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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.
Background:
Although several studies have discussed some of the molecular and cellular changes associated with hereditary gingival fibromatosis (HGF), its pathogenesis is still largely unclear. This study was directed to detect and outline the degree of relationship between the immunophenotyped macrophages (M2) expressing CD163 and TGF-β1 in patients with gingival overgrowth due to HGF.
Methods:
Biopsies from 20 patients suffering from HGF and 20 normal control subjects were harvested, histologically and immunohistochemically stained then, analyzed and statistically compared and correlated for CD163 immunoexpression and TGF-β1.
Results:
All HGF specimens expressed TGF-β1 by most of the connective tissue fibroblasts, with statistically high significant mean of area % (2.61 ± 0.41) compared to normal controls (0.11 ± 0.06; P = .001). All control specimens revealed negligible CD163 immunostaining of the few inflammatory cells found with a mean area of % (0.69 ± 0.12), while the specimens of HGF cases showed statistically significant higher CD163 expression (3.39 ± 0.75) at (P = .007). A statistically significant higher mean % of M2 cells expressing CD163 in relation to the total number of the inflammatory cells was revealed in HGF (34.46 ± 2.04) compared to the control group (16.36 ± 2.39; P-value ≤ .05). Moderate correlation between CD163 and TGF-β1 was detected in HGF (r = .451; P-value < .05).
Conclusions:
CD163 and TGF-β1 were clearly expressed in HGF cases compared to healthy control patients, with significant correlation. In HGF, the increase in CD 163-positive cells was specific and not dependent on the chronic gingival inflammation.
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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