生物钟蛋白Bmal1对实验性牙周炎相关肾损伤的影响

目的 通过建立大鼠牙周炎模型,探讨生物钟蛋白Bmal1对慢性牙周炎相关肾损伤的影响。方法 将12只雄性Wistar大鼠随机分为对照组和牙周炎组,每组6只。采用正畸结扎丝对牙周炎组大鼠双侧上颌第一磨牙进行结扎处理,对照组大鼠不进行任何干预措施。8周后,检测2组大鼠的牙周临床指标,包括牙周探诊深度、牙龈出血指数和牙齿松动度。采用Micro-CT对大鼠上颌骨进行扫描和三维图像重建,评估牙槽骨吸收情况。采用苏木精-伊红（HE）和过碘酸雪夫（PAS）染色对牙周组织和肾组织进行病理学观察。采用生化试剂盒检测肾脏功能指标肌酐、白蛋白、血尿素氮的水平,以及氧化应激指标超氧化物歧化酶、谷胱甘肽和丙二醛的水平。MitoSOX red染色检测肾组织内活性氧（ROS）含量。实时荧光定量聚合酶链反应（RT-qPCR）和免疫组织化学染色检测大鼠肾组织中Bmal1、核因子-E2相关因子2 (Nrf2)和血红素加氧酶1 (HO-1)的基因及蛋白表达水平。结果 与对照组相比,牙周组织Micro-CT及HE染色结果显示,牙周炎组上颌第一磨牙区出现明显的骨吸收和附着丧失;肾组织HE及PAS染色结果表明,牙周炎组大鼠肾组织有...     

间歇性低氧对牙周炎大鼠牙周组织中 NF-κB、IL-6及 PGE2含量的影响

目的：建立慢性间歇性低氧（CIH）及牙周炎大鼠模型,研究 NF-κB、IL-6及 PGE2水平的变化。方法：将32只普通级6周龄雄性 SD 大鼠随机分为4组（n ＝8）：A：常氧空白组、B：常氧牙周炎组、C：CIH 组、D：CIH 合并牙周炎组。B、D 组大鼠上颌第二磨牙进行结扎处理,辅以高糖饮食;A、C 组正常饮食。C、D 组置于低氧舱8 h／d。8周后处死,HE 染色,免疫组化检测牙周组织 NF-κB 含量,ELISA 检测牙龈组织 IL-6、PGE2。结果：HE 染色：8周后 B 组、D 组牙周炎症表现明显。免疫组化：B、C、D 组 NF-κB 表达均高于 A 组（P ＜0．05）;ELISA 检测：B、C、D 组 IL-6、PGE2含量高于 A 组（P ＜0．05）,且 D 组 IL-6、PGE2和NF-κB 表达较其他各组明显升高。结论：CIH 导致炎症因子升高,加重牙周组织破坏,使牙周炎症加剧。     

壳寡糖对骨质疏松伴牙周炎大鼠骨代谢及IKK/NF-κB通路的影响

目的：探讨壳寡糖对骨质疏松伴牙周炎模型小鼠骨代谢和IKK/NF-κB通路的影响。方法：将30只大鼠随机分为3组，每组10只，分为对照组、去势牙周炎组和壳寡糖治疗组。除对照组外，其余2组大鼠均切除卵巢并涂抹牙龈卟啉单胞菌液，建立骨质疏松伴牙周炎模型。结扎手术后4周，以200 mg/kg灌胃壳寡糖治疗组大鼠，另2组灌胃等体积生理盐水，每天1次，连续90天。观察各组牙周组织变化，给药前、给药结束后检测大鼠骨密度。给药结束后，尾静脉采血，采用酶联免疫吸附法测定各组血清碱性磷酸酶（ALP）、骨钙素（BGP）和抗酒石酸酸性磷酸酶5b(TRACP5b)的含量。采用视诊和探诊相结合的方法得到各组大鼠的牙龈指数和牙周附着丧失；处死大鼠，取出上颌骨，测量釉-牙骨质界到牙槽嵴顶的距离，得到牙槽骨吸收值。采用H-E染色，对各组大鼠上颌骨牙体、牙周组织进行病理学观察。采用RT-PCR和蛋白免疫印迹法分别检测各组大鼠牙周组织中核因子κB (NF-κB)、IκB激酶（IKK）mRNA和蛋白表达水平。采用SPSS 22.0软件包对数据进行统计学分析。结果：对照组大鼠牙龈呈粉红色，探诊不出血；去势牙周炎组大鼠牙龈红肿，...     

IGF-1对体外培养髁突软骨细胞增殖与凋亡的影响

目的：：研究IGF-1对IL-1β诱导的颞下颌关节软骨细胞增殖与凋亡的影响。方法：组织块培养法分离培养人髁突软骨细胞,通过细胞形态观察和免疫细胞化学染色进行鉴定。将培养的细胞分为：对照组、IL-1β组(10μg/L)、 IL-1β+IGF-1组(0、1、10、50、100μg/L), MTT法检测各组细胞增殖能力变化,流式细胞仪检测细胞周期分布以及细胞凋亡情况,Western blot检测各组细胞中凋亡相关因子Bcl-2、Bax和Caspase-3以及p38 MAPK/NF-κB蛋白表达变化。结果：人髁突软骨细胞生长状态良好,甲苯胺蓝染色胞质呈深蓝色,II型胶原呈阳性表达。与对照组比较,IL-1β组细胞增殖能力、Bcl-2/Bax比值明显降低,早凋与晚凋细胞百分数、Caspase-3、p38 MAPK/NF-κB蛋白表达均明显增加;与IL-1β组比较,1~100μg/L IGF-1预处理组细胞增殖能力、Bcl-2/Bax比值逐渐上升(P<0.05),细胞凋亡率、Caspase-3、p38 MAPK /NF-κB蛋白表达则逐渐下调(P<0.05),均呈现一定的浓度依赖性。结论：IGF-1可抑制IL-1β诱导的髁突软骨细胞凋亡并减轻p38 MAPK/NF-κB的活化。     

阿奇霉素对牙周炎大鼠牙槽骨影响的Micro?CT研究

目的通过Micro-CT研究阿奇霉素对牙周炎大鼠牙槽骨微结构的影响。方法雄性SD大鼠随机分为3组:对照组、结扎组、阿奇霉素组。结扎组和阿奇霉素组大鼠均采用丝线结扎左侧上颌第一磨牙,建立实验性牙周炎模型。从结扎起阿奇霉素组大鼠每天腹腔注射阿奇霉素3.5 mg/kg。注射2周后,将大鼠处死,取上颌骨。采用Micro-CT分析大鼠上颌第一磨牙牙槽骨吸收和微结构的改变。结果结扎组与对照组比较上颌第一磨牙周围牙槽骨的高度明显减少,而阿奇霉素组在药物诱导下牙槽骨吸收明显减小,阿奇霉素对牙槽骨高度降低起抑制作用。大鼠结扎后,牙槽骨微结构发生明显改变,其中BV/TV、Tb.N、Tb.Th和BMD值均明显降低,而Tb.Sp值增加。而阿奇霉素组牙槽骨微结构参数能恢复到一定水平,与对照组的差异明显减少。结论阿奇霉素可阻止实验性大鼠牙周炎的牙槽骨继续破坏,对实验性大鼠牙周炎有治疗作用。     

