Abstract
BackgroundApoptosis, 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)MethodsEight 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 immunohistochemistryResultsThere 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.ConclusionThe higher frequency of Bcl-2 expression in GAP group indicates and delayed apoptosis can lead to increasing resident inflammatory cells in periodontal tissues and resulting in progressive periodontal destruction.
Highlights
Apoptosis, or programmed cell death is a form of physiological cell death
The local host response to aa includes the recruitment of neutrophils and the subsequent release of inflammatory mediators and cytokines, which appear to play an important role in the pathogenesis of periodontal disease
Based on a direct effect of bacteria in cell cultures, it has been suggested that apoptosis might play an important role in periodontitis
Summary
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. Inflammatory periodontal diseases are characterized as local and peripheral infection involving multiple species of gram-negative organisms. The local host response to aa includes the recruitment of neutrophils and the subsequent release of inflammatory mediators and cytokines, which appear to play an important role in the pathogenesis of periodontal disease. The mechanisms responsible for gingival tissue damage are poorly understood, and both immune-mediated reactions and direct cytopathic effects of bacteria may be involved. Based on a direct effect of bacteria in cell cultures, it has been suggested that apoptosis might play an important role in periodontitis. The nature of molecular mechanisms participating in this process remain unknown (page number not for citation purposes)
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