Severity Of Periodontal Destruction Research Articles

Comparative analysis of GCF β-glucuronidase level in diabetic and nondiabetic patients with chronic periodontitis: A clinicobiochemical study

Recent evidences prove that, release of potent lysosomal enzymes e.g. β-Glucuronidase by degranulation of polymorponuclear leukocytes in host gingiva may contribute significantly to tissue destruction and the pathogenesis of periodontal disease. The purpose of the present study was to compare and correlate GCF β-Glucuronidase with periodontal status among diabetic and non-diabetic patients with chronic periodontitis. A total number of 75 patients were equally divided into Group I (control group), Group II (non diabetic with chronic periodontitis) and Group III (diabetic with chronic periodontitis). Clinical parameters like Plaque index, Gingival index, Probing Pocket Depth and RBS were recorded. The β-Glucuronidase level in GCF of all three groups was determined by spectrophotometric analysis. It was observed that the periodontitis patients irrespective of their diabetic status, showed increased periodontal destruction with elevated level of β-Glucuronidase than the controls. Also, the diabetic patients showed increased severity of periodontal destruction and the elevated level of β-Glucuronidase, thus indicating diabetics at a higher risk for progressive periodontal destruction.

Human β defensin‐1 and ‐2 expression in the gingiva of patients with specific periodontal diseases

beta defensin antimicrobial peptides are important in epithelial innate immunity, and their differential expression is associated with periodontal diseases. The aims of this study were to determine the mRNA expression of human beta defensin-1 and -2 in the gingival tissue of patients with gingivitis, aggressive periodontitis and chronic periodontitis, and to evaluate the relationship between defensin expression and type and/or severity of periodontal destruction. Fifteen patients in each group with gingivitis, aggressive periodontitis and chronic periodontitis, and 10 healthy subjects, were included in the study (n=55). The periodontal status of the subjects was determined by periodontal clinical measurements and radiographical evaluations. Transcriptional levels of human beta defensin-1 and -2 genes in gingival samples were assessed by using the quantitative real-time polymerase chain reaction technique, and the data were evaluated statistically by the relative expression Software Tool 2 for groupwise comparisons. Expression of the human beta defensin-1 gene was lower in gingivitis and aggressive periodontitis groups, and significantly higher in the chronic periodontitis group, than in the control group (p<0.001). Human beta defensin-2 mRNA expression in the gingivitis group was lower than in the control group; however, the difference was statistically significant only in half of the gingivitis patients (p<0.001). Human beta defensin-2 mRNA levels were higher in some chronic periodontitis patients, but lower in the others when compared with the control group (p<0.001). Expression of the human beta defensin-2 gene increased in the aggressive periodontitis group relative to the control group. This study suggests that human beta defensin-1 and -2 genes in the gingival epithelium show differential expression in patients with specific periodontal diseases, and aggressive and chronic periodontitis types demonstrate different gingival beta defensin-1 and -2 expression patterns.

IL-1 gene polymorphisms in Korean periodontitis patients

The primary cause for developing periodontitis is bacteria, but host factors such as diabetes, smoking, and genetics could contribute to the clinical appearance as well as the extent and severity of periodontal destruction. The host inflammatory response to the bacterial challenge is one of the factors contributing to the destruction of periodontal tissue1,2). The role of proinflammatory cytokines has been studied extensively in periodontal diseases. Involvement of interleukin-1 (IL-1) in the pathogenesis of periodontal disease has been suspected because of association between the known biological effects of the cytokine and the manifestations of the disease. IL-1 level has been reported to be elevated in inflamed periodontal tissues and gingival crevicular fluid associated with periodontitis3,4). Masada et al.3) reported that IL-1 might serve as a marker of periodontal tissue destruction because IL1 was produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 enables ingress of inflammatory cells into sites of infection; stimulates eicosanoid release by monocytes and fibroblasts; stimulates matrix metralloproteinases; and contributes to the inflammatory cascade of the microbial immune response5,6). Proinflammatory cytokine IL-1 exists in 2 forms, IL1α, and IL-1β. There are 3 genes that regulate the production of IL-1 variants: IL-1A, IL-1B, and IL-1 receptor antagonist (IL-1 RN)7). These genes are located close to each other on chromosome 2q13. Genes IL-1A and IL-1B control the production of proinflammatory proteins, IL-1αand IL-1β, respectively. IL-1 RN controls the synthesis of an antagonist protein (IL-ra) that impedes IL-1αand IL-1β8,9). The specific forms alleles of each IL-1A and IL-1B gene present in an individual vary. The term “genetic polymorphism”refers to a change in the sequence

Analysis of the relationship between the severity of periodontal destruction and proteoglycan metabolism of gingiva and gingival crevicular fluid

