How?
The stages of deterioration of the ACL observed intraoperatively in OA knees suggest the following sequence, which we have used to grade the damage:
- Normal
- Loss of synovial covering, usually starting distally
- Longitudinal splits in the substance of the exposed ligament
- Friable and fragmented with stretching and loss of strength of the collagen bundles
- Absent or ruptured.
Why?
Among the knee’s ligaments, the ACL is peculiarly at risk because of two anatomical features.
1. Its intra-articular course puts it at risk of nutritional insufficiency from chronic synovitis of any type. For instance, the ACL is frequently damaged by chronic rheumatoid synovitis. The importance of the ligament’s synovial investment is also suggested by the observation that the ACL is always healthy in knees in which the ligamentum mucosum is intact (Dr RD Scott, personal communication). Experimental stripping of the synovium from rabbit ACL causes a succession of changes very like those seen in human OA joints, culminating in structural disintegration of the ligament (Robinson et al., 1992).
2. The ligament is at risk of physical damage from osteophytes at the margins of the condyles. In knees with anteromedial OA, osteophytes are almost always present on the lateral side, and sometimes on both sides of the intercondylar notch, and the lower part of the ligament may be damaged by them as the knee approaches full extension (Fig. 4.6).
Figure 4.6 Intraoperative picture of an ACL that is partly denuded of synovium, has longitudinal splits and is surrounded by osteophytes. Chronic synovitis and osteophytosis, which are both common in antereomedial OA, probably represent the response throughout the joint cavity to material shed into it from the cartilage erosions in the medial compartment.
Summary of pathology
The primary pathological lesions of anteromedial OA are focal erosions of the cartilage on the inferior surface of the medial femoral condyle and on the anterior and central parts of the medial tibial plateau, areas that make contact with one another in extension.
Chronic synovitis and marginal osteophytosis are secondary pathological changes. The articular cartilage of the lateral compartment is functionally intact. The cruciate and collateral ligaments are of normal length.
While the ACL remains effective, the orderly flexion–extension movements of the femur on the tibia in the sagittal plane are preserved, maintaining the separation of the flexion areas from the extension areas. Progressive loss of bone causes increasing varus deformity in extension but not in flexion.
Failure of the ACL allows posterior subluxation of the femur on the tibia and offers a sufficient explanation for the progression from anteromedial arthritis to posteromedial disease, with an associated fixed varus deformity.
If this is the natural history, resurfacing the medial compartment while the ACL is still intact may cure the symptoms and recover the normal kinematics and mechanics of the joint. If the osteophytes have been removed, and cartilage debris is no longer shed into the joint cavity, later failure of the ACL and spread of the disease to the other compartments may be avoided.
These are the theoretical reasons for employing unicompartmental arthroplasty as the treatment for anteromedial OA.
