Subchondral bone cysts, osteochondritis dissecans, and Legg-Calvé-Perthes disease: a correlation and proposal of their possible common etiology and pathogenesis.

Various theoretical hypotheses have been proposed for the nontraumatic etiology of osteochondritis dissecans, subchondral bone cyst formation, and Legg-Calvé-Perthes disease. Although a direct relationship between these distinct clinical entities has sparse referral in the literature, their common theories of etiology and evolution have been extensively documented, although not correlated. The various etiologic theories of osteochondritis dissecans, Legg-Calvé-Perthes disease, and subchondral bone cyst formation have been individually presented. The conclusion drawn upon review of these theories would prove that all of the proposed etiologies for the above syndromes are remarkably similar. Furthermore, as referred to in the contents of this paper, the signs, symptoms, and roentgenographic findings also appear to be common to all three syndromes. Various clinicopathologic studies have demonstrated similar gross pathologic and histologic findings between osteochondritis dissecans, subchondral bone cysts formation, and Legg-Calvé-Perthes disease. The authors, therefore, contend that the most likely nontraumatic etiology of this condition is a common multifactorial causation with an identical pathogenesis. They propose a common etiology resulting in a pathologic process, originating in subchondral cyst formation. Eventually, a communication between the cysts and the joint will occur secondary to either the duration and progression of the cystic process, endogenous, or exogenous stress resulting in collapse of the articular surface. A complete or partially detached osteochondral fragment results from these forces. Osteochondritis dissecans and Legg-Calvé-Perthes disease may represent the same stage in the pathologic process. Degenerative joint disease is the final stage of this pathologic process. Further studies need to be performed to explore this relationship and the proposed pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)