Objective: The lack of dystrophin in the mouse mutant mdx leads to muscle degeneration and is the most used animal model for Duchenne muscular dystrophy (DMD). The DMD patients have distorted dentofacial morphology which could be a result of changed masticatory mechanics due to muscular damage and dysfunction. The aim of this study is to investigate the regeneration process in the masticatory muscles of mdx-mouse due to the analysis of mRNA expression of the Myosin heavy chain (MyHC) isoforms. METHODS: In a mouse model (mdx and controls; 100 days old, n=10 each group) we examined myosin heavy chain - isoforms expression mRNA in the masticatory mucles and taking samples from masseter (MAS), temporalis (TEM) and tongue (TON) muscles. RESULTS: In control mice IIx isoforms are more expressed as IIb in MAS (65% vs. 30%, p<0.05) and TEM (83% vs. 12%, p<0.05), in TON that relation being inversed (26% vs. 72%, p<0.05). The fiber type distribution in MAS did not change in mdx, as compared to the controls although slight insignificant increase in IIb was observed. In TEM the content of IIb MyHC isoforms was reduced in comparison to the controls (12% resp. 37%; p < 0.01). The TON muscle in the mdx group represents a strongly reduced expression of IIx (26%; controls 31%, p<0.05) and IIb isoforms (74%; controls 69%, p<0.05). All masticatory muscles appeared to have very small amounts of type IIa and no content of type I. These findings were also confirmed by immunohistochemistry and Western blot analysis. CONCLUSION: The observed down regulation of the expression of IIx and IIb MyHC isoforms is an evidence for muscle adaptation process due to dystrophin absence and may be responsible for functional misbalance of masticatory muscles resulting in morphological changes that are observed in DMD patients.