本文關(guān)鍵詞： 牙周炎 心理應(yīng)激 高壓氧 低氧誘導(dǎo)因子-α　出處：《中國病理生理雜志》2016年02期 　論文類型：期刊論文

【摘要】：目的:探討高壓氧(hyperbaric oxygen,HBO)治療對心理應(yīng)激相關(guān)牙周炎牙周組織低氧誘導(dǎo)因子1α(hypoxia-inducible factor-1α,HIF-1α)表達的影響。方法:清潔級4周齡雄性Wistar大鼠120只,隨機分為4組:正常對照組;單純應(yīng)激組;牙周炎組:用浸有牙齦卟啉單胞菌株的絲線結(jié)扎左側(cè)上頜第二磨牙牙頸部,復(fù)制實驗性牙周炎模型;牙周炎+應(yīng)激組。于實驗后第9周停止應(yīng)激刺激,對除正常對照組外其它各組大鼠每組選取6只進行HBO治療。于實驗后2、4和8周末分批處死未治療動物,每組處死6只;于實驗后10周末處死HBO治療及未治療動物。處死前測量術(shù)區(qū)的牙周附著情況,制作牙體牙周聯(lián)合切片,觀察牙周的組織學(xué)改變。免疫組化法檢測各組大鼠牙周組織HIF-1α的表達水平,計算平均陽性細胞率。結(jié)果:大體觀察見正常對照組及單純應(yīng)激組牙周附著位置正常;牙周炎組出現(xiàn)牙齦萎縮,附著喪失明顯;牙周炎+應(yīng)激組附著喪失明顯,根分叉暴露,HBO治療后,牙齦水腫減輕,牙周袋變淺;組織學(xué)觀察見牙周炎+應(yīng)激組牙周組織破壞程度在各時點均重于牙周炎組;經(jīng)HBO治療后,牙周組織炎癥程度減輕,炎癥細胞浸潤減少;牙齦指數(shù)(gingival index,GI)及牙周附著喪失(attachment loss,AL)檢查見單純應(yīng)激組與正常對照組在各時點均無顯著差異;在第4、8周時牙周炎+應(yīng)激組GI、AL明顯高于牙周炎組(P0.01);HBO治療結(jié)束后牙周炎組及牙周炎+應(yīng)激組GI、AL明顯低于未治療組(P0.05);單純應(yīng)激組與正常對照組HIF-1α免疫組化平均陽性細胞率在各時點均無顯著差異;牙周炎+應(yīng)激組HIF-1α平均陽性細胞率在第4、8周時均明顯高于牙周炎組(P0.01);HBO治療結(jié)束后牙周炎組及牙周炎+應(yīng)激組HIF-1α平均陽性細胞率較未治療組降低(P0.01)。結(jié)論:心理應(yīng)激可加重牙周組織缺氧程度從而加重牙周炎癥狀,HBO通過增加牙周組織的氧供應(yīng)量對大鼠實驗性牙周炎及心理應(yīng)激相關(guān)牙周炎有顯著的治療效果。
[Abstract]:Objective: to study hyperbaric oxygen with hyperbaric oxygen. HBO) treatment on hypoxia-inducible factor-1 偽 and hypoxia-inducible factor-1 偽 in periodontal tissue of periodontitis associated with psychological stress. Methods: 120 male Wistar rats of clean grade 4 weeks old were randomly divided into 4 groups: normal control group; Simple stress group; In the periodontitis group, experimental periodontitis model was established by ligating the neck of the left maxillary second molar with filaments impregnated with porphyromonas gingivalis. Periodontitis stress group. At the 9th week after the experiment, the stress stimulation was stopped, and 6 rats in each group except the normal control group were treated with HBO. 2. At the end of 4 and 8 weeks, the untreated animals were killed in batches and 6 animals were killed in each group. HBO and untreated animals were killed at the end of 10 weeks after the experiment. Periodontal attachment was measured before death and periodontal joint sections were made. Immunohistochemical method was used to detect the expression of HIF-1 偽 in periodontal tissues of rats. Results: the normal periodontal attachment was observed in normal control group and simple stress group. In periodontitis group, gingival atrophy and loss of attachment were observed. After HBO treatment, gingival edema was alleviated and the periodontal bag shallowed in the stress group of periodontitis. Histological observation showed that the degree of periodontal tissue destruction in periodontitis stress group was more serious than that in periodontitis group at each time point. After HBO treatment, the degree of periodontal inflammation was reduced and the infiltration of inflammatory cells was decreased. Gingival index (GI) and periodontal attachment attachment (loss). There was no significant difference between the simple stress group and the normal control group at all time points. At the 4th week, GIIA AL in periodontitis stress group was significantly higher than that in periodontitis group (P 0.01). After HBO treatment, the levels of GI AL in periodontitis group and periodontitis stress group were significantly lower than those in untreated group (P 0.05). There was no significant difference in the average positive rate of HIF-1 偽 immunohistochemistry between the simple stress group and the normal control group at each time point. The average positive rate of HIF-1 偽 in periodontitis stress group was significantly higher than that in periodontitis group at the 8th week. The average positive rate of HIF-1 偽 in periodontitis group and periodontitis stress group after HBO treatment was lower than that in untreated group (P 0.01). Conclusion: psychological stress can aggravate the degree of hypoxia in periodontal tissue and aggravate the symptoms of periodontitis. HBO has a significant therapeutic effect on experimental periodontitis and psychological stress-related periodontitis in rats by increasing oxygen supply in periodontal tissue.
【作者單位】： 暨南大學(xué)醫(yī)學(xué)院口腔醫(yī)學(xué)系;
【基金】：廣東省社會發(fā)展領(lǐng)域科技計劃項資助項目(No.2013B021800043;No.2014A020212212)
【分類號】：R781.42
【正文快照】： 牙周炎是侵犯牙齦和牙周組織的一種慢性炎癥性疾病,主要特征為牙周袋的形成、袋壁的炎癥和牙槽骨吸收,是導(dǎo)致成年人牙齒喪失的主要原因[1]。研究表明,微生物是牙周病的啟動因子,心理應(yīng)激與炎癥性疾病如類風(fēng)濕性關(guān)節(jié)炎和牙周病之間有關(guān)聯(lián)[2],是牙周病潛在的重要的風(fēng)險因子[3]。

【參考文獻】

相關(guān)期刊論文 前1條

1 劉金波;方飛;易娟;易莉;;人牙髓組織缺氧耐受機制的初步研究[J];臨床口腔醫(yī)學(xué)雜志;2007年05期

【共引文獻】

相關(guān)期刊論文 前1條

1 龔啟梅;凌均h，

本文編號：1442417