sclerostin在2型糖尿病伴牙周炎大鼠牙槽骨骨重建过程中的表达及意义

目的： 观察2型糖尿病（T2DM）伴牙周炎大鼠牙槽骨骨重建过程中骨硬化蛋白（sclerostin）的表达。方法： 将54只SD大鼠随机分为健康组、牙周炎组、T2DM伴牙周炎组,每组各18只。牙周炎组建立牙周炎大鼠模型,T2DM伴牙周炎组先建立T2DM模型,再建立牙周炎模型。腹腔注射STZ后1、5、10 d,检测糖代谢指标。结扎后8周,检测牙周指标。建模成功后1、3、6个月,免疫组织化学染色检测牙槽骨组织中sclerostin的表达。采用SPSS 21.0软件包对数据进行统计学分析。结果： 与未建模大鼠相比,T2DM建模大鼠腹腔注射STZ后1、5、10 d空腹血糖（FBG）,腹腔注射STZ后10 d空腹胰岛素（FINS）及胰岛素抵抗指数（HOMA-IR）均显著升高（P<0.05）。与未建模大鼠相比,牙周炎建模大鼠牙龈出血指数（SBI）、菌斑指数（PLI）、探针深度（PD）均显著增加（P<0.05）。与健康组相比,牙周炎组、T2DM伴牙周炎组建模成功后1、3、6个月牙槽骨组织中sclerostin表达显著增加（P<0.05）,且T2DM伴牙周炎组显著高于牙周炎组（P<0.05）。与建模成功后1个月相比,牙周炎组、T2DM伴牙周炎组建模成功后3、6个月牙槽骨组织中sclerostin表达显著增加（P<0.05）。与建模成功后3个月相比,牙周炎组、T2DM伴牙周炎组建模成功后6个月牙槽骨组织中sclerostin表达显著减少（P<0.05）。结论： sclerostin在牙周炎中表达增加,且合并T2DM进一步上调sclerostin的表达,但在骨重建过程中逐渐下调。     

胰岛素治疗对糖尿病大鼠牙槽骨RANKL/OPG mRNA影响的研究

目的通过研究胰岛素治疗对糖尿病大鼠牙周组织病理改变及牙槽骨中NF-κB受体活化因子配体(Receptor activator of nuclear factor-κB ligand,RANKL)和骨保护素(osteoprotegerin,OPG)mRNA水平比值情况的影响,探讨糖尿病影响牙周病时牙槽骨吸收的机理。方法将12只大鼠采用静脉注射链脲佐菌素的方法建立糖尿病模型,并随机分为治疗组和对照组。治疗组给予胰岛素皮下注射,对照组注射等量生理盐水。分别于实验开始时、造模成功后和8周后处死时测量大鼠体重和血糖。右下磨牙区牙周组织脱钙后HE染色观察组织病变状况;应用RT-PCR检测左下磨牙区牙槽骨RANKL和OPG mRNA表达情况,并比较两组大鼠RANKL/OPG比值差异。结果胰岛素治疗组较糖尿病组牙周组织炎症反应减轻,牙槽骨吸收减弱;血糖值(P<0.05)及RANKL/OPGmRNA比值(P<0.01)降低。结论胰岛素治疗可能增加牙周组织修复和再生能力,降低糖尿病大鼠的牙槽骨RANKL/OPGmRNA比值。提示血糖水平增高可能是影响糖尿病大鼠的牙槽骨吸收危险因素之一。     

