Oral Dis. 2025 Dec 12. doi: 10.1111/odi.70168. Online ahead of print.
ABSTRACT
OBJECTIVE: Botulinum toxin type A (BTXA) is widely used in oral and maxillofacial surgery to treat masseter hypertrophy and bruxism, inducing transient masseter atrophy, but the underlying mechanisms remain unclear. Mitophagy, essential for muscle fiber homeostasis, plays a critical role in muscle atrophy. This study aims to investigate whether mitophagy mediates BTXA-induced masseter muscle atrophy.
METHODS: Rats received BTXA injections into masseter for 2 and 8 weeks. Muscle fiber composition was assessed via histology and immunofluorescence. Mitophagy markers (LC3-II, p62, beclin-1, Tomm20) were quantified by western blot. Mitochondrial function was evaluated via ATP content and mitochondrial DNA (mtDNA) copy number.
RESULTS: BTXA injection led to transient masseter muscle atrophy. During this process, the proportion of type IIA muscle fibers significantly increased, while the proportion of type IIB fibers decreased. Additionally, at 2 weeks post-BTXA injection, the expression levels of LC3-II, p62, and beclin-1 were notably upregulated, whereas Tomm20 expression was downregulated. Furthermore, a significant reduction in ATP content and mtDNA copy number was observed at the same time point, indicating impaired mitochondrial function.
CONCLUSION: These findings suggest that mitophagy plays a crucial role in BTXA-induced masseter muscle atrophy, providing new insights into the mechanisms underlying BTXA treatment.
PMID:41388353 | DOI:10.1111/odi.70168