Periodontitis, dental plaque, and atrial fibrillation in the Hamburg City Health Study.

BACKGROUND/AIM: Atrial fibrillation (AF) is a major health problem and causes heart failure and stroke. Pathophysiological mechanisms indicate a link with oral health including periodontitis (PD), but supporting data are scarce. The aim was to investigate the link between features of oral health and the prevalence of AF. METHODS: This cross-sectional analysis of the Hamburg City Health Study included 5,634 participants with complete data on their PD and AF status. AF was assessed via self-reported questionnaire or medically diagnosed by standard 12-lead resting ECG. The oral health examination included full-mouth measurements of the dental plaque index (PI), the clinical attachment loss (CAL) at 6 sites per tooth, the bleeding on probing (BOP) and the decayed, missing and filled teeth (DMFT) index. Descriptive analyses for all variables stratified by the status of PD were performed. To test for an association between prevalent PD and prevalent AF, multivariable logistic regression models were used. Mediation analysis was used to test if interleukin-6 (IL-6) and/or C-reactive protein (CRP) mediated the association between PD and AF. RESULTS: Atrial fibrillation (prevalence: 5.6%) and the severity of PD (prevalence: moderate: 57.7%, severe: 18.9%) increased with age in men and women. Prevalent severe PD, CAL ≥3 mm, PI, and BOP were all associated with prevalent AF in unadjusted regression analysis. However, no association except for PI (odds ratio (OR): 1.22, 95% confidence interval (CI): 1.1-1.35, p<0.001) could be observed after adjusting for age, sex, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), body mass index, diabetes, smoking, and educational level. Participants brushing their teeth at least twice daily had a lower AF prevalence compared with those brushing only once daily. Hs-CRP, IL-6, and the odds of AF increased as a function of PD severity grades in unadjusted analysis. However, neither the DMFT index nor IL-6 or CRP was associated with AF after adjusting for age and sex. Mediation analyses could not provide support for the hypothesis that IL-6 or CRP acted as mediator of the association between prevalent PD and prevalent AF. CONCLUSION: The study shows an association between prevalent AF and increased dental plaque levels indicated by a higher PI. In contrast, an association of prevalent PD with prevalent AF after adjustments for several confounders could not be demonstrated. Further studies are necessary to investigate the mechanisms underlying poor oral hygiene and AF as well as the influence of improved oral hygiene on AF onset.

Orally administered ovine serum immunoglobulins modulate dental plaque in cats.

The effects of orally administered ovine serum immunoglobulin on dental plaque and associated oral immunity in cats were investigated. The two treatment groups consisted of 1) cats that were fed unsupplemented kibble (control diet) and 2) cats that were fed the same kibble but coated with a freeze-dried ovine serum immunoglobulin preparation (ovine Ig) (test diet). The adult cats were randomly allocated to one of the two diets (n = 15) and received their respective kibble for a 28-day experimental period. When compared to the ovine Ig-supplemented kibble, cats consuming the unsupplemented kibble had significantly (p < 0.05) higher dental plaque scores. Cat IgA and IgG concentrations in the saliva and serum were significantly (p < 0.05) higher for cats fed the unsupplemented kibble when compared to cats receiving the ovine Ig supplement. Similarly, myeloperoxidase activity in the saliva was significantly (p < 0.05) higher for cats fed the unsupplemented kibble when compared to cats receiving the Ig-supplement. Orally administered ovine serum Ig positively influenced oral health and oral immunity in cats as evidenced by preventing an increase of dental plaque formation, salivary and serum IgA and IgG concentrations and salivary myeloperoxidase activity.

Bis-enoxacin blocks rat alveolar bone resorption from experimental periodontitis.

Periodontal diseases are multifactorial, caused by polymicrobial subgingival pathogens, including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Chronic periodontal infection results in inflammation, destruction of connective tissues, periodontal ligament, and alveolar bone resorption, and ultimately tooth loss. Enoxacin and a bisphosphonate derivative of enoxacin (bis-enoxacin) inhibit osteoclast formation and bone resorption and also contain antibiotic properties. Our study proposes that enoxacin and/or bis-enoxacin may be useful in reducing alveolar bone resorption and possibly bacterial colonization. Rats were infected with 10(9) cells of polymicrobial inoculum consisting of P. gingivalis, T. denticola, and T. forsythia, as an oral lavage every other week for twelve weeks. Daily subcutaneous injections of enoxacin (5 mg/kg/day), bis-enoxacin (5, 25 mg/kg/day), alendronate (1, 10 mg/kg/day), or doxycycline (5 mg/day) were administered after 6 weeks of polymicrobial infection. Periodontal disease parameters, including bacterial colonization/infection, immune response, inflammation, alveolar bone resorption, and systemic spread, were assessed post-euthanasia. All three periodontal pathogens colonized the rat oral cavity during polymicrobial infection. Polymicrobial infection induced an increase in total alveolar bone resorption, intrabony defects, and gingival inflammation. Treatment with bis-enoxacin significantly decreased alveolar bone resorption more effectively than either alendronate or doxycycline. Histologic examination revealed that treatment with bis-enoxacin and enoxacin reduced gingival inflammation and decreased apical migration of junctional epithelium. These data support the hypothesis that bis-enoxacin and enoxacin may be useful for the treatment of periodontal disease.

