Abstract
Background Mast cells are indigenous connective tissue cells that function in the process of inflammation and edema. Their numbers were studied in a quantitative morphological study of the soleus muscles from 32-week-old and 56-week-old normal and genetically dystrophic dy2J and mdx mice to determine the incidence of mast cells in muscle to increasing age and to normal and myopathic conditions. Methods Soleus muscles from normal C57Bl/J and from dystrophic C57Bl/SnJ (dy2J/dy2J) and C57BL/10ScSn mdx mice were processed for examination by light and electron microscopy. Quantitation of mast cells was performed on semi-thick sections and expressed as an average of cells per millimeter squared of muscle tissue. Results Mast cells were observed in the connective tissue interstitium that normally separates skeletal muscle into fascicles. Their cytoplasmic granules stained metachromatically with toluidine blue and often obscured the single, centrally placed nucleus. They occurred singly or in small groups and were most frequently seen adjacent to neurovascular elements within the muscle, and in many cases were closely associated with the outer capsular regions of muscle spindles. Between the 32- and 56-week-old groups in each strain, an age-related increase in mast cell numbers was observed. In the dystrophic conditions, the dy2J and mdx skeletal muscles exhibited a two- to four-fold increase in mast cells when compared to normals in both age groups. Extensive connective tissue proliferation and sites of necrotic and regenerating muscle were common features in both myopathies. Conclusions Results of this study indicate that a significantly higher number of mast cells which exist in dy2J and mdx murine skeletal muscles may be related to the high amount of connective tissue infiltration and extensive muscle fiber remodelling in these conditions. Moreover, the close proximity of mast cells to muscle spindles and nerve fascicles suggests that these cells may play a role in modulating their activities. Anat. Rec. 247:341–349, 1997. © 1997 Wiley-Liss, Inc.
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