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1.
目的 研究免疫低下对青少年牙周炎(JP)特异性病原菌感染的影响。方法 二次60Co全身照射制备免疫低下豚鼠及正常豚鼠各36只,随机分组,下前牙龈沟接种伴放线放线杆菌(Aa)和/或牙龈卟啉单胞菌(Pg),于2、3、 6周分批处死,进行组织病理学及破骨细胞计数对比研究。结果 免疫低下Aa、Pg、Aa+Pg组2、3周时牙周破坏明显,重于免疫正常组,破骨细胞计数高于免疫正常组,有统计学差异(P<0·05)。结论 免疫低下加重Aa、Pg对牙周组织破坏,机体免疫状态是JP发生发展的重要环节。  相似文献   

2.
目的:探讨慢性不可预知性复合心理应激对大鼠实验性牙周炎模型牙周组织愈合的影响。方法:雄性SD大鼠128只,随机抽取32只作为正常对照组。其余96只大鼠用丝线结扎右上颌第二磨牙颈部,4周后,采用龈沟出血指数和牙周探诊深度验证牙周炎模型。同时将大鼠结扎丝线去除,随机分为牙周炎对照组、牙周炎+应激组、牙周炎+应激+应激对抗药物组,每组32只。实验第5周起,应激组和药物组大鼠每日给予慢性不可预知性应激,同时药物组每日按5 mg/kg腹腔注射氟西汀。于实验第4、5、6、8周进行大鼠体质量测量、行为学测试、血清学检测;采用组织学观察牙周组织炎症反应、牙槽骨丧失、附着丧失以及破骨细胞计数。结果:心理应激大鼠出现体质量增长减慢、行为异常、血清皮质酮与促肾上腺皮质激素浓度升高(P<0.05),心理应激影响下大鼠牙周炎的愈合进程减慢,炎细胞浸润面积、牙槽骨吸收量与破骨细胞计数在实验第6周和8周、附着丧失在第8周高于对照组(P<0.05)。抗应激药物可逆转心理应激对牙周炎愈合过程的影响,该组炎细胞浸润面积与牙槽骨吸收在第6周和8周、破骨细胞计数在第8周明显低于应激组(P<0.05)。结论:慢性不可预知性心理应激能影响牙周组织的愈合,影响牙周炎的预后。而药物对抗应激能够减轻这种影响。  相似文献   

3.
Th2极化对牙周炎保护作用的实验研究   总被引:2,自引:0,他引:2  
目的:探讨稳定机体免疫反应对牙周组织病变的免疫调节作用,为牙周炎的免疫防治提供实验依据.方法:选用36 只SPF级12周龄雄性KM小鼠,随机分成3 组:正常对照组;牙周炎组,采用丝线结扎牙颈部并接种牙周炎患者病变区域龈缘下细菌诱导实验性牙周炎模型;Th2极化组,同上法复制实验性牙周炎模型,于术后第0 d感染低剂量旋毛虫.正常对照组及各实验组分别于术后第1、4、8、12 周分批处死动物,进行组织学观察和血清细胞因子IFN-γ、IL-4检测.结果:牙周炎组的牙周组织表现为中等程度的炎症破坏,而Th2极化组的牙周破坏程度较牙周炎组轻.牙周炎组血清IFN-γ含量较Th2极化组明显升高(P<0.01); Th2极化组IL-4含量较牙周炎组明显升高(P<0.01).结论:牙周炎的发病过程与Th1/Th2免疫应答平衡的失调有密切关系,表现为Th1细胞功能相对亢进,Th2细胞功能不足;Th2型细胞因子可有效减轻病变程度,对牙周组织具有保护作用.  相似文献   

4.
Th1极化反应与牙周炎病理改变的实验研究   总被引:3,自引:0,他引:3  
目的:观察增强机体Th1型细胞功能对牙周炎的影响,探讨机体免疫平衡失调在牙周炎发病中的作用.方法:SPF级KM 12 周龄雄性小鼠36 只,随机分成3 组:正常对照组;牙周炎组,采用丝线结扎牙颈部并接种牙周炎患者病变区龈缘下细菌诱导实验性牙周炎模型;Th1极化组,同法复制牙周炎模型,并于术后第0天感染紫外线减毒弓形虫.正常对照组及各实验组分别于术后第1、4、8、12 周分批处死动物,进行组织学观察和血清细胞因子TNF-α、IL-10检测.结果:Th1极化组牙周破坏程度较牙周炎组为重, 血清TNF-α含量较牙周炎组明显升高(P<0.01), IL-10含量较牙周炎组明显降低(P<0.01).结论:牙周炎的发病过程与Th1/Th2免疫应答平衡的失调有密切关系,表现为Th1细胞功能相对亢进,Th2细胞功能不足;Th1型细胞因子可加重牙周组织疾病和增加牙槽骨的吸收量.  相似文献   

