Stress-Periodontitis-Relationships-A Case for Psychoneuroimmunology?

Article excerpt

Summary

The present paper discusses psychoimmunological aspects of periodontitis, an inflammatory disease with high prevalence in adult western communities. A brief introduction into epidemiology and pathogenesis of periodontitis precedes a review of current data on stressperiodontitis relationships. The role of interleukin-16 in the pathogenesis of periodontitis is explained and we briefly summarize data on the effects of stress on interleukin-16. We describe the methods we use to assess the local immune response within the periodontium as well as the experimental gingivitis model we employ to study the interactions between stress and accumulation of microbial plaque. The results of two studies assessing stress effects on local interleukin 113 levels under conditions of continuous plaque accumulation vs. perfect oral hygiene are shown and their implications for the risk of periodontal breakdown in patients discussed. Finally we deal with some interesting aspects of the temporal dynamics of stress-induced immune alterations. Concluding remarks give some ideas of what we believe future PNI research on stress-periodontitis relationships should involve.

Key words: stress, periodontitis, psychoneuroimmunology.

Periodontitis - epidemiology and pathogenesis About 15% of the adult western communities suffer from periodontitis, an inflammation of the periodontal tissue which results in irreversible damage to the alveolar bone and the periodontal tissue. The disease causes attachment loss of the affected teeth and - if untreated - ends up with tooth loss. Indeed, the major reason for tooth loss in German and North American adults seems to be periodontitis and not - as one might assume - caries (Johnson et al., 1988; Micheelis & Reich, 1999). The most prevalent form of periodontitis is adult periodontitis which progresses slowly over years and very often remains undetected for a long time since the clinical signs can be very decent until gingival recessions and increased tooth motility result from the chronic inflammatory process.

The fundamental steps in the etiopathogenesis of marginal periodontitis are well known: Accumulation of supragingival microbial plaque induces gingivitis which results in pseudopockets further hampering oral hygiene. This facilitates subgingival plaque growth which then may result in inflammation of the whole periodontium at the site of infection including the alveolar bone; bacterial enzymes and toxins and the immune reponse of the host induce irreversible tissue damage especially to the alveolar bone. The gingivitis has now become a periodontitis. Periodontal pockets evidence the former inflammation and, even with professional treatments a restitutio ad integrum is not possible anymore at this stage of the disease. Periodontal patients need lifelong professional help in cleaning their periodontal pockets. Accumulation of supragingival plaque is a conditio sine qua non in the pathogenesis of periodontitis. However, once periodontal pockets have established subgingival plaque may exist in the absence of supragingival plaque and thus may further impair periodontal health. Although a gingivitis precedes the first manifestation of periodontitis it seems as if further development of the disease may occur independently of whether clinical signs of gingivitis can be observed or not (Johnson et al., 1988).

Stress - a risk factor in periodontitis? For many years attempts have been made to prevent periodontitis mainly by improving oral hygiene. However, it has now been realized that the level of oral hygiene which is necessary to completely prevent periodontal inflammations, i.e. removement of any plaque at least once daily, cannot be achieved on a community level (Seymour, 1991). Furthermore, while nearly 100% of the western communities show insufficient oral hygiene only about 15% suffer from periodontal disease (Griffiths et al., 1988; Johnson et al., 1988; Micheelis & Reich, 1999). …