牙周病,牙周组织的慢性炎症性疾病,不仅是牙齿脱落的主要原因,但它也已知会加剧/与各种代谢紊乱有关,比如肥胖,糖尿病,血脂异常,和心血管疾病。最近,越来越多的证据表明,牙周病对肝病的病理生理有不利影响。特别是,非酒精性脂肪性肝病,代谢综合征的肝脏表现,与牙周病有关.非酒精性脂肪性肝病的特征是在没有习惯性饮酒史的情况下肝脏脂肪沉积,病毒感染,或自身免疫性疾病。非酒精性脂肪性肝病的一个子集可以发展成更严重和进行性的形式,即非酒精性脂肪性肝炎。后者可导致肝硬化和肝细胞癌,这是终末期肝病。广泛的研究提供了合理的机制来解释牙周病如何对非酒精性脂肪性肝病和非酒精性脂肪性肝炎产生负面影响。即通过血行或肠内途径。在牙周炎期间,肝脏不断暴露于从口腔全身扩散的各种致病因素,如细菌及其副产品,炎性细胞因子,和活性氧,这些可能参与非酒精性脂肪性肝病和非酒精性脂肪性肝炎的疾病促进。此外,由牙周病菌的肠内易位引起的肠道菌群失调可能会损害肠壁屏障功能,并促进肝毒素和肠杆菌通过肠肝循环转移到肝脏。此外,在代谢综合征人群中,牙周炎与胰岛素抵抗相关的全身疾病之间的相互作用进一步加强了与非酒精性脂肪性肝病的相关性.然而,人类牙周炎和非酒精性脂肪性肝病之间的大多数病理联系是由流行病学观察研究提供的,因果关系尚未建立。一些系统和荟萃分析研究也显示出相互矛盾的结果。此外,牙周治疗对非酒精性脂肪性肝病的影响几乎没有研究。尽管有这些限制,牙周病的全球负担以及近期非酒精性脂肪性肝病的流行具有重要的临床和公共卫生意义.新出现的证据表明牙周疾病和肝脏疾病之间存在关联,因此,我们提出术语牙周病相关的非酒精性脂肪性肝病或牙周病相关的非酒精性脂肪性肝炎。在这一领域的持续努力将为基于牙周学观点的新诊断和治疗方法铺平道路,以解决这种危及生命的肝病。
Periodontal disease, a chronic inflammatory disease of the periodontal tissues, is not only a major cause of tooth loss, but it is also known to exacerbate/be associated with various metabolic disorders, such as obesity, diabetes, dyslipidemia, and cardiovascular disease. Recently, growing evidence has suggested that periodontal disease has adverse effects on the pathophysiology of liver disease. In particular, nonalcoholic fatty liver disease, a hepatic manifestation of metabolic syndrome, has been associated with periodontal disease. Nonalcoholic fatty liver disease is characterized by hepatic fat deposition in the absence of a habitual drinking history, viral infections, or autoimmune diseases. A subset of nonalcoholic fatty liver diseases can develop into more severe and progressive forms, namely nonalcoholic steatohepatitis. The latter can lead to cirrhosis and hepatocellular carcinoma, which are end-stage liver diseases. Extensive research has provided plausible mechanisms to explain how periodontal disease can negatively affect nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, namely via hematogenous or enteral routes. During periodontitis, the liver is under constant exposure to various pathogenic factors that diffuse systemically from the oral cavity, such as bacteria and their by-products, inflammatory cytokines, and reactive oxygen species, and these can be involved in disease promotion of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Also, gut microbiome dysbiosis induced by enteral translocation of periodontopathic bacteria may impair gut wall barrier function and promote the transfer of hepatotoxins and enterobacteria to the liver through the enterohepatic circulation. Moreover, in a population with metabolic syndrome, the interaction between periodontitis and systemic conditions related to insulin resistance further strengthens the association with nonalcoholic fatty liver disease. However, most of the pathologic links between periodontitis and nonalcoholic fatty liver disease in humans are provided by epidemiologic observational studies, with the causal relationship not yet being established. Several systematic and meta-analysis studies also show conflicting results. In addition, the effect of periodontal treatment on nonalcoholic fatty liver disease has hardly been studied. Despite these limitations, the global burden of periodontal disease combined with the recent nonalcoholic fatty liver disease epidemic has important clinical and public health implications. Emerging evidence suggests an association between periodontal disease and liver diseases, and thus we propose the term periodontal disease-related nonalcoholic fatty liver disease or periodontal disease-related nonalcoholic steatohepatitis. Continued efforts in this area will pave the way for new diagnostic and therapeutic approaches based on a periodontologic viewpoint to address this life-threatening liver disease.