Serum high-density lipoprotein cholesterol level associated with the extent of periodontal inflammation in type 1 diabetic subjects.

AIM: High-density lipoprotein (HDL) cholesterol is known for its anti-inflammatory and antioxidant activities in protection against cardiovascular diseases. We investigated whether a protective association also exists between serum HDL and periodontal inflammation in type 1 diabetic subjects (T1DM). METHODS: Plaque and periodontal inflammation (bleeding and PD ≥ 4 mm) were examined in 80 subjects with T1DM. The serum levels of glycosylated haemoglobin (HbA1c, %) and HDL (mmol/l) were determined. Adjusted associations between inflammation and serum HDL were analysed using linear regression analysis. To study the linearity of the association, the subjects were categorized into HDL tertiles (I-III). RESULTS: A statistically significant negative association was observed between serum HDL level and the extent of bleeding and PD ≥ 4 mm. Subjects in HDL tertiles II and III (high HDL) presented significantly fewer inflamed sites when compared with the subjects in tertile I (low HDL), whereas no significant difference in the number of inflamed sites was observed between tertiles II and III. CONCLUSIONS: Based on the finding of a negative association between serum HDL and periodontal inflammation, HDL may be considered a marker of susceptibility to periodontal inflammation. A longitudinal study is needed to verify possible causal relationship between serum HDL and inflammation.

Salivary blood group antigens and microbial flora.

OBJECTIVE: Secretor is an individual with ability to produce blood group reactive substances in the exocrine glands and to secrete these substances in the body fluids such as saliva. In saliva the blood reactive antigens are found primarily on mucins which exhibit microheterogenicity and different subtypes of these molecules. This study was done to find out if the salivary blood group antigens have any role in the adherence of certain selected microorganism in the oral cavity. METHODS: Unstimulated whole saliva and sub gingival plaque samples were collected from subjects with clinically healthy gingival, chronic gingivitis and chronic periodontitis with probing pocket depth ≥4mm and attachment loss ≥1mm. Secretor status was determined by using Haemagglutination Inhibition Assay. Unstimulated whole saliva and sub gingival plaque samples were collected to culture and isolate the selected microorganisms. The clinical scores, secretor status and the presence or absence of selected microorganisms were compared within the groups using Chi-square test and students unpaired t-test. RESULTS: The numbers of secretors were more in the healthy group (22.2%) and non secretors were more in the chronic periodontitis group (22.2%). The clinical scores were higher in the in non secretors compared to the secretors in all the three groups. P intermedia and P gingivalis were prevalent among non secretors in chronic gingivitis group. (P=0.075 and P=0.032) and chronic periodontitis group (P=0.068 and P=0.009).

Serum cytokine and periodontal profiles in relation to disease activity of rheumatoid arthritis in Japanese adults.

BACKGROUND: Rheumatoid arthritis (RA) and periodontitis are common chronic inflammatory conditions and share many pathologic features. A similar profile of cytokines is involved in the pathogenesis of the two diseases. The relationship between the disease activity of RA and the periodontal condition remains unclear. This study examines whether the disease activity of RA affects serum cytokine and periodontal profiles. METHODS: The study subjects consisted of 84 Japanese adults with RA and 22 race-matched control individuals. After periodontal and rheumatologic examination, the disease activity of RA was determined with the Disease Activity Score including 28 joints using C-reactive protein (DAS28-CRP). Serum levels of cytokines including interleukin (IL)-1beta, IL-6, IL-12, IL-12 p40, IL-18, and tumor necrosis factor-alpha (TNF-alpha) were determined by an enzyme-linked immunosorbent assay. High-sensitive CRP was also measured with a latex particle-enhanced nephelometric method. RESULTS: Of 84 patients with RA, 28 and 56 patients exhibited low and moderate to high disease activity, respectively. Serum levels of IL-6, TNF-alpha, and CRP were significantly different between the two groups (P <0.05). Additionally, a significant correlation was observed between DAS28-CRP and percentage of sites with bleeding on probing (BOP) (P = 0.008) and between serum TNF-alpha levels and percentage of sites with BOP (P = 0.01) in 56 patients with RA with moderate to high activity. CONCLUSION: These results suggest that the disease activity of RA correlated with serum levels of IL-6, TNF-alpha, and CRP, and it might influence BOP in the patients with moderate to high disease activity.

