雌激素缺乏对大鼠实验性牙周炎骨吸收的影响

目的评价雌激素缺乏及雌激素替代治疗(ERT),对大鼠实验性牙周炎牙槽骨吸收的影响。方法选取Wistar雌性大鼠24只,随机分成三组,Ⅰ组假手术组(n=8)、Ⅱ组卵巢摘除(OVX)组(n=8),Ⅲ组OVX 雌激素给药组(n=8)。21天后,将大鼠一侧上颌第一磨牙的牙周结扎,60天后,处死动物,取材,测得双侧磨牙的骨吸收量。结果结扎侧Ⅱ组的骨吸收量显著高于Ⅰ、Ⅲ组,有统计学意义,P<0.05;Ⅰ、Ⅲ组相比无统计学差别,P>0.05。结论ERT可能有效地防止雌激素缺乏状态下的牙槽骨吸收,但对于伴有菌斑刺激引起的牙周炎,ERT尚不能有效地阻止牙槽骨的吸收。     

固齿膏抑制大鼠实验性牙周炎形成的初步研究

用丝线缝扎大鼠前牙颈部形成实验性牙周炎的同时,分别用消炎痛和固齿膏治疗以抑制炎症的形成,以盐水作对照,结果发现在治疗的第7d和21d,固齿膏和消炎痛组与盐水对照组和未用药的牙周炎对照组相比,牙龈指数(GI)和牙周袋深(PD)明显降低,炎细胞浸润和骨吸收减少。与未缝扎的正常对照组无显著差异。提示固齿膏和消炎痛对实验性牙周炎都有一定的抑制作用。     

大鼠实验性牙周炎动物模型研究

首次用丝线缝扎大鼠牙颈部，喂高良物以观察牙周炎的形成。结果发现，丝线缝扎组，高糖喂养组，丝线缝扎和高糖喂养在实验１周和４周时牙龈指数和牙周袋深均增加。丝线缝扎组和高糖组在１周时牙龈固有层淋巴细胞和巨噬细胞增多，４周时可见破骨细胞和牙槽骨吸收，４周时丝线缝扎组破骨细胞较糖喂养组明显。     

内源性甲状旁腺激素抑制实验性小鼠牙周炎牙槽骨的吸收

目的探讨内源性甲状旁腺激素在实验性小鼠牙周炎牙槽骨吸收过程中的作用。方法大肠杆菌内毒素脂多糖牙龈局部注射法建立小鼠实验性牙周炎牙槽骨吸收模型,通过组织形态学、骨总胶原染色、耐酒石酸酸性磷酸酶染色等方法,比较分析甲状旁腺激素基因敲除小鼠和野生型小鼠牙槽骨吸收的差异。结果和野生型小鼠相比,甲状旁腺激素基因敲除小鼠的牙周骨丧失值、牙槽骨内单位长度骨小梁破骨细胞数以及骨面上破骨细胞的总长度占骨面长度的百分比则明显增加,牙周单位面积骨量明显降低。结论内源性甲状旁腺激素在实验性牙周炎牙槽骨吸收过程中起着重要的抑制作用。     

环肌酸抑制大鼠牙周炎周围牙槽骨吸收的实验研究

目的:通过体外和体内实验探讨环肌酸对牙周炎造成的牙槽骨吸收的抑制作用.方法:体外实验通过细胞活力测定、碱性磷酸酶染色和茜素红染色、抗酒石酸酸性磷酸酶染色和实时反转录聚合酶链反应(RT-PCR)等检测,评价环肌酸对成骨细胞和破骨细胞增殖和分化的影响.动物实验将20只大鼠分为4组,A组为对照组,B组采用牙周结扎+生理盐水注...     

