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目的:通过建立大鼠实验性牙周炎模型,探讨慢性心理应激影响牙周炎的致病机制。方法:清洁级4周龄雌性Wistar大鼠80只,随机分为4组:(1)正常对照组;(2)实验性牙周炎组:用浸有牙周致病菌的丝线结扎左侧上颌第二磨牙牙颈部复制牙周炎模型;(3)单纯应激组:牙周不作特殊处理,给予应激刺激;(4)牙周炎+应激组:按上法复制牙周炎模型,并予以应激刺激。各组动物分别于实验后第2、4、6和8周分批处死,各时点每组处死动物5只。大鼠处死前尾静脉采血检测血糖浓度、心脏采血检测血清促肾上腺皮质激素(ACTH)、乳酸脱氢酶(LDH)及其同工酶LDH1。制作组织切片,HE染色观察大鼠左侧上颌第二磨牙牙周组织的炎性变化及牙槽骨的吸收情况。结果:(1)单纯应激组及牙周炎+应激组血糖及血清ACTH水平在2和4周时明显高于正常对照组和实验性牙周炎组(P<0.01),牙周炎+应激组在6和8周时血糖及血清ACTH水平仍较正常对照组和实验性牙周炎组高(P<0.01);(2)牙周炎+应激组血清LDH水平在各时点明显高于正常对照组和实验性牙周炎组(P<0.01),牙周炎+应激组血清LDH1水平在各时点均明显低于正常对照组和实验性牙周炎组(P<0.01);(3)组织学观察显示与正常对照组和单纯应激组牙龈及牙槽骨均无明显改变;牙周炎+应激组牙龈组织的炎症及牙槽骨破坏程度在4、6和8周时明显高于牙周炎组。结论:应激刺激可能通过降低牙周组织氧代谢水平加重大鼠牙周炎症程度。
OBJECTIVE: To establish a rat experimental periodontitis model to explore the pathogenesis of chronic psychological stress on periodontitis. Methods: Eighty-four-week-old female Wistar rats were randomly divided into 4 groups: (1) normal control group; (2) experimental periodontitis group: the left side (3) Simple stress group: periodontal without special treatment, given stress stimulation; (4) periodontitis + stress group: According to the law copy periodontitis Model, and be stimulated by stress. Animals in each group were sacrificed in batches at 2, 4, 6 and 8 weeks after the experiment, and 5 animals were sacrificed at each time point. Blood was taken from the caudal vein before the sacrifice to determine the blood glucose level. Serum adrenocorticotropic hormone (ACTH), lactate dehydrogenase (LDH) and its isoenzyme LDH1 were detected by blood sampling in the heart. Tissue sections were made and the inflammatory changes of periodontal tissues of the maxillary second molar on the left and the absorption of alveolar bone were observed by HE staining. Results: (1) The levels of blood glucose and serum ACTH in simple stress group and periodontitis + stress group were significantly higher than those in normal control group and experimental periodontitis group at 2 and 4 weeks (P <0.01), periodontitis + Stress group at 6 and 8 weeks, blood glucose and serum ACTH levels are still higher than the normal control group and experimental periodontitis group (P <0.01); (2) periodontitis + stress group serum LDH levels at each time (P <0.01). The levels of serum LDH1 in periodontitis + stress group were significantly lower than those in normal control group and experimental periodontitis group at each time point (P <0.01) <0.01). (3) Histological observation showed no significant changes in the gingiva and alveolar bone between the normal control group and the simple stress group. The inflammation of gingival tissue and the degree of alveolar bone destruction in periodontitis + stress group were at 4, 6 and 8 weeks was significantly higher than the periodontitis group. Conclusion: Stress stimulation may aggravate periodontal inflammation in rats by decreasing the level of oxygen metabolism in periodontal tissues.