Risk Indicators for Periodontitis in a Military Treatment Population

Horning, Gregory M.; Hatch, Craig L.; Cohen, Mark E.

doi:10.1902/jop.1992.63.4.297

Cited by 91 publications

(60 citation statements)

References 19 publications

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“…The strong association found between smoking and advanced periodontal diseased is consistent with the hypothesis that smoking has cumulative detrimental effects on periodontal health (Horning et al, 1992) thus there is good evidence that the more a patient smokes the greater the degree of periodontal disease. In this study results has shown that current smokers represent a mean duration of 15 years while former smokers represent 21 years.…”

Section: Discussionsupporting

confidence: 81%

“…In addition, former smokers were 1.68 times more likely to suffer from periodontitis (Tomar and Asma, 2000). Horning et al (1992) reported an association between smoking and advanced periodontitis. This is consistent with the hypothesis that smoking has a cumulative effect on periodontal health i.e., the more a patient smokes, the greater the degree of chronic inflammatory periodontal disease.…”

Section: Introductionmentioning

confidence: 99%

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The Relationship between Serum Cotinine Levels and Periodontal Status

Al-Bayaty

Baharuddin

Abdulla

2010

OnLine Journal of Biological Sciences

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Problem statement:Smoking plays a significant role in the development of periodontal disease. Quantitative relation between smoking and increased severity of periodontal disease, by means of biochemical marker has not been described in Malaysian population. The present study was designed to apply serum cotinine measurement as a quantitative method to evaluate smoking levels in Malaysian patients and to correlate these levels with the severity of periodontal disease. Approach: The study group consisted of 80 healthy individuals (20-64) year, Current Smokers 26, Non Smokers 27 and Former Smokers 27. The subjects were then asked to complete a questionnaire including the demographic, socioeconomic status, medical history and history of cigarette smoking. The periodontal variables recorded were amount of Visible Plaque score, gingival bleeding Index and community periodontal index. Samples of blood "10 mL" were obtained in vacutainer tubes containing EDTA for quantitative analysis of serum levels of cotinine. The serum samples were analyzed for cotinine content by means of a competitive-inhibition ELISA technique. Results: Current smokers represent the highest mean cotinine serum level, 95.5 ng mL −1 , compared to former smokers, 35.5 ng mL −1 and non smokers, 22.9 ng mL −1 . The mean serum cotinine level in periodontally healthy patient showed the highest cotinine level (84 ng mL −1 ) followed by the gingivitis patients (68 ng mL −1 ) and (50 ng mL −1 ) for periodontitis patients. Conclusion: The present observations clearly indicate an association between smoking, periodontal disease clinical parameters "plaque, gingival bleeding scores" and cotinine serum levels in current smokers. Cotinine serum levels doesn't affected by the existence or the severity of periodontal disease.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

The Relationship between Serum Cotinine Levels and Periodontal Status

Al-Bayaty

Baharuddin

Abdulla

2010

OnLine Journal of Biological Sciences

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“…17 Horn ing's study in 1992 found similar results, reporting males to have increased risk of moderate or advanced periodontitis (OR 1.78, 95% CI: 1.42-2.46). 20 Male gender deserves consideration in a risk model for periodontal disease, the effects of which must be addressed through behaviour modifi cation.…”

Section: Gendermentioning

confidence: 99%

Who is at risk? Periodontal disease risk analysis made accessible for the general dental practitioner

2008

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“…Cross-sectional and longitudinal studies have detailed the consistent, positive association between smoking and periodontal attachment loss (Bergstrom 1989, Preber & Bergstrom 1990, Haber & Kent 1992, Horning et al 1992, Haber et al 1993, Ah et al 1994. A meta-analysis of the literature conducted by Papapanou (1996) for the 1996 World Workshop in Periodontics revealed that smokers have an almost 3-fold increase in their risk for severe periodontal disease vs non-smokers.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of dioxin effects on bone formation in vitro by a newly described aryl hydrocarbon receptor antagonist, resveratrol

Singh¹,

Casper²,

Fritz³

et al. 2000

Journal of Endocrinology

131

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Aryl hydrocarbon receptor (AhR) ligands are environmental contaminants found in cigarette smoke and other sources of air pollution. The prototypical compound is TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), also known as dioxin. There is an increasing body of knowledge linking cigarette smoking to osteoporosis and periodontal disease, but the direct effects of smokeassociated aryl hydrocarbons on bone are not well understood. Through the use of resveratrol (3,5,4 -trihydroxystilbene), a plant antifungal compound that we have recently demonstrated to be a pure AhR antagonist, we have investigated the effects of TCDD on osteogenesis. It was postulated that TCDD would inhibit osteogenesis in bone-forming cultures and that this inhibition would be antagonized by resveratrol. We employed the chicken periosteal osteogenesis (CPO) model, which has been shown to form bone in vitro in a pattern morphologically and biochemically similar to that seen in vivo, as well as a rat stromal cell bone nodule formation model. In the CPO model, alkaline phosphatase (AP) activity was reduced by up to 50% (P<0·01 vs control) in the presence of 10 9 M TCDD and these effects were reversed by 10 6 M resveratrol (P<0·05 vs TCDD alone). TCDD-mediated inhibition of osteogenesis was restricted primarily to the osteoblastic differentiation phase (days 0-2) as later addition did not appear to have any effects. Message levels for important bone-associated proteins (in the CPO model) such as collagen type I, osteopontin, bone sialoprotein and AP were inhibited by TCDD, an effect that was antagonized by resveratrol. Similar findings were obtained using the rat stromal bone cell line. TCDD (at concentrations as low as 10 10 M) caused an approximately 33% reduction in AP activity, which was abrogated by 3·5 10 7 M resveratrol. TCDD also induced a marked reduction in mineralization (75%) which was completely antagonized by resveratrol. These data suggest that AhR ligands inhibit osteogenesis probably through inhibition of osteodifferentiation and that this effect can be antagonized by resveratrol. Since high levels of AhR ligands are found in cigarette smoke, and further since smoking is an important risk factor in both osteoporosis and periodontal disease, it may be postulated that AhR ligands are the component of cigarette smoke linking smoking to osteoporosis and periodontal disease. If so, resveratrol could prove to be a promising preventive or therapeutic agent for smoking-related bone loss.

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Risk Indicators for Periodontitis in a Military Treatment Population

Cited by 91 publications

References 19 publications

The Relationship between Serum Cotinine Levels and Periodontal Status

The Relationship between Serum Cotinine Levels and Periodontal Status

Who is at risk? Periodontal disease risk analysis made accessible for the general dental practitioner

Inhibition of dioxin effects on bone formation in vitro by a newly described aryl hydrocarbon receptor antagonist, resveratrol

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