In this study, using MOAKS, we found the pre-ACLR waiting period length was positively associated with MM extrusion, medial cartilage loss, and medial and lateral osteophyte formation. There were significant moderate correlations between the pre-ACLR waiting period and medial and lateral osteophyte formation, PFJ osteophyte formation, and cartilage loss. This indicates that degenerative changes progress with the passing of time from ACL injury.
The general mechanism of OA progression after ACL injury is as follows: First, joint instability leads to secondary meniscal abnormalities. Later, meniscal extrusion occurs, and the area of femoral and tibial cartilage contact increases, causing joint instability and overload with cartilage degeneration. Subsequently, inflammation is induced in the synovium in the knee joint, leading to osteophyte formation, and tibiofemoral joint deformity.[11],[12],[13] These early changes are radiographically occult.
Various OA scoring systems using MRI have emerged in recent years. Scoring systems such as WORMS and BLOKS have been well-established and are widely used, but both instruments have certain limitations. For example, the WORMS method mixes multiple different constructs in meniscal scoring, and BLOKS is cumbersome and complex.[14],[15],[16] MOAKS has been developed from WORMS and BLOKS to improve semi-quantitative scoring and has been reported as highly reliable. MOAKS has been used in several recent studies.[17],[7],[18]
Several MRI studies evaluating early OA changes in meniscal morphology and cartilage degeneration have been published.[19],[20] To the best of our knowledge, there has been no study comparing MOAKS pre- and post-ACLR. In this study, early knee OA was easily quantified using MOAKS in ACL-injured knees .
The occurrence and progression of OA is known as a long-term complication after ACL injury or reconstruction. Barenius et al. reported that if ACL injury is treated conservatively, 20% of cases had KL grade 3 OA changes on X-ray in 10 years, and 60% cases had KL grade 2 OA changes on X-ray in 15 years.[11] Potter et al reported risk of cartilage loss doubled from year 1 for the lateral compartment and medial femoral condyle and tripled for the patella. By years 7 to 11, the risk for the lateral femoral condyle was 50 times baseline, 30 times for the patella, and 19 times for the medial femoral condyle using morphologic MRI and quantitative T2 mapping.[21] In our study, MOAKS revealed early OA changes in 34 cases after 20.5 ± 6.3 months from ACL injury, with a significant correlation between waiting period and OA progression. In other words, knee OA after ACL injury progresses gradually the time of injury. OA changes are irreversible. Over the past few years, regenerative treatments for articular cartilage and meniscus are advancing rapidly, but there is insufficient evidence that they avoid knee OA changes.[22] So an approach that treats ACL injuries early would allow less time for OA progression. Several studies have recommended early ACL reconstruction after ACL injury for this reason.[12] Nishida et al have confirmed a phenomenon in which the relative position of the tibia with respect to the femur shifts anteriorly as the waiting time from ACL injury to reconstruction increases.[23] In addition, rotational instability and joint laxity increased one year after ACL injury, which may be complicated by meniscal injury.[24] OA progression in ACL injured knees is thought to be due to meniscal or other soft tissue injuries and ligamentous laxity. Early ACLR within 6 months to 1 year of injury is considered desirable to prevent the occurrence of such complications after ACL injury. The present results uphold this recommendation.
Previous studies have reported that reconstructed ligaments or tendons are not histologically ligament-like even one year after ACLR.[25] Nageli et al. reported that considering the biological maturation of the transplanted graft and the functional recovery of the knee, it is better not to return to sports for up to 2 years after ACLR.[26] Jonsson et al. reported that pivot shift-positive patients after ACLR had inferior subjective knee functional outcome and experienced the onset of early knee OA. They found that about 20% of patients are positive for pivot shift even two years after ACLR, and these long-term complications have not been completely preventable.[27] In our study cases, patients had returned to sports after approximately 1 year. The results of two-way repeated measure ANOVA showed no significant time effect on MOAKS score, possibly due to the sample size. But there was a tendency that a concomitant MM abnormality was associated with a worse outcome after ACLR. Whether it is too early to return to sports in one year cannot be determined from our results, but increased caution may be advisable in cases with concomitant MM abnormality.
Several studies have reported some evidence that meniscal damage is a component of osteoarthritis.[28],[29] Our result showed that there was no significant difference in each MOAKS score between pre-ACLR and 20.5 ± 6.3 months after ACLR. However, the post-ACL MOAKS of medial cartilage loss tended to be worse than the pre-ACL MOAKS in the MM group.
Knee OA is primarily due to medial meniscal injury and can occur independently of ACL injury. Even after ACL reconstruction, MM abnormality is considered to result in progression of medial knee medial cartilage loss. Our results showed that MM abnormality affected medial cartilage but not PFJ cartilage.
Normally, PFJ OA progression follows femorotibial (FT) OA. This FT joint incongruity causes knee joint stiffness and greater sagittal dynamic joint stiffness would particularly stress and overload the patellofemoral compartment and thereby contribute to PFJ OA worsening.[30] Justin et al. recommended FT joint mobilization for successful management of the patellofemoral pain syndrome.[31]
In other words, it takes some time to develop PFJ OA. PFJ OA had not developed within the follow-up period of this study even in the MM abnormality group. To prevent knee OA progression, some factors and indicators have been clarified below. Several authors have reported the importance of knee extension torque for knee OA. Dell’isola et al. indicated that knee extension torque weakness is associated with radiographic (medial and/or lateral) OA progression in neutrally aligned knees.[32] Katsuragi et al. suggested that radiographically occult osteophyte formation is a sign of early knee OA.[5] Based on these reports, and taking irreversible changes into account, in order to prevent the progression of OA, it is desirable to detect early OA using MRI as early as possible, and to perform early intervention in ACL reconstructed knees, such as knee muscle strength training.
We found that BMI is strongly associated with knee OA, as also found by several other studies.[33],[34] Based on these, high-BMI patients with ACL injury should undergo surgery as soon as possible, or, if that is not possible, should be monitored carefully and encouraged to lose weight.
Limitations
Patients of different ages and activity levels participated in this study, and the number of patients may have been insufficient. In this study, the muscle strength pre- and post-ACLR was not evaluated. It is generally said that muscle weakness around the knee joint increases knee instability and increases the risk of knee OA.[32] The influence of the muscle strength on the results could not be considered. In some cases, menisci were resected, however the extent of the resection was not evaluated.