骨保护素对犬牙齿萌出过程中[牙合]方组织内破骨细胞的影响

目的：在体研究骨保护素对正常犬牙齿萌出过程中[牙合]方组织内破骨细胞的影响,并分析其机制。方法：同一窝6只出生7d本地犬随机分成对照组和骨保护素组,后者皮内注射骨保护素每日1．5mg／kg,连续3d。自注药起5d取其下颌骨,制备石蜡切片,分别用酶组织化学和免疫组织化学的方法检测犬下颌第三前磨牙牙胚[牙合]方组织中破骨细胞、RANKL阳性细胞的变化情况。结果：骨保护素组中平均破骨细胞数、RANKL表达较对照组明显降低（P〈0．05）。结论：骨保护素对正常犬牙齿萌出过程中[牙合]方组织内的破骨细胞可能有抑制作用,这可为牙齿萌出的研究提供一定参考。     

降钙素对小鼠牙齿萌出途中破骨细胞的影响

目的:在体研究降钙素对正常小鼠牙齿萌出过程中破骨细胞的影响,并分析其机制。方法:同一窝10只出生3d小鼠随机分成对照组和降钙素组,后者皮内注射鲑鱼降钙素每日1U/100g,连续3d。自注药起7d取其下颌骨,分别用酶组织化学和免疫组织化学的方法检测破骨细胞、RANKL阳性细胞在牙胚周围组织中的变化情况。结果:降钙素组的平均破骨细胞数、RANKL表达较对照组明显降低。结论:降钙素对正常小鼠牙齿萌出过程中的破骨细胞可能有抑制作用,这可为牙齿萌出的研究提供一定参考。     

牙齿萌出过程及机制的研究进展

牙齿的萌出是一个复杂而且受到严密调控的过程,这一过程受到多种细胞因子的调控,国内外学者研究较多。该文就牙齿的萌出过程及作用机制作一概述。     

JNK在牙囊细胞破骨细胞向分化的实验研究

目的　通过特异性抑制剂SP600125抑制JNK信号通路,探究大鼠牙齿萌出中JNK信号在成熟破骨细胞形成过程中的相关调控机制。方法 分离培养SD大鼠牙囊细胞。用不同浓度的SP600125对细胞预处理,实时定量PCR检测DFCs中核因子κB受体活化剂配体、骨保护素基因表达量。DFCs和BMMs建立共培养体系,TRAP染色观察OC的数量。结果 SP600125在20μmol/L浓度范围内对DFCs的增殖无显著影响（P﹥0.05）,RT-PCR结果示：SP600125干预72h后,RANKL基因表达量下降,OPG上升,与对照组比较差异均有统计学意义（P﹤0.05）。TRAP染色阳性计数结果：各组均有OC生成,9d较7d产生的OC数显著增加,加入不同浓度的抑制剂组破骨细胞数均有减少,与对照组相比差异有统计学意义（P﹤0.05）。结论 本研究阐明了在大鼠牙齿萌出中,SP600125通过抑制JNK信号通路,对OC形成具有一定的抑制作用,可为牙齿萌出、牙槽骨改建等破骨细胞相关性口腔疾病提供研究基础。     

骨保护素对犬牙齿萌出过程(牙合)中方组织内破骨细胞的影响

目的:在体研究骨保护素对正常犬牙齿萌出过程中(牙合)方组织内破骨细胞的影响, 并分析其机制.方法:同一窝 6 只出生7 d本地犬随机分成对照组和骨保护素组, 后者皮内注射骨保护素每日1.5 mg/kg, 连续3 d.自注药起 5 d取其下颌骨, 制备石蜡切片,分别用酶组织化学和免疫组织化学的方法检测犬下颌第三前磨牙牙胚方组织中破骨细胞、RANKL阳性细胞的变化情况.结果:骨保护素组中平均破骨细胞数、RANKL表达较对照组明显降低(P<0.05).结论:骨保护素对正常犬牙齿萌出过程中(牙合)方组织内的破骨细胞可能有抑制作用,这可为牙齿萌出的研究提供一定参考.     

牙齿萌出调控因子的研究进展

多种组织、细胞及调控因子参与了牙齿萌出这一复杂的过程。其中调控因子在牙齿萌出中的作用，受到了广泛关注，本文就调控因子在牙齿萌出过程中的作用作一综述。     

RANKL在人乳牙根生理性吸收过程中的表达

目的:探讨核因子κB受体活化剂配体RANKL在人乳牙根生理性吸收过程中的表达及作用。方法:运用免疫组织化学的方法检测人乳牙根生理性吸收过程中RANKL蛋白的表达。结果:乳牙的破牙细胞、牙髓成纤维细胞及成牙本质细胞胞浆中RANKL免疫组化染色阳性,且表达高于恒牙组,差异有统计学意义(P<0.05),乳牙牙周韧带成纤维细胞RANKL染色结果与恒牙组相比较差异无统计学意义(P>0.05)。结论:RANKL在人乳牙牙根生理性吸收过程中有表达,其可能对乳恒牙替换起到一定的促进作用。     

