interleukin-8 and Pulpitis

Inflammatory biomarkers are potentially useful targets for pulpal diagnostic tests that can identify pulp status and predict vital pulp treatment (VPT) outcome, however, their accuracy is unknown.. (1) Calculate sensitivity, specificity and diagnostic odds ratio (DOR) of previously investigated pulpitic biomarkers; (2) Determine if biomarker levels discriminate between clinical diagnoses of pulpitis based on the presence or absence of spontaneous pain (3) Evaluate if biomarker level can predict VPT outcome.. Searches: PubMed/MEDLINE, Ovid SP, Cochrane Central Register of Controlled Trials (CENTRAL), International Clinical Trials Registry Platform (ICTRP), ClinicalTrials.gov, Embase, Web of Science and Scopus in May 2023.. prospective and retrospective observational studies and randomized trials. Participants were humans with vital permanent teeth and a well-defined pulpal diagnosis.. deciduous teeth, in vitro and animal studies. Risk of bias was assessed with modified-Downs and Black quality assessment checklist. Meta-analysis was performed using bivariate random effect model in Meta-DiSc 2.0 and RevMan and the quality of the evidence was assessed using Grading of Recommendations Assessment, Development and Evaluation.. Fifty-six studies were selected, reporting >70 individual biomolecules investigating pulpal health and disease at the gene and protein level. Most studies were of low and fair quality. Among the biomolecules investigated, IL-8 and IL-6 demonstrated a level of diagnostic accuracy with high sensitivity, specificity and DOR to discriminate between healthy pulps and those exhibiting spontaneous pain suggestive of IRP (low-certainty evidence). However, none was shown to have high DOR and the ability to discriminate between pulpitic states (very low certainty evidence). Limited data suggests high levels of matrix metalloproteinase 9 correlate with poorer outcomes of full pulpotomy.. The inability of identified molecular inflammatory markers to discriminate between dental pulps with spontaneous and non-spontaneous pain should shift the focus to improved study quality or the pursuit of other molecules potentially associated with healing and repair.. Low-quality evidence suggests IL-8 and IL-6 demonstrated level of diagnostic accuracy to discriminate between healthy pulps and those exhibiting spontaneous pain. There is a need for standardized biomarker diagnostic and prognostic studies focusing on solutions that can accurately determine the degree of pulp inflammation.. PROSPERO CRD42021259305.

Topics: Biomarkers; Humans; Interleukin-6; Interleukin-8; Pain; Prospective Studies; Pulpitis; Retrospective Studies

Recent advances in immunology have disclosed the enormous complexity of the immune regulatory system. The dental pulp is equipped to mount adaptive immune responses to caries, which include at least antigen-presenting cells, lymphocytes, mast cells and their cytokines, and chemokines. The purpose of this review is to summarize our current understanding of the roles of these cellular and molecular components in the irreversibly inflamed pulp. The immunopathology of abscess formation and the mechanisms for painless pulpitis are also discussed.

Topics: Animals; B-Lymphocytes; Chemokines; Cytokines; Dendritic Cells; Dental Caries; Dental Pulp; Humans; Immunity, Innate; Interleukin-8; Macrophages; Periapical Abscess; Pulpitis; T-Lymphocytes; Toothache

The purpose of this prospective, randomized, double-blind study was to evaluate the pulpal concentrations of prostaglandin E2 (PGE2) and interleukin-8 (IL-8) in untreated teeth with irreversible pulpitis after the administration of an intraosseous injection of Depo-Medrol. Forty emergency patients with a clinical diagnosis of irreversible pulpitis experiencing moderate to severe pain participated. After receiving local anesthesia, patients randomly received, in a double-blind manner, an intraosseous injection of either 1 ml of Depo-Medrol (40 mg) (20 patients) or 1 ml of sterile saline placebo (control) (20 patients). No endodontic treatment was initiated. At 1 or 3 days after the intraosseous injection, the teeth were extracted and the pulpal tissue harvested. Prostaglandin E2 and interleukin-8 concentrations were determined by enzyme immunoassay. Results demonstrated a significantly (p < 0.05) lower concentration of prostaglandin E2 compared to the saline group at day 1. There were no significant (p > 0.05) differences between the two groups at day 3. The pulpal concentrations of prostaglandin E2 were reduced at 1 day after the intraosseous injection of Depo-Medrol.

Topics: Adult; Anti-Inflammatory Agents; Bone and Bones; Chi-Square Distribution; Dental Pulp; Dinoprostone; Double-Blind Method; Female; Humans; Injections; Interleukin-8; Male; Methylprednisolone; Methylprednisolone Acetate; Pain Measurement; Prospective Studies; Pulpitis; Statistics, Nonparametric; Toothache

The signaling mechanisms for Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammation in human dental pulp cells are not fully clarified. This in vitro study aimed to evaluate the involvement of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in PgLPS-induced pulpal inflammation.. Human dental pulp cells (HDPCs) were challenged with PgLPS with or without pretreatment and coincubation with a PI3K/Akt inhibitor (LY294002). The gene or protein levels of PI3K, Akt, interleukin (IL)-6, IL-8, alkaline phosphatase (ALP), osteocalcin and osteonectin were analyzed by reverse transcription polymerase chain reaction (PCR), real-time PCR, western blotting, and immunofluorescent staining. In addition, an enzyme-linked immunosorbent assay was used to analyze IL-6 and IL-8 levels in culture medium.. In response to 5 μg/ml PgLPS, IL-6, IL-8, and PI3K, but not Akt mRNA expression of HDPCs, was upregulated. IL-6, IL-8, PI3K, and p-Akt protein levels were stimulated by 10-50 μg/ml of PgLPS in HDPCs. PgLPS also induced IL-6 and IL-8 secretion at concentrations higher than 5 μg/ml. Pretreatment and co-incubation by LY294002 attenuated PgLPS-induced IL-6 and IL-8 mRNA expression in HDPCs. The mRNA expression of ALP, but not osteocalcin and osteonectin, was inhibited by higher concentrations of PgLPS in HDPCs.. P. gingivalis contributes to pulpal inflammation in HDPCs by dysregulating PI3K/Akt signaling pathway to stimulate IL-6 and IL-8 mRNA/protein expression and secretion. These results are useful for understanding the pulpal inflammation and possible biomarkers of inflamed pulp diagnosis and treatment.

