Histological changes in masticatory muscles of mdx mice

Objective ne muscular dystrophy (DMD) patients have distorted dentofacial morphology that could be a result of changed force balance of masticatory muscles due to unequal dystrophic changes in various masticatory muscles. Skeletal muscles of DMD patients and those of murine model of DMD – mdx mice – are both characterized by Ca2+ induced muscle damage, muscle weakness and characteristic histological changes. Therefore, to determine the pathological changes in this animal model of DMD, we examined the masticatory muscles of the mdx mice for histological abnormalities including nuclei localization, fibre diameters, and collagen expression. sections from masseter (MAS), temporal (TEM), tongue (TON) and soleus (SOL) of mdx and control normal mice were stained with hemalaun/eosin or with Sirius Red and morphometrically analysed. Levels of collagen staining in normal and mdx muscles were measured using image analysis and the mean optical density (mod) was determined. s phin deficient masticatory muscles contained 11–75% fibres with centralised nuclei. In mdx mice an increased mean fibre diameter was observed as compared to the age-matched control muscles (control vs. mdx; MAS: 33.44 ± 0.49 μm vs. 37.76 ± 0.68 μm, p < 0.005; TEM: 32.93 ± 0.4 μm vs. 42.93 ± 0.68 μm, p < 0.005; SOL: 33.15 ± 0.29 μm vs. 40.62 ± 0.55 μm, p < 0.005; TON: 13.44 ± 0.68 μm vs. 15.63 ± 0.18 μm, p < 0.005). Increased expression of collagen was found in MAS (mod control vs. mdx: 1.34 vs. 3.99, p < 0.005), TEM (mod control vs. mdx: 3.11 vs. 4.73, p < 0.01) and SOL (mod control vs. mdx: 2.36 vs. 3.49, p < 0.01). sion ndings revealed that mdx masticatory muscles are unequally affected by the disease process. The masticatory muscles of the mdx mice could present a useful model for further investigating the influence of dystrophin deficiency on muscles function.