The new theory first required an extensive set of exclusion criteria: inflammatory diseases of the hip (such as rheumatoid arthritis, ankylosing spondylitis, Reiter’s syndrome, or lupus) as well as calcium pyrophosphate disease, diffuse idiopathic skeletal hyperostosis, gout, and hemochromatosis. Also excluded were osteonecrosis and fractures around the joint, including fracture of the acetabulum, femoral head, or femoral neck. Similarly, cases of damage to the cartilage from infection or resulting from penetration of a fixation device into the joint space were excluded. This set of exclusions was necessary to narrow the definition of hip OA to those causes that arise within the joint itself without extraneous inflammatory, traumatic, and metabolic causes, such as OA that can develop after an earlier septic damage or after rheumatoid arthritis has damaged the joint at an earlier time and has burned out as an active rheumatoid process.
Second, within this redefined group, several additional key observations were made. Clearly, many cases of hip OA result from severe developmental or acquired deformities of the hip that occurred in infancy or childhood. Children with developmental dysplasia resulting in a hypoplastic acetabular articulation coupled to a deformed femoral head often develop progressive and severe arthritis of the hip in late adolescence or young adult life. Similarly, some patients with severe SCFE or Legg-Calvé-Perthes disease may develop late OA. It is generally agreed hip OA in these examples is causally related to the gross deformity. In contrast, the focus of the new concept addressed those remaining cases of hip OA in which the deformity was considered mild, slight or even, in the eyes of casual observers, nonexistent. In the past, such cases have been commonly considered “primary” (ie, without known etiology).
It was in this group of patients with mild deformities that the hypothesis developed. Murray’s [46
] work suggested hip OA could develop secondary to rather subtle, sometimes previously unrecognized deformities that occurred before full skeletal maturation. One example was the development of hip OA secondary to a mild, unrecognized, and untreated SCFE. Harris and Solomon and their coworkers presented additional longitudinal data on documented cases of mild developmental hip disease unrecognized as abnormal by many radiologists and orthopaedic surgeons, which led years later to hip OA [20
]. The leading conditions contributing to these subtle deformities were developmental hip dysplasia, SCFE, Legg-Calvé-Perthes disease, multiple epiphyseal dysplasia, and spondyloepiphyseal dysplasia.
This concept was subsequently supported in retrospective analyses of patients presenting in adult life with hip OA, without any of the excluded conditions, for whom prior radiographs were available for analysis after adulthood had been reached, but before any radiographic signs of arthritis were visible. From these studies, a striking observation was made: 79% of these cases had antecedent subtle but definite signs of an underlying developmental abnormality [21
Among women, unrecognized and untreated developmental dysplasia predominated [61
]. Among men, the dominant abnormality was femoral, not acetabular, and had the characteristic of the “tilt” deformity on AP radiographs [62
]. When assessed using three radiographic views (AP, frog lateral, and crosstable lateral), this femoral deformity was more fully described and named the “pistol grip” deformity [21
]. Detailed longitudinal followup studies of long duration confirmed this characteristic configuration of the femoral head and neck could be produced by several etiologies, namely SCFE, Legg-Calvé-Perthes disease, multiple epiphyseal dysplasia, and spondyloepiphyseal dysplasia. This same femoral deformity also existed in many patients, both male and female, who had developmental acetabular dysplasia. Thus, this common femoral deformity can exist both with and without an acetabular dysplasia. Moreover, as is well known, longitudinal studies show some cases of Legg-Calvé-Perthes disease that began as a purely femoral abnormality producing a pistol grip deformity can secondarily lead to acetabular deformity [21
Thus, this concept is reinforced by evidence from both longitudinal studies following known cases of developmental dysplasia of the hip, SCFE, and Legg-Calvé-Perthes disease into adulthood and retrospective studies of adult cases of OA, which showed a high correlation between these hip deformities resulting from infantile, childhood, and adolescent conditions and the subsequent adult hip OA.
A retrospective study of Caucasian cases in the United States suggested 79% of the cases of adult OA were associated with these deformities, and when the remaining 21% of cases were further examined over a longer time span, an additional 10% had or subsequently developed signs of rheumatoid arthritis, hemochromatosis, or calcium pyrophosphate disease [21
]. Thus, after eliminating the excluded conditions listed above that lead to degenerative changes in the hip, approximately 90% of the cases of adult hip OA were associated with some developmental abnormality.
Solomon et al. [54
] made similar observations in Caucasians living in South Africa. Moreover, they made other relevant observations. They found a markedly lower incidence of hip OA in Africans in South Africa compared to Caucasians. This difference also correlated with a markedly lower incidence of those related developmental conditions listed above, conditions that were common among Caucasian children and adolescents in South Africa but uncommon among Africans. These parallel differences in Africans further suggested a causal role of developmental deformities of the hip in leading to adult hip OA [55
]. This relationship between developmental deformities and subsequent OA was further reinforced by the identification by Solomon and coworkers of two “geographically isolated African communities in whom hip OA was unexpectedly common; in both, there is also a high incidence of hip dysplasia” [56
A relationship between developmental deformities and hip OA is not new. For decades, many cases of hip OA have been called “secondary,” for example, secondary to severe dysplasia. The distinction here lies in the novel concept that more subtle deformities, often unrecognized in the past as meaningful deformities, can produce hip OA (Fig. ). This hypothesis proposes most, if not all, hip OA is secondary, often secondary to subtle but definite and commonly overlooked, ignored, or not recognized dysplasia or pistol grip deformities.
Fig. 3A–C (A) FAI is shown in a 34-year-old man with an apparently normal AP radiograph. (B) The nonspherical femoral head leading to reduced offset at the neck and predisposition to cam FAI is visible on the lateral radiograph. (C) The MRI scan confirmed the (more ...)