Recent knee injuries spark rapid cascade to joint failure

PARIS – Recent knee injuries are strongly associated with accelerated knee osteoarthritis, according to an analysis from the prospective, multicenter Osteoarthritis Initiative.

"Certain injuries may initiate or coincide with an accelerated cascade towards joint failure in as little as 12 months," Jeffrey Driban, Ph.D., said at the World Congress on Osteoarthritis. "In fact, 76% of individuals with an injury and accelerated knee osteoarthritis experienced their injury in the 12 months prior to the study outcome."

The study defined accelerated knee OA as progression from a Kellgren-Lawrence grade 0 or 1 on baseline bilateral radiographs to end-stage KL grade 3 or 4 within 48 months.

Although knee OA typically has been a slowly progressive disorder, 5%-17% of patients now experience accelerated forms of OA.

"If we can better characterize this phenomenon and its potential risk factors, we can provide more insights into the nature of progression in hopes of identifying an at-risk subset," said Dr. Driban of the division of rheumatology at Tufts Medical Center, Boston.

The study by Dr. Driban and his colleagues was published in Arthritis Care & Research (2014 April 29 [doi:10.1002/acr.22359]).

A total of 1,930 participants in the Osteoarthritis Initiative, all with a KL grade of 0 or 1 on baseline bilateral radiographs, were asked at baseline and at each annual visit whether they had ever been "injured enough to limit ability to walk for at least 2 days."

On follow-up, 1,325 had no knee OA, 54 had accelerated knee OA, and 187 had typical knee OA, defined as at least one knee increased in radiographic scoring within 48 months (excluding accelerated OA).

After exclusion of 12 patients with missing data, 30% of the accelerated OA group, 28% in the typical OA group, and 35% in the no OA group had a history of knee injury before baseline. A new knee injury was reported by 32%, 13%, and 11%, respectively, with data missing from 59 persons.

In univariate analyses, participants with accelerated knee OA were significantly older than were those with typical OA or no OA (61.8 years vs. 58 years vs. 59.2 years; P = .023) and had a greater body mass index (28.9 kg/m² vs. 27.9 kg/m² vs. 27.1 kg/m²; P = .002), Dr. Driban said.

In multinomial logistic regression analyses that adjusted for age, sex, BMI, presence of static knee malalignment, and systolic blood pressure, there was no association between prior knee injury and accelerated OA (odds ratio, 0.84) or typical OA (OR, 0.76).

However, when the investigators looked further, participants with accelerated OA were almost 3.5 times more likely to report a recent knee injury during the observation period (OR, 3.37; 95% confidence interval, 1.82-6.25) than were those with typical OA (OR, 0.99) or no OA (reference), he said.

Moreover, if a participant experienced a knee injury 1 year before the study outcome, the risk of accelerated OA increased ninefold (OR, 9.22; CI, 4.50-18.90) versus threefold for typical OA (OR, 3.04; CI, 1.66-5.58).

Despite the focus on injuries leading to accelerated OA, the analyses can’t rule out that accelerated OA may also cause an injury or that there could be a "vicious cycle," in which an injury can cause accelerated OA, associated with joint space loss, increased symptoms, and increased risk for subsequent injury, Dr. Driban said.

This line of thought helps explain why prior injury was not associated with accelerated knee OA, but recent injury was. As patients were free of radiographic OA at baseline, those with a history of a prior injury that could cause accelerated knee OA would already have been eliminated from the study, he explained in an interview.

Secondly, if accelerated knee OA can increase the risk of injury, knee injuries from years ago would not be related to accelerated knee OA because the disorder did not exist at the time of the injury.

Finally, there also could be a recall bias, as patients often have a hard time recalling injuries that may have happened years ago.

Despite the limitations of self-reported injuries and insufficient data regarding the type, severity, status of the meniscus, mechanism, or subsequent treatment of the knee injury, the findings represent an important "starting point" in understanding the association between injuries and accelerated osteoarthritis, Dr. Driban said.

"We need to monitor older adults who report an injury, as this may initiate accelerated OA or indicate an individual experiencing accelerated OA, and we need to determine which injuries may be related to accelerated osteoarthritis," he said at the meeting, sponsored by the Osteoarthritis Research Society International.

During the discussion following the formal presentation, Dr. David Felson, professor of medicine and epidemiology at Boston University, said, "I think what you are saying is exactly right," but suggested that the investigators exclude patients with spontaneous osteonecrosis of the knee and osteochondritis dissecans, as both conditions are more common than anticipated and can drive very rapid development of OA. Conversely, inclusion of patients with osteophyte-only knee OA would increase the number likely identified with accelerated OA, he said.

