Abstract
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.
Highlights
Chronic periodontitis (CP) [1] is the most frequent form of periodontitis [2,3]
Factor XIIIa+ immature dendritic cells (DC) could be observed only in the LP (Figure 2A and 2D); CD1a+ immature DCs could only be observed in the oral epithelium (OE), sulcular epithelium (SE), and LP (Figure. 2B, 2E and 2F); while CD83+ mature DCs could be observed in the OE and LP regions (Figure 2C, 2G, 2H)
Prior reports have shown that, in regions such as the lymph nodes, spleen, and liver, where DCs are continually exposed to potential antigens, IL-6 avoids a state of perpetual inflammation and protects central immune organs from overstimulation [34,35]
Summary
Chronic periodontitis (CP) [1] is the most frequent form of periodontitis [2,3]. The bacterial biofilm is required, but not sufficient, for disease initiation. The host inflammatory immune reaction begins when the recognition of the bacterial pathogens occurs by means of antigen-presenting cells, such as dendritic cells (DCs) [7]. Myeloid DCs, known as conventional DCs, present a strong capability of capturing antigens, which enables them to stimulate T cells [8]. In this context, in CP, DC activation occurs after coming into contact with lipopolysaccharide (LPS) [9,10] or immune complexes [11] produced by periodontal pathogens [12,13]. These DCs become mature, express costimulatory molecules, and produce distinct cytokine patterns, such a INF- and IL-17, which will determine the selective migration of CD4 T-helper subsets and the subsequent production of characteristic cytokines [7,11]
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