Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease primarily of the joints that, if lelt untreated, results in functional disebility concordant with radiographic progression. It is well recognized that strking pathogenic similarities exist between periodontitis and RA. Proinflammatory cytokines such as tumor necrosis factoralpha (TNF a) and interleukin (IL) as well as microbial enzymes and host matrix metalloproteianses (MMP-8 and -9) appear to play important roles in both conditions | One of the strengths of our study was the inclusion of a control group of patients with OA in whom there was no other inflammatory arthritis and who were demographically similar to the patients with RA. We were also able to control for many of the potential confounder of the relationship between RA and periodontitis inflammation. Such as smoking, DM, gender, race, medication use, and age. Limitations of our study include the ralatively low number of patients, particularly in the comparator group with OA. Also, the exact effect of the medications used to treat both RA and OA on periodontitis requires a larger cohort that also includes normal controls. In addition, one-third of the patients with RA had inactive disease as measureed by DAS28(4v), which, albeit an important clinical goal, may have limited our ability to dectect significant correlations with periodontitis severity. In addition, this piot study does not include relevant genotyping and serologic analyses, efforts that will be critical in future studies examining these clinical association. Also, given the unique attibutes of this veteran cohort (predonminantly older men), it is possible that our findings are not applicable to other RA populations, specifically, younger women.
