雌激素缺乏对大鼠牙槽骨吸收影响的实验研究

目的观察雌激素缺乏对大鼠牙槽骨吸收的影响。方法34只雌性SD大鼠随机分为4组。第1组假手术(n=8),第2组卵巢切除(n=9),第3组卵巢切除加牙周结扎(n=9),第4组卵巢切除、牙周结扎加雌激素治疗(n=8)。适应性喂养7天后行假手术或双侧卵巢切除术。第4组于术后第二天起皮下注射苯甲酸雌二醇．20μg／kg体重／次,三天一次。第3、4两组于卵巢切除术后28天,结扎丝结扎上颌第一磨牙诱导牙周炎。第63天处死全部大鼠。常规取材。观察牙用组织组织学改变。测量牙用骨丧失值(PBL)。比较牙用骨支持率(PBS)。检测血清碱性磷酸酶(ALP)。结果采用成组f检验,第1、2两组的PBL分别为0．398±O．147mm,0．663±0．132哪。PBS分别为O．588±O．058。0．440±0．197,组间差异均有统计学意义(P<0．05);第2、3两组的PBL、PBS组间差异均有统计学意义(P<0．05)。第3组的PBL为0．875±0．197mm,PBS为0．336±O．087;第3、4两组的PBL、PBS组间差别没有统计学意义(P>0．05),第4组的PBL为O．823±0．119mm,PBS为0．360±0．950。结论雌激素缺乏促进牙槽骨吸收,茵斑刺激加剧骨质疏松大鼠牙槽骨的吸收,雌激素替代治疗不能预防骨质疏松大鼠因茵斑刺激引发的牙槽骨吸收。     

Micro‐computerized tomography analysis of alveolar bone loss in ligature‐ and nicotine‐induced experimental periodontitis in rats

Liu Y‐F, Wu L‐A, Wang J, Wen L‐Y, Wang X‐J. Micro‐computerized tomography analysis of alveolar bone loss in ligature‐ and nicotine‐induced experimental periodontitis in rats. J Periodont Res 2010; 45: 714–719. © 2010 John Wiley & Sons A/S Background and Objective: Nicotine reportedly is a risk factor for periodontitis, but accurate data regarding nicotine‐induced alveolar bone loss is lacking. The aim of this study was to quantitatively assess alveolar bone loss in ligature‐ and nicotine‐induced periodontitis in rats using micro‐computerized tomography (micro‐CT). Material and Methods: Thirty‐six adult male rats were treated by placing silk ligatures around the cervixes of the right second maxillary molar; the contralateral tooth was untreated. After ligation, the animals were randomly divided into three groups: group A received intraperitoneal injections of saline solution, group B received 0.83 mg of nicotine/kg/d, and group C received 1.67 mg of nicotine/kg/d. Six animals in each group were killed on days 14 and 28 after ligature placement, and then micro‐CT examinations were conducted. Results: In all groups, bone mineral density (BMD), bone volume fraction (BVF), trabecular number (Tb.N) and trabecular thickness (Tb.Th) values of the ligated sides were significantly lower than those of the unligated sides (p < 0.001), whereas alveolar bone height loss (ABHL) and trabecular separation (Tb.Sp) of the ligated sides were significantly higher than those of the unligated sides (p < 0.001). Compared with the control group, nicotine administration increased the ABHL value and decreased the BMD, BVF and Tb.Th values of both sides in a dose‐dependent manner (p < 0.05). Conclusion: Our results confirmed that ligature could cause significant loss in the trabecula of alveolar bone, and daily administration of nicotine resulted in further bone loss and microstructure deterioration.     

Impact of cannabis sativa (marijuana) smoke on alveolar bone loss: a histometric study in rats

Background: Cannabis sativa (marijuana) can interfere with bone physiopathology because of its effect on osteoblast and osteoclast activity. However, its impact on periodontal tissues is still controversial. The present study evaluates whether marijuana smoke affects bone loss (BL) on ligature‐induced periodontitis in rats. Methods: Thirty male Wistar rats were used in the study. A ligature was placed around one of the mandible first molars (ligated teeth) of each animal, and they were then randomly assigned to one of two groups: control (n = 15) or marijuana smoke inhalation ([MSI] for 8 minutes per day; n = 15). Urine samples were obtained to detect the presence of tetrahydrocannabinol. After 30 days, the animals were sacrificed and decalcified sections of the furcation area were obtained and evaluated according to the following histometric parameters: bone area (BA), bone density (BD), and BL. Results: Tetrahydrocannabinol was positive in urine samples only for the rats of the MSI group. Non‐significant differences were observed for unligated teeth from both groups regarding BL, BA, and BD (P >0.05). However, intragroup analysis showed that all ligated teeth presented BL and a lower BA and BD compared to unligated teeth (P <0.05). The intergroup evaluation of the ligated teeth showed that the MSI group presented higher BL and lower BD (P <0.05) compared to ligated teeth from the control group. Conclusion: Considering the limitations of this animal study, cannabis smoke may impact alveolar bone by increasing BL resulting from ligature‐induced periodontitis.     

The influence of thyroid hormones on periodontitis-related bone loss and tooth-supporting alveolar bone: a histological study in rats

Background and Objective: Recent studies have pointed to potentially periodontal risk indicators, however no information is available on the impact of changes in thyroid hormone levels on the progression of periodontitis and on the quality of alveolar bone. Thus, the aim of the present study was to evaluate histologically, in rats, the influence of thyroid hormones on the rate of periodontal bone loss resulting from ligature placement and on the quality of tooth‐supporting alveolar bone. Material and Methods: Thirty‐six male Wistar rats were randomly assigned to the following groups: healthy (control, n = 12), hypothyroidism (n = 12) and hyperthyroidism (n = 12). Once alterations were confirmed by total serum levels of triiodothyronine and thyroxine, ligatures were randomly placed around one of the first mandibular molars. Thirty days later, the animals were killed and specimens routinely processed for serial decalcified sections. The parameters assessed were periodontitis‐related bone loss, quality of tooth‐supporting alveolar bone and the number of cells positive for tartrate‐resistant acid phosphatase (TRAP), a marker of bone resorption. Results: At the ligated sites, intergroup analysis revealed that hypothyroidism significantly increased the bone loss resulting from ligature‐induced periodontitis (p = 0.02) and the number of TRAP‐positive cells on the linear surface of bone crest (p = 0.01). In addition, no significant differences were detected regarding the quality of the bone (p = 0.24) or the number of TRAP‐positive cells in the area of the interradicular bone for ligated teeth among the groups (p = 0.17). Conclusion: It may be concluded that decreased serum levels of thyroid hormones may enhance periodontitis‐related bone loss, as a function of an increased number of resorbing cells, whereas the tooth‐supporting alveolar bone seems to be less sensitive to alterations in hormone levels.     

雌孕激素缓释凝胶对去势牙周炎大鼠牙槽骨吸收部位修复再生作用的研究

目的:研究雌孕激素缓释凝胶对去势牙周炎大鼠牙槽骨修复再生的作用。方法:选取6月龄雌性大鼠,随机分为去势组和假手术组,去势术后12周检测血清钙、磷、碱性磷酸酶和E2浓度。用0.2 mm结扎线于单侧第一磨牙牙颈部结扎,结扎4周后,建立大鼠牙周炎模型,用Micro-CT观察骨丧失情况。移除结扎线,将大鼠分为假手术生理盐水组,假手术上药组,去势生理盐水组和去势上药组。将配制好的雌孕激素缓释凝胶和生理盐水分别注入大鼠牙周袋内,治疗8周后,进行Micro-CT分析和HE组织学染色。结果:去势大鼠骨密度降低,血清钙、磷浓度降低,碱性磷酸酶活性升高,E2浓度降低。牙周结扎后,假手术组牙槽骨有水平吸收,去势组牙槽骨不仅水平方向上的吸收,垂直方向上也同样有吸收,牙槽嵴高度降低明显,根分叉暴露。雌孕激素缓释凝胶联合应用后,牙槽骨骨密度(BMD)升高、骨小梁数量(Tb.n)增加、骨小梁分离度(Tb.Th)增加、骨小梁连接数(Tb.Pf)增多,破骨细胞减少,新骨形成。结论:雌孕激素缓释凝胶能够促进去势大鼠牙槽骨吸收部位的修复再生。     

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。     

Low- and high-yield cigarette smoke inhalation potentiates bone loss during ligature-induced periodontitis

BACKGROUND: It is well recognized that cigarette consumption is a strong risk factor for periodontitis. Tobacco companies have developed a cigarette with low levels of toxic compounds; however, its effect on periodontium has not been investigated. The aim of this study was to verify the impact of smoke produced by low- and high-yield cigarettes on bone loss resulting from ligature-induced periodontitis. METHODS: A total of 36 male Wistar rats were used in the study. A ligature was placed around one of the mandibular first molars (ligated teeth) of each animal, and they were assigned randomly to one of three groups: group 1: control (N = 10), group 2: 30 days' inhalation of smoke produced by high-yield cigarettes (N = 13), and group 3: 30 days' inhalation of smoke produced by low-yield cigarettes (N = 13). The animals were sacrificed 30 days after ligature placement, and the specimens were processed for decalcified sections. RESULTS: Intergroup analysis of unligated teeth (without periodontal disease) did not show a significant difference regarding periodontal ligament area (2.40 +/- 0.5 mm(2), 2.72 +/- 0.7 mm(2), and 2.61 +/- 0.4 mm(2) for groups 1, 2, and 3, respectively; P >0.05). Conversely, significant differences were noted in ligated teeth (with periodontitis); bone loss was directly proportional to the level of toxic compounds in the cigarettes (5.74 +/- 0.5 mm(2), 7.40 +/- 0.50 mm(2), and 6.51 +/- 0.50 mm(2) for groups 1, 2, and 3, respectively; P <0.05). CONCLUSION: Low- and high-yield cigarettes potentiated bone loss during experimental periodontitis in a directly proportional fashion.     

Effect of cyclosporin A on alveolar bone homeostasis in a rat periodontitis model

OBJECTIVES: The administration of cyclosporin A has been associated with significant bone loss and increased bone remodeling. The present investigation was designed to evaluate the effects of cyclosporin A on alveolar bone of rats subjected to experimental periodontitis, using serum, stereometric and radiographic analysis. METHODS: Twenty-four rats were divided into one of the following groups with six animals each: group I, control rats; group II, in which the animals received a cotton ligature around the lower first molars; group III, in which the rats received a cotton ligature around the lower first molars and were treated with 10 mg/(kg body weight day) of cyclosporin A; group IV, in which the rats were treated with 10 mg/(kg body weight day) of cyclosporin A. At the end of experimental period, at 30 days, animals were killed and the serum calcium and alkaline phosphatase levels were measured in all groups. The distance from the alveolar bone crest to the cemento-enamel junction was measured radiographically for each mesial surface of the lower first molars of each rat. After histological processing, the stereological parameters: volume densities of multinucleated osteoclasts (V(o)), alveolar bone (V(b)), marrow (V(m)), and relation of eroded surface/bone surface (Es/Bs) were assessed at the mesial region of the alveolar bone. RESULTS: Significant decreases in serum calcium were observed in those groups that received cyclosporin A therapy. No significant changes in serum alkaline phosphatase were observed. The therapy with cyclosporin A combined with the ligature placement decreased the V(b) and increased the V(o), V(m) and Es/Bs at the mesial surface of lower first molars. On the other hand, the radiographic data showed that cyclosporin A therapy diminished the alveolar bone loss at the mesial surface of the lower first molars. CONCLUSIONS: Therefore, within the limits of this study, we suggest that cyclosporin A at immunosuppressive levels can bring about an imbalance in the alveolar bone homeostasis in rats. However, in the presence of inflammatory stimulation, the inhibition of the immune system by cyclosporin A may decrease the initial periodontal breakdown.     

N‐acetylcysteine decreases alveolar bone loss on experimental periodontitis in streptozotocin‐induced diabetic rats

Toker H, Ozdemir H, Balc? H, Ozer H. N‐acetylcysteine decreases alveolar bone loss on experimental periodontitis in streptozotocin‐induced diabetic rats. J Periodont Res 2012; 47: 793–799. © 2012 John Wiley & Sons A/S Background and Objective: The purpose of this study was to evaluate the morphometric and histopathological changes associated with experimental periodontitis in diabetic rats in response to systemic administration of N‐acetylcysteine (NAC), a sulfhydryl‐containing thiol antioxidant. Material and methods: Sixty Wistar rats were divided into six experimental groups: nonligated (NL) group; ligature‐only (L) group; streptozotocin‐only (STZ) group; STZ and ligature (STZ + L) group; and systemic administration of NAC and ligature (70 and 100 mg/kg body weight per day, respectively) (NAC70 and NAC100 groups). Diabetes mellitus was induced by 60 mg/kg of streptozotocin. Silk ligatures were placed at the gingival margin of the lower first molars of the mandibular quadrant. The study duration was 30 d and the animals were killed 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 the 30‐d study period, alveolar bone loss was significantly higher in the STZ + L group compared with the other groups (p < 0.05). Also, alveolar bone loss in all the NAC groups was significantly lower than in the STZ + L and L groups (p < 0.05). The osteoblastic activity in the NAC100 group was significantly higher than in the other groups (p < 0.05). Conclusion: Within the limits of this study, it can be suggested that NAC, when administered systemically, prevents alveolar bone loss in the diabetic rat model.     

Effect of obesity on alveolar bone loss in experimental periodontitis in Wistar rats

Obesity has been linked to higher inflammatory status and periodontal breakdown.

Objective

The purpose of this study was to investigate the effect of obesity on alveolar bone loss in experimental periodontitis in rats.

Material and Methods

Twenty-four female Wistar rats were randomly divided into two groups: obese (n=13), which were fed with "cafeteria diet" (CAF diet - high amounts of sucrose and fat) for 90 days in order to gain weight, and non-obese (n=11) regularly fed rats. Ligature-induced experimental periodontitis was created in all animals. Body weight differed statistically between obese and non-obese groups (277.59 and 223.35 g, respectively) at the moment of the ligature placement. Morphometric registration of alveolar bone loss was carried out after 30 days of ligature placement to determine the effect of obesity on the progression of experimental periodontitis.

Results

Intra-group comparisons showed significantly higher alveolar bone loss mean values in maxillary teeth with ligature (P<0.05). Alveolar bone loss [mean (SD), mm] was not statistically different between obese and non-obese groups [0.71 (0.09) and 0.65 (0.07) mm, respectively]. However, when palatal sides are analyzed separately, obese group presented significantly higher alveolar bone loss (P<0.05) as compared to non-obese [0.68 (0.12) and 0.53 (0.13) mm, respectively].

Conclusions

In spite of the weak differences, it is possible to conclude that the progression of alveolar bone loss in ligature-induced periodontitis can be potentially influenced by body weight in rats.     

实验性牙周炎动物模型研究

目的：建立一种近似人类临床牙周炎动物模型。方法：将大鼠随机分成对照组及实验组，并分别给予生理盐水肌肉注射、左上颌第2磨牙钢丝结扎和醋酸泼尼松龙肌肉注射。于实验第6周及第8周分2批处死大鼠。结果：实验组动物激素注射第4天后便出现了进食减少、倦怠少动等表现，符合中医肾虚的症状，并且出现了牙槽骨疏松、牙槽嵴吸收、牙周袋形成及破骨细胞活跃等病理性改变。对照组大鼠则无上述表现。结论：牙间结扎加糖皮质激素注射的方法可成功地建立近似于人类临床牙周炎的动物模型，为研究牙周炎提供了很好的方法。     

Decrease of Pericytes is Associated With Liver Disease Caused by Ligature‐Induced Periodontitis in Rats

Background: Damage caused by periodontitis not only affects periodontal tissues, but also increases the severity of various illnesses such as rheumatoid arthritis, diabetes, and liver diseases. The aim of this study is to investigate the association between induced periodontitis and damage caused through its systemic effects on the liver. Methods: Twenty rats were divided into two groups: control and periodontitis. The following parameters were evaluated: gingival bleeding index (GBI), probing depth (PD), myeloperoxidase (MPO) activity, alveolar bone loss (ABL) for periodontal tissues; histopathologic examination of gingival and liver tissues; immunohistochemistry to cells positive for neural/glial antigen 2 (NG2) expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA) concentrations in liver; and serum levels of alanine aminotransferase and aspartate aminotransferase. Results: GBI, PD, MPO, ABL, and histopathologic examinations demonstrated the development of periodontitis. There was a significant increase in microvesicular steatosis accompanied by a marked reduction in NG2+ pericytes in the periodontitis group compared with the control group. The periodontitis group had significantly lower GSH and higher MDA concentration in the liver compared with the control group. Conclusions: The present study results link the systemic effects of induced periodontitis with changes in hepatic tissues such as microvesicular steatosis, likely caused by an increase in oxidative stress and lipid peroxidation. The findings from the present study implicate an association between a decrease of pericytes and liver disease caused by ligature‐induced periodontitis in rats.     

Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis

Tokunaga K, Seto H, Ohba H, Mihara C, Hama H, Horibe M, Yoneda S, Nagata T. Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis. J Periodont Res 2011; 46: 655–662. © 2011 John Wiley & Sons A/S Background and Objective: Periodontitis is characterized by periodontal tissue inflammation and alveolar bone loss. The intermittent administration of parathyroid hormone (PTH), a major regulator of bone remodeling, has been demonstrated to stimulate osteoblastic activity. Although the systemic administration of PTH has been reported to protect against periodontitis‐associated bone loss, the effect of the topical administration of PTH is unclear. In this study, the effect of intermittent administration of PTH on osteoblastic differentiation was examined in cultured calvaria cells and then the effect of topical and intermittent administration of PTH was determined by measuring the recovery of alveolar bone loss after inducing experimental periodontitis in rats. Material and Methods: Alkaline phosphatase activity and bone nodule formation were measured in fetal rat calvaria cells. Experimental periodontitis was induced by placing nylon ligature around rat maxillary molars for 20 d. After ligature removal (day 0), PTH was topically injected into buccal gingiva three times a week for 10 wk. Micro‐computed tomography analysis and histological examination were performed on days 35 and 70. Results: Intermittent exposure of PTH in calvaria cells increased alkaline phosphatase activity and bone nodule formation by 1.4‐ and 2.4‐fold, respectively. Ligature procedures induced marked alveolar bone loss around the molars on day 0 and greater bone recovery was observed in the PTH‐treated rats on day 70. An increase in osteoid formation on the surface of alveolar bone was detected in the PTH‐treated rats. Conclusion: Intermittent treatment with PTH stimulated osteoblastic differentiation in fetal rat calvaria cell cultures, and topical and intermittent administration of PTH recovered alveolar bone loss in rat experimental periodontitis.     

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...     

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.     

Effects of Polycan,a β‐glucan,on experimental periodontitis and alveolar bone loss in Sprague‐Dawley rats

Kim YS, Kang SJ, Kim JW, Cho HR, Moon SB, Kim KY, Lee HS, Han CH, Ku SK, Lee YJ. Effects of Polycan, a β‐glucan, on experimental periodontitis and alveolar bone loss in Sprague‐Dawley rats. J Periodont Res 2012; 47: 800–810. © 2012 John Wiley & Sons A/S Background and Objective: Polycan is a promising candidate for the treatment of periodontal disease. This study was undertaken to examine whether Polycan, a type of β‐glucan, has a protective effect on ligature‐induced experimental periodontitis and related alveolar bone loss in Sprague‐Dawley rats. Material and Methods: Polycan was orally administered, daily, for 10 d, at 21.25, 42.5 or 85 mg/kg, beginning 1 d after ligation. Changes in body weight and alveolar bone loss were monitored, and the anti‐inflammatory effects of Polycan were determined by measuring the levels of myeloperoxidase (MPO), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) in gingival tissue. We also evaluated inducible nitric oxide synthase (iNOS) activity and malondialdehyde (MDA) concentrations as a measure of the antioxidant effect. Results: Ligature placement led to a marked decrease in body weight, increased alveolar bone loss and increased concentrations of MPO, IL‐1β, TNF‐α and MDA, as well as increased iNOS activity and inflammatory cell infiltration and decreased collagen‐fiber content. Histological examination revealed increases in the number and activity of osteoclast cells, decreases in alveolar bone volume and elevated percentages of osteclasts on the alveolar bone surface. Daily oral treatment with 42.5 or 85 mg/kg of Polycan for 10 d led to significant, dose‐dependent inhibition of the effect of ligature placement. Conclusion: Taken together, these results suggest that 10 d of oral treatment with Polycan effectively inhibits ligature placement‐induced periodontitis and related alveolar bone loss via an antioxidant effect.     

Estrogen deficiency and periodontal condition in rats: a radiographic and macroscopic study

The purpose of this study was to evaluate the impact of ovariectomy-induced estrogen deficiency as a risk factor of periodontal disease in rats. Forty 90-day old female rats were either ovariectomized (OVX; n=20) or sham operated (SHAM; n=20). After 30 days, periodontitis was induced by placement of a cotton ligature around the upper second molars of 10 OVX and 10 SHAM animals. All animals were sacrificed 5 weeks later. Body weight was assessed before all surgical procedures. The left hemimaxillas were removed and the percentage of periodontal bone support was determined radiographically and buccal alveolar bone loss was determined macroscopically using an image-analysis software. Furcation involvement was also evaluated. Data were analyzed statistically by ANOVA at 5% significance level. Within the evaluated period, the ovariectomized rats gained more weight than the sham-operated animals (p<0.001). The animals in which periodontitis was induced had less bone support, greater alveolar bone loss and furcation involvement than those without ligature (p<0.001). However, there was no difference between ovariectomized and sham-operated animals (p>0.05). Based on the findings of this study, estrogen deficiency could not be considered as a risk factor for periodontal disease.     

Matrix metalloproteinase-2 may be involved with increased bone loss associated with experimental periodontitis and smoking: a study in rats

BACKGROUND: Smoking has been associated with periodontitis severity and is considered a risk factor for its development. It has been reported that matrix metalloproteinase (MMP) produced by host cells plays a major role in periodontal tissue destruction. Thus, the present study tested, in rats, the hypothesis that local increased levels of MMP-2 would be associated with the enhanced periodontitis-related bone loss after intermittent cigarette smoke inhalation (CSI). METHODS: Twenty-seven adult male Wistar rats were used. A ligature was placed around one of the mandibular first molars of each animal and they were randomly assigned to the following control (N = 13) or CSI (N = 14) group. Sixty days later, the animals were sacrificed, the gingival tissues harvested, and the specimens processed for decalcified sections. Extracts from the gingival tissues were prepared and assayed for MMP-2 expression. RESULTS: Intergroup comparisons (unligated sites) showed that CSI might directly affect alveolar bone (0.16 +/- 0.03 mm2 versus 0.24 +/- 0.09 mm2 for non-smokers and smokers, respectively; P = 0.001). Moreover, CSI significantly enhanced bone loss resulting from experimental periodontitis (0.64 +/- 0.36 mm2 versus 1.50 +/- 0.50 mm2 for non-smokers and smokers, respectively; P<0.05). In addition, zymography demonstrated that CSI also enhanced both MMP-2 levels and activity in the gingival tissues around ligated teeth. CONCLUSION: Within the limits of the present investigation, it can be assumed that the effect of CSI on MMP-2 levels and activity may account for the increased periodontitis progression rate observed in smokers.     

Morphometric, histomorphometric, and microcomputed tomographic analysis of periodontal inflammatory lesions in a murine model

BACKGROUND: Porphyromonas gingivalis is recognized as one of the major periodontal pathogens in chronic periodontitis, a common infectious disease characterized by inflammation and destruction of periodontal tissues. Several animal models with P. gingivalis have been used in periodontitis studies. Additionally, multiple approaches have also been applied to measuring alveolar bone loss in periodontitis models, including histomorphometry, morphometry, and radiography. The aims of this study were to assess periodontal inflammatory lesions after P. gingivalis-induced periodontitis and use this model to compare three approaches for assessing alveolar bone loss. METHODS: Twelve-week-old male C57BL/6 mice were divided into two groups: 48 P. gingivalis-infected and 52 untreated control mice. Periodontitis was induced by wrapping P. gingivalis-soaked ligatures around the left maxillary second molar and changing the ligatures every other day. Mice were euthanized on days 0, 3, 7, and 10 after ligature placement, for a total of 12 experimental and 13 control mice per time point. Epithelial downgrowth, inflammation, and osteoclast activity were evaluated; alveolar bone loss was determined by histomorphometry, morphometry, and microcomputed tomography. RESULTS: The P. gingivalis-infected group showed significantly increased epithelial downgrowth (P <0.05), inflammation (P <0.05), alveolar bone loss (P <0.05), and osteoclast activity (P <0.05) throughout the experimental period compared to the controls. All three methods yielded efficient evaluation of alveolar bone loss. CONCLUSIONS: Our results show evidence that the P. gingivalis-soaked ligature-induced murine model mounts an adequate inflammatory response and exhibits periodontal tissue breakdown compatible with other models of periodontal disease. In addition, alveolar bone loss can accurately be quantified using any of the three alveolar bone analyses presented in this article.