〔Abstract〕 To investigate the effects of occlusal alterations on masseter muscle atrophy after the applica⁃tion of excessive orthodontic tension , and the role and mechanism of prophylactic nitrate supplementation in the pre⁃vention and treatment of masseter muscle atrophy. Methods Eight⁃week⁃old male SD rats were selected. An ortho⁃dontic appliance was placed in the oral cavity of the rats to obtain a rat model of occlusal alterations , and the mas⁃seter muscles were taken at various times after excessive orthodontic force application for relevant tests. Masseter muscle weighing , HE staining , Western blot and immunohistochemistry assays were used to detect the atrophic state of the masseter muscle. Meanwhile , immunofluorescence staining was used to detect the hypoxic status of the mas⁃[ cluster of differentiation 31 (CD31) , vascular endothelial growth factor (VEGF)] . After 28 days of prophylactic nitrate supplementation and application of orthodontic tension , the status of masseter muscle atrophy , tissue hypoxi⁃ growth factor receptor (EGFR) , protein kinase B (AKT ) , extracellular signal⁃regulated kinases 1/2 (ERK1/2) to detect masseter muscle apoptosis. Results The molar displacement caused by overload traction could lead to masseter muscle atrophy , accompanied by hypoxia in the masseter tissue and decreased expression of angiogenesis⁃related proteins. Preventive nitrate supplementation could prevent masseter muscle atrophy , alleviate tissue hypoxi⁃a , and promote angiogenesis. The anti⁃apoptotic effects of the EGFR⁃AKT/ERK1/2 signaling pathway contributed to the preventive effects of nitrate on masseter muscle atrophy. Conclusion Occlusal alterations brought about by excessive orthodontic tension exertion in rats may lead to masseter muscle atrophy , and prophylactic nitrate supple⁃mentation may resist hypoxia and atrophy of masseter muscle tissues by promoting angiogenesis through the anti⁃ap⁃optotic effects of the EGFR⁃AKT/ERK1/2 pathway.