快速上颌扩弓后局部应用二磷酸盐对腭中缝复发率的影响

目的 :探讨快速上颌扩弓后二磷酸盐 (BP)对大鼠腭中缝复发率的影响。方法 :6周龄SD雄性大鼠 88只 ,随机分为 11组 ,进行快速上颌扩弓实验 :快速扩弓 1周、保持 2周或 4周、复发后 4周。在保持期大鼠根据保持时间和注射BP的剂量不同分为 5种不同的处理方式 ,分别在扩弓结束、保持结束、复发结束时处死大鼠 ,制作脱钙及不脱钙切片 ,比较 5种处理方法大鼠扩弓后的复发率 (RR)、矿化沉积速率 (MAR )、破骨细胞的数量 (ON )。结果 :保持期注射BP的剂量不同明显影响扩弓后的复发率。结论 :快速上颌扩弓后局部应用二磷酸盐能减少大鼠腭中缝区破骨细胞的数量 ,加快新骨的矿化沉积速率 ,形成更多的新骨以减少扩弓后的复发率     

双膦酸盐对大鼠腭中缝快速扩弓后骨缝重建的影响

目的研究双膦酸盐对大鼠腭中缝快速扩开后骨缝重建的影响。方法将7周龄雄性wisrar大鼠42只随机分成3组，每组14只，所有大鼠均进行快速上颌扩大1周，再保持4周时，对照组不给药，实验一组双膦酸盐灌胃2周，实验二组双膦酸盐灌胃4周，保持结束后拆除所有大鼠的保持器，并且处死各组的一半大鼠，其余的大鼠复发4周，结束时再全部处死。测量每个实验步骤结束时腭中缝的宽度。所有大鼠取材后制做脱钙骨切片，光镜下观察计算各组大鼠扩弓后的复发率及破骨细胞数量。结果对照组腭中缝处破骨细胞数量及扩弓后腭中缝复发率明显高于实验一组和实验二组。结论大鼠上颌快速扩大后机械保持配合使用双膦酸盐能减少腭中缝处破骨细胞的数量，抑制新生骨质吸收，减少扩弓后的复发率。     

上颌快速扩弓腭中缝骨改建效果及其辅助方法研究进展

上颌快速扩弓是矫治青少年上颌横向发育不足的重要手段。如何有效促进腭中缝骨改建、增加扩弓稳定性、缩短保持期、减少扩弓复发一直是正畸学者探究的问题。本文简述上颌快速扩弓后腭中缝生物学改变, 并对上颌快速扩弓及促进腭中缝骨改建的辅助方法进行综述。     

雷尼酸锶对大鼠上颌快速扩弓影响的实验研究

目的 探讨雷尼酸锶对大鼠上颌快速扩弓的影响。方法 36只6周龄雄性Wistar大鼠,随机分为3组,空白对照（A）组﹑扩弓（B）组﹑扩弓并给药雷尼酸锶（C）组,每组12只。A组不扩弓,也不给药雷尼酸锶;B﹑C组用双眼圈簧扩弓器扩弓,力值1 N;C组扩弓开始即每天定时给药雷尼酸锶（600 mg•kg-1）。实验第4﹑7﹑10天分批处死大鼠,测量上颌宽度,并对大鼠腭中缝进行组织学观察和成骨细胞计数。结果 扩弓结束后,A组大鼠上颌宽度无明显变化（P>0.05）,B﹑C组上颌宽度较扩弓前均增加（P<0.05）,而B﹑C两组间的上颌宽度无明显差异（P>0.05）。组织学观察,A组腭中缝见少量红染的纤维组织,可见间充质样细胞、软骨细胞及成骨细胞。B﹑C组腭中缝处见较多红染的纤维组织,成纤维细胞﹑软骨细胞增多,腭中缝近骨边缘处多见成骨细胞;C组成骨细胞计数多于B组。结论 上颌快速扩弓可开大发育期大鼠腭中缝,增加上牙弓及上颌宽度;雷尼酸锶可以促进大鼠上颌快速扩弓时腭中缝处成骨细胞分化,加速新骨形成及骨质沉积钙化,减少复发。     

