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PubMed2002

Coping with stress: its influence on periodontal disease.

BACKGROUND: Various forms of stress behavior were documented and in patients with periodontitis their relationship with periodontal disease was investigated. METHODS: Eighty-nine patients with different forms of chronic periodontitis were included in this retrospective case-control study. They were all undergoing periodontal treatment at the Department of Dental Prosthetics, University of Graz, or a private dental practice. The control group consisted of 63 persons employed in health care at the Clinic of Graz. All participants completed a stress coping questionnaire of 114 items and 19 actional and intrapsychic stress coping modes. The questionnaire served as a psychodiagnostic survey aimed at collecting data on stress coping strategies. Clinical attachment loss (CAL) served as the clinical parameter. RESULTS: With the help of a factor analysis with a factorization and Varimax rotation, 5 factors were extracted from the 19 subtests. The reliability of the questionnaire was less than 0.70 only for subtests "escape" and "pharmaceutical drugs." Otherwise the internal consistency ranged between 0.74 and 0.92, and the retest reliability between 0.72 and 0.84. Subsequent assessment with the t test for independent random samples at the 5% level showed that patients differ significantly from controls in regard of factor 2 (active coping, P = 0.40) and 3 (distractive coping, P = 0.033), and that they differ very significantly from controls in regard of factor 4 (defensive coping, P = 0.000) and 5 (coping through aggression and pharmaceutical drugs, P = 0.007). In the statistical analysis of factors with regard to the severity of periodontal disease, the patients were divided into 2 groups (mild to moderate and severe). The t test for independent random samples showed significance for factor 4 (defensive coping) in that patients with a defensive coping style had greater attachment loss (pF4 = 0.04). CONCLUSIONS: The data corroborate the thesis that periodontitis patients with inadequate stress behavior strategies (defensive coping) are at greater risk for severe periodontal disease. However, further investigations are required to confirm the significance of inappropriate coping styles with respect to the advancement of periodontal disease.

Adaptation, Psychological↗
PubMed1998

The East London Study of Maternal Chronic Periodontal Disease and Preterm Low Birth Weight Infants: study design and prevalence data.

The influence of subject-based and environmental factors on the balance between the subgingival microbial challenge and the host response in periodontal diseases illustrates the intimate link between oral and systemic health. From this stems the hypothesis that the persistent Gram-negative challenge and associated inflammatory sequelae in periodontal disease may have consequences extending beyond the periodontal tissues themselves. This paper addresses the design of a case-control study to examine the relationship between preterm low birth weight (PLBW) and maternal periodontal disease. We present preliminary data on the prevalence of these 2 conditions in a group of mothers at the Royal Hospitals Trust, London, U.K. Cases are defined as mothers delivering an infant weighing less than 2,500g before 37 weeks gestation and controls as mothers delivering an infant of more than 2,500g after 38 weeks. We estimated that a study involving 800 mothers (1:3 case:control) should have sufficient power to detect an association with a minimum odds ration of 3 at the 5% significance level. Demographic details of 177 subjects demonstrated that they were representative of the local population, and the prevalence of PLBW was within the expected range. However, the extent and severity of periodontal disease were higher than predicted and may have reflected elevations in gingival inflammation associated with pregnancy. The final outcome of the study should help determine the need for further interventionist studies to demonstrate a causal relationship between periodontal disease and PLBW, as well as provide information on the prevalence of periodontal diseases in this study population.

Adolescent↗
PubMed1987

Immunologic dysfunction in the pathogenesis of periodontal diseases.

Despite significant progress in our understanding of the pathogenesis and etiology of periodontal diseases, the nature and contribution of the immune system to this disorder remains unclear. Several studies provide evidence for either a protective or destructive rôle. These conflicting findings are difficult to reconcile, since most interpretations tend to argue for a static contributory rôle (i.e., either protective or destructive) of the immune system. Current theories on the rôle of the immune response do not address these conflicting findings as well as the contradictory observation of a detectable immune response in the face of persistent infection in these patients. In this article, we present a model, based on available data, for the contribution of the immune system to the pathogenesis of periodontal disease. This model ascribes a dynamic rôle for the immune response. As documented in other infectious diseases, it is entirely possible, for example, that a state of immunologic dysfunction may occur in the earliest stages of periodontal disease progression; this may then be followed by a period of active immune reactivity (humoral and/or cellular) that would represent either a delayed or depressed response. This model is discussed in conjunction with recent findings that several suspected periodontal pathogens are capable of producing immunosuppressive agents. Many of the apparently contradictory clinical observations concerning the host immune response to oral pathogens and its correlation (or lack of) with both the progression and severity of periodontal disease may be accounted for in this model.

Humans↗
PubMed1990

[Non-plaque related periodontal diseases].

Non-plaque related periodontal diseases are rather rare, and may be based on a wide range of lesions, both benign and malignant. The clinical and radiographic signs often mimic those of the common plaque-related diseases and, therefore, may significantly postpone proper diagnosis and treatment.

Dental Plaque↗
PubMed2004

Smoking, periodontal disease and the role of the dental profession.

Epidemiological investigations support a firm relationship between smoking and periodontal disease. The likely benefits of smoking cessation programmes are considerable for periodontal disease, cancers and nearly all chronic systemic diseases. The mechanisms by which smoking may influence the development and progression of periodontal disease are as yet unclear, but may include changes in the vasculature, the immune and inflammatory systems, tissue oxygenation and the healing processes. Unfortunately, although dental professionals have more opportunities to encourage smokers to quit (most people visit their dentist more frequently than their doctor), dentists claim that they are not well informed on this subject. The purpose of this review is to describe the evidence for a link between smoking and periodontal disease, the possible pathology induced by smoking on the periodontal tissues and its impact on therapy, and to outline the smoking cessation techniques that are currently available.

Dentists↗
PubMed1993

Risk indicators and risk markers for periodontal disease experience in older adults living independently in Ontario, Canada.

This study examined risk indicators and risk markers for periodontal disease experience in 624 adults aged 50 years and over living independently in four communities in Ontario, Canada. The data were collected as part of the baseline phase of a longitudinal study of the oral health and treatment needs of this population. Periodontal disease experience was assessed in terms of attachment loss, measured at two sites on each remaining tooth. Bivariate and multivariate analyses were used to examine the relationship between a number of sociodemographic, general health, psychosocial, and oral health variables and three indicators of periodontal disease experience. These were: mean attachment loss, the proportion of sites examined with loss of 2 mm or more, and the probability of the subjects having severe disease, arbitrarily defined as a mean attachment loss in the upper 20th percentile of the distribution. Mean attachment loss was 2.95 mm (SD = 1.41 mm), and 76.6% of sites examined had loss of 2 mm or more. In bivariate analyses, the most consistent predictors of periodontal disease experience were: age, education, income, smoking, dental visiting, the number of remaining teeth, the number of decayed coronal surfaces, and the number of decayed root surfaces. In multivariate analyses, age, education, current smoking status, and the number of teeth had the most consistent independent effects. These data confirm the results of recent US studies indicating that periodontal disease experience is influenced by social and behavioral factors.

Age Factors↗
PubMed1995

Smoking and periodontal disease severity.

This study was performed to assess the influence of smoking on periodontal disease severity. Data concerning periodontal status and smoking habits were collected from 889 periodontal patients: 340 male and 549 female, 21 to 76 years of age, 47.4% being non smokers and 52.6% smokers. Periodontal parameters, recorded by the same examiner (PMC), were: gingival recession (GR), Pocket depth (PD), Probing attachment level (PAL), and mobility (M). The influence of age, sex and tobacco consumption on these periodontal parameters was statistically evaluated using an analysis of variance (ANOVA) with covariates. A non-linear effect model was also fitted by taking the natural logarithms of the response variables (GR, PD, PAL) closer to biomedical phenomena. Mobility was analyzed by a chi2-test. The effect of smoking on periodontitis showed no association with age or with sex. Smoking, age and sex were shown to be statistically significant for periodontitis, by performing both univariate (t-test for equal means) and multivariate tests. p-values for smoking and periodontitis were: GR (p=0.000), PD (p=0.000), PAL (p=0.000) and M (P=0.015). Smoking one cigarette per day, up to 10, and up to 20, increased PAL by 0.5%, 5% and 10%, respectively. The impact of tobacco is comparable to the impact resulting from the factor of age in this sample, increasing PAL by 0.7% for each year of life. Comparison between smokers of less than 10 cigarettes per day (PAL mean 3.72 mm +/-0.86) and non-smokers (PAL mean 3.84 +/- 0.89) showed no differences in PAL (p=0.216), while comparison for smokers from 11 to 20 cigarettes (PAL mean 4.36 +/- 1.23) and for more than 20 cigarettes (PAL mean 4.50 +/- 1.04) demonstrated significant differences (p=0.000). These findings suggest that: (1) tobacco increases periodontal disease severity; (2) this effect is clinically evident above consumption of a certain quantity of tobacco.

Adult↗
PubMed2000

Hormonal factors in periodontal disease.

This article discusses the effects of sex steroid hormones, glucocorticoids and insulin deficiency on periodontal tissues, and the possible consequences on periodontal disease progression. The androgens and oestrogens have predominantly anabolic functions in stimulating matrix synthesis, which is applicable to periodontal repair and medication-induced gingival overgrowth. Oestrogen and progesterone can contribute to pregnancy gingivitis; long-term use of hormonal contraceptives can accelerate progression of periodontal disease. Higher levels of circulating cortisol, associated with stress, can influence the onset of acute necrotic ulcerative gingivitis. Gingivitis and periodontal disease are reported to be more prevalent in type 1 and type 2 diabetes mellitus (periodontal disease, particularly in older, less well controlled subjects) than in non-diabetic individuals.

Adult↗
PubMed1993

Non-human primates used in studies of periodontal disease pathogenesis: a review of the literature.

The inability to examine initiation and progression of periodontal disease and to assess certain therapies in humans has led to a great interest in the use of animal models in periodontal research. Some of the most prominent animals used are non-human primates. This article reviews the characteristics of non-human primate models in periodontal health, in the transition from health to gingivitis to periodontitis, and in experimental gingivitis and periodontitis. Where possible, the results of these studies are compared with results from human studies. Only a few studies have compared in detail the anatomy, physiology, immunology, and tissue interactions in monkeys with those of humans. With the exceptions of differences and variations in size of the dentition, the number of each tooth type as well as larger canines, presence of diastemata between anterior teeth, and an edge-to-edge relationship of the incisors, the dental and periodontal anatomy of non-human primates seem quite similar to that of humans. Clinically healthy gingiva can be established and maintained in non-human primates, and gingivitis as well as periodontitis occur in these animals. It is possible to induce experimental periodontitis by placement of peri-dental silk ligatures or orthodontic elastics as well as by surgical removal of alveolar bone. Although the most appropriate model for studies of periodontal disease pathogenesis in non-human primates appears to involve the application of silk ligatures, some difficulties may occur in establishing periodontal break-down by using this model. Many clinical, histological, microbiological, and immunological characteristics of spontaneous and experimental marginal inflammation in most non-human primates are similar to those in humans. The most significant differences between small non-human primates and humans are the very limited number of lymphocytes and plasma cells in the inflammatory infiltrate of squirrel monkeys (Saimiri sciureus) and marmosets. Therefore, the use of squirrel monkeys and marmosets may not be appropriate in many studies of periodontal disease pathogenesis. The most significant microbial differences between macaque species and humans are a lower proportion of Actinomyces species, the presence of a catalase-producing Prevotella melaninogenica strain, and the high carrier rate for Actinobacillus actinomycetemcomitans in subgingival plaque of macaque species. The significance of these differences is presently unknown. It is concluded that the use of many non-human primate species due to the apparent close anatomic and biologic similarities to humans is appropriate in experimental studies of periodontal disease, provided the use of laboratory animals is requisite and lower species are not applicable.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Chronic treatment with the glutamate receptor antagonist MK-801 alters periodontal disease susceptibility.

OBJECTIVE: Previous experiments in rats suggest that hypothalamic-pituitary-adrenal (HPA) axis over-responsiveness, which leads to increased secretion of immunoregulatory glucocorticoid hormones, increases periodontal disease susceptibility, whereas HPA axis under-responsiveness is associated with increased resistance to the disease. The present study was designed to investigate whether MK-801 (dizocilipine malate), an antagonist of the glutamate receptor N-methyl-D-aspartate (NMDA) in the brain, which has been found to play an important role in the regulation of the HPA axis, would influence the outcome of experimental ligature-induced periodontal disease in a rat model. METHODS: Experimental periodontal disease was induced in periodontal disease susceptible and HPA axis high-responding Fischer 344 rats 2 days before chronic treatment with MK-801(1 mg/kg intraperitoneally). The periodontal breakdown was assessed after the ligatures had been in place for 23 days. Following intraperitoneal Gram-negative bacterial lipopolysaccharide stimulation (Escherichia coli, 250 microg/kg), concentrations of glucocorticoid receptors (GRs) in the hippocampus, and levels of the cytokine tumour necrosis factor alpha (TNF-alpha), as well as the HPA axis-derived hormone corticosterone, were measured in serum. RESULTS: Compared to vehicle-treated controls, MK-801-treated rats had significantly increased periodontal tissue destruction (p < 0.01). MK-801-treated rats also showed significantly increased expression of GRs in the hippocampus (p < 0.05), elevated levels of corticosterone (p < 0.001) and reduced levels of TNF-alpha (p < 0.01) in serum 2 h after lipopolysaccharide stimulation. CONCLUSION: These findings may implicate glutamate receptor-dependent mechanisms in periodontal disease, and support the concept of a bidirectional immune-brain-immune regulatory network with importance for periodontal health and disease.

Animals↗
PubMed1977

[Therapy of periodontal diseases].

An analysis of general periodontal treatment carried out in the Departement of Cardiology, Periodontology and Preventive Dental Medicine of the University of Zurich, Dental Institute was undertaken with the aid of 50 randomly selected patient case histories. Immediately following therapy, it was found that a normal marginal periodontium had been established in all cases. A prerequisite for this success was effective patient oral hygiene. The duration of total treatment depended upon diagnosis and treatment plan and ranged from 18 to 62 h. Documentation of each phase of treatment was responsible for a significant part of the total therapy time. In view of the relatively large amount of time necessary to treat periodontal disease, future emphasis should be placed upon the refinement and propagation of preventive measures.

Adult↗
PubMed1989

[Periodontal disease--specific or nonspecific infection?].

The concept of a non-specific etiology of periodontal disease has been predominant during the last century. It was believed that this disease was caused by the normal oral microbial flora and dependent on the state of the immune system of the host. The specific plaque hypothesis, which is currently discussed, claims that specific oral bacteria cause different forms of periodontal disease. High counts of these bacteria have been found in association with different forms of periodontal disease. These bacteria have also been found to have stronger pathogenic potential than other members of the oral microbiota. It is concluded that there are different forms of periodontal disease and that some of these forms are probably opportunistic infections associated with different microbial etiologies.

Humans↗
PubMed2003

Meta-analysis of periodontal disease and risk of coronary heart disease and stroke.

