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Genetic Susceptibility Testing in Periodontal Therapy

For several centuries the dental profession has evolved in the recognition and treatment of periodontal disease. Patients arrive at the dental office, receive a diagnosis of existing periodontal pathology and, hopefully, complete a course of treatment to restore as nearly as possible the original state of health. This has become know as the treatment-based approach to controlling disease.

During the 1920's, Churchill discovered that individuals in areas with high natural fluoride concentrations in their drinking water experienced much less decay. Subsequent study revealed that the fluoride content of enamel constituted a risk factor for caries. Controlling this risk factor, in this case optimizing fluoride levels in the drinking water, resulted in large reductions in decay. This information-based, risk reduction approach to controlling disease has been termed the "prevention" or "medical" model. Risk factor control has become commonplace in trying to treat chronic diseases such as coronary artery disease, osteoporosis, diabetes and arthritis. Periodontal disease is a chronic disease, multifactorial in origin. As we become better aware and can identify those factors which put people at high risk, our periodontal treatment approaches can be selected with much greater accuracy. Consequently, we will become more sophisticated at providing the proper level of preventive services to individuals. Previous editions of the newsletter have dealt with smoking as one significant risk factor in the etiology of periodontal disease. Recently, a genetic susceptibility marker for periodontal disease has been identified which may improve our ability to decide who must receive extensive periodontal therapy and more stringent post-treatment preventive services. This newsletter capsulizes genetic risk assessment in periodontal therapy.

Clinicians have recognized for years that some individuals get lots of plaque and calculus, but experience little loss of periodontal support. Other patients seem to have really clean mouths, but experience extensive bone loss. Their disease is not so much related to the quantity of bacteria as to some other factor. While the presence of certain bacteria have been correlated with more extensive periodontal disease (juvenile periodontitis, localized juvenile periodontitis), other forms of extensive disease are not so clearly identified with specific bacteria (like refractory periodontal disease). Research scientists reason that the spread of disease may also be dependent on the host response. In 1989, Garrison and Nichols reported a marked difference between the monocyte cell's response to bacteria in patients with advanced periodontal destruction and those who were resistant to disease. In patients with advanced periodontal disease, blood monocytes (which transform to macrophages once into the tissues and attack toxins produced by bacteria) were two to three times more likely to gravitate towards endotoxin produced by gram negative bacteria than were blood monocytes in those with little disease. This effect was sustained in spite of the stage of treatment of the patient's periodontal disease, indicating a genetic response factor was responsible. And within the past two years, research has indeed identified a genetic marker that can be correlated with the degree of tissue destruction that occurs in some periodontal patients with advanced disease.

Genetic testing for periodontal disease susceptibility hinges on measuring a gene which regulates the production of an inflammation mediator called Interleukin 1B. Interleukin 1B is a strong stimulator of host cells, which destroy bone and soft tissue in an attempt to limit the spread of infection. This destruction happens more as a result of the intensity of the response to a bacterial challenge than to the quantity of bacteria challenging the system. The intensity of the response is determined by the gene makeup dictating the quantity of interleukin 1B cells produce in response to a bacterial challenge. Think of it this way. Each parent contributes chromosomal material to the gene that determines if interleukin 1B will be produced in small or large quantities. Each parent can have, from their parents, a gene makeup which possesses either a negative molecular base for extra interleukin 1B production or a positive molecular base for extra interleukin 1B. When parents have a child, the child can then have three possible combinations of interleukin 1B molecular bases. They can have negative-negative, negative-positive or positive-positive combinations. Jotwani, researching gene types, has shown that positive-positive gene combination individuals produce four times as much interleukin 1B as do those individuals with a negative-negative combination. Kornman has calculated periodontal disease progression to be seven times more likely in positive-positive gene combinations than in negative-negative combinations. Currently, only smoking overrides this genetic risk marker as a predictor of periodontal destruction.

This effect on periodontal disease is so pronounced because interleukin 1B participates in the response to a bacterial challenge in several ways. Interleukin 1B is one of a class of local tissue response modifiers called interleukins (older terms taught in dental schools were cytokines and lymphokines) whose role is to facilitate cell-to-cell communications. The potentiating effect of Interleukin 1B in bone destruction is enhanced disproportionally in positive-positive gene combination individuals.

The trade name of this test is PST (for periodontal sensitivity testing). It requires the clinician to do a finger stick on the patient and place 3 drops of blood on a sampling card. (A more recent version allows for saliva samples to be used.) The card is sent to a commercial laboratory in Flagstaff, Arizona where the genetic makeup of the interleukin 1B gene site is determined. Currently the test costs $210.00.

What does a positive test mean in terms of care? A positive test would first advise the clinician that supportive therapy at shortened intervals is essential. Perhaps these patients may need professional deplaquing at four to six week intervals. It might also indicate a benefit to be gained with the use of connective tissue stabilizing medications, inflammatory reaction suppressants and/or periodic antibiotics as well as organism susceptibility testing. Initial preparation procedures with closer monitoring may be completed first, but where pockets persist surgical care followed by stringent maintenance may be the most effective treatment because it will produce the greatest reduction in Interleukin 1B production.

This is a new process which will require some time to become cost effective, but could prove in the near future to be highly beneficial as a screening tool in predicting disease potential. Prevention (and perhaps gene manipulation) could then be better tailored to individual needs. We look forward to any questions you might have regarding this advance in periodontal diagnosis.
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