牙囊在牙齿萌出时的调控作用

牙囊起源于外胚间充质 ,是包绕在成釉器外围的一层致密的结缔组织 ,在牙齿发育后期形成牙骨质、牙周膜和固有牙槽骨。牙齿萌出是牙齿从颌骨中迁移至功能位的一个复杂的生理过程。以往的研究证明 ,牙齿萌出需要依赖牙囊的存在 ,但其机制一直未明了。以下就近几年来关于牙囊从整体、细胞、分子水平上对牙齿萌出的调控作用所做的研究进行综述。1　牙囊在牙齿萌出时的整体调控作用牙齿的萌出需要依赖牙囊的存在。ＣａｈｉｌｌＤＲ的研究表明 ,以手术方法去除小鼠牙囊牙齿不能萌出 ,而保留牙囊用其它物质置换牙胚结果置换物可以萌出[1] 。Ｌａｒ…     

人乳牙根生理性吸收中RANKL的mRNA表达

目的：探求核因子κB受体活化剂配体-RANKL在人乳牙根生理性吸收过程中的表达和作用。方法：临床收集牙根吸收期人乳牙10个,运用原位杂交方法检测乳牙和牙周膜细胞中RANKL的mRNA表达情况。结果：吸收期乳牙中牙周韧带成纤维细胞、牙髓成纤维细胞、成牙本质细胞表达RANKL。乳牙吸收区陷窝内可见大量破牙细胞,RANKL表达不显著。结论：乳牙根生理性吸收过程由破牙细胞调节,RANKL可能促进破牙细胞的生成和活性。     

调控牙萌出的细胞及分子机制研究进展

牙萌出是指牙冠形成后向平面移动,穿过牙槽骨和口腔黏膜到达功能位置的一系列复杂生理过程。目前研究认为,牙萌出由牙槽骨、牙囊、破骨细胞、成骨细胞及多种细胞因子等共同调控,其中牙囊参与调控牙槽骨吸收与形成,是牙萌出的必要条件;同时,牙根形成及牙周韧带在牙齿持续萌出阶段发挥作用。牙萌出的具体调控机制尚不明确,本文就牙萌出过程中发挥调控作用的细胞及分子机制的研究现状作一综述。     

不同正畸力对大鼠牙周组织压力侧核因子κB受体活化因子配基表达影响研究

目的探讨大鼠实验性牙齿移动中不同正畸力对牙槽骨核因子KB受体活化因子配基（RANKL）表达的影响。方法本研究于2010年9-12月在山西医科大学寄生虫实验室完成。选用健康雄性Wistar大鼠36只,随机分为对照组、轻力组、中力组、大力组（各9只）,分别施加0、0．29、0．49、0．98N正畸力,建立大鼠牙齿移动模型。免疫组化法检测大鼠牙周组织压力侧RANKL的表达。结果对照组RANKL有少量表达,主要分布于破骨细胞的胞核,正畸加力各组RANKL表达主要分布于压力侧牙周膜及骨改建区的破骨细胞,在基质细胞和牙周膜成纤维细胞也有表达,且其黄染程度强于对照组。各实验组牙周组织压力侧不同程度地出现血管被挤压、玻璃样变区和骨吸收陷窝。正畸力与RANKL的表达呈正相关（r=O．834,P〈0．01）。结论正畸力与大鼠牙槽骨压力侧RANKL的表达呈正相关,且0．49N为促进RANKL表达的最佳力值。     

正畸移动狗乳磨牙对其恒牙胚的影响

目的:研究正畸力作用下,狗乳磨牙移动对恒牙胚以及恒牙萌出的影响。方法:选用健康15～16周龄雄性中国狗20只,左侧下颌为实验侧,右侧下颌为对照侧,以狗乳尖牙为支抗移动第二乳磨牙。观察正畸加力0d、7d、14d和21d后狗第二乳磨牙的移动以及第三恒前磨牙牙胚的变化。同时对乳牙牙周组织、恒牙牙胚的牙囊、周围牙槽骨进行组织学观察,并对牙槽骨内的破骨细胞进行计数。结果:正畸加力21d后,与对照侧相比,实验侧第二乳磨牙近移31.5%,X线片显示第三恒前磨牙牙胚位置与对照侧相比近移31.9%,二者有明显差异。恒牙萌出后近移30.3%。组织学观察:第二乳磨牙和第三恒前磨牙牙胚近中侧均见骨质吸收,可见破骨细胞;远中侧可见新骨形成。第三恒前磨牙牙胚牙囊近中侧纤维受压、变窄,远中侧纤维受到牵张、变宽。结论:正畸力移动乳牙对其继承恒牙的萌出具有诱导作用,可以使恒牙胚在牙槽骨中有同方向移动趋势,萌出位置改变。     