5.
大鼠实验性牙周炎牙龈组织中一氧化氮含量改变的研究   总被引:3,自引:0,他引:3  
目的:探讨NO在牙周炎病理进程中的作用。方法:健康Sprague-Dawley大鼠共72只,随机分为正常对照组和牙周炎组,每组36只。参照DiPaola法复制大鼠牙周炎动物模型。分别于术后1、4和8周时处死动物,每个时间点每组处死动物12只。采用分光光度仪测量大鼠牙龈组织中亚硝酸盐(NO2-)和硝酸盐(NO3-)的含量,以间接确定NO含量;采用组织切片法观察牙周组织的组织病理学改变;应用Tiger细胞图象仪测量附着丧失(AL)。结果:术后4周和8周时,牙周炎组牙龈组织NO2-/NO3-含量明显高于正常对照组(P<0.01);在牙周炎组,术后8周牙龈组织NO2-/NO3-含量明显高于术后4周(P<0.01)。在牙周炎组,术后4周和8周与术后1周比较,AL显著增加(P<0.01);术后8周与4周比较,AL显著增加(P<0.01)。结论:NO2-/NO3-含量与牙周组织的破坏程度、AL直接相关。NO的合成在牙周组织疾病的进程中发挥作用,提示在牙周炎的治疗中控制NO的合成具有临床应用价值。  相似文献   

6.
实验性糖尿病牙周炎骨丧失动物模型研究   总被引:3,自引:2,他引:1  
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.  相似文献   

7.
实验性糖尿病牙周炎诱导骨细胞凋亡的初步研究   总被引:2,自引:0,他引:2  
目的初步探讨糖尿病牙周炎条件下骨细胞的凋亡情况。方法选用6wk雄性SD大鼠62只,随机分为糖尿病牙周炎组(DP,n=22)、牙周炎(P,n=20)以及正常对照组(N,n=20)。采用一次性腹腔注射STZ(55mg/kg)的方法建立大鼠糖尿病模型,注射STZ后1wk检测血糖,血糖≥16.65mmol/L者定为糖尿病大鼠。采用丝线结扎大鼠上颌第二磨牙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3wk和6wk分批处死,进行HE染色和原位细胞凋亡检测。观察指标包括:牙槽骨丧失(ABL),骨细胞计数,骨细胞凋亡百分率。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意义(P〈0.05),牙槽骨丧DP组〉P组〉N组。与N组比较,P组和DP组单位面积骨细胞数均减少,与P组比较,DP组单位面积骨细胞数亦显著减少(P〈0.05)。在丝线结扎后3周和6周,糖尿病牙周炎组(DP)骨细胞凋亡百分率均达到牙周炎组(P)的2倍左右。结论糖尿病条件下牙周炎骨丧失明显增加,糖尿病可加强牙周炎条件下牙周组织中骨细胞的凋亡,降低骨细胞的数量。  相似文献   

8.
目的:观察放线共生放线杆菌表面相关物质在骨吸收破坏中的作用。方法:用成年健康犬的C8、C7、C6、D6、D7、D8,去髓后将含500mg/mL的放线共生放线杆菌表面相关物质溶解物过滤除菌后的无菌生理盐水注入根管中,对照组加入等量无菌生理盐水,术后1个月后观察。结果:实验组可见犬牙槽骨尖周骨质吸收,牙周膜纤维排列受到破坏,对照组无明显改变,两组均未见到细菌污染。结论:此物质有极强的骨吸收诱导活性,在细菌未到达组织时其可溶性对尖周组织产生连续的毒性作用。  相似文献   

