S100, bcl2 and myeloperoxid protein expirations during periodontal inflammation

Abstract

BackgroundPeriodontal inflammation is characterized by injuries in collagen, epithelial, bone tissues. The hypotheses to be tested were relationship between the s100, bcl2 and myeloperoxidase in gingival tissues (MPO does affect the level of s100, bcl2). The object of this study was to investigate of s100 expression, bcl2 expression and myeloperoxidase expression in periodontal inflammation.Methods27 patients (giant-cell epulis) and 30 patients (acute and chronic inflammations) were included in the study for s100 expression, bcl2 expression and myeloperoxidase expression by immunohistochemistry and hematoxylin - eosin.ResultsGiant-cells in epulis positivity for myeloperoxidase has been observed in 100 % However, only 75.31 % of giant-cells were positive for bcl2 expression. Acute 98.2 %, and chronic 89.28 % inflammation was a significant positive for myeloperoxidase. The immunohistochemical findings of s100, bcl 2 and myeloperoxidase in epithelial layers have showed the result of 100 %, 82,2 %, 100 % positive cells in acute and 100 %, 78.25 %, 100 % in chronic process of inflammation respectively.ConclusionThe results indicate that the pathogenesis of periodontal inflammation might involve inhibition of cell death, through the overexpression of bcl-2, due to identifying factors myeloperoxidase (result in the DNA damage by the product of catalysis). The highest levels of s100 activity have been found at sites with chronic inflammation.

Characteristics of cellular composition of periodontal pockets

“…In the future without timely intervention will lead to more severe damage of periodontal tissues, premature loss of teeth, and changes in temporomandibular joints. Results from the previous research indicate the role of periodontal pathological processes in the development of systemic inflammation [ 4–6 ].…”

Body temperature-dependent microRNA expression analysis in rats: rno-miR-374-5p regulates apoptosis in skeletal muscle cells via Mex3B under hypothermia

“…Bcl-2 family proteins regulate apoptosis through protein–protein interactions. Previous reports suggest that overexpression of Bcl‐2 inhibits apoptosis and plays an important role in the development of inflammation-related disorders 33 , 34 . Accordingly, these results suggest activation of a novel rno-miR-374-5p / Mex3B / Kras pathway to elevate cell viability in extreme hypothermia.…”

The RAS‐PI3K‐AKT‐NF‐κB pathway transcriptionally regulates the expression of BCL2 family and IAP family genes and inhibits apoptosis in fibrous epulis

“…Limited studies have been carried out to delineate the pathogenesis of epulis and gingival hyperplasia. Several studies have found that apoptosis inhibition through overexpression of bcl‐2 might play an important role in the development of epulis . Extracellular matrix degradation and remodeling are also important aspects, and matrix metalloproteinases (MMPs) play an important role in periodontal tissue destruction …”

“…that apoptosis inhibition through overexpression of bcl-2 might play an important role in the development of epulis. [7][8][9] Extracellular matrix degradation and remodeling are also important aspects, and matrix metalloproteinases (MMPs) play an important role in periodontal tissue destruction. 10 Systems biology approaches such as whole-genome expression profiling may provide new insights into the molecular mechanisms of fibrous epulis.…”