The Rise of Structural Osteoarthritis of the Hip

Commentary By the creative use of 80-year-old serial radiographs from the longitudinal Brush growth study in Cleveland, Ohio, Morris et al. have made an important contribution to our understanding of the evolution of proximal femoral cam morphology. One obvious potential limitation is the extrapolation of data from the 1940s to the present growth patterns of the proximal femoral physeal plate in adolescents, given improved nutrition, changing activity levels, and other unknown factors. However, the study participants were presumably children of parents with the financial capacity to have them monitored regularly by a pediatrician, and they participated in “health contests,” thereby permitting us to presume that they were comparable with today’s adolescents. Over fifty years ago, Murray1 described the “tilt deformity” of the femoral head and neck as a precursor of osteoarthritis of the hip. Numerous other studies have supported the theory that a substantial proportion of noninflammatory osteoarthritis is secondary to anatomical variations in hip development2. It is now 15 years since Ganz et al.3,4 linked femoroacetabular impingement to cam morphology as a cause of hip pain and early-onset progressive osteoarthritis. Studies by Siebenrock et al.5,6 identified high-level sports activities in adolescence as a cause of growth modulation of the proximal part of the femur, leading to abnormal epiphyseal extension and cam morphology. The current study lends support to the hypothesis that the cam deformity develops from chronic impingement before rather than after proximal femoral physeal closure as there was no increase in the deformity on radiographs after physeal closure; however, this was determined from a subset of only 25 patients who had radiographs made after closure. Thus, cam morphology does not appear to develop as a genetic aberration of normal development but instead requires additional environmental factors such as repetitive trauma in adolescence as a result of participation in an undefined level of sports activities. Presumably, there is individual variability in this response to activity, and the threshold for generating epiphyseal extension is likely a combination of individual susceptibility and the intensity of the offending activities. The authors concluded that “the exact mechanism for epiphyseal extension is unclear,” and they “propose[d] that it may represent a physiologic response to increased shear stresses across the physis and serve as a protective mechanism to prevent SCFE [slipped capital femoral epiphysis].” In addition, they noted that “while this would be a beneficial adaptive response during adolescence, the subsequent development of cam morphology as a result of this epiphyseal extension may be the unfortunate long-term consequence of a short-term adaptive response.” Their conclusions are likely appropriate, but their additional observation that “further studies are needed to investigate this theory” is equally valid. What are the clinical and health policy implications of this and other related published studies? First, we need to know to what extent this “structural” arthritis constitutes a substantial proportion of the causes of osteoarthritis of the hip. It would seem to be a relatively small amount compared with the frequency of other causes such as congenital disorders (skeletal dysplasias), genetic disorders (familial osteoarthritis), defects in cartilage metabolism, developmental dysplasia of the hip, and posttraumatic arthritis of the hip. There is little doubt that surgery for femoroacetabular impingement is currently very fashionable among hip surgeons focusing on young adults; however, the extent of the problem needs to be better defined as it is premature to make recommendations for surgical treatment that could be implied by these recent publications. Second, how should evolving cam morphology be monitored in elite adolescent athletes? Morris et al. sensibly stated that “we do not recommend radiographic screening for this marker,” referring to the epiphyseal extension ratio. Indeed, except for symptomatic individuals, radiographic monitoring cannot be justified and should not be encouraged. Magnetic resonance imaging is expensive from a cost-resource utilization perspective so is not an appealing screening tool; however, the refinement of ultrasonography may have some promise as a less costly monitoring technique. Third, should certain athletic activities be restricted for adolescents on the basis of this information? With the current epidemic of childhood obesity that is partly due to a lack of sufficient exercise, it would not seem to be common sense to recommend limitations on sports activities except for symptomatic adolescents who have demonstrated cam morphology and clinical signs of impingement. Finally, there has been an explosion of arthroscopic and open surgery in recent years for symptomatic cam lesions of the proximal part of the femur, with gratifying short-term relief of pain in some individuals. Reports of its efficacy are anecdotal, have inadequate long-term follow-up, or lack scientific rigor. Furthermore, there are insufficient numbers of long-term studies to establish whether the onset of symptomatic osteoarthritis is actually prevented or delayed. To what extent may some of this surgery be justified? While our understanding of the evolution of osteoarthritis is steadily improving, the quality of evidence to support widespread surgery for femoroacetabular impingement has not kept pace with current practice.

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