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OSTEOCHONDRITIS DISSECANS

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Osteochondritis dissecans (OCD) is a poorly characterized process that involves a fragmentation of articular cartilage and/or subchondral bone resulting in focal devitalization that can result in debilitating pain, inflammation, and degeneration. If left untreated, end-stage arthritis may occur as a result of abnormal wear patterns and continued cartilaginous injury.

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Originally thought to be the primary result of inflammation, the condition was termed “osteochondritis”; although, its true underlying cause is not known, trauma appears to be a predisposing factor. Other contributing causes may include genetic predisposition, ischemia, or ligamentous abnormality/laxity. “Dissecans” refers to the Latin root “to dissect” and is reflected by the separation of cartilage and subchondral bone.

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Pathology

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At the cartilage-bone interface, chondrocytes form articular cartilage, which is composed of hydrated proteoglycan and collagen. In OCD, it is thought that damage to this protective layer of proteoglycans results in disintegration and desiccation of the cartilage. Cartilage lacks innervation; however, progressive damage results in exposure of the underlying bone, which causes pain and disability. Thus, by the time that the disorder becomes clinically apparent, significant cartilaginous damage has already occurred.1

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OCD affects children as well as adults. The incidence of juvenile OCD, in which the physis is unfused, is increasing. This is likely owing to participation in competitive sports, especially those involving jumping and axial loading. Males represent the majority of patients with juvenile OCD, although the incidence among females is also rising. Adult OCD is unusual over the age of 50 years, although it can affect patients of any age. It is unclear if adult OCD results from prior/juvenile injury, although de novo adult cases have been reported. There is likely some overlap in the two forms of the disease, although the general distinction remains the presence (or absence) of an open physis. Chondrocytes have very little capacity for regeneration, although in the juvenile form of the disease, approximately 50% will heal, whereas in the adult form, very few will heal without intervention and often progress to osteoarthritis.

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Anatomy

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The knee (Figure 9-1) is the most commonly affected joint, representing approximately 75% of the cases, although other joints including the ankle (Figure 9-2) and elbow are also commonly seen. Rarely, OCD can present in the shoulder, hand, wrist, or hip. The defect is usually seen in a single joint, although it is bilateral in approximately 20–30% of cases.

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Figure 9-1.

Osteochondritis dissecans (OCD) of the medial femoral condyle. AP view (A) of the knee shows flattening and sclerosis of the medial femoral condyle. There is minimal associated joint space narrowing. Coronal T1 image (B) of the same knee demonstrates low T1 signal. Coronal T2 image (C) demonstrates high signal in the medial femoral condyle compatible with edema. A fracture and unstable osteochondral bony fragment (arrow) are noted.

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