Periodontal disease, periodontal pathogens, and rheumatoid arthritis update

The concept of a relationship between periodontal disease and rheumatoid arthritis (RA) was discussed more than 50 years ago. There is much about the origin of rheumatoid arthritis that is still unknown. The anatomic site at which RA-related autoimmunity is initiated and the timing are also elusive currently. Systemic inflammation and the autoimmune processes begin long before the onset of perceptible joint inflammation.

Feb 26th, 2015

Richard H. Nagelberg, DDS

The concept of a relationship between periodontal disease and rheumatoid arthritis (RA) was discussed more than 50 years ago. There is much about the origin of rheumatoid arthritis that is still unknown. The anatomic site at which RA-related autoimmunity is initiated and the timing are also elusive currently. Systemic inflammation and the autoimmune processes begin long before the onset of perceptible joint inflammation.

Research suggests that RA-related autoimmunity may be initiated at a mucosal site years before the onset of joint symptoms. Potential sites of initiation include gastrointestinal, lung, and oral mucosa. Additional studies of individuals in the preclinical period of RA that can provide insight into the relationship between mucosal inflammation, RA-related autoantibody generation, and subsequent joint inflammation in RA are needed. An improved understanding of the initial steps in the development of RA would provide insights into disease pathogenesis leading to more effective treatments and/or novel preventive strategies in RA (Demoruelle et al. 2014).

Since the publication of the first study in 2009 (Smolik et al.), which revealed the association between Porphyromonas gingivalis (Pg) and rheumatoid arthritis, a number of additional studies have been conducted that reach the same conclusion as the original one. The Smolik study indicated that further studies were needed to affirm their findings, and that affirmation is well under way.

The body produces a number of enzymes called peptidylarginine deiminases (PADs). These enzymes convert the amino acid arginine within a peptide (i.e., protein building blocks) into peptidylcitrulline in a process known as citrullination. Protein citrullination plays a vital role in normal physiology, in which it is involved in the formation of rigid structures such as skin, hair, and myelin sheaths, as well as other normal physiological effects in the body. So the enzyme PAD and the process of protein citrullination are important components of normal physiology. P. gingivalis is the only microbe known also to produce the enzyme PAD. Aberrant citrullination has been observed in a variety of diseases, including RA and diseases of the skin and nervous system.

Research findings indicate that oral citrullination of human and bacterial proteins by the PAD enzyme produced by P. gingivalis triggers an antibody response to the modified protein. This citrullination by the bacterial PAD occurs within the inflammatory context of periodontal diseases, including periodontitis and gingivitis. The body mounts an inflammatory response to the citrullinated proteins. This inflammatory response occurs throughout the body, including the joints. The prevailing theory indicates that P. gingivalis-mediated citrullination triggers the autoimmunity typically seen in individuals who are genetically susceptible to rheumatoid arthritis. The autoimmune processes lead to the soft and hard tissue joint damage in individuals with RA.

The sequence of events in which the disease process is initiated long before the onset of detectable joint damage in RA is reminiscent of the same long time frame for the development of type 2 diabetes. In that case, the insulin-producing beta cells in the pancreas can be burning out long before the signs of diabetes are noticed by the individual or their health-care provider.

Research also suggests that individuals with RA have a higher incidence and severity of periodontal disease, and that treatment of gum disease can improve the symptoms of RA. These findings are very preliminary and cannot be understood to be conclusive. However, it is not premature to provide the status of research to patients as long as it is done in an accurate, ethical manner. Promises of improvement in joint signs and symptoms would be examples of inappropriate verbiage. It would be ethical and appropriate to indicate that research suggests an association between periodontal disease, Pg, and rheumatoid arthritis, but that conclusive evidence does not yet exist. It would be appropriate to use salivary DNA testing to identify the presence of Pg. It is appropriate and our responsibility to control every bit of periodontal disease. If a patient tests positive for Pg and does not have periodontal disease, it is appropriate to recommend a power toothbrush such as the Philips Sonicare FlexCare Platinum.

It is not too soon for responsible education, treatment, and recommendations. Our patients need not be in the dark about what the scientific community is discovering.


Richard Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at gr82th@aol.com.

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