At surgery, knees with the above mentioned physical signs regularly demonstrate the following anatomical features, some of which are visible in the intraoperative photograph shown in Figure 4.2(g) and all of which are illustrated in the diagrams in Figure 4.3.
Figure 4.3 Diagrammatic explanation of the physical signs of anteromedial OA in the right knee .
1. Both cruciate ligaments are functionally normal, though the ACL may have suffered some damage and may have longitudinal splits.
2. The cartilage on the tibia is eroded, and eburnated bone is exposed, anteriorly and/or centrally on the medial plateau. An area of full-thickness cartilage is always preserved at the back of the plateau (Fig. 4.3(a)).
3. The cartilage on the inferior articular surface of the medial femoral condyle is eroded, and eburnated bone is exposed. The posterior surface of the condyle retains its full-thickness cartilage (Fig. 4.3(a)).
4. The weight bearing articular cartilage of the lateral compartment, although often fibrillated, preserves its full thickness (Fig. 4.3(b)). In many cases, a full thickness ulcer can be present on the medial border of the lateral femoral condyle (see Fig 5.4) (Kendrick et al., 2010).
5. The medial collateral ligament (MCL) is of normal length (Figs. 4.3(d–f )).
6. The posterior capsule is shortened (Fig. 4.3(a)).
Correlations
The observed sites of articular surface damage, together with the intact status of the cruciate ligaments and the MCL, explain the symptoms and physical signs.
1. The cruciate ligaments maintain the normal pattern of ‘rollback’ of the femur on the tibia in the sagittal plane (see Chapter 3) and thereby preserve the distinction between the damaged contact areas in extension (the anterior tibial plateau and the inferior surface of the medial femoral condyle) (Figs. 4.3(a) and (b)) and the intact contact areas in flexion (the posterior tibial plateau and the posterior surface of the femoral condyle) (Figs. 4.3(c) and (d)). The short posterior capsule causes the flexion deformity (Fig. 4.3(a)).
2. The varus deformity of the extended leg, (and the pain felt on standing and walking), are caused by loss of cartilage and bone from the contact areas in extension (Figs. 4.3(a) and 4.3(b)).
The angle of varus depends on the amount of material lost. To expose bone on both surfaces, the total thickness of cartilage lost is about 5 mm, causing about 5° of varus. At least this degree of deformity is usual on presentation because pain seldom becomes severe until there is bone-on-bone contact during weight bearing. Thereafter, each millimetre of bone eroded increases the deformity by about 1°.
3. The varus deformity corrects spontaneously at 90° as the articular cartilage is intact in the areas of contact in flexion (Figs. 4.3(c) and (d)). Therefore the MCL is drawn out to its normal length every time the patient bends the knee (Fig. 4.3(d)), and structural shortening of the ligament does not occur. Thus an intact ACL ensures an MCL of normal length, as demonstrated by manual correction of the varus (Fig. 4.3(f)) when the posterior capsule is relaxed (Fig. 4.3(e)) with the knee flexed.