Expression of caspase-3, p53 and Bcl-2 in generalized aggressive periodontitis

<p>Abstract</p> <p>Background</p> <p>Apoptosis, or programmed cell death is a form of physiological cell death. It is increased or decreased in the presence of infection, inflammation or tissue remodelling. Previous studies suggest that apoptosis is involved in the path...

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Bibliographic Details
Main Authors: Özdemir B Handan, Uslu Hilal, Bulut Şule, Bulut Ömer
Format: Article
Language:English
Published: BMC 2006-06-01
Series:Head & Face Medicine
Online Access:http://www.head-face-med.com/content/2/1/17
Description
Summary:<p>Abstract</p> <p>Background</p> <p>Apoptosis, or programmed cell death is a form of physiological cell death. It is increased or decreased in the presence of infection, inflammation or tissue remodelling. Previous studies suggest that apoptosis is involved in the pathogenesis of inflammatory periodontal disease. The aim of the present study was to investigate the clinical features and known indicators of apoptosis (p53, Bcl-2, Caspase-3) in patients with generalized aggressive periodontitis (GAP)</p> <p>Methods</p> <p>Eight patients with GAP, who had sites with probing depths (PD) > 5 mm, and 10 periodontally-healthy persons were included in the study. Clinical examinations and PD were performed, and the plaque index and gingival index were recorded. Gingival tissues biopsies were obtained from active site of each patient and from healthy individuals. The expression of caspase-3, Bcl-2, and p53 was evaluated by immunohistochemistry</p> <p>Results</p> <p>There were no significant differences between GAP and control group with respect to levels of caspase-3 and p53 expression (P > 0.05). Contrary, the frequency of grade 3 expression of Bcl-2 was higher in GAP group than the control group.</p> <p>Conclusion</p> <p>The higher frequency of <it>Bcl-2 </it>expression in GAP group indicates and delayed apoptosis can lead to increasing resident inflammatory cells in periodontal tissues and resulting in progressive periodontal destruction.</p>
ISSN:1746-160X