The natural history of hip OA in athletes

Understanding the natural history of hip OA across the lifespan (figure 1), could empower clinicians and athletes/patients to prioritise appropriate evidence-based interventions (eg, education, clinician-led incremental exercise rehabilitation or surgery) for better hip health:

1. Adolescence: Changes in articular cartilage composition—a biomarker of early-stage OA—are evident in elite adolescent football players, possibly affecting its tolerance to high joint loads and increasing susceptibility to pathological change.2 This concept is supported by a recent longitudinal study of adolescent athletes where cartilage damage increased over 24 months.3 Primary cam morphology develops due to load-related femoral capital growth plate changes during maturation—from around 9 to 10 years of age in girls and 11 to 12 years in boys.4 This developmental process is more pronounced (ie, larger cam morphology) in elite-level athletes and continues until growth plate closure with likely no further development after maturation.4 5 We do not fully understand the pathological interaction between cam morphology and joint structures, although it appears to be inconsequential in most athletes.2 6 Cam morphology might not influence joint structure until after skeletal growth.2

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Figure 1

Hip OA in athletes, natural history and research recommendations. OA, osteoarthritis; THA, total hip arthroplasty.

1. Adulthood: Roughly 50% of athletes (men and women) have intra-articular hip joint pathology (often only seen on MRI) by the third decade.7 It is unclear if hip joint pathology progresses over time or if specific factors expediate structural joint change. When and how rapidly hip pathology progresses in adulthood—if at all—likely pivots on multiple intrinsic and extrinsic factors including the extent of hip morphology, exposure to high joint impact exercise and/or occupational load, and other biological factors.

2. Older age: Former male and female elite athletes have a higher prevalence of hip OA and are more likely to undergo total hip arthroplasty when compared with the general population.1 However, not all older athletes will progress to end-stage hip OA, with many still benefiting from evidence-based treatments.

When considering the natural history of OA in athletes, research has largely focused on primary cam morphology development and associated chondrolabral pathologies.2 7 This neglects the complex aetiology of OA, the role of other hip conditions (eg, hip dysplasia) and the part of symptoms and disability in athlete burden. To progress our knowledge of hip OA in athletes, we require longitudinal studies investigating the importance of, and interrelationship between, joint structures and symptoms.

Cam morphology and aetiology of symptomatic hip OA

Primary cam morphology is a causal factor for hip OA in older non-athletic adults (mean age, 59 years).8 Despite being common in athletes, the role of primary cam morphology in hip OA development in younger athletes is still unclear. Recent evidence supports the role of cam morphology in early hip OA.6 However, primary cam morphology and structural changes should not be made scapegoats for painful hips—it is likely more complicated.6 Primary cam morphology and associated soft-tissue pathology are equally present in athletes with and without hip pain.6 7 Repetitive hip movements (eg, combined hip flexion and internal rotation) may also play a key role in symptom and OA development in athletes with cam morphology. Further work is needed to understand why only some athletes with cam morphology develop symptoms. We suggest that clinicians consider intra-articular findings together with injury history, athlete characteristics, physical examination, athletic demands and wider physiological, psychological and social factors.

Can we prevent the high rates of intra-articular hip damage among young, physically active adults?

Hip OA is not exclusively a disease of older people. We cannot ignore the high incidence of intra-articular hip damage in more than half of athletes by the third decade.7 Should clinicians wait until patients present with symptoms, or should they intervene in asymptomatic individuals? While primary prevention represents the ultimate goal for athletes and clinicians, preventing primary cam morphology development is complex. For example, recommendations to reduce external (athletic) loads during adolescence may conflict with recommendations for young individuals to engage in regular exercise and sports. Such a prevention programme may coincide with a time of skill development and talent identification in some sports, which can jeopardise a young athlete’s ability to reach the elite level. Until we know if primary cam morphology can or should be prevented, we cannot recommend a reduction of exercise loads during adolescence.9 The challenges associated with primary prevention make secondary prevention more attractive. However, the optimal secondary prevention programme for hip OA has not been determined, with research efforts often hampered by the lengthy follow-up needed to evaluate OA development and consensus on definitions for symptom and structural progression.10 It is likely a programme consisting of education, exercise-based interventions, and, in some, surgery, may be useful, as recommended for the knee.10 Interventions—including education (eg, identification of symptoms, risk factors for early hip OA development and the effectiveness of different treatment approaches) of all stakeholders—to prevent hip OA, should be implemented across the lifespan, particularly in athletes participating in high joint impact sports.

The increasing burden of hip OA in athletes and its complex natural history, including, the development and prognosis of primary cam morphology makes prevention challenging. Clinicians and researchers—with athlete and patient partners—have prioritised research to grapple with these complexities.9 To prevent hip OA in all athletes, we should: (1) work to better understand how primary cam morphology and other relevant hip morphologies develop and their causal role in early hip OA; (2) develop and evaluate secondary prevention strategies to slow/prevent hip OA development; and (3) perform qualitative research of athletes with hip OA to understand the lived experience. Hip OA prevention in athletes might then become ever more possible!