Gingivitis and periodontitis are thought to result from an imbalance between those oral microorganisms which normally colonize tooth surfaces in close contact with the gingival margin, and the nature and efficiency of the host response. The bacteria are the triggering agents, but host defence mechanisms within the gingival/periodontal tissues seem to be responsible for most of the tissue damage and for the outcome and progression of the diseases. It has recently been shown that emotional or psychological load (stress) may influence immune activities directly via nerve messenger substances (neurotransmitters and neuropeptides) and/or indirectly via neuroendocrine (hormone) substances. This review discusses how emotional stressors and nervous and neuroendocrine responses to psychological stressors may modulate the immune response to bacteria, and thus be expected to influence the progression and course of gingivitis and periodontitis.

The aim of this study was to test the hypothesis of an association between hypothalamic-pituitary-adrenal (HPA) axis reactivity and progression of periodontal disease. Histocompatible Lewis and Fischer 344 rats respond to stressful stimuli with low and high HPA axis reactivity, respectively. Experimental periodontitis was induced by tying a silk ligature around the neck of maxillary 2nd right molar teeth in 10 Lewis and 10 Fischer 344 rats with contralateral non-manipulated teeth as controls. Twenty non-manipulated animals were included. Also, experimental periodontitis was induced in 10 adrenalectomized Wistar rats and in 10 sham-operated rats. Furthermore, corticosterone pellets were subcutaneously implanted in 9 Lewis rats, while placebo pellets were implanted in 8 animals. Disease progression was evaluated histometrically and radiographically. The low-responding Lewis rats developed significantly less periodontal breakdown than did the high-responding Fischer 344 rats. Administration of corticosterone increased the disease development. while adrenalectomy reduced the disease severity. Our findings demonstrate the importance of genetic factors in the development of periodontal disease, and suggest that HPA axis hyper-activation is one mechanism by which periodontal disease susceptibility may be increased.

The findings support recent studies suggesting that traumatic life events such as the loss of a spouse may increase the risk for periodontal disease. Above all, the present results indicate that an individual's ability to cope with stressful stimuli (coping behavior), as measured by the beliefs of locus of control of reinforcements may play a role in the progression of periodontal disease.

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These experimental results are consistent with an emerging literature showing that life stress, anxiety, depression, pathological grief, and poor coping behaviour may dysregulate regulatory mechanisms within the brain involved in immune regulation, and thereby alter immune responses and influence the susceptibility/resistance to inflammatory disorders.