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Periodontal Bone Loss (periodontal + bone_loss)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Nicotinic acetylcholine receptor activation mediates nicotine-induced enhancement of experimental periodontitis

JOURNAL OF PERIODONTAL RESEARCH, Issue 3 2009
T. Breivik
Background and Objective:, Smokers have an increased risk of developing periodontitis as well as showing more rapid progression and resistance to treatment of the disease, but the biological mechanisms are poorly understood. This study was designed to investigate putative biological mechanisms by which nicotine may enhance the susceptibility and thus the course of periodontitis in an animal model. Material and Methods:, Ligature-induced periodontitis was applied in periodontitis-susceptible Fischer 344 rats. The animals were either given daily intraperitoneal injections of the nicotinic acetylcholine receptor antagonist mecamylamine (1 mg/kg) 45 min before subcutaneous injections in the neck skin of nicotine (0.8 mg/kg), or treated with the same amount of saline intraperitoneally and nicotine subcutaneously, or treated with mecamylamine and saline. Control animals received intraperitoneal and subcutaneous injections of saline only. Periodontal bone loss was assessed when the ligatures had been in place for 3 wk. Two hours before decapitation, all rats received lipopolysaccharide (LPS; 100 ,g/kg, intraperitoneally) to induce a robust immune and stress response. Results:, Compared with saline/saline-treated control animals, saline/nicotine-treated rats developed significantly more periodontal bone loss, and LPS provoked a significantly smaller increase in circulating levels of the cytokines tumour necrosis factor-,, transforming growth factor-1, and interleukin-10. Mecamylamine pretreatment of nicotine-treated rats abrogated the increased periodontal bone loss and the LPS-induced decrease in tumour necrosis factor-,, but had no significant effects on the levels of transforming growth factor-1, and interleukin-10, or the stress hormone corticosterone. Conclusion:, The results indicate that nicotine enhances the susceptibility to periodontitis via nicotinic acetylcholine receptors, which may act by suppressing protective immune responses through the cholinergic anti-inflammatory pathway. [source]

Periodontitis and incidence of cerebrovascular disease in men,

ANNALS OF NEUROLOGY, Issue 4 2009
Monik Jimenez SM
Objective To identify associations between periodontitis and incidence of cerebrovascular disease. Methods We analyzed data of 1,137 dentate men in the Veterans Affairs Normative Aging and Dental Longitudinal Study who were followed with triennial medical/dental exams for up to 34 years (mean, 24 years). We evaluated incidence of cerebrovascular events consistent with stroke or transient ischemic attack in relation to mean radiographic alveolar bone loss (a measure of periodontitis history) and cumulative periodontal probing depth (a measure of current periodontal inflammation). Cox proportional hazards models were fit controlling for age, baseline socioeconomic status, and time-varying effects of established cardiovascular risk factors. Results Eighty incident cases of cerebrovascular disease occurred from 27,506 person-years. Periodontal bone loss was significantly associated with an increased hazard rate (HR) of cerebrovascular disease (HR, 3.52; 95% confidence interval [CI], 1.59,7.81 comparing highest to lowest bone loss category; p for trend, <0.001). There was a stronger effect among men aged <65 years (HR, 5.81; 95% CI, 1.63,20.7) as compared with men aged ,65 years (HR, 2.39; 95% CI, 0.91,6.25). Periodontal probing depth was not associated with a significantly increased rate of cerebrovascular disease in the combined or age-stratified analyses. Interpretation These results support an association between history of periodontitis,but not current periodontal inflammation,and incidence of cerebrovascular disease in men, independent of established cardiovascular risk factors, particularly among men aged <65 years. Ann Neurol 2009;66:505,512 [source]

Tobacco smoking and periodontal bone height in a Saudi Arabian population

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 9 2005
Suzan Natto
Abstract Aim: To study the association between tobacco smoking, in particular water pipe smoking, and periodontal bone height. Methods: A study sample of 355 individuals in the age range 17,60 years was recruited from Jeddah, Saudi Arabia. The smoking behavior was registered through a questionnaire during interview. Participants were stratified into water pipe smokers (33%), cigarette smokers (20%), mixed smokers (19%) and non-smokers (28%). The periodontal bone height was measured from digital panoramic radiographs mesially and distally to each tooth and expressed as a percentage of the root length. Results: The mean periodontal bone height was 76.2% for water pipe smokers, 75.8% for cigarette smokers, 80.2% for mixed smokers and 80.9% for non-smokers. The association between smoking and mean bone height was statistically significant controlling for age (p<0.001). The association between life-time smoking exposure and mean bone height controlling for age was statistically significant in water pipe smokers and cigarette smokers (p<0.01). The prevalence of bone loss in excess of 30% of the bone height was 27% in water pipe smokers, 24% in cigarette smokers, 9% in mixed smokers and 6% in non-smokers. The prevalence was significantly greater in water pipe smokers and cigarette smokers compared with non-smokers (p<0.001). The relative risk of periodontal bone loss associated with water pipe and cigarette smoking after adjustment for age was 3.5-fold and 4.3-fold elevated, respectively, compared with non-smoking (p<0.01). Conclusion: An association between tobacco smoking and periodontal bone height reduction is observed. The impact of water pipe smoking is of the same magnitude as that of cigarette smoking. [source]

Nicotinic acetylcholine receptor activation mediates nicotine-induced enhancement of experimental periodontitis

Effect of adoptive transfer of antigen-specific B cells on periodontal bone resorption

JOURNAL OF PERIODONTAL RESEARCH, Issue 2 2006
Y. Harada
Background and Objectives:, Host immune responses to periodontal pathogens have been considered to contribute to the alveolar bone destruction in periodontitis. However, the role of B lymphocytes in the pathogenesis of periodontal bone loss is not clear. Methods:, We examined the effect of adoptive transfer of antigen-specific B cells from rat spleens on experimental periodontal bone resorption. Donor rats were immunized intraperitoneally (i.p.) with formalin-killed Actinobacillus actinomycetemcomitans. Antigen-specific B cells were prepared from splenocytes by first binding CD43+ cells to Petri dishes coated with anti-CD43 antibody to remove T cells, and non-binding cells were passed through a nylon wool column to deplete accessory cells. The retained cells were then collected and bound to A. actinomycetemcomitans- coated Petri dishes for enrichment of A. actinomycetemcomitans -binding B cells (AAB). A. actinomycetemcomitans non-binding B cells (ANB) and B cells from non-immunized donor rats (NIB) were also collected from these procedures. Each type of B cell was injected into a group of recipient rats that were then orally infected with live A. actinomycetemcomitans. Results:, At termination, the antibody levels to A. actinomycetemcomitans in serum and gingival wash fluids were significantly higher in the recipients transferred with AAB when compared to the recipients transferred with ANB or NIB. A markedly elevated number of antibody-forming cells were observed in the spleens of the recipients transferred with AAB, and these recipient rats also exhibited significantly increased bone resorption when compared to the other groups. Conclusions:, It is suggested that B cells can contribute to periodontal bone resorption and that antigen-triggering of B cells is required for the bone resorption. [source]