9.
目的:通过观测实验性牙周炎大鼠胰岛组织形态、检测外周血胰岛素水平和胰岛环氧化酶(cyclooxygenase,COX-2)表达情况,探讨慢性牙周炎对胰岛的影响。方法:将25只SD大鼠随机分为对照组10只和慢性牙周炎组15只,慢性牙周炎组行双侧上颌磨牙结扎法建立牙周炎模型。基线和12周采集外周血,12周处死大鼠,取颌骨和胰腺组织标本做切片,观察牙周和胰腺的组织学改变,测量牙槽骨吸收高度,并采用免疫组织化学法检测胰岛COX-2表达情况。结果:12周时牙周炎组外周血中肿瘤坏死因子(tumor necrosis factor-α,TNF-α)达(10.02±2.16)pg/mL,较对照组(7.64±1.59)pg/mL有明显升高(P<0.05)。但牙周炎组的血清胰岛素水平、胰岛形态和COX-2的表达水平均未见明显差异。结论:中等程度慢性牙周炎尚不足以造成大鼠胰岛组织形态和功能的改变。  相似文献   

10.
目的探讨冠心病患者牙周状况与牙龈卟啉单胞菌(Pg)和伴放线放线杆菌(Aa)的关系。方法试验分4组:冠心病伴慢性牙周炎组(A组)34例,冠心病组(B组)28例,慢性牙周炎组(C组)30例和对照组(D组)31例。记录各组牙周状况,取龈下菌斑进行Pg和Aa的分离培养及生化鉴定,检测牙周袋或龈沟内Pg和Aa阳性率。结果牙周状况A组比B组、C组差,C组比D组差。Pg、Aa阳性率A组比B组高,C组比D组高。结论冠心病患者的牙周健康状况较非冠心病患者差,提示慢性牙周炎可能是冠心病的又一危险因素。  相似文献   

11.
目的:探讨应激性唾液标志物嗜铬粒蛋白A(chromogranin A,CgA)、皮质醇、α淀粉酶、β内啡肽与牙周炎临床参数龈沟出血指数(sulcus bleeding index,SBI)、牙周探诊深度(periodontal probing depth,PD)、附着丧失(attachment loss,AL)的相关性。方法:选择2017年12月-2018年12月江西省中西医结合医院口腔科收治的慢性牙周炎患者105例为牙周炎组,同期在院健康体检者105例为对照组,检测2组唾液中CgA、皮质醇、α淀粉酶、β内啡肽水平及SBI、PD、AL。采用SPSS 22.0软件包分析应激性唾液标志物与牙周炎临床参数的相关性,利用多因素Logistic回归分析明确牙周炎有关的危险因素。结果:牙周炎组唾液中CgA、皮质醇、α淀粉酶、β内啡肽水平显著高于对照组(P<0.05),牙周炎组SBI、PD、AL显著高于对照组(P<0.05),唾液中CgA、皮质醇、α淀粉酶、β内啡肽水平与SBI均呈正相关 (P<0.05),唾液中CgA、皮质醇、α淀粉酶、β内啡肽水平与PD均呈正相关 (P<0.05),唾液中CgA、皮质醇、α淀粉酶、β内啡肽水平与AL均呈正相关 (P<0.05),CgA、皮质醇、α淀粉酶、β内啡肽是牙周炎的独立危险因素(P<0.05)。结论:应激性唾液标志物CgA、皮质醇、α淀粉酶、β内啡肽与牙周炎临床参数显著相关,提示应激性唾液标志物能在一定程度上反映牙周炎的病情进展,为牙周炎诊断和疗效监测提供有益参考。  相似文献   

12.
Background: The aim of this study is to investigate effects of strontium ranelate (SR) on alveolar bone loss (ABL) in rats with experimental periodontitis. Methods: Forty Wistar rats were randomly divided into five groups: 1) control (n = 8); 2) ligated (n = 8); 3) 300 mg/kg SR (SR300, n = 8); 4) 625 mg/kg SR (SR625, n = 8); and 5) 900 mg/kg SR (SR900, n = 8). To create experimental periodontitis, 4/0 silk ligatures were inserted submarginally around first molars at the right mandible. After 11 days, rats were sacrificed. ABL was calculated by measuring cemento‐enamel junction and alveolar crest distance. Interleukin (IL)‐1β, osteoprotegerin (OPG), and bone‐specific alkaline phosphatase (BALP) serum levels were determined by enzyme‐linked immunosorbent assay. Histopathologic analysis was used to evaluate inflammatory cell infiltration, numbers of osteoblasts and osteoclasts, and receptor activator of nuclear factor‐kappa B ligand (RANKL) activity. Results: ABL was significantly lower in SR900 group than in the ligated group (P <0.05). Osteoclast numbers in ligated group were significantly higher than in the control, SR300, and SR900 groups (P <0.05). In ligated, SR625, and SR900 groups, significantly higher osteoblast numbers were detected than in control group (P <0.05). Osteoblast numbers in SR625 group were significantly higher than in the SR300 group (P <0.05). RANKL activities in SR900 and control groups were close to each other (P >0.05). Serum IL‐1β, OPG, and BALP levels revealed no significant difference (P >0.05). Conclusion: It can be concluded that SR can reduce RANKL activity and osteoclast numbers, as well as ABL.  相似文献   

