BACKGROUND: Previous literature showed contrasting results regarding dendritic cell (DC) counts in patients with periodontal diseases. Although smoking decreases the number of DCs in the lungs, the effect of smoking on the quantitative distribution of Langerhans cells (LCs) and DCs in patients with chronic gingivitis has not been investigated to our knowledge. METHODS: Gingival samples were obtained from 30 patients (15 smokers and 15 non-smokers). Immunohistochemical staining was performed to identify CD1a+ immature LCs and CD83+ mature DCs. The inflammatory infiltrate was evaluated and counted. Densities of cells were calculated within the oral epithelium (OE), sulcular epithelium (SE), and lamina propria (LP) for CD1a+ cells and within the LP for CD83+ cells. Results were compared between groups. This study evaluates whether the high number of cigarettes and smoking years affects densities of cells. Correlations among densities of LCs and DCs with densities of inflammatory infiltrate, number of cigarettes, and smoking years were performed. RESULTS: Densities of inflammatory infiltrate and CD1a+ cells from the SE and LP were significantly lower for smokers than for non-smokers (P <0.05). This result could not be identified for CD1a+ cells from the OE and for CD83+ cells from the LP. The number of cigarettes and smoking years did not affect densities of cells. No statistically significant correlations could be drawn among densities of LCs and DCs and inflammatory infiltrate, number of cigarettes, and smoking years. CONCLUSION: Smoking proved to affect the quantitative distribution of LCs and DCs in patients with chronic gingivitis.
BACKGROUND: Previous literature showed contrasting results regarding dendritic cell (DC) counts in patients with periodontal diseases. Although smoking decreases the number of DCs in the lungs, the effect of smoking on the quantitative distribution of Langerhans cells (LCs) and DCs in patients with chronic gingivitis has not been investigated to our knowledge. METHODS: Gingival samples were obtained from 30 patients (15 smokers and 15 non-smokers). Immunohistochemical staining was performed to identify CD1a+ immature LCs and CD83+ mature DCs. The inflammatory infiltrate was evaluated and counted. Densities of cells were calculated within the oral epithelium (OE), sulcular epithelium (SE), and lamina propria (LP) for CD1a+ cells and within the LP for CD83+ cells. Results were compared between groups. This study evaluates whether the high number of cigarettes and smoking years affects densities of cells. Correlations among densities of LCs and DCs with densities of inflammatory infiltrate, number of cigarettes, and smoking years were performed. RESULTS: Densities of inflammatory infiltrate and CD1a+ cells from the SE and LP were significantly lower for smokers than for non-smokers (P <0.05). This result could not be identified for CD1a+ cells from the OE and for CD83+ cells from the LP. The number of cigarettes and smoking years did not affect densities of cells. No statistically significant correlations could be drawn among densities of LCs and DCs and inflammatory infiltrate, number of cigarettes, and smoking years. CONCLUSION: Smoking proved to affect the quantitative distribution of LCs and DCs in patients with chronic gingivitis.