实验性糖尿病牙周炎骨丧失动物模型研究

目的:建立实验性糖尿病牙周炎骨丧失动物模型,以进一步揭示糖尿病加重牙周炎骨丧失的细胞学机制.方法:选用6周龄雄性SD大鼠62只,随机分为糖尿病牙周炎组(DP)、牙周炎组(P)以及正常对照组(N).采用一次性腹腔注射链脲佐菌素(streptozotocin,STZ)的方法诱导大鼠糖尿病模型,采用丝线结扎联合口内接种细菌的方法建立牙周炎模型.动物分别于丝线结扎后3周和6周分批处死,进行HE染色、TRAP染色.观测指标包括:牙槽骨丧失,组织病理学比较,炎症区破骨细胞计数等.资料采用单因素方差分析统计学处理.结果:丝线结扎后3周和6周,大鼠牙槽骨丧失在N组与P组、N组与DP组、P组与DP组不同,组间两两比较均有统计学差异(P＜0.05),牙槽骨丧失DP组＞P组＞N组.炎症区单位长度破骨细胞数在N组、P组、DP组不同,N组与P组比较,N组与DP组比较、P组与DP组比较均有统计学差异(P＜0.05),其炎症区单位长度破骨细胞数DP组＞P组＞N组.结论:糖尿病可加重牙周炎牙周组织破坏,糖尿病条件下牙周炎骨丧失明显增加.糖尿病可能通过促进炎症部位破骨细胞生成,增强骨吸收,促进牙周炎骨丧失.     

大黄素治疗实验性牙周炎的骨计量学研究

目的:观察不同浓度大黄素对实验性牙周炎大鼠附着丧失和牙槽骨吸收的治疗作用.方法:选取纯种雌性SD大鼠随机分为4 组,各30 只: 正常对照组(N组)、牙周炎组(P组)、低浓度大黄素治疗组(PL组)及高浓度大黄素治疗组(PH组).建立牙周炎动物模型并按分组用药,分别于4、 6、 8 周时处死动物,取上颌骨标本进行骨计量学观察.结果:PL组和PH组结缔组织附着丧失量、牙槽骨嵴高度丧失量和破骨细胞个数均明显小于P组,成骨细胞个数均明显大于P组(P<0.05).结论:大黄素可抑制牙周附着丧失和牙槽骨吸收,并能促进牙槽骨形成.     

正畸力作用下垂直型骨吸收牙周炎大鼠牙槽骨改建的实验研究

目的：观察正畸力作用下牙周炎大鼠垂直吸收的牙槽骨改建,为牙周炎的临床正畸治疗提供依据。方法：将75只10周龄雄性SD大鼠,随机分为3组,正常加力对照组（ A）、牙周炎垂直骨吸收对照组（ B）、牙周炎垂直骨吸收加力实验组（ C）,每组各25只,各组动物分别于加力后8 h,1、7、14、21 d处死,取动物模型上颌左侧第一磨牙近中牙槽骨进行组织学及免疫学检测,所得结果进行对比研究。结果：正畸加力至7d时,实验组大鼠垂直吸收侧牙周膜纤维排列紊乱,出现无细胞结构,结缔组织可见少量炎症细胞,牙槽骨表面还可见功能活跃的多核破骨细胞,与对照组相比较无显著差异,实验组大鼠牙周组织中IGF?1表达达到峰值,光密度值最高,与对照组比较有显著差异（ P＜0．05）;加力至14 d时,实验组大鼠垂直吸收侧牙周组织中RUNX2的表达达到峰值,其光密度值最高,明显高于正常加力对照组,其变化有统计学意义（P＜0．05）。结论：控制牙周炎症和消除咬合创伤后,正畸力能刺激牙周炎大鼠垂直缺损牙槽骨区域的RUNX2和IGF?1的表达增强,合成骨胶原和骨基质的能力增强,从而促进牙槽骨的改建。     

