In this section, some of the criteria listed above are discussed in more detail.
Flexion deformity
There may be several contributory causes for the (usually small) flexion deformity commonly seen in knees with anteromedial OA.
1. The posterior capsule is structurally shortened, perhaps from the effect of chronic synovitis and/or the patient’s prolonged reluctance to straighten the painful knee.
2. Osteophytes at the posterior margin of the medial femoral condyle can ‘tent’ the posterior capsular ligament.
3. Osteophytes at the top of the intercondylar notch of the femur can impinge, near full extension, on an osteophyte arising from the tibia in front of the attachment of the ACL.
It seems likely that there is always some structural shortening of the posterior capsule because removal of the osteophytes at surgery, although it often improves the deformity, does not immediately restore full extension. However, unlike TKA, unicompartmental replacement is followed in the postoperative period by spontaneous improvement of extension, probably from stretching of the shortened posterior capsule.
Weale et al. (1999) reported that 28 knees with a mean preoperative flexion deformity of 8° (SD 8) reduced to a mean of 1° (SD 2) 1–2 years after OUKA (p< 0.001). At 10+ years, the mean deformity was not significantly changed (3° (SD 4)).
Provided that anterior and posterior osteophytes are removed, some correction will occur during the operation and improvement will continue in the succeeding year so that a preoperative flexion deformity of as much as 15° is considered acceptable. In fact, it is unusual to encounter as great a deformity as this in an OA knee with an intact ACL. However, in avascular necrosis (AVN or SONK), with severe collapse of the femoral condyle, greater degrees of flexion deformity are encountered and have been found to correct spontaneously after OUKA (Langdown et al., 2005; Marmor, 1993).
Why does flexion deformity correct spontaneously after UKA and not after TKA?
In TKA, ‘balancing the ligaments’ in flexion means equalising the lengths of the MCL and the lateral collateral ligament (LCL) to create a quadrilateral flexion gap (Fig. 4.14(d)). This is achieved by lengthening the MCL (Fig 4.14(e)), which leaves the flexion gap wider than before and the posterior capsule relatively too short. Therefore, spontaneous correction of residual flexion deformity after TKA would require the posterior capsule to stretch beyond its physiological length.
Figure 4.14 (a) In the normal knee above 20° flexion fibres within the MCL, ACL & PCL are tight and the LCL is slack. (b) During OUKA, no ligaments are released so postoperatively the MCL, ACL & PCL are tight and the LCL is slack. There is no distraction of the joint.
Figure 4.14 (c) During TKA, the ACL is removed and the PCL is defunctioned. (d) For the knee to be balanced, both LCL & MCL have to be tight so the lateral side is distracted. (e) Following bone cuts, a rectangular gap usually can only be achieved with a medial release (f) so when the TKA is implanted the joint is distracted.
In UKA, the cruciate mechanism and the MCL are both preserved intact and the flexion gap is the same after the operation as before, so that the posterior capsule is required only to stretch back to its physiological length for the flexion deformity to correct. Alteration of the interstriational angle of the lattice-like structure of the posterior capsule provides a mechanism whereby it could shorten, and lengthen again, but only within the limit set by the physiological lengths of its constituent fibres (Fig. 4.15).