13.
目的探讨Toll样受体?4(Toll like receptor?4,TLR?4)抑制剂TAK?242对大鼠重度牙周炎骨质吸收的影响,为重度牙周炎寻找辅助治疗手段提供实验基础。方法18只3周龄雄性Wistar大鼠随机分为3组(n=6),其中1组为正常对照组,另外2组以含有牙龈卟啉单胞菌(P.gingivalis)ATCC33277的5?0丝线结扎大鼠双侧上颌磨牙行重度牙周炎建模,分为牙周炎组、TAK?242组;TAK?242组从丝线结扎第1天起,通过尾静脉隔天注射1次溶于DMSO的TAK?242(2 mg/kg),另外两组注射相同体质量比例的DMSO溶剂,连续8周;第8周末处死3组大鼠,获取大鼠上颌骨标本,采用micro?CT扫描后三维重建,测量特定位点釉牙骨质界?牙槽嵴顶的距离评估骨丧失量,并对牙槽骨骨质相关参数和骨质微结构进行分析;组织学切片苏木精?伊(HE)染色观察牙周组织病理改变;甲基绿染色观察牙槽骨吸收情况;抗酒石酸酸性磷酸酶(TRAP)染色观察破骨细胞分布情况。结果Micro?CT定量分析显示:牙周炎组与TAK?242组牙槽骨吸收显著高于对照组;与牙周炎组相比,TAK?242组大鼠上颌第一磨牙近、远中根吸收位点的骨丧失均显著减轻(P<0.001),骨密度(P<0.05)与骨体积/总体积分数(P<0.01)显著增高,骨小梁数目与骨小梁厚度(P<0.01)相对增多,骨小梁分离度(P<0.01)和骨小梁结构模式指数显著降低。牙周炎组骨质呈现疏松多孔的蜂窝状结构,骨小梁结构恶化,向杆状结构转变;TAK?242组骨质微结构改善,骨量改善,骨小梁分布相对更致密,骨小梁结构与对照组更相似。HE染色发现牙周炎组与TAK?242组牙周附着丧失与牙槽骨吸收较对照组显著;与牙周炎组相比,甲基绿染色表明TAK?242组骨吸收减轻,TRAP染色显示破骨细胞浸润减少(P<0.001)。结论TLR?4抑制剂TAK?242能缓解大鼠重度牙周炎骨吸收,改善其多孔、稀疏、排列紊乱的炎症性骨小梁结构。  相似文献   

14.
IntroductionOrthodontic relapse occurs after orthodontic treatment and shifting of teeth to unfavorable positions. Bisphosphonates’ effects on bone resorption and relapse prevention have been extensively investigated. However, topical administration, which results in local effect, is still a problem.ObjectiveThis study aimed to investigate the effect of risedronate with gelatin hydrogel as a carrier to prevent relapse movement by inhibiting osteoclast activity.MethodsLower incisors of 75 guinea pigs were moved distally using an orthodontic appliance until ±3 mm length. Gelatin hydrogel was fabricated to obtain a semisolid controlled release of 250 (Bis-CR250) and 500 mmol/L risedronate (Bis-CR500) and then applied intrasulcularly into the mesial subperiosteal area of 50 guinea pigs (25 in each group) every 3 days; the rest were the control (Bis-CR000). After 14 days of stabilization, the apparatus was removed. The distance decrease between incisors and the osteoclast number with TRAP staining at 0, 3, 7, 14, and 21 days were measured. ANOVA was used to determine the differences among the different time and experimental groups.ResultsBoth treatments showed significantly less relapse movement compared to the control (p < 0.05) at 14 and 21 days. Bis-CR500 more effectively inhibited the relapse movement than Bis-CR250 on day 21, indicating a dose dependency in the inhibition. Both treatments showed less osteoclast numbers than control (p < 0.05).ConclusionControlled release of bisphosphonate risedronate with a topically administered gelatin hydrogel has shown to be effective in decreasing the tooth relapse movement and osteoclast activity.  相似文献   

