for the coming year is really that of spokesperson for a leadership group that has developed a 4-year presidential line and governance structure to ensure a solid platform for continuity and to achieve the goals of the AAOS Strategic Plan year after year. While the Academy president does not set his or her own agenda for the year, David has several priority goals during his tenure, which include ensuring that the rules governing the repeal and replacement of the Medicare Sustainable Growth Rate (SGR) formula treat our patients fairly, opening of the new digital and modular Orthopaedic Learning Center (OLC), preventing the harmful effects of unnecessary and premature ICD-10 (International Classification of Diseases, Tenth Revision) implementation, leading a cultural change in surgical patient safety, and advances in AAOS technology offerings in education and online lifelong learning.

Dr. Teuscher stated that the repeal of the SGR formula this year was a major step forward for orthopedic surgeons. Averting a 21% reduction in physician reimbursement in 2015, the new legislation will increase physician payments by 0.5% annually through 2019, at which time the Centers for Medicare and Medicaid Services (CMS) will begin a new payment system, based not on the traditional fee-for-service model, but on a new incentive: the quality and value of care.¹ David firmly believes that the AAOS has a major role to assist the practicing orthopedic surgeon manage this new payment system by:

• establishing standards of performance and quality that will drive payment for medical services.
• helping the practicing orthopedic surgeon report useful quality outcomes in a simple and accessible format.
• linking these new reporting measures to satisfy Maintenance of Certification (MOC) requirements.

David is especially proud of the recently opened OLC. This cutting-edge facility, sponsored by the AAOS and its equity partners (Arthroscopy Association of North America, American Orthopaedic Society for Sports Medicine, American Association of Hip and Knee Surgeons, OLC), is clear evidence of the Academy’s commitment to the highest quality of musculoskeletal care and lifelong learning for its members.

Dr. Teuscher is concerned that CMS may not be fully prepared for implementation of the new ICD-10 codes on October 1, 2015. In the spirit of advocacy for its members, the AAOS is actively engaged to recommend delay of ICD-10 implementation until reliable operating systems to process this new system can be ensured.

David and orthopedic patient safety experts are working with national perioperative stakeholders to plan and implement a National Surgical Patient Safety Summit in 2016. This will cause a cultural change in how we lead treatment teams to deliver a highly reliable and safe surgical experience for all our patients.

Finally, Dr. Teuscher is extremely excited about improvements in technology offered to Academy members. Many of us enjoyed the new AAOS My Academy app available this year at the Las Vegas meeting that enabled review of the 2015 program on your smartphone. Dr. Teuscher anticipates that upgrades to the AAOS Access app will provide the most comprehensive mobile platform for continuing medical education and educational videos available to all Academy members. The AAOS website is undergoing a complete update and expansion of offerings by the end of this year.

Over the years of interviewing current presidents of the AAOS, I have been impressed by consistent characteristics of our leaders: enormously energetic, engaging, articulate, and tirelessly committed to the Academy and its members. David Teuscher processes all these qualities. We are very fortunate to have someone of David’s organizational and leadership skills navigate our course through the turbulent health care waters that lie ahead of us in the coming years.◾

For the past 9 years, I have interviewed the president of the American Academy of Orthopaedic Surgeons (AAOS) to better understand the roles the AAOS and its president play in our professional lives.

At the 2015 AAOS Annual Meeting in Las Vegas this past March, David D. Teuscher, MD, assumed leadership of the AAOS as its 83rd president. Dr. Teuscher is a partner and past president of the Beaumont Bone & Joint Institute in Beaumont, Texas, and has had a broad experience in leadership positions in both Texas medical professional societies and the AAOS. Dr. Teuscher obtained his undergraduate degree from the University of Illinois at Champaign/Urbana and his medical degree from the University of Texas Medical School at San Antonio. He completed his orthopedic residency at the Brooke Army Medical Center, in Fort Sam Houston, and, following 13 years of military service, he entered private practice in 1993.

He has led numerous AAOS committees over the years, most notably the team that in 2014 completed a revision of the AAOS Strategic Plan, “Vision 20/20,” which outlines the Academy’s goals over the next 6 years, including the following elements:

• AAOS Mission: Serving our profession to provide the highest-quality musculoskeletal care.
• AAOS Vision: Keeping the world in motion through the prevention and treatment of musculoskeletal conditions.
• Core Values: Excellence, Professionalism, Leadership, Collegiality, Lifelong Learning.
• Strategic Domains: Advocacy, Education, Membership, Organizational Excellence, Quality and Patient Value.

Read more at: http://www.aaos.org/about/strategicplan.asp.

Dr. Teuscher explained that his role as president for the coming year is really that of spokesperson for a leadership group that has developed a 4-year presidential line and governance structure to ensure a solid platform for continuity and to achieve the goals of the AAOS Strategic Plan year after year. While the Academy president does not set his or her own agenda for the year, David has several priority goals during his tenure, which include ensuring that the rules governing the repeal and replacement of the Medicare Sustainable Growth Rate (SGR) formula treat our patients fairly, opening of the new digital and modular Orthopaedic Learning Center (OLC), preventing the harmful effects of unnecessary and premature ICD-10 (International Classification of Diseases, Tenth Revision) implementation, leading a cultural change in surgical patient safety, and advances in AAOS technology offerings in education and online lifelong learning.

Dr. Teuscher stated that the repeal of the SGR formula this year was a major step forward for orthopedic surgeons. Averting a 21% reduction in physician reimbursement in 2015, the new legislation will increase physician payments by 0.5% annually through 2019, at which time the Centers for Medicare and Medicaid Services (CMS) will begin a new payment system, based not on the traditional fee-for-service model, but on a new incentive: the quality and value of care.¹ David firmly believes that the AAOS has a major role to assist the practicing orthopedic surgeon manage this new payment system by:

• establishing standards of performance and quality that will drive payment for medical services.
• helping the practicing orthopedic surgeon report useful quality outcomes in a simple and accessible format.
• linking these new reporting measures to satisfy Maintenance of Certification (MOC) requirements.

David is especially proud of the recently opened OLC. This cutting-edge facility, sponsored by the AAOS and its equity partners (Arthroscopy Association of North America, American Orthopaedic Society for Sports Medicine, American Association of Hip and Knee Surgeons, OLC), is clear evidence of the Academy’s commitment to the highest quality of musculoskeletal care and lifelong learning for its members.

Dr. Teuscher is concerned that CMS may not be fully prepared for implementation of the new ICD-10 codes on October 1, 2015. In the spirit of advocacy for its members, the AAOS is actively engaged to recommend delay of ICD-10 implementation until reliable operating systems to process this new system can be ensured.

David and orthopedic patient safety experts are working with national perioperative stakeholders to plan and implement a National Surgical Patient Safety Summit in 2016. This will cause a cultural change in how we lead treatment teams to deliver a highly reliable and safe surgical experience for all our patients.

Finally, Dr. Teuscher is extremely excited about improvements in technology offered to Academy members. Many of us enjoyed the new AAOS My Academy app available this year at the Las Vegas meeting that enabled review of the 2015 program on your smartphone. Dr. Teuscher anticipates that upgrades to the AAOS Access app will provide the most comprehensive mobile platform for continuing medical education and educational videos available to all Academy members. The AAOS website is undergoing a complete update and expansion of offerings by the end of this year.

Over the years of interviewing current presidents of the AAOS, I have been impressed by consistent characteristics of our leaders: enormously energetic, engaging, articulate, and tirelessly committed to the Academy and its members. David Teuscher processes all these qualities. We are very fortunate to have someone of David’s organizational and leadership skills navigate our course through the turbulent health care waters that lie ahead of us in the coming years.◾

First-line treatments for osteoarthritis (OA) are targeted at the inflammatory reaction that occurs after breakdown of articular cartilage through regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, or surgical intervention. Associated activity restrictions and chronic pain have spurred a search for alternative treatments, commonly daily supplements such as glucosamine, chondroitin, and fish oil, to name a select few of the innumerable products reported to benefit patients with OA.

Background

Fish oil is 1 of the 2 most popular supplements among patients with OA. However, its effectiveness and precise benefit are still debated,^1,2 and there is confusion about the definition of the product, the nature of investigations into its effectiveness, and the standardization of research unique to OA. Most fish oil research relates to patients with rheumatoid arthritis (RA). The anti-inflammatory benefits seen in patients with RA are generally applied to characterize fish oils as anti-inflammatory agents with a logical benefit in reducing OA symptoms. However, there is a dearth of independent and focused clinical results justifying that assumption. Further, lack of federal regulation of the supplement industry hinders conducting generalizable studies regarding medical benefit in a regulated and verified dose and form.³

The benefits of fish oil in RA treatment are well supported and accepted. In patients with RA, daily fish oil supplementation has been shown to reduce use of other medications and improve pain scores reported by both physicians and patients.^4-10 The clinical efficacy of fish oil use in RA has been determined to be “reasonably strong,” with multiple studies confirming suppression of inflammatory cytokines in vitro and in vivo.^11,12 The mechanism by which the inflammatory processes are augmented by fish oil supplementation suggests potential benefit to patients with OA, though review articles as recent as 2011 have concluded that research in that capacity is not sufficient to warrant recommendation.^13,14

Most studies of OA-specific use of fish oils have been conducted in in vitro models. Treatment of bovine chondrocytes with omega-3 fatty acids causes reductions in inflammatory markers induced by interleukin 1, one of several proinflammatory cytokines that induce inflammation in OA at the gene and plasma levels, and these reductions have been reproduced.^15-17 Although a preventive benefit was found in a study of pig medial collateral ligament fibroblasts, findings of later studies have been inconsistent.¹⁸ It also appears that fish oils may alter lipid composition in membranes, favoring incorporation of anti-inflammatory precursor n-3 fatty acids over proinflammatory precursor n-6 fatty acids in these model systems.^19,20

Animal in vivo models have also been used to describe the effects of fish oil supplementation on OA. Assessment of dogs with OA before and after supplementation with the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) revealed improvement in clinical signs observed by owners, improvement in weight-bearing measured by veterinary clinicians, and decreased use of NSAIDs.^21-24

Fish oil studies using osteoarthritic cartilage samples harvested during surgical procedures have demonstrated results consistent with other model systems described thus far. They have demonstrated a dose-dependent decrease in induced inflammatory destruction of tissue associated with fish oil supplementation. In addition, finding a lack of cellular toxicity, they have validated the safety of supplements.^25,26 Proposed but unproven mechanisms for the anti-inflammatory actions of EPA and DHA include competition with n-6 fatty acids; presence of resolvins (anti-inflammatory molecules derived from EPA and DHA); presence of n-3 products that compete with proinflammatory molecules for receptors; reduction in gene expression of cytokines, cyclo-oxygenase 2, and degrading proteinases; interference in the signaling pathways of inflammation; and reduction in lymphocyte proliferation.^26,27

Reduction in the n-6/n-3 ratio has been correlated with reduced inflammatory conditions such as OA, stemming from the epidemiologic evidence that higher n-3 intake in Eastern diets and lower intake of n-6 result in a lower incidence of these diseases.^18,28,29 Studies have found sufficient evidence to suggest that this ratio has a role in OA, though not sufficient to recommend supplement use over diet modification.¹⁹ One study demonstrated an ability to favorably alter bone marrow lipid composition with n-3 fatty acid supplementation.¹⁰

The evidence leads to a conclusion of anti-inflammatory benefits from fish oils in these abstracted models. The multitude of basic science studies conducted on the anti-inflammatory properties of omega-3 fatty acids, only briefly reviewed here, supports the potential benefits colloquially ascribed to fish oil in the treatment of OA yet also implies the need for human clinical trials to address these properties clinically.

We reviewed the literature to address claims that fish oil supplementation can prevent or decrease severity of OA. We hypothesized there would be insufficient clinical studies to justify recommending supplementation to patients. Of note, the degree of heterogeneity in the evidence precluded performing a meta-analysis with any statistical validity.

Literature Review

In the PubMed database, we targeted the subject of fish oils and OA by using search terms that included omega-3, DHA, EPA, and alpha-linolenic acid. The MedLine and Google Scholar databases were searched as well. Results were limited to those reported in English and involving human subjects and clinical trials; results were excluded if they primarily involved patients with RA. Studies cited or mentioned in articles found through the PubMed search were evaluated according to the criteria mentioned, such that all relevant articles available at time of search are thought to be included, and these articles represent a reasonable presentation of the available evidence.

Findings

Our search revealed 6 clinical trials in which omega-3–containing supplements were used in the treatment of human OA with differing endpoints. We reviewed these trials in detail. One study, which used alteration of bone marrow lipids as an endpoint, was included for completeness of the evaluation of the relevant evidence.²⁰ In addition, the study by Wang and colleagues,³⁰ who assessed patients without clinical evidence of OA for development of bone marrow lesions, was reviewed. This study was deemed relevant to examine the process by which n-3 fatty acids alter knee structure, as subsequent risk of OA has not been elucidated, and effects on bone marrow lesions may indeed have a direct impact on the OA process. Results of the trials that were identified were varied between no significant difference in OA symptoms between treatment and control groups, implied benefits, and substantial benefits.

The first clinical study of omega-3 supplementation in OA treatment was conducted in 1992.³¹ The study compared 10 g of cod liver oil (containing 786 mg of EPA) with 10 g of olive oil, both taken daily over 24 weeks by 86 patients with OA. Effects were assessed by NSAID use (recorded in patient diary) and pain score (evaluated by clinician) every 4 weeks. The trial found no significant difference in effects between the oils.

Wang and colleagues³⁰ used a food questionnaire to measure the n-3 intake of 293 healthy adults and quantified their bone marrow lesions after 10 years in an effort to describe how n-3 intake correlates with development of OA or pre-OA lesions. Higher intake of n-6 fatty acids was positively associated with presence of bone marrow lesions; n-3 intake had no association.

In a study of 84 patients who had joint replacement, Pritchett²⁰ evaluated lipid alterations resulting from a regimen of 3 g of fish oil containing 11% DHA daily for a 6-month trial period, measuring lipids before and after the trial period. Pritchett²⁰ found a 20% increase in long-chain fatty acids and a corresponding decrease in saturated fatty acids, as measured in bone marrow.

The supplement Phytalgic (Phythea Laboratories), which is advertised for OA, includes n-3 fatty acids, n-6 fatty acids, extract from Urtica dioica (the common nettle), zinc, and vitamin E. In a study by Jacquet and colleagues,³² this supplement was given 3 times daily over 3 separate 4-week periods to 81 patients with knee or hip OA. Measuring NSAID use with patient diaries and assessing pain with the WOMAC (Western Ontario and McMaster Universities) Osteoarthritis Index every 4 weeks for 12 weeks, the authors found a significant decrease in NSAID use and, according to WOMAC results, a more than 50% reduction in pain and stiffness, and improved function.

One study compared the effects of glucosamine with and without omega-3 fatty acids in 182 patients with knee or hip OA.³³ Each day, patients took 500 mg of glucosamine plus 3 capsules each containing either 444 mg of omega-3 fatty acids or 444 mg of an oil mixture. Pain was assessed with visual analog scale and the WOMAC scale 3 times over the 26-week study. More than 90% reductions in morning stiffness and pain were found for the combination of fish oil and glucosamine.

The Multicenter Osteoarthritis Study (MOST), published in February 2012, demonstrated that plasma levels of n-3 and n-6 polyunsaturated fatty acids (PUFAs) may be related to knee structural findings.³⁴ This study confirmed that dietary modification of n-3 and n-6 PUFAs altered plasma concentration predictably. Higher DHA intake was associated with less evidence of OA on patellofemoral cartilage, though no association was found on tibiofemoral cartilage.³⁴

Discussion

The lack of human clinical trials detailing the effects of fish oil supplementation in patients with OA is arguably the most significant hindrance to fish oil being routinely recommended. Since 1992, only 6 studies have addressed this topic, and their endpoints and results were inconsistent. These interventional trials had their limitations, including short duration, insufficient dosage, inappropriate n-3 choice, dietary interactions, genotype, and medication interactions.¹⁸ The present review is limited as well, by the quantity of evidence on the topic and by the focus (of the majority of the studies) on short-term alterations in pain and mobility instead of on disease-modifying potential. Short-term evaluation is unlikely to capture such an effect, which may require long-term supplementation to become evident.

The results of the study by Stammers and colleagues³¹ must be examined critically, as the likelihood of detection bias is high. Highly subjective assessments of effect, lack of standardized NSAID treatments, and limitations in patient numbers and disease severity raise concerns about validity. In addition, confounding variables (eg, medication interactions, alternative treatments, olive oil use) undermine the design. It is therefore difficult to interpret the results of this trial.

The study by Wang and colleagues³⁰ did not involve supplementation, and intake was assessed only with food frequency questionnaires. It is therefore difficult to apply their results or findings to this review. In addition, the authors did not obtain baseline magnetic resonance imaging for comparison with that obtained at study completion—that is, they did not address any subclinical disease before dietary recording.

Pritchett²⁰ acknowledged study limitations of small sample size and use of 1 subject as both patient and control. Although the study seemed to demonstrate that omega-3 supplementation augmented the lipid profile of joints, it did not directly demonstrate improvement in or prevention of OA. Identification of bone marrow lesions is not definitive proof of OA but an alteration that may correlate with development. The logical supposition is that altering the local environment may alter development of disease within that environment, though this is not proven.

An article reviewing the Phytalgic study highlighted the suspect nature of its results—claims that the supplement is 76% more effective than gold-standard corticosteroid injection.³⁵ Also highlighted were lack of confirmed mechanism, questionable control, detection bias caused by aftertaste, and the high attrition rate in the placebo group. It is difficult to apply these results to fish oil supplementation, as Phytalgic contains other potentially confounding substances.

Of note, the findings of MOST were observational; n-3 and n-6 levels were not altered or supplemented. Altered disease process was demonstrated in patellofemoral cartilage but not in tibiofemoral cartilage in the same patient. The inconsistencies may be explained by the observational nature of the study and the lack of supplementation that would have produced a more significant increase in n-3 PUFA levels and thus more uniform conclusions, if in fact n-3 PUFAs were the significant factor in the altered cartilage structure. Although supportive of a preventive or disease-altering benefit, the results do not speak to supplementation.

Perhaps the most convincing evidence supporting fish oil for OA comes from a 2009 study by Gruenwald and colleagues.³³ However, this 2-supplement study addressing synergy was financed by Seven Seas, a company with industry ties. The study was not placebo-controlled and was registered only after completion. The authors omitted baseline values, apparently did not correct for baseline in the statistical analysis, and did not report the distribution of results. The implication is that the results were overstated, or that, at minimum, the supporting data were not reported. Nevertheless, this study demonstrated benefits consistent with the animal and human laboratory studies. However, research is needed to repeat and validate these results, elucidate the mechanism of action, and quantify the benefit unique to fish oil.

Conclusion

Despite the overwhelming popularity of fish oil supplements and the assumption of benefit for patients with arthritis, there appears to be insufficient clinical evidence to justify use of fish oils in the treatment or prevention of OA. Possible efficacy in laboratory and animal studies has yet to be sufficiently observed and verified in clinical trials. Although it is impossible to refute the promise of these agents as beneficial adjuncts to anti-inflammatory regimens, there remains a need for significant, well-designed clinical trials to evaluate the efficacy, safety, and clinical parameters of omega-3 fatty acids in a standardized form before they can in good faith be recommended to patients with OA.

First-line treatments for osteoarthritis (OA) are targeted at the inflammatory reaction that occurs after breakdown of articular cartilage through regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, or surgical intervention. Associated activity restrictions and chronic pain have spurred a search for alternative treatments, commonly daily supplements such as glucosamine, chondroitin, and fish oil, to name a select few of the innumerable products reported to benefit patients with OA.

Background

Fish oil is 1 of the 2 most popular supplements among patients with OA. However, its effectiveness and precise benefit are still debated,^1,2 and there is confusion about the definition of the product, the nature of investigations into its effectiveness, and the standardization of research unique to OA. Most fish oil research relates to patients with rheumatoid arthritis (RA). The anti-inflammatory benefits seen in patients with RA are generally applied to characterize fish oils as anti-inflammatory agents with a logical benefit in reducing OA symptoms. However, there is a dearth of independent and focused clinical results justifying that assumption. Further, lack of federal regulation of the supplement industry hinders conducting generalizable studies regarding medical benefit in a regulated and verified dose and form.³

The benefits of fish oil in RA treatment are well supported and accepted. In patients with RA, daily fish oil supplementation has been shown to reduce use of other medications and improve pain scores reported by both physicians and patients.^4-10 The clinical efficacy of fish oil use in RA has been determined to be “reasonably strong,” with multiple studies confirming suppression of inflammatory cytokines in vitro and in vivo.^11,12 The mechanism by which the inflammatory processes are augmented by fish oil supplementation suggests potential benefit to patients with OA, though review articles as recent as 2011 have concluded that research in that capacity is not sufficient to warrant recommendation.^13,14

Most studies of OA-specific use of fish oils have been conducted in in vitro models. Treatment of bovine chondrocytes with omega-3 fatty acids causes reductions in inflammatory markers induced by interleukin 1, one of several proinflammatory cytokines that induce inflammation in OA at the gene and plasma levels, and these reductions have been reproduced.^15-17 Although a preventive benefit was found in a study of pig medial collateral ligament fibroblasts, findings of later studies have been inconsistent.¹⁸ It also appears that fish oils may alter lipid composition in membranes, favoring incorporation of anti-inflammatory precursor n-3 fatty acids over proinflammatory precursor n-6 fatty acids in these model systems.^19,20

Animal in vivo models have also been used to describe the effects of fish oil supplementation on OA. Assessment of dogs with OA before and after supplementation with the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) revealed improvement in clinical signs observed by owners, improvement in weight-bearing measured by veterinary clinicians, and decreased use of NSAIDs.^21-24

Fish oil studies using osteoarthritic cartilage samples harvested during surgical procedures have demonstrated results consistent with other model systems described thus far. They have demonstrated a dose-dependent decrease in induced inflammatory destruction of tissue associated with fish oil supplementation. In addition, finding a lack of cellular toxicity, they have validated the safety of supplements.^25,26 Proposed but unproven mechanisms for the anti-inflammatory actions of EPA and DHA include competition with n-6 fatty acids; presence of resolvins (anti-inflammatory molecules derived from EPA and DHA); presence of n-3 products that compete with proinflammatory molecules for receptors; reduction in gene expression of cytokines, cyclo-oxygenase 2, and degrading proteinases; interference in the signaling pathways of inflammation; and reduction in lymphocyte proliferation.^26,27

Reduction in the n-6/n-3 ratio has been correlated with reduced inflammatory conditions such as OA, stemming from the epidemiologic evidence that higher n-3 intake in Eastern diets and lower intake of n-6 result in a lower incidence of these diseases.^18,28,29 Studies have found sufficient evidence to suggest that this ratio has a role in OA, though not sufficient to recommend supplement use over diet modification.¹⁹ One study demonstrated an ability to favorably alter bone marrow lipid composition with n-3 fatty acid supplementation.¹⁰

The evidence leads to a conclusion of anti-inflammatory benefits from fish oils in these abstracted models. The multitude of basic science studies conducted on the anti-inflammatory properties of omega-3 fatty acids, only briefly reviewed here, supports the potential benefits colloquially ascribed to fish oil in the treatment of OA yet also implies the need for human clinical trials to address these properties clinically.

We reviewed the literature to address claims that fish oil supplementation can prevent or decrease severity of OA. We hypothesized there would be insufficient clinical studies to justify recommending supplementation to patients. Of note, the degree of heterogeneity in the evidence precluded performing a meta-analysis with any statistical validity.

Literature Review

In the PubMed database, we targeted the subject of fish oils and OA by using search terms that included omega-3, DHA, EPA, and alpha-linolenic acid. The MedLine and Google Scholar databases were searched as well. Results were limited to those reported in English and involving human subjects and clinical trials; results were excluded if they primarily involved patients with RA. Studies cited or mentioned in articles found through the PubMed search were evaluated according to the criteria mentioned, such that all relevant articles available at time of search are thought to be included, and these articles represent a reasonable presentation of the available evidence.

Findings

Our search revealed 6 clinical trials in which omega-3–containing supplements were used in the treatment of human OA with differing endpoints. We reviewed these trials in detail. One study, which used alteration of bone marrow lipids as an endpoint, was included for completeness of the evaluation of the relevant evidence.²⁰ In addition, the study by Wang and colleagues,³⁰ who assessed patients without clinical evidence of OA for development of bone marrow lesions, was reviewed. This study was deemed relevant to examine the process by which n-3 fatty acids alter knee structure, as subsequent risk of OA has not been elucidated, and effects on bone marrow lesions may indeed have a direct impact on the OA process. Results of the trials that were identified were varied between no significant difference in OA symptoms between treatment and control groups, implied benefits, and substantial benefits.

The first clinical study of omega-3 supplementation in OA treatment was conducted in 1992.³¹ The study compared 10 g of cod liver oil (containing 786 mg of EPA) with 10 g of olive oil, both taken daily over 24 weeks by 86 patients with OA. Effects were assessed by NSAID use (recorded in patient diary) and pain score (evaluated by clinician) every 4 weeks. The trial found no significant difference in effects between the oils.

Wang and colleagues³⁰ used a food questionnaire to measure the n-3 intake of 293 healthy adults and quantified their bone marrow lesions after 10 years in an effort to describe how n-3 intake correlates with development of OA or pre-OA lesions. Higher intake of n-6 fatty acids was positively associated with presence of bone marrow lesions; n-3 intake had no association.

In a study of 84 patients who had joint replacement, Pritchett²⁰ evaluated lipid alterations resulting from a regimen of 3 g of fish oil containing 11% DHA daily for a 6-month trial period, measuring lipids before and after the trial period. Pritchett²⁰ found a 20% increase in long-chain fatty acids and a corresponding decrease in saturated fatty acids, as measured in bone marrow.

The supplement Phytalgic (Phythea Laboratories), which is advertised for OA, includes n-3 fatty acids, n-6 fatty acids, extract from Urtica dioica (the common nettle), zinc, and vitamin E. In a study by Jacquet and colleagues,³² this supplement was given 3 times daily over 3 separate 4-week periods to 81 patients with knee or hip OA. Measuring NSAID use with patient diaries and assessing pain with the WOMAC (Western Ontario and McMaster Universities) Osteoarthritis Index every 4 weeks for 12 weeks, the authors found a significant decrease in NSAID use and, according to WOMAC results, a more than 50% reduction in pain and stiffness, and improved function.

One study compared the effects of glucosamine with and without omega-3 fatty acids in 182 patients with knee or hip OA.³³ Each day, patients took 500 mg of glucosamine plus 3 capsules each containing either 444 mg of omega-3 fatty acids or 444 mg of an oil mixture. Pain was assessed with visual analog scale and the WOMAC scale 3 times over the 26-week study. More than 90% reductions in morning stiffness and pain were found for the combination of fish oil and glucosamine.

The Multicenter Osteoarthritis Study (MOST), published in February 2012, demonstrated that plasma levels of n-3 and n-6 polyunsaturated fatty acids (PUFAs) may be related to knee structural findings.³⁴ This study confirmed that dietary modification of n-3 and n-6 PUFAs altered plasma concentration predictably. Higher DHA intake was associated with less evidence of OA on patellofemoral cartilage, though no association was found on tibiofemoral cartilage.³⁴

Discussion

The lack of human clinical trials detailing the effects of fish oil supplementation in patients with OA is arguably the most significant hindrance to fish oil being routinely recommended. Since 1992, only 6 studies have addressed this topic, and their endpoints and results were inconsistent. These interventional trials had their limitations, including short duration, insufficient dosage, inappropriate n-3 choice, dietary interactions, genotype, and medication interactions.¹⁸ The present review is limited as well, by the quantity of evidence on the topic and by the focus (of the majority of the studies) on short-term alterations in pain and mobility instead of on disease-modifying potential. Short-term evaluation is unlikely to capture such an effect, which may require long-term supplementation to become evident.

The results of the study by Stammers and colleagues³¹ must be examined critically, as the likelihood of detection bias is high. Highly subjective assessments of effect, lack of standardized NSAID treatments, and limitations in patient numbers and disease severity raise concerns about validity. In addition, confounding variables (eg, medication interactions, alternative treatments, olive oil use) undermine the design. It is therefore difficult to interpret the results of this trial.

The study by Wang and colleagues³⁰ did not involve supplementation, and intake was assessed only with food frequency questionnaires. It is therefore difficult to apply their results or findings to this review. In addition, the authors did not obtain baseline magnetic resonance imaging for comparison with that obtained at study completion—that is, they did not address any subclinical disease before dietary recording.

Pritchett²⁰ acknowledged study limitations of small sample size and use of 1 subject as both patient and control. Although the study seemed to demonstrate that omega-3 supplementation augmented the lipid profile of joints, it did not directly demonstrate improvement in or prevention of OA. Identification of bone marrow lesions is not definitive proof of OA but an alteration that may correlate with development. The logical supposition is that altering the local environment may alter development of disease within that environment, though this is not proven.

An article reviewing the Phytalgic study highlighted the suspect nature of its results—claims that the supplement is 76% more effective than gold-standard corticosteroid injection.³⁵ Also highlighted were lack of confirmed mechanism, questionable control, detection bias caused by aftertaste, and the high attrition rate in the placebo group. It is difficult to apply these results to fish oil supplementation, as Phytalgic contains other potentially confounding substances.

Of note, the findings of MOST were observational; n-3 and n-6 levels were not altered or supplemented. Altered disease process was demonstrated in patellofemoral cartilage but not in tibiofemoral cartilage in the same patient. The inconsistencies may be explained by the observational nature of the study and the lack of supplementation that would have produced a more significant increase in n-3 PUFA levels and thus more uniform conclusions, if in fact n-3 PUFAs were the significant factor in the altered cartilage structure. Although supportive of a preventive or disease-altering benefit, the results do not speak to supplementation.

Perhaps the most convincing evidence supporting fish oil for OA comes from a 2009 study by Gruenwald and colleagues.³³ However, this 2-supplement study addressing synergy was financed by Seven Seas, a company with industry ties. The study was not placebo-controlled and was registered only after completion. The authors omitted baseline values, apparently did not correct for baseline in the statistical analysis, and did not report the distribution of results. The implication is that the results were overstated, or that, at minimum, the supporting data were not reported. Nevertheless, this study demonstrated benefits consistent with the animal and human laboratory studies. However, research is needed to repeat and validate these results, elucidate the mechanism of action, and quantify the benefit unique to fish oil.

Conclusion

Despite the overwhelming popularity of fish oil supplements and the assumption of benefit for patients with arthritis, there appears to be insufficient clinical evidence to justify use of fish oils in the treatment or prevention of OA. Possible efficacy in laboratory and animal studies has yet to be sufficiently observed and verified in clinical trials. Although it is impossible to refute the promise of these agents as beneficial adjuncts to anti-inflammatory regimens, there remains a need for significant, well-designed clinical trials to evaluate the efficacy, safety, and clinical parameters of omega-3 fatty acids in a standardized form before they can in good faith be recommended to patients with OA.

First-line treatments for osteoarthritis (OA) are targeted at the inflammatory reaction that occurs after breakdown of articular cartilage through regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroid injections, or surgical intervention. Associated activity restrictions and chronic pain have spurred a search for alternative treatments, commonly daily supplements such as glucosamine, chondroitin, and fish oil, to name a select few of the innumerable products reported to benefit patients with OA.

Background

Fish oil is 1 of the 2 most popular supplements among patients with OA. However, its effectiveness and precise benefit are still debated,^1,2 and there is confusion about the definition of the product, the nature of investigations into its effectiveness, and the standardization of research unique to OA. Most fish oil research relates to patients with rheumatoid arthritis (RA). The anti-inflammatory benefits seen in patients with RA are generally applied to characterize fish oils as anti-inflammatory agents with a logical benefit in reducing OA symptoms. However, there is a dearth of independent and focused clinical results justifying that assumption. Further, lack of federal regulation of the supplement industry hinders conducting generalizable studies regarding medical benefit in a regulated and verified dose and form.³

The benefits of fish oil in RA treatment are well supported and accepted. In patients with RA, daily fish oil supplementation has been shown to reduce use of other medications and improve pain scores reported by both physicians and patients.^4-10 The clinical efficacy of fish oil use in RA has been determined to be “reasonably strong,” with multiple studies confirming suppression of inflammatory cytokines in vitro and in vivo.^11,12 The mechanism by which the inflammatory processes are augmented by fish oil supplementation suggests potential benefit to patients with OA, though review articles as recent as 2011 have concluded that research in that capacity is not sufficient to warrant recommendation.^13,14

Most studies of OA-specific use of fish oils have been conducted in in vitro models. Treatment of bovine chondrocytes with omega-3 fatty acids causes reductions in inflammatory markers induced by interleukin 1, one of several proinflammatory cytokines that induce inflammation in OA at the gene and plasma levels, and these reductions have been reproduced.^15-17 Although a preventive benefit was found in a study of pig medial collateral ligament fibroblasts, findings of later studies have been inconsistent.¹⁸ It also appears that fish oils may alter lipid composition in membranes, favoring incorporation of anti-inflammatory precursor n-3 fatty acids over proinflammatory precursor n-6 fatty acids in these model systems.^19,20

Animal in vivo models have also been used to describe the effects of fish oil supplementation on OA. Assessment of dogs with OA before and after supplementation with the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) revealed improvement in clinical signs observed by owners, improvement in weight-bearing measured by veterinary clinicians, and decreased use of NSAIDs.^21-24

Fish oil studies using osteoarthritic cartilage samples harvested during surgical procedures have demonstrated results consistent with other model systems described thus far. They have demonstrated a dose-dependent decrease in induced inflammatory destruction of tissue associated with fish oil supplementation. In addition, finding a lack of cellular toxicity, they have validated the safety of supplements.^25,26 Proposed but unproven mechanisms for the anti-inflammatory actions of EPA and DHA include competition with n-6 fatty acids; presence of resolvins (anti-inflammatory molecules derived from EPA and DHA); presence of n-3 products that compete with proinflammatory molecules for receptors; reduction in gene expression of cytokines, cyclo-oxygenase 2, and degrading proteinases; interference in the signaling pathways of inflammation; and reduction in lymphocyte proliferation.^26,27

Reduction in the n-6/n-3 ratio has been correlated with reduced inflammatory conditions such as OA, stemming from the epidemiologic evidence that higher n-3 intake in Eastern diets and lower intake of n-6 result in a lower incidence of these diseases.^18,28,29 Studies have found sufficient evidence to suggest that this ratio has a role in OA, though not sufficient to recommend supplement use over diet modification.¹⁹ One study demonstrated an ability to favorably alter bone marrow lipid composition with n-3 fatty acid supplementation.¹⁰

The evidence leads to a conclusion of anti-inflammatory benefits from fish oils in these abstracted models. The multitude of basic science studies conducted on the anti-inflammatory properties of omega-3 fatty acids, only briefly reviewed here, supports the potential benefits colloquially ascribed to fish oil in the treatment of OA yet also implies the need for human clinical trials to address these properties clinically.

We reviewed the literature to address claims that fish oil supplementation can prevent or decrease severity of OA. We hypothesized there would be insufficient clinical studies to justify recommending supplementation to patients. Of note, the degree of heterogeneity in the evidence precluded performing a meta-analysis with any statistical validity.

Literature Review

In the PubMed database, we targeted the subject of fish oils and OA by using search terms that included omega-3, DHA, EPA, and alpha-linolenic acid. The MedLine and Google Scholar databases were searched as well. Results were limited to those reported in English and involving human subjects and clinical trials; results were excluded if they primarily involved patients with RA. Studies cited or mentioned in articles found through the PubMed search were evaluated according to the criteria mentioned, such that all relevant articles available at time of search are thought to be included, and these articles represent a reasonable presentation of the available evidence.

Findings

Our search revealed 6 clinical trials in which omega-3–containing supplements were used in the treatment of human OA with differing endpoints. We reviewed these trials in detail. One study, which used alteration of bone marrow lipids as an endpoint, was included for completeness of the evaluation of the relevant evidence.²⁰ In addition, the study by Wang and colleagues,³⁰ who assessed patients without clinical evidence of OA for development of bone marrow lesions, was reviewed. This study was deemed relevant to examine the process by which n-3 fatty acids alter knee structure, as subsequent risk of OA has not been elucidated, and effects on bone marrow lesions may indeed have a direct impact on the OA process. Results of the trials that were identified were varied between no significant difference in OA symptoms between treatment and control groups, implied benefits, and substantial benefits.

The first clinical study of omega-3 supplementation in OA treatment was conducted in 1992.³¹ The study compared 10 g of cod liver oil (containing 786 mg of EPA) with 10 g of olive oil, both taken daily over 24 weeks by 86 patients with OA. Effects were assessed by NSAID use (recorded in patient diary) and pain score (evaluated by clinician) every 4 weeks. The trial found no significant difference in effects between the oils.

Wang and colleagues³⁰ used a food questionnaire to measure the n-3 intake of 293 healthy adults and quantified their bone marrow lesions after 10 years in an effort to describe how n-3 intake correlates with development of OA or pre-OA lesions. Higher intake of n-6 fatty acids was positively associated with presence of bone marrow lesions; n-3 intake had no association.

In a study of 84 patients who had joint replacement, Pritchett²⁰ evaluated lipid alterations resulting from a regimen of 3 g of fish oil containing 11% DHA daily for a 6-month trial period, measuring lipids before and after the trial period. Pritchett²⁰ found a 20% increase in long-chain fatty acids and a corresponding decrease in saturated fatty acids, as measured in bone marrow.

