一氧化碳释放分子对牙周炎大鼠动脉粥样硬化的影响

目的 研究一氧化碳释放分子(carbon monoxide releasing molecule-2, CORM-2)对实验性大鼠牙周炎模型中动脉粥样硬化的作用。方法 40只8周龄Wistar大鼠,随机分为正常组、一氧化碳组(carbon monoxide group, CO组)、牙周炎组(chronic periodontitis group, CP组)和溶剂组(dimethylsulfoxide group, DMSO组)。CP组和CO组采用丝线结扎并注射内毒素法建立牙周炎模型。建模当天,CO组经腹腔注射CORM-2(10 mg/kg/d),DMSO组注射等体积DMSO溶液(0.05%V),正常组不做任何处理。分别于建模后1、3、7、14、28 d用酶联免疫吸附法检测血清内C反应蛋白(C-reactive protein, CRP)、可溶性血管细胞黏附分子1(soluble vascular cell adhesion molecule-1, sVCAM-1)、氧化型低密度脂蛋白(oxidized low density lipoprotein, ox-LDL)及白介素10( interleukin-10 ,IL-10)的含量。4周后处死大鼠,取大鼠降主动脉行油红O染色,观察脂质沉积情况,并检测牙槽骨吸收情况。采用SPSS 17.0软件包对所得数据进行统计学分析。结果 CO组大鼠牙周组织中炎细胞浸润及牙槽骨吸收程度均较CP组大鼠低,CP组大鼠血清CRP、sVCAM-1及ox-LDL水平显著高于CO组,CO组大鼠血清中IL-10水平显著高于其他各组（P<0.05）。28天后,在CP组大鼠降主动脉中可发现脂质沉积,而CO组大鼠血管中则无脂质沉积。结论 CORM-2能够抑制实验性牙周炎大鼠的炎性反应及动脉粥样硬化的形成。     

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。     

人β防御素3基因转染及金纳米颗粒处理后的牙周膜细胞对大鼠牙周炎形成影响研究

目的    探讨人β防御素3基因转染大鼠牙周膜细胞,并经金纳米颗粒处理后,局部注射对SD大鼠慢性牙周炎形成的影响。方法    丝线结扎法构建SD大鼠慢性牙周炎模型,酶消化法提取大鼠牙周膜细胞并鉴定,用携带人β防御素3基因的腺病毒转染细胞并经金纳米颗粒处理,在慢性牙周炎构建同期局部注射细胞悬液到腭侧牙龈,对照组分别注射生理盐水和空载体腺病毒转染后的细胞悬液。2周后处死大鼠取材。通过Micro-CT和免疫组化染色观察大鼠牙周炎形成情况。结果    单纯结扎组第二磨牙周围牙槽骨明显吸收,牙龈上皮钉突向内增生,棘层增厚,炎细胞浸润,胶原纤维变性、局部断裂。局部注射经转染和金纳米颗粒处理的牙周膜细胞后,结扎区域牙槽骨吸收水平降低,骨密度和骨体积分数增加;牙龈上皮炎症细胞浸润和上皮钉突增生减少,胶原纤维断裂和排列紊乱等病理变化得到改善。结论    人β防御素3基因转染及金纳米颗粒处理后的大鼠牙周膜细胞局部注射后,可减轻SD大鼠的牙周组织炎症,降低牙周组织破坏,从而在牙周炎的形成过程中起到保护作用。     

人骨保护素质粒转染抑制大鼠实验性牙周炎骨吸收的研究

目的:将自行构建的质粒载体pcDNA3.1-h OPG,通过体内转染,评价OPG直接基因转染疗法对大鼠实验性牙周炎牙槽骨吸收的影响,为牙周炎以及种植体周炎的生物治疗提供实验依据.方法:将30只SD大鼠随机分为3组,即I组生理盐水组(n=10,100μg/只)、Ⅱ组pcDNA3.1(-)组(n=10,100μg/只)、Ⅲ组pcDNA3.1-hOPG组(n=10,100μg/只).通过丝线结扎、接种牙周炎可疑致病菌、喂高糖软食诱发实验性牙周炎.结扎28d后处死,通过大体标本、组织学等观察牙槽骨吸收、OPG及破骨细胞变化.结果:Ⅲ组结扎侧OPG表达强度增加,牙槽骨吸收量减少(P＜0.05),活化破骨细胞数降低(P＜0.05).结论:OPG重组质粒转染,减少破骨细胞数量,有效减缓实验性牙周炎引起的牙槽骨吸收破坏.     