15.
目的:探究生命早期负性应激对大鼠成年后实验性牙周炎进展的影响。方法:在3周龄雄性SD大鼠建立慢性温和不可预知应激(unpredictable chronic mild stress, UCMS)模型,以正常饲养大鼠为对照。应激5周后对所有大鼠右上第二磨牙进行实验性牙周炎处理。通过行为学实验评估大鼠情绪状态;ELISA检测血清皮质酮、IL-1β和TNF-α水平;HE染色观察破骨细胞数目,测量牙槽骨丧失量。结果:UCMS大鼠出现糖水偏好下降(P<0.001)、强迫游泳实验中不动时间增加(P<0.01)等抑郁样行为;血清皮质酮及炎性细胞因子水平升高(P<0.05)。HE染色可见UCMS大鼠牙周炎侧牙槽骨吸收量最大,其次为对照组牙周炎侧,再次为对照组正常侧(P<0.001);破骨细胞数目变化趋势与之类似(P<0.001)。血清皮质酮含量与牙周破坏程度呈正相关关系(P<0.05)。结论:生命早期负性应激可能通过HPA轴增强体液免疫,加剧大鼠实验性牙周炎病变程度。  相似文献   

16.
目的:建立慢性牙周炎(chronic periodontitis,CP)合并高脂血症(hyperlipidemia,HL)的SD大鼠模型并对其进行牙周基础治疗,观察血清白介素-6(interleukin 6,IL-6)炎症因子及牙槽骨的影响。方法:SD大鼠随机分为4组,对照组(A)、HL组(B)、CP组(C)、HL+CP组(D);进行相应的建模处理,从建模开始15周后随机处死B组大鼠1只,取颈动脉分叉血管组织进行油红O染色,观察到泡沫细胞形成,则建模成功。再将C/D组随机分为2小组,C1/D1为自然进程组,C2/D2为牙周基础治疗组,进行2次牙周干预,分别于干预前1周、第1次干预后1周、第2次干预后1、3、5周采血,酶联免疫吸附法测定血清IL-6含量。实验结束后处死所有大鼠,取单侧上颌骨,剥离牙龈,进行亚甲基蓝染色,使用电子数显卡尺在徕卡显微镜(16X)下测量离体上颌骨实验牙釉质牙骨质界至牙槽嵴顶(cementoenamel junction and alveolar bone crest,CEJ- ABC)的距离(第一、二磨牙共12个位点)作为牙槽骨吸收值以检测牙槽骨吸收情况。使用SPSS21.0软件对所得数据进行统计学分析。结果:血清IL-6含量C、D组明显高于A组(P<0.05),其中,C1/D1组随时间推移一直呈现上升趋势,C2/D2组则在第2次干预后1周血清IL-6含量达到高峰,随观察时间延长则逐渐下降并低于基线水平(P<0.05);牙槽骨丧失量:C、D组>A组(P<0.001),而C2/D2组较C1/D1组牙槽骨丧失略有改善,但差异无统计学意义;牙槽骨吸收与血清IL-6水平呈Pearson正相关关系(P<0.01)。结论:高脂血症可加重牙周炎病变,牙周干预后短期内表现为机体炎症反应加重,远期则可能因炎症因子水平的降低而减轻全身病变进程。血清IL-6水平升高后,牙周局部表现为牙槽骨的吸收量增加。牙周基础治疗一定程度上可改善伴或不伴有高脂血症的牙周炎大鼠牙槽骨丧失的进程。  相似文献   

