Patellofemoral OA After ACL Reconstruction
Patellofemoral OA After ACL Reconstruction
The present study provides unique insights into the individual contribution of patellofemoral and tibiofemoral OA severity to symptoms and functional performance after ACLR. Patellofemoral OA (47%) was more common than tibiofemoral OA (31%) 5–10 years after ACLR, with OA being frequently isolated to the patellofemoral joint (20%). This compartmental distribution pattern of OA reflects previous community-based studies and is identical to the reported prevalence from BPTB ACLR, suggesting that a HT autograft does not protect the patellofemoral joint from degenerative change. Our recent literature review proposed a number of explanations for the high rate of patellofemoral OA after ACLR, including concomitant damage to the patellofemoral compartment at the time of injury, which we confirmed in the current study and altered frontal and transverse plane knee kinematics, which we observed in our recent kinematic study. While it is possible that knee movement restrictions and prolonged quadriceps weakness also contribute to patellofemoral OA development, we did not observe any movement deficits in those with patellofemoral OA and muscle strength was not specifically evaluated. The prevalence of tibiofemoral OA in our study is similar to that in other studies with a 5-year to 10-year follow-up of HT ACLR. Lower rates of patellofemoral and tibiofemoral OA after ACLR have also been reported in the literature, which most likely reflect the different radiological methods and structural features of OA assessed. We chose to define OA using the OARSI atlas because other classification systems are limited to the tibiofemoral joint or JSN. It is also possible that the high prevalence of OA in our study may relate to the older age (mean 35 years) at surgery of our cohort, especially as our results ( Table 1 ) support previous findings that older age at ACLR predicts OA.
Debate surrounds the impact of radiographic knee OA severity on pain and function. We found that KOOS-pain was influenced by combined compartmental disease severity, while subscales such as KOOS-symptoms and KOOS-QOL were influenced by increasing patellofemoral OA severity alone. Not unexpectedly, worse score on the AKPS, used predominantly for patellofemoral pain conditions, was only associated with increasing patellofemoral disease severity. The KOOS-ADL subscale was not associated with severity of OA in either compartment, which may partly relate to this subscale's measurement properties. The KOOS-ADL subscale was the only one that did not satisfy the regression assumptions due to its large ceiling effect, a feature observed in other studies. The greater association of patellofemoral OA severity with most patient-reported outcomes, even when tibiofemoral changes were accounted for, may reflect the findings in community-based studies, which suggest that the patellofemoral joint may be a more potent source of knee OA symptoms than the tibiofemoral joint. It is possible that, for people who have undergone ACLR, interventions targeting the patellofemoral joint may have a greater impact on KOOS-symptoms and KOOS-QOL than those targeting the tibiofemoral joint. Considering the bias of ACLR rehabilitation programmes towards addressing tibiofemoral symptoms and function, further investigation is required.
Patellofemoral OA severity was independently associated with poorer performance on all three functional tasks. One factor that may underpin this finding is quadriceps strength. Although we did not measure quadriceps strength, patellofemoral OA and associated structural features have been associated with lower quadriceps function. Furthermore, any quadriceps strength benefits of a HT, compared to BPTB autografts, resolve at 12 months postsurgery with no difference observed up to 10 years postsurgery. Therefore, it is plausible that quadriceps weakness was a feature of patellofemoral OA after HT autograft, contributing to decreased performance on the functional tasks. The probability of radiographic OA progression in these individuals could be heightened by quadriceps weakness.
Patellofemoral chondral injuries noted at surgery significantly increased the odds of patellofemoral OA at the 5-year to 10-year follow-up, which is consistent with previous reports. In contrast, we found no association between chondral injuries and tibiofemoral OA. Owing to our relatively low numbers, further larger studies are needed to confirm the presence or absence of associations between tibiofemoral chondral lesions and OA, particularly in the lateral compartment where we observed large CIs. This is important, since previous studies provide conflicting results on the association between chondral damage and tibiofemoral OA. Our results support previous reports of an association between medial meniscectomy and tibiofemoral OA in the respective compartment, but not an association with lateral meniscectomy. However, we did not confirm previous findings of an association between meniscectomy and patellofemoral OA following ACL injury. The association between meniscal injury and long-term patellofemoral OA development is likely to be mediated by other factors, such as altered loading patterns, that require further investigation.
We observed that those who underwent an early ACLR developed less patellofemoral OA than those who waited 1 year or more for an ACLR. This relationship was not observed in the tibiofemoral compartment. Our findings are consistent with previous reports of a relationship between patellofemoral OA and cartilage damage and longer duration from injury to ACLR. While this may indicate that surgical delay is suboptimal for patellofemoral joint health, the patellofemoral cartilage has been shown to continue to deteriorate despite an ACLR and randomised controlled trials are required to determine whether reconstruction reduces the long-term development of patellofemoral OA.
