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牙周病相关的牙槽骨丧失与环境低氧下铅中毒大鼠

Alveolar bone loss associated to periodontal disease in lead intoxicated rats under environmental hypoxia.

机构信息

Department of Physiology, Faculty of Dentistry, University of Buenos Aires, Argentina.

出版信息

Arch Oral Biol. 2013 Oct;58(10):1407-14. doi: 10.1016/j.archoralbio.2013.06.010. Epub 2013 Jul 9.

DOI:10.1016/j.archoralbio.2013.06.010
PMID:23845752
Abstract

Previously reported studies from this laboratory revealed that rats chronically intoxicated with lead (Pb) under hypoxic conditions (HX) impaired growth parameters and induced damages on femoral and mandibular bones predisposing to fractures. We also described periodontal inflammatory processes under such experimental conditions. Periodontitis is characterised by inflammation of supporting tissues of the teeth that result in alveolar bone loss. The existence of populations living at high altitudes and exposed to lead contamination aimed us to establish the macroscopic, biochemical and histological parameters consistent with a periodontal disease in the same rat model with or without experimental periodontitis (EP). Sixty female rats were divided into: Control; Pb (1000ppm of lead acetate in drinking water); HX (506mbar) and PbHX (both treatments simultaneously). EP was induced by placing ligatures around the molars of half of the rats during the 14 days previous to the autopsy. Hemi-mandibles were extracted to evaluate bone loss by histomorphometrical techniques. TNFα plasmatic concentration was greater (p<0.01) in Pb and HX animals. TBA-RS content was significantly higher in gums of rats with or without EP only by means of Pb. The SMG PGE2 content increased by Pb or HX was higher in PbHX rats (p<0.01). Pb and HX increased EP induced alveolar bone loss, while Pb showed spontaneous bone loss also. In conclusion, these results show that lead intoxication under hypoxic environment enhanced not only alveolar bone loss but also systemic and oral tissues inflammatory parameters, which could aggravate the physiopathological alterations produced by periodontal disease.

摘要

先前本实验室的研究报告显示,在缺氧条件下(HX)慢性铅中毒(Pb)的大鼠会损害生长参数,并导致股骨和下颌骨受损,易发生骨折。我们还描述了在这种实验条件下的牙周炎症过程。牙周炎的特征是牙齿支持组织的炎症,导致牙槽骨丧失。由于存在生活在高海拔地区并受到铅污染的人群,我们旨在建立与牙周病一致的宏观、生化和组织学参数,该模型使用相同的大鼠,无论是否存在实验性牙周炎(EP)。将 60 只雌性大鼠分为以下几组:对照组;Pb(饮用水中 1000ppm 的醋酸铅);HX(506mbar)和 PbHX(同时进行两种处理)。在尸检前的 14 天,通过结扎一半大鼠的磨牙来诱导 EP。提取半下颌骨,通过组织形态计量学技术评估骨丢失。Pb 和 HX 动物的 TNFα 血浆浓度更高(p<0.01)。仅通过 Pb,有或没有 EP 的大鼠牙龈中的 TBA-RS 含量明显更高。Pb 或 HX 增加的颌下腺 PGE2 含量在 PbHX 大鼠中更高(p<0.01)。Pb 和 HX 增加了 EP 诱导的牙槽骨丢失,而 Pb 也显示出自发性骨丢失。总之,这些结果表明,缺氧环境下的铅中毒不仅增强了牙槽骨丢失,而且还增强了全身和口腔组织的炎症参数,这可能会加重牙周病引起的生理病理改变。

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