Department of Orthodontics, Osaka Dental University.
Department of Oral Anatomy, Osaka Dental University.
Dent Mater J. 2024 Jun 1;43(3):430-436. doi: 10.4012/dmj.2023-262. Epub 2024 Apr 19.
The delayed mucosal healing of tooth extraction sockets in diabetes has few known effective treatment strategies, and its underlying mechanism remains unknown. Senescent cells may play a pivotal role in this delay, given the well-established association between diabetes, senescent cells, and wound healing. Here, we demonstrated an increase in p21- or p16-positive senescent cells in the epithelial and connective tissues of extraction sockets in type 2 diabetic rats compared to those in control rats. Between 7 and 14 days after tooth extraction, a decrease in senescent cells and improvement in re-epithelialization failure were observed in the epithelium, while an increase in senescent cells and persistence of inflammation were observed in the connective tissue. These results suggest that cellular senescence may have been induced by diabetes and contributed to delayed mucosal healing by suppressing re-epithelization and persistent inflammation. These findings provide new targets for treatment using biomaterials, cells, and drugs.
糖尿病患者拔牙后黏膜愈合延迟,目前针对这种情况,治疗策略收效甚微,其潜在机制也尚不明确。鉴于糖尿病、衰老细胞与伤口愈合之间存在明确关联,衰老细胞可能在这种延迟中发挥关键作用。本研究在 2 型糖尿病大鼠的拔牙窝上皮组织和结缔组织中观察到 p21 或 p16 阳性衰老细胞增加,与对照组大鼠相比,这一现象更为明显。拔牙后 7 至 14 天,上皮组织中的衰老细胞减少,上皮再上皮化失败得到改善,而结缔组织中的衰老细胞增加,炎症持续存在。这些结果表明,细胞衰老可能是由糖尿病引起的,并通过抑制再上皮化和持续炎症而导致黏膜愈合延迟。这些发现为使用生物材料、细胞和药物治疗提供了新的靶点。