The supplement Phytalgic (Phythea Laboratories), which is advertised for OA, includes n-3 fatty acids, n-6 fatty acids, extract from Urtica dioica (the common nettle), zinc, and vitamin E. In a study by Jacquet and colleagues,³² this supplement was given 3 times daily over 3 separate 4-week periods to 81 patients with knee or hip OA. Measuring NSAID use with patient diaries and assessing pain with the WOMAC (Western Ontario and McMaster Universities) Osteoarthritis Index every 4 weeks for 12 weeks, the authors found a significant decrease in NSAID use and, according to WOMAC results, a more than 50% reduction in pain and stiffness, and improved function.

One study compared the effects of glucosamine with and without omega-3 fatty acids in 182 patients with knee or hip OA.³³ Each day, patients took 500 mg of glucosamine plus 3 capsules each containing either 444 mg of omega-3 fatty acids or 444 mg of an oil mixture. Pain was assessed with visual analog scale and the WOMAC scale 3 times over the 26-week study. More than 90% reductions in morning stiffness and pain were found for the combination of fish oil and glucosamine.

The Multicenter Osteoarthritis Study (MOST), published in February 2012, demonstrated that plasma levels of n-3 and n-6 polyunsaturated fatty acids (PUFAs) may be related to knee structural findings.³⁴ This study confirmed that dietary modification of n-3 and n-6 PUFAs altered plasma concentration predictably. Higher DHA intake was associated with less evidence of OA on patellofemoral cartilage, though no association was found on tibiofemoral cartilage.³⁴

Discussion

The lack of human clinical trials detailing the effects of fish oil supplementation in patients with OA is arguably the most significant hindrance to fish oil being routinely recommended. Since 1992, only 6 studies have addressed this topic, and their endpoints and results were inconsistent. These interventional trials had their limitations, including short duration, insufficient dosage, inappropriate n-3 choice, dietary interactions, genotype, and medication interactions.¹⁸ The present review is limited as well, by the quantity of evidence on the topic and by the focus (of the majority of the studies) on short-term alterations in pain and mobility instead of on disease-modifying potential. Short-term evaluation is unlikely to capture such an effect, which may require long-term supplementation to become evident.

The results of the study by Stammers and colleagues³¹ must be examined critically, as the likelihood of detection bias is high. Highly subjective assessments of effect, lack of standardized NSAID treatments, and limitations in patient numbers and disease severity raise concerns about validity. In addition, confounding variables (eg, medication interactions, alternative treatments, olive oil use) undermine the design. It is therefore difficult to interpret the results of this trial.

The study by Wang and colleagues³⁰ did not involve supplementation, and intake was assessed only with food frequency questionnaires. It is therefore difficult to apply their results or findings to this review. In addition, the authors did not obtain baseline magnetic resonance imaging for comparison with that obtained at study completion—that is, they did not address any subclinical disease before dietary recording.

Pritchett²⁰ acknowledged study limitations of small sample size and use of 1 subject as both patient and control. Although the study seemed to demonstrate that omega-3 supplementation augmented the lipid profile of joints, it did not directly demonstrate improvement in or prevention of OA. Identification of bone marrow lesions is not definitive proof of OA but an alteration that may correlate with development. The logical supposition is that altering the local environment may alter development of disease within that environment, though this is not proven.

An article reviewing the Phytalgic study highlighted the suspect nature of its results—claims that the supplement is 76% more effective than gold-standard corticosteroid injection.³⁵ Also highlighted were lack of confirmed mechanism, questionable control, detection bias caused by aftertaste, and the high attrition rate in the placebo group. It is difficult to apply these results to fish oil supplementation, as Phytalgic contains other potentially confounding substances.

Of note, the findings of MOST were observational; n-3 and n-6 levels were not altered or supplemented. Altered disease process was demonstrated in patellofemoral cartilage but not in tibiofemoral cartilage in the same patient. The inconsistencies may be explained by the observational nature of the study and the lack of supplementation that would have produced a more significant increase in n-3 PUFA levels and thus more uniform conclusions, if in fact n-3 PUFAs were the significant factor in the altered cartilage structure. Although supportive of a preventive or disease-altering benefit, the results do not speak to supplementation.

Perhaps the most convincing evidence supporting fish oil for OA comes from a 2009 study by Gruenwald and colleagues.³³ However, this 2-supplement study addressing synergy was financed by Seven Seas, a company with industry ties. The study was not placebo-controlled and was registered only after completion. The authors omitted baseline values, apparently did not correct for baseline in the statistical analysis, and did not report the distribution of results. The implication is that the results were overstated, or that, at minimum, the supporting data were not reported. Nevertheless, this study demonstrated benefits consistent with the animal and human laboratory studies. However, research is needed to repeat and validate these results, elucidate the mechanism of action, and quantify the benefit unique to fish oil.

Conclusion

Despite the overwhelming popularity of fish oil supplements and the assumption of benefit for patients with arthritis, there appears to be insufficient clinical evidence to justify use of fish oils in the treatment or prevention of OA. Possible efficacy in laboratory and animal studies has yet to be sufficiently observed and verified in clinical trials. Although it is impossible to refute the promise of these agents as beneficial adjuncts to anti-inflammatory regimens, there remains a need for significant, well-designed clinical trials to evaluate the efficacy, safety, and clinical parameters of omega-3 fatty acids in a standardized form before they can in good faith be recommended to patients with OA.