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Integrated hypothesis of dental caries and periodontal diseases

机译:龋齿和牙周疾病的综合假设

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摘要

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:这篇综述考虑了基于理论生态学原理的龋齿和牙周疾病的综合假设。该假说的主旨是基于口腔微生物群的动态稳定性阶段,在此阶段内在的(主要是唾液和龈沟液)和细菌的(主要是代谢的)弹性因子保持生态动力学的稳定性,与临床健康相适应。但是,固有回弹性因子的丧失和/或微生物代谢底物可用性的长期变化可能会导致微生物群的生态平衡转变为糖解(产酸)阶段或氨基酸降解/蛋白水解(碱化)阶段,具体取决于主要的底物,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,例如唾液流量和细菌营养素向口腔的流入。与传统观点相反,过量摄入可发酵碳水化合物可能会导致因高血糖而引起的牙周组织炎症。综合假说强调,龋齿和牙周疾病均起源于动态稳定阶段,并响应微生物群的营养失衡而出现。牙周疾病可能属于糖引起的炎性疾病,类似于糖尿病,肥胖症和心血管疾病。

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