Role of IL-6, TNF-A and LT-A variants in the modulation of the clinical expression of plaque-induced gingivitis.

AIM: The purpose of the present study was to assess the association of interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-A) and lymphotoxin alpha (LT-A) gene polymorphisms with the clinical parameters of gingivitis in a large experimental gingivitis trial and with each of two subgroups, "high responder" (HR, n=24) and "low responder" (LR, n=24), with distinct susceptibility to gingivitis. MATERIAL AND METHODS: Ninety-six systemically and periodontally healthy non-smokers, 46 males (mean age: 23.9+/-1.7) and 50 females (mean age: 23.3+/-1.6), were included in a randomized split-mouth localized 21-day experimental gingivitis trial. Plaque index, gingival index, gingival crevicular fluid volume and angulated bleeding score were recorded. HR and LR subgroups were characterized by substantially different severities of gingival inflammation despite a similar plaque accumulation rate. All subjects were genetically characterized for IL-6(-174), IL-6(-597), TNF-A(-308) and LT-A(+252) polymorphisms. RESULTS: None of the variants analysed, either as single polymorphisms or as a combined genotype, was associated with the clinical parameters in the overall population. For the polymorphisms studied, genotypic distributions in HR and LR subjects were not significantly different. CONCLUSIONS: The present results suggest an absence of association between IL-6, TNF-A and LT-A polymorphisms and subject-based clinical behaviour of the gingiva in response to de novo plaque accumulation.

Total antioxidant capacity and antioxidant enzymes in serum, saliva, and gingival crevicular fluid of preeclamptic women with and without periodontal disease.

BACKGROUND: The aim of this study was to investigate the total antioxidant capacity, superoxide dismutase and glutathione peroxidase activities, and malondialdehyde levels in serum, saliva, and gingival crevicular fluid (GCF) in preeclamptic and normotensive pregnant women with and without periodontal disease. METHODS: Forty pregnant women, consisting of 10 preeclamptic subjects with periodontal disease, 10 preeclamptic periodontally healthy subjects, 10 normotensive subjects with periodontal disease, and 10 normotensive periodontally healthy subjects, were included in this study. After clinical measurement and samplings, total antioxidant capacity, superoxide dismutase, glutathione peroxidase activities, and malondialdehyde levels in serum, saliva, and GCF of preeclamptic and normotensive pregnant women were determined, and the data were tested by non-parametric tests. Total antioxidant capacity of the clinical samples was measured using a novel automated colorimetric measurement method. Superoxide dismutase and glutathione peroxidase activities and malondialdehyde levels were determined spectrophotometrically. RESULTS: Superoxide dismutase and glutathione peroxidase activities in GCF and serum and total antioxidant capacity in saliva, GCF, and serum were the lowest in preeclamptic women with periodontal disease. However, serum and GCF levels of malondialdehyde were the highest in this group of pregnant women. CONCLUSIONS: Systemic and local antioxidant and total antioxidant capacities are affected by periodontal disease in addition to the impact of preeclamptic status. Similar comments may be made for the increases in systemic and local malondialdehyde levels.

The diagnosis of periodontal disease in private practice.

BACKGROUND: Periodontal disease is an inflammatory reaction to the bacteria in dental plaque. The present study compared the prevalence of periodontal disease in patients using as a diagnostic either probing depth measurements, an inflammatory marker such as numbers of white blood cells in plaque samples, or microbiological markers such as the microscopic count and the benzoyl-DL-arginine naphthylamide (BANA) test. METHODS: Teeth with the most inflammation and/or deepest pockets in each quadrant were probed and subgingival plaque was sampled from 1,043 consecutive new patients enrolled in a private practice. Multivariate "diagnostic" models were developed based upon the probing depth (general linear models), percentage of white blood cell-positive and percentage of BANA-positive plaques (logistic regression models) to determine the prevalence of patients with periodontal disease. RESULTS: Plaque samples were removed from 3,694 sites. Fifty-two percent of sampled pockets were >4 mm; 49% of sites were inflamed, using the presence of white blood cells, and 28% were infected using the BANA test. Diagnostic models were highly significant at P<0.0001. The white blood cell model was the most parsimonious as demonstrated by the lowest Akaike information criteria statistic and had the highest receiver operator characteristic (ROC) curve relative to the probing depth and BANA models. CONCLUSIONS: Periodontal disease can be diagnosed chairside by the presence of white blood cells in plaque samples, a finding that reflects the inflammatory nature of the disease process. This approach would reduce the misclassification of subjects as having periodontal disease (130 patients in the present study who had pockets) but minimal evidence of an inflammatory response.