Topics: Dental Pulp; Humans; Interleukin-6; Interleukin-8; Lipopolysaccharides; Osteonectin; Phosphatidylinositol 3-Kinase; Phosphatidylinositol 3-Kinases; Porphyromonas gingivalis; Proto-Oncogene Proteins c-akt; Pulpitis; Signal Transduction

To investigate the regulatory role of miR-155 and Kinesin Superfamily Proteins-5C (KIF-5C) in the progression of pulpitis based on bioinformatic analysis.. Normal pulp tissues and pulpitis pulp tissues were collected and subjected to high-throughput sequencing and the differentially expressed miRNAs were determined. An in vitro and in vivo pulpitis model was established. HE, IHC staining and histological evaluation were used to verify the inflammatory state of human and mouse pulp tissues. The mRNA expression of IL-1β and TGF-β1 were determined by RT-qPCR and protein expression of IL-1α, IL-4, IL-8, IL-13, IFN-γ, IL-6, IL-10 and MCP-1 were determined by protein chip. The target genes of miR-155 were predicted by miRanda database and verified by Dual-luciferase reporter assay, RT-qPCR and western blotting. MiR-155 lentivirus were used to upregulate or downregulate miR-155 and the siRNA of KIF-5C was used to downregulate KIF-5C. The expression of miR-155 or KIF-5C was determined by RT-qPCR. All statistics were analysed using GraphPad prism 8.2.. The high-throughput sequencing results showed that 6 miRNAs (miR-155, miR-21, miR-142, miR-223, miR-486, miR-675) were significantly upregulated in diseased human pulp tissues, and miR-155 was significantly elevated among the six miRNAs. RT-qPCR results demonstrated that miR-155 expression was upregulated in human pulpitic tissue, mice pulpitic tissue and LPS-HDPCs. IL-1β was increased while TGF-β1 was decreased in lenti-miR-155 transfected LPS-HDPCs. Analysis of protein chip results indicated that lenti-miR-155 transfected LPS-HDPCs produced higher levels of IL-8, IL-6, MCP-1. The opposite results were obtained when miR-155 was inhibited. Through miRanda database screen and Dual-luciferase reporter assay, the target gene (KIF-5C) of miR-155 was identified. In lenti-miR-155 transfected LPS-HDPCs, the expression of KIF-5C was downregulated. However, when shRNA-miR-155 was transfected to LPS-HDPCs, the opposite result was obtained. Silent RNA was used to knock down KIF-5C, the results showed that when both KIF-5C and miR-155 were knocked down simultaneously, the downregulated expression of inflammatory factors observed in LPS-HDPCs following miR-155 knockdown was rescued.. MiR-155 plays an important role in promoting pulpitis through targeting KIF-5C and may serve as a potential therapeutic target.

Topics: Animals; Dental Pulp; Humans; Interleukin-6; Interleukin-8; Kinesins; Lipopolysaccharides; Luciferases; Mice; MicroRNAs; Pulpitis; Transforming Growth Factor beta1

This research aims to quantify pro-inflammatory cytokines from the exudates of dental pulp tissues are helpful in the diagnosis of pulpitis, thus, laying down the foundation for further vital pulp therapy on irreversible pulpitis.. The authors selected patients admitted to Beijing Stomatological Hospital from October 2016 to March 2018. Exudates were collected from pulp exposure and were divided into four groups, which encompass normal pulps (Group 1), early stage of chronic pulpitis (Group 2), late stage of chronic pulpitis (Group 3) and acute attack of chronic pulpitis (Group 4).. The cytokines IL-1β, IL-6, IL-8 and TNF from the exudates of dental pulp tissues were quantified by cytometric bead array using enhanced sensitivity flex sets. All statistical analyses were performed using SPSS 22.0 and the 2-sided significance level was set at p < 0.05. The Kruskal-Wallis test, Mann-Whitney U test and Spearman correlation analysis were employed to process data.. There were 32, 37, 14, 29 samples in Groups 1, 2, 3 and 4, respectively. Only small amount of IL-1β, IL-8 was expressed in normal pulps and almost no TNF, IL-6 could be detected in Group 1. No difference was observed in the concentration of TNF between Group 2, 3, 4.

Topics: Cytokines; Dental Pulp; Exudates and Transudates; Humans; Interleukin-6; Interleukin-8; Pulpitis

Nel-like molecule type 1 (Nell-1) is a secreted protein that plays an important role in osteoinduction in multiple animal models. A previous study has suggested the anti-inflammatory effect of Nell-1 on bone inflammation inhibition. However, its role in pulpitis has not been investigated. The present study aims to explore the effect of human recombinant Nell-1 (Nell-1) on rat pulp inflammation response, and its effect on lipopolysaccharide-induced inflammation in human dental pulp cells and its related intracellular signaling pathways. 30 Wistar rats with healthy non-carious maxillary first molars were chosen, Nell-1 was absorbed onto a sterile collagen sponge and capped onto exposed pulps. The expression of IL-6 and IL-8 were detected by immunohistochemical staining. Human dental pulp cells (hDPCs) were isolated from healthy extracted premolars and third molars. hDPCs were co-cultured with Escherichia coli lipopolysaccharide (LPS), Nell-1 protein, and mitogen-activated protein kinase (MAPK) inhibitors. The expression of pro-inflammatory cytokines and chemokines, such as IL-6 and IL-8, was examined via quantitative real-time PCR and enzyme-linked immunosorbent assay. The results showed that Nell-1 inhibited the inflammatory response of rat pulp. LPS treatment contributed to the expression of inflammatory factors in hDPCs, whereas Nell-1 obviously suppressed the LPS-induced inflammation. p38 MAPK and extracellular signal-regulated kinase (ERK) MAPK inhibitors attenuated the anti-inflammatory effect of hrNell-1, whereas the c-Jun N-terminal kinases (JNK) MAPK inhibitor exerted minimal effect. Therefore Nell-1 could inhibit LPS-induced inflammation in human dental pulp cells, and this effect may be mediated by p38 and ERK MAPK signaling pathways, but not JNK MAPK signaling pathway.

Topics: Adolescent; Adult; Animals; Cells, Cultured; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Humans; Inflammation; Interleukin-6; Interleukin-8; Lipopolysaccharides; Nerve Tissue Proteins; Pulpitis; Rats, Wistar; Real-Time Polymerase Chain Reaction; Recombinant Proteins; Young Adult

The aim of this study was to compare levels of neurokinin A (NKA), substance P (SP), interleukin (IL)-8, and matrix metalloproteinase-8 (MMP-8) in pulp tissue and gingival crevicular fluid (GCF) samples of healthy and symptomatic irreversible pulpitis teeth.. Forty patients diagnosed with healthy and symptomatic irreversible pulpitis teeth were included in this study. NKA, SP, IL-8, and MMP-8 levels were measured using the enzyme-linked immunosorbent assay test after pulp and GCF samples were obtained from healthy (n = 20) and symptomatic irreversible pulpitis teeth (n = 20). GCF sampling of 40 teeth was repeated 1 week later. Routine root canal treatment procedures of the teeth were performed, and the treatment process was completed. As a control group, GCF samples were taken from the contralateral teeth in both groups. Statistical analysis was performed using dependent and independent t tests, analysis of variance, Kruskal-Wallis, Mann-Whitney U tests, and Pearson correlation analysis.. Comparing the groups, all mediator levels were significantly higher in the pulp samples in the pulpitis group compared with the healthy group (NKA: P < .001, SP: P = .005, IL-8: P < .001, and MMP-8: P < .001). Likewise, in the pulpitis group, all mediator levels were significantly higher in the first GCF samples compared with the healthy group (NKA: P = .01, SP: P < .001, IL-8: P = .001, and MMP-8: P < .001).. It was observed that NKA, SP, IL-8, and MMP-8 increased significantly in pulp tissue and GCF specimens of symptomatic irreversible pulpitis teeth compared with pulp tissue and GCF specimens of healthy teeth. Second, it was determined that NKA, SP, IL-8, and MMP-8 levels decreased significantly in GCF samples in teeth diagnosed with symptomatic irreversible pulpitis 1 week after the removal of inflamed pulp. Finally, SP, IL-8, and MMP-8 levels were found to be higher in pulp tissue samples of the patients with symptomatic irreversible pulpitis with higher pain scores than those with low pain scores.

Topics: Gingival Crevicular Fluid; Humans; Interleukin-8; Matrix Metalloproteinase 8; Neurokinin A; Pulpitis; Substance P

The aim of this study was to assess the influence of ketorolac tromethamine and dexamethasone on substance P and IL-8 expression when used as a root canal irrigant for single visit root canal treatment for acute irreversible pulpitis. A total of 42 patients with pain due to acute irreversible pulpitis in carious premolar and molar teeth were included in this study. The four irrigation groups were as follows: saline (n = 11), 3% sodium hypochlorite (n = 11), ketorolac tromethamine (n = 10) and dexamethasone (n = 10). Blood samples S1 and S2 were collected upon access opening and after canal preparation, respectively. Quantification of substance P and IL-8 were done using ELISA test. Post-operative pain was assessed by questioning the patients. The difference between S1 and S2 sample values for the four different irrigant groups was not significant. The sodium hypochlorite group had a higher mean expression of substance P and IL-8 values. Dexamethasone irrigation was more effective in controlling post-operative pain.

Topics: Dental Pulp Cavity; Humans; Interleukin-8; Pulpitis; Root Canal Irrigants; Root Canal Preparation; Root Canal Therapy; Sodium Hypochlorite; Substance P

Our study aimed to investigate the role of interleukin (IL)-17 in dental pulp inflammation and the relationship between WNT5A and IL-17.. Immunohistochemical staining was used to detect the expression of tumor necrosis factor-α (TNF-α), WNT5A and IL-17 in pulp tissues. Anti-IL-17 neutralizing antibody was used in rat pulpitis model and to study the role of IL-17 in pulpitis. TNF-α, WNT5A or IL-17 recombinant protein were used to treat human dental pulp cells. RT-PCR, Western blot, and Enzyme linked immunosorbent assay were used to detect the expression of mRNA and protein. Transwell assay was used to measure the migration of THP-1 cells, which is a human monocytic cell line.. IL-17 and WNT5A are co-expressed in TNF-α high-expressed region in human and rat pulpitis tissue. IL-17 mainly contributes to its positive regulatory role in inflammation through up regulate cytokines and mediated macrophages migration. Anti-IL-17 neutralizing antibody can suppress the inflammatory cell infiltration and TNF-α expression in dental pulpitis. TNF-α promotes the expression of IL-17 partly through WNT5A and WNT5A regulates IL-17 expression by mitogen-activated protein kinase (MAPK)-(P38 and ERK) pathway.. IL-17 acts as an inflammatory mediator in dental pulp inflammation. The expression of IL-17 can be partially regulated by WNT5A.

Topics: Animals; Dental Pulp; Gene Expression Regulation; Humans; Inflammation; Interleukin-17; Interleukin-8; Pulpitis; Rats; Tumor Necrosis Factor-alpha; Wnt-5a Protein

The process of pulpitis is characterized by extracellular matrix imbalance and inflammatory cell infiltration. As an essential transcription factor, sex-determining region Y-box 9 (SOX9) is significantly inhibited by tumor necrosis factor alpha in inflammatory joint diseases. The aim of this study was to explore the role of SOX9 in extracellular matrix balance, cytokine expression, and the immune response in dental pulp.. The expression of SOX9 in normal and inflamed pulp tissue/human dental pulp cells (HDPCs) was detected by immunohistochemistry, Western blot, and quantitative polymerase chain reaction (qPCR). SOX9 small interfering RNA was used to knock down SOX9 expression of dental cells in vitro; extracellular matrix imbalance was analyzed by qPCR, Western blot, and gelatin/collagen zymography, and the secretion of cytokines was scanned by antibody arrays. The immune response of THP-1 was investigated by cell migration assay, cell attachment assay, phagocytosis assay, and enzyme-linked immunosorbent assay. The interaction of SOX9 with target genes was explored by chromatin immunoprecipitation (ChIP).. SOX9 was strongly expressed in normal dental pulp tissue and HDPCs and reduced in inflamed pulp. SOX9 knockdown could inhibit the production of type I collagen, stimulate the enzymatic activities of MMP2 and MMP13, and regulate the production of interleukin (IL) 8 of HDPCs. SOX9 knockdown also effectively suppressed the differentiation and functional activities of THP-1. ChIP showed that the binding of the SOX9 protein with matrix metalloproteinase (MMP)-1, MMP-13, and IL-8 gene promoters was reduced after being treated with recombinant human tumor necrosis factor alpha.. SOX9 was inhibited in inflamed dental pulp and may participate in the regulation of extracellular matrix balance, the inflammatory process, and the immune response.