17.
Background: The present study aims to investigate the effects of systemic melatonin administration on alveolar bone resorption in experimental periodontitis in rats. Methods: Twenty‐four male Sprague‐Dawley rats were divided into three groups (control, experimental periodontitis [Ped], and experimental periodontitis treated with melatonin [Mel‐Ped]). For periodontitis induction, first molars were ligatured submarginally for 4 weeks. After ligature removal, rats in the Mel‐Ped group were treated with a daily single dose of 10 mg/kg body weight melatonin for 15 consecutive days. At the end of the study, intracardiac blood samples and mandible tissues were obtained for histologic, biochemical, and radiographic analysis. Serum markers related to bone turnover, calcium, phosphorus, bone alkaline phosphatase (b‐ALP), and terminal C telopeptide of collagen Type I (CTX) were analyzed. Myeloperoxidase levels were determined in gingival tissue homogenates, and receptor activator of nuclear factor‐kappa B ligand (RANKL) activation was analyzed in the mandible samples stereologically. Alveolar bone loss was also evaluated radiographically in the mandible samples of each group. Results: Melatonin treatment decreased serum CTX levels and increased b‐ALP levels. Serum calcium and phosphorus levels were not statistically different among groups (P >0.05). Alveolar bone resorption and myeloperoxidase activity were statistically higher in the Ped group compared to the Mel‐Ped group (P <0.05). Immunohistochemical staining of RANKL and osteoclast activity were significantly lower in the Mel‐Ped group compared to the Ped group (P <0.05). Conclusion: This study reveals that melatonin treatment significantly inhibits regional alveolar bone resorption and contributes to periodontal healing in an experimental periodontitis rat model.  相似文献   

18.
Ozdemir H, Kara MI, Erciyas K, Ozer H, Ay S. Preventive effects of thymoquinone in a rat periodontitis model: a morphometric and histopathological study. J Periodont Res 2012; 47: 74–80. © 2011 John Wiley & Sons A/S Background and Objective: Thymoquinone has a variety of pharmacologic properties, including antihistaminic, antibacterial, antihypertensive, hypoglycemic, anti‐inflammatory and anti‐oxidative activities. Through its anti‐inflammatory and antioxidant properties, thymoquinone may play an important role in preventing periodontal diseases. The aim of this study was to evaluate the effectiveness of thymoquinone in preventing the initiation and progression of periodontitis in a rat periodontitis model. Material and Methods: Twenty‐four rats were randomly divided into three experimental groups: a nonligated (NL) treatment group (n = 8), a ligature‐only (LO) treatment group (n = 8) and a ligature plus thymoquinone (10 mg/kg, daily for 11 d) (TQ) treatment group. In order to induce experimental periodontitis, a 4/0 silk suture was placed at the gingival margin of the right‐mandibular first molars of the rats. Thymoquinone was administered by gastric feeding until the animals were killed on day 11. Changes in the alveolar bone levels of rats in each group were measured clinically, and tissues of rats in each group were examined histopathologically to determine inflammatory cell infiltration (ICI), osteoblast and osteoclast activities, and osteoclast morphology. Results: Alveolar bone loss around the mandibular molar tooth was significantly higher in the LO group compared with NL and TQ groups (p < 0.05). The ratio of the presence of ICI and osteoclast numbers was significantly higher in the LO group than in the NL and TQ groups (p < 0.05). Osteoblastic activity was significantly lower in the LO group than in the NL and TQ groups (p < 0.05). Conclusion: The present study showed that the oral administration of thymoquinone diminishes alveolar bone resorption in a rat periodontitis model.  相似文献   

19.
何建明 《口腔医学》2005,25(2):80-82
目的 评价骨形成蛋白复合物联合胶原膜治疗牙周组织缺损的临床效果。方法 将骨形成蛋白复合物即重组合异种骨应用于引导组织再生(GTR)技术中,与传统的GTR技术和牙周翻瓣术对照研究。选择经过牙周基础治疗的35例4 5处牙周组织缺损,分为3组,BMP组:牙周缺损处植入骨形成蛋白复合物和胶原膜;GTR组:牙周缺损处植入胶原膜;OFD组:做牙周翻瓣术,为对照组。术后12、2 4周分别观察各组的牙周探诊深度(PPD)、临床牙周附着丧失(CAL)和龈沟出血指数(SBI)等临床指标变化。结果 3组术后PPD、CAL和SBI均有明显减少和降低。BMP组、GTR组与OFD组相比较,PPD和CAL减少、SBI降低,差异均有显著性(术后12周时P <0 .0 5 ,术后2 4周时P <0 .0 1) ;BMP组与GTR组相比,PPD和CAL减少,差异有显著性(P<0 .0 1) ,而SBI降低,差异无显著性(P >0 .0 5 )。结论 骨形成蛋白复合物联合胶原膜是治疗牙周组织缺损较为理想的方法  相似文献   

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