Physical activity assessed with the Tegner Activity Scale was lower in those with knee OA (median 4) compared to those free of OA (median 5). While measuring and quantifying physical activity remains a challenge, post hoc analysis revealed that the difference in Tegner scores was mostly observed in those with tibiofemoral OA, as those with patellofemoral OA did not differ in activity level from those with no OA (data not presented). Physical activity may protect the patellofemoral joint of uninjured knees by decreasing the rate of patellar cartilage volume loss over time. However, Neuman et al found that individuals with patellofemoral OA 15 years after ACLR rated higher on the Tegner Activity Scale than those with no OA. Physical activity levels before and after ACLR, as well as the extent of postoperative rehabilitation performed, may be confounding factors in the development of patellofemoral OA. However, owing to the retrospective nature of the current study, no data on these factors were available. Perhaps staying physically active is a risk factor for patellofemoral OA after ACLR because of the altered patellofemoral loading patterns that occur after injury and persist following ACLR.
The present study has limitations. While participants were self-selected, which may have resulted in a selection bias towards those with more symptoms and functional limitations, the OA prevalence was similar to previous reports. The relatively large number of invitation letters that did not reach potential participants (n=105, 14%) occurred due to individuals changing address since surgery, which is common in individuals of this age group. Although not strictly interval data, for the purposes of evaluating their relative contribution to symptoms and function, tibiofemoral and patellofemoral OA severity were treated as such in the regression models. Furthermore, this was a cross-sectional study, and thus we did not have information on baseline (preinjury or pre-ACLR) radiographic status. It is possible that the presence of OA in this cohort may have been pre-existing and not associated with the ACL injury or reconstruction. However, no overt degeneration was observed arthroscopically at the time of ACLR, and the rate of patellofemoral and tibiofemoral OA found in the current study is much higher than that observed in the uninjured contralateral knee of patients 12 years after ACLR of a similar age (2.5% and 15%, respectively), making it unlikely that the prevalence of OA was independent of ACLR. Considering our findings of high patellofemoral OA, future prospective studies evaluating the development of OA after ACLR should also investigate the patellofemoral joint.
Orthopaedic and sports medicine clinicians should be aware of the high prevalence of patellofemoral OA (47%) and tibiofemoral OA (31%), 5–10 years after HT autograft ACLR. Importantly, patellofemoral OA severity was associated with worse symptoms and decreased functional performance, independent of tibiofemoral OA severity. Although most radiographic changes observed in the patellofemoral joint were mild, clinicians should consider the patellofemoral joint during postoperative rehabilitation, in an attempt to address long-term symptoms and degenerative joint disease.
Discussion
The present study provides unique insights into the individual contribution of patellofemoral and tibiofemoral OA severity to symptoms and functional performance after ACLR. Patellofemoral OA (47%) was more common than tibiofemoral OA (31%) 5–10 years after ACLR, with OA being frequently isolated to the patellofemoral joint (20%). This compartmental distribution pattern of OA reflects previous community-based studies and is identical to the reported prevalence from BPTB ACLR, suggesting that a HT autograft does not protect the patellofemoral joint from degenerative change. Our recent literature review proposed a number of explanations for the high rate of patellofemoral OA after ACLR, including concomitant damage to the patellofemoral compartment at the time of injury, which we confirmed in the current study and altered frontal and transverse plane knee kinematics, which we observed in our recent kinematic study. While it is possible that knee movement restrictions and prolonged quadriceps weakness also contribute to patellofemoral OA development, we did not observe any movement deficits in those with patellofemoral OA and muscle strength was not specifically evaluated. The prevalence of tibiofemoral OA in our study is similar to that in other studies with a 5-year to 10-year follow-up of HT ACLR. Lower rates of patellofemoral and tibiofemoral OA after ACLR have also been reported in the literature, which most likely reflect the different radiological methods and structural features of OA assessed. We chose to define OA using the OARSI atlas because other classification systems are limited to the tibiofemoral joint or JSN. It is also possible that the high prevalence of OA in our study may relate to the older age (mean 35 years) at surgery of our cohort, especially as our results ( Table 1 ) support previous findings that older age at ACLR predicts OA.
Debate surrounds the impact of radiographic knee OA severity on pain and function. We found that KOOS-pain was influenced by combined compartmental disease severity, while subscales such as KOOS-symptoms and KOOS-QOL were influenced by increasing patellofemoral OA severity alone. Not unexpectedly, worse score on the AKPS, used predominantly for patellofemoral pain conditions, was only associated with increasing patellofemoral disease severity. The KOOS-ADL subscale was not associated with severity of OA in either compartment, which may partly relate to this subscale's measurement properties. The KOOS-ADL subscale was the only one that did not satisfy the regression assumptions due to its large ceiling effect, a feature observed in other studies. The greater association of patellofemoral OA severity with most patient-reported outcomes, even when tibiofemoral changes were accounted for, may reflect the findings in community-based studies, which suggest that the patellofemoral joint may be a more potent source of knee OA symptoms than the tibiofemoral joint. It is possible that, for people who have undergone ACLR, interventions targeting the patellofemoral joint may have a greater impact on KOOS-symptoms and KOOS-QOL than those targeting the tibiofemoral joint. Considering the bias of ACLR rehabilitation programmes towards addressing tibiofemoral symptoms and function, further investigation is required.
