Olsen Ingar
Department of Oral Biology, Faculty of Dentistry, University of Oslo , Oslo , Norway.
Acta Odontol Scand. 2015;73(8):563-8. doi: 10.3109/00016357.2015.1007480. Epub 2015 Apr 20.
To give an overview of the periodontal-systemic connection seen from a microbiologist.
Original research papers, review articles and workshop proceedings were consulted.
Periodontal bacteria can cross epithelial cells, enter the circulation, invade endothelial cells, induce endothelial cell dysfunction and activate inflammatory and immune responses. Several studies support the association between periodontitis (PD) and cardiovascular disease. Severe PD involves a risk for development of type 2 diabetes. Maternal PD is moderately associated with adverse pregnancy outcome and pre-eclampsia. Dental plaque can contain respiratory pathogens able to promote chronic obstructive pulmonary disease and pneumonia. Periodontal bacterial DNA has been detected in synovial fluid of patients with rheumatoid arthritis. Minor evidence exists for associations between PD and chronic kidney disease, obesity, cancer, metabolic syndrome and cognitive impairment. Concerns can be raised as to the interpretation of some study results due to heterogeneity in definitions used for PD, too much weight upon in vitro studies with a few selected organisms and failing recognition that the majority of the periodontal microbiota is not yet cultivated.
Periodontal bacteria may participate in extra-oral infections such as CVD, diabetes, APO, pre-eclampsia, COPD, pneumonia, RA, CKD, obesity, cancer, MetS and cognitive impairment. Most knowledge is based on associations which do not necessarily imply causality. Future studies should reach consensus on the definition of PD and systemic disease outcomes, recognize the full spectrum of the microbiota in PD and bacteremia, including not-yet-cultivated organisms and delineate the clinical significance of genetic strain variations and the role of periodontopathogenic vs gut organisms within atheromatous lesions. For demonstration of causality, large, long-term clinical studies should use well-defined criteria for PD and robust disease outcomes to elucidate the importance of PD intervention and prevention.
从微生物学家的角度概述牙周-全身联系。
查阅原始研究论文、综述文章和研讨会论文集。
牙周细菌可穿过上皮细胞,进入循环系统,侵袭内皮细胞,诱导内皮细胞功能障碍并激活炎症和免疫反应。多项研究支持牙周炎(PD)与心血管疾病之间的关联。重度牙周炎会增加2型糖尿病发生的风险。孕妇患牙周炎与不良妊娠结局和先兆子痫中度相关。牙菌斑可能含有能够引发慢性阻塞性肺疾病和肺炎的呼吸道病原体。在类风湿性关节炎患者的滑液中已检测到牙周细菌DNA。关于牙周炎与慢性肾病、肥胖、癌症、代谢综合征和认知障碍之间的关联仅有少量证据。由于牙周炎定义的异质性、对少数选定微生物的体外研究权重过大以及未认识到大多数牙周微生物群尚未培养,因此对一些研究结果的解释可能存在问题。
牙周细菌可能参与口腔外感染,如心血管疾病、糖尿病、动脉粥样硬化、先兆子痫、慢性阻塞性肺疾病、肺炎、类风湿性关节炎、慢性肾病、肥胖、癌症、代谢综合征和认知障碍。大多数知识基于关联性,不一定意味着因果关系。未来的研究应就牙周炎和全身疾病结局的定义达成共识,认识到牙周炎和菌血症中微生物群的全貌,包括尚未培养的微生物,并阐明基因菌株变异的临床意义以及牙周致病微生物与肠道微生物在动脉粥样硬化病变中的作用。为了证明因果关系,大型长期临床研究应使用明确的牙周炎标准和可靠的疾病结局来阐明牙周炎干预和预防的重要性。