The pathogenesis of Dupuytren's contracture: contractile mechanisms of the myofibroblasts.
The role of myofibroblasts in the pathogenesis of Dupuytren's contracture was investigated by light and electron microscopic histochemical methods. Dupuytren's myofibroblasts contain an intracellular contractile mechanism that is driven by the dephosphorylation of adenosine triphosphate. Our study of calcium adenosinetriphosphatase (ATPase) activities verifies that the site of this energy system is on the myofilaments of the myofibroblasts. The degree of ATPase activity, as determined by cell counts, appeared to correlate with the residual contracture as predicted by the Legge and McFarlane Outcome Standard Formula. Further, alcian blue staining on the ultrastructural level indicates that the myofibroblasts are associated with each other and with surrounding collagen by a glycosaminoglycan matrix 300 to 1000 A thick. Collagen fibrils are attached by a similar matrix comprised of 100 A thick fibrils. The dynamic cellular architecture of the multiple adjacent myofibroblasts with their connections to surrounding collagen may be partially responsible for the residual clinical deformities seen in this disease.
D000328:Adult; D000368:Aged; D003599:Cytoskeleton / Q000502:physiology / Q000648:ultrastructure; D004387:Dupuytren Contracture / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005347:Fibroblasts / Q000502:physiology / Q000648:ultrastructure*; D006225:Hand / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction