Hip Osteoarthritis: Etiopathogenesis and Implications for Management

Abstract

Highly prevalent among the elderly, hip osteoarthritis (OA) carries a heavy burden of disease. Guidelines for the management of hip OA are often extrapolated from knee OA research, despite clear differences in the etiopathogenesis and response to treatments of OA at these sites. We propose that hip OA requires specific attention separate from other OA phenotypes. Our understanding of the etiopathogenesis of hip OA has seen significant advance over the last 15 years, since Ganz and colleagues proposed femoroacetabular impingement (FAI) as an important etiological factor. This narrative review summarizes the current understanding of the etiopathogenesis of hip OA and identifies areas requiring further research. Therapeutic approaches for hip OA are considered in light of the condition's etiopathogenesis. The evidence for currently adopted management strategies is considered, especially those approaches that may have disease-modifying potential. We propose that shifting the focus of hip OA research and public health intervention to primary prevention and early detection may greatly improve the current management paradigm.

Keywords: Etiology; FAI; Femoroacetabular impingement; Hip; Management; Osteoarthritis; Rheumatology; Risk factors; Therapy.

Figures

Fig. 1

Risk factors for hip osteoarthritis

Fig. 2

Developmental dysplasia of the hip (DDH). The femoral head is less stable within the shallow acetabulum (image on left), causing the distribution of shear forces that damage the articular cartilage and predispose to labral tears (image on right) [31] (reprinted by permission from Macmillan Publishers Ltd)

Fig. 3

Cam impingement. The cam lesion abuts against the labrum, pushing it outwards and compressing the acetabular cartilage inwards. The labrum separates from the cartilage and the acetabular cartilage delaminates from the bone [46] (reproduced with permission from Springer)

Fig. 4

Pincer impingement. Owing to acetabular over-coverage, the femoral neck abuts against the hip labrum, damaging the labrum and eventually the underlying cartilage. A contre-coup lesion can also occur, where continued flexion of the hip, after the femoral neck is already abutting against the acetabular rim, causes subtle joint subluxation and damage to the acetabular cartilage. The labrum separates from the cartilage and the acetabular cartilage delaminates from the bone [46] (reproduced with permission from Springer)

Fig. 5

Diagnosis of FAI morphology. The a alpha angle and b lateral center edge angle are two of the imaging parameters commonly used to classify FAI morphology. The alpha angle (a), shown here on a modified Dunn X-ray view, is the angle formed by the femoral neck axis and a line connecting the center of the femoral head to the point at which the head–neck contour becomes aspherical. Greater than 50° or 55° is often considered suggestive of cam morphology. The lateral center edge angle (b), measured on an AP pelvic X-ray, is the angle formed by a vertical line connecting the center of the femoral head with the lateral edge of the acetabulum. Greater than 40° is often considered suggestive of pincer morphology

Fig. 6

The genes responsible for the development of OA have been proposed to exist on a continuum related to joint morphology. Some defective genes are expressed in markedly abnormal joint morphology, such as in some chondrodysplasias, causing early-onset OA. Other more common genetic defects are expressed in subtle morphological aberrations that cause late-onset OA, previously considered primary OA [31] (reprinted with permission from Macmillan Publishers Ltd)