THE ROLE OF STRESS IN PERIODONTAL DISEASE

In 1878, Louis Pasteur observed that chickens that were normally resistant to anthrax become susceptible following immersion in cold water. This discovery probably marked the beginning of research on the relationship between stress and infectious diseases. Over the last decade, the field of psychoneuroimmun-
ology has provided more and more evidence about how the immune system communicates with the nervous and endocrine (hormone) systems durning periods of stress - evoking changes to the body that are clinically profound.

Evidence of the damaging effects of stress on the tissues surrounding teeth (periodontium) has been accumulating for over 50 years. However, because the lack of multiple longitudinal studies preventing stress from being labeled a "risk factor" per se as it relates to periodontal disease, it is widely acknowledged that it is a "risk indicator" for the onset, progression and severity of periodontal disease ("pyorrhea") which is, basically, an infection of the bone that can lead to tooth loss. Other risk indicators such as osteoporosis, HIV, and immunocompromised conditions are commonly accepted as other variables that influence the bone degredation around the teeth.

As with other chronic infections, the onset and progression of periodontal disease is largely programmed by the influence of certain local and systemic risk factors that have a dramatic effect on the resistance of the host to certain pathogenic (disease-producing) germs (bacteria). These germs are called "periodontal pathogens" and the factors that increase the chance that they will cause disease are called "risk factors" among which smoking, diabetes and a genetic variable called "interleukin-1 polymorphism" (IL-1 genotype) are examples. Smokers are four times more likelly to have periodontal disease than non-smokers and diabetics with poorly controlled blood sugar levels have a much greater bone loss probability than those under control at about five times more. The IL-1 genotype is a specific genetic marker that identifies patients who have an increased risk for severe periodontal disease. Non-smokers or former light smokers who are also IL-1 genotype positive are more than three times more likely to acquire moderate to severe disease than those who are genotype negative; patients who are both smokers and genotype positive may be 7.7 times more likely to have tooth loss than non-smokers who are negative. (Patients can be tested for this IL-1 polymorphism).

It is generally recognized that microorganisms (germs) possess the ability to recognize hormones within their hosts and to utilize them in order to adapt to their surroundings. This supports the supposition that psychological stress may favor the development of many bacerial infections. Researchers have learned that two hormones - adrenaline and noradrenaline (the "catacholamines") - are released during the human stress response (from the adrenal glands and the autonomic nervous system) and these agents act as environmental cues to alter the growth of forty three microorganisms found within the colonies of plaque that live under the gumline (pockets) around the teeth (called "biofilm"). They found that a little under half of these bacterial species were stimulated to grow when the noradrenalin was injected into the mass and a little over half showed an increase in growth when inoculated with adrenalin. There was also a difference in growth response within bacterial species and within and between the biofilm complexes. It is thought that this variations may influence the composition of the biofilm allowing the more pathogenic bacteria to thrive which, in turn, creates an environment for a more severe form of periodontal disease.