IGF-1信号通路相关蛋白在大鼠髁突软骨细胞增殖分化中的表达

目的:研究胰岛素样生长因子-1(IGF-1)信号转导通路在大鼠髁突软骨细胞增殖分化调控过程中相关基因的表达。方法:体外单层培养并鉴定出生后1、7、14、28 d共4组SD大鼠髁突软骨细胞。免疫组织化学方法检测细胞内IGF-1表达情况,Real-time PCR及Western印迹法检测细胞内IGF-1R、Bcl-2、Bax mRNA及蛋白表达。饥饿培养24 h后,实验组加入质量浓度为100 ng/mL的重组大鼠IGF-1细胞因子(rrIGF-1)继续培养24、48 h,CCK-8检测细胞增殖情况,Real-time PCR技术检测各组髁突软骨细胞内IGF-1R、IGF-2R、Raf1、GSK-3、IGFBP3、NF-κB、Bcl-2、Bax、integrin、TGF-βmRNA表达情况;对照组培养液不加rrIGF-1。结果:各鼠龄组SD大鼠髁突软骨细胞内IGF-1表达均阳性,IGF-1R mRNA及蛋白表达相对平稳,Bcl-2、Bax mRNA及蛋白表达逐渐增强,在出生14 d后表达下降(P<0.05)。加入100 ng/mL rrIGF-1后,髁突软骨细胞增殖速度显著增加,细胞凋亡减少,Real-time PCR结果显示实验组IGF-1R、GSK-3、Bax、integrin mRNA表达整体呈下降趋势;IGF-2R、Raf1、IGFBP3、NF-κB、Bcl-2、TGF-βmRNA表达水平总体呈上调趋势,差异有统计学意义。结论 :IGF-1介导的信号转导途径参与了髁突软骨细胞的增殖、分化以及软骨形成早期的调控,并可能与integrin、TGF-β等其他蛋白相互作用,共同参与髁突发育过程。     

壳寡糖对牙周炎大鼠牙槽骨吸收及Th17/Treg平衡和OPG/RANKL/RANK通路的影响

目的: 探讨壳寡糖对牙周炎大鼠牙槽骨吸收及Th17/Treg平衡和OPG/RANKL/RANK通路的影响。方法: 建立牙周炎大鼠模型,随机分为模型组、壳寡糖低剂量组、壳寡糖中剂量组、壳寡糖高剂量组和甲硝唑组,每组12只,另取12只作为对照组。分组处理后,评估牙龈指数、牙槽骨吸收值;H-E染色观察牙周组织病理形态学变化;流式细胞术检测外周血中Th17/Treg细胞比值;酶联免疫吸附试验（ELISA）检测各组大鼠血清中IL-17、TGF-β、RANKL、OPG水平,实时荧光定量PCR（qRT-PCR）检测各组大鼠牙周组织OPG、RANKL mRNA表达水平。采用SPSS 24.0软件包对数据进行统计学分析。结果: 与对照组相比,模型组大鼠牙周组织呈现牙周膜纤维束断裂、排列紊乱,毛细血管扩张、增生,炎症细胞浸润等病理损伤;牙龈指数、牙槽骨吸收值、Th17/Treg比值、血清RANKL及IL-17水平、牙周组织RANKL mRNA水平显著升高（P<0.05）,血清OPG及TGF-β水平、牙周组织OPG mRNA水平显著降低（P<0.05）。与模型组相比,壳寡糖低、中、高剂量组和甲硝唑组大鼠牙周组织病理损伤减轻;牙龈指数、牙槽骨吸收值、Th17/Treg比值、血清RANKL及IL-17水平、牙周组织RANKL mRNA水平显著降低（P<0.05）,血清OPG及TGF-β水平、牙周组织OPG mRNA水平显著升高（P<0.05）,且壳寡糖各组呈剂量依赖性,壳寡糖高剂量组与甲硝唑组相比,差异无统计学意义（P>0.05）。结论: 壳寡糖可促使Th17/Treg平衡恢复正常,上调OPG表达,下调RANKL表达,抑制牙周炎大鼠牙槽骨吸收,改善其临床症状。     

用放射免疫测定法分析豚鼠牙龈和牙槽骨中前列腺素E2含量及与牙周炎的关系

将２０只豚鼠分为对照组和牙周炎组，每组１０只，用丝线缝扎十高糖食料喂养形成牙周炎，用放射免疫测定法（ＲＩＡ）分析牙周炎形成后两组牙龈和牙槽骨中前列腺素Ｅ２（ＰＧＥ２）含量。结果表明牙周炎组和对照组牙龈组织中ＰＧＥ２含量均高于牙槽骨中的含量，对照组牙龈组织中ＰＧＥ２（３９４．９７±１１８．２７ｐｇ／ｍｇ）为牙槽骨中（１８２．９１±３３．２９ｐｇ／ｍｇ）的２．１倍，牙周炎组龈组织中ＰＧＥ２（９４６．５８±１０６．８６ｐｇ／ｍｇ）为牙槽骨中（３１０．３７±４６．５８ｐｇ／ｍｇ）的３倍。牙周炎组牙龈和牙槽骨中ＰＧＥ２含量与对照组相应组织的ＰＧＥ２比均有非常显著性差异，牙周炎组牙龈组织中ＰＧＥ２为对照组的２．４倍，而牙槽骨中的ＰＧＥ２为对照组牙槽骨的１．７倍。提示豚鼠牙周炎时牙龈和牙槽骨中ＰＧＥ２升高，ＰＧＥ２与牙龈炎症和牙槽骨吸收有密切关系，使用抑制ＰＧＥ２合成的药物消炎痛等治疗豚鼠牙周炎将有显著的治疗效果     

HDAC5-Mediated Acetylation of p100 Suppresses Its Processing

IntroductionPeriodontitis is a condition involving chronic inflammation in the gums, periodontal ligaments, cementum, and alveolar bone. Nuclear factor-κB (NF-κB) activation is the prominent mediator of inflammation and osteoclast differentiation. The role of histone deacetylase 5 (HDAC5) in periodontitis development and NF-κB regulation is not fully understood.MethodsWe used primary mouse bone marrow–derived osteoclast cultures in vitro and a mouse model of chronic periodontists (CPD) treated with the HDAC4/5 inhibitor LMK-235. Real-time polymerase chain reaction, micro computed tomography, flow cytometry, western blot, and immunoprecipitation were used to study proinflammatory cytokines, NF-κB activation, HDAC5 activity, and the interaction of HDAC5 with NF-κB p100.ResultsLMK-235, a selective inhibitor of HDAC4 and HDAC5, reduced osteoclast marker gene expression (Cstk, Acp5, and Calcr) and tartrate-resistant acid phosphatase activity in primary osteoclast cultures. LMK-235 reduced the increase in cementoenamel junction–alveolar bone crest distance, inflammatory cell infiltration of gingival tissues, and expression levels of interleukin (IL)-1β, tumor necrosis factor alpha, IL-6, and IL-23a, indicating an ameliorative effect on CPD. Immunoprecipitation experiments have further confirmed p100–HDAC5 interaction, acetylation levels of p100, and NF-κB activation.ConclusionsThese results indicate that HDAC5 binds and deacetylates p100, leading to its activation, increased proinflammatory cytokine production, gingival infiltration, and osteoclast differentiation, thus promoting alveolar bone resorption. HDAC5 inhibition is therefore a potentially promising therapeutic strategy for the treatment of periodontitis.     

Vitamin C intake inhibits serum lipid peroxidation and osteoclast differentiation on alveolar bone in rats fed on a high-cholesterol diet

Objective

A high-cholesterol diet stimulates osteoclast differentiation, which may be induced by increased serum lipid peroxidation. The inhibition of serum lipid peroxidation by vitamin C may offer beneficial effects on osteoclast differentiation including increased expression of receptor activator of nuclear factor (NF)-κB ligand (RANKL) and NF-κB. This study investigated the effects of vitamin C intake on RANKL and NF-κB expression in periodontal tissue of rats fed a high-cholesterol diet.

Design

Twenty-four rats (8 weeks old) were divided into four groups: a control group (fed a regular diet) and three experimental groups (fed a high-cholesterol diet supplemented with 0, 1 and 2 g/l vitamin C/day) in this 12-week study. Vitamin C was provided by its addition to drinking water. As an index of serum lipid peroxidation, hexanoyl-lysine (HEL) level was determined by a competitive enzyme-linked immunosorbent assay method. Immunohistological analysis was performed to evaluate RANKL and NF-κB expression on the alveolar bone surface. The number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts was also counted.