一氧化碳对炎症环境下人牙龈成纤维细胞黏附分子表达影响的机制研究

目的 研究一氧化碳对炎症环境下人牙龈成纤维细胞（HGF）黏附分子表达影响的分子机制。方法 体外培养HGF,以50 ng•mL-1的TNF-α和10 ng•mL-1的IL-1β刺激加入或不加入500 μmol•L-1一氧化碳释放分子-3（CORM-3）的HGF;分别在刺激10、20 min后收集部分细胞,用Western blot法检测丝裂原激活蛋白激酶（MAPK）通路中细胞外调节蛋白激酶（ERK）、c-Jun氨基末端激酶（JNK）和p38的磷酸化水平;在刺激4 h后用Western blot法检测核转录因子-κB（NF-κB）的核内表达;在部分实验中,HGF在TNF-α、IL-1β及CORM-3刺激前以鸟苷酸环化酶特异性抑制剂1H-[1,2,4]噁二唑[4,3-α]喹喔啉-1-酮（ODQ）预处理8 h,刺激24 h后用Western blot法检测细胞间黏附分子-1（ICAM-1）的表达。结果 在TNF-α和IL-1β刺激细胞10 min后,MAPK通路中p38、ERK和JNK的磷酸化水平即有明显升高,CORM-3能够明显抑制p38的磷酸化,而对ERK和JNK的磷酸化水平无明显影响;4 h后,CORM-3可明显抑制NF-κB-p65的核内表达。ODQ不能改变CORM-3对TNF-α和IL-1β共同刺激下ICAM-1表达水平的影响,说明CORM-3的作用并非通过鸟苷酸环化酶系统实现。结论 一氧化碳对炎症环境下HGF黏附分子表达的抑制作用可能是通过对NF-κB的活性抑制和对MAPK p38磷酸化水平的抑制作用来实现的。     

盐酸小檗碱对大鼠牙周组织中白细胞介素-1β和肿瘤坏死因子-α表达的影响

目的探讨盐酸小檗碱对大鼠实验性牙周炎模型牙周组织中白细胞介素- 1β（IL- 1β）和肿瘤坏死因子- α（TNF- α）表达的影响。方法在成功建立大鼠实验性牙周炎模型的基础上，实验动物在分别灌服盐酸小檗碱后第1、2、3、4周处死，取牙周组织标本作切片，行常规苏木精- 伊红染色，观察牙周组织病理变化状况，并采用免疫组织化学SABC法检测IL- 1β、TNF- α水平变化。结果牙周炎组牙周组织中IL- 1β、TNF- α表达明显高于正常组（P<0.05）；各时间段牙周炎治疗组牙周组织中IL- 1β、TNF- α表达明显低于牙周炎组（P<0.05），但牙周炎治疗组各时间段之间IL- 1β、TNF- α表达无显著差异。结论大鼠实验性牙周炎模型牙周组织中TNF- α、IL- 1β表达水平较正常对照组明显升高，应用盐酸小檗碱能抑制实验性牙周炎模型牙周组织中TNF- α、IL- 1β的表达。     

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.     

慢性不可预知性应激对大鼠实验性牙周炎预后的影响

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。     

实验性糖尿病牙周炎诱导骨细胞凋亡的初步研究

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。     

阻塞性睡眠呼吸暂停综合征对大鼠牙周组织影响的研究

目的：建立大鼠间歇低氧动物模型模拟阻塞性睡眠呼吸暂停综合征（OSAS）以及牙周炎的动物模型，探讨OSAS与牙周炎发病的相关性。方法???将20只SD大鼠随机分为常氧对照组（A组）和间歇低氧组（B组）。间歇低氧模型是将O2和N2循环通入实验舱，使O2浓度为（10%±0.5%）~（21%±0.5%），每天循环通气8?h。同时，采用正畸结扎丝结扎SD大鼠左侧上颌第二磨牙，建立牙周炎的动物模型。8周后处死动物，采用X线、组织学方法观察各组大鼠牙周组织的破坏情况。结果???各组大鼠结扎侧牙相对于非结扎侧牙的牙周探诊深度、龈沟出血指数升高，牙槽骨明显吸收。B组结扎侧牙的牙周组织炎症更显著。结论???间歇低氧环境可加重牙周组织的炎症反应，这就提示OSAS可能是牙周炎的危险因素之一。     

