MD Matthew A. Popa, MD Victor M. Goldberg, MD Glenn D. Wera
Springer New York
The study of the etiology of osteoarthritis (OA) of the hip has developed into a dynamic field over the past 50 years. Epidemiological, genetic, anatomical, and biological research indicates that hip osteoarthritis appears to be a distinct entity in comparison to arthritis that affects other joints. Significant racial and ethnic differences exist in the prevalence of hip OA. Several gene single nucleotide polymorphisms (SNPs) have been discovered that are associated with an increased risk for the development of hip OA. The ethnic distribution of these SNPs also supports the differences seen in hip OA prevalence. The notion of hip OA as a “primary” disease has been challenged by the continued development of the theory of femoroacetabular impingement (FAI). This theory posits that hip OA develops secondary to subtle anatomical differences compared to “normal” hips. The identification and surgical treatment of these differences may postpone or possibly prevent hip OA development. Advances in the understanding of important signaling pathways in OA progression, such as the Wnt and TGF-β pathways, provide potential targets for new therapeutic agents.