Autophagy: A Key Regulator of Oral Bone Regeneration

The alveolar bone, maxilla, and mandible are critical hard tissues that provide support in the oral cavity. However, inflammation, tumors, trauma, congenital or acquired deformities, and other factors can lead to bone structure destruction. Therefore, maintaining bone tissue homeostasis through regeneration is crucial for oral tissue structure and function. Numerous studies have demonstrated that the basal level of autophagy plays a vital role in regulating the functional state of osteoblasts, osteoclasts, and osteocytes. Additionally, autophagy is required to maintain the stemness, replication, and differentiation capacities of BMSCs. If autophagy is deficient, abnormal bone conditions may occur.

As previously mentioned, autophagy plays a crucial role in stem cell differentiation and the regulation of antioxidant processes. These processes involved in stem cell osteogenic differentiation also affect oral bone regeneration. Furthermore, bone regeneration requires coordination and cooperation among various bone cells. Evidence has shown that osteoblast differentiation and mineralization are accompanied by autophagy up-regulation. Autophagy-like vesicles are often present within the cytoplasm of mineralized cells, and these vesicles can transport calcium and phosphate crystals to promote bone matrix mineralization. If autophagy is inhibited, impaired bone mineralization and decreased bone mass may occur. Autophagy ablation has also been found to contribute to ER stress and an increase in RANKL secretion, which promotes the activation of osteoclasts and bone resorption. Moreover, suppressing autophagy inhibits the terminal differentiation of osteoblasts.