Patellofemoral OA severity was independently associated with poorer performance on all three functional tasks. One factor that may underpin this finding is quadriceps strength. Although we did not measure quadriceps strength, patellofemoral OA and associated structural features have been associated with lower quadriceps function. Furthermore, any quadriceps strength benefits of a HT, compared to BPTB autografts, resolve at 12 months postsurgery with no difference observed up to 10 years postsurgery. Therefore, it is plausible that quadriceps weakness was a feature of patellofemoral OA after HT autograft, contributing to decreased performance on the functional tasks. The probability of radiographic OA progression in these individuals could be heightened by quadriceps weakness.
Patellofemoral chondral injuries noted at surgery significantly increased the odds of patellofemoral OA at the 5-year to 10-year follow-up, which is consistent with previous reports. In contrast, we found no association between chondral injuries and tibiofemoral OA. Owing to our relatively low numbers, further larger studies are needed to confirm the presence or absence of associations between tibiofemoral chondral lesions and OA, particularly in the lateral compartment where we observed large CIs. This is important, since previous studies provide conflicting results on the association between chondral damage and tibiofemoral OA. Our results support previous reports of an association between medial meniscectomy and tibiofemoral OA in the respective compartment, but not an association with lateral meniscectomy. However, we did not confirm previous findings of an association between meniscectomy and patellofemoral OA following ACL injury. The association between meniscal injury and long-term patellofemoral OA development is likely to be mediated by other factors, such as altered loading patterns, that require further investigation.
We observed that those who underwent an early ACLR developed less patellofemoral OA than those who waited 1 year or more for an ACLR. This relationship was not observed in the tibiofemoral compartment. Our findings are consistent with previous reports of a relationship between patellofemoral OA and cartilage damage and longer duration from injury to ACLR. While this may indicate that surgical delay is suboptimal for patellofemoral joint health, the patellofemoral cartilage has been shown to continue to deteriorate despite an ACLR and randomised controlled trials are required to determine whether reconstruction reduces the long-term development of patellofemoral OA.
Physical activity assessed with the Tegner Activity Scale was lower in those with knee OA (median 4) compared to those free of OA (median 5). While measuring and quantifying physical activity remains a challenge, post hoc analysis revealed that the difference in Tegner scores was mostly observed in those with tibiofemoral OA, as those with patellofemoral OA did not differ in activity level from those with no OA (data not presented). Physical activity may protect the patellofemoral joint of uninjured knees by decreasing the rate of patellar cartilage volume loss over time. However, Neuman et al found that individuals with patellofemoral OA 15 years after ACLR rated higher on the Tegner Activity Scale than those with no OA. Physical activity levels before and after ACLR, as well as the extent of postoperative rehabilitation performed, may be confounding factors in the development of patellofemoral OA. However, owing to the retrospective nature of the current study, no data on these factors were available. Perhaps staying physically active is a risk factor for patellofemoral OA after ACLR because of the altered patellofemoral loading patterns that occur after injury and persist following ACLR.
The present study has limitations. While participants were self-selected, which may have resulted in a selection bias towards those with more symptoms and functional limitations, the OA prevalence was similar to previous reports. The relatively large number of invitation letters that did not reach potential participants (n=105, 14%) occurred due to individuals changing address since surgery, which is common in individuals of this age group. Although not strictly interval data, for the purposes of evaluating their relative contribution to symptoms and function, tibiofemoral and patellofemoral OA severity were treated as such in the regression models. Furthermore, this was a cross-sectional study, and thus we did not have information on baseline (preinjury or pre-ACLR) radiographic status. It is possible that the presence of OA in this cohort may have been pre-existing and not associated with the ACL injury or reconstruction. However, no overt degeneration was observed arthroscopically at the time of ACLR, and the rate of patellofemoral and tibiofemoral OA found in the current study is much higher than that observed in the uninjured contralateral knee of patients 12 years after ACLR of a similar age (2.5% and 15%, respectively), making it unlikely that the prevalence of OA was independent of ACLR. Considering our findings of high patellofemoral OA, future prospective studies evaluating the development of OA after ACLR should also investigate the patellofemoral joint.
Orthopaedic and sports medicine clinicians should be aware of the high prevalence of patellofemoral OA (47%) and tibiofemoral OA (31%), 5–10 years after HT autograft ACLR. Importantly, patellofemoral OA severity was associated with worse symptoms and decreased functional performance, independent of tibiofemoral OA severity. Although most radiographic changes observed in the patellofemoral joint were mild, clinicians should consider the patellofemoral joint during postoperative rehabilitation, in an attempt to address long-term symptoms and degenerative joint disease.
