935 resultados para Tooth Diseases


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This third part of a series of publications from the Swiss task force "Smoking--Intervention in the private dental office" on the topic "tobacco use and dental medicine" describes the clinical and radiographic changes of the periodontium within smokers as well as the consequences of tobacco use on periodontal and implant therapy. With increased use of tobacco, patients show higher periodontal probing depths, increased clinical attachment loss, more alveolar bone resorption, a higher prevalence of gingival recessions, and a higher risk for tooth loss. In contrast to this, with smokers, the clinical characteristics of gingival inflammation or bleeding on periodontal probing are less established. Smokers show less positive results after conventional, surgical and regenerative periodontal therapy. The benefits of mucogingval surgery are reduced and less successful in smokers. Moreover, smoking impairs the osseointegration of oral implants and is at least partly responsible for a majority of biological complications in implant dentistry, such as periimplantitis. Based on the present understanding of periodontal diseases, the clinical findings, and the specific therapeutic outcomes with smokers, it appears to be reasonable, next to the current classification of periodontal diseases, to use the term "smokers periodontitis".

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This literature review represents the second in a series of articles from the Swiss task force "Smoking--Intervention in the private dental office" on the topic "tobacco use and dental medicine". In this article, the epidemiological background as well as some pathogenetic processes are described and discussed critically for tobacco-related periodontal diseases. Earlier publications confirmed tobacco consumption as a risk factor for periodontal diseases. Over the last few years, oral health research has significantly contributed to the understanding of the mechanisms leading to the deterioration of the hard and soft tissues supporting the teeth. With the recording of the number of cigarettes smoked per day and the amount of years tobacco was used, a dose response relationship was established. Various, potentially significant pathogenic effects of tobacco-related substances may exist on the periodontal tissues, the immune response system or the composition of the oral flora. Moreover, there is reference that tobacco consumption may change the genetically determined susceptibility for periodontal diseases.

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The clinical diagnosis 'erosion' is made from characteristic deviations from the original anatomical tooth morphology, thus, distinguishing acid induced tissue loss from other forms of wear. Primary pathognomonic features are shallow concavities on smooth surfaces occurring coronal from the enamel-cementum junction. Problems from diagnosing occlusal surfaces and exposed dentine are discussed. Indices for recording erosive wear include morphological as well as quantitative criteria. Currently, various indices are used making the comparison of prevalence studies difficult. The most important and frequently used indices are described. In addition to recording erosive lesions, the assessment of progression is important as the indication of treatment measures depends on erosion activity. A number of evaluated and sensitive methods for in vitro and in situ approaches are available, but the fundamental problem for their clinical use is the lack of re-identifiable reference areas. Tools for clinical monitoring are described.

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Dental erosion is often described solely as a surface phenomenon, unlike caries where it has been established that the destructive effects involve both the surface and the subsurface region. However, besides removal and softening of the surface, erosion may show dissolution of mineral underneath the surface. There is some evidence that the presence of this condition is growing steadily. Hence, erosive tooth wear is becoming increasingly significant in the management of the long-term health of the dentition. What is considered as an acceptable amount of wear is dependent on the anticipated lifespan of the dentition and, therefore, is different for deciduous compared to permanent teeth. However, erosive damage to the permanent teeth occurring in childhood may compromise the growing child's dentition for their entire lifetime and may require repeated and increasingly complex and expensive restoration. Therefore, it is important that diagnosis of the tooth wear process in children and adults is made early and adequate preventive measures are undertaken. These measures can only be initiated when the risk factors are known and interactions between them are present. A scheme is proposed which allows the possible risk factors and their relation to each other to be examined.

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AIM: The purpose of this randomized split-mouth clinical trial was to determine the active tactile sensibility between single-tooth implants and opposing natural teeth and to compare it with the tactile sensibility of pairs of natural teeth on the contralateral side in the same mouth (intraindividual comparison). MATERIAL AND METHODS: The hypothesis was that the active tactile sensibilities of the implant side and control side are equivalent. Sixty two subjects (n=36 from Bonn, n=26 from Bern) with single-tooth implants (22 anterior and 40 posterior dental implants) were asked to bite on narrow copper foil strips varying in thickness (5-200 microm) and to decide whether or not they were able to identify a foreign body between their teeth. Active tactile sensibility was defined as the 50% threshold of correct answers estimated by means of the Weibull distribution. RESULTS: The results obtained for the interocclusal perception sensibility differed between subjects far more than they differed between natural teeth and implants in the same individual [implant/natural tooth: 16.7+/-11.3 microm (0.6-53.1 microm); natural tooth/natural tooth: 14.3+/-10.6 microm (0.5-68.2 microm)]. The intraindividual differences only amounted to a mean value of 2.4+/-9.4 microm (-15.1 to 27.5 microm). The result of our statistical calculations showed that the active tactile sensibility of single-tooth implants, both in the anterior and posterior region of the mouth, in combination with a natural opposing tooth is similar to that of pairs of opposing natural teeth (double t-test, equivalence margin: +/-8 microm, P<0.001, power >80%). Hence, the implants could be integrated in the stomatognathic control circuit.

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Objectives: To assess the ability to predict tooth loss on the basis of clinical and radiographic parameters. Methods: Clinical and radiographic data from a five year prospective cohort were studied to identify cause of progressive tooth loss in older subjects. Results: 363 subjects with a baseline mean age of 67.1 years (S.D. + 4.7, range : 60-75), and 51.4% women were studied including 59.5% never smokers, and 33.0% current smokers. At baseline the subjects had, on average, 22.4 teeth (S.D. + 6.4). Self-assessed tooth loss risk was identified by 16.0 % of subjects while 34% of subjects lost teeth. Tooth loss due to caries was found in 24.7% (178 teeth), periodontitis in 15.4% (133 teeth), peri-apical lesions 5.9% (32 teeth), combined periodontal/peri-apical in 3.4% (18 teeth), and teeth irrational to treat in 7.5% (58 teeth) of the subjects. 122 of the extracted teeth (34%) should have been possible to save but were extracted. At year five severe caries, periodontitis, peri-apical lesions, periodontal/peri-apical, irrational to treat were found in 6.3%, 7.2%, 2.6%, 4.6%, and 1.2% of subjects, respectively. Signs of osteoporosis increased by 11.2 % (Klemetti index). Linear regression analysis failed to include smoking habits as being explanatory. Explanatory factors were researcher prediction of extraction needs, subject self assessment of risk and change in ostoporosis status (r2 = 0.39, ANOVA, F=22.6, p< 0.001). Conclusions: Caries and periodontitis are primary causes for extraction. Progressive osteoporosis is associated with tooth loss. Radiographs, and subjects self-assessment of risk for tooth loss are robust predictors.

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The absence or deficiency of specific platelet glycoprotein receptors has a well-defined role in causing several rare bleeding disorders such as Bernard-Soulier syndrome or Glanzmann's thrombasthenia. Several new rare disorders caused by defects in other receptors or their signalling pathways have recently been described. Platelet receptors are also often targets for antibodies in pathological conditions. The roles of platelet receptors or their polymorphism variants in diseases such as cardiovascular disorders have started to be intensively investigated over the last 5 years. Many of these findings still remain controversial. Recent evidence points to a fundamental role for platelets and their receptors in the origins of atherosclerosis. Studies on the role of platelet receptors in diseases such as asthma, diabetes and HIV are still at an early stage.

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Polymorphisms in coagulation factors leading to altered susceptibility to cardiovascular diseases have been known for some time and some are now well-established risk factors. More recently, an increasing number of polymorphisms have been identified in platelet receptors and a series of studies indicate that these too may play a role as individual risk factors for stroke and myocardial infarction. The effect of these platelet polymorphisms appears less clear-cut than some of the coagulation factor effects and other, associated, risk factors may be important in defining their role. In this review platelet receptor polymorphisms and their role as risk factors are surveyed and their possible relevance discussed.

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The role of platelet glycoprotein receptors in disorders caused by their absence or defects such as in Bernard-Soulier syndrome or Glanzmann's thrombasthenia has been known for many decades now. Their function as targets for pathological antibodies is also well established. The possible roles of platelet receptors or their polymorphism variants in the origins of diseases such as cardiovascular disorders are less well studied. Investigation of this area began about five years ago and many findings still remain controversial. The involvement of platelet receptors in other diseases like asthma, diabetes and HIV are only starting to be studied.

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OBJECTIVE: To analyse the performance of a new M. tuberculosis-specific interferon gamma (IFNgamma) assay in patients with chronic inflammatory diseases who receive immunosuppressive drugs, including tumour necrosis factor alpha (TNFalpha) inhibitors. METHODS: Cellular immune responses to the M. tuberculosis-specific antigens ESAT-6, CFP-10, TB7.7 were prospectively studied in 142 consecutive patients treated for inflammatory rheumatic conditions. Results were compared with tuberculin skin tests (TSTs). Association of both tests with risk factors for latent M. tuberculosis infection (LTBI) and BCG vaccination were determined and the influence of TNFalpha inhibitors, corticosteroids, and disease modifying antirheumatic drugs (DMARDs) on antigen-specific and mitogen-induced IFNgamma secretion was analysed. RESULTS: 126/142 (89%) patients received immunosuppressive therapy. The IFNgamma assay was more closely associated with the presence of risk factors (odds ratio (OR) = 23.8 (95% CI 5.14 to 110) vs OR = 2.77 (1.22 to 6.27), respectively; p = 0.009), but less associated with BCG vaccination than the TST (OR = 0.47 (95% CI 0.15 to 1.47) vs OR = 2.44 (0.74 to (8.01), respectively; p = 0.025). Agreement between the IFNgamma assay and TST results was low (kappa = 0.17; 95% CI 0.02 to 0.32). The odds for a positive IFNgamma assay strongly increased with increasing prognostic relevance of LTBI risk factors. Neither corticosteroids nor conventional DMARDs significantly affected IFNgamma responses, but the odds for a positive IFNgamma assay were decreased in patients treated with TNFalpha inhibitors (OR = 0.21 (95% CI 0.07 to 0.63), respectively; p = 0.006). CONCLUSIONS: These results demonstrate that the performance of the M. tuberculosis antigen-specific IFNgamma ELISA is better than the classic TST for detection of LTBI in patients receiving immunosuppressive therapy for treatment of systemic autoimmune disorders.