黄芩苷对大鼠实验性牙周炎的保护效应及作用机制研究

目的 观察黄芩苷对丝线结扎诱导的大鼠牙周组织炎性破坏的保护作用,并探讨这一作用是否与牙龈组织中基质金属蛋白酶(matrix metalloproteinases,MMP)表达水平的改变有关.方法 将SD大鼠按随机数字表法分为3组,每组9只.用丝线结扎方法建立牙周炎模型,建模第7天处死动物.用药组(B200组)每天灌胃给予黄芩苷200 mg/kg;阴性对照组(L组)每天灌胃药物媒介0.5%羧甲基纤维素钠;空白对照组(C组)不予牙周炎诱导.评价牙槽骨吸收和胶原纤维的面积分数.免疫组化方法检测牙龈组织中MMP-1、MMP-2和MMP-9的表达.结果 B200组的骨吸收值[(0.93±0.04)mm]显著低于L组[(1.03±0.07)mm,P=0.009)];B200组的胶原纤维面积分数[(48.13±18.69)%]显著高于L组[(31.08±14.85)%,P=0.047];与L组相比,应用黄芩苷显著下调了MMP-1(P=0.023)及MMP-9(P=0.042)的水平,并降低了MMP-2的表达(P=0.099).结论 黄芩苷能够减少丝线结扎诱导的大鼠牙周炎的组织破坏,这一作用可能与其抑制MMP-1、MMP-2和MMP-9的表达有关.     

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目的研究能够快速建立稳定、可靠、重复性好的大鼠实验性牙周炎模型的方法,摸索建模的最佳时间并对比研究结扎与非结扎区域的牙槽骨破坏情况。方法本研究于2010年7月至2011年1月在中国医科大学基础医学院微生物学实验室及口腔医学院中心实验室完成。将18只SD大鼠随机分为对照组和4周、8周实验组。采用牙颈部结扎合并口腔接种牙周致病菌的方法,建立大鼠实验性牙周炎模型。分别于4周、8周时进行牙周检查,并利用放射影像和体视显微镜检查对比大鼠的牙周骨组织破坏情况。结果4周和8周实验组大鼠结扎区都出现牙龈红肿,探诊出血,均可探及较深的牙周袋。对照组和4周、8周实验组大鼠上颌三颗磨牙平均骨丧失量分别为（357．63±284．96）μm、（929．56±366．43）μm和（941．80±354．87）μm。与对照组相比,4周和8周实验组大鼠上颌磨牙的骨丧失量均显著增加,差异有统计学意义（P〈0．05）,但4周与8周实验组之间差异无统计学意义（P〉0．05）。结论采用牙颈部结扎合并口腔接种牙周致病菌的方法,4周左右即可形成稳定可靠的大鼠牙周炎模型。大鼠的牙周骨破坏在4周之后速度减缓。     

Effect of sodium alendronate on alveolar bone resorption in experimental periodontitis in rats

BACKGROUND: Bisphosphonates are potent inhibitors of bone resorption and were shown to inhibit bone resorption in experimental periodontitis by unknown mechanisms. We studied the effect of the aminobisphosphonate sodium alendronate (SA) in experimental periodontitis. Wistar rats were subjected to ligature placement around the second upper left molars. METHODS: Animals were treated with SA 0.01 to 0.25 mg/kg subcutaneously (sc), either 1 hour before (prophylactic) or starting 5 days after (therapeutic) periodontitis induction and daily until the rats were sacrificed (11 days). Controls received saline. Animals were weighed daily. Alveolar bone loss was measured as the difference (in millimeters) between the cusp tip and the alveolar bone. The periodontium and the surrounding gingivae were examined at histopathology, and the neutrophil influx into the gingivae was assayed using myeloperoxidase activity. The local bacterial flora was assessed through culture of the gingival tissue in standard aerobic and anaerobic media. RESULTS: Alveolar bone loss was significantly and dose dependently inhibited by SA either as a prophylactic or therapeutic treatment compared to the control. SA reduced tissue lesion at histopathology, with partial preservation of the periodontium, coupled to decreased myeloperoxidase activity compared to the control. The reduced neutrophil influx was also shown in carrageenan-induced peritonitis, used as a control experiment for this parameter. SA also significantly inhibited the growth of pigmented bacilli and Fusobacterium nucleatum, which are important in the pathogenesis of periodontal disease. SA also inhibited the in vitro growth of isolated Peptostreptococcus sp. CONCLUSION: Sodium alendronate preserves alveolar bone resorption and has anti-inflammatory and antibacterial activities in experimental periodontitis.     