Topics: Cell Line; Dental Pulp; Extracellular Matrix; Gene Knockdown Techniques; Humans; Interleukin-8; Matrix Metalloproteinases; Pulpitis; Real-Time Polymerase Chain Reaction; Recombinant Proteins; SOX9 Transcription Factor; Tumor Necrosis Factor-alpha

To investigate IL-17 expression in human pulpitis and to study the effects of IL-17 on the secretion of the chemokines IL-6 and IL-8 and the related signalling pathways.. Samples of human dental pulp tissue were obtained from healthy controls and patients with pulpitis. Cytokine IL-17 messenger RNA (mRNA) expression in the pulp tissue was detected by real-time polymerase chain reaction. In addition, human dental pulp fibroblasts (HDPFs) were stimulated with IL-17. Production of IL-6 and IL-8 was determined by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. Aspects of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) signalling pathways were examined by Western blot analysis.. Increased levels of IL-17 mRNA were found in inflamed dental pulp tissue (pulpitis). Stimulation of dental pulp tissue with IL-17 induced the production of IL-6 and IL-8 in a dose-dependent manner. In addition, IL-17 stimulation resulted in rapid activation of nuclear factor-kappaB (NF-κB), phosphorylation of p38 MAPK, extracellular signal-regulated kinase (ERK) and Jun N-terminal kinase (JNK) in HDPFs.. IL-17 may participate in pulp tissue inflammation through chemokine production and NF-κB and MAPKs signalling pathways.

Topics: Adult; Blotting, Western; Case-Control Studies; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Female; Fibroblasts; Humans; Interleukin-17; Interleukin-6; Interleukin-8; Male; MAP Kinase Signaling System; NF-kappa B; Pulpitis; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Signal Transduction

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-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 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.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Bone Resorption; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Female; Humans; Inflammation; Interleukin-8; Male; Middle Aged; Osteoprotegerin; Periapical Periodontitis; Periapical Tissue; Pulpitis; RANK Ligand; Young Adult

Dental pulp has limited capability to regenerate, which happens in the early stage of pulpitis. An ambiguous relationship exists; inflammation may impair or support pulp regeneration. Epigenetics, which is involved in cell proliferation and inflammation, could regulate human dental pulp cell (HDPCs) regeneration. The aim of this study was to determine the role of the epigenetic mark, enhancer of zeste homolog 2 (EZH2), in the inflammation, proliferation, and regeneration of dental pulp. We used trimethylated histone H3 lysine 27(H3K27me3) and its lysine demethylase 6B (KDM6B) to monitor functional effects of altered EZH2 levels.. We detected epigenetic marks (EZH2, H3K27me3, and KDM6B) in pulp tissue by immunohistochemistry and immunofluorescence. EZH2 levels in HDPCs in inflammatory responses or differentiation were analyzed by quantitative polymerase chain reaction and Western blot. Quantitative polymerase chain reaction was used to assess the effects of EZH2 inhibition on interleukins in HDPCs upon tumor necrosis factor alpha stimulation. Cell proliferation was tested by cell counting kit-8, cell cycle, and apoptosis analysis. HDPC differentiation was investigated by quantitative polymerase chain reaction, alkaline phosphatase activity, and oil red O staining.. EZH2 and H3K27me3 were decreased, whereas KDM6B was increased in infected pulp tissue and cells, which were similar to HDPC differentiation. EZH2 inhibition suppressed IL-1b, IL-6, and IL-8 messenger RNA (mRNA) in HDPCs upon inflammatory stimuli and impeded HDPC proliferation by decreasing cell number, arresting cell cycle, and increasing apoptosis. Suppressed EZH2 impaired adipogenesis, peroxisome proliferator-activated receptor r (PPAR-r), and CCAAT-enhancer binding protein a (CEBP/a) mRNA in adipogenic induction while enhancing alkaline phosphatase activity, Osx, and bone sialoprotein (BSP) mRNA in mineralization induction of HDPCs.. EZH2 inhibited HDPC osteogenic differentiation while enhancing inflammatory response and proliferation, suggesting its role in pulp inflammation, proliferation, and regeneration.

Topics: Adipogenesis; Alkaline Phosphatase; Apoptosis; Calcification, Physiologic; CCAAT-Enhancer-Binding Protein-alpha; Cell Differentiation; Cell Proliferation; Cells, Cultured; Dental Pulp; Enhancer of Zeste Homolog 2 Protein; Epigenesis, Genetic; Histones; Humans; Integrin-Binding Sialoprotein; Interleukin-1beta; Interleukin-6; Interleukin-8; Jumonji Domain-Containing Histone Demethylases; Osteogenesis; Peroxisome Proliferator-Activated Receptors; Polycomb Repressive Complex 2; Pulpitis; Regeneration; Sp7 Transcription Factor; Transcription Factors; Tumor Necrosis Factor-alpha

