Potential Link Between Periodontal Disease and Prostatitis

By Nabil F. Bissada, BDS, DDS, MSD

Periodontitis may contribute to an increased level of PSA level in patients with common prostatitis, which probably occurs through dissemination of various cytokines that can further exaggerate the preexisting inflammation. In our research, which was published in the Journal of Periodontology, we examined 35 men, all of whom had some kind of prostatitis (ie, either mild or a more serious form) as confirmed by a clinical urological and rectal examination, as well as prostate-specific antigen (PSA) levels and needle biopsy of the prostate. Those studied had not received dental care in 3 months, and their gum health was examined and evaluated. The groups were then broken into two, including those who demonstrated high PSA levels or malignancies and those who demonstrated low to normal PSA levels. We found that in patients with both severe prostatitis and severe periodontitis, their PSA levels were significantly higher than those with only periodontitis or prostatitis alone.

This is significant because this is the first of kind of study relating inflammation of the prostate to periodontal disease in the oral cavity. Conventional thought has been that PSA is very specific to the prostate gland, with nothing to do with periodontal disease, because PSA is really produced by the epithelial cells of the acini of the prostate gland itself. Because it is processed, formed, and excreted into the bloodstream, we postulated that too much of it would be an indicator or a marker for inflammation of the prostate, among other things.

What’s surprising is that when we divided our patients into groups of mild to no periodontitis and moderate to severe periodontitis, we found that the PSA levels in the bloodstreams of those patients with more severe periodontitis was higher than the normal range or than those with no or a very mild form of periodontal disease. Based on this observation, we have concluded that PSA is not a marker or a screening marker for inflammation of the prostate only, but probably also is an inflammatory marker like others we know in the body, such as cytokines and C-reactive proteins, which are good inflammatory markers for the presence of systemic inflammation in the body.

A longitudinal study is needed to determine causality. Which one comes first: inflammation of the mouth or inflammation of the prostate? Another study already underway is an interventional study to provide more concrete answers concerning the link between inflammation of the prostate and inflammation of the periodontia in the mouth. If those patients with chronic prostatitis and chronic periodontitis are treated for chronic periodontitis, would this have an impact on (1) lowering the PSA level; and (2) reducing the signs and symptoms of the prostatitis?

About the Author

Nabil F. Bissada, BDS, DDS, MSD
Professor and Chairman
Department of Periodontics
School of Dental Medicine
Case Western Reserve University
Cleveland, Ohio
nabil.bissada@case.edu