Thereare very few facts from which to develop cogent conceptsabout pathogenesis of periodontal disease and the role ofthe host, making it very difficult to make predictions todayas to which host factors may be useful in diagnosis.These, and as yet undescribed factorswhich play a key role in resolution of inflammation and healing, may be valuable indicators of periodontal disease in remission, or of subjects who are resistant to periodontal disease.Finally, due to an improved understanding of the pathogenesis of periodontal diseases, an additional approach to therapy with respect to modulation of host response has received attention.The future will see a range of host response modulators developed as adjunctive treatments for periodontitis. ![]() Our understanding of host responsesin periodontal disease is at a very early level. Many of the concepts presentedare already being challenged and will likely be changedwith more information. However, there may be considerable loss ofthe alveolar bone and connective tissue supporting the teeth.Concepts have been presented based on recent developmentsin immunobiology, but this is only a current pictureof a rapidly-developing field. Usually survives and the infection is controlled. However, further large-scale studies on both genders are recommended to confirm their role as prognostic markers. Conclusion: As Pentraxin-3 is more positively correlated with clinical parameters of chronic periodontitis than tumor necrosis factor-α, it could be a better diagnostic and prognostic marker for the disease. Positive correlations between the mean values of both markers levels, and clinical parameters were found whereas, Pentraxin-3 was more positively correlated. Furthermore, these levels were reduced after treatment with a highly statistically significant difference. Mean Pentraxin-3 and tumor necrosis factor-α levels were higher in chronic periodontitis patients than in the control group with a significant difference between both groups. Results: The mean values of periodontal parameters were significantly reduced after treatment. ![]() Differences between both groups regarding clinical parameters and tested biomarkers were assessed and correlations between them were calculated. Methods: Pentraxin-3 and tumor necrosis factor-α levels were measured by Enzyme-Linked Immunosorbent Assay for Gingival Crevicular Fluid samples of 53 chronic periodontitis patients before and after periodontal treatment as well as from 50periodontally healthy subjects as a control group. ![]() The Aim: Investigating the role of Pentraxin-3 in comparison to tumor necrosis factor-α as a diagnostic and prognostic marker for chronic periodontitis. No differences were detected between the aforementioned conditions regarding the density of the T and B lymphocytes and to the number of the dendritic cells. ![]() The density of macrophages was greater in CG and the level of cellular activation of the lymphocyte infiltrate was greater in CP. However, significant differences (p<0.05) were found between the groups in the density of CD25+ and CD68+ cells. The statistical analysis showed no significant differences (p>0.05) between CG and CP regarding the density of the CD4+ and CD20+ cells and the number of S-100+ cells. The S-100+ cells were identified in the epithelium and the lamina propria, exhibiting distinct morphology and number. CD20+ cell distribution was predominantly in groups and the CD25+ cells exhibited a diffuse or focal distribution. The CD4+ and CD68+ cells exhibited a diffuse distribution in the connective tissue. In order to contribute to the knowledge of the pathogenesis of periodontal disease, an immunohistochemical analysis of the density of inflammatory mononucleated cells and the number of dendritic cells was performed using anti-CD4, anti-CD20, anti-CD25, anti-CD68 and anti-protein S-100 antibodies in 17 cases of chronic gingivitis (CG) and 25 of chronic periodontitis (CP).
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