A healthy knee may develop OA due to a meniscus tear and an intact meniscus can degenerate in an arthritic knee

Observation 

A cadaveric specimen of left knee was dissected. Upon observation before dissection, there was an obvious presence of a moderate degree of valgus malalignment of the knee joint. Medial side of the knee was dissected carefully to look over all the soft tissue layers as they maintain functionally important connections with the medial meniscus(10). Upon dissection, the first layer was a superficial fascia covering the vastus medialis and Sartorius’ tendon. Sartorius tendon was blended with gracilis and semitendinosus muscles to form a pes anserinus and vastus medialis was blended with quadriceps tendon. Superficial layers of a medial collateral ligament (MCL) were then exposed. Deep fibers of MCL and coronary ligament or meniscotibial ligaments were attached to the peripheral rim of the posteromedial corner of the knee. The medial meniscus (MM) is also found firmly attached to the tibia throughout its circumference by the coronary ligaments. These firm attachments of MM periphery and its horns attachment to the tibia provide rigidity to the MM movement and hence is more prone to injury than more movable lateral meniscus (LM) 16,22.

Upon exposure to medial meniscus, there was a marked presence of a degenerated medial meniscus with reddish color and significant calcification. There was evidence of ample white crystals around the medial meniscus and few in lateral meniscus and tibial plateau (FIG 2). These crystals were predicted to be the crystals of calcium pyrophosphate dihydrate (CPPD) which is the surrogate clinical presentation of chondrocalcinosis 2, 3. However, there was no evidence of the presence of crystals in the joint ligaments. There were abundant severe tissue disruptions, fraying and small meniscal tears mostly in the inner concave fold of meniscus. There was also a significant meniscal tear at the postero-lateral corner of the lateral meniscus. However, morphological dimensions of the meniscus were within the normal range as reported by many studies. Measurements: anterior-posterior length, 40mm; medial-lateral width, 25mm; anterior horn, SH-4mm, CW-5mm; midbody, CH-6mm, CW-8mm; posterior horn, SH-7mm, CW-10mm.

The anterior Insertional ligament of the medial meniscus was attached in a fan-shaped to the transverse intermeniscal ligament as mentioned by Kohn et al in 64% of the cases in their study and a transverse ligament type variant in AHMM reported by McDermott et al 2010. Both anterior and posterior meniscofemoral ligaments were present in the knee joint. However, several studies have reported less incidence of the presentation of anterior meniscofemoral ligament or both anterior and posterior ligaments in the knee joint(5).

There was significant bone degeneration in the posterior inferior aspect of the lateral femoral condyle and in a lateral tibial plateau. This is a distinct clinical presentation of osteoarthritis of the lateral femoral condyle of the joint. Degeneration of bone started from 3cm posteroinferiorly from the anterior margin of the lateral femoral condyle. The length of the bony degeneration was 2.2cm from anterior to posterior, extending up to 1.5 cm margin from the posteriormost margin of the condyle. The width of the bone involved was 1.5 cm at its widest area. Interestingly, there was not any evidence of bone degeneration in the medial compartment of the joint despite the marked presentation of severe calcification of medial meniscus. We predicted age, valgus malalignment and calcification of menisci and tears may be the major causative factors for the resultant lateral osteoarthritis in the joint.

Discussion

Lateral OA is strongly associated with the increasing valgus malalignment. Our observation also supports this association but it counters some earlier studies like Johnson et al reported that the transmission of a center of pressure is more medially in the knee joint with valgus deformity and thus lateral compartment is rarely affected. However, their study has focused only on the medial compartment of the knee and load transmission which cannot explain the complex biomechanics of the knee joint. Due to the more concave surface of a medial tibial plateau and less mobile medial meniscus, there is even distribution of load across the medial compartment compared to flat or even slightly complex lateral tibial plateau. Also, lateral meniscus carries higher loads than medial meniscus both in static and dynamic weight bearing. More forces are transmitted through the posterior region of LM often with subluxation of the posterior horn of LM during deep flexion of the knee as femoral condyles roll back on the tibial plateau.

Meniscal damage or tears is one of the major risk factors for the initiation and progression of OA. Valgus malalignment increases the risk of lateral meniscus degeneration. Our observation of significant lateral meniscus tear and widest bone degeneration of lateral femoral condyle both in the postero-lateral corner may explain and support this association between meniscal tear and OA. Malalignment of the joint and meniscal tear might have changed the normal mobility of lateral meniscus affecting the normal load transmission and shock absorption and hence more contact stress or friction between the bones resulting into a progression of OA. Altering or correcting the mechanical alignment of the joint by various means of therapeutic approach, lifestyle modification and or surgical approach can stop the progression of Knee OA.

“A healthy knee may develop OA due to a meniscus tear and an intact meniscus can degenerate in an arthritic knee.” The mechanistic relationship between knee OA and meniscal damage is conflicting. However, many studies have agreed upon the higher incidence of degenerated menisci in knees with OA. Katsura et al reported more involvement or degeneration of medial meniscus in OA knees. They demonstrated that mechanical properties of medial meniscus deteriorated 4 fold greater than that of control medial menisci while little change in lateral meniscus. We predicted that obesity(due to ample amount of fat seen during dissection), valgus malalignment, lateral OA and possible lifestyle with more of squatting activities (due to more involvement of posterior aspect of lateral femoral condyle) might have increased contact stress significantly in the medial meniscus causing severe wear and tear, degeneration  and resultant chondrocalcinosis of medial meniscus.

Proper diagnosis of chondrocalcinosis of menisci is clinically important as it could mimic a meniscal tear in radiographic interpretations like MRI, resulting in unnecessary surgeries. To rule out the extent of OA and meniscal damage is clinically important for better prognosis. Treatment of OA is basically to improve functionally ability and pain. Only outer 3^rd of the meniscus has pain fibers when most often meniscal damage only involve the innermost avascular region of menisci. 21 et al reported no difference in functional and pain scores by OA knee with or without the meniscal tear. So, treatment or rehabilitation for OA may produce better prognosis than meniscectomy in patients with severe OA with meniscal damages.

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