The changes in T lymphocyte subsets following periodontal treatment in patients with chronic periodontitis

Ercıyas, Kamile; Orbak, Recep; Kavrut, Fahri; Demir, Turgut; Kaya, Hasan

doi:10.1111/j.1600-0765.2005.00855.x

Cited by 15 publications

(15 citation statements)

References 41 publications

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“…Flow cytometry has traditionally been used in immunological studies to identify immune cells on the basis of their fluorescent characteristics (5,19). Recent investigations have mod- ified this methodology to quantify fluorescent polycarboxylate microspheres that are bound to DNA (bead-based flow cytometry).…”

Section: Discussionmentioning

confidence: 99%

Response of Subgingival Bacteria to Smoking Cessation

et al. 2010

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It has been demonstrated that smoking cessation alters the subgingival microbial profile; however, the response of individual bacteria within this ecosystem has not been well studied. The aim of this investigation, therefore, was to longitudinally examine the effect of smoking cessation on the prevalence and levels of selected subgingival bacteria using molecular approaches for bacterial identification and enumeration. Subgingival plaque was collected from 22 smokers at the baseline and 12 months following periodontal nonsurgical management and smoking cessation counseling. The prevalence and abundance of selected organisms were examined using nested PCR and multiplexed bead-based flow cytometry. Eleven subjects successfully quit smoking over 12 months (quitters), while 11 continued to smoke throughout (smokers). Smoking cessation led to a decrease in the prevalence of Porphyromonas endodontalis and Dialister pneumosintes at 12 months and in the levels of Parvimonas micra, Filifactor alocis, and Treponema denticola. Smoking cessation also led to an increase in the levels of Veillonella parvula. Following nonsurgical periodontal therapy and smoking cessation, the subgingival microbiome is recolonized by a greater number of health-associated species and there are a significantly lower prevalence and abundance of putative periodontal pathogens. The results indicate a critical role for smoking cessation counseling in periodontal therapy for smokers in order to effectively alter the subgingival microbiome.It is established that bacterial consortia within the subgingival microbiome play a critical role in the etiology of chronic periodontitis. Although tobacco smoking has been shown to preferentially enrich this microbiome for pathogenic species (26, 29), it is not known if smoking cessation is capable of reversing this pathogenic colonization, since current evidence is based only on cross-sectional comparisons of former and current smokers (10,25). A longitudinal examination of subgingival bacteria following smoking cessation would allow us to determine how the individual bacteria within this ecosystem respond to smoking cessation.We have previously shown, using a cultivation-independent, open-ended approach, that smoking cessation results in a shift in the subgingival microbial profile during recolonization following periodontal therapy (7). In order to identify the individual organisms that contributed to this compositional shift, it is necessary to use a targeted, sensitive, and quantitative approach to measure the levels of these species.Bead-based flow cytometry has recently been used to measure the abundance of target organisms in complex bacterial communities (24,28). This cultivation-independent approach is capable of simultaneously measuring the levels of several organisms, both cultivated and uncultivated. It also has a wide dynamic range; that is, it is capable of quantifying both the less numerous and the numerically dominant members of a microbial community.The goals of the present investigation were to ...

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Section: Discussionmentioning

confidence: 99%

Response of Subgingival Bacteria to Smoking Cessation

et al. 2010

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“…The role of CD8 + T‐cells in periodontitis has been analyzed in patients with different forms of periodontitis . CD8 + T‐cell clones from inflamed periodontal tissues were analyzed in early studies, by stimulation with phytohemagglutinin, for their production of different cytokines and their biological functions.…”

Section: Role Of Cytotoxic T‐cell Subsets In Periodontitismentioning

confidence: 99%

T‐ and B‐cell subsets in periodontitis

Gonzáles¹

2015

Periodontology 2000

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A large amount of information is available, in the medical literature, on the molecular and immunological mechanisms in which T- and B-cells are involved in the pathogenesis of inflammatory diseases. This review attempts to describe the most important features of the T-cell subsets and their cytokine networks in periodontitis, including the interaction of pathogens with different cell subsets and their gene-expression profiles. Additionally, the known interactions of T- and B-cell subsets in periodontitis are described. The purpose of this article was to provide an overview of the cell interactions and cytokine networks specifically involved in the pathogenesis of periodontitis, and models and paradigms from recent research in this area are presented. However, the review of the literature also revealed that relatively little is known about the genetic or structural factors that confer cross-reactivity of natural and/or autoreactive antibodies in the immunopathogenesis of periodontitis. Pathogens, in turn, are continuously evolving and creating mechanisms to evade immunological reactions controlled and modulated by T- and B-cells.

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“…Bacterial antigens causing periodontitis activate CD4 + T cells and lead to expression of the RANK ligand (RANKL) on CD4 + T cells. RANKL binds to RANK on preosteoclasts or osteoclasts, and enhances the differentiation of preosteoclasts into osteoclasts and the activation of mature osteoclasts (Brunetti et al, 2005;Erciyas et al, 2006;Kawai et al, 2006). Surface proteins expressed on monocytic cells interact with their corresponding receptors or ligands, and modulate the functions of T cells.…”

Section: Introductionmentioning

confidence: 99%