Chondral Injuries

Chondral lesions exist on a spectrum from acute isolated fragments to diffuse degenerative disease. Acute articular fragmentation is increasingly recognized as a cause of hip pain following trauma.36 Propagation of a displaced fragment superimposed on underlying degenerative disease may also occur and sometimes explains the acute exacerbation of symptoms in the presence of degenerative arthritis. Preexisting degeneration should always be suspected when the history of trauma is minimal.

A common mechanism for acute articular fragmentation is a direct blow to the greater trochanter, such as that sustained from a fall landing on the lateral aspect of the hip.36 This trauma is especially seen in athletic young adult men. These individuals are apt to be participating in contact and collision activities in which this type of mechanism is common. Physically fit men have less adipose tissue directly over the trochanter; thus, there is less soft tissue to cushion the blow and, with solid bone structure, the force is delivered unchecked to the joint surface. This trauma results in either a full-thickness articular fragment from the medial aspect of the femoral head, due to the shear forces, or chon-drocyte cell death and focal chondromalacia in the superomedial acetabulum as a result of the impact. Elderly patients or patients with osteopenia would more likely sustain a hip fracture.

As noted previously, 48% to 73% of aceta-bular labral tears have associated articular dam-

age.12,21,26,27 These lesions occur at the articular labral junction. The extent of articular damage may be the limiting factor in the response to arthroscopy and should be suspected in almost any patient undergoing arthroscopy with an identifiable labral tear. Also, remember that investigative studies are best at showing labral pathology and poorest at showing articular damage. Noguchi et al. have shown that, in the presence of dysplasia, articular wear uniformly begins at the anterolateral margin of the ac-etabulum.37 We have observed this to be a common site of origin of articular deterioration both with and without associated acetabular dysplasia. Grade IV articular lesions in this area with surrounding healthy articular surface are sometimes amenable to microfracture. With critical patient selection, as much as 35 points improvement (100-point modified Harris Hip Score) has been reported.31 For these lesions, microfracture may actually influence the natural history of the process, slowing the degeneration that eventually occurs.

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