OBJECTIVE: The purpose of this study was to analyze published studies and abstracts in order to provide a quantitative summary of periodontal disease as a risk factor for cardiovascular disease and to explore the possible causes for conflicting results in the literature. STUDY DESIGN: We searched all published literature on the Medline literature search engine since 1980. An additional search was performed with bibliographic citations from each article. Nine cohort studies (8 prospective and 1 retrospective), in which relative risks (RRs), CIs, and P values were reported or could be calculated were included. Four researchers independently extracted RRs, CIs, and P values from each study and evaluated the degree of confounding adjustment. The combined result was calculated with weighted average, and sources of disparity were tested with regression analyses. RESULTS: The summary RR was 1.19 (95% CI, 1.08 1.32), indicating a higher risk of future cardiovascular events in individuals with periodontal disease compared with those without. In an analysis stratified to individuals of </=65 years of age, the RR was 1.44 (95% CI, 1.20 to 1.73). When the outcome was restricted to stroke only, the RR was 2.85 (95% CI, 1.78 to 4.56). In the metaregression analysis, the effects of residual confounding caused an overestimate of the results by 12.9% and, with a proxy for periodontal disease, caused an underestimate of 29.7%. CONCLUSIONS: Periodontal disease appears to be associated with a 19% increase in risk of future cardiovascular disease. This increase in RR is more prominent (44%) in persons aged </=65 years. Although the increment of risk between subjects with or without periodontal disease in the general population is modest, at around 20% because nearly 40% of population has periodontal disease, this modest increase may have a profound public health impact.

Adult↗
PubMed1991

[Influence of saliva components on periodontal disease in insulin-dependent diabetics].

In diabetic patients an increased incidence of periodontal disease has been demonstrated. This study was to elucidate the influence of saliva constituents on periodontal alterations. 31 insulin-dependent type-I diabetics and a control group were submitted to oral examination. During daytime salivary samples were collected at regular intervals for analysis of glucose, sodium, potassium, calcium and the pH values. Additional information on relevant blood values and organic complications were obtained from the diabetic group. The results revealed a significant correlation between the degree of diabetes control and periodontal disease. The saliva concentrations of glucose and potassium were significantly elevated as against the controls. However, no correlation was found between the saliva components and periodontal disease.

Adolescent↗
PubMed2005

Relationship between obesity, glucose tolerance, and periodontal disease in Japanese women: the Hisayama study.

BACKGROUND: Recent studies have reported a relationship between obesity and periodontal disease. Obesity is the strongest risk factor for type 2 diabetes, which is, in turn, a risk factor for periodontal disease. An oral glucose tolerance test is necessary to diagnose diabetes; however, no study has examined the relationship between obesity and periodontal disease by taking oral glucose tolerance test results into consideration. METHODS: In all, 584 Japanese women aged between 40 and 79 years old, with at least 10 teeth, underwent health examinations. Body mass index, waist-hip ratio, body fat, and oral glucose tolerance test results were used as independent variables with known risk factors for periodontal disease. Mean probing pocket depth and mean attachment loss were used as the dependent variables. RESULTS: In all of the analyses, body mass index, body fat, and waist--hip ratio were significantly associated with the highest quintile of mean probing pocket depth, even when adjusted for oral glucose tolerance test results. In the multivariate analysis, the subjects with the highest quartile of body mass index had a significantly higher odds ratio (OR) for the highest quintile of mean probing pocket depth [OR, 4.3; 95% confidence interval (CI), 2.1--8.9; p<0.001], whereas neither impaired glucose tolerance nor diabetes were significantly associated with deep pockets. The relationships between the obesity indexes and mean attachment loss did not reach statistical significance. CONCLUSION: Obesity was associated with deep pockets in Japanese women, even after adjusting for oral glucose tolerance test.

Adult↗
PubMed2002

Maternal periodontal disease and preterm low birthweight: case-control study.

Periodontal disease has been suggested to be an important risk factor for preterm low birthweight (PLBW). Here we report a case-control study of 236 cases (infants < 37 wks and weighing < 2499 g) and a daily random sample of 507 controls (> or = 38 wks and weighing > or = 2500 g). Clinical periodontal indices were measured on the labor wards. Associated risk factors for periodontal disease and PLBW were ascertained by means of a structured questionnaire and maternity notes. The risk for PLBW decreased with increasing pocket depth (odds ratio [OR] 0.83, 95% confidence interval [CI] 0.68 to 1.00). After adjustment for maternal age, ethnicity, maternal education, smoking, alcohol consumption, infections, and hypertension during pregnancy, this decreased further (OR 0.78, 95% CI 0.64 to 0.99). We found no evidence for an association between PLBW and periodontal disease. Our results do not support a specific drive to improve periodontal health of pregnant women as a means of improving pregnancy outcomes.

Adolescent↗