Autophagy's Role in Oral Mucosa Regeneration: A Review

Oral skin and mucosa possess a robust regenerative ability due to their abundant vascularization and unique repair mechanism. Numerous studies have examined the role of autophagy in oral mucosa regeneration. This article focuses on the impact of autophagy on oral mucosa regeneration.

A study by Vescarelli [154] suggests that autophagy activation in oral mucosa results in increased production of αSMA and collagen 1α1, leading to a fibrotic repair outcome. However, in the attached gingiva, autophagy is not activated during wound healing, resulting in scarless repair.

Autophagy is also involved in regulating pathological conditions such as oral submucous fibrosis, hypertonicity, and carcinogenesis. In oral submucous fibrosis, the overactivation of autophagy by arecoline leads to apoptosis and dysregulation in human oral keratinocytes, causing atrophic epithelium. Autophagy suppression can ameliorate fibrosis by promoting apoptosis and suppressing proliferation of fibroblasts. Autophagy levels are also increased during oral carcinogenesis and are correlated with poorer behavior of the leukoplakias.

Interestingly, Liu Q's study [159] found that cigarette smoke extract induces oral mucosa epithelial cells, and autophagy inhibition aggravates oral epithelial cell apoptosis, while enhanced autophagy protects oral epithelial cells. Furthermore, oral epithelial cells are often exposed to hypertonic environments induced by food, and autophagy activation can protect them from high osmolarity-induced cell death.

In conclusion, autophagy acts as a positive regulator of oral mucosa repair and regeneration. However, autophagy defects can significantly affect cell viability and ultimately cause cell death, especially under certain stress conditions. Further exploration is needed to regulate autophagy to facilitate oral mucosa regeneration.