Anjana, R., Joseph, L. & Suresh, R. Immunohistochemical localization of CD1a and S100 in gingival tissues of healthy and chronic periodontitis subjects. Oral Dis. 18, 778-785
Department of Periodontology, Faculty of Dental Sciences, Sri Ramachandra University, Chennai Department of General Pathology, Sri Ramachandra Medical College, Sri Ramachandra University, Chennai, India. Oral Diseases
(Impact Factor: 2.43).
05/2012; 18(8):778-85. DOI: 10.1111/j.1601-0825.2012.01945.x
The aim of this study was to evaluate the presence and distribution of CD1a and S100 protein markers in states of gingival health and chronic periodontitis in human subjects.
Materials and methods:
Gingival tissue samples were derived from 10 healthy and 10 chronic periodontitis-affected human subjects. The presence and distribution of CD1a and S100 protein was assessed using immunohistochemistry, and the cell types involved in their expression was determined.
The presence and distribution of CD1a was confined only to the gingival epithelium, whereas S100 was seen in the epithelium and connective tissue. However, increased expression of both CD1a and S100 protein was seen in periodontitis-affected gingival tissues compared with healthy gingiva. Immunohistochemistry demonstrated that CD1a- and S100-positive cells in the epithelium are Langerhans cells (LCs) and S100 positive cells in the connective tissue are dendritic cells (DCs).
Our findings suggest the transition of CD1a-positive LCs to S100-positive DCs from epithelium to connective tissue in response to an antigenic challenge. Demonstration of increased number of S100-positive DCs in the gingival connective tissue in chronic periodontitis possibly suggests their involvement in bone resorption in addition to their antigen presentation property.
Available from: Sreenatha S Kirakodu
- "As the lesion progresses, increasing numbers of mononuclear cells emigrate into the affected tissues and into the subgingival sulcus, consistent with a more chronic inflammatory lesion (Smith et al., 2010). The cellular profiles of these apparent established lesions include various phenotypes of T cells, B cells and plasmacytes producing antibody (Ebersole et al., 2013), and antigen-presenting cells including macrophages (Bartold et al., 2010; Hajishengallis, 2010; Merry et al., 2012) and dendritic cells (DC) (Anjana et al., 2012; Cutler & Teng, 2007). "
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ABSTRACT: Recent evidence has determined a phenotypic and functional heterogeneity for macrophage populations. This plasticity of macrophage function has been related to specific properties of subsets (M1 and M2) of these cells in inflammation, adaptive immune responses and resolution of tissue destructive processes. This investigation hypothesized that targeted alterations in the distribution of macrophage phenotypes in aged individuals, and with periodontitis would be skewed towards M1 inflammatory macrophages in gingival tissues. The study used a non-human primate model to evaluate gene expression profiles as footprints of macrophage variation in healthy and periodontitis gingival tissues from animals 3-23 years of age and in periodontitis tissues in adult and aged animals. Significant increases in multiple genes reflecting overall increases in macrophage activities were observed in healthy aged tissues, and were significantly increased in periodontitis tissues from both adults and aged animals. Generally, gene expression patterns for M2 macrophages were similar in healthy young, adolescent and adult tissues. However, modest increases were noted in healthy aged tissues, similar to those seen in periodontitis tissues from both age groups. M1 macrophage gene transcription patterns increased significantly over the age range in healthy tissues, with multiple genes (e.g. CCL13, CCL19, CCR7 and TLR4) significantly increased in aged animals. Additionally, gene expression patterns for M1 macrophages were significantly increased in adult health versus periodontitis and aged healthy versus periodontitis. The findings supported a significant increase in macrophages with aging and in periodontitis. The primary increases in both healthy aged tissues and, particularly periodontitis tissues appeared in the M1 phenotype.
Available from: nature.com
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ABSTRACT: The oral cavity contains distinct mucosal surfaces, each with its own unique distribution of dendritic cell (DC) subsets. In addition to tissue-specific properties, such organization might confer differential immune outcomes guided by tissue-resident DCs, which translate in the lymph node into an overall immune response. This process is further complicated by continual exposure and colonization of the oral cavity with enormous numbers of diverse microbes, some of which might induce destructive immunity. As a central cell type constantly monitoring changes in oral microbiota and orchestrating T-cell function, oral DCs are of major importance in deciding whether to induce immunity or tolerance. In this review, an overview of the phenotype and distribution of DCs in the oral mucosa is provided. In addition, the role of the various oral DC subsets in inducing immunity vs. tolerance, as well as their involvement in several oral pathologies is discussed.Mucosal Immunology advance online publication, 12 June 2013; doi:10.1038/mi.2013.42.
Available from: Ricardo Alves Mesquita
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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-[Formula: see text], 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-[Formula: see text], 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-[Formula: see text], 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.
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