Breivik T, Sluyter F, Hof M, Cools A
Department of Periodontology, Faculty of Dentistry, University of Oslo, Norway.
Behav Genet. 2000 Mar;30(2):123-30. doi: 10.1023/a:1001903221046.
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.
本研究对Breivik等人（1996年）之前提出的模型进行了测试，该模型根据下丘脑-垂体-肾上腺（HPA）轴的反应性来预测牙周炎（一种炎症性疾病）的程度。简而言之，该模型表明，血浆皮质酮水平升高会通过将辅助性T细胞平衡转向更多的Th2反应来调节免疫系统，而这反过来又会增加对牙周炎的易感性。为了验证该模型，对两种基因不同的大鼠进行了比较，这两种大鼠在行为和内分泌方面对压力的反应有所不同（高皮质酮反应的APO-SUS大鼠和低皮质酮反应的APO-UNSUS大鼠）。通过结扎诱导实验性牙周炎，并通过组织学和影像学测量组织（纤维和骨）丧失的程度。结果表明，正如预期的那样，APO-SUS动物比APO-UNSUS动物对牙周炎更敏感，即表现出更多的纤维和骨丧失。这些数据与在Fischer大鼠和Lewis大鼠以及接受皮质酮治疗和肾上腺切除的动物中的发现一致，并表明HPA轴反应性变化背后的遗传因素（以及它们对压力的行为反应）在炎症性疾病的发展中起重要作用。