iTRAQ-based quantitative analysis of alveolar bone resorption in rats with experimental periodontitis

ObjectivePeriapical periodontitis results in alveolar bone resorption around the root apex. During the progression of inflammation, host cells release various inflammatory mediators and pro-inflammatory cytokines through immune responses. However, the pathological mechanisms associated with periapical bone destruction remain unclear. This study was objected to identify differentially regulated proteins in periapical periodontitis via a quantitative proteomics approach using isobaric tags for relative and absolute quantification (iTRAQ) labelling of peptides.MethodsA model of periapical periodontitis by sealing LPS into the pulp chambers of rats was established. iTRAQ was employed to screen differentially expressed proteins in alveolar bone between periapical lesions and healthy controls. These proteins were further analysed by bioinformatics. And four proteins were validated by western bolt.ResultsWe identified 4398 proteins, of which 7 were up-regulated and 151 were down-regulated in periapical periodontitis compared to normal tissue. Using bioinformatics tools such as GO and KEGG pathway analysis, we found that our proteomics strategy could identify and quantify differentially expressed proteins that were not described in previous studies examining periapical periodontitis; these proteins included hexokinase, legumain and members of the keratin family.ConclusionIn summary, our results represent potential biomarkers for the detection of periapical periodontitis and demonstrate that quantitative proteomics is a robust discovery tool for the identification of differentially regulated proteins in periapical periodontitis.     

Nitric oxide synthase inhibition prevents alveolar bone resorption in experimental periodontitis in rats

BACKGROUND: Periodontitis is the most frequent cause of tooth loss in adults. Nitric oxide (NO) has been linked to bone resorption mechanisms during inflammation processes. The aim of this study was to investigate the effect of NOS (NO synthase) inhibitors in the alveolar bone loss in an experimental periodontitis disease (EPD) model. METHODS: Wistar rats were subjected to a ligature placement around the second upper left molars and were sacrificed at 11 days. Alveolar bone loss was evaluated by the sum of distances between the cusp tips and the alveolar bone along the axis of each molar root, subtracting from the contralateral side. Histopathological analysis was based on cell influx, alveolar bone, and cementum integrity. Leukogram was performed at 6 hours and 1, 7, and 11 days after the EPD induction. Groups were treated with the NOS inhibitors, aminoguanidine (AG) (2.5 to 10 mg/kg/d), or L-arginine methyl ester (L-NAME, 5 to 20 mg/kg/d) intraperitoneally (i.p.), 1 hour before the EPD induction and daily for 11 days. Controls received only saline (EPD group). As controls for L-NAME specificity, groups were co-treated with either L-arginine (150 to 600 mg/kg/d) or D-arginine (600 mg/kg/d) and L-NAME (20 mg/kg/d). Different groups were used for morphometric and histopathological analysis. RESULTS: Both L-NAME and AG significantly and dose-dependently inhibited the alveolar bone loss as compared to EPD group. L-NAME (20 mg/kg/d) reduced the alveolar bone loss by 50%, whereas AG (5 mg/kg/d) reduced it by 47% compared to EPD. This result was coupled to a significant reduction of cell influx to the periodontium, as well as to the preservation of alveolar bone and cementum, seen at histopathology, for both compounds. The co-administration of L-arginine, but not of D-arginine reversed L-NAME effects. CONCLUSION: These data provide evidence that NOS inhibitors prevent inflammatory bone resorption in experimental periodontitis.     