Although it is well-described that proteoglycans (PGs) are among the major non-collagenous components of the matrix which are degraded during periodontal diseases, the relationship between PG metabolism and seventy of periodontal breakdown, the extent of degradation of PGs together with the resulting end-products, and the elimination pathways of these catabolic end-products is likely to need further clarification. The main aim of the present study was to analyze the possible impact of severity of periodontal destruction on PG metabolism of gingiva and gingival crevicular fluid (GCF). For this purpose, gingiva and GCF samples obtained from patients (n = 45) exhibiting sites (n = 57) with moderate periodontal breakdown (MP) or severe periodontal breakdown (SP) were analyzed for PG metabolism via spectrophotometric determination of uronic acid levels. Gingiva and GCF samples were obtained from the same sites in every patient to analyze the possible relationship between uronic acid content of gingival tissue and GCF. No significant differences were found in uronic acid levels between sites with MP and SP (p > 0.05). The uronic acid content of GCF and gingiva showed significant overlaps between MP and SP sites and uronic acid levels did not present any constant correlation with the clinical parameters (p > 0.05). In a similar manner, uronic acid content of GCF and gingival tissue was not correlated (p > 0.05). The lack of a significant correlation between the uronic acid content of gingival tissue and GCF may suggest that the passage of PG metabolites from gingiva to GCF is likely to be under the influence of multifactorial interactions rather than being linear. As a general measure of PG metabolism, uronic acid levels do not seem to be related with the severity of periodontal destruction and tend to act as different measures when compared to traditional clinical parameters.

Prevalence and severity of periodontal disease at mandibular molar teeth in smokers with regular oral hygiene habits.

Smoking appears to be detrimental to health because it has been associated with several diseases including cancer and cardiovascular diseases. Smoking also appears to be a major environmental factor associated with periodontal disease progression. The objective of this study was to evaluate the prevalence and severity of periodontal destruction as influenced by smoking in a Thai population. Gingival health and periodontal conditions at mandibular molar furcation sites in 120 Thai dental patients (60 smokers and 60 never-smokers, age range 31 to 60 years) with generally high oral hygiene standards and regular dental care habits were evaluated. Smokers exhibited more frequent and severe mandibular molar periodontal destruction than never-smokers. The prevalence and severity of gingival recession, periodontal pocket formation, clinical attachment loss, furcation involvement, and tooth mobility were significantly increased in smokers compared to never-smokers. Seventy-three percent of the smokers exhibited furcation involvement in contrast to only 20% of the never-smokers. The results of this study suggest that smoking appears to be a major environmental factor associated with accelerated periodontal destruction in adult smokers with generally high oral hygiene standards and regular dental care habits in a Thai population.

Smoking cessation strategies and periodontal disease in young adults.

Previous studies have related tobacco consumption to an increased prevalence, extent and severity of periodontal destruction and to a poorer response to therapy.

Periodontal manifestations of systemic disease.

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.

The periodontal status of irregular dental attenders

The aim of this investigation was to assess the prevalence and severity of periodontal destruction in irregular dental attenders. 50 subjects aged between 20 and 49 years completed a questionnaire and had a periodontal examination. Measurements of plaque, calculus, bleeding, probing depth and clinical attachment level were made at 4 proximal sites per tooth. Results were compared to those for 132 regular attenders. The irregular attenders had more sites with plaque (46.3 +/- 27% versus 17.3 +/- 21.1%) than the regulars and significantly more sites which bled (53.7 +/- 20.4% versus 33.6 +/- 20.7%) and with calculus (35 +/- 21.1% versus 13.4 +/- 12.8%). However, the irregulars had virtually the same number of teeth as the regular attenders, 25.6 +/- 3.3 compared with 25.4 +/- 4.3. Irregular attenders had slightly deeper mean probing depths (2.9 +/- 0.4 versus 2.7 +/- 0.4 mm) but the prevalence and extent of attachment loss was no different between the groups. It was concluded that the prevalence and severity of destructive periodontal disease as indicated by periodontal attachment loss was not related to the regularity of dental attendance in the groups studied.

The periodontal condition of regular dental attenders in Northern Ireland.

The aim of this study was to assess the prevalence and severity of periodontal destruction in regular dental attenders in Northern Ireland. 132 individuals aged between 20 and 49 years who had recently had a course of routine treatment in the General Dental Service completed a questionnaire and had a periodontal examination. Measurements of plaque, subgingival calculus, bleeding, probing pocket depth and periodontal attachment level were made at 4 proximal sites per tooth. Plaque was present at an average of 17%, subgingival calculus at 13%, and bleeding on probing at 34% of interproximal surfaces examined. The mean probing pocket depth was 2.7 mm and the mean probing attachment level was 1.0 mm. Incipient periodontal destruction was common with all subjects having at least 1 pocket of greater than or equal to 3 mm and 90% having at least 1 site with greater than or equal to 2 mm attachment loss. Only 24 (18%) of those examined had deep pocketing or severe loss of periodontal attachment (greater than or equal to 6 mm). The extent of deep pocketing and severe attachment loss was low at only 0.2% and 0.6%, respectively, of the sites examined. It was concluded that gingivitis and incipient periodontitis were prevalent and extensive in the regular dental attenders investigated, but that severe periodontal destruction was uncommon.

Evaluation of a radiographic partial recording system assessing the extent and severity of periodontal destruction

The purpose of the present study was to evaluate the validity and reliability of a partial radiographic bivariate index system (PESI-2). The principles of the index were applied to data from a random sample of 192 industrial employees aged 30-65 yr. Estimates of Extent and Severity of radiographic bone loss provided by the PESI-2, as well as adjusted estimates by means of simple regression models, were compared to values obtained by a full mouth radiographic examination. It was shown that the values provided by the PESI-2 were of rather high validity and reliability. The use of the adjusting models resulted in increased validity of the severity estimates and enhanced reliability of both components of the bivariate. The results verified the applicability of the PESI-2 in epidemiologic research of destructive periodontal disease.