Results

Feeding a high-cholesterol diet increased not only the serum HEL level but also the number of TRAP-positive osteoclasts on the alveolar bone surface, with an increase in RANKL and NF-κB expression on alveolar bone surface. Intake of vitamin C reduced the serum HEL level and osteoclast differentiation, with decreasing RANKL and NF-κB expression.

Conclusions

Vitamin C intake could suppress osteoclast differentiation, including RANKL and NF-κB expression on the alveolar bone surface, by decreasing serum lipid peroxidation in rats fed a high-cholesterol diet.     

PPARγ在脂多糖刺激牙周膜细胞中调控NF-κB信号通路的作用研究

目的:探讨PPARγ在牙周炎中调控作用机制。方法:组织块法培养健康人牙周膜细胞(human periodontal ligament cells, hPDLCs)并鉴定。细胞处理分为以下4组,A组:对照组;B组:脂多糖(lipopolysaccharide,LPS )刺激组;C组:罗格列酮对照组,即二甲基亚砜(dimethylsulfoxide, DMSO)处理组;D组:罗格列酮处理组。免疫印迹法检测过氧化物酶体增殖物激活受体γ(peroxisome proliferator activated receptor γ,PPARγ)和核因子κB(nuclear factor κB, NF-κB) p65胞核、胞浆及总蛋白含量,细胞免疫荧光检测NF-κB p65表达部位。实时定量PCR和酶联免疫法检测白细胞介素1β(interleukin-1β,IL-1β)和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)RNA和蛋白表达。结果:LPS刺激下,胞核PPARγ表达降低NF-κB p65表达升高,相应的IL-1β和TNF-α RNA及蛋白表达量均升高。同时加入罗格列酮后,胞核PPARγ表达升高NF-κB p65表达降低,且IL-1β和TNF-α RNA及蛋白表达量均降低。差异均有统计学意义(P<0.01)。结论:PPARγ通过下调NF-κB信号通路抑制脂多糖刺激下牙周膜细胞炎症因子RNA表达和蛋白分泌,进而调节牙周炎症反应。     

罗格列酮对牙周炎大鼠牙龈脂联素受体表达的影响

目的:探讨罗格列酮(ROS)对牙周炎大鼠牙龈脂联素受体1(AdipoRl) mRNA、脂联素受体2(AdipoR2) mRNA和TNF-α等炎症因子表达的影响及在牙周炎中对牙槽骨保护的潜能.方法:50只SD大鼠随机分为5组(n=10),大鼠不干预处理作为空白对照,40只大鼠用于制作牙周炎模型后分别用蒸馏水(牙周炎组)、1、3、10 mg/kg ROS(低、中、高剂量组)灌胃1次/d,持续4周.然后取样,RT-PCR测定牙龈组织AdipoR1和AdipoR2 mRNA表达水平,ELISA测牙龈组织TNF-α、MMP-9和血浆脂联素浓度,标准化的数码摄影测量釉牙骨质界到牙槽骨嵴顶(CEJ-A)距离.结果:牙周炎组和空白对照组相比,牙龈组织AdipoR1和AdipoR2的mRNA表达水平显著降低(P＜0.01),血浆脂联素水平无差异(P＞0.05),TNF-α和MMP-9浓度显著上升(P＜0.01).和牙周炎组相比,低、中、高剂量治疗组牙龈组织AdipoRl mRNA表达均升高(P＜0.05),TNF-α浓度显著降低(P＜0.01);中、高剂量治疗组牙龈组织AdipoR2 mRNA表达显著升高(P＜0.01),MMP-9浓度显著降低(P＜0.01),血浆脂联素浓度升高(P＜0.05),牙槽骨吸收量显著降低(P＜0.01).结论:ROS可能通过上调牙龈组织中AdipoR1和AdipoR2 mRNA表达水平,降低TNF-α、MMP-9浓度,缓解牙周组织炎症,降低牙槽骨吸收.     

