RUSSELL BODIES DEVELOPMENT IN ASSOCIATION WITH APOPTOTIC CHANGES IN DIABETIC HUMAN GINGIVA

Citation:
Abbass, M. M. S., and R. A. A. Moneim, "RUSSELL BODIES DEVELOPMENT IN ASSOCIATION WITH APOPTOTIC CHANGES IN DIABETIC HUMAN GINGIVA", Egyptian Dental Journal, 2014.

Abstract:

Background: Periodontal disease is considered the sixth major complication of diabetes mellitus. Apoptosis plays a functional role in limiting diabetic repair through diabetes-enhanced caspase-3 activity. The immune system has been shown to play an important role in the initiation and progression of periodontal disease. The fact that diabetics are more susceptible to infections suggests that immunologic capability may be deranged and the inflammatory process is enhanced in term of increased level of immunoglobulins. Russell bodies, an uncommon finding that may be associated with chronic inflammatory conditions. T-cells might promote the formation of Russell bodies (Mott cells) through the release of soluble factors, such as IL-2 which acts in a paracrine fashion to support the survival and function of regulatory T – cells (Tregs).
Methods: The aim of the study was to determine the adaptive apoptotic and inflammatory alterations accompanying diabetes in human gingival. To fulfill this objective, gingival biopsies (one per person) were collected from 10 diabetic patients (Type 2 diabetes mellitus) with periodontitis (Diabetic group) and from 10 donors with no known history of diabetes mellitus or periodontitis (Control group).The sections were examined histologically, immunohistochemically and by the direct immunofluorescence technique.
Results: Histopathological examination of the diabetic gingiva showed the association of Russell bodies with the numerous inflammatory cells detected in the lamina propria. This was further assured by increased reaction for CD138. Also, there was increased immunoreactivity for caspase-3 and IL-2. The histomorphometric analysis data supported the immunohistochemical results as there has been a high significant increase in the area percentage of caspase-3, CD-138 and IL-2 immunoreaction in the gingiva of diabetic group in comparison to the control group. Immunofluorescence labeling revealed increased reaction for IgA and IgM in the inflammatory cells and Russell bodies.
Conclusions: Diabetes enhanced apoptosis results in a cascade of events; starting by inflammation and formation of Mott cells (Russell bodies) in addition to deterioration of the immune system in the form of increased immunoglobulins.