有位署名为a3511260的博友留言，提供了一条非常有价值的线索：一种口腔细菌被证明是诱发类风湿性关节炎的“祸根”！据外国媒体报道，认真刷牙可保口腔健康，医学界也发现，刷牙刷得好，对心脏健康也有关联益处。最近美国一项研究又发现，认真刷牙可以帮助对抗关节炎。美国路易斯维尔大学研究人员在《科学公共图书馆·病原卷》上介绍说，诱发牙周疾病的一种主要细菌“牙龈卟啉单胞菌”，会产生一种特定的酶。
在这种酶的催化下，某些特定蛋白质的“残基”会转变为瓜氨酸。这时机体就会把这样的蛋白质误认作“入侵者”，诱发免疫反应。对于风湿性关节炎患者来说，这种免疫反应就会带来慢性炎症，引起关节内的硬骨质及软骨损伤。研究人员说，关节炎患者如果口腔内存有上述病菌，就会连锁反应般加速关节炎的病程，加重病情。研究者因此认为，认真刷牙可以帮助对抗关节炎。
我根据这条线索找到了它的原文，这是2013年9月12日发表于PLoS Pathogens上的一篇原创论文，为Open Access，点击以下论文题目即可打开阅读并下载全文：Porphyromonas gingivalis Facilitates the Development and Progression of Destructive Arthritis through Its Unique Bacterial Peptidylarginine Deiminase (PAD)。
为便于介绍，下面分别列出该文的Abstract和Author Summary。
Abstract
Rheumatoid arthritis and periodontitis are two prevalent chronic inflammatory diseases in humans and are associated with each other both clinically and epidemiologically. Recent findings suggest a causative link between periodontal infection and rheumatoid arthritis via bacteria-dependent induction of a pathogenic autoimmune response to citrullinated epitopes. Here we showed that infection with viable periodontal pathogen Porphyromonas gingivalis strain W83 exacerbated collagen-induced arthritis (CIA) in a mouse model, as manifested by earlier onset, accelerated progression and enhanced severity of the disease, including significantly increased bone and cartilage destruction. The ability of P. gingivalis to augment CIA was dependent on the expression of a unique P. gingivalis peptidylarginine deiminase (PPAD), which converts arginine residues in proteins to citrulline. Infection with wild type P. gingivalis was responsible for significantly increased levels of autoantibodies to collagen type II and citrullinated epitopes as a PPAD-null mutant did not elicit similar host response. High level of citrullinated proteins was also detected at the site of infection with wild-type P. gingivalis. Together, these results suggest bacterial PAD as the mechanistic link between P. gingivalis periodontal infection and rheumatoid arthritis.
Author Summary
Clinical and epidemiological data indicates that chronic periodontal disease (PD), one of the most prevalent infectious inflammatory disease of mankind, is linked to systemic inflammatory diseases such as cardiovascular diseases (CVD), rheumatoid arthritis (RA) and chronic obstructive pulmonary disease (COPD). Nevertheless, the causative mechanisms of association between PD and chronic inflammatory diseases are very poorly understood. Recent findings suggest a causative link between periodontal infection and rheumatoid arthritis via bacteria-dependent induction of a pathogenic response to citrullinated epitopes. In present study we show that infection with viable periodontal pathogen Porphyromonas gingivalis but not another oral bacterium (Prevotella intermedia), exacerbated CIA, as manifested by earlier onset, accelerated progression and enhanced severity of the disease, including significantly increased bone and cartilage destruction. The ability of P. gingivalis to augment CIA was dependent on the expression of a unique enzyme peptidylarginine deiminase, which converts arginine residues in proteins to citrulline. This knowledge may create new perspectives in the treatment and prevention of RA in susceptible individuals.