Masseter response to long-term experimentally induced anterior crossbite in Sprague-Dawley rats

•Twenty-week aberrant occlusion caused rat masseter atrophy.•Twenty-week aberrant occlusion did not cause atrophy in rat lateral pterygoid muscle.•Twenty-week aberrant occlusion upregulated Fbxo32 expression in rat masseter.•Twenty-week aberrant occlusion did not change Fbxo32 in rat lateral pterygoid muscle.•Increased Fbxo32 expression would be a candidate biomarker of rat masseter atrophy. To detect the long-term response to unilateral anterior crossbite (UAC) in masticatory muscles and in molecular biomarkers of peripheral blood leukocytes. Fifty-six six-week-old Sprague-Dawley rats were used. The gene-fold changes in peripheral blood leukocytes were detected by the microarray analysis to compare the rats that received 20-week UAC treatment with age-matched controls (n = 4). Muscle atrophy-related gene Fbxo32 was selected based on the data of the microarray analysis verified by using real-time PCR. The remaining 36 rats were randomly separated in the UAC and control groups at 12 and 20 weeks (n = 12). The protein expression of Fbxo32 and the muscle injury and myogenesis-related markers, αB-crystallin and desmin, were detected in the masseter and lateral pterygoid muscles by western blot assay. In the 20-week UAC group, the masseter muscle weight was lower than that in the age-matched control group, and the expression level of Fbxo32 gene in peripheral blood leukocytes was increased according to the microarray analysis confirmed by real-time PCR detection. The increased protein expression levels of Fbxo32 were detected in the masseter in the 20-week UAC group, and the protein expression levels of desmin and αB-crystallin were decreased at this time point. No similar changes were detected in the lateral pterygoid muscle. Masseter atrophy is induced by long-term stimulation of UAC. The increased expression of the Fbxo32 gene in peripheral blood leukocytes may be a candidate biological marker of masseter atrophy.