Effects of topical administration of clodronate on alveolar bone resorption in rats with experimental periodontitis

BACKGROUND: We examined whether topical administration of a bisphosphonate clodronate could prevent alveolar bone loss in rats with experimental periodontitis. METHODS: On day 0, elastic rings were placed around the cervix of the right and left maxillary first molars (M1) to induce inflammatory periodontitis. Fifty microl of clodronate solution at a concentration of either 0 (0.9% NaCl), 20, 40, or 60 mM was injected into the subperiosteal palatal area adjacent to the interdental area between M1 and M2 on either the left or right (experimental) side on days 0, 2, 4, and 6. The contralateral side served as a control and received 0.9% NaCl solution without clodronate. The animals were sacrificed on day 7. RESULTS: Histological examination and determination of bone mineral density in the interdental alveolar bone area between M1 and M2 revealed that placement of an elastic ring caused severe vertical and horizontal bone resorption on the control side, while the topical administration of clodronate significantly prevented such alveolar bone loss. The number of osteoclasts on the experimental side was decreased compared with the control side. Furthermore, many of the osteoclasts on the experimental side were detached from the surface of the alveolar bone and had degenerated appearances, such as rounded shapes and a loss of polarity. CONCLUSIONS: These results suggest that topical administration of clodronate may be effective in preventing osteoclastic bone resorption in periodontitis.     

Disodium chlodronate prevents bone resorption in experimental periodontitis in rats

BACKGROUND: Periodontitis is a chronic disease characterized by alveolar bone loss and inflammatory changes. We studied the effect of disodium chlodronate (CD), a bisphosphonate used in metastatic and metabolic bone disease as a bone resorbing drug, in an experimental periodontitis model (EPD) focusing on anti-resorptive and anti-inflammatory parameters. METHODS: A nylon thread ligature was placed around the left maxillary molars of 72 male Wistar rats who were sacrificed after 7 or 11 days. Groups were treated daily with CD (1, 5, or 25 mg/kg/sc) starting at day 0 until day 7 (prophylactic CD) or from day 5 until day 11 (curative CD) after periodontitis induction. Non-treated group (NT) consisted of rats subjected to periodontitis that received no pharmacological treatment. Alveolar bone loss (ABL) was measured as the distance between the cuspid tips and the alveolar bone. The right jaw was used as control. The hemiarcades were processed for histopathologic analysis. RESULTS: In NT group there was significant ABL, severe mononuclear cells influx, and increase in osteoclast numbers. Prophylactic CD treatment decreased the ABL 25.8%, 61.6%, and 75.5% as compared to NT for the 1, 5, and 25 mg/kg CD doses, respectively. Curative CD treatment decreased the ABL 20%, 62%, and 69% as compared to NT for the 1, 5 and 25 mg/kg CD doses, respectively. Both prophylactic and curative CD decreased histological changes, as compared to NT rats (P <0.01). CONCLUSIONS: CD has both bone sparing and anti-inflammatory activity in EPD in rats when administered as a pretreatment or in an ongoing process. The possibility of using CD as an alternative treatment in human periodontitis should be considered.     

唑来磷酸对实验性牙槽骨吸收抑制作用的研究

目的:在实验性牙槽骨吸收动物模型基础上,研究唑来磷酸局部应用对实验性牙槽骨吸收的影响,旨在找出一种效果理想的防治牙槽骨吸收的局部应用药物,为其局部应用于临床提供实验依据。方法:40只SD大鼠,随机分为5组,每组8只,一组为正常对照组,其余4组为实验组,分别为造模对照组、唑来磷酸低剂量、中剂量和高剂量治疗组(0.8mg/mL,1.0mg/mL和1.2mg/mL);实验组均采用牙周翻瓣术建立牙槽骨吸收模型,治疗组在翻瓣局部处分别给予不同浓度的唑来磷酸药物。所有大鼠在给药21天后处死,取牙体牙周组织标本,进行X线片拍摄、常规病理切片观察。结果:低剂量组、中剂量组和高剂量组牙槽骨吸收程度明显低于造模对照组,差异有统计学意义(P<0.05);牙槽骨病理切片显示中剂量组和高剂量组破骨细胞数量均较造模对照组明显减少(P<0.05);且骨小梁面积均优于造模对照组(P<0.05)。结论:唑来磷酸局部应用对牙周翻瓣术诱导的牙槽骨吸收具有一定的抑制作用。