Niederauer Ana Js, Guimarães Renan Ab, Oliveira Kepler Ls, Pires Adalberto R, Demasi Ana Pd, Ferreira Heloísa Ha, Sperandio Marcelo, Napimoga Marcelo H, Peruzzo Daiane C
Faculdade São Leopoldo Mandic, Departamento de Biologia Molecular,Campinas, Sao Paulo, Brasil.
Faculdade São Leopoldo Mandic, Departamento de Periodontia, Campinas, Sao Paulo - Brasil.
Acta Odontol Latinoam. 2019 Dec 1;32(3):164-171.
Halitosis is highly prevalent in periodontitis and attributed mainly to the presence of volatile sulfur compounds (VSC), where hydrogen sulfide (H2S) is the chief culprit in the characteristic malodor of periodontitis and thus may play an active role in its pathogenesis. The aim of this study was to evaluate the effect of H2S in the acute, intermediate and chronic immuneinflammatory host response and alveolar bone loss in vivo by using an animal model of induced periodontal disease. Thirtysix rats were divided into 2 groups: test group (n = 18), rats exposed to H2S (NaHS H2S donor molecule) and control group (n = 18), rats treated with saline only (Ctrl). All animals had one of their lower second molars ligated to induce periodontal disease (PD). The sound contralateral molar was used as control (H). Each group was subdivided into 3 (n = 6), according to followup time (3h, 5 days and 14 days). The gingival tissue was used for mRNA expression analysis (IL1, IL6, RANKL, OPG and SOFAT) by realtime PCR and the mandibles were analyzed morphometrically. Data analysis showed that the ligature promoted alveolar bone loss, observed mainly at 14 days, both in the group exposed to H2S and in the Ctrl group. H2S administration did not result in additional bone loss. Gene expression showed a significant increase in IL1, IL6, RANKL and SOFAT only in the CtrlPD group (p<0.05). A significant downregulation in OPG expression was observed over time in the CtrlPD group (p<0.05). In conclusion, H2S had no effect on alveolar bone loss in the absence of a ligature. In the presence of a ligature, however, exposure to H2S had an immunoregulatory effect on the expression of proinflammatory and proresorptive cytokines.
口臭在牙周炎中非常普遍，主要归因于挥发性硫化物（VSC）的存在，其中硫化氢（H2S）是牙周炎特征性恶臭的主要元凶，因此可能在其发病机制中发挥积极作用。本研究的目的是通过使用诱导性牙周疾病动物模型，评估H2S在体内急性、中期和慢性免疫炎症宿主反应及牙槽骨丧失中的作用。36只大鼠分为2组：试验组（n = 18），暴露于H2S（NaHS，H2S供体分子）的大鼠；对照组（n = 18），仅用生理盐水处理的大鼠（Ctrl）。所有动物均结扎其一颗下第二磨牙以诱导牙周疾病（PD）。对侧健康磨牙用作对照（H）。根据随访时间（3小时、5天和14天），每组再分为3组（n = 6）。牙龈组织用于通过实时PCR进行mRNA表达分析（IL-1、IL-6、RANKL、OPG和SOFAT），下颌骨进行形态计量分析。数据分析表明，结扎促进了牙槽骨丧失，主要在14天时观察到，暴露于H2S的组和Ctrl组均如此。给予H2S并未导致额外的骨丧失。基因表达显示，仅在Ctrl-PD组中IL-1、IL-6、RANKL和SOFAT显著增加（p<0.05）。在Ctrl-PD组中，随时间观察到OPG表达显著下调（p<0.05）。总之，在没有结扎的情况下，H2S对牙槽骨丧失没有影响。然而，在存在结扎的情况下，暴露于H2S对促炎和促吸收细胞因子的表达具有免疫调节作用。
