Effects of nicotine administration in rats on MMP2 and VEGF levels in periodontal membrane

Deveci, B; Ayna, Buket; Tacir, İbrahim Halil; Deveci, Engin; Tuncer, Mehmet Cudi; Pala, Ayşegül

doi:10.5603/fm.a2018.0004

Cited by 10 publications

(11 citation statements)

References 39 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nicotine has an additive effect on human gingival fibroblast-mediated collagen degradation when combined with the presence of P. gingivalis 31 . Deveci et al 32 found that nicotine reduces the production of MMPs, disrupts collagen synthesis and causes periodontitis in rats. They observed that nicotine increases periodontitis by disrupting the periodontal membrane and prevents the anchorage of teeth in the dental alveoli by disrupting the epithelial structure.…”

Section: Resultsmentioning

confidence: 99%

“…Nicotine, which is the major ingredient of cigarette smoke, up-regulates MMP-1, MMP-2 and MMP-3 gene expression in arterial smooth muscle cells, vascular endothelial cells, periodontal ligament fibroblasts and osteoclasts. Nicotine administration also causes a change in fibroblast activity due to the change of collagen fiber synthesis and decreased MMP2 expression 32 .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Effect of tobacco on periodontal disease and oral cancer

Zhang¹,

He²,

He³

et al. 2019

Tob. Induc. Dis.

105

View full text Add to dashboard Cite

INTRODUCTION Periodontal disease and oral cancer are common health hazards. Epidemiological investigations show that smoking, periodontal disease and oral cancer are closely related. Tobacco is one of the major risk factors for periodontitis and oral cancer. METHODS A systematic literature review was performed. To identify relevant studies, the following online databases were searched using specific keywords: PubMed, Web of Science and CNKI. RESULTS Tobacco not only possesses an addictive effect, but it aggravates periodontal disease by promoting the invasion of pathogenic bacteria, inhibiting autoimmune defense, aggravating the inflammatory reaction, and aggravating the loss of alveolar bone. According to current evidence, tobacco significantly aggravates the development and progression of periodontal disease and oral cancer, and periodontal disease may be related to the prevalence of oral cancer. CONCLUSIONS Clinicians should strongly recommend that smokers undertake a strategy to stop smoking to avoid the exacerbation of nicotine-related periodontal disease and to reduce the incidence of oral cancer.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Effect of tobacco on periodontal disease and oral cancer

Zhang¹,

He²,

He³

et al. 2019

Tob. Induc. Dis.

105

View full text Add to dashboard Cite

show abstract

“…2016, Deveci et al . 2018). The period of 28 days of nicotine application was sufficient to observe its effects on alveolar bone (Liu et al .…”

Section: Discussionmentioning

confidence: 99%

“…2013, Deveci et al . 2018). In this study, the IP injections were initiated 7 days before pulp access, to simulate the induction of apical periodontitis in an organism already exposed to nicotine.…”

Section: Discussionmentioning

confidence: 99%

“…A greater proliferation of inflammatory cells, increased angiogenic activity, cell degeneration and changes in collagen synthesis were also previous observed in the periodontal apparatus of rats exposed to nicotine (Deveci et al . 2018). Besides that, the chronic consumption of the both substances leads to an extensive inflammatory response on the alveolar bone loss (Pereira Vasconcelos et al .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of alcohol and nicotine consumption on the development of apical periodontitis in rats: a correlative micro‐computed tomographic, histological and immunohistochemical study

et al. 2020

View full text Add to dashboard Cite

AimTo evaluate the effects of alcohol and nicotine, when used alone or simultaneously, in the development of apical periodontitis induced in rats, using a correlative analytic approach with micro‐CT, histological and immunohistochemical analysis.MethodologyTwenty‐eight male Wistar rats were arranged into four groups: Control, Nicotine, Alcohol and Alcohol + Nicotine. The alcohol groups were exposed to self‐administration of a 25% alcohol solution, whilst the other groups drunk only filtered water. The nicotine groups received daily intraperitoneal injections of a solution with 0.19 μL of nicotine per mL, whilst the other groups received saline solution. The pulps of the left mandibular first molars were exposed for 28 days to induce periapical lesions. Throughout the experiment, drug administration was maintained, and the animals had their weight and solid and liquid consumption measured. After euthanasia, the mandibles were removed and the area, volume and major diameter of the periapical lesions were measured using micro‐computed tomography images. The samples were submitted to histopathological evaluation and immunohistochemistry for RANKL and PTHrP. Statistical analysis was undertaken with a significance level of 5%. Nonparametric data were analysed using the Kruskal–Wallis test followed by Dunn's test, whilst one‐way anova followed by Tukey's test was performed for parametric data.ResultsThe alcohol groups had lower solid and liquid consumption and gained less weight when compared to the nonalcohol groups (P < 0.05). The Alcohol + Nicotine group had lesions with significantly larger volume and area when compared to the other groups (P < 0.05), whilst the Alcohol or Nicotine groups had significantly larger lesions than the control group (P < 0.05). There was no significant difference in the largest diameter of the lesions amongst groups (P > 0.05). The experimental groups had greater inflammatory response scores than the control group (P < 0.05), and the representative samples had more pronounced immunoreaction against RANKL and PTHrP antibodies.ConclusionsAlcohol and nicotine consumption exacerbated the inflammatory response and the development of periradicular lesions in rats. The association of both substances enhanced their harmful effects.

show abstract