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This study tests the model presented previously by Breivik et al. (1996), in which the extent of periodontitis, an inflammatory disease, is predicted from the reactivity of the HPA-axis. Briefly, the model implies that elevated plasma levels of corticosterone modulate the immune system by shifting the T-helper balance toward a more Th2 response, which, alternately, increases the sensitivity to periodontitis. To test this model, two genetically distinct types of rats that differ both behaviorally and endocrinologically in their response to stress (high corticosterone responding APO-SUS rats and low corticosterone responding APO-UNSUS rats) were compared. Periodontitis was experimentally induced through the placement of a ligature and measured as the extent of tissue (fiber and bone) loss, both histologically and radiographically. The results show that, as expected, APO-SUS animals are more sensitive to periodontitis, i.e., show more fiber and bone loss, than APO-UNSUS animals. These data are in agreement with findings in Fischer and Lewis rats, as well as with corticosterone treated and adrenalectomized animals and suggest that genetic factors underlying the variation in the reactivity of the HPA-axis (and, accordingly, their behavioral response to stress) play an important a role in the development of inflammatory diseases.

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