Dr. Driban reported no conflicting interests.

[email protected]

PARIS – Recent knee injuries are strongly associated with accelerated knee osteoarthritis, according to an analysis from the prospective, multicenter Osteoarthritis Initiative.

"Certain injuries may initiate or coincide with an accelerated cascade towards joint failure in as little as 12 months," Jeffrey Driban, Ph.D., said at the World Congress on Osteoarthritis. "In fact, 76% of individuals with an injury and accelerated knee osteoarthritis experienced their injury in the 12 months prior to the study outcome."

The study defined accelerated knee OA as progression from a Kellgren-Lawrence grade 0 or 1 on baseline bilateral radiographs to end-stage KL grade 3 or 4 within 48 months.

Although knee OA typically has been a slowly progressive disorder, 5%-17% of patients now experience accelerated forms of OA.

"If we can better characterize this phenomenon and its potential risk factors, we can provide more insights into the nature of progression in hopes of identifying an at-risk subset," said Dr. Driban of the division of rheumatology at Tufts Medical Center, Boston.

The study by Dr. Driban and his colleagues was published in Arthritis Care & Research (2014 April 29 [doi:10.1002/acr.22359]).

A total of 1,930 participants in the Osteoarthritis Initiative, all with a KL grade of 0 or 1 on baseline bilateral radiographs, were asked at baseline and at each annual visit whether they had ever been "injured enough to limit ability to walk for at least 2 days."

On follow-up, 1,325 had no knee OA, 54 had accelerated knee OA, and 187 had typical knee OA, defined as at least one knee increased in radiographic scoring within 48 months (excluding accelerated OA).

After exclusion of 12 patients with missing data, 30% of the accelerated OA group, 28% in the typical OA group, and 35% in the no OA group had a history of knee injury before baseline. A new knee injury was reported by 32%, 13%, and 11%, respectively, with data missing from 59 persons.

In univariate analyses, participants with accelerated knee OA were significantly older than were those with typical OA or no OA (61.8 years vs. 58 years vs. 59.2 years; P = .023) and had a greater body mass index (28.9 kg/m² vs. 27.9 kg/m² vs. 27.1 kg/m²; P = .002), Dr. Driban said.

In multinomial logistic regression analyses that adjusted for age, sex, BMI, presence of static knee malalignment, and systolic blood pressure, there was no association between prior knee injury and accelerated OA (odds ratio, 0.84) or typical OA (OR, 0.76).

However, when the investigators looked further, participants with accelerated OA were almost 3.5 times more likely to report a recent knee injury during the observation period (OR, 3.37; 95% confidence interval, 1.82-6.25) than were those with typical OA (OR, 0.99) or no OA (reference), he said.

Moreover, if a participant experienced a knee injury 1 year before the study outcome, the risk of accelerated OA increased ninefold (OR, 9.22; CI, 4.50-18.90) versus threefold for typical OA (OR, 3.04; CI, 1.66-5.58).

Despite the focus on injuries leading to accelerated OA, the analyses can’t rule out that accelerated OA may also cause an injury or that there could be a "vicious cycle," in which an injury can cause accelerated OA, associated with joint space loss, increased symptoms, and increased risk for subsequent injury, Dr. Driban said.

This line of thought helps explain why prior injury was not associated with accelerated knee OA, but recent injury was. As patients were free of radiographic OA at baseline, those with a history of a prior injury that could cause accelerated knee OA would already have been eliminated from the study, he explained in an interview.

Secondly, if accelerated knee OA can increase the risk of injury, knee injuries from years ago would not be related to accelerated knee OA because the disorder did not exist at the time of the injury.

Finally, there also could be a recall bias, as patients often have a hard time recalling injuries that may have happened years ago.

Despite the limitations of self-reported injuries and insufficient data regarding the type, severity, status of the meniscus, mechanism, or subsequent treatment of the knee injury, the findings represent an important "starting point" in understanding the association between injuries and accelerated osteoarthritis, Dr. Driban said.

"We need to monitor older adults who report an injury, as this may initiate accelerated OA or indicate an individual experiencing accelerated OA, and we need to determine which injuries may be related to accelerated osteoarthritis," he said at the meeting, sponsored by the Osteoarthritis Research Society International.

During the discussion following the formal presentation, Dr. David Felson, professor of medicine and epidemiology at Boston University, said, "I think what you are saying is exactly right," but suggested that the investigators exclude patients with spontaneous osteonecrosis of the knee and osteochondritis dissecans, as both conditions are more common than anticipated and can drive very rapid development of OA. Conversely, inclusion of patients with osteophyte-only knee OA would increase the number likely identified with accelerated OA, he said.

Dr. Driban reported no conflicting interests.

