Giovanna Ribeiro Souto

Effect of Smoking on Langerhans and Dendritic Cells 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.

Tobacco use increase the number of aneuploid nuclei in the clinically healthy oral epithelium.

BACKGROUND The most important risk factor linked to the development of oral leukoplakia (OL) and oral squamous cell carcinoma (OSCC) is tobacco use. Tobacco contains carcinogens that influence the DNA repair, cell cycle control and may produce chromosomal aberrations. The loss or acquisition of one or more chromosomes is defined as aneuploidy. METHODS Aneuploidy was determined by means of the DNA-content included in cells obtained by exfoliative cytology and Feulgens staining. The cells were collected from the clinically healthy lateral margin of the tongue of non-smokers without oral lesions, smokers without oral lesions, smokers with OL, and smokers with OSCC, using the CytoBrush(®). Each group was composed of 20 individuals. A Carl Zeiss image analyzer system and the KS300 software were used. Statistical analysis was performed with BioEstat(®) software. RESULTS The mean percentage of aneuploid nuclei was statistically higher in the smokers (79.65%), smokers with OL (68.4%), and smokers with OSCC (93.65%), as compared to non-smokers (39.3%) (P<0.05). A trend toward an increase in the aneuploidy of the smokers with OSCC group (P=0.02), as compared to the non-smoker group, could be observed. No significant difference could be observed as regards the mean percentage of aneuploid nuclei in relation to duration of tobacco use or the number of the cigarettes smoked. CONCLUSIONS Tobacco use is responsible for an increased number of aneuploid nuclei in the oral epithelium.

Effect of smoking on immunity in human chronic periodontitis.

AIM Evaluate the effects of smoking on dendritic cells (DCs), cytokines, clinical periodontal parameters, and number of teeth in samples of human chronic periodontitis (CP). MATERIAL AND METHODS Gingival samples were obtained from 24 smokers and 21 non-smokers with CP. Periodontal examination was carried out. Immunohistochemical staining was performed to identify Factor XIIIa+ immature, CD1a+ immature, and CD83+ mature DCs. The inflammatory infiltrate was counted, and IL-2, IL-10, IL-4, IL-6, IFN-γ, TNF-α, and IL-17A were measured using the cytometric bead array (CBA). Inflammatory infiltrate, DCs, cytokines, classification of CP, clinical periodontal parameters, number of teeth, smoking habit in years (SH/years), and number of cigarettes smoked per day (C/day) were correlated and compared. RESULTS CD83+ mature DCs decreased in the smokers group. Negative correlations could be observed between the number of C/day with levels of IL-17A and number of teeth. Correlations between smoking, periodontal disease status, and other cytokines were not observed. CONCLUSIONS Smoking decreases mature DCs in chronic periodontitis. Moreover, a dose-dependent relation can be observed between C/day and number of teeth and levels of IL17A observed. Smokers show a different modulation of the CP immune response.

Pro-inflammatory, Th1, Th2, Th17 Cytokines and Dendritic Cells: A Cross-sectional Study in Chronic Periodontitis

There are a limited number of studies correlating the different stages of dendritic cells (DC) maturation with cytokines in individuals presented chronic periodontitis (CP). The aim of the study was to evaluate the correlation among the expression of IL-2, IL-10, IL-4, IL-6, IFN-, TNF-α, and IL-17A with the presence of DC and mild-moderate or advanced CP. Gingival samples were obtained from 24 individuals with CP and six samples of normal mucosa (NM) overlapping third molar for controls of the levels of cytokines. Periodontal examination was performed. Immunohistochemical staining was carried out, revealing CD1a+ immature, Fator XIIIa+ immature, and CD83+ mature DCs. The inflammatory infiltrate was counted, and the cytokines were measured by flow cytometry. Densities of DCs and inflammatory infiltrate, cytokines, subtypes of CP, and clinical periodontal parameters were correlated and compared. IL-6 expression was correlated positively with the increased numbers of CD1a+ immature DCs. Levels of IL-2, TNF-α, IFN-, IL-10, and IL-17A were increased when compared with NM. The percentage of sites with clinical attachment level (CAL)>3 were positively correlated with densities of inflammatory infiltrate and negatively correlated with densities of immature DCs. IL-6 can contribute to the increase of the immature DCs in the CP. Higher levels of IL-2, TNF-α, IFN-, IL-10, and IL-17A cytokines were observed in CP. Higher densities of inflammatory infiltrate as well as lower densities of immature DCs can result in a more severe degree of human CP.

Smoking effect on chemokines of the human chronic periodontitis.

AIM Evaluate the effects of smoking on chemokines of the human chronic periodontitis (CP). MATERIALS AND METHODS Gingival samples were obtained from 23 smokers (S) and 20 non-smokers (NS) diagnosed with CP. Periodontal examination was performed. The CCL2, CCL3, CCL5, CCL19, CCL20, and CXCL8 chemokine levels were measured in gingival tissues using enzyme-linked immunosorbent assay. Chemokines were compared between S and NS, and were correlated with the number of cigarettes per day (C/day) and time of the smoking habit in years (SH/years). RESULTS CCL3 and CXCL8 of S were significantly smaller than that found in NS subjects, whereas the CCL5 levels increased in the S group. Negative correlations could be observed between CCL19 levels and SH/year. CONCLUSION Smoking suppresses the immune response which may contribute to an increased susceptibility to periodontal disease in smokers.

