Ultrastructural changes in inherited cardiac calcinosis of DBA/2 mice.
Cardiac dystrophic calcinosis, an inherited condition in DBA/2 mice, produced extensive calcific lesions in the right ventricular myoepicardium of affected mice. The morphogenesis of the cardiac alterations was evaluated by microscopic and ultrastructural studies. The initial event was necrosis and mineralization of subepicardial myocytes. Mineral deposits were seen as dense granular and spicular deposits in mitochondria only, mitochondria and adjacent sarcoplasm, or the entire sarcoplasm in necrotic myocytes. In mature myoepicardial calcific lesions, the remnants of necrotic myocytes were seen as scattered dense masses of mineralized debris with surrounding fibroplasia and occasional macrophages and giant cells. Male weanling DBA/2 mice (n = 135) were fed either a commercial diet adequate in selenium-vitamin E (Se-E) content, or a basal semipurified Se-E-deficient diet with or without silver acetate for 15, 20 or 25 weeks. Cardiac calcinosis severity seemed to increase in mice which developed concurrent Se-E deficiency. Cardiac calcinosis in the DBA/2 mouse is a useful model of cardiac calcification.
D000818:Animals; D002114:Calcinosis / Q000235:genetics / Q000473:pathology / Q000662:veterinary*; D009202:Cardiomyopathies / Q000235:genetics / Q000473:pathology / Q000662:veterinary*; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA