scholarly journals Effects of cigarette smoking on periodontium

2002 ◽  
Vol 55 (5-6) ◽  
pp. 229-232 ◽  
Author(s):  
Marija Bokor-Bratic

Introduction The exact mechanisms by which smoking effects the periodontal tissues are not known. Studies in which plaque or calculus are taken into consideration come to conflicting conclusions regarding effects of smoking. Aim The aim of this study was to examine the oral hygiene and periodontal status in smokers and compare them with nonsmokers. Material and methods The study group comprised 83 smokers and 83 nonsmokers. The mean age (SD) of smokers and nonsmokers was 42,4?7,0 years and 43,7?6,4 years, respectively. The age difference was not statistically significant. The average tobacco consumption of the smokers at the time of investigation was 14 cigarettes a day and they had been regular smokers for 21 years on average. Results The amount of dental plaque was evaluated in accordance with the criteria of Green-Vermillion by using disclosing solution. The periodontal condition was evaluated by Ramfjord Periodontal Disease Index. For gingival recession the distance from the cemento-enamel junction to the gingival margin was determined on mid-buccal and mid-lingual surfaces of all teeth. Each subject was radiographically examined with a full mouth intraoral survey. Alveolar bone loss was determined as the distance from the cemento-enamel junction to the point where lamina dura became continuous with the compact bone of the interdental septum. Mean alveolar bone loss based on all mesial and distal measurements was calculated for each subject. The amount of dental plaque was high in both smokers (2,60,60) and nonsmokers (1,50,70), whereas the differences were statistically significant (p<0.001). Conclusion Periodontal destruction, alveolar bone loss and gingival recession were significantly increased in smokers compared to nonsmokers (p<0.001). It is concluded that differences observed between smokers and nonsmokers with regard to periodontal condition are attributable to differences in oral hygiene. Smoking is a risk factor for periodontal health.

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.


1959 ◽  
Vol 17 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Arnulk Arno ◽  
Olav Schei ◽  
Arne Lovdal ◽  
Jens Wæehaug

Endocrinology ◽  
2013 ◽  
Vol 154 (2) ◽  
pp. 773-782 ◽  
Author(s):  
Masanori Koide ◽  
Yasuhiro Kobayashi ◽  
Tadashi Ninomiya ◽  
Midori Nakamura ◽  
Hisataka Yasuda ◽  
...  

Periodontitis, an inflammatory disease of periodontal tissues, is characterized by excessive alveolar bone resorption. An increase in the receptor activator of nuclear factor-κB ligand (RANKL) to osteoprotegerin (OPG) ratio is thought to reflect the severity of periodontitis. Here, we examined alveolar bone loss in OPG-deficient (OPG−/−) mice and RANKL-overexpressing transgenic (RANKL-Tg) mice. Alveolar bone loss in OPG−/− mice at 12 weeks was significantly higher than that in RANKL-Tg mice. OPG−/− but not RANKL-Tg mice exhibited severe bone resorption especially in cortical areas of the alveolar bone. An increased number of osteoclasts was observed in the cortical areas in OPG−/− but not in RANKL-Tg mice. Immunohistochemical analyses showed many OPG-positive signals in osteocytes but not osteoblasts. OPG-positive osteocytes in the cortical area of alveolar bones and long bones were abundant in both wild-type and RANKL-Tg mice. This suggests the resorption in cortical bone areas to be prevented by OPG produced locally. To test the usefulness of OPG−/− mice as an animal model for screening drugs to prevent alveolar bone loss, we administered an antimouse RANKL antibody or risedronate, a bisphosphonate, to OPG−/− mice. They suppressed alveolar bone resorption effectively. OPG−/− mice are useful for screening therapeutic agents against alveolar bone loss.


Author(s):  
JordanaHeidemann Pandini ◽  
Lais Fernanda Pasqualotto ◽  
Pedro Henrique de Carli Rodrigues ◽  
João Paulo Gonçalves De Paivaa ◽  
Patricia Oehlmeyer Nassar ◽  
...  

The resveratrol is a polyphenol known for its health benefits, which includes the ability to interfere in the osteoblastogenesis, which may foster adverse immunomodulators effects in the host response to periodontal disease. In the present study we evaluated the appearance of periodontal tissues of rats with experimentally induced periodontitis, by using resveratrol. Twenty-four male Wistar rats were used, in which half of the animals received a ligature around the first lower molars, then forming the groups with experimental periodontitis. Next, four groups were created: 1) Control Group (CON); 2) The Ligature Group (LIG); 3) Group Resveratrol (RSV); 4) Ligature-Resveratrol Group (LIG-RSV). The animals of the Resveratrol groups were daily dosed with 10 mg/kg of body weight of polyphenol orally, during four weeks. After 105 days of experimental period, euthanasia was performed. The results showed a significantly lower alveolar bone loss (p<0.05) in animals that received resveratrol, and still, the polyphenol was able to reduce concentration of interleukin 17 (IL-17) in the groups dosed with it. Our conclusion is that dosing rats with experimental periodontitis with resveratrol could cause a protective effect on the alveolar bone loss, in addition to act positively on the IL-17.


1959 ◽  
Vol 30 (1) ◽  
pp. 7-16 ◽  
Author(s):  
Olav Schei ◽  
Jens Waerhaug ◽  
Arne Lovdal ◽  
Arnulf Arno

2016 ◽  
Vol 144 (5-6) ◽  
pp. 273-279 ◽  
Author(s):  
Aysun Akpınar ◽  
Nebı Karakan ◽  
Aysan Alpan ◽  
Suat Dogan ◽  
Fahrettin Goze ◽  
...  

Introduction. Periodontitis is a chronic inflammatory and osteolytic disease. Vitamin B complex is a class of water-soluble vitamins that play important roles in cell metabolism. Objective. The aim of this study was to evaluate the effects of riboflavin (RBF), nicotinamide (NA), and folic acid (FA) on alveolar bone loss in experimental periodontitis rat model. Methods. Sixty-four male Wistar rats were randomly divided into the following eight groups: Control, Ligated, RBF50 (RBF, 50 mg/kg daily), NA50 (NA, 50 mg/kg daily), FA50 (FA, 50 mg/kg daily), RBF100 (RBF, 100 mg/kg daily), NA100 (NA, 100 mg/kg daily), and FA100 (FA, 100 mg/kg daily). Periodontitis was induced using silk ligature around the right first mandibular molar. After 11 days the rats were sacrificed. Mandible and serum samples were collected. Changes in alveolar bone levels were measured clinically, and periodontal tissues were examined histopathologically. Serum IL-1? (pg/ml) levels were analyzed by using ELISA. Results. Mean alveolar bone loss in the mandibular first molar tooth revealed to be significantly lower in RBF100 group than in the Control group. In the Ligated group, alveolar bone loss was significantly higher than in all other groups. The ratio of presence of inflammatory cell infiltration in the Ligated group was significantly higher than in the Control group. The differences in the serum IL-1? levels between the groups were not statistically significant. Osteoclasts that were observed in the Ligated group were significantly higher than those of the Control and FA100 groups. The osteoblastic activity in the Ligated group, RBF100, and NA100 groups were shown to be significantly higher than those in the Control group. Conclusion. This study has demonstrated that systemic administration of RBF, NA, and FA in different dosages (50-100 mg/kg) reduced alveolar bone loss in periodontal disease in rats.


2021 ◽  
Author(s):  
Hua Liu ◽  
Yingjie Xu ◽  
Qi Cui ◽  
Ning Liu ◽  
Fuhang Chu ◽  
...  

Abstract ObjectivesTo study the effects of psoralen on the intestinal barrier and alveolar bone loss (ABL) in rats with chronic periodontitis.MethodsFifty-two 8-week-old specific pathogen-free (SPF) male Sprague-Dawley (SD) rats were randomly divided into the following four groups: Control group (Control), Psoralen group of healthy rats (Pso), Periodontitis model group (Model), and Psoralen group of periodontitis rats (Peri+Pso). The alveolar bone resorption of maxillary molars was observed via hematoxylin-eosin staining and micro-computed tomography. The expression level of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal tissues were evaluated by immunofluorescence staining. The changes in serum tumour necrosis factor (TNF)-α, interleukin (IL)-10, IL-6, intestinal mucosal occludin and claudin-5 were detected using enzyme-linked immunosorbent assay (ELISA). The level of intestinal mucosal NOD2 was detected using immunohistochemical methods. DNA was extracted from the intestinal contents and the 16s rRNA gene was sequenced using an Illumina Miseq platform.ResultsThe expression of NOD2 protein in the intestinal tract of periodontitis rats decreased after intragastric psoralen administration. Psoralen increased the intestinal microbiota diversity of rats. The level of serum pro-inflammatory factor TNF-α decreased and the level of anti-inflammatory factor IL-10 increased. ABL was observed to be significantly decreased in rats treated with psoralen. Psoralen decreased the RANKL/OPG ratio of periodontitis rats.ConclusionsPsoralen may affect the intestinal immune barrier and ecological barrier, mediate immune response, promote the secretion of anti-inflammatory factor IL-10, and reduce the secretion of the pro-inflammatory factor TNF-α, thus reducing ABL in experimental periodontitis in rats.


Author(s):  
Bianca Caroline Custodio dos Santos ◽  
Jossinelma Camargo Gomes ◽  
Angela Esmeralda Zaparolli Miola ◽  
Simone Karine Rothen ◽  
Célia Patricia Muller Rodrigues ◽  
...  

Objective: To analyze the effects of melatonin administration on the periodontal tissues of rats, linked or not with ligature-induced periodontal disease. Materials and Methods: 40 male Wistar rats aged eight weeks, divided into Control Group (GCON), Ligature Group (GLIG), Melatonin Group (GMEL) and Ligature and Melatonin Group (GLIGMEL). GLIG and GLIGMEL were induced to experimental periodontitis by placing a ligature on the lower molars for 30 days. During the experiment, after 16 days with the ligature, melatonin was administered orally for 10 mg/kg for 14 days in GMEL and GLIGMEL. In the end, euthanasia was performed and the hemi-mandibles were collected for the respective histological and radiographic analyzes; for the results, Shapiro-Wilk, ANOVA-One-Way and Tukey's multiple comparison tests were used. Results: A significantly lower alveolar bone loss (p<0.05) was demonstrated in the animals that received the administration of melatonin, in which it had a prophylactic function against the effects of the disease, evidenced in radiographic, histomorphometric and histological analyzes in the bone cell count. Conclusion: Results show that the therapy with administration of melatonin promotes a protective effect on the alveolar bone tissue of rats with induced experimental periodontitis.


2020 ◽  
Vol 19 (3) ◽  
pp. 497-503
Author(s):  
Fang Wang ◽  
Ping Sun ◽  
Qiang Sun

Purpose: To investigate the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 32) weighing 180 - 200 g (mean weight, 190 ± 10 g) were randomly assigned to four groups of eight rats each: control group, periodontitis group, bisleuconothine A (50 mg/kg) group and bisleuconothine A (100 mg/kg) group. Rats in the treatment groups received bisleuconothine intraperitoneally for two weeks. Periodontitis was induced in the rats using standard procedures. Serum and tissue samples were used for biochemical analysis. Alveolar bone loss was measured in rat maxillae, while the activity of bone alkaline phosphatase (BALP) was determined in serum. Tumor necrosis factor α (TNF-α) interleukin-1β and interleukin-6 (IL-1β and IL-6) were determined in gingival tissue using enzyme-linked immunosorbent assay (ELISA) kit. Gene and protein expressions of receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), and matrix metallopeptidase-9 (MMP-9) were measured in gingival tissue using real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting, respectively. Results: Bisleuconothine A treatment significantly and dose-dependently reduced alveolar bone loss, as well as serum levels of TNF-α, IL-1β and IL-6, but increased BALP activity in periodontitis rats (p < 0.05). It also significantly and dose-dependently reduced mRNA expressions of RANKL and MMP-9, but significantly increased OPG mRNA expression (p < 0.05). Similarly, treatment with bisleuconothine A significantly and dose-dependently down-regulated RANKL, p-NF-kB, p-IkBα and iNOS proteins in gingival tissue of periodontitis rats (p < 0.05). The results of histopathological examination indicated that bisleuconothine A treatment significantly reversed histological changes in periodontal tissues of periodontitis rats. It also significantly reduced the degree of polymorphonuclear (PMN) cell infiltration in periodontal tissue. Conclusion: The results obtained show that bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells. Keywords: Bisleuconothine A, Expression, Inflammation, Periodontitis, RANKL


Sign in / Sign up

Export Citation Format

Share Document