The association of an intact ACL with the focal pattern of cartilage erosions described above is striking. White et al. (1991) described 46 medial tibial plateaux excised sequentially from a series of OA knees treated by OUKA, all of them with an intact ACL and with cartilage erosions exposing bone (Ahlback stages 2, 3, and 4) (Ahlback, 1968). The erosions were all anterior and central (Fig. 4.4). They rarely extended to the posterior quarter of the plateau and never reached the posterior joint margin.
Harman et al. (1968) examined the tibial plateaux excised from 143 osteoarthritic knees during operations for TKA. They found that wear in ACL-deficient varus knees was located a mean 4 mm more posterior on the medial plateau than wear in ACL-intact knees (p < 0.05). The ACL-deficient knees also exhibited more severe varus deformity. The authors stated: ‘… it is evident that anterior cruciate ligament integrity is a dominant factor affecting the location of tibiofemoral contact and the resulting cartilage wear patterns in patients with osteoarthritis’. Similar findings were reported by Mullaji et al. (2008). The authors assessed tibial articular cartilage wear intraoperatively in 100 consecutive patients with varus OA. They noted that the posterior half of the medial tibial plateau was more commonly involved in ACL deficiency with predominant anteromedial wear in ACL-intact knees. Moschella et al. (2006) reached very similar conclusions from their examination of 70 excised medial plateaux from varus osteoarthritic knees, the lesion in ACL intact knees lying centrally and medially on the medial plateau.
The site and extent of the tibial erosions can be determined reliably from lateral radiographs (see Fig. 4.11) (White et al., 1991). Based on this, Keyes et al. (1992) studied the preoperative lateral radiographs of 50 OA knees in which the state of the ACL had been recorded at surgery (25 ACL deficient and 25 ACL intact). Using four blinded observers, they found 95% correlation between preservation of the posterior part of the medial tibial plateau on the radiograph and an intact ACL at surgery, and 100% correlation of erosion of the posterior plateau on the radiograph with an absent or badly damaged ACL.
Figure 4.4 Typical tibial plateau lesions of anteromedial OA. The graph compares radiographic data with data from 46 intraoperative specimens. (The graph is reproduced with permission and copyright © of the British Editorial Society of Bone and Joint Surgery [White SH, Ludkowski PF, Goodfellow JW. Anteromedial osteoarthritis of the knee. J Bone Joint Surg [Br] 1991; 73-B: 582–6].)
These correlations show that, as long as the ACL remains intact, the tibiofemoral contact areas in flexion remain distinct from the areas of contact in extension. Progressive loss of bone causes the varus deformity in extension to increase but, while the ACL continues to function, the deformity corrects spontaneously in flexion and structural shortening of the MCL does not occur.
Failure of the ACL may be the event that causes the transition from anteromedial OA to the posteromedial form of the disease, with posterior subluxation of the femur and structural shortening of the MCL. Deschamps and Lapeyre (1987) observed that absence of the ACL in an osteoarthritic knee was associated with posterior subluxation of the femur on the tibia in extension. Figure 4.5 demonstrates how this subluxation results in abrasion of the cartilage at the back of the tibial plateau by the exposed bone on the inferior surface of the femoral condyle. Thereafter, in flexion, the cartilage on the posterior surface of the femoral condyle is also destroyed by abrasion on the tibial plateau, now devoid of cartilage. The varus deformity is then present in flexion as well as in extension, and the MCL can shorten structurally.
Figure 4.5 (a) The intact ACL holds the femur forward on the tibia in extension. (b) Rupture (or stretching) of the ACL allows posterior subluxation of the femur on the tibia and secondary damage to the posterior articular surface of the tibial plateau. Thereafter, the cartilage on the posterior surface of the femur is damaged when the femur flexes.
The sequence described above does not require us to assume any ‘spread’ of the original disease to adjacent intact cartilage. Failure of the ACL alone is enough to explain how the original lesions in the ‘extension areas’ of the medial compartment could cause secondary physical damage to the cartilage of its ‘flexion areas’ and start a process that results in a subluxed knee with progressive bone loss posteromedially and fixed varus deformity.