Interleukin‐1β and tumour necrosis factor‐α levels in periapical exudates

Ataoğlu, Tamer; Üngör, Mete; Serpek, Behiç; Haliloğlu, Seyfullah; Ataoğlu, Hanife; Arı, Hale

doi:10.1046/j.1365-2591.2002.00467.x

Cited by 74 publications

(64 citation statements)

References 20 publications

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“…As a potent immunologic mediator of acute and chronic inflammatory responses, TNF-a has the capability to increase bone resorption (25). Our findings are in accordance with previous reports that showed higher levels of TNF-a in root canal exudates and periapical lesions in human cases of chronic apical periodontitis (21,26). IL-1 has been shown to play a pivotal role in several chronic diseases, and it is known to be one of the most active stimulators of osteoclastic bone resorption (27,28).…”

Section: Discussionsupporting

confidence: 91%

Cytokine Analysis in Lesions Refractory to Endodontic Treatment

Henriques

Brito

Tavares

et al. 2011

Journal of Endodontics

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Section: Discussionsupporting

confidence: 91%

Cytokine Analysis in Lesions Refractory to Endodontic Treatment

Henriques

Brito

Tavares

et al. 2011

Journal of Endodontics

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“…Consequently, cytokines such as tumor necrosis factor alpha (TNF-α) and interleukins (1a, 1b, 6, 8 and 12p40) probably take part in the development of AP. TNF-α has been reported in human AP and root canal exudate, which reinforces the hypothesis that this cytokine is involved in pulp and periapical pathogenesis, including the concomitant bone loss (1)(2)(3)(4)(5)(6)(7).…”

Section: Introductionsupporting

confidence: 76%

Association Between Apical Periodontitis and TNF-α -308 G>A Gene Polymorphism: A Systematic Review and Meta-Analysis

et al. 2017

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Currently, investigations have focused on the identification of Single Nucleotide Polymorphisms (SNP) involved in host response and its ability to generate an immunity deficiency. The aim of this study was to perform a systematic review (SR) and metaanalysis to evaluate the association between TNF-α -308 G>A polymorphism and apical periodontitis (AP) phenotypes. A broad search for studies was conducted. The following databases were used: PubMed, Scopus, Web of Science, and VHL (Medline, SciELO, Ibecs, and Lilacs). The MeSH terms "Periapical Periodontitis," "Periapical Abscess," "Polymorphism, Genetic," and "Polymorphism, Single Nucleotide" were used. MeSH synonyms, related terms, and free terms were included. Clinical investigations of individuals with different AP phenotypes in permanent teeth were selected. After application of the eligibility criteria, selected studies were qualified by assessing their methodological quality. A fixed effect model was used for the meta-analysis. The initial search identified 71 references. After excluding duplicate abstracts, 33 were selected. From these, two were eligible for quality assessment and were classified as being of moderate evidence. The included studies did not demonstrate association between AP and TNF-α -308 G>A SNP. However, the meta-analysis demonstrated an association between the genotype distribution and AP phenotype (OR= 0.49; confidence interval= 0.25, 0.96; p=0.04). The role of TNF-α -308 G>A SNP in AP phenotypes is debatable. Further studies are needed to confirm and understand the underlying mechanisms of the identified association.

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“…Cytokines such as TNF-␣, IL-6, and IL-23␣ are soluble mediators and are released from immunocompetent cells in the periapical inflammatory processes. These cytokines can stimulate bone resorption in periapical lesion areas (38). Proinflammatory cytokines, such as TNF-␣, have been reported to have a key role in regulating the inflammatory response (39).…”

Section: Discussionmentioning

confidence: 99%

A Small Molecule, Odanacatib, Inhibits Inflammation and Bone Loss Caused by Endodontic Disease

et al. 2015

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dPeriapical disease, an inflammatory disease mainly caused by dental caries, is one of the most prevalent infectious diseases of humans, affecting both children and adults. The infection travels through the root, leading to inflammation, bone destruction, and severe pain for the patient. Therefore, the development of a new class of anti-periapical disease therapies is necessary and critical for treatment and prevention. A small molecule, odanacatib (ODN), which is a cathepsin K (Ctsk) inhibitor, was investigated to determine its ability to treat this disease in a mouse model of periapical disease. While Ctsk was originally found in osteoclasts as an osteoclast-specific lysosomal protease, we were surprised to find that ODN can suppress the bacterium-induced immune response as well as bone destruction in the lesion area. X rays and microcomputed tomography (micro-CT) showed that ODN treatment had significant bone protection effects at different time points. Immunohistochemical and immunofluorescent staining show that ODN treatment dramatically decreased F4/80؉ macrophages and CD3 ؉ T cells in the lesion areas 42 days after infection. Consistent with these findings, quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) analysis showed low levels of proinflammatory mRNAs (for tumor necrosis factor alpha, interleukin 6, and interleukin 23␣) and corresponding cytokine expression in the ODN-treated disease group. The levels of mRNA for Toll-like receptors 4, 5, and 9 also largely decreased in the ODN-treated disease group. Our results demonstrated that ODN can inhibit endodontic disease development, bone erosion, and immune response. These results indicate that application of this small molecule offers a new opportunity to design effective therapies that could prevent periapical inflammation and revolutionize current treatment options. P eriapical lesions result from microbial infection of the dental pulp tissue by members of the autogenous oral microflora, which induce inflammation in the pulp tissue (1). This inflammatory process, much like periodontitis, increases in magnitude in the apical region of the root canal system and subsequently in the periapical area, leading to periapical bone resorption as the infection spreads throughout the canal system toward the apical foramen and into the adjacent bone (2). Furthermore, periapical lesions that present with radiographic bone lesions are preceded by necrotic pulp tissues. Unlike periodontal disease inflammation (3, 4), endodontic lesions exhibit differences in the character of the immune response (5).Despite many studies aimed at discovering ways to alleviate the effects of oral disease, there is still an urgent need to improve the health of millions with periapical disease who suffer from oralbacterial-infection-induced periapical inflammation, oral bone erosion, and the potential loss of teeth. The discovery of the critical roles of cathepsin K (Ctsk) in osteoclastic bone resorption is the fruit of decades of investigation on bone biol...

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Interleukin‐1β and tumour necrosis factor‐α levels in periapical exudates

Abstract: Periapical exudate levels of both cytokines failed to reflect periapical disease state.

Cited by 74 publications

References 20 publications

Cytokine Analysis in Lesions Refractory to Endodontic Treatment

Cytokine Analysis in Lesions Refractory to Endodontic Treatment

Association Between Apical Periodontitis and TNF-α -308 G>A Gene Polymorphism: A Systematic Review and Meta-Analysis

A Small Molecule, Odanacatib, Inhibits Inflammation and Bone Loss Caused by Endodontic Disease

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