Expression of CD163 in hereditary gingival fibromatosis: A possible association with TGF-β1

Hala H Hazzaa1,2, Ossama M Gouda2,3,4, Naglaa M Kamal5

  • 1Department of Oral Medicine, Diagnosis and Periodontology, Faculty of Dentistry, Al Azhar University (Girls Branch), Cairo, Egypt.

Abstract

Insights

Hereditary gingival fibromatosis (HGF) involves increased CD163-positive M2 macrophages and TGF-β1. These markers correlate moderately, suggesting a specific role in HGF pathogenesis beyond general inflammation.

Area of Science:

  • Oral pathology
  • Immunohistochemistry
  • Molecular biology

Background:

  • Hereditary gingival fibromatosis (HGF) pathogenesis remains unclear despite known molecular and cellular changes.
  • This study investigates the relationship between M2 macrophages (CD163+) and TGF-β1 in HGF-induced gingival overgrowth.

Purpose of the Study:

  • To detect and outline the relationship between CD163-expressing macrophages and TGF-β1 in HGF patients.
  • To compare these markers in HGF patients versus healthy controls.

Main Methods:

  • Histological and immunohistochemical analysis of gingival biopsies from 20 HGF patients and 20 controls.
  • Statistical comparison and correlation of CD163 immunoexpression and TGF-β1 levels.

Main Results:

  • Significantly higher TGF-β1 expression in HGF fibroblasts (2.61±0.41) vs. controls (0.11±0.06).
  • Significantly higher CD163 expression on inflammatory cells in HGF (3.39±0.75) vs. controls (0.69±0.12).
  • Increased M2 macrophages (CD163+) in HGF (34.46±2.04%) compared to controls (16.36±2.39%), with moderate correlation (r=0.451) between CD163 and TGF-β1.

Conclusions:

  • CD163 and TGF-β1 are significantly expressed in HGF cases compared to controls.
  • The increase in CD163-positive cells in HGF is specific and not solely due to chronic inflammation.

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