Hip osteoarthritis: Definition and etiology

Abstract

Hip osteoarthritis (OA) is a degenerative process where continued cartilage breakdown results from mechanical overload, causing secondary bony and synovial changes and characteristic clinical and radiographic findings. Evidence is accumulating that primary hip OA is actually secondary to a subtle mechanical problem like mild dysplasia or femoroacetabular impingement (FAI). Dysplasia causes increased cartilage stress at the lateral acetabular rim, with labral hypertrophy and cartilage breakdown. FAI causes damage when the hip is flexed. Cam-ype FAI causes cartilage delamination and separation of the labral-chondral junction, while pincer-type FAI causes a crushing injury to the labrum and a linear pattern of cartilage damage. Family history is a known risk factor for hip OA, and both FAI and dysplasia can be inherited. In addition, certain genotypes appear to make the cartilage more vulnerable to mechanical overloading. Nonetheless, not all radiographic hip OA is symptomatic, and not everyone with FAI or dysplasia ultimately develops hip OA. Thus, it appears that end-stage hip OA is a multifactorial process, caused by a combination of a structural deformity, wear due to activity, the inherent “robustness” of the cartilage, and the amount of inflammation that the individual experiences. The understanding of the structural factors that contribute to hip OA is advancing rapidly. It also appears that identification and treatment of FAI and dysplasia help symptoms that result from early chondrolabral damage.