Etiology
Controversy surrounds the etiology of osteochondritis dissecans of the knee. Causes including inflammation, genetic predisposition, ischemia, a defect in ossification, and repetitive trauma have been postulated, but there are insufficient data to conclusively support any of these.
Genetic predisposition was originally proposed, suggesting that the condition represented a variation of epiphyseal dysplasia.[9] Later reports of genetic predisposition have varied.[10][11] There is an important subgroup of patients with familial multiple osteochondritis dissecans and associated short stature. This subgroup should be identified both for adequate treatment, as individuals within a family, and for genetic counselling.[12]
History of trauma is reported in up to 40% of patients with osteochondritis dissecans in the knee and up to 90% in patients with osteochondritis involving the talus.[6] Even without history of direct trauma, the condition appears to be related to repetitive microtrauma similar to stress fracture.[2][13]
Pathophysiology
Osteochondritis dissecans of the knee
The relationship between osteochondritis dissecans, abnormal ossification, and the “normal variant” appearance of epiphyseal maturation remains unclear. The appearance on plain film x-rays of irregularities of ossification in the distal femoral growth plate, termed the “normal variant of ossification,” was originally reported in 1958 and remains a common finding seen on plain film x-rays of young knees.[14] There is no evidence to suggest that the “normal variant” develops into osteochondritis.
The role of ischemia and vascular supply is unclear. Early speculation linked osteochondritis dissecans to avascular necrosis; although studies do not support this theory.[15][16] Studies have, however, demonstrated decreased blood supply near the insertion of the posterior cruciate ligament on the medial femoral condyle.[17] This region corresponds to the site of the classic osteochondritis lesion.
Reports of micro-tissue findings in stable juvenile osteochondritis dissecans lesions indicate an underlying instability at deeper layers of articular cartilage and poor healing at areas of separation. Histological examination from biopsied tissue revealed two distinct patterns:[18]
Thick, homogeneous hyaline cartilage alone with little fibrous tissue surrounding areas of separation.
Nearly normal, thin hyaline cartilage above a mixed layer of hyaline cartilage and subchondral trabeculae along with fibrous/fibro-cartilaginous tissue at the areas of separation, indicating delayed union or nonunion between the articular surface, hyaline cartilage, and subchondral bone.
Biomechanical abnormalities, such as repetitive impingement from the medial tibial spine on the lateral aspect of the medial femoral condyle with knee abduction, have been proposed to contribute to this condition.[19][20] Analysis of the location of osteochondritis dissecans and the position of the mechanical axis within the same knee compartment has been linked for both knees, with medial (varus axis) as well as lateral (valgus axis) compartment osteochondritis dissecans. This indicates higher loading within the affected knee compartment and, therefore, axial alignment may be a cofactor in osteochondritis dissecans of the femoral condyles.[21]
Osteochondritis dissecans of the talus (ankle)
A large percentage of lesions of the talus appear to be directly related to trauma. In a large meta-analysis, 96% of lesions on the lateral aspect and 62% of lesions on the medial aspect of the talus were related to a traumatic event, typically a lateral/inversion ankle sprain.[6]
Osteochondritis dissecans of the capitellum (elbow)
The presence of bad throwing mechanics and overuse at an age corresponding to mid-stage osseous development at the elbow are the likely combination of factors resulting in osteochondritis at the elbow. The ossific nucleus of the capitellum is supplied primarily by posterior vessels that function as end arteries in skeletally immature individuals.[22]
Cellular viability in the chondroepiphysis may be compromised by repetitive microtrauma to the interosseous recurrent artery, middle collateral artery, radial collateral artery, and radial recurrent artery as they traverse the soft cartilage matrix. This continued injury may result in a disorder of endochondral ossification, leading to osteochondritis dissecans.[23]
Classification
Clinical classification[4]
1. Juvenile
Immature skeleton with open physes
2. Adult
Mature skeleton with closed physes
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