Immunolocalization of bone‐resorptive cytokines in rat pulp and periapical lesions following surgical pulp exposure

Tani‐Ishii, Nobuyuki; Wang, C.-Y.; Stashenko, Philip

doi:10.1111/j.1399-302x.1995.tb00145.x

Cited by 148 publications

(130 citation statements)

References 26 publications

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“…However, in previous studies the kinetics of apical periodontitis has been investigated mainly employing rodent models where the pulp gets exposed to the oral environment (17). Pro-inflammatory cytokines, such as IL-1 and TNF-α, are expressed at a very early stage of the disease in rodent's periapical tissues (18). Especially IL-1 plays a pivotal role in development and progression of apical periodontitis (8).…”

Section: Discussionmentioning

confidence: 99%

Periapical fluid RANKL and IL-8 are differentially regulated in pulpitis and apical periodontitis

et al. 2014

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The dental pulp space can become infected due to a breach in the surrounding hard tissues. This leads to inflammation of the pulp (pulpitis), soft tissue breakdown, and finally to bone loss around the root apex (apical periodontitis). The succession of the molecular events leading to apical periodontitis is currently not known. The main inflammatory mediator associated with neutrophil chemotaxis is interleukin-8 (IL-8), and with bone resorption the dyad of receptor activator of NF-B ligand (RANKL) and osteoprotegerin (OPG). The levels of RANKL, OPG and IL-8 were studied in periapical tissue fluid of human teeth (n = 48) diagnosed with symptomatic irreversible pulpitis (SIP) and asymptomatic apical periodontitis (AAP). SIP represents the starting point, and AAP an established steady state of the disease. Periapical tissue fluid samples were collected using paper points and then evaluated using enzyme-linked immunosorbent assays (ELISAs). Target protein levels per case were calibrated against the corresponding total protein content, as determined fluorometrically. RANKL was expressed at significantly higher levels in SIP compared to AAP (P < 0.05), whereas OPG was under the detection limit in most samples. In contrast, IL-8 levels were significantly lower in SIP compared to AAP (P < 0.05). Spearman's correlation analysis between RANKL and IL-8 revealed a significantly (P < 0.05) negative correlation between the two measures (rho = -.44). The results of this study suggest that, in the development of apical periodontitis, periapical bone resorption signaling, as determined by RANKL, occurs prior to inflammatory cell recruitment signaling, as determined by IL-8. AbstractThe dental pulp space can become infected due to a breach in the surrounding hard tissues. This leads to inflammation of the pulp (pulpitis), soft tissue breakdown, and finally to bone loss around the root apex (apical periodontitis). The succession of the molecular events leading to apical periodontitis is currently not known. The main inflammatory mediator associated with neutrophil chemotaxis is interleukin-8 (IL-8), and with bone resorption the dyad of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG). The levels of RANKL, OPG and IL-8 were studied in periapical tissue fluid of human teeth (n=48) diagnosed with symptomatic irreversible pulpitis (SIP) and asymptomatic apical periodontitis (AAP). SIP represents the starting point, and AAP an established steady state of the disease. Periapical tissue fluid samples were collected using paper points and then evaluated using enzyme-linked immunosorbent assays (ELISAs). Target protein levels per case were calibrated against the corresponding total protein content, as determined fluorometrically. RANKL was expressed at significantly higher levels in SIP compared to AAP (P<0.05), whereas OPG was under the detection limit in most samples. In contrast, IL-8 levels were significantly lower in SIP compared to AAP (P<0.05). Spearman's correlation analysis between RANKL and IL-8 rev...

