It was osteoarthritis that discovered femoroacetabular impingement

That morphological abnormalities of the hip could be a cause rather than a result of osteoarthritis (OA) was observed many years before the actual mechanism of femoroacetabular impingement (FAI) was described. Morphological abnormalities, currently termed as cam and pincer, were often present in people with hip OA. Ganz et al1 first described how these morphological abnormalities may cause intra-articular hip damage by a motion-dependent process called FAI.

Epidemiological studies

Although FAI is a motion-dependent process, valid techniques to quantify the dynamic nature of FAI are still elusive. For epidemiological purposes, a cam-type femoral head or acetabular overcoverage on X-ray is often used to study its relationship with OA. In several cohort studies, there is conflicting evidence regarding the association between pincer deformity and OA. Importantly, the higher quality prospective cohort studies fail to demonstrate an association between the two.2 ,3 It is unknown whether this is due to the relatively high prevalence of pincer deformities in the general population that remain asymptomatic, or because the heterogeneous definition of a pincer deformity makes quantification difficult.

For cam deformities, most epidemiological studies show an association with the development of OA.4 One should consider, however, that most cam deformities remain asymptomatic for a lifetime since positive predictive values for the development of OA range between 6% and 25%. Interestingly, these percentages are similar to the proportion of people with a cam deformity who become symptomatic.5 Clearly not all cam deformities lead to cam-type FAI.

However, when a person has both a cam deformity and limited hip internal rotation, the positive predictive value for developing OA rises to over 50%.6 For future studies and clinical practice, it is essential to better quantify the cam deformity as well as the dynamic process of FAI. This will allow improved and earlier characterisation, and identification of participants who will develop symptoms; this is a group in which to test preventive measures.

A few decades are missing

There is now strong evidence that cam deformities develop during skeletal maturation and are present immediately after growth is complete. However, participants in epidemiological studies that evaluated the relationship between cam deformity and OA are generally over 45 years of age. No epidemiological studies can shed light on the natural history of a cam deformity from skeletal growth until late adulthood. Does a cam deformity only lead to OA from the age of 45 years, or also earlier in life? Is the association between cam deformity and intra-articular hip pathology more or less strong before the age of 45 years? Does this relationship depend on physical activity? Do any interacting cofactors such as, for example, femoral version, acetabular orientation, hamstring tightness or other unknown factors contribute to the development of hip OA?

There are indications that the strength of association between a cam deformity and OA becomes weaker as the patient becomes older. In a prospective cohort study in people with a mean age of 55 years, cam deformity was strongly associated with fast progressing hip OA; in other cohorts with older people, the association was weaker.6 ,7 Thus, participants with a cam deformity who have reached a certain age without developing OA, appear to have other protective cofactors. There may also likely be additional factors, besides a cam deformity, that play a role in the development of OA at an older age.

The age group that usually presents with first symptoms resulting from FAI generally consists of young adults. Many surgical studies have confirmed that these young adults with symptomatic FAI can already have extremely damaged hip joints.8 In cam-type FAI, the most common finding is labral damage with or without acetabular cartilage delamination at the site where the cam deformity is forced into the acetabulum. One interesting finding from the few epidemiological studies in this young population showed an association between the presence of a cam deformity and labral tears as well as decreased cartilage thickness in asymptomatic individuals of a mean age of only 20 years.9

A very interesting question is whether symptomatic FAI in young adults should be considered as early hip OA. The period in between cam development and apparent clinical or radiological hip OA is characterised by a continuum of marked tissue changes. The point until which this intra-articular damage is still reversible remains to be determined.

Can we prevent OA by joint preserving surgery or other strategies?

The strong association between a cam deformity and the development of hip OA leads to the question of whether hip pathology can be prevented. One method suggested is the surgical removal of the cam deformity, but there are no data on the structural (long term) joint preservation following surgery. Additionally, the timing of surgery poses a dilemma, as the severity of chondropathy is associated with worse outcomes following surgery and more rapid progression to total hip replacement.10 Conversely, surgery at the very early stage is undesirable as it may be considered over treatment because not everybody with (symptomatic) cam deformity develops OA. Other strategies could be to preclude the (yet unknown) cofactors that are likely to be involved in developing OA via the FAI pathway or, even better, prevent the cam deformity from developing, but for this purpose, we require greater knowledge on its aetiology.