Dental pulp inflammation and repair are closely related. Osteocalcin (OCN), a glycoprotein present in dentin matrix, is expressed by odontoblasts. Although OCN is considered a reparative molecule inside the dental pulp, it is not clear if it is involved in pulpal inflammation. The objective of this study was to localize OCN in reversible and irreversible pulpitis and to describe its possible function in inflammation.. Pulp tissues in the form of reversible and irreversible pulpitis were collected from the endodontic clinic. Those from impacted teeth were used as controls. Immunohistochemistry was used to localize OCN. Samples were analyzed for OCN and inflammatory mediator expression using multiplex assay.. OCN in inflamed tissues was localized in cells and matrix around calcification areas and in cells around blood vessels but not in normal tissues. The plex assay (Bio-Plex 200, Bio-Rad Laboratories Ltd, Mississauga, ON, Canada) showed OCN expression in reversible pulpitis significantly higher than in irreversible pulpitis, and both were significantly higher than in the controls. A panel of inflammatory mediators showed an increase in reversible and irreversible pulpitis. Another panel was decreased in both stages compared with the controls. OCN expression in reversible pulpitis was positively correlated to the expression of vascular endothelial growth factor, fibroblast growth factor, macrophage inflammatory protein-1β, monocyte-derived chemokine, monocyte chemoattractant protein-1, interleukin (IL)-17, and soluble IL-2 receptor α and negatively correlated to that of IL-1α, IL-1β, IL-8, granulocyte macrophage colony-stimulating factor, and macrophage inflammatory protein-1α.. Profound understanding of the pulp inflammatory process would lead to new molecular treatment strategies. Our data indicate that OCN expression in reversible pulpitis is associated with angiogenic markers, suggesting its potential use in regenerative treatment.

Topics: Chemokine CCL2; Chemokine CCL3; Chemokine CCL4; Collagen; Dental Pulp; Dental Pulp Calcification; Dentin; Fibroblast Growth Factors; Fibrosis; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Inflammation Mediators; Interleukin-17; Interleukin-1alpha; Interleukin-1beta; Interleukin-2 Receptor alpha Subunit; Interleukin-8; Odontoblasts; Osteocalcin; Pulpitis; Vascular Endothelial Growth Factor A

Previous studies have suggested that odontoblasts sense gram-positive bacteria components through Toll-like receptor 2 (TLR2) and trigger dental pulp immunity by producing proinflammatory cytokines. Currently, the factors that modulate odontoblast TLR2 activation are unknown. Our aim was to investigate lipopolysaccharide-binding protein (LBP) effects on the TLR2-mediated odontoblast response.. Human odontoblast-like cells were stimulated with lipoteichoic acid (LTA) (a TLR2 ligand), LBP, CD14 (a TLR2 cofactor), or various combinations of LTA/LBP, LTA/CD14, or LTA/CD14/LBP. CXCL8, IL6, and TLR2 gene expression was assessed by real-time polymerase chain reaction. CXCL8 and interleukin (IL)-6 production was determined by enzyme-linked immunosorbent assay in culture supernatants of cells stimulated with LTA, LTA/CD14, or LTA/CD14/LBP. LBP effects on nuclear factor kappa B (NF-κB), p38, JNK, ERK, STAT3, and p70S6 signaling pathways were determined in LTA-stimulated odontoblast-like cells with a multiplex biometric immunoassay. LBP effects were compared with specific inhibitors of these signaling pathways. LBP transcript and protein were investigated in vivo in healthy and inflamed dental pulps by real-time polymerase chain reaction and immunohistochemistry.. Activation of CXCL8, IL6, and TLR2 gene expression and CXCL8 and IL-6 secretion in LTA- and LTA/CD14-stimulated odontoblast-like cells was significantly decreased by LBP. LBP inhibited NF-κB and p38 signaling pathways in LTA-stimulated cells in a similar way to NF-κB and p38 inhibitors. LBP transcript and protein were detected in vivo in inflamed dental pulps but not in healthy ones.. These results demonstrate that LBP reduces TLR2-dependent production of inflammatory cytokines by odontoblast-like cells. We suggest that in this way it could modulate host defense in human dental pulp.

Topics: Acute-Phase Proteins; Carrier Proteins; Cell Culture Techniques; Extracellular Signal-Regulated MAP Kinases; Gram-Positive Bacteria; Humans; Interleukin-6; Interleukin-8; Lipopolysaccharide Receptors; Lipopolysaccharides; MAP Kinase Kinase 4; MAP Kinase Signaling System; Membrane Glycoproteins; NF-kappa B; Odontoblasts; p38 Mitogen-Activated Protein Kinases; Pulpitis; Ribosomal Protein S6 Kinases, 70-kDa; STAT3 Transcription Factor; Teichoic Acids; Toll-Like Receptor 2

To find possible reagents to minimize inflammatory responses by using an established pulpitis models for the purpose of developing new pulp-capping materials, and to test the possible use of phosphorylated pullulan as a carrier for such an anti-inflammatory reagent.. Co-culturing was performed using transwell systems. Inflammatory responses were evaluated by measuring cytokines produced by the cells. The effects of two flavonoids, luteolin and quercetin, as anti-inflammatory reagents, and phosphorylated pullulan, which potentially achieves a sufficient marginal sealing to hydroxyapatite and slowly releases luteolin, as a carrier for flavonoids, were tested.. Flavonols, particularly luteolin, dramatically attenuated inflammatory cytokine production, which was augmented by co-cultures. Luteolin was successfully enclosed by phosphorylated pullulan. Finally, it was confirmed that luteolin released from phosphorylated pullulan was effective in reducing cytokine production by co-cultures.. Combination of phosphorylated pullulan and luteolin could be potentially used in the treatment of dental pulp inflammation.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cell Line, Transformed; Cells, Cultured; Chemokine CCL2; Chemokine CCL5; Coculture Techniques; Dental Pulp; Drug Carriers; Drug Combinations; Flavonoids; Glucans; Interleukin-6; Interleukin-8; Luteolin; Materials Testing; Pulp Capping and Pulpectomy Agents; Pulpitis; Quercetin; Tumor Necrosis Factor-alpha

To measure and compare the levels of the cytokines IL-2, IL-6, IL-8, IL-10, TNF-α and IFN-γ in pulpal blood from irreversible pulpitis, asymptomatic caries exposure and normal pulps.. Blood was obtained from pulp exposure sites using cotton pellets. Twenty-five samples were obtained from normal teeth, 40 from asymptomatic caries-exposed pulps and 43 from irreversible pulpitis teeth. Cytokine levels were determined by high-sensitivity ELISA. Data were statistically analysed using Kruskal-Wallis and Mann-Whitney U-tests.. Significantly higher levels (P < 0.05) of IL-6, IL-8, IL-10, TNF-α and IFN-γ were detected in caries-exposed pulps and irreversible pulpitis as compared to normal teeth. IL-2 and IL-10 levels were significantly higher (P < 0.05) in caries-exposed pulps as compared to irreversible pulpitis, whilst IL-8 was significantly higher (P < 0.001) in irreversible pulpitis as compared to caries-exposed teeth. Most interestingly, IL-6/IL-10 and IL-8/IL-10 ratios were significantly higher (P < 0.001) in irreversible pulpitis compared with both caries-exposed and normal teeth.. Levels of IL-8 and the ratios of IL-6/IL-10 and IL-8/IL-10 have the potential to be indicators of pulpal inflammation in caries exposure cases. Cytokine estimation in pulpal blood may help in the diagnosis of pulpal inflammation.

