[Study of orthodontic problems in patients with periodontal disease. 2. The malposition of teeth in periodontal disease].
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UNLABELLED: Periodontal medicine defines a rapidly emerging branch of periodontology focusing on the wealth of new data establishing a strong relationship between periodontal health or disease and systemic health or disease. The aim of this paper is to critically examine the evidence for an association between periodontal infections and cardiovascular disease. MATERIAL AND METHODS: Literature and data on periodontal diseases and their links to cardiovascular disease. Medline and Pub-Med search. Review of relevant information and data. RESULTS: There is increasing evidence that individuals with periodontal disease may be at higher risk for adverse medical outcomes, including cardiovascular disease. A number of studies to date indicate that this increased risk appears to be independent of other known behavioral and medical risk factors and also appears to be related to the severity of periodontal disease. This article evaluates the inflammatory mechanisms of periodontal disease and cardiovascular disease and examines the potential role of local inflammation in systemic inflammatory disease. CONCLUSIONS: Periodontal diseases may be risk factors for cardiovascular diseases.
A patient had the benign form of Albers-Schönberg disease complicated by periodontitis. Review of the patient's 36-year history revealed that the long-term prognosis can be good. Determining factors in the prognosis are the severity of bony involvement and proper periodontal and dental maintenance.
Feline periodontal disease has many elements in common with human and canine disease. Anatomic, physiologic, microbiologic, and immunologic differences between the three species make it impossible to predict with certainty whether successful approaches to controlling and treating canine oral disease will also prove successful in cats. We have developed methods for reproducible, quantitative evaluation of feline dental plaque and calculus. Our studies demonstrated that feline plaque accumulation peaks at 1 week after prophylaxis and that calculus peaks at 4 weeks after prophylaxis. These methods should be adequately sensitive to document control of plaque and calculus accumulation by efficacious chemical or antimicrobial agents.
The aim of this study was to estimate the incidence of periodontal disease activity (PDA) in treated periodontitis patients in a longitudinal survey. Seven periodontitis patients with 170 teeth (970 sites) participated in this 6 to 12 month study. After initial therapy, the clinical parameters including attachment level (AL) were recorded as the baseline data and then repeated every two months. Occlusal stents were used for each patient to assure the accuracy and reproductivity of the attachment level measurements. Detection of > or = 2 mm of new AL between two consecutive visits was required to designate a site as PDA. During the study period, 21 sites out of 970 sites showed PDA. For better accuracy, we calculated the yearly PDA rate based on the 6-month data because not all the seven patients finished the 12-month observation. The estimated PDA rate per year was 2.8%. Data also showed that maxillary bicuspids and molars on both jaws were more susceptible to PDA. Interproximal sites and sites with > or = 6 mm pockets before treatment showed significantly greater PDA rate than buccal (lingual) sites and sites with < or = 4 mm initial pocket depth. Our data supports the tooth specific and site specific concept in periodontal disease.
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Cytokines present during immune responses have a tremendous influence on resistance/susceptibility to oral diseases including periodontal disease and oral opportunistic infections in the immunocompromised individual, as seen by altered Th cytokines in saliva with human immunodeficiency virus (HIV) disease progression and oropharyngeal candidiasis. This study was designed to evaluate whether the presence of severe periodontal disease has any influence on Th cytokines in saliva of HIV-positive persons. For this, saliva from a cohort of HIV-positive persons with mild or severe periodontitis was evaluated for Th cytokines. A dominant Th2-type cytokine profile in saliva was validated in HIV-positive subjects with considerable immune suppression, irrespective of periodontal disease status. However, no significant differences in concentrations of Th1- or Th2-type cytokines in saliva were observed when stratified by periodontal status. Thus, the lack of salivary influences by periodontitis eliminates periodontal disease as a variable in interpretations regarding correlates of local cytokines during oral manifestations of HIV.
Tests for periodontal disease that are able to detect both ongoing and future loss of clinical attachment would be valuable assets in determining the diagnosis and treatment of periodontal diseases. We hypothesized that connective tissue-associated proteins could be detected in crevicular fluid and would reflect the biochemical activity of the periodontium in health and disease. To test this hypothesis, crevicular fluid samples obtained from patients with various states of periodontal disease were analyzed for the presence of several connective tissue-associated proteins using a dot blot assay. Two such proteins, osteonectin and N-propeptide alpha I type I collagen, were detected in crevicular fluid samples of patients with periodontal disease. Furthermore, the amount of these proteins detected in crevicular fluid appeared to increase with increased probing depth at the sampled site. These studies indicate that measurements of connective tissue-associated proteins in crevicular fluid may prove to be a valuable tool for diagnosing periodontal diseases.
BACKGROUND: Human periodontal diseases are inflammatory disorders that are the result of complex interactions between periodontopathogens and the host's immune response. Two important and interrelated factors are involved in the pathophysiological progression of periodontal diseases, i.e. the activation of immune system and the production of oxygen radicals and their related metabolites. Increased production of oxygen radicals may contribute to oxidative stress, which is reported to be involved in many diseases, including periodontal diseases. OBJECTIVES: The objective of this study was to investigate glutathione peroxidase, lactoferrin and myeloperoxidase, which play an essential role in free radical production and defenses, and the proinflammatory cytokine interleukin-1beta (IL-1beta), which is important in the regulation of immunological and inflammatory reactions in human periodontal diseases. METHODS: Gingival crevicular fluid (GCF) samples were collected from 27 subjects, 19 periodontitis patients and eight healthy controls, ranging in ages from 24 to 62 years. Clinical parameters were recorded. GCF glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta were analyzed by enzyme-linked immunosorbent assays (ELISA). RESULTS: The periodontitis sites exhibited significantly greater total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta than healthy sites. Total amount of glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta was positively correlated with plaque index, gingival index, probing depth and probing attachment level (p < 0.05). CONCLUSION: The imbalance between the levels of myeloperoxidase/IL-1beta and glutathione peroxidase/lactoferrin could result in tissue damage of reactive oxygen species (ROS) in periodontitis which is initiated and perpetuated by the chronic insults of periodontopathogens.
The present study shows that 14C-arachidonic acid metabolism in gingiva of patients with periodontal disease is mainly via the lipoxygenase pathway. In two pools of gingival tissue homogenates, the lipoxygenase products contained 22.65% and 23.38%, while the prostaglandins (PGs), products of the cyclooxygenase pathway, contained only 4.85% and 3.98% of the total radioactivity incubated. 12-hydroxy-eicosatetraenoic acid (12-HETE), a lipoxygenase product, was detected as a major metabolite of arachidonic acid in gingiva.
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BACKGROUND: Cigarette smoking is a significant risk factor for both coronary heart disease and periodontal disease. The goal of this study was to better understand the role of smoking in the relationship between periodontal disease and heart attack history. METHODS: The study population consisted of 5,285 participants in the Third National Health and Nutrition Examination Survey (NHANES) during 1988-1994 and who were age 40 years or older when examined. The data analysis employed logistic regression models and accounted for the complex sampling design used in NHANES. RESULTS: After adjustment for potential confounders, we only found significant associations between periodontal loss of attachment (LOA) and heart attack history for smokers, with odds ratios and 95% confidence interval (CI) of 2.64 (1.48 to 4.71), 3.84 (1.22 to 12.10) and 5.87 (1.91 to 18.00) for those with 2.0 to 2.99, 3.0 to 3.99, and 4 mm or more mean LOA, respectively. When the analysis was stratified by smoking status and tertile of age at heart attack, the statistically significant associations were limited to smokers who had a heart attack between the ages of 25 and 50 years, with odds ratios and 95% Cl associated with increasing mean LOA for this group of 3.29 (1.35 to 8.04), 7.32 (1.60 to 33.51), and 8.04 (1.91 to 18.00), respectively. CONCLUSIONS: These results suggest that cigarette smoking is a necessary cofactor in the relationship between periodontal disease and coronary heart disease, and the increase in risk appears to be age dependent. However, the key role played by smoking in the etiology of both periodontal and heart diseases makes it difficult to determine how much of the observed association resulted from periodontal disease.
Mycoplasma have been identified in one case of juvenile periodontitis by size, morphology, hemadsorption and cultural techniques. These microorganisms were found on the surface of the tooth, on the surface of pocket epithelium and invading the gingival epithelium and adjacent connective tissue. These observations suggest the need for further studies on the role of Mycoplasma in the pathogenesis of advanced periodontal infections. The role of Mycoplasma in periodontal disease is discussed.
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BACKGROUND: The periodontal disease status of 320 dentate adults, diagnosed 23.7 years previously with Type 1 insulin dependent diabetes mellitus, was evaluated. These patients had been monitored at 2-year intervals as part of a large University of Pittsburgh longitudinal study assessing the medical complications associated with insulin dependent diabetes. METHODS: During one of their regularly scheduled medical examinations, a group of 320 adult dentate subjects (mean age of 32.1 years) received a periodontal examination as part of a comprehensive oral health assessment. The oral health assessment collected data regarding demographics, oral health behaviors, tooth loss, coronal and root caries, salivary functions, and soft tissue pathologies. For the periodontal assessments, 3 facial sites (mesial, midcervical, distal) of the teeth in the right maxillary/left mandibular or left maxillary/right mandibular quadrants were evaluated for calculus, bleeding on probing (BOP) and loss of gingival attachment (LOA). RESULTS: Attachment loss was significantly greater for older patients whereas BOP and calculus levels were relatively constant across age categories. Univariate analyses of factors possibly related to extensive periodontal disease (LOA > or =4 mm for at least 10% of sites examined) indicated an association with older age; lower income and education; past and current cigarette smoking; infrequent visits to the dentist; tooth brushing less than once per day; older age of onset; longer duration of diabetes; and the diabetic complication of neuropathy. A multivariate regression model of all possibly significant factors found current cigarette use (odds ratio [OR] = 9.73), insulin dependent diabetes onset after 8.4 years of age (OR = 3.36), and age greater than 32 years (OR = 3.00) explained the majority of the extensive periodontal disease in this group of diabetic patients. CONCLUSIONS: Management and prevention of extensive periodontal disease for Type 1 diabetic patients should include strong recommendations to discontinue cigarette smoking.
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