Abstract

m c t d s w w p o c d t c hysicians have known for over 250 years that articular cartilage damage is a “troublesome thing nd once destroyed, it is not repaired.”1 Although hondral lesions that penetrate to or through the subhondral bone may fill with fibrocartilage, the biomehanical and biochemical features remain inferior to yaline cartilage.2-4 Unlike the recognized poor progosis of the meniscectomized knee, the natural history f chondral lesions remains far more speculative. At his juncture, treatment recommendations are for those esions believed to be contributing to a patient’s sympoms and are not generally directed toward asymptomtic lesions. Clinical experience has taught us that fter these lesions become symptomatic (a cause of ain, swelling, mechanical symptoms), they tend to ersist or inexorably progress over an indeterminate ime course. On one end of the spectrum, small full-thickness artilage lesions in low-demand patients can fill in ith fibrocartilage and may render a patient asympomatic. On the other end, large osteochondral lesions n higher-demand patients are less likely to develop a linically significant fibrocartilagenous healing reponse and more frequently result in pain and disabilty.3,5 The treatment algorithm is evolving and may be onstrued as a spectrum of options ranging from those hat are considered palliative (arthroscopic debrideent and lavage), reparative (marrow stimulation

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