[email protected]

PARIS – Recent knee injuries are strongly associated with accelerated knee osteoarthritis, according to an analysis from the prospective, multicenter Osteoarthritis Initiative.

"Certain injuries may initiate or coincide with an accelerated cascade towards joint failure in as little as 12 months," Jeffrey Driban, Ph.D., said at the World Congress on Osteoarthritis. "In fact, 76% of individuals with an injury and accelerated knee osteoarthritis experienced their injury in the 12 months prior to the study outcome."

The study defined accelerated knee OA as progression from a Kellgren-Lawrence grade 0 or 1 on baseline bilateral radiographs to end-stage KL grade 3 or 4 within 48 months.

Although knee OA typically has been a slowly progressive disorder, 5%-17% of patients now experience accelerated forms of OA.

"If we can better characterize this phenomenon and its potential risk factors, we can provide more insights into the nature of progression in hopes of identifying an at-risk subset," said Dr. Driban of the division of rheumatology at Tufts Medical Center, Boston.

The study by Dr. Driban and his colleagues was published in Arthritis Care & Research (2014 April 29 [doi:10.1002/acr.22359]).

A total of 1,930 participants in the Osteoarthritis Initiative, all with a KL grade of 0 or 1 on baseline bilateral radiographs, were asked at baseline and at each annual visit whether they had ever been "injured enough to limit ability to walk for at least 2 days."

On follow-up, 1,325 had no knee OA, 54 had accelerated knee OA, and 187 had typical knee OA, defined as at least one knee increased in radiographic scoring within 48 months (excluding accelerated OA).

After exclusion of 12 patients with missing data, 30% of the accelerated OA group, 28% in the typical OA group, and 35% in the no OA group had a history of knee injury before baseline. A new knee injury was reported by 32%, 13%, and 11%, respectively, with data missing from 59 persons.

In univariate analyses, participants with accelerated knee OA were significantly older than were those with typical OA or no OA (61.8 years vs. 58 years vs. 59.2 years; P = .023) and had a greater body mass index (28.9 kg/m² vs. 27.9 kg/m² vs. 27.1 kg/m²; P = .002), Dr. Driban said.

In multinomial logistic regression analyses that adjusted for age, sex, BMI, presence of static knee malalignment, and systolic blood pressure, there was no association between prior knee injury and accelerated OA (odds ratio, 0.84) or typical OA (OR, 0.76).

However, when the investigators looked further, participants with accelerated OA were almost 3.5 times more likely to report a recent knee injury during the observation period (OR, 3.37; 95% confidence interval, 1.82-6.25) than were those with typical OA (OR, 0.99) or no OA (reference), he said.

Moreover, if a participant experienced a knee injury 1 year before the study outcome, the risk of accelerated OA increased ninefold (OR, 9.22; CI, 4.50-18.90) versus threefold for typical OA (OR, 3.04; CI, 1.66-5.58).

Despite the focus on injuries leading to accelerated OA, the analyses can’t rule out that accelerated OA may also cause an injury or that there could be a "vicious cycle," in which an injury can cause accelerated OA, associated with joint space loss, increased symptoms, and increased risk for subsequent injury, Dr. Driban said.

This line of thought helps explain why prior injury was not associated with accelerated knee OA, but recent injury was. As patients were free of radiographic OA at baseline, those with a history of a prior injury that could cause accelerated knee OA would already have been eliminated from the study, he explained in an interview.

Secondly, if accelerated knee OA can increase the risk of injury, knee injuries from years ago would not be related to accelerated knee OA because the disorder did not exist at the time of the injury.

Finally, there also could be a recall bias, as patients often have a hard time recalling injuries that may have happened years ago.

Despite the limitations of self-reported injuries and insufficient data regarding the type, severity, status of the meniscus, mechanism, or subsequent treatment of the knee injury, the findings represent an important "starting point" in understanding the association between injuries and accelerated osteoarthritis, Dr. Driban said.

"We need to monitor older adults who report an injury, as this may initiate accelerated OA or indicate an individual experiencing accelerated OA, and we need to determine which injuries may be related to accelerated osteoarthritis," he said at the meeting, sponsored by the Osteoarthritis Research Society International.

During the discussion following the formal presentation, Dr. David Felson, professor of medicine and epidemiology at Boston University, said, "I think what you are saying is exactly right," but suggested that the investigators exclude patients with spontaneous osteonecrosis of the knee and osteochondritis dissecans, as both conditions are more common than anticipated and can drive very rapid development of OA. Conversely, inclusion of patients with osteophyte-only knee OA would increase the number likely identified with accelerated OA, he said.

Dr. Driban reported no conflicting interests.

[email protected]