Morphometric evaluation of keratocystic odontogenic tumor before and after marsupialization

The aim of the present study was the morphometric evaluation of the epithelial lining and fibrous capsule in histological specimens of keratocystic odontogenic tumors (KOTs) before and after marsupialization. Histological sections from six KOTs that had undergone marsupialization followed by enucleation were photographed. The thickness and features of the capsule and of the epithelial lining of the tumor were evaluated upon marsupialization and upon subsequent enucleation using Axion Vision software. The histological specimens taken upon marsupialization presented an epithelial lining that is typical of KOTs. After marsupialization, the enucleated specimens had a modified epithelial lining and a fibrous capsule that both presented a greater median thickness (p = 0.0277 and p = 0.0212, respectively), morphological changes, and significant enlargement. These modifications can facilitate full surgical treatment and may well be related to a low KOT recurrence rate.

Relationship Between Chemokines and Dendritic Cells in Human Chronic Periodontitis

BACKGROUND The purpose of this study was to evaluate the relationship between chemokines and dendritic cells (DCs) in human chronic periodontitis (CP). METHODS Gingival samples were obtained from 23 individuals with CP, and six samples of normal mucosa (NM) overlapping the third molar were used to control for the chemokine levels. Periodontal examination was conducted. Immunohistochemistry was performed for Factor XIIIa(+) and cluster of differentiation (CD)1a(+) immature DCs and CD83(+) mature DCs. Levels of the CC chemokine ligand (CCL)2, CCL3, CCL5, CCL19, CCL20, and CXC chemokine ligand (CXCL)8 were measured in gingival tissues using enzyme-linked immunosorbent assay. Inflammatory infiltrate, DCs, chemokines, classification of human CP, and clinical parameters were correlated and compared. RESULTS The expression of CCL2 and CCL20 was positively correlated with increased densities of CD1a(+) DCs. CCL3 and CXCL8 were positively related to the clinical attachment level. CCL3, CCL5, CCL19, and CXCL8 levels increased in the gingival samples of patients with CP compared with NM, whereas CCL20 levels increased in advanced CP compared with mild-moderate CP. CONCLUSIONS More CD1a(+) immature DCs are related to CCL2 and CCL20. CCL3 and CXCL8 chemokines are related to a greater severity of human CP.

Solitary fibrous tumor of the parotid gland: case report

Solitary fibrous tumor (SFT) is a rare spindle cell neoplasm that usually develops in the pleura and peritoneum. The head and neck region is involved in only 6% of the cases. Involvement of the parotid gland is a rare phenomenon, with only 24 cases reported in the literature. The aim of this study is to report an additional case of SFT affecting the parotid gland, and to review the literature on previously reported cases. The patient was a 42-year-old male with a 4-cm, fibro-elastic, movable, painless nodule in the inferior lobe of the parotid gland. The lesion was surgically excised and, following histopathological and immunohistochemical analysis, a diagnosis of SFT was rendered. The patient has been followed-up for ten months, with no signs of recurrence. Clinical, histopathological, immunohistochemical and treatment aspects of the tumor are discussed. Key words:Solitary fibrous tumor, parotid gland, case report.

Lesão liquenóide oral relacionada ao amálgama

Amalgam-related oral lichenoid lesion, a rare disorder in dental practice, is an important differential diagnosis among oral leukoplastic lesions. We report two cases with rapid clinical resolution following the replacement of amalgam fillings.

Metallothionein immunoexpression in selected benign epithelial odontogenic tumors.

BACKGROUND Odontogenic tumors exhibited variable biologica behaviors. Metallothionein (MT) is correlated with the cellular homeostasis of essential metals, cellular differentiation, and proliferation. The core goals of this study are (i) to report and to compare MT expression among benign epithelial odontogenic tumors; (ii) to correlate MT with cellular proliferation index; and (iii) to evaluate the influence of the inflammatory infiltrate on MT expression. MATERIALS AND METHODS Ten cases of solid ameloblastomas (SABs), 4 squamous odontogenic tumors (SOTs), 5 adenomatoid odontogenic tumors (AOTs), and 3 calcifying epithelial odontogenic tumors (CEOTs) were subjected to immunohistochemical to anti-MT, anti-Ki-67, and anti-PCNA. Statistical analysis was performed using BioEstat(®) 4.0. RESULTS Metallothionein staining was found to be the highest in the SABs (93.1%), followed by SOTs (52.9%), AOTs (38.4%), and CEOTs (0%). MT staining exhibited statistically significant differences between the SABs and the SOTs (P = 0.0047) and the AOTs (P = 0.0022). A weak-to-strong positive correlation between IMT and IK or IP was observed in SABs and SOTs, whereas a strong negative correlation was observed in AOTs. No differences in IMT, IK, and IP were observed between inflammation groups A and B. CONCLUSIONS The increased MT expression observed in the SABs might be correlated with clinical behavior (local invasiveness and high rate of recurrence). In the SABs and SOTs, MT plays a role in the stimulation of cellular proliferation. In contrast, MT can inhibit cellular proliferation in the AOT. The IMT, IK, and IP are not affected by inflammation.