Correlation between Clinical/Radiographic Features and Inflammatory Cytokine Networks Produced by Macrophages Stimulated with Endodontic Content

Martinho, Frederico Canato; Chiesa, Wanderson Miguel Maia; Leite, Fábio Renato Manzolli; Cirelli, Joni Augusto; Gomes, Brenda Paula Figueiredo de Almeida

doi:10.1016/j.joen.2012.02.021

Cited by 80 publications

(102 citation statements)

References 44 publications

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“…In fact, the development of symptomatic apical abscesses has been associated with the high IL-6 transcription rate GG genotype and G allele of IL-6 polymorphism in locus À174 (16). Additionally, IL-6 protein levels were shown to increase along with ALEO size in apical exudates (17).…”

Section: Discussionmentioning

confidence: 98%

C-Reactive Protein Expression Is Up-regulated in Apical Lesions of Endodontic Origin in Association with Interleukin-6

Garrido

Dezerega

Bordagaray

et al. 2015

Journal of Endodontics

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Section: Discussionmentioning

confidence: 98%

C-Reactive Protein Expression Is Up-regulated in Apical Lesions of Endodontic Origin in Association with Interleukin-6

Garrido

Dezerega

Bordagaray

et al. 2015

Journal of Endodontics

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“…Also, Th1 responses are known to be regulated by T regulatory cells, IL-10 (11), and transforming growth factor-b (27). The correlation between inflammatory biomarkers and development of clinical/radiographic features is of interest for establishment of therapy (7,28). Clinically, TTP and POP are indicative parameters of the presence of inflammation in periradicular tissues (28).…”

Section: Discussionmentioning

confidence: 99%

“…The correlation between inflammatory biomarkers and development of clinical/radiographic features is of interest for establishment of therapy (7,28). Clinically, TTP and POP are indicative parameters of the presence of inflammation in periradicular tissues (28). The presence of POP was positively associated with TNF-a and IFN-g, whereas higher levels of IL-4 and IL-13 decreased the chance of POP.…”

Section: Discussionmentioning

confidence: 99%

“…Further activation of macrophages causes a cycle of further killing of intracellular bacteria, further presentation of antigens to Th1-helper cells, with further release of IFN-g. IFN-g, in combination with other stimuli such as lipopolysaccharide, frequently recovered from primarily infected root canals with apical periodontitis (28), up-regulates IL-1 and TNF expression (29,30). Thereby, TNF induces the production of IL-1 (31), which in turn stimulates its synthesis in a positive feedback loop (32).…”

Section: Discussionmentioning

confidence: 99%

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Clinical Influence of Different Intracanal Medications on Th1-type and Th2-type Cytokine Responses in Apical Periodontitis

Martinho

Nascimento

Leite

et al. 2015

Journal of Endodontics

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“…High levels of TNF-α have been identified in the tissue and gingival crevicular fluid of patients with advanced periodontitis and chronic periapical periodontitis (2–4). Increased TNF-α levels have also been identified in primarily infected root canals and the infected periapical tissue of patients with pulpitis and chronic periapical periodontitis (5,6). Therefore, the expression of TNF-α is considered to be correlated with the progression of bone resorption in periodontal and periapical diseases.…”

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor-α induces interleukin-34 expression through nuclear factor-κB activation in MC3T3-E1 osteoblastic cells

Yang

Qiu

et al. 2014

Molecular Medicine Reports

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Osteoblasts produce various types of cytokines under pathological conditions and control osteoclast differentiation. Tumor necrosis factor-α (TNF-α) has been demonstrated to exert complex effects in osteoblasts under local inflammatory conditions, including in periodontal and periapical diseases. Interleukin-34 (IL-34) has been recently identified as a novel regulatory factor for the differentiation and function of osteoclasts. The present study provides the first evidence, to the best of our knowledge, that the expression of IL-34 is induced by TNF-α through nuclear factor-κB (NF-κB) activation in MC3T3-E1 osteoblastic cells. TNF-α induced IL-34 expression in a dose- and time-dependent manner. Immunocytochemistry with an NF-κB antibody demonstrated that NF-κB was mainly localized in the cytoplasm of the untreated MC3T3-E1 cells. Rapid translocation of NF-κB from the cytoplasm to the nucleus was observed in the cells treated with TNF-α for 15 min. Translocation and transcriptional activity of NF-κB were also determined by western blotting and a luciferase reporter assay, respectively. Pretreatment with 100 μM CAPE, an inhibitor of NF-κB, significantly inhibited TNF-α-induced IL-34 expression. These results indicate that TNF-α induces IL-34 expression via NF-κB in osteoblasts.

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Correlation between Clinical/Radiographic Features and Inflammatory Cytokine Networks Produced by Macrophages Stimulated with Endodontic Content

Cited by 80 publications

References 44 publications

C-Reactive Protein Expression Is Up-regulated in Apical Lesions of Endodontic Origin in Association with Interleukin-6

C-Reactive Protein Expression Is Up-regulated in Apical Lesions of Endodontic Origin in Association with Interleukin-6

Clinical Influence of Different Intracanal Medications on Th1-type and Th2-type Cytokine Responses in Apical Periodontitis

Tumor necrosis factor-α induces interleukin-34 expression through nuclear factor-κB activation in MC3T3-E1 osteoblastic cells

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