Effects of boric acid on experimental periodontitis and alveolar bone loss in rats

ObjectiveThe goal of the present study was to evaluate the histopathologic and morphometric effects of systemic boric acid in a rat periodontitis model.DesignTwenty-four Wistar rats were divided into three groups of eight animals each: non-ligated (NL), ligature only (LO), and ligature and treated with boric acid (BA) (3 mg/kg per day for 11 days). A 4/0 silk suture was placed in a subgingival position around the mandibular first molars; after 11 days the rats were sacrificed, and changes in alveolar bone levels were measured clinically and tissues were histopathologically examined to assess the differences amongst the study groups.ResultsThe ratio of presence of inflammatory cell infiltration (ICI) and osteoclast number in the LO group was significantly higher than that of the NL and BA groups (p < 0.05). The ratio of presence of osteoblastic activity in the LO group was significantly lower than that of the NL and BA groups (p < 0.05). Alveolar bone loss was also significantly higher in the LO group compared to the BA and NL groups (p < 005).ConclusionsThis study has demonstrated that systemic administration of boric acid reduced periodontal inflammation and alveolar bone loss in periodontal disease in rats.     

Effect of sumac extract on serum oxidative status,RANKL/OPG system and alveolar bone loss in experimental periodontitis in rats

Objectives

Sumac (Rhus coriaria L.) is widely used spice which has several properties such as antioxidant, anti-inflammatory and antimicrobial. The purpose of this animal study was to evaluate the effects of sumac extract on levels of receptor activator of nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG) expression, serum oxidative status, and alveolar bone loss in experimental periodontitis.

Material and Methods

Twenty-four Wistar rats were separated into three groups: non-ligated (NL, n=8), ligature only (LO, n=8), and ligature and treated with sumac extract (S, n=8) (20 mg/kg per day for 11 days). A 4/0 silk suture was placed around the mandibular right first molars subgingivally; after 11 days, the rats were sacrificed, and alveolar bone loss was histometrically measured. The detection of RANKL and OPG were immunohistochemically performed. Levels of serum total antioxidant status (TAS)/total oxidant status (TOS), and oxidative stress index (OSI) were also analyzed.

Results

Alveolar bone loss was significantly greater in the LO group compared to the S and NL groups (p<0.05). The number of inflammatory cell infiltrate (ICI) and osteoclasts in the LO group was significantly higher than that of the NL and S groups (p<0.05). The number of osteoblasts in the LO and S groups was significantly higher than that of the NL group (p<0.05). There were significantly more RANKL-positive cells in the LO group than in the S and NL groups (p<0.05). OPG-positive cells were higher in S group than in LO and NL groups (p<0.05). TOS and OSI levels were significantly reduced in S group compared to LO group (P<0.05) and TAS levels were similar in S and NL group (p>0.05).

Conclusions

The present study showed that systemic administration of sumac extract may reduce alveolar bone loss by affecting RANKL/OPG balance, TOS and OSI levels in periodontal disease in rats.     

The histopathological and morphometric investigation of the effects of systemically administered boric acid on alveolar bone loss in ligature-induced periodontitis in diabetic rats

Objective. The purpose of this study was to evaluate the effects of systemically administered boric acid on alveolar bone loss, histopathological changes and oxidant/antioxidant status in ligature-induced periodontitis in diabetic rats. Materials and methods. Forty-four Wistar rats were divided into six experimental groups: (1) non-ligated (NL, n = 6) group, (2) ligature only (LO, n = 6) group, (3) Streptozotocin only (STZ, n = 8) group, (4) STZ and ligature (STZ+LO, n = 8) group, (5) STZ, ligature and systemic administration of 15 mg/kg/day boric acid for 15 days (BA15, n = 8) group and (6) STZ, ligature and systemic administration of 30 mg/kg/day boric acid for 15 days (BA30, n = 8) group. Diabetes mellitus was induced by 60 mg/kg streptozotocin. Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 15 days after diabetes induction and the animals were sacrificed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were histopathologically examined. Serum total antioxidant status (TAS), total oxidant status (TOS), calcium (Ca) and magnesium (Mg) levels and oxidative stress index (OSI) were evaluated. Primary outcome was alveolar bone loss. Seconder outcome (osteoblast number) was also measured. Results. At the end of 15 days, the alveolar bone loss was significantly higher in the STZ+LO group compared to the other groups (p < 0.05). There was no significant difference in alveolar bone loss between the STZ+LO 15 mg/kg boric acid and STZ+LO 30 mg/kg boric acid groups (p > 0.05). Systemically administered boric acid significantly decreased alveolar bone loss compared to the STZ+LO group (p < 0.05). The osteoblast number in the BA30 group was significantly higher than those of the NL, STZ and STZ+LO groups (p < 0.05). Inflammatory cell infiltration was significantly higher in the STZ+LO group the other groups (p < 0.05). Serum TAS levels were significantly higher in the NL and LO groups than the other groups (p < 0.05). The differences in TOS levels were not found to be significant among all the groups (p > 0.05). The OSI values of the BA30 group were significantly lower than the STZ+LO group (p < 0.05). Also, the differences in serum calcium and magnesium levels were insignificant among the all groups (p > 0.05). Conclusion. Within the limits of this study, it can be suggested that BA, when administered systemically, may reduce alveolar bone loss in the diabetic rat model.     

