Ateeq Hira, Zia Afaf, Husain Qayyum, Khan Mohd Sajid, Ahmad Mohd
Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh-202002, India.
Dr. Ziauddin Ahmad Dental College, Aligarh Muslim University, Aligarh-202002, India.
J Diabetes Metab Disord. 2022 Jan 29;21(1):1003-1009. doi: 10.1007/s40200-021-00960-7. eCollection 2022 Jun.
Diabetes mellitus and periodontitis are inflammatory diseases, the severity of inflammation results in the progression and persistence of both the disorders and affects bones. Diabetic complications aggravate in diabetic subjects having periodontitis; similarly, diabetic patients are more prone to developing gingivitis and periodontitis. Periodontal and diabetic inflammation disturbs bone homeostasis, which possibly involves both innate and adaptive immune responses. The pathogenic processes that link the two diseases are the focus of much research and it is likely that upregulated inflammation arising from each condition adversely affects the other. RANKL/OPG pathway plays a prominent role in periodontal and diabetic inflammation and bone resorption.
This review article summarises the literature on the link between inflammatory cytokines and the prevalence of disturbed bone homeostasis in diabetic patients with periodontitis. An extensive search was done in PubMed, Scopus, Medline and Google Scholar databases between April 2003 and May 2021.
A total of 27 articles, including pilot studies, case-control studies, cross-sectional studies, cohort studies, randomized control trials, longitudinal studies, descriptive studies and experimental studies, were included in our literature review.
Since RANKL/OPG are cytokines and have immune responses, regulating these cytokines expression will help control diabetes, periodontitis and bone homeostasis. The growing evidence of bone loss and increased fracture risk in diabetic patients with periodontitis makes it imperative that health professionals carry out planned treatment focusing on monitoring oral health in diabetic patients; bone markers should also be evaluated in patients with chronic periodontitis with an impaired glycemic state.
糖尿病和牙周炎均为炎症性疾病,炎症的严重程度会导致这两种疾病的进展和持续,并影响骨骼。患有牙周炎的糖尿病患者的糖尿病并发症会加重;同样,糖尿病患者更容易患牙龈炎和牙周炎。牙周炎和糖尿病引发的炎症会扰乱骨稳态,这可能涉及先天性和适应性免疫反应。连接这两种疾病的致病过程是众多研究的焦点,很可能每种疾病引发的炎症上调都会对另一种疾病产生不利影响。核因子κB受体活化因子配体/骨保护素(RANKL/OPG)信号通路在牙周炎、糖尿病炎症及骨吸收过程中发挥着重要作用。
这篇综述文章总结了有关炎性细胞因子与患有牙周炎的糖尿病患者骨稳态紊乱患病率之间联系的文献。于2003年4月至2021年5月期间在PubMed、Scopus、Medline和谷歌学术数据库中进行了广泛检索。
我们的文献综述共纳入了27篇文章,包括初步研究、病例对照研究、横断面研究、队列研究、随机对照试验、纵向研究、描述性研究和实验研究。
由于RANKL/OPG是细胞因子并具有免疫反应,调节这些细胞因子的表达将有助于控制糖尿病、牙周炎和骨稳态。越来越多的证据表明,患有牙周炎的糖尿病患者存在骨质流失且骨折风险增加,这使得医疗保健专业人员必须开展有计划的治疗,重点是监测糖尿病患者的口腔健康;对于血糖状态受损的慢性牙周炎患者,也应评估其骨标志物。