Topics: Adolescent; Adult; Biomarkers; Dental Caries; Dental Pulp; Dental Pulp Exposure; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interferon-gamma; Interleukin-10; Interleukin-2; Interleukin-6; Interleukin-8; Interleukins; Male; Middle Aged; Pulpitis; Tumor Necrosis Factor-alpha; Young Adult

Dentin matrix protein-1 (DMP-1) is involved in the mineralization of hard dental tissues. DMP-1 is localized in several soft tissues, but its role is unclear.. Human inflamed dental pulps were collected from the endodontic clinic and human normal pulps from impacted teeth. Dental pulp cells from 8 subjects were explanted to test the effect of DMP-1 on interleukin-6 (IL-6) and IL-8 production by using enzyme-linked immunosorbent assay.. DMP-1 was localized in pulp inflammation by using immunohistochemistry but was not present in impacted root pulps. Wherever found, areas of calcification were positively stained against DMP-1, suggesting its possible involvement in pulp inflammation and in pathologic calcification. To test this hypothesis, primary human pulp fibroblasts were cultured. The fibroblasts were identified on the basis of their morphology, immunoreactivity against vimentin and collagen 1a1 by immunofluorescence and negative staining to CD45, CD34, and cytokeratin by flow cytometry. DMP-1 (10 ng/mL) stimulated the production of IL-6 and IL-8 from pulp fibroblasts. DMP-1 showed an additive effect with lipopolysaccharide in IL-6 and IL-8 production. Inhibition of the p38 mitogen-activated protein kinase pathway blocked the proinflammatory effect of DMP-1 on pulp fibroblasts.. Our data indicate that DMP-1 might participate in the development of inflammatory changes in the dental pulp. DMP-1 inhibition might be a new therapeutic strategy to target pulp inflammation and pathologic calcification.

Topics: Calcinosis; Cell Culture Techniques; Dental Pulp; Enzyme Inhibitors; Extracellular Matrix Proteins; Fibroblasts; Humans; Imidazoles; Inflammation Mediators; Interleukin-6; Interleukin-8; Lipopolysaccharides; MAP Kinase Signaling System; p38 Mitogen-Activated Protein Kinases; Phosphoproteins; Pulpitis; Pyridines; Tooth, Impacted

To establish an ex vivo pulpitis model by co-culturing dental pulp cells with macrophages.. As dental pulp cells, immortalized human dental pulp cells, named DP-1, were used, whilst as macrophage cell lines, the differentiated human monocytic cell line, THP-1, was used. In some experiments, primary dental pulp cells were isolated and used to confirm the results obtained in the experiments using immortalized cells. Co-culturing was performed using transwell systems. Inflammatory responses were evaluated by measuring cytokines produced by the cells.. Co-culturing both cell types markedly up-regulated inflammatory cytokine production as compared with the cells cultured independently, suggesting that both cell types interact with each other to synergistically produce higher amounts of inflammatory cytokines. Interestingly, both DP-1 and primary dental pulp cells appeared to produce molecules stimulating macrophages to produce tumour necrosis factor-α-.. Co-culturing immortalized dental pulp cells and macrophages may be a new ex vivo model for studying the pathophysiology of reversible pulpitis.

Topics: Cell Line, Transformed; Cells, Cultured; Chemokine CCL2; Chemokine CCL5; Coculture Techniques; Cytokines; Dental Pulp; Humans; Interleukin-6; Interleukin-8; Macrophages; Models, Biological; Pulpitis; Tumor Necrosis Factor-alpha

Human odontoblasts trigger immune response s to oral bacteria that invade dental tissues during the caries process. To date, their ability to regulate the expression of the nucleotide-binding domain leucine-rich repeat containing receptor NOD2 when challenged by Gram-positive bacteria is unknown. In this study, we investigated NOD2 expression in healthy and inflamed human dental pulps challenged by bacteria, and in cultured odontoblast-like cells stimulated with lipoteichoic acid (LTA), a Toll-like receptor (TLR) 2 agonist which is specific for Gram-positive bacteria. We found that NOD2 gene expression was significantly up-regulated in pulps with acute inflammation compared to healthy ones. In vitro, LTA augmented NOD2 gene expression and protein level in odontoblast-like cells. The increase was more pronounced in odontoblast-like cells compared to dental pulp fibroblasts. Blocking experiments in odontoblast-like cells with anti-TLR2 antibody strongly reduced the NOD2 gene expression increase, whereas stimulation with the synthetic TLR2 ligand Pam(2)CSK(4) confirmed NOD2 gene up-regulation following TLR2 engagement. These data suggest that NOD2 up-regulation is part of the odontoblast immune response to Gram-positive bacteria and might be important in protecting human dental pulp from the deleterious effects of cariogenic pathogens.

Topics: Antibodies, Monoclonal; Carrier Proteins; Cells, Cultured; Dental Pulp; Fibroblasts; Gene Expression; Humans; Interleukin-8; Lipopolysaccharides; Molar; Nod2 Signaling Adaptor Protein; Odontoblasts; Pulpitis; Teichoic Acids; Toll-Like Receptor 2; Tumor Necrosis Factor-alpha