Longitudinal alveolar bone loss in postmenopausal osteoporotic/osteopenic women.

The purpose of this 2-year longitudinal clinical study was to investigate alveolar (oral) bone height and density changes in osteoporotic/osteopenic women compared with women with normal lumbar spine bone mineral density (BMD). Thirty-eight postmenopausal women completed this study; 21 women had normal BMD of the lumbar spine, while 17 women had osteoporosis or osteopenia of the lumbar spine at baseline. All subjects had a history of periodontitis and participated in 3- to 4-month periodontal maintenance programs. No subjects were current smokers. All patients were within 5 years of menopause at the start of the study. Four vertical bitewing radiographs of posterior sextants were taken at baseline and 2-year visits. Radiographs were examined using computer-assisted densitometric image analysis (CADIA) for changes in bone density at the crestal and subcrestal regions of interproximal bone. Changes in alveolar bone height were also measured. Radiographic data were analyzed by the t-test for two independent samples. Osteoporotic/osteopenic women exhibited a higher frequency of alveolar bone height loss (p<0.05) and crestal (p<0.025) and subcrestal (p<0.03) density loss relative to women with normal BMD. Estrogen deficiency was associated with increased frequency of alveolar bone crestal density loss in the osteoporotic/osteopenic women and in the overall study population (p<0.05). These data suggest that osteoporosis/osteopenia and estrogen deficiency are risk factors for alveolar bone density loss in postmenopausal women with a history of periodontitis.

Antibodies to Treponema pallidum in serum from subjects with periodontitis: relationship to pathogen-related oral spirochetes.

Pathogen-related oral spirochetes were identified in dental plaque using monoclonal antibodies to putative Treponema pallidum-specific proteins, and serum from subjects with necrotizing ulcerative gingivitis contained immunoglobulin G to molecules thought to be restricted to T. pallidum. The purpose of this study was to determine whether subjects with periodontitis were more likely to have serum antibodies to T. pallidum if pathogen-related oral spirochetes were present. Pathogen-related oral spirochetes were detected in subgingival plaque from 27 of 40 subjects, and 33 subjects had serum antibodies that bound T. pallidum proteins in immunoblots. Subjects with pathogen-related oral spirochetes were no more likely to have IgA, IgG or IgM to 15-, 37- or 47-kDa proteins than were subjects without pathogen-related oral spirochetes. In contrast to subjects with necrotizing ulcerative gingivitis, subjects with periodontitis had no detectable antibodies to 37- or 12-kDa proteins. Further research is needed to identify the stimulus for antibodies that cross-react with T. pallidum proteins.

Denture stomatitis and ABO blood types.

To determine the interrelation between ABO blood types of denture wearers, denture plaque accumulation, and denture stomatitis, 442 denture wearers were studied using a simplified culture method, which is convenient to use in the dental office. The degree of plaque accumulation and the occurrence of denture stomatitis varied depending on the blood type of the patients. Especially in blood group O compared with other types, both denture plaque accumulation and denture stomatitis were found to be higher or more severe. These results suggest that the ABO blood group is one of the etiologic factors of denture stomatitis and that denture wearers of blood group O are more susceptible to denture stomatitis.

Human serum antibody responses to oral microorganisms. IV. Correlation with homologous infection.

Recent microbiological studies of periodontal disease in humans have supported the concept of a specific bacterial etiology. While individual agents have not been unequivocally identified, numerous Gram-negative members of the subgingival microflora have been implicated. In addition, elevations in systemic antibody responses have been consistent with certain oral microorganisms being involved in an infectious process associated with the disease. This report delineates the relationship between elevated systemic antibody levels and oral colonization with the homologous microorganism at active disease sites. Thirty-four patients with various types of periodontal disease were examined. Using ELISA, each patient was shown to have an elevated antibody response to at least one organism from a battery of 18 oral microorganisms that were tested. Subsequently, subgingival plaque was cultured from disease-active and -inactive sites of each subject. The results demonstrated that the same microorganism to which the individual exhibited elevated serum antibody responses was detected in nearly 55% of the disease-active sites, while only 18% of the inactive sites showed the microorganism. Certain microorganisms including Actinobacillus actinomycetemcomitans, Bacteroides gingivalis, Eikenella corrodens and Wolinella recta were primarily or exclusively correlated with active disease lesions. These findings support the hypothesis that elevated systemic antibodies to periodontopathic bacteria are reflective of subgingival colonization and exist as a response to a bacterial infection at disease-active sites.