Effect of non-surgical periodontal therapy on the levels of Th17/Th1/Th2 cytokines and their transcription factors in Chinese chronic periodontitis patients

Zhao, Lu; Zhou, Yan; Xu, Yan; Sun, Ying; Li, Lü; Wu, Chen

doi:10.1111/j.1600-051x.2011.01712.x

Cited by 90 publications

(100 citation statements)

References 51 publications

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“…Conversely, serum levels of various cytokines in patients with periodontitis were investigated in several previous studies and the results were often controversial (Duarte et al, 2010;Andrukhov et al, 2011;Zhao et al, 2011). The contradictions in the existing data are probably caused by the heterogeneity among the various individuals, differences in susceptibility to periodontitis, differences in the oral microbiota and low levels of cytokines in the serum (Andrukhov et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…and reveals some important aspects of the systemic reach of periodontal inflammation (Fitzsimmons et al, 2010;Zhao et al, 2011). However, it is emphasized that the mechanical removal of the dental biofilm by scaling and root planning, with or without another supporting modality, does not mean that, at any magnitude, inflammation/infection does not persist.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the amount of Th17 cells in peripheral blood was reduced, especially the IL-17+ and IFN-γ+ subpopulations. These results suggested that Th17 cells play a destructive role in the immune balance in periodontitis, the effect of Th1 cells was not significant, while Th2 cells had a protective effect (Zhao et al, 2011). In addition, it is known that individuals with better response to periodontal therapy decreased their inflammatory risk category (OR 4.8, 95% CI 1.4 to 15.8) after correction for age, gender, ethnicity and tobacco use (D'Aiuto et al, 2004a).…”

Section: Local and Systemic Responses In Periodontal Diseasementioning

confidence: 96%

“…The expansion of human Th17 cells is regulated by IL-23, whereas IL-1, TGF-β1 and IL-6 initiate the differentiation of Th17 (Konermann et al, 2012). Moreover, IL-21, as an autocrine-regulating factor for Th17 cells, plays an important role in inducing the differentiation of Th17 cells and inhibition of Th1 and Treg function (Zhao et al, 2011).…”

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

confidence: 99%

See 3 more Smart Citations

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Leite¹,

Carneiro²,

Nunes

et al. 2015

American Journal of Immunology

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Periodontal Diseases (PD) are characterized by pathological manifestation of host immune response to bacterial infection at the tooth/gingival interface. Evidences points periodontitis as a risk factor for pathological systemic conditions, such as, cardiovascular diseases and diabetes. The identification of host factors that determine their susceptibility to immune subversion can provide useful information in the pathogenesis of periodontitis. Protective acute inflammatory response fails to remove inflammatory cells, especially neutrophils, evolving to chronic, destructive and pathological lesions. T and B cells actively participate in pathogenesis of the disease. CD4+ naive T cells are activated by antigenic stimulation and differentiate into subpopulations of distinct effector cells, characterized by its specific cytokine production profiles and functions. In periodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) play antagonistic roles as effector and suppressor cells, respectively. In presence of Tregs, there is a decrease in the levels of pro-inflammatory cytokines, such as, Interferon gamma (IFN-γ), Interleukin (IL) -17, Tumor Necrosis Factor (TNF) and IL-1 β, at sites of disease. Absence of Tregs may cause a variety of disorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG) are modulators of bone resorption in periodontitis. The balance between periodontal bone resorption by osteoclasts and bone formation by osteoblasts controls bone mass. RANKL induces osteoclast differentiation and maturation and OPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNA and the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis. Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors were explored. Therapies for periodontitis involving cellular and molecular biology are not specific and have many side effects. Current therapies to successfully control the PD reduces clinical signs of inflammation at local sites of the disease; however, new treatments for periodontitis should address the contribution of immune cells in bone resorption, particularly in the natural course of the disease, considering its periods of remission and progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Local and Systemic Responses In Periodontal Diseasementioning

confidence: 96%

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

confidence: 99%

See 2 more Smart Citations

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Leite¹,

Carneiro²,

Nunes

et al. 2015

American Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…IL-21 is a pleiotropic cytokine highly expressed in gingival biopsies of chronic periodontitis [77,78], and it has been implicated in osteoclastogenesis and bone resorption [79], as well as in the development of Th17 cells [80]. It has also been implicated in the inhibition of Tregs polarization in low-grade chronic inflammatory disorders, such as obesity [81].…”

Section: Th9 Th22 and T Follicular Helpermentioning

confidence: 99%

Cytokine Networks Regulating Inflammation and Immune Defense in the Oral Cavity

Cavalla

Araujo-Pires

Biguetti

et al. 2014

Curr Oral Health Rep

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The host/pathogen interaction in infectious oral diseases is characterized by complex and precisely orchestrated host response mechanisms aimed to protect the host against the microbial challenge with minimal collateral damage to host cells and tissues. Central to the host response in this battlefront is the expression of cytokines. The resulting cytokine networks, which ultimately regulate the host response at multiple levels, thereby determine the clinical outcome of the disease and explain most of its defining features from a mechanistic viewpoint. This review intends to present a structured view of the intricate cytokine networks that regulate inflammation and immune defense in the oral cavity, guiding the reader throughout the evolving paradigms that describe how the simultaneous action of multiple cytokines shapes the nature of the immune response to oral infection.

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Exosomal microRNA‐155‐5p from PDLSCs regulated Th17/Treg balance by targeting sirtuin‐1 in chronic periodontitis

Zheng

Dong

Yang

et al. 2019

Journal Cellular Physiology

113

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The mechanism of local inflammation and systemic injury in chronic periodontitis is complicated, in which and exosomes play an important role. In our study, we found that T helper cell 17 (Th17)/regulatory T cell (Treg) balance is destabilized in the peripheral blood of patients with periodontitis, with upregulated Th17 or downregulated Treg, respectively. Porphyromonas gingivalis lipopolysaccharide (LPS) was used to simulate the inflammatory microenvironment of chronic periodontitis. The exosomes were extracted from periodontal ligament stem cells (PDLSCs) in LPSinduced periodontitis environment, which inversely effected on CD4+ T cells under normal and inflammatory conditions. Furthermore, compared with exosomes from normal PDLSCs, lower expression of microRNA-155-5p (miR-155-5p) and higher expression of Sirtuin-1 (SIRT1) were observed in exosomes from LPS-stimulated PDLSCs. Exosomes from PDLSCs alleviated inflammatory microenvironment through Th17/Treg/miR-155-5p/SIRT1 regulatory network. This study aimed to find the "switching" factors that affected the further deterioration of periodontitis to maximally control the multiple downstream damage signal factors to further understand periodontitis and find new targets for its treatment.

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Effect of non-surgical periodontal therapy on the levels of Th17/Th1/Th2 cytokines and their transcription factors in Chinese chronic periodontitis patients

Abstract: These results suggest that Th17 cells play a destructive role in the immune balance of periodontitis, and the effect of Th1 cells is not significant, while Th2 cells have a protective effect.

Cited by 90 publications

References 51 publications

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Cytokine Networks Regulating Inflammation and Immune Defense in the Oral Cavity

Exosomal microRNA‐155‐5p from PDLSCs regulated Th17/Treg balance by targeting sirtuin‐1 in chronic periodontitis

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