The innate immune response is activated by recognition of microbial components through specific pattern recognition receptors including nucleotide-binding oligomerization domain (NOD)-like receptors. However, the regulation of NOD-1 in inflamed human dental pulp remains poorly understood. This study aimed to evaluate the expression of NOD-1 in healthy and inflamed human dental pulps. In addition, the secretion of chemokines induced by NOD-1 and the related signaling pathways were studied.. Samples of human dental pulp tissues were obtained from freshly extracted wisdom teeth. The protein localization of NOD-1 in the pulp tissues was detected by immunohistochemistry. In addition, human dental pulp fibroblasts were stimulated with NOD-1 agonist γ-D-glutamylmeso-diaminopimelic acid. Production of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was determined by an enzyme-linked immunosorbent assay. The involvement of mitogen-activated protein kinase (MAPK) signaling pathways was examined by Western blot analysis, and the association of MAPK signaling with chemokine production was determined.. The results demonstrated the expression of NOD-1 in normal dental pulp, and up-regulated NOD-1 expression was observed in inflamed dental pulp. On stimulation with NOD-1 agonist, production of IL-8 and MCP-1 was induced in a dose-dependent manner. Moreover, phosphorylation of p38 MAPK and Jun N-terminal kinase (JNK) was enhanced by stimulation of NOD-1. With the treatment of p38 MAPK and JNK inhibitors, the NOD-1-induced IL-8 production was suppressed.. In response to microbial invasion, the expression of NOD-1 can be regulated in a ligand-inducible manner. NOD-1 might participate in pulp inflammation through chemokine production via MAPK signaling pathways.

Topics: Analysis of Variance; Cells, Cultured; Chemokine CCL2; Dental Pulp; Fibroblasts; Gene Expression Regulation; Humans; Interleukin-8; JNK Mitogen-Activated Protein Kinases; MAP Kinase Signaling System; Nod1 Signaling Adaptor Protein; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Pulpitis; Statistics, Nonparametric; Up-Regulation

Prostaglandin F(2alpha) (PGF(2alpha)) and interleukin-1beta (IL-1beta) levels are elevated in inflamed dental pulp. The roles of IL-1beta and PGF(2alpha) in the pathogenesis of pulpal inflammation await investigation. We found that IL-1beta stimulated PGF(2alpha) production of human dental pulp cells. IL-1beta and PGF(2alpha) (0.5-10 mumol/L) also induced IL-8 production and mRNA expression in pulp cells. Aspirin inhibited IL-1beta-induced PGF(2alpha), but not IL-8 production. PGF(2alpha)-induced IL-8 production and mRNA expression were inhibited by U0126 (an inhibitor of mitogen-activated protein kinase kinase [MEK1/2]) inhibitor), whereas SQ22536 (an adenylate cyclase inhibitor) enhanced this event. These results indicate that IL-1beta-induced IL-8 production in pulp cells is not mainly via direct activation of cyclooxygenase and PGF(2alpha) generation. PGF(2alpha)-induced IL-8 production is possibly via activation of MEK/extracellular signal-regulated kinase signaling, but not by activation of adenylate cyclase. IL-1beta and PGF(2alpha) might involve the pathogenesis of pulpal inflammation via induction of IL-8 production.

Topics: Activating Transcription Factor 1; Adenine; Butadienes; Cells, Cultured; Cyclic AMP Response Element-Binding Protein; Dental Pulp; Dinoprost; Extracellular Signal-Regulated MAP Kinases; Humans; Interleukin-1beta; Interleukin-8; MAP Kinase Signaling System; Mitogen-Activated Protein Kinase Kinases; Nitriles; Protein Kinase Inhibitors; Pulpitis

Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E(2) and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis.

Topics: Acetylmuramyl-Alanyl-Isoglutamine; Apoptosis; Cells, Cultured; Chemokine CCL2; Chemokine CXCL10; Cyclooxygenase 2; Dental Pulp; Diaminopimelic Acid; Dinoprostone; Escherichia coli; Fibroblasts; Humans; Inflammation Mediators; Interleukin-6; Interleukin-8; Lipopeptides; Lipopolysaccharides; Nod1 Signaling Adaptor Protein; Nod2 Signaling Adaptor Protein; Pulpitis; Signal Transduction; Streptococcus mutans; Toll-Like Receptor 2; Toll-Like Receptor 4; Vascular Cell Adhesion Molecule-1

Pulpitis is characterized by the marked infiltration of inflammatory cells in response to an invasion of caries-related bacteria. It is well known that chemokines regulate the trafficking of lymphocytes, and CC chemokine ligand 20 (CCL20) has been recently shown to play a crucial role in the recruitment of memory T cells and immature dendritic cells into inflammatory lesions. We previously reported that CCL20 was mainly expressed in microvascular endothelial cells and macrophages that accumulated in inflamed pulp tissues and that its specific receptor, CCR6, was expressed on infiltrated lymphocytes. However, the mechanism of CCL20 expression remains unclear.. In this study, we investigated the expression of CCL20 in monocytes/macrophages, endothelial cells, and pulpal fibroblasts after stimulation with Streptococcus mutans, a representative of caries-related bacteria, or proinflammatory cytokines. CCL20 messenger RNA was detected by reverse transcription-polymerase chain reaction in inflamed pulp, but not in clinically normal pulp. By enzyme-linked immunosorbent assay, S. mutans induced a human monocytic cell line, differentiated macrophage-like THP-1 cells, and human umbilical vein endothelial cells (HUVEC) to produce an increased amount of CCL20. Lipoteichoic acid from S. mutans also elicited CCL20 production by HUVEC. Moreover, CCL20 production from pulpal fibroblasts was increased by stimulation with inetrleukin-1beta and tumor necrosis factor-alpha.. Our results indicate that CCL20 expression is induced by stimulation with caries-related bacteria that have invaded deeply into the dentinal tubules as well as by proinflammatory cytokines in the inflamed pulpal lesions. It may be involved in the progression of pulpitis via accumulation of inflammatory cells.

