Although Smith-Petersen described impingement of the native hip in 1936 [1], the success of replacement arthroplasty of the hip dominated the orthopaedic literature until the early contemporary reports of femoroacetabular impingement (FAI) at the turn of the millennium [2]. Subsequently, an exponential increase in interest in the subject has occurred, as demonstrated by the annual number of Pubmed hits for FAI, which reached 168 in 2010 alone. This interest is perhaps not surprising when one considers that FAI represents a new diagnosis for young adults with hip pain, an opportunity for advanced imaging and surgical techniques, and perhaps most tantalisingly, the possibility of altering the natural history of degenerative joint disease and limiting progression to endstage osteoarthritis (OA). With the explosion of recent interest in FAI, there are many controversies and unresolved issues that will be the targets for research over the next decade.
Aetiology of FAIFemoroacetabular impingement may occur secondary to paediatric hip disease or trauma, but the vast majority of cases have no underlying known cause and may be considered "primary FAI". A hip with symptomatic FAI is likely to differ from a "normal" hip through a combination of its morphology, durability of its articular cartilage and labrum, and demands placed upon it, with regard to the range of movement and activity level of the patient. Recent evidence suggests a strong genetic component to FAI [3], which is in keeping with the known genetic predisposition to hip OA. Whether abnormal morphology is determined at conception, or is acquired during skeletal development, is not known. It is conceivable that there is a genetic predisposition to subclinical slipped capital femoral epiphysis, for example. However, not all hips with abnormal joint morphology develop symptoms. A cam deformity is a common finding (approximately 20% incidence) in asymptomatic male subjects [4][5][6][7] and patients with FAI often have similar deformities in the contralateral asymptomatic hip [8]. This supports the notion that additional variables, such as the vulnerability of the labrum and articular cartilage to injury, and activity level, are important in modulating whether abnormal morphology results in symptoms. The importance of activity type and intensity needs further investigation. It stands to reason that an activity such as hurdling will potentially damage an at-risk hip by increasing the frequency and severity of impingement episodes. Better ways of grading activity are required in order to classify individuals. With regard to morphology, very little is known regarding the development of the nondysplastic hip through childhood and adolescence, and prospective studies during skeletal development may help to determine whether morphology is dependent on activity or other factors. Longitudinal studies of well-characterised cohorts will improve our understanding of how FAI develops.
Difficulties with imagingIt is crucial to appreciate that making a diagnosis of FAI relies on...