Effects of tobacco smoke on the secretion of interleukin-1beta,tumor necrosis factor-alpha,and transforming growth factor-beta from peripheral blood mononuclear cells

Alterations of the host response caused by short-term exposure to high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream of smokers (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. In this study, we examined the secretion of three cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and transforming growth factor (TGF)-beta] from mononuclear blood cells from current smokers and non-smokers exposed to in vitro tobacco smoke (which may be comparable to in vivo acute smoke exposure) and mononuclear blood cells from current smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure). Peripheral blood mononuclear cells were isolated from eight healthy current smokers and eight healthy non-smokers, plated in culture wells, exposed in vitro for 1-5 min to cigarette smoke in a smoke box system or not exposed (baseline controls), and then incubated without further smoke exposure for another 24 h. Supernatants from each well were then collected and assayed for the concentrations of the three cytokines by enzyme-linked immunosorbent assay (ELISA). At baseline, mean IL-1beta levels were higher in smokers than in non-smokers (mean: 10.6 vs. 5.9 pg/ml, anova: P < 0.05). In both smokers and non-smokers, secreted levels of IL-1beta increased from 0 to 5 min of in vitro smoke exposure (mean: 5.9-9.9 pg/ml, t-test: P < 0.05 for non-smokers only) with levels in smokers higher than in non-smokers (P > 0.05). Mean TNF-alpha levels increased from 0 to 2 min of smoke exposure and decreased from 2 to 5 min in smokers and non-smokers, with higher levels in non-smokers than smokers at all time-points (P > 0.05). Mean TGF-beta levels were higher in smokers than in non-smokers at all time-points (mean: 180.5 vs. 132.0 pg/ml, P < 0.05 at 5 min only) with no significant alteration of the pattern of secretion with cigarette smoke exposure. These observed alterations in the secretion of cytokines from mononuclear blood cells in smokers, relative to non-smokers, and with in vitro smoke exposure may play a role in the pathogenesis of periodontal diseases in smokers.     

Analysis of tumor necrosis factor-alpha, transforming growth factor-beta, interleukin-10, IL-6, and interferon-gamma gene polymorphisms in patients with chronic periodontitis

BACKGROUND: Cytokine gene polymorphisms may have an impact on the susceptibility to and progression of chronic periodontitis. In this study, we analyzed the -1082 interleukin-10 (IL-10), -308 tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta 1 (TGF-beta1) (codons 10 and 25), -174IL-6, and +874 interferon-gamma (IFN-gamma) gene single-nucleotide polymorphisms in a cohort of patients with chronic periodontal disease. METHODS: The diagnosis was made on the basis of standardized clinical and radiographic criteria. A total of 122 adult patients with chronic periodontitis and 114 unrelated, ethnically and age-matched white control subjects were genotyped by a polymerase chain reaction-sequence-specific primer. RESULTS: The number of individuals carrying the -174IL-6 CC genotype was significantly higher in the group of patients than in the control group (odds ratio [OR] = 1.896; 95% confidence interval [CI] = 1.106 to 3.250; P = 0.0283). The TGF-beta1 (codon 25) GG (Arg(25)/Arg(25)) genotype was detected more frequently in control subjects than in periodontitis patients (OR = 0.459; 95% CI = 0.230 to 0.920; P = 0.0421). CONCLUSION: The -174IL-6 and TGF-beta1 (codon 25) single-nucleotide polymorphisms are associated with susceptibility to chronic periodontitis in the population studied.     

Tumor necrosis factor-alpha and transforming growth factor-beta1 in chronic periapical lesions

OBJECTIVE: Proinflammatory cytokines are involved in the pathogenesis of periapical lesions. The purpose of this study was to evaluate the presence of the cytokines tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta(1) (TGF-beta(1)) in periapical pathosis and to determine their relationship to the size of the lesions.Study Design: One tooth from each of 25 patients was root-end resected, and the periapical lesion was collected. The amounts of TNF-alpha and TGF-beta(1) were assessed by enzyme-linked immunosorbent assay. RESULTS: TGF-beta(1) was detected in 21 of 25 lesions. In samples with scar tissue, no TGF-beta(1) activity was detected. A statistically significant correlation was found between TGF-beta(1) per milligram of tissue and the diameter of the lesions. TNF-alpha was detected in only 2 samples. CONCLUSIONS: TGF-beta(1) was present in periapical granulomas and cysts but not in lesions with scar tissue. The correlation between the amount of TGF-beta(1) per milligram of tissue and the size of the lesion was significant.     

Lipopolysaccharide from Actinobacillus actinomycetemcomitans stimulates production of interleukin-1beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-1 receptor antagonist in human whole blood

Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) is supposed to be an important etiological agent in localized juvenile periodontitis (LJP). We have studied the effect of lipopolysaccharide (LPS) extracted from these periodontopathogenic bacteria on synthesis of the proinflammatory cytokines, interleukin-1beta(IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and the anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra) in human whole blood. LPS from A. actinomycetemcomitans in concentrations > or =1 ng/ml induced a significant production of all these proinflammatory cytokines, whereas LPS from Escherichia coli (E. coli), strain 026:B6 had to be added in concentrations > or =1 microg/ml to obtain a similar effect. Similarly, LPS from A. actinomycetemcomitans > or =0.1 ng/ml resulted in production of IL-1ra, while LPS from E. coli 026:B6 had to be added at > or =10 ng/ml to obtain similar effects. It has been suggested that the ratio between production of proinflammatory and anti-inflammatory cytokines may influence the outcome of periodontal diseases. Other in vitro and in vivo studies have, however, indicated that very large excesses (100-1000 times) of IL-1ra compared to IL-1beta are required to shift the IL-1ra:IL-1beta ratio in favor of an inhibition of IL-1 bioactivity. In our ex vivo system, we found that stimulation with extremely low doses of A. actinomycetemcomitans LPS (0.1-1 ng/ml) resulted in IL-1ra production solely, without concomitant production of IL-1beta, the excess of IL-1ra over IL-1beta peaking at 1 ng/ml, which accordingly should suggest that LPS from A. actinomycetemcomitans primarily has proinflammatory effects.     

Behavior of human dental pulp cells exposed to transforming growth factor-beta1 and acidic fibroblast growth factor in culture

The development of methods for regenerative endodontic procedures requires an understanding of the factors regulating the development of odontoblasts from adult cell populations such as pulpal cell lines. In this study, we exposed cultures of human pulp cells (7th passage) to growth factors including transforming growth factor-beta1 (TGF-beta1, at 1 or 5 ng/mL), acidic fibroblast growth factor (aFGF, 5 ng/mL), or a combination of the 2 growth factors and evaluated cellular morphology and markers of cell phenotype including alkaline phosphatase activity, osteocalcin, bone sialoprotein (BSP), and dentin sialophosprotein (DSPP). The mean number of nucleoli in the 1 ng/mL TGF-beta1 group was significantly higher than with 5 ng/mL aFGF. Alkaline phosphatase activity was significantