Effects of lactation on alveolar bone loss in experimental periodontitis

BACKGROUND: The development and progression of periodontitis are accelerated by various systemic conditions. The present study was designed to determine whether lactation affects alveolar bone loss in rat models of experimental periodontitis. METHODS: Sixty-two female Wistar rats were bred with male rats and divided into three groups that were fed diets containing 0.9%, 0.3%, and 0.02% calcium. They were divided further into two subgroups of lactating and non-lactating animals. An elastic ring was placed around the neck of the right mandibular first molar to induce periodontitis (experimental side) on day 32 after mating. The left first molar was not fitted with an elastic ring (control side). After the lactation period, bone mineral density (BMD) was determined, and a histologic examination of the interdental alveolar bone was performed. RESULTS: On the experimental and control sides, BMD decreased significantly according to the amount of calcium in the diet; however, the magnitude of this decrease was much greater in the lactating group. Histologic examination revealed that in lactating and non-lactating rats, the decrease in BMD was accompanied by a decrease in alveolar bone height on the experimental side, whereas similar results were not seen on the control side. CONCLUSIONS: Lactation could be a risk factor for alveolar bone loss, especially under conditions of calcium insufficiency. Increased systemic demand for calcium and an insufficient supply of calcium might enhance the development of alveolar bone loss in periodontitis.     

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.     

Effects of experimental osteoporosis on alveolar bone loss in rats

A study was conducted to investigate the relationship between osteoporosis and alveolar bone loss. Alveolar bone loss was evaluated by radiographic and visual inspection of rats with experimental osteoporosis. Twenty 4-week-old female Sprague-Dawley rats were divided into the following groups: Group A-ovariectomized and given a standard solid diet; Group B-ovariectomized and given a calcium-deficient diet; Group C-sham-ovariectomized and given a standard solid diet; and Group D-sham-ovariectomized and given a calcium-deficient diet. After 4 weeks, the rat were euthanatized. The maxillae, mandibles, femurs, and tibias were removed carefully and fixed in 10% neutral buffered formalin. The bone mineral density of each bone and the alveolar bone loss were measured. The bone mineral densities of the maxillae, mandibles, femurs and tibias in Group C were significantly higher than those in Groups B and D, but not higher than those in Group A. However, there were no significant differences between any of the groups with regard to alveolar bone loss from the cemento-enamel junction to the molar bone crest. Therefore, it was concluded that osteoporosis itself may not be capable of causing periodontal destruction, and thus may not be a major factor in periodontal disease.     

Age-related periodontitis and alveolar bone loss in rice rats

ObjectiveTo characterize in rice rats: (a) periodontitis (PD) progress with feeding of standard laboratory rat chow (STD) during ages 4–80 weeks; and (b) PD progress with feeding of a high sucrose-casein (H-SC) diet during young adulthood.MethodsOne group (N = 12) was euthanized at age 4 weeks (Baseline). Four groups (N = 8-16) consumed a STD diet from baseline and were necropsied at ages 22, 30, 52, and 80 weeks. Three groups (N = 10-16) consumed an H-SC diet from baseline. Two were necropsied at ages 22 and 30 weeks, respectively. The third switched to the STD diet at age 22 weeks and was necropsied at age 30 weeks. All mandibles/maxillae were assessed by histometry for degree of periodontal inflammation (PD Score), alveolar crest height (ACH, mm), and horizontal alveolar bone height (hABH, mm²).ResultsIn STD diet rats aged ≥30 weeks, all endpoints were worse (P < 0.05) than at Baseline. In H-SC diet rats aged ≥22 weeks, all endpoints were worse than at Baseline (P < 0.05). At age 22 weeks, all endpoints were worse in the H-SC group than in the STD group (P < 0.05). By age 30 weeks, the STD and H-SC groups did not differ.Conclusions1) STD diet fed rice rats develop moderate/severe PD by age 30 weeks; 2) an H-SC diet accelerates moderate/severe PD development; and 3) switching to a STD diet does not halt/reverse PD that was accelerated by an H-SC diet. These data further clarify use of the rice rat as a PD model.     

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.     

Selective cyclooxygenase-2 inhibition prevents alveolar bone loss in experimental periodontitis in rats

BACKGROUND: Prostaglandins are implicated in periodontal bone destruction. We investigated the effect of a non-selective cyclooxygenase (COX) inhibitor (indomethacin-IND) or a type 2 COX inhibitor (meloxicam-MLX) in an experimental periodontal disease (EPD) model. METHODS: Wistar rats were subjected to placement of a nylon thread ligature around the maxillary molars and sacrificed after 7 days. Alveolar bone loss (ABL) was measured in one quadrant as the distance between the cemento-enamel junction and the alveolar bone. The other quadrant was processed for histopathologic analysis. Daily weight and white blood cell count were recorded. Groups were treated subcutaneously for 7 days with either IND (0.5, 1, or 2 mg/kg) or MLX (0.75, 1.5, or 3 mg/kg). Controls received no treatment. Macroscopic analysis of the gastric mucosa was done. The control group did not receive any manipulation, and a non-treated group consisted of rats subjected to periodontitis that received no pharmacological treatment. RESULTS: In the non-treated (NT) group, there was significant ABL, severe mononuclear influx, and an increase in osteoclast numbers. Significant neutrophilia and lymphomonocytosis occurred at 6 hours and at 7 days, respectively, as compared to controls. Significant weight loss persisted until the seventh day in the NT group. Both IND and MLX reduced ABL and histopathologic changes. Neutrophilia and lymphomonocytosis were also significantly reversed. Both IND and MLX induced earlier weight recovery. The stomachs of the IND (1 and 2 mg/kg) groups presented hemorrhage and ulcers, whereas in the MLX-treated groups, there were mild petechiae just in the 3 mg/kg group. CONCLUSIONS: COX inhibition prevented ABL in this experimental periodontal disease model. MLX displays similar efficacy and less gastric damage than IND. MLX may provide a better risk/benefit ratio in the treatment of human periodontitis than non-selective COX inhibitors.     

The effect of indomethacin on alveolar bone loss in experimental periodontitis

This study was undertaken to determine if prostaglandins play a role in the events leading to loss of bone in the ligature model of periodontitis. Periodontitis was induced by placement of the ligatures around mandibular teeth on one side of the jaw of squirrel monkeys ( Saimiri sciureus ). From one day prior to ligature placement, half the animals were administered indomethacin (5 mg/kg/day), a potent inhibitor of prostaglandin synthesis. Animals were sacrificed after one and two weeks of experimental periodontitis. It was found that indomethacin treatment abolished the significant losses of alveolar bone height and bone mass seen in non-indomethacin-treated (NIT) animals following ligature placement. Indomethacin also depressed the large increase in osteoclast density measured at one week in the NIT animals. The results support the hypothesis that prostaglandins are an important mediator of bone loss in the ligature model of periodontitis. Evidence is also presented for the coupling of bone resorption with osteoblastic neo-osteogenesis on both periodontal ligament and endosteal bone surfaces.     

Effects of colchicine on gingival inflammation,apoptosis, and alveolar bone loss in experimental periodontitis

1 Background

The aim of the study was to investigate the effects of colchicine on cytokine production, apoptosis, alveolar bone loss, and oxidative stress in an experimental model of periodontitis in rats.

2 Methods

Forty‐eight rats were divided equally into four groups: healthy (H); periodontitis (P); periodontitis+colchicine low dose (CL, 30 μg/kg/day), and periodontitis+colchicine high dose (CH, 100 μg/kg/day). After 11 days, interleukin (IL) ‐1β, IL‐8, and IL‐10 were analyzed in gingival samples using Enzyme‐Linked ImmunoSorbent Assay. Receptor activator of nuclear factor kappa‐B ligand (RANKL), osteoprotegerin (OPG), total oxidative stress (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) were measured in gingiva and serum. Alveolar bone volume was evaluated via micro‐CT. Apoptotic cells were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay in histological sections.

3 Results

Colchicine treatment significantly reduced IL‐1β, IL‐8, RANKL, RANKL/OPG, TOS, OSI, and bone volume ratio levels, and increased TAS levels compared to group P (p < 0.05). High dose colchicine treatment (CH) significantly decreased TUNEL+ cell counts compared to group P (p < 0.05).

4 Conclusions

These finding suggest that colchicine has a prophylactic potential for the prevention of periodontal tissue destruction through anti‐inflammatory, anti‐oxidative, anti‐apoptotic, and bone‐protective effects.     

Effects of chlorpromazine on alveolar bone loss in experimental periodontal disease in rats

Chlorpromazine (CPZ), a phenothiazine derivative, possesses anti-inflammatory properties, inhibition of tumor neurosis factor-alpha (TNF-alpha) synthesis and bone resorption. TNF-alpha promotes inflammatory changes and bone resorption in periodontitis. We have studied the effect of CPZ in experimental periodontitis. Wistar rats were subjected to a ligature placement around the cervix of the right second upper molars. Alveolar bone loss was evaluated by the sum of the distances between the cusp tip and the alveolar bone along the axis of each molar root, which was subtracted from the contralateral side. Histopathological analysis of the periodontium was based on cell influx, osteoclast number, and alveolar bone and cementum integrity. Animals were weighed daily and total and differential peripheral white blood cell counts were performed 6 h and 1, 7 and 11 d after periodontitis induction. Groups were treated with CPZ 1 h before and daily up to the 11th d of periodontitis. Alveolar bone loss was inhibited 46%, 55.4%, and 76.5% by CPZ at 1, 3 and 9 mg/kg, respectively. Histological analysis showed a significant reduction of cell influx and osteoclast number, as well as preservation of the alveolar process and cementum. CPZ reversed leukocytosis but not weight loss. In conclusion, CPZ reduces bone loss in experimental periodontitis, probably via TNF-alpha blockade.     

Intermittent administration of parathyroid hormone ameliorated alveolar bone loss in experimental periodontitis in streptozotocin-induced diabetic rats

ObjectiveIntermittent administration of parathyroid hormone (PTH) has been demonstrated to have anabolic effects on bone metabolism and is approved for use in the treatment of osteoporosis. This study evaluates the role of intermittent PTH administration on alveolar bone loss in streptozotocin (STZ)-induced diabetic rats.DesignFifty male Sprague Dawley rats were randomly divided into the following five groups: (1) a control group (saline placebo without ligature and STZ injection), (2) a PTH group (PTH administration without ligature and STZ injection), (3) an L group (saline placebo with ligature), (4) an L + STZ group (saline placebo with ligature and STZ injection), and (5) an L + STZ + PTH group (PTH administration with ligature and STZ injection). PTH was administered at 75 μg/kg per dose four times a week for 28 days. Subsequently, all rats were sacrificed, and their mandibles were extracted for micro-computed tomography (micro-CT) scanning, as well as histological and immunochemical evaluation.ResultsMicro-CT scanning demonstrated the anabolic effect of PTH on alveolar bone metabolism in STZ-induced diabetic rats (P < 0.05), and histomorphometry indicated that PTH inhibited inflammation of the periodontium and increased the level of osteoblastic activity (P < 0.05). Immunochemical evaluation showed that rats subjected to both ligature placement and STZ injection had the highest receptor activator of nuclear factor kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio and that PTH administration decreased this ratio.ConclusionIntermittent systemic PTH administration effectively reduced alveolar bone loss and ameliorated the manifestation of experimental periodontitis in STZ-induced diabetic rats.     

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.     

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.     

尼古丁对实验性牙周炎大鼠牙槽骨影响的显微CT观察

目的 建立牙周炎大鼠的牙槽骨三维模型,采用显微CT观察尼古丁对大鼠牙槽骨的影响.方法 36只SD大鼠,丝线结扎上颌右侧(实验侧)第二磨牙颈部,左侧不予结扎,作为自身对照(对照侧),使用完全随机分组方法分为对照组(A)及尼古丁注射低剂量(B)和高剂量(C)组,每组12只.分别给予生理盐水和尼古丁0.83、1.67 mg·kg-1·d-1腹腔注射.每组分别于给药后第14、28天各处死6只,取双侧上颌磨牙区牙体牙周复合组织,行显微CT扫描、重建、测最和分析.结果 随尼古丁给药剂量增加,双侧牙槽骨骨密度、骨体积分数、骨小梁厚度逐渐降低,牙槽骨高度丧失与骨小梁间隙逐渐升高.28 d时C组牙槽骨高度丧失[对照侧和实验侧分别为(0.61±0.14)、(1.39±0.09)mm]显著高于B组[对照侧和实验侧分别为(0.39±0.10)、(1.31±0.06)mm]和A组[对照侧和实验侧分别为(0.30±0.06)、(0.94±0.07)mm];C组牙槽骨骨密度[对照侧和实验侧分别为(617.86±34.27)、(572.46±31.62)mg/cm3]显著低于B组[对照侧和实验侧分别为(660.04±36.73)、(604.97±32.59)mg/cm3]和A组[对照侧和实验侧分别为(709.15±34.95)、(657.04±30.06)mg/cm3].结论 尼古丁可加重丝线结扎造成的大鼠牙槽骨骨量丧失和骨质微观结构的变化,导致牙槽骨骨质疏松.     

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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.