Decoupling periodontal infection and inflammation

Jan. 1, 2012
The factors, events, and conditions required for the development and progression of periodontal disease are well understood at this point.

By Richard H. Nagelberg, DDS

The factors, events, and conditions required for the development and progression of periodontal disease are well understood at this point. The infectious and inflammatory components of periodontal disease occur in a linear manner in which the inflammatory response necessarily follows the infection of the gingival tissues by bacteria, including the periodontal pathogens.

We now know that the body’s inflammatory response is primarily responsible for periodontal tissue breakdown. In other words, the body is doing it to itself.

The other necessary player in the process is genetics. People must be genetically susceptible to periodontitis for it to occur. Those who are not genetically programmed for periodontal disease can withstand much higher oral bacterial loads than those who are genetically prone to periodontitis. We also now know that gingivitis is not an early form of periodontitis, but rather the gatekeeper to it. Not all cases of gingivitis progress to full-blown periodontal disease.

Bacteria are necessary, but not capable on their own of producing periodontal disease. The body’s response to the bacteria is required for tissue breakdown to occur. As an analogy, consider the effect of cigarettes on heart disease and lung cancer. The cigarette, on its own, unlit, cannot cause disease. It has to be lit and smoked; the body’s response to the burning tobacco and paper is what will potentially cause pulmonary and cardiovascular diseases. The bacteria cannot cause periodontal disease on their own. It is the interplay between the bacteria and the body’s response to those bacteria that determines the level of periodontal disease manifested.

In order to reduce biofilm aggregation, we provide professional care for our patients and make home-care recommendations. If successful, the oral bacterial load will be held to a level the body can handle. If the immune system is not ignited, tissue damage will not occur. This does not constitute decoupling the infectious and inflammatory components of periodontal disease, but rather the absence of signaling the immune system into action to combat a bacterial infection, since an infection has not occurred.

Decoupling periodontal infection and inflammation would involve a failure of the inflammatory response to mobilize despite a significant bacterial challenge. This is substantially what occurs in individuals who are not genetically programmed for periodontitis. They can have lots of biofilm in the mouth, but do not progress past gingivitis because the genetic coding necessary for periodontitis expression does not exist.

The ability to decouple periodontal infection and inflammation may provide something that realistically approaches a cure for periodontal disease. There is a global or whole body immune system and localized immune systems for various organs and areas of the body, including the oral cavity. Turning off the entire immune system would prevent periodontal tissue breakdown, but is not consistent with life. If we could, however, turn off the local immune system for the oral cavity, then biofilm accumulation could occur, even to considerable levels, and periodontal tissue destruction could not occur since the immunoinflammatory response is not capable of being switched on.

When this approach to a cure for periodontal disease or some other mechanism becomes available to the profession, this does not mean that unchecked biofilm accumulation will be our recommendation. Research has shown an association between specific periodontal pathogens and an increased risk for acute myocardial infarction, atherosclerosis, coronary obstruction, rheumatoid arthritis, and hypertension, among others. These associations were observed independently of periodontal disease; in other words, the bacteria themselves are implicated.

At this time when there is no cure for periodontal disease, except edentulousness, we are now capable of providing highly individualized periodontal treatment rather than a one-size-fits-all approach. This is made possible by salivary diagnostics, host modulatory meds, oral probiotics, lasers, and chemotherapeutics, to name a few. If the eventual cure for periodontal disease is achieved through decoupling periodontal infection from inflammation, then we may be back to optimal treatment for periodontal disease by a one-size-fits-all approach.

Dr. Richard Nagelberg has practiced general dentistry in suburban Philadelphia for more than 29 years. He is a speaker, advisory board member, consultant, key opinion leader for several dental companies and organizations, and lecturer on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at [email protected].

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