Department of Microbiology, Faculty of Biochemistry, Biophysics, and Biotechnology, Jagiellonian University, ul. Gronostajowa 7, 30-387, Krakow, Poland,
Curr Rheumatol Rep. 2014 Mar;16(3):408. doi: 10.1007/s11926-014-0408-9.
Porphyromonas gingivalis is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme, P. gingivalis peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host's signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.
牙龈卟啉单胞菌是慢性牙周炎的主要病原体,这是一种涉及支持牙齿的组织进行性破坏的疾病过程。最近,该生物体被报道产生一种独特的细菌酶,即牙龈卟啉单胞菌肽精氨酸脱亚氨酶(PPAD),它具有将蛋白质中的精氨酸残基转化为瓜氨酸的能力。蛋白质瓜氨酸化改变了蛋白质的结构和功能;因此,PPAD 可能参与宿主信号网络的失调和免疫逃避。此外,越来越多的证据表明,针对瓜氨酸化蛋白的自身免疫在类风湿关节炎 (RA) 的发展中起作用。由于吸烟者肺部的炎症状态导致对瓜氨酸化表位的免疫耐受被打破,因此在牙周炎部位慢性暴露于瓜氨酸化蛋白也可能使易感个体易患自身抗体并引发 RA。在这篇综述中,我们讨论了证据表明 PPAD 可能代表牙周炎和 RA 之间的一种机制联系,这两种疾病在流行病学水平上已知有显著的相关性。