Masseter myopathy following systemic corticosteroid administration: an experimental study.

Abstract

Immature A/J mice were treated with a series of alternate (every 4 days) doses of triamcinolone hexacetonide, a long-acting synthetic analogue of cortisol, and their masseter muscles were studied ultrastructurally. Various degrees of degenerative changes were found in most myofibers of triamcinolone-treated animals. These changes ranged from local alterations in the configuration of the Z discs to a complete disarray of the myofibrilar architecture. Severely affected myofibers revealed areas with total disintegration of myofilaments, loss of mitochondria, and an almost total depletion of glycogen. In addition, some nuclei were centrally located and an obvious enhancement of collagen fibrillogenesis was found in the endomysial spaces. The latter comprised a mixture of banded collagen fibrils and slender filaments which lacked any specific orientation of organization. Endothelial cells of intramuscular capillaries were hypertrophic, thus evoking a marked occlusion of the vascular lumen. Ultrastructural changes were also noted in axon terminals and in the sole-plate sarcoplasm: loss of synaptic vesicles along with shrinkage of axon terminals, partial loss of postsynaptic folds, and a decrease in the number of mitochondria within the sole-plate sarcoplasm. It is proposed that triamcinolone, even if administered on an alternate schedule, promotes myopathic changes in the masseter muscles of immature mice which, in turn, might possibly contribute to the hormone-retardive effect upon the growth potential of the developing mandible.