Gingival levels of monocyte chemoattractant protein-1 (MCP-1) in diabetes mellitus and periodontitis: an experimental study in rats

The objectives of this study were to investigate and compare the monocyte chemoattractant protein-1 (MCP-1) levels of gingival tissues in diabetes mellitus (DM) and periodontitis and to reveal the effects of MCP-1 on periodontal inflammation and destruction in these diseases. DM was created in 15 rats (group 1) by streptozotocin injection, and periodontitis was obtained by ligature induction in 15 rats (group 2). Fifteen systemically and periodontally healthy rats were used as control (group 3). Gingival MCP-1 levels were measured by enzyme-linked immunosorbent assay (ELISA). Periodontal inflammation was quantified by the inflammatory cell infiltration in the gingival samples, whereas periodontal destruction was assessed by the alveolar bone loss in the experimental regions. MCP-1 concentrations were higher in groups 1 and 2 than in group 3 (p < 0.001). Increased gingival inflammatory cell infiltration and alveolar bone loss were observed in groups 1 and 2 compared to group 3 (p < 0.001). There were positive correlations among the MCP-1 level, gingival inflammatory cell infiltration, and alveolar bone loss in groups 1 and 2 (p < 0.001). Our results suggest that (1) DM may lead to enhanced MCP-1 production in periodontal tissues likewise for periodontitis and (2) there may be a positive correlation between the MCP-1 concentration and diseased nature of periodontium in both diseases.     

Accuracy of radiographic pixel linear analysis in detecting bone loss in periodontal disease: Study in diabetic rats

IntroductionPeriodontitis, a complex infectious disease that may lead to irreversible loss of periodontium, is considered a predisposing agent for developing insulin resistance due to the release of inflammatory mediators, showing a bilateral relationship with diabetes mellitus. The investigation of periodontal disease requires a clinical approach and complete intraoral radiographs, even with increasing concerns about radiation exposure. Thus, this study assesses pixel linear analysis accuracy using digital radiography via Digora® in detecting alveolar bone destruction in diabetic rats with periodontal disease.Methodology40 rats were divided into groups (n = 10): control (C), rats with periodontal disease (PD), experimental diabetic rats (ED), experimental diabetic rats with periodontal disease (ED-PD). Diabetes was induced by streptozotocin and periodontal disease by periodontal ligature. After 30 days, maxillae bone destruction was obtained by linear analysis of vertical bone loss using digital radiography and then assessed by micro-CT and histology. Data were analyzed by ANOVA and Tukey’s test (p < 0.05).ResultsRadiographic, micro-CT and histological analysis presented accurate and similar results. PD and ED-PD groups showed higher bone destruction than C and ED groups (p < 0.05). Moreover, the ED-PD group had higher bone loss than the PD group (p < 0.05).ConclusionThe pixel linear analysis via digital radiography was an accurate, low-cost alternative in detecting alveolar bone loss in this rat model. Micro-CT and histological analysis may also be used to obtain linear measures to assess and compare periodontal bone destruction in diabetic rats.     

Preventive effects of thymoquinone in a rat periodontitis model: a morphometric and histopathological study

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.     

Alveolar bone loss associated to periodontal disease in lead intoxicated rats under environmental hypoxia

Previously reported studies from this laboratory revealed that rats chronically intoxicated with lead (Pb) under hypoxic conditions (HX) impaired growth parameters and induced damages on femoral and mandibular bones predisposing to fractures. We also described periodontal inflammatory processes under such experimental conditions. Periodontitis is characterised by inflammation of supporting tissues of the teeth that result in alveolar bone loss. The existence of populations living at high altitudes and exposed to lead contamination aimed us to establish the macroscopic, biochemical and histological parameters consistent with a periodontal disease in the same rat model with or without experimental periodontitis (EP). Sixty female rats were divided into: Control; Pb (1000 ppm of lead acetate in drinking water); HX (506 mbar) and PbHX (both treatments simultaneously). EP was induced by placing ligatures around the molars of half of the rats during the 14 days previous to the autopsy. Hemi-mandibles were extracted to evaluate bone loss by histomorphometrical techniques. TNFα plasmatic concentration was greater (p < 0.01) in Pb and HX animals. TBA-RS content was significantly higher in gums of rats with or without EP only by means of Pb. The SMG PGE₂ content increased by Pb or HX was higher in PbHX rats (p < 0.01). Pb and HX increased EP induced alveolar bone loss, while Pb showed spontaneous bone loss also. In conclusion, these results show that lead intoxication under hypoxic environment enhanced not only alveolar bone loss but also systemic and oral tissues inflammatory parameters, which could aggravate the physiopathological alterations produced by periodontal disease.     

A morphometric and histopathologic evaluation of the effects of propolis on alveolar bone loss in experimental periodontitis in rats

BACKGROUND: Propolis collected by honeybees from various plant sources is a resinous hive product possessing a broad spectrum of biologic activities. Propolis has been used extensively in the diet to improve health and prevent disease. The purpose of this study was to analyze the morphometric and histopathologic changes associated with experimental periodontitis in rats in response to the systemic administration of propolis. METHODS: Forty Wistar rats were divided into four experimental groups: non-ligated (NL; N = 10); ligature only (LO; N = 10); and systemic administration of ligature and propolis (100 mg/kg body weight per day [Pro100; N = 10] or 200 mg/kg body weight per day [Pro200; N = 10]). Silk ligatures were placed at the gingival margin of the lower first molars in both mandibular quadrants. The study duration was 11 days, and the animals were sacrificed at the end of this period. Changes in alveolar bone levels were clinically measured, and tissues were histopathologically examined to assess the differences among the study groups. RESULTS: At the end of 11 days, alveolar bone loss was significantly higher in the LO group compared to the NL, Pro100, and Pro200 groups (P <0.05). Osteoclast numbers in the LO group were significantly higher than those of the NL, Pro100, and Pro200 groups (P <0.05). Both dosages of propolis significantly reduced the periodontitis-related bone loss, but the differences between the two propolis groups were not statistically significant (P >0.05). CONCLUSION: The findings of this study provide morphologic and histologic evidence that propolis, when administered systemically, prevents alveolar bone loss in the rat model.     

Self‐perceived oral symptoms and periodontal status among young intravenous heroin addicts: A cross‐sectional case‐control study

1 Background

It is hypothesized that (a) self‐perceived oral symptoms (OSs) are worse in intravenous heroin addicts (IHA) than controls; and (b) clinical periodontal inflammatory parameters (plaque index [PI], bleeding on probing [BOP], PD and clinical attachment loss [AL]), number of missing teeth (MT), and radiographic marginal bone loss (MBL) are higher in IHA compared with controls. The aim was to compare the self‐perceived OSs and periodontal parameters among young IHA and controls.

2 Methods

Sociodemographic data, self‐perceived OSs and duration and daily frequency of intravenous heroin use was gathered using a structured questionnaire. Full‐mouth PI, BOP, PD, and clinical AL were measured, and number of MT were recorded. Mesial and distal MBL on all teeth was measured on digital radiographs. Odds ratios (OR) with 95% confidence intervals (CI) were computed for self‐perceived OSs and periodontal parameters were assessed using the Mann Whitney U‐test and logistic regression analysis. Sample‐size was estimated, and level of significance was set at P < 0.05.

3 Results

OR (95% CI) for self‐perceived loose teeth (P < 0.001), pain in teeth (P < 0.001), dry mouth (P < 0.001), burning sensation in mouth (P < 0.001), bleeding gums (P < 0.001) and pain during chewing (P < 0.001) were significantly higher in the test than control group. Number of MT (P < 0.05), PI (P < 0.05), clinical AL (P < 0.05), and mesial (P < 0.05) and distal (P < 0.05) MBL were statistically significantly higher among individuals in the test group compared with the control group.

4 Conclusion

Self‐perceived OSs and periodontal inflammatory parameters were worse in IHA than controls.