骨保护素/核因子-κB受体活化因子/核因子κB-受体活化因子配体信号分子调控牙萌出的研究进展

牙萌出是牙胚、牙槽骨以及多种类细胞系及多条通路信号分子相互作用共同调控的、复杂有序的生理过程。牙齿萌出需要在牙胚的方形成萌出通道,穿过牙槽骨和口腔黏膜到达功能位置。这一过程主要由破骨细胞直接执行,而骨保护素/核因子-κB受体活化因子/核因子κB-受体活化因子配体信号分子(OPG/RANK/RANKL)信号分子则可通过调节破骨细胞的分化与成熟来调控牙槽骨的改建,以保证牙萌出时方牙槽骨能被正常吸收。牙萌出的具体调控机制尚不明确,该文就OPG/RANK/RANKL信号分子调控牙萌出的研究现状作一综述。     

In situ expression of RANKL, RANK, osteoprotegerin and cytokines in osteoclasts of rat periodontal tissue

OBJECTIVES: This study examined the in situ expression of receptor activator of nuclear factor-kappaB ligand (RANKL), receptor activator of nuclear factor-kappaB (RANK), osteoprotegerin, interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in the osteoclasts of rat periodontal tissue. BACKGROUND: In periodontal disease, osteoclasts cause resorption of the alveolar bone. The function of osteoclasts is regulated by interaction with periodontal ligament cells (PDLs). Furthermore, various kinds of molecules such as RANKL, RANK, osteoprotegerin, IL-1beta and TNFalpha are known to be related to the osteoclasts differentiation and function. It is therefore important to observe the expression of RANKL, RANK, osteoprotegerin and cytokines in osteoclasts and PDLs. METHODS: Four-week-old Wistar rats were used. Tooth movement was performed by the Waldo method, and the pathological bone resorption was induced. The demineralized maxillae and mandiblae were embedded with paraffin. In situ hybridization was performed to detect RANKL, RANK, osteoprotegerin, IL-1beta, and TNFalpha mRNAs in osteoclasts and other cells using the specific RNA probes, respectively. RESULTS: Both RANKL and RANK were concomitantly expressed in some osteoclasts. RANKL was also positive in osteoblasts and PDLs. No IL-1beta- and TNFalpha-positive osteoclast was noted. The positive signals of osteoprotegerin were detected in almost all osteoblasts, PDLs and odontoblasts. No osteoprotegerin-positive osteoclasts were observed. The number and the distribution pattern of RANKL- and RANK-expressing osteoclasts changed when orthodontic excessive force was applied to periodontal tissue. In addition, IL-1beta and TNFalpha were shown to be expressed in osteoclasts under pathological status. CONCLUSION: These findings suggest that an autocrine mechanism of RANKL-RANK exists in osteoclast, which is heightened in the pathological conditions. Furthermore, the autocrine mechanism of IL-1beta and TNFalpha is also provided in osteoclast under pathological condition. These autocrine mechanisms therefore seem to regulate the osteoclast function in both physiological and pathological conditions.     

Reduction of orthodontic tooth movement by experimentally induced periodontal inflammation in mice

Orthodontic therapy is known to have an aggravating effect on the progression of destructive periodontitis if oral hygiene is not maintained. However, it is largely unknown how active periodontitis affects the velocity of orthodontic tooth movement. In this study, we examined the effect of periodontal inflammation on orthodontic tooth movement using a mouse model. Orthodontic force was applied on the maxillary first molar of mice, with or without ligature wire to induce experimental periodontitis. The distance moved by the first molar was significantly reduced by the ligature-induced experimental periodontitis. Tartrate-resistant acid phosphatase staining revealed that the number of osteoclasts present during orthodontic treatment was lower in the pressure zone of alveolar bone in the presence of periodontal inflammation. Consistently, the expression level of receptor activator of nuclear factor-κB ligand (RANKL) in the pressure zone was decreased in the ligature group. By contrast, experimental periodontitis increased the expression of cyclooxygenase-2 mRNA in the periodontal tissues, while in vitro treatment with prostaglandin E₂ decreased extracellular signal-regulated kinase phosphorylation and RANKL expression induced by mechanical stress in osteoblasts. Taken together, these results suggest that the orthodontic force-induced osteoclastogenesis in alveolar bone was inhibited by the accompanying periodontal inflammation, at least partly through prostaglandin E₂, resulting in reduced orthodontic tooth movement.     

Effects of aging on RANKL and OPG levels in gingival crevicular fluid during orthodontic tooth movement

OBJECTIVES: To compare the levels of the receptor activator of NFkB ligand (RANKL) and osteoprotegerin (OPG) in the gingival crevicular fluid (GCF) during orthodontic tooth movement in juvenile and adult patients. DESIGN: Fifteen juveniles and 15 adults served as subjects. GCF was collected from the distal cervical margins of the experimental and control teeth at 0, 1, 24, and 168 h after application of a retracting force. Enzyme-linked immunosorbent assay kits were used to determine RANKL and OPG levels in the GCF samples. RESULTS: The amount of tooth movement for juveniles was larger than for adults after 168 h. Further, after 24 h RANKL levels were increased and those of OPG decreased in GCF samples from the compression side during orthodontic tooth movement in both juveniles and adults. The RANKL/OPG ratio in GCF from adult patients was lower than that in the juvenile patient samples. CONCLUSION: Our results suggest that the age-related decrease in amount of tooth movement may be related to a decrease in RANKL/OPG ratio in GCF during the early stages of orthodontic tooth movement.