By A. G. Moore
There are, it seems, two major types of gum inflammation: one is caused by plaque formation and irritation. This is called gingivitis and is the kind of gum disease most people experience; gingivitis is usually resolved by prophylaxis in the dentist’s office. In a small percentage of cases,unresolved gingivitis leads to periodontitis, which is a more serious condition. Periodontitis is a chronic, inflammatory, autoimmune response to pathogens. Although inflammation occurs with gingivitis, it is localized; tooth structure and underlying bone are not involved as they are with periodontitis.(See: Columbia College of Dental Medicine, http://www.simplestepsdental.com/SS/ihtSS/r.==/st.32477/t.35030/pr.3.html)
The disease process in periodontitis is similar to that in other autoimmune diseases and the condition is just as recalcitrant to treatment. As with systemic autoimmune diseases, the condition can wax and wane and responds more or less to to medical intervention on a case by case basis.
While I could find a very weak, if any, association between periodontitis and systemic lupus, there was a strong correlation between this kind of gum disease and other systemic inflammations. Periodontitis of the autoimmune variety has been implicated in the development of rheumatoid arthritis (see NIH article: http://www.ncbi.nlm.nih.gov/pubmed/11453241), atherosclerosis and diabetes (see Periodontitis and Diabetes Interrelationships: Role of Inflammation. http://www.ncbi.nlm.nih.gov/pubmed/11887455). Periodontitis has also been shown to be associated with end stage renal disease (see: Effect of Periodontitis on Overt Nephropathy and End-stage Renal Disease in Type 2 Diabetes http://www.ncbi.nlm.nih.gov/pubmed/17259499).
Although the evidence I uncovered for a link between SLE and periodontitis was weak, there was one kind of lupus that did correlate strongly with this gum condition: acute cutaneous lupus erythematosus. (see Aggressive Periodontitis and Chronic Cutaneous Lupus http://www.lupus.org/webmodules/webarticlesnet/templates/new_donatenow.aspx?articleid=457&zoneid=43).
It’s tempting, when finding associations between conditions, to suggest that one causes the other. But many of the articles I’ve cited in this post are careful to draw a distinction between cause and correlation. In the National Institutes of Health piece on end-stage renal disease, for example, the authors point out that it is not yet determined whether treatment of periodontitis will affect the course of renal disease.
On the other hand, in the instance of the diabetes/periodontitis correlation, the author of the NIH article suggests that causation goes both ways: having type 2 diabetes predisposes someone toward development of periodontitis and chronic periodontitis can instigate kidney inflammation.
How does this help us, besides adding to our understanding of our bodies? Established protocols for treating autoimmune diseases depend heavily on immune suppression. This brings with it a host of problems, as we all know. A significant possibility exists, we learn now, that specific pathogens (infectious agents) may be implicated in the development of lupus. Therefore, instead of suppressing the entire immune system–which is kind of like spraying shotgun pellets at a scurrying mouse–we might be able to target specific antagonists.
Wouldn’t that be a wonderful revolution in lupus treatment?