by Jonathan Richter, DDS, FAGD
Rheumatoid arthritis (RA) is the most common type of autoimmune arthritis, affecting more than 1.3 million Americans. Of these, 75 percent are women, with the disease most often beginning between 40 to 60 years of age. RA is a chronic disease that causes pain, stiffness, swelling, and limited motion and function of many joints.
Being an autoimmune disease means that certain cells of the immune system do not work properly and start attacking healthy tissues — in the case of RA, the joints in the human body. Although there is no known specific cause of RA, new research is giving us a better idea of what might be the underlying cause. Johns Hopkins researchers have found a bacterium that causes chronic inflammatory gum infections, which also triggers the inflammatory autoimmune response characteristic of RA.
First author on this research Maximilian Konig, M.D., a former Johns Hopkins University School of Medicine fellow, stated: “The idea that RA, although an autoimmune disease, may be initiated by a microbial infection is not novel but has been speculated on for more than a century. One intriguing clinical observation is the fact that patients with RA frequently have severe periodontal disease and that some patients with periodontal disease may be at increased risk of developing RA.”
In recent years, the scientific understanding of the abnormal immune response in RA has grown exponentially, and is now known to be when disease-specific autoantibodies (ACPAs) target and attack proteins that had been transitioned as a result of the attack. The abnormal immune response to the transition of the proteins appears to drive the joint inflammation and destruction seen in RA.
Recent studies from Johns Hopkins suggest that neutrophils (a type of white blood cell) appear to be the source of many of these proteins targeted in this disease. The study has identified a process where the neutrophils drive pathways that create pores in the neutrophil membrane, thereby activating the cell to generate autoantigens.
The study demonstrated that the periodontal pocket in patients infected with the periodontal pathogen Aa (Actinobacillus actinomycetemcomitans) mimics the rheumatoid joint—in that they harbor the same specified proteins targeted by ACPAs in patients with RA. The researchers realized that the mechanism by which Aa drives the generation of RA autoantigens was very similar to what they saw before in the inflamed joints of patients with RA. At this point, how these findings are best applied to patients with RA remains uncertain; however, it is clear that good hygiene and proactive steps to minimize periodontal disease could offer a way of preventing RA.
Source: Jonathan Richter, DDS, FAGD, of Cardiodontal (310 E. Shore Rd., Ste. 101, Great Neck). For more information or to schedule an appointment, call 516-282-0310 or visit Cardiodontal.com.
