Laxity in healthy and osteoarthritic knees

Authors


Abstract

Objective

Although it is a cause of osteoarthritis (OA) in animal models, laxity in human knee OA has been minimally evaluated. Ligaments become more compliant with age; whether this results in clinical laxity is not clear. In theory, laxity may predispose to OA and/or result from OA. Our goals were to examine the correlation of age and sex with knee laxity in control subjects without OA, compare laxity in uninvolved knees of OA patients with that in older control knees, and examine the relationship between specific features of OA and knee laxity.

Methods

We assessed varus–valgus and anteroposterior laxity in 25 young control subjects, 24 older control subjects without clinical OA, radiographic OA, or a history of knee injury, and 164 patients with knee OA as determined by the presence of definite osteophytes. A device was designed to assess varus–valgus laxity under a constant varus or valgus load while maintaining a fixed knee flexion angle and thigh and ankle immobilization. Radiographic evaluations utilized protocols addressing position, beam alignment, magnification, and landmark definition; the semiflexed position was used, with fluoroscopic confirmation.

Results

In the controls, women had greater varus–valgus laxity than did men (3.6° versus 2.7°; 95% confidence interval [95% CI] of difference 0.38, 1.56; P = 0.004), and laxity correlated modestly with age (r = 0.29, P = 0.04). Varus–valgus laxity was greater in the uninvolved knees of OA patients than in older control knees (4.9° versus 3.4°; 95% CI of difference 0.60, 2.24; P = 0.0006). In OA patients, varus–valgus laxity increased as joint space decreased (slope −0.34; 95% CI −0.48, −0.19; P < 0.0001) and was greater in knees with than in knees without bony attrition (5.3° versus 4.5°; 95% CI of difference 0.32, 1.27; P = 0.001).

Conclusion

Greater varus–valgus laxity in the uninvolved knees of OA patients versus older control knees and an age-related increase in varus–valgus laxity support the concept that some portion of the increased laxity of OA may predate disease. Loss of cartilage/bone height is associated with greater varus–valgus laxity. These results raise the possibility that varus–valgus laxity may increase the risk of knee OA and cyclically contribute to progression.

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