Department of Prosthodontics, New York University College of Dentistry, 345 East 24th Street, 4W, New York, NY 10010, USA.
J Craniomaxillofac Surg. 2013 Mar;41(2):e42-8. doi: 10.1016/j.jcms.2012.08.001. Epub 2012 Sep 7.
Healing of tooth extraction sockets in poorly controlled diabetic patients is often delayed and accompanied by severe infection. The exact cellular and molecular mechanisms underlying the pathogenesis of this complication are still not fully understood.
The purpose of this study was to investigate molecular changes associated with delayed oral wound healing in diabetes.
Six to eight weeks old male type 2 diabetes and age matched control inbred mice were used and maxillary molar tooth extractions were performed. At 4 and 7 days after tooth extraction, the edentulous mucosa of the mice were harvested, and analyzed for histology and gene expression of key wound healing factors.
In the diabetic model, histological analysis showed that epithelial tissue migration for wound closure was delayed after tooth extraction compared to the control. Quantitative real-time PCR revealed that expression of the TGF-β1, TGF-β2, TGF-β3, TGFβRII and TGFβRIII genes was significantly downregulated in the diabetic model at 4 and 7 days after tooth extraction.
These results suggest that delayed wound healing of oral mucosa in diabetes may be associated with decreased expression levels of these regulatory genes which play important roles in controlling epithelial wound closure.
在血糖控制不佳的糖尿病患者中,拔牙创口的愈合常常会延迟,并伴有严重的感染。导致这种并发症的发病机制的确切细胞和分子机制尚未完全阐明。
本研究旨在探讨与糖尿病口腔伤口愈合延迟相关的分子变化。
使用 6 至 8 周龄的雄性 2 型糖尿病和年龄匹配的近交系小鼠,并进行上颌磨牙拔牙。拔牙后 4 天和 7 天,采集无牙黏膜,分析关键伤口愈合因子的组织学和基因表达。
在糖尿病模型中,组织学分析显示,与对照组相比,拔牙后上皮组织迁移以封闭伤口的速度较慢。实时定量 PCR 显示,在拔牙后 4 天和 7 天,糖尿病模型中 TGF-β1、TGF-β2、TGF-β3、TGFβRII 和 TGFβRIII 基因的表达明显下调。
这些结果表明,糖尿病患者口腔黏膜愈合延迟可能与这些调节基因的表达水平降低有关,这些基因在控制上皮伤口闭合中发挥着重要作用。