Introduction: Human masseter muscle fiber type properties associate with variations in vertical growth of the face, highlighting clinically significant relationships between musculoskeletal function and malocclusion. MYO1H is an unconventional myosin whose function is not fully understood, but its paralog MYO1C regulates glucose metabolism and intracellular transport. We have recently determined that a variation in the MYO1H gene associates with mandibular prognathism in Caucasians. To better understand the role MYO1H and MYO1C play in facial growth we examined their gene expression in masseter muscle from dentofacial deformity subjects undergoing surgery for treatment jaw skeleton-based malocclusions.
Methods: Muscle samples were cut and stained with myosin heavy chain (MHC) antibodies to determine fiber type properties. RNA was isolated to determine expression levels for the unconventional Class I myosin genes, MYO1H and MYO1C, and sarcomeric MHC genes by TaqMan ® RT-PCR. Fiber type properties, gene expression quantities and subject malocclusion classification were compared.
Results: Although not significant, there was a data trend for increased MYO1H and MYO1C expression in class III malocclusion compared to class II malocclusion. Since mRNA (messenger RiboNucleic Acid) quantities for MYO1H were limited, the majority of comparisons were made for MYO1C, which was found in greater abundance. There were significant correlations ( p < 0.05) between MYO1C expression and fiber type percent occupancy in masseter muscle from subjects with normal and deep bite malocclusions. Significant correlations were also identified between MYO1C and MHC gene expression.
Conclusions: Differences in MYO1C gene expression associate with variations in mandibular length and fiber type properties. Altered glucose transport during condylar cartilage growth may be one of the cellular mechanisms which helps produce mandibular prognathism. This same cellular mechanism appears to be important in masseter muscle fiber type differences, which contribute to development of open and deep bite skeletal malocclusions in the vertical dimension. Further experiments are required to support these trends.