Immunocytochemical indicators of apoptosis in gingival tissues of patients with chronic periodontitis

Aldona Kasprzak; Miłosz Hausmann; Agata Małkowska-Lanzafame; Joanna Surdyk-Zasada; Wiesława Przybyszewska; Elżbieta Siodła; Anna Surdacka

doi:10.20883/medical.e42

Authors

Aldona Kasprzak Chair and Department of Histology and Embryology, Poznan University of Medical Sciences, Poland
Miłosz Hausmann Chair and Department of Histology and Embryology, Poznan University of Medical Sciences, Poland
Agata Małkowska-Lanzafame Department and Clinics of Conservative Dentistry and Periodontology, Poznan University of Medical Sciences, Poland
Joanna Surdyk-Zasada Chair and Department of Histology and Embryology, Poznan University of Medical Sciences, Poland
Wiesława Przybyszewska Chair and Department of Histology and Embryology, Poznan University of Medical Sciences, Poland
Elżbieta Siodła Chair and Department of Histology and Embryology, Poznan University of Medical Sciences, Poland
Anna Surdacka Department and Clinics of Conservative Dentistry and Periodontology, Poznan University of Medical Sciences, Poland

DOI:

https://doi.org/10.20883/medical.e42

Keywords:

chronic periodontitis, apoptosis, immunocytochemistry

Abstract

Introduction. Inflammatory mechanisms of chronic periodontitis (CP) may be linked to various forms of disturbances in apoptosis.
Aim. The study aimed at comparison of tissue expression of anti-apoptotic protein (Bcl-2) and proapoptotic proteins (p53, caspase-3) in gingival tissues of 30 patients with CP and of 15 with healthy periodontium.
Material and methods. Gingival samples (n = 68) were obtained during the open curettage procedure with gingivectomy of adult patients (18 women and 12 men) with CP. Classical immunocytochemical (IHC) method was used to detect apoptotic proteins, and the obtained expression was evaluated using semi-quantitative IRS scale.
Results. No differences could be revealed in expression intensity or reciprocal correlations between apoptotic proteins within the group of patients with CP. Greater expression of the two apoptotic proteins (Bcl-2 and p53) were detected in patients with CP than in control individuals. Moreover, a more pronounced expression of Bcl-2 was demonstrated in gingival samples of patients with localised form as compared to generalised form of CP. Expression of caspase-3 (effector phase of apoptosis) manifested no differences between CP and control individuals. Greater expression of the anti-apoptotic protein Bcl-2 and caspase-3 was detected in cells of inflammatory infiltrates in lamina propria than in keratinocytes.
Conclusions. In CP significant alterations developed in expression of indicators of apoptosis, with prevalence of Bcl-2 and p53 expression, as compared to the control. The localised form of CP was linked to higher proportion of Bcl-2-positive cells of inflammatory infiltrates, suggesting that apoptosis was inhibited mainly in this form of CP. The comparable expression of caspase-3 in gingival cells with CP and in control and absence of correlation with clinical data suggested that the process of apoptosis did not play a significant role in destruction of periodontium tissues in CP.

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