槲皮素在大鼠上颌快速扩弓时对腭中缝骨改建的影响

目的：研究槲皮素对大鼠上颌快速扩弓时腭中缝骨质改建的作用。方法：18只6周龄SPF级雄性Wistar大鼠,随机分为3组,A组为空白对照组,B组为扩弓组,C组为扩弓并灌服槲皮素组,每组均6只。其中,A组不扩弓,也不灌服槲皮素;B﹑C组用双眼圈簧扩弓器扩弓,力值0.98 N,C组扩弓后每天灌服槲皮素（100 mg/kg）,A、B组根据体重灌服同剂量的生理盐水。14 d后处死大鼠,标本进行石蜡切片,行常规苏木精-伊红染色、Masson三色染色、免疫组织化学染色。利用Image-pro plus软件对切片吸光度进行分析,采用SPSS 19.0 软件包对数据进行统计学分析。结果：实验第14天,H-E染色和Masson染色显示,A组腭中缝见少量纤维组织,可见软骨细胞、间充质样细胞及成骨细胞等;B﹑C组腭中缝处纤维组织较多,成纤维细胞﹑软骨细胞增多,腭中缝近骨区域处多见成骨细胞;C组成骨细胞数量明显多于B组,有新骨钙化沉积。免疫组织化学染色显示,B组大鼠腭中缝组织中的BMP-2表达量在第14天时显著高于A组（P<0.01）,C 组大鼠腭中缝组织中BMP-2 的表达量显著高于B组（P<0.05）。结论：上颌快速扩弓可扩大生长发育期大鼠的腭中缝;槲皮素能够促进大鼠上颌快速扩弓时腭中缝BMP-2的表达,使骨质沉积钙化,加速新骨形成。     

锂盐对大鼠腭中缝扩张成骨的影响

目的：观察锂盐对腭中缝扩张后新骨形成的影响。方法：使用扩大簧对Wistar大鼠作快速扩弓,腭中缝扩大3d后每日给予LiCl灌胃,对照组使用NaCl。通过甲苯胺蓝染色定量分析新骨的形成,免疫组化染色检测β-catenin的表达。结果：腭中缝扩大后第3天开始有新骨形成,应用LiCl后新骨边缘成骨细胞表达β-catenin增加。半定量分析显示实验组7d新骨形成量显著增加,是对照组的1.36倍（P〈0.05）。结论：锂盐能够通过激活β-catenin信号,促进大鼠腭中缝扩大后的新骨形成。     

上颌牙弓反复快速扩缩的动物模型的建立及初步研究

目的建立上颌牙弓反复快速扩缩的动物模型并进行初步研究。材料和方法选择6周龄健康雄性SD大鼠22只，随机分成3组：实验一组（单纯扩弓组）9只，连续扩弓5天；实验二组（反复扩缩组）9只，先扩弓5天，再缩弓5天，然后再扩弓5天…，如此反复25天，扩三次，缩两次；对照组4只，不进行任何处理。实验组在实验前、扩弓结束、缩弓结束时，拍腭中缝X线片，取大鼠上颌石膏模型。结果大鼠上颌咬合片中可以看到：扩弓后，大鼠腭中缝被打开，而缩弓结束后，腭中缝回复到扩弓前水平。模型测量发现：单纯扩弓组扩弓结束时中切牙间距离及第一磨牙间的距离比扩弓前增大（P〈0．05）。反复扩缩组每次扩弓结束时中切牙间距离及第一磨牙间的距离均增大（P〈0．05）；每次缩弓结束时，中切牙间距离及第一磨牙间的距离均缩小，与扩弓前水平相当（P〉0．05）。对照组腭中缝宽度、中切牙间距离及第一磨牙间的距离均无变化。结论本研究利用扩弓和缩弓装置成功建立了上颌牙弓反复快速扩缩的动物模型；腭中缝宽度、中切牙间距离及第一磨牙间的距离随着扩弓或缩弓而增大或回复，并且随着扩弓次数的增加，每次扩弓后中切牙间距离及第一磨牙间的距离均比前一次扩弓增大，第一扩弓和第三次扩弓的差异有显著性。     

快速扩弓对上颌第三磨牙萌出的影响[英]

快速扩弓是一种正畸临床上广泛应用的矫形治疗方法.尽管快速扩弓旨在通过打开腭中缝以矫治上颌骨牙弓狭窄,但由于上颌骨与头面部诸多骨块相连接,因此快速扩弓对牙和骨骼的生长均有一定的影响.     

种植钉辅助上颌快速扩弓治疗年轻成人上颌牙弓狭窄的CBCT分析

目的 探讨种植钉辅助上颌快速扩弓治疗年轻成人上颌狭窄的效果.方法 样本包括15.5～28.0岁上颌骨性狭窄病例10例(男3例,女7例),平均年龄(20.1±5.4)岁.使用种植钉辅助上颌快速扩弓技术,分别于治疗前、扩弓后和保持3个月后拍摄CBCT,并对资料进行统计分析.结果 扩弓后腭中缝前部和后部分别增加3.49 mm和2.94 mm,后部腭中缝增量占扩弓器扩大量的47.9％,后部腭中缝增量占第一磨牙间宽度增量的52.3％.鼻腔宽度、上颌基骨和牙槽宽度扩弓后增加(P＜0.05),且保持三个月后增加量无明显改变.牙槽骨高度变化无统计学意义(P＞0.05).结论 种植钉辅助上颌快速扩弓能有效开展年轻成人腭中缝,矫正骨性牙弓狭窄,并减少牙支抗扩弓引起的副作用.     

手术辅助腭扩展技术的应用进展

手术辅助腭扩展技术是通过外科手术方法进行上颌骨颊侧及腭中缝骨皮质切开,术后采用固定扩弓矫治器扩弓。本文对由于各种原因特别是唇腭裂引起的上颌骨横向发育不足的病例进行手术辅助腭扩展的适应证、手术方式、术后并发症及其对颅颌面的影响进行了综述。     

抑制核因子-κB受体活化因子及其配体通路治疗牙周炎的研究进展

核因子-κB受体活化因子(RANK)及其配体(RANKL)在牙周炎患者的牙槽骨吸收中具有重要的作用,抑制RANKL/RANK通路,可有效抑制破骨细胞的分化和激活,从而抑制牙槽骨的吸收。骨保护蛋白(OPG)可和RANKL结合,干扰RANKL和RANK的结合,从而防止骨组织的过度破坏。本文就RANKL/RANK/OPG轴、RANKL/RANK/OPG与牙周炎、抑制RANKL/RANK通路治疗牙周炎的可行性等研究进展作一综述。     

抑制核因子-κB受体活化因子及其配体通路治疗牙周炎的研究进展

核因子-κB受体活化因子（RANK）及其配体（RANKL）在牙周炎患者的牙槽骨吸收中具有重要的作用,抑制RANKL／RANK通路,可有效抑制破骨细胞的分化和激活,从而抑制牙槽骨的吸收。骨保护蛋白（OPG）和RANKL结合,干扰RANKL和RANK的结合,从而防止骨组织的过度破坏。本文就RANKL／RANK／OPG轴、RANKL／RANK／OPG与牙周炎、抑制RANKL／RANK通路治疗牙周炎的可行性等研究进展作一综述。     

Low-energy laser stimulates tooth movement velocity via expression of RANK and RANKL

OBJECTIVE: Recent studies have demonstrated that low-energy laser irradiation stimulates bone formation in vitro and in vivo. However, very little is known about the effects of laser irradiation on osteoclastogenesis. The receptor activator of the nuclear factor-kB (RANK) / RANK ligand (RANKL) / osteoprotegerin (OPG) system is essential and sufficient for osteoclastogenesis. The present study was designed to examine the effects of low-energy laser irradiation on expressions of RANK, RANKL, and OPG during experimental tooth movement. DESIGN: To induce experimental tooth movement in rats, 10 g of orthodontic force was applied to the molars. Next, a Ga-Al-As diode laser was used to irradiate the area around the moved tooth and the amount of tooth movement was measured for 7 days. Immunohistochemical staining with RANK, RANKL, and OPG was performed. Real time PCR was also performed to elucidate the expression of RANK in irradiated rat osteoclast precursor cells in vitro. RESULTS: In the irradiation group, the amount of tooth movement was significantly greater than in the non-irradiation group by the end of the experimental period. Cells that showed positive immunoreactions to the primary antibodies of RANKL and RANK were significantly increased in the irradiation group on day 2 and 3, compared with the non-irradiation group. In contrast, the expression of OPG was not changed. Further, RANK expression in osteoclast precursor cells was detected at an early stage (day 2 and 3) in the irradiation group. CONCLUSION: These findings suggest that low-energy laser irradiation stimulates the velocity of tooth movement via induction of RANK and RANKL.     

GaAs半导体激光对狗的上颌骨快速扩弓后新骨形成的促进效果

目的:通过GaAs半导体激光对狗的上颌骨快速扩弓后进行一定剂量的照射,探讨GaAs半导体激光对狗的上颌骨腭中缝处新骨形成的促进效果,为今后口腔正畸利用激光促进新骨形成的临床工作提供一定的实验依据。方法:随机选3只狗定为实验组,采用快速螺旋扩弓器打开腭中缝,并同时用GaAs半导体激光MDC-500型进行照射;另选3只狗定为对照组,只采用快速螺旋扩弓器打开腭中缝,不进行GaAs半导体激光的照射。快速扩弓3周,机械保持4周,自然保持8周。制作组织学标本,行光镜观察。结果:组织切片显示实验组腭中缝处新生类骨质的数量和面积都大于对照组,统计学有意义。结论:GaAs半导体激光对腭中缝处扩弓后新骨形成有一定的促进作用,成骨面积平均增加35%,为今后临床应用提供基础理论依据。     

