This 2008 synthesis by Ganz, Leunig, and Harris integrates four decades of epidemiologic observation with the FAI concept to argue that most hip OA results from subtle developmental deformities acting through a mechanical impingement mechanism. It defines cam and pincer FAI, their distinct damage signatures, and the rationale for early surgical correction before cartilage damage becomes irreversible.
For 40 years, a large fraction of hip OA was labeled 'idiopathic' because the underlying deformities were subtle enough to be dismissed on plain films. This paper closes that gap by linking the Murray-Harris-Solomon epidemiologic hypothesis directly to surgically observed FAI damage patterns, providing both a mechanism and a treatment target.
In clinic, this reframes how you evaluate a 28-year-old athletic man with hip pain and a borderline-normal AP radiograph. Get a cross-table lateral. Look for head-neck offset loss. Check internal rotation at 90° flexion — each 10° of loss doubles his rim pathology risk.
When you see limited internal rotation plus MRI evidence of rim or cartilage damage, this paper is why we act early. FAI treatment is most effective before secondary degenerative changes are established; waiting until the patient has joint space narrowing on radiograph is waiting too long.
The paper also explains a clinical paradox worth knowing: cam FAI patients often have less pain than pincer patients despite more cartilage destruction, because the labrum. Which carries nociceptive fibers. Is spared early in cam disease.
This 2008 synthesis by Ganz, Leunig, and Harris integrates four decades of epidemiologic observation with the FAI concept to argue that most hip OA results from subtle developmental deformities acting through a mechanical impingement mechanism. It defines cam and pincer FAI, their distinct damage signatures, and the rationale for early surgical correction before cartilage damage becomes irreversible.
For 40 years, a large fraction of hip OA was labeled 'idiopathic' because the underlying deformities were subtle enough to be dismissed on plain films. This paper closes that gap by linking the Murray-Harris-Solomon epidemiologic hypothesis directly to surgically observed FAI damage patterns, providing both a mechanism and a treatment target.
In clinic, this reframes how you evaluate a 28-year-old athletic man with hip pain and a borderline-normal AP radiograph. Get a cross-table lateral. Look for head-neck offset loss. Check internal rotation at 90° flexion — each 10° of loss doubles his rim pathology risk.
When you see limited internal rotation plus MRI evidence of rim or cartilage damage, this paper is why we act early. FAI treatment is most effective before secondary degenerative changes are established; waiting until the patient has joint space narrowing on radiograph is waiting too long.
The paper also explains a clinical paradox worth knowing: cam FAI patients often have less pain than pincer patients despite more cartilage destruction, because the labrum. Which carries nociceptive fibers. Is spared early in cam disease.