Local and cardiorenal effects of periodontitis in nitric oxide-deficient hypertensive rats

Objective

In this study we have assessed the renal and cardiac consequences of ligature-induced periodontitis in both normotensive and nitric oxide (NO)-deficient (L-NAME-treated) hypertensive rats.

Materials and methods

Oral L-NAME (or water) treatment was started two weeks prior to induction of periodontitis. Rats were sacrificed 3, 7 or 14 days after ligature placement, and alveolar bone loss was evaluated radiographically. Thiobarbituric reactive species (TBARS; a lipid peroxidation index), protein nitrotyrosine (NT; a marker of protein nitration) and myeloperoxidase activity (MPO; a neutrophil marker) were determined in the heart and kidney.

Results

In NO-deficient hypertensive rats, periodontitis-induced alveolar bone loss was significantly diminished. In addition, periodontitis-induced cardiac NT elevation was completely prevented by L-NAME treatment. On the other hand L-NAME treatment enhanced MPO production in both heart and kidneys of rats with periodontitis. No changes due to periodontitis were observed in cardiac or renal TBARS content.

Conclusions

In addition to mediating alveolar bone loss, NO contributes to systemic effects of periodontitis in the heart and kidney.     

S100A9在糖尿病大鼠牙周组织中的表达及其作用研究

目的 研究S100A9蛋白在糖尿病大鼠牙周组织中的表达,探讨其在糖尿病诱发的牙周病变中可能的作用机制。方法 本实验通过对SD大鼠腹腔注射链脲佐菌素（STZ）构建糖尿病大鼠模型,通过苏木精-伊红（HE）染色观察糖尿病大鼠牙周结构的变化,免疫组织化学染色观察糖尿病大鼠牙周组织中S100A9的表达与分布,同时检测其配体Toll受体4（TLR4）和核转录因子κB（NF-κB）/p-P65蛋白的表达。通过分析上述蛋白的表达规律,探讨S100A9蛋白在糖尿病诱发的牙周病变中的作用机制。结果 糖尿病大鼠的牙槽骨骨小梁结构稀疏,硬骨板消失;免疫组织化学染色显示牙周膜、牙槽骨及牙龈上皮中S100A9的表达水平比对照组明显上调,TLR4在牙槽骨、牙周膜、牙龈中的表达水平相较于对照组也显著增强;p-P65在对照组中没表达,但在糖尿病组中牙周膜和牙槽骨中呈阳性表达。结论 糖尿病导致大鼠牙周组织结构病变,其原因可能与S100A9介导的TLR4和NF-κB信号通路的活化有关。     

Immunohistochemical expression of RANKL, RANK and OPG in gingival tissue of patients with periodontitis

Abstract Objectives. To evaluate the expression of the receptor activator of NF-κB (RANK), the receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG), in the gingival tissue of patients with periodontitis. Materials and methods. Gingival tissue was obtained from 14 systemically healthy subjects with chronic periodontitis during conventional periodontal surgery. Immunohistochemistry was used to detect the expression of RANK, RANKL and OPG in the oral and periodontal pocket epithelium as well as in the connective tissue cells. Results. RANKL was negatively expressed in both oral and periodontal pocket epithelium. OPG was also negative or weakly positive in the whole epithelium. RANK showed moderate/strong positive staining mainly in the basal and suprabasal layer of oral and periodontal pocket epithelium. In most of the cases, more than 60% of the inflammatory cell infiltrate stained for RANK and RANKL. In these cases the intensity of the stained cells ranged from moderate-to-strong. In less than half of the cases, OPG was positive in more than 60% of the stained cells of the inflammatory cell infiltrate. Conclusion. The RANK, RANKL and OPG proteins are differentially expressed in periodontal tissues and may play a major role in the bone loss occurring in periodontitis.