Femoroacetabular impingement: question-driven review of hip joint pathophysiology from asymptomatic skeletal deformity to end-stage osteoarthritis

Femoroacetabular impingement (FAI), together with its two main pathomechanisms, cam and pincer, has become a trending topic since the end of the 1990s. Despite massive academic research, this hip disorder still conceals obscure aspects and unanswered questions that only a question-driven approach may settle. The pathway that leads a FAI asymptomatic morphology through a FAI syndrome to a FAI-related osteoarthritis is little known. Contact mechanics provides a shareable and persuasive perspective: cam FAI is based on shear contact stress at joint level with consequent cartilage wear; pincer FAI, contrariwise, determines normal contact stress between acetabular rim and femoral neck and squeezes the labrum in between, with no cartilage wear for many years from the onset. Pincer prognosis is then far better than cam. As a matter of fact, cartilage wear releases fragments of extracellular matrix which in turn trigger joint inflammation, with consequently worsening lubrication and further enhanced wear. Inflammation pathobiology feeds pathotribology through a vicious loop, finally leading to hip osteoarthritis. The association of cam and pincer, possibly overdiagnosed, is a synergic combination that may damage the joint rapidly and severely. The expectations after FAI surgical correction depend strictly on chondral layer imaging, on time elapsed from the onset of symptoms and on clinic-functional preoperative level. However, preemptive surgical correction is not recommended yet in asymptomatic FAI morphology.

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