Autophagy in Maxillofacial Muscle Regeneration: A Review of Recent Findings

The maxillofacial muscle is comprised of two types of muscles: masticatory and expression muscles. The trigeminal nerve innervates the masticatory muscles, while the facial nerve innervates the expression muscles. Although autophagy has been extensively studied in skeletal muscle regeneration, little attention has been paid to its role in maxillofacial muscle regeneration. However, given that both masticatory and expression muscles are skeletal muscles, it is reasonable to assume that the autophagy process in maxillofacial muscle regeneration is similar to that of other skeletal muscle regeneration processes.

To study the effects of traditional oral surgery, which involves the removal of masseter and temporal muscles, Seki Y developed a rat trigeminal nerve denervation model. Rab24, an autophagy marker involved in autophagosome formation, was found to be upregulated in the injured trigeminal motor nucleus after surgical denervation. In the klotho mouse, a model for aging, the masseter and tongue muscles showed decreased weight and myofiber diameter, accompanied by activation of the autophagic-lysosomal pathway, which helps maintain survival activities such as mastication, swallowing, and respiration. Another study found that sleep deprivation increased LC3 expression in both masseter and temporal muscles, but prolonged sleep deprivation decreased autophagy levels. Additionally, autophagy has been found to act as an important regulator under hypoxic stress in genioglossus muscle-derived stem cells, with sustained hypoxia promoting the expression of LC3II and Beclin1, as well as the HIF-1α/BNIP3 signaling pathway.

These limited studies suggest that autophagy plays a protective role in maintaining the normal function of maxillofacial muscles, but overstressed stimulation may decrease autophagy levels. Further investigation is needed to fully understand the role of autophagy in maxillofacial muscle function and regeneration.