牙周病的治疗和糖尿病的控制:对证据的评估和未来研究的需要

Sara G. Grossi Dr.
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引用次数: 178

摘要

有证据表明,2型糖尿病患者的细胞因子反应增加,尤其是促炎细胞因子白介素(IL)-1β、IL-6和肿瘤坏死因子(TNF)-α。遗传、年龄和营养是这种反应增强的重要信号,最近也有报道称,是感染和炎症的重要信号。糖尿病状态下IL-1β、IL-6和TNF-α的持续升高对肝脏有影响,刺激急性期蛋白的释放,产生与2型糖尿病相关的特征性脂质代谢失调,并且对胰腺β细胞也有影响。此外,TNF-α是胰岛素受体酪氨酸激酶活性的有效抑制剂,已被认为是胰岛素抵抗的病因之一。总之,证据支持细胞因子升高在与糖尿病相关的病理生理和代谢异常中的作用。牙周炎是一种感染,糖尿病患者的发病率是非糖尿病患者的两倍。牙龈卟啉单胞菌是引起这种感染的微生物之一,它能够侵入内皮细胞,是单核细胞和巨噬细胞激活的有力信号。因此,一旦在糖尿病宿主中建立,这种慢性感染使糖尿病控制复杂化,并增加微血管和大血管并发症的发生和严重程度。与急性感染的治疗不同,慢性感染的治疗方式是一个有争议的问题。有证据表明,机械去除牙龈下感染并不能完全消除牙周感染,因此对糖化血红蛋白的降低对糖尿病控制没有影响。另一方面,研究将全身抗生素作为机械清创的辅助手段,导致牙龈卟啉卟啉菌减少到无法检测的水平,并伴随糖化血红蛋白的减少,这与糖尿病药物或胰岛素的降糖作用无关。证据支持慢性牙周感染治疗对糖尿病患者至关重要的观点。糖尿病患者感染状况的评估是适当治疗决策的基础。牙周病杂志2001;6:138-145。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Treatment of Periodontal Disease and Control of Diabetes: An Assessment of the Evidence and Need for Future Research

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1β, IL-6, and TNF-α in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-α, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions. Ann Periodontol 2001;6:138-145.

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