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Results for “Chronic Periodontitis”

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At least 19 recordsLinked to original sources
PubMed1978

Prevalence of chronic periodontitis in 13-15-year-old children. A radiographic study.

The bitewing radiographs of 1,731 English and Danish schoolchildren aged 13--15 years were examined to assess the prevalence of chronic periodontitis. Only one child (0.06%) was found to be affected in comparison with the high prevalence of 51.5% reported by Hull et al. (1975). Minute qualitative changes in the radiographic appearance of the alveolar crest, or changes in the visual representation of the width of the periodontal ligament space are not reliable or valid criteria for assessing chronic periodontitis. Horizontal bone loss observed on radiographs, which can be accurately measured using the cemento-enamel junction as a reference point, is a useful diagnostic criterion for the measurement of chronic periodontitis.

Adolescent↗
PubMed2026

Causal effect of chloride intracellular channel protein 5 on chronic periodontitis: A Mendelian randomization study.

This study aimed to evaluate the potential causal effect of chloride intracellular channel protein 5 (CLIC5) on the risk of chronic periodontitis (CP) using a Mendelian randomization (MR) approach. MR analysis was conducted utilizing publicly available summary statistics from genome-wide association studies summary statistics for CLIC5 and CP. Multiple MR methods, including inverse variance weighted, MR Egger, weighted median and weighted mode, were employed to estimate the causal effects. Sensitivity analyses, comprising leave-one-out and heterogeneity assessments were performed to evaluate the robustness of our findings. This MR analysis consistently revealed a negative association between CLIC5 and CP, with statistical significance achieved using the inverse variance weighted and weighted median methods. The concordant effect estimates obtained from all methodological approaches collectively indicated a potential protective effect of CLIC5 against CP. The sensitivity analyses further confirmed the robustness of these findings. This study provides genetic evidence suggesting a potential causal association between increased CLIC5 levels and decreased risk of CP. These findings augment the existing literature implicating chloride channel proteins in modulating the inflammatory processes pertinent to periodontal health. Further investigation is warranted to decipher the underlying biological mechanisms and to explore the potential of CLIC5 as a therapeutic target for CP.

Chloride Channels↗
PubMed1978

The effect of a 1% chlorhexidine gel in the initial therapy of chronic periodontal disease.

Thirty patients took part in a 4 week 'double-blind' clinical trial. Following initial oral hygiene instruction and scaling, half the patients were instructed to brush with a 1% Chlorhexidine gel in the evenings, the other half to use placebo. A standard dentifrice was used in the morning. In both groups there was a marked improvement in all parameters recorded, and although final plaque scores showed a statistically significant difference in favor of the test group, there was virtually no difference in rate or degree of resolution of gingivitis. The use of standard dentifrice was only partially successful in preventing staining.

Adolescent↗
PubMed1979

The immunopathogenesis of progressive chronic inflammatory periodontal disease.

Natural, humoral and cellular immune mechanisms have all been implicated in the pathogenesis of chronic inflammatory periodontal disease. However, confusion still exists as to the role played by each of these immunological mechanisms. Recently, characterization of the cell types within the progressive lesion has been established, in which four recognizable zones were described. Immediately subjacent to the epithelium lining the periodontal pocket both polymorphonuclear leukocytes (PMN's) and macrophages were seen, while cells deeper in the tissues had the morphological appearance of lymphocytes. The majority of these lymphocytes had a B-cell phenotype although a few T-cells and macrophages were found. On the advancing front of the lesion the cells had the morphological appearance of plasma cells, the majority of which contained IgG. Other cells found in this region had the morphology of plasma cells yet contained no cytoplasmic immunoglobulin, but they did contain substantial amounts of lysosomal enzymes. Similar cells have previously been described in periodontal disease; their frequent association with fibroblasts may suggest that they are important in the pathogenesis. Deposits of IgG and fibrin were found in the fibrous tissue band surrounding the lesion. These results are reviewed and, although the zones described were not anatomically distinct, by describing the lesion in this way it was possible to establish a convenient model to explain the immunopathogenesis of progressive chronic inflammatory periodontal disease. In this respect, progressive chronic inflammatory periodontal disease in man should be considered as a B-cell lesion.

Animals↗
PubMed1979

Conversion of a stable T-cell lesion to a progressive B-cell lesion in the pathogenesis of chronic inflammatory periodontal disease: an hypothesis.

Changes in the host's immunological response or, alternatively, changes in the oral microflora have been implicated as possible mechanisms by which a stable lesion of chronic inflammatory periodontal disease may become a progressive lesion leading to tissue destruction and tooth loss. It has recently been established that the progressive lesion in humans can be unequivocally considered as a B-cell response. Circumstantial evidence exists which suggests that the stable lesion is in fact a T-cell-mediated mechanism. An hypothesis is presented to explain the change from a stable to a progressive state in terms of a shift from a predominantly T-cell lesion to one involving large numbers of B-cells. Mechanisms of this shift in cell populations are considered together with a discussion of possible means of preventing such a shift.

Animals↗
PubMed1977

[Therapy of chronic apical periodontitis in traumatically injuring front teeth with ongoing root growth].

Because of the patient's age and the width of the apical foramen, conventional or surgical root canal fillings are frequently not indicated for the treatment of chronic apical periodontitis in teeth whose roots have not yet fully grown. Therefore resorbable paste fillings are applied either to induce deposition of apical hard substance or to bridge the time until root canal filling is possible. In a comparative clinical and radiological study in 171 young patients, Walkhoff's iodoform paste and calcium hydroxide were examined with regard to their inductive effect on the formation of an apical hard substance barrier.

Adolescent↗