Topics: Adult; Aged; Cell Differentiation; Cell Line; Cells, Cultured; Chemokine CCL20; Cytokines; Dental Pulp; Endothelial Cells; Endothelium, Vascular; Female; Fibroblasts; Humans; Inflammation Mediators; Intercellular Adhesion Molecule-1; Interleukin-1beta; Interleukin-8; Lipopolysaccharides; Macrophages; Male; Middle Aged; Monocytes; Pulpitis; Streptococcus mutans; Teichoic Acids; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1

Irreversibly inflamed pulp (IIP) constitutes both a pathophysiologic and a diagnostic challenge. Gingival crevicular fluid (GCF) samples were obtained with Periopaper strips from IIP and adjacent and contralateral teeth for interleukin-8 (CXCL8) and tumor necrosis factor-alpha (TNF-alpha) measurements. Pain intensity was reported by using a verbal numeric scale (1-10). TNF-alpha (n = 25) was not detectable in GCF, whereas CXCL8 (n = 17) was significantly greater in IIP (302.1 +/- 164.9 pg/mL) compared with adjacent (139 +/- 138.58 pg/mL; P = .0072) or contralateral (173.8 +/- 166.4 pg/mL; P = .0231) teeth. A subgroup of high pain (>5) patients (n = 7) had CXCL8 IIP levels (323.6 +/- 148.4 pg/mL) that were significantly different from the contralateral teeth (P = .0262); however, they did not differ from the adjacent teeth (P = .1649), suggesting that neighboring teeth might also have inflammation. Another group of patients (n = 7) who had received local anesthesia before sampling had very low IIP CXCL8 levels. GCF CXCL8 levels might be a useful measurement for staging patients with acute pulpitis.

Topics: Acute Disease; Adult; Anesthetics, Local; Female; Gingival Crevicular Fluid; Humans; Interleukin-8; Lidocaine; Male; Mandibular Nerve; Middle Aged; Nerve Block; Pain Measurement; Pulpitis; Tumor Necrosis Factor-alpha

This study examined the effect of nitric oxide (NO) on interleukin-8 (IL-8) production and the involvement of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappaB) signaling pathways in primary cultured human pulp cells.. IL-8 production was measured using enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. MAPK activation and IkappaB degradation and phosphorylation were determined by western blotting.. Sodium nitroprusside (SNP), an NO donor, has increased IL-8 secretion and mRNA expression in a dose- and time-dependent manner. SNP induced the phosphorylation of p38 MAPK and extracellular-regulated kinase (ERK), degradation and phosphorylation of IkappaB, and activation of NF-kappaB. Furthermore, inhibition of the ERK, p38, and NF-kappaB pathways blocked SNP-induced IL-8 secretion.. Human pulp cells showed NO-induced IL-8 expression via the MAPK and NF-kappaB pathways, which may play an important role in the inflammatory responses of pulp and periapical lesions.

Topics: Blotting, Western; Cells, Cultured; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Extracellular Signal-Regulated MAP Kinases; Humans; I-kappa B Proteins; Interleukin-8; MAP Kinase Signaling System; NF-kappa B; Nitric Oxide; Nitric Oxide Donors; Nitroprusside; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Pulpitis; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction

To determine whether leucocyte infiltration during neurogenic inflammation in the pulp is regulated by neuropeptides via inducing the release of proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) from human dental pulp.. Cultured primary pulp cells and pulp tissue explants were stimulated with substance P (SP) and/or calcitonin gene-related peptide (CGRP). IL-8 or MCP-1, secreted from cultured cells or produced in pulp explants, was analysed by enzyme-linked immunosorbent assay.. Substance P induced IL-8 secretion from cultured pulp cells (approximately threefold increase over control, P < 0.05) and from pulp tissue explants (two- to three fold). SP only minimally to moderately induced MCP-1 (approximately two fold) in cultured pulp cells. While MCP-1 induction in cultured pulp cells was detected after 24 h of SP stimulation, no induction was observed in pulp tissue. CGRP did not induce IL-8, but moderately increased MCP-1 production (approximately three fold) in cultured pulp cells. There was no synergistic induction of MCP-1 by SP plus CGRP stimulation of pulp cells.. Substance P is a stronger inducer of IL-8 production in dental pulp than CGRP. IL-8 is more strongly induced than MCP-1 by SP, suggesting a more important role for IL-8 than MCP-1 in leucocyte infiltration during neurogenic inflammation in dental pulp.

Topics: Calcitonin Gene-Related Peptide; Cells, Cultured; Chemokine CCL2; Culture Techniques; Dental Pulp; Humans; Interleukin-8; Neurogenic Inflammation; Pulpitis; Substance P

The purpose of this study was to investigate the level of IL-8 in exudates clinically obtained from normal and inflamed human dental pulp tissues so as to reveal the possible relationship between IL-8 and pulpitis.. Samples of 2 microliters of pulpal exudate from each normal or clinically diagnosed as acute or chronic pulpitis teeth was obtained by filter paper strips and IL-8 level was measured by ELISA method.. No IL-8 was detected in the samples from normal pulp, but significant amount of IL-8 appeared in inflamed pulp tissues, and the level of IL-8 in exudates of acute stage of pulpitis was higher than that of chronic stage (P < 0.01).. This study demonstrates that IL-8 is produced and accumulated in pulp inflammation and may play a role in the occurrence and development of human pulpitis.

Topics: Acute Disease; Chronic Disease; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Exudates and Transudates; Humans; Inflammation Mediators; Interleukin-8; Methylcellulose; Pulpitis

Elevated levels of interleukin-8, a potent chemoattractant and activator of neutrophils, are associated with infectious and inflammatory diseases. However, little is known about interleukin-8 expression in human dental pulp. The purpose of this study was to determine whether tissue levels of interleukin-8 are elevated in irreversibly inflamed human pulps.. Experimental samples were from teeth clinically diagnosed with irreversible pulpitis (diseased pulps). Controls were from freshly extracted, caries-free third molars (normal pulps). Samples were subjected to enzyme-linked immunosorbent assay and/or immunohistochemical analysis with specific antibodies to interleukin-8.. The enzyme-linked immunosorbent assay studies showed elevated levels of interleukin-8 in diseased pulps (mean, 1.82+/-0.79 pg/mL/microg protein), as compared to detectable interleukin-8 levels in samples from normal pulps (mean, 0.08+/-0.04 pg/mL/microg protein; P<.05). Immunohistochemical analyses demonstrated that diseased samples exhibited a higher density of localized interleukin-8 staining in areas with heavy infiltration of inflammatory cells. In contrast, normal pulps showed negative or weak interleukin-8 staining.. Interleukin-8 concentration was higher in pulps diagnosed with irreversible pulpitis; only negligible amounts of interleukin-8 were present in normal pulps.

Topics: Antibodies; Coloring Agents; Dental Pulp; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Humans; Immunoenzyme Techniques; Immunohistochemistry; Interleukin-8; Molar, Third; Proteins; Pulpitis