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Section: Discussionmentioning

confidence: 99%

Periapical fluid RANKL and IL-8 are differentially regulated in pulpitis and apical periodontitis

et al. 2014

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“…Macrophages are prominent in inflammatory periapical tissues, and produce large quantities of IL-1 (7,8). Therefore, we tested the ability of the four infecting pathogens to induce IL-1␣ by macrophages in vitro.…”

Section: Macrophage Il-1␣ Responses To Pathogensmentioning

confidence: 99%

IL-10, But Not IL-4, Suppresses Infection-Stimulated Bone Resorption In Vivo

Sasaki¹,

Hou²,

Belani³

et al. 2000

The Journal of Immunology

169

171

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Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1α in the murine model. The production and activity of IL-1α is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10−/− mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4−/− exhibited no increased resorption. IL-10−/− had markedly elevated IL-1α production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4−/− exhibited decreased IL-1α production (p < 0.05). IL-10 also suppressed IL-1α production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1α expression.

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“…Recently large amount of interleukin-1 and tumor necrosis factor-αhave been demostrated to induce rat pulpitis. 12 These findings highlighted the significance of proinflammatory cytokines in pulpal injury. It is well established that interleukin-1 and tumor necrosis factor-αcan mediate inflammatory tissue destruction by stimulating MMP-1 and TIMP-1 production in several cell types.…”

Section: Introductionmentioning

confidence: 92%

The effect of tumor necrosis factor (TNF)-α to induce matrix metalloproteinase (MMPs) from the human dental pulp, gingival, and periodontal ligament cells

Rhim

Park

Kim

et al. 2011

J Korean Acad Conserv Dent

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Objectives: In the present study, three kinds of tissues cells (pulp, gingiva, and periodontal ligament) were investigated if those cells express MMP and TIMP when they were stimulated with neuropeptides (substance P, CGRP) or proinflammatory cytokine, TNF-α . Materials and Methods:The cells cultured from human dental pulp (PF), gingiva (GF) and periodontal ligament were (PDLF) stimulated with Mock, SP, TNF-α , and CGRP for 24 hrs and 48 hrs. for an RNase protection assay and Enzyme Linked Immunosorbent Assay. Cells (PF, GF and PDLF) seeded in 100 mm culture dish were stimulated with SP (10 -5, 10 -8 M) or only with medium (Mock stimulation) for 4hrs and for 24 hrs for RNase Protection Assay, and they were stimulated with CGRP (10 -5 M) and TNF-α(2 ng/mL) for 24 hrs and with various concentraion of TNF-α(2, 10, and 100 ng/mL) for Rnase Protection Assay with a human MMP-1 probe set including MMP 1, 2, 8, 7, 8, 9, 12, and TIMP 2, 3. In addition, cells (PF, GF and PDLF) were stimulated with Mock and various concentraion of TNF-α(2, 10, and 100 ng/mL) for 24 hrs and with TNF-α(10 ng/mL) for 48 hrs, and the supernatents from the cells were collected for Enzyme Linked Immunosorbent Assay (ELISA) for MMP-1 and MMP-13. Results: The expression of MMPs in PF, GF, PDLF after stimulation with SP and CGRP were not changed compared with Mock stimulation for 4 hrs and 24 hrs. The expression of MMP-1, -12, -13 24 hrs after stimulation with TNF-αwere upregulated, however the expression of TIMP-3 in PF, GF, PDLF after stimulation with TNF-αwere downregulated. TNF-α(2 ng/mL, 10 ng/mL, 100 ng/mL) increased MMP-1 and MMP-12 expression in PF dose dependently for 24 hrs. Conclusions: TNF-αin the area of inflammation may play an important role in regulating the remodeling of dentin, cementum, and alveolar bone.

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Immunolocalization of bone‐resorptive cytokines in rat pulp and periapical lesions following surgical pulp exposure

Cited by 148 publications

References 26 publications

Periapical fluid RANKL and IL-8 are differentially regulated in pulpitis and apical periodontitis

Periapical fluid RANKL and IL-8 are differentially regulated in pulpitis and apical periodontitis

IL-10, But Not IL-4, Suppresses Infection-Stimulated Bone Resorption In Vivo

The effect of tumor necrosis factor (TNF)-α to induce matrix metalloproteinase (MMPs) from the human dental pulp, gingival, and periodontal ligament cells

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