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Integrated hypothesis of dental caries and periodontal diseases

机译:牙科龋病和牙周病的综合假设

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ABSTRACT This review considers an integrated hypothesis of dental caries and periodontal diseases that builds on theoretical ecological principles. The backbone of the hypothesis is based on the dynamic stability stage of the oral microbiota, at which intrinsic (mainly saliva and gingival crevicular fluid) and bacterial (mainly metabolic) resilience factors maintain ecological dynamic stability, compatible with clinical health. However, loss of intrinsic resilience factors and/or prolonged changes in the availability of microbial metabolic substrates may shift the ecological balance of the microbiota into either saccharolytic (acidogenic) or amino acid-degrading/proteolytic (alkalinogenic) stages, depending on the nature of the predominant substrates, leading to clinical diseases. Therefore, to maintain and restore the dynamic stability of the oral microbiota, it is necessary to control the drivers of disease, such as salivary flow and influx of bacterial nutrients into the oral cavity. Contrary to conventional wisdom, excessive intake of fermentable carbohydrates may contribute to inflammation in periodontal tissues resulting from hyperglycaemia. An integrated hypothesis emphasizes that both dental caries and periodontal diseases originate in the dynamic stability stage and emerge in response to nutritional imbalances in the microbiota. Periodontal diseases may belong to the sugar driven inflammatory diseases, similar to diabetes, obesity, and cardiovascular diseases.
机译:摘要本综述考虑了牙科龋齿和牙周病的综合假设,这些假设构建了理论生态原则。假设的骨干是基于口腔微生物的动态稳定性阶段,其中固有(主要是唾液和牙龈沟槽)和细菌(主要代谢)弹性因素保持生态动态稳定性,与临床健康相容。然而,微生物代谢底物可用性的内在弹性因素和/或延长变化的丧失可以将微生物群的生态平衡转化为糖类溶解(酸性)或氨基酸降解/蛋白水解(碱性原酸)阶段,这取决于本质主要的底物,导致临床疾病。因此,为了维持和恢复口腔微生物群的动态稳定性,有必要控制疾病的驱动因素,例如唾液流动和细菌营养素的流入口腔。与传统智慧相反,过量摄入可发酵的碳水化合物可能导致高血糖血症导致的牙周组织中的炎症。综合假设强调,龋齿和牙周病疾病都源于动态稳定阶段,并响应微生物群中的营养不平衡而出现。牙周病可能属于糖驱动的炎性疾病,类似于糖尿病,肥胖症和心血管疾病。

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