基于RANKL-RANK-OPG轴研究丹参素防治牙槽骨骨质疏松的作用

目的:探讨RANKL-RANK-OPG轴在丹参素防治牙槽骨骨质疏松中的作用。方法:SD大鼠随机分为3组:对照组、去卵巢组和丹参素治疗组。实验90 d后取大鼠牙槽骨,HE染色观察牙槽骨组织形态学改变,组织化学染色方法检测牙槽骨组织中TRAP的活性,免疫组化的方法检测牙槽骨组织中RANKL和OPG的表达情况。结果:与去卵巢组相比:丹参素治疗组牙槽骨骨量明显增多,TRAP阳性的破骨细胞数减少,RANKL/OPG减小。结论:丹参素防治牙槽骨骨质疏松可能与其调控RANKL-RANK-OPG轴有关。     

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。     

The effect of etidronate on the periodontium of ovariectomized rats

Background: Bisphosphonates are indicated for the treatment of osteoporosis. However, they could have an adverse effect on specific sites, such as the bisphosphonate‐related osteonecrosis of the jaw. The aim of this study is to investigate the effect of etidronate on the resorption and apposition sides of the periodontium in ovariectomized rats. Methods: Twenty‐four female Wistar rats were randomly subjected to either ovariectomy or sham operation. After 8 weeks, six animals of each group were sacrificed. The other 12 rats received 5 mg/kg/day etidronate subcutaneously during 4 weeks. Tartrate‐resistant acid phosphatase reaction and immunohistochemical staining for receptor activator of nuclear factor‐κB (RANK), RANK‐ligand (RANKL), osteoprotegerin (OPG), and osteocalcin was performed. Immunoreactivity was evaluated using a semiquantitative analysis. Results: In ovariectomized rats, osteoclasts were noticed in the root socket of molars, including the apposition side of the periodontium, in which RANKL expression was significantly evidenced. In the etidronate‐treated group, OPG expression was significantly expressed and osteoclasts that were noticed in the resorption side remained undetected in the apposition side even under ovariectomy. RANK was significantly expressed in ovariectomized rats treated with etidronate. Osteoid formation and osteocalcin expression were described on the alveolar bone surfaces in etidronate‐treated rats, with or without ovariectomy. Conclusions: Etidronate has specific site and bone cell actions in the periodontium. It inhibits the osteoclast differentiation induced by ovariectomy in the apposition side of the periodontium but maintains bone formation over all the socket surfaces. Such specificity may be related to the pathogenesis of the bisphosphonate‐induced osteonecrosis of the jaw.     

Protective Mechanisms of Simvastatin in Experimental Periodontal Disease

Background: Simvastatin is a cholesterol‐lowering drug whose pleiotropic effects may have a therapeutic impact on bone. This study evaluates the effect of simvastatin on rats subjected to experimental periodontal disease. Methods: Periodontitis was induced by ligature placement around the maxillary left second molar of rats for 11 days. Groups of six animals received oral saline or simvastatin (3, 10, and 30 mg/kg/day) until sacrifice on day 11. Alveolar bone loss was determined by macroscopic and histologic examination. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total alkaline phosphatase (TAP) were evaluated. Gingival myeloperoxidase activity and gingival levels of interleukin‐1β (IL‐1β), tumor necrosis factor‐α, IL‐10, reduced glutathione, malonaldehyde, and nitrate/nitrite were analyzed to investigate oxidative stress and inflammation. Expression of inducible nitric oxide synthase (iNOS), matrix metalloproteinases 1 and 8 (MMP‐1 and ‐8), bone morphogenetic protein‐2 (BMP‐2), receptor activator of nuclear factor κB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also investigated by immunohistochemistry to assess bone turnover and metabolism. Immunofluorescence microscopy was used to confirm the expression of RANKL in rats’ maxillae. Results: Treatment with simvastatin improved alveolar bone loss within all of the parameters studied, thus demonstrating anti‐inflammatory and antioxidant activity. Simvastatin reduced expression of iNOS, MMP‐1 and ‐8, RANK, and RANKL and increased BMP‐2 and OPG levels in the periodontal tissue. Simvastatin (30 mg/kg) increased TAP activity on day 11 compared with the saline group. No differences were found in the levels of AST and ALT in any of the groups studied. Conclusion: The present data suggest that simvastatin prevents inflammatory bone resorption in experimental periodontitis, which may be mediated by its anti‐inflammatory and antioxidant properties.