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      The Antimicrobial Treatment of Periodontal Disease: Changing the Treatment Paradigm

      Critical Reviews in Oral Biology & Medicine
      SAGE Publications

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          Periodontal disease and cardiovascular disease.

          It is our central hypothesis that periodontal diseases, which are chronic Gram-negative infections, represent a previously unrecognized risk factor for atherosclerosis and thromboembolic events. Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis. We further suggest that periodontal disease, once established, provides a biological burden of endotoxin (lipopolysaccharide) and inflammatory cytokines (especially TxA2, IL-1 beta, PGE2, and TNF-alpha) which serve to initiate and exacerbate atherogenesis and thromboembolic events. A cohort study was conducted using combined data from the Normative Aging Study and the Dental Longitudinal Study sponsored by the United States Department of Veterans Affairs. Mean bone loss scores and worst probing pocket depth scores per tooth were measured on 1,147 men during 1968 to 1971. Information gathered during follow-up examinations showed that 207 men developed coronary heart disease (CHD), 59 died of CHD, and 40 had strokes. Incidence odds ratios adjusted for established cardiovascular risk factors were 1.5, 1.9, and 2.8 for bone loss and total CHD, fatal CHD, and stroke, respectively. Levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease.
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            Polymerase chain reaction detection of 8 putative periodontal pathogens in subgingival plaque of gingivitis and advanced periodontitis lesions.

            A 16S rRNA-based polymerase chain reaction (PCR) detection method was used to determine the prevalence of Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Eikenella corrodens, Porphyromonas gingivalis, Prevotella intermedia. Prevotella nigrescens and Treponema denticola in subgingival specimens of 50 advanced periodontitis, 50 adult gingivitis and 50 pediatric gingivitis subjects. The optimal PCR conditions were determined for each study species. Agarose gel electrophoresis of PCR products from each study species revealed a single band of the predicted size. Restriction enzyme digestion of amplicons confirmed the specificity of the amplification. PCR detection limits were in the range of 25-100 cells. No cross-reactivity with other oral micro-organisms or nonspecific amplification was observed. The prevalence by PCR in advanced periodontitis, adult gingivitis and pediatric gingivitis subjects was 30%, 14% and 14% for A. actinomycetemcomitans, 86%, 18% and 8% for B. forsythus, 74%, 52% and 78% for C. rectus, 80%, 70% and 66% for E. corrodens, 70%, 10% and 14% for P. gingivalis, 58%, 12% and 18% for P. intermedia, 52%, 20% and 22% for P. nigrescens, and 54%, 16% and 16% for T. denticola, respectively. The prevalence was higher in the advanced periodontitis group than in both adult gingivitis and pediatric gingivitis for A. actinomycetemcomitans, B. forsythus, P. gingivalis, P. intermedia, P. nigrescens and T. denticola at P < 0.01, and for E. corrodens at P < 0.05. The prevalence of C. rectus was significantly higher in the advanced periodontitis group than in the adult gingivitis group at P < 0.01. Matching results between PCR and culture occurred in 28% (B. forsythus) to 71% (A. actinomycetemcomitans) of the samples; the major discrepancy occurred in the PCR-positive/culture-negative category. Matching results between PCR and DNA probe methods were found in 84% of the subjects (B. forsythus) and 70% (P. gingivalis). Odds ratio analysis revealed statistically significant positive associations between 17 of the 28 possible combinations (P < 0.01). This study demonstrated the utility of a 16S rRNA-based PCR detection method for identifying important subgingival microorganisms. The results indicated a strong association between the study species and periodontitis. Several previously unreported symbiotic relationships were found between the 8 species tested.
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              Dental disease and risk of coronary heart disease and mortality.

              To investigate a reported association between dental disease and risk of coronary heart disease. National sample of American adults who participated in a health examination survey in the early 1970s. Prospective cohort study in which participants underwent a standard dental examination at baseline and were followed up to 1987. Proportional hazards analysis was used to estimate relative risks adjusted for several covariates. Incidence of mortality or admission to hospital because of coronary heart disease; total mortality. Among all 9760 subjects included in the analysis those with periodontitis had a 25% increased risk of coronary heart disease relative to those with minimal periodontal disease. Poor oral hygiene, determined by the extent of dental debris and calculus, was also associated with an increased incidence of coronary heart disease. In men younger than 50 years at baseline periodontal disease was a stronger risk factor for coronary heart disease; men with periodontitis had a relative risk of 1.72. Both periodontal disease and poor oral hygiene showed stronger associations with total mortality than with coronary heart disease. Dental disease is associated with an increased risk of coronary heart disease, particularly in young men. Whether this is a causal association is unclear. Dental health may be a more general indicator of personal hygiene and possibly health care practices.
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                Author and article information

                Journal
                Critical Reviews in Oral Biology & Medicine
                Critical Reviews in Oral Biology & Medicine
                SAGE Publications
                1045-4411
                1544-1113
                December 2016
                December 2016
                : 10
                : 3
                : 245-275
                Article
                10.1177/10454411990100030101
                10759408
                aa33197d-b5de-4820-8491-5ca40a802e61
                © 2016
                History

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