Hala H Hazzaa1,2, Ossama M Gouda2,3,4, Naglaa M Kamal5, Shereen Abdel Moula Ali6, Marwa A M El Shiekh7, Marwa M Tawfik8. 1. Department of Oral Medicine, Diagnosis and Periodontology, Faculty of Dentistry, Al Azhar University (Girls Branch), Cairo, Egypt. 2. Department of Oral Medicine, Diagnosis and Periodontology, Faculty of Dentistry, Nahda University, Beni-Suef, Egypt. 3. Department of Oral Medicine, Diagnosis and Periodontology, Faculty of Dentistry, Suez Canal University, Ismailea, Egypt. 4. Nahda University, Beni-Suef, Egypt. 5. Department of Oral Patholology, Faculty of Oral and Dental Medicine, Ahram Canadian University, 6th of October, Egypt. 6. Department of Oral Medicine and Periodontology, Faculty of Dentistry, Tanta University, Tanta, Egypt. 7. Department of Oral Biology, Faculty of Dentistry, Al Azhar University (Girls Branch), Cairo, Egypt. 8. Department of Oral Medicine and Periodontology, Faculty of Dentistry, Beni-Suef University, Beni-Suef, Egypt.
Abstract
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.
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.