Abstract
Purpose: Cam-type femoroacetabular impingement characterized by extra bone formation at the anterolateral head-neck junction of the hip creates a non-spherical femoral head, known as a cam deformity. The cam deformity is forced into the acetabulum during flexion and internal rotation of the hip, leading to structural damage as acetabular labrum tears and cartilage delamination. This damage might gradually lead to osteoarthritis. Cam deformity and subtle acetabular dysplasia are recently recognized as relevant risk factors for hip osteoarthritis (HOA). In subtle acetabular dysplasia, the femoral head has contact with a small area of the shallowacetabulum. Therefore, more focal stress is put on this small area, which provides insufficient coverage for the femur. Cumulative articular surface contact stress above a critical threshold in dysplastic joints causes joint degeneration. However, the influence of these deformities on HOA incidence compared with other risk factors including age, gender, and body mass index (BMI) and the effect modification of other known determinants on these associations are not yet known. Methods: Participants of Rotterdam Study (RS-I: n = 2960, RS-II: n = 1470) including men and women aged >55 years with a Kellgren and Lawrence (K/L) grade ≥1 at baseline and mean follow-up of 9.2 years were included in the study. Incident radiographic HOA was defined as a K/L grade of ≥2 or a total joint replacement at follow-up. The shape of the proximal femur and the acetabulumwere outlined by a set of points (23 points, Figure 1) that were positioned on pre-defined anatomical landmarks on the anteroposterior pelvic radiographs using statistical shape modeling software. Using this point set, alpha and center-edge (CE) angles, parameters that quantify these deformities were calculated. Acetabular dysplasia and cam deformity were defined as the presence of a CE angle 60°, respectively (Figure 1). Using generalized estimating equation models, odds ratios were calculated to assess the associations between both hip deformities and the development of HOA. Results: At the follow-up times, 234 and 179 cases of HOAwere identified for RS-I and RS-II, respectively. Incident OA was defined in 281 hips within RS-I among that 12.2% (n = 34) had cam deformity and 8.3% (n = 23) had acetabular dysplasia, while out of 218 hips with incident OA in RS-II,16.1% (n = 35) had cam deformity and 7.3% (n = 16) had dysplasia. In pooled data analyses (Table 1), individuals with cam deformity had a two-fold increased risk for developing osteoarthritis (OR = 2.0, 95% CI= 1.48-2.71, p = 0.00001) compared with individuals without cam deformity. Moreover, subtle acetabular dysplasia was significantly associated with increased risk of HOA (OR = 1.96, 95% CI = 1.35-2.84, p = 0.0004). Both associations were independent of known risk factors of HOA such as age, sex, and BMI and were only significantly associated with development of OA in younger individuals. These bony deformities were independently related to the outcomewhen included in the samemodel (camdeformity: OR (95% CI) = 2.03 (1.50-2.76), hip dysplasia: OR (95% CI) = 2.03 (1.41-2.92)). The results were almost consistent in both cohorts. Conclusions: Individuals with cam deformity and acetabular dysplasia are strongly predisposed to progression to HOA independently from other well known risk factors of age, sex, and BMI. Interestingly, both deformities were only predisposing to OA in relatively young individuals. Therefore, early identification of these conditions is important and might provide an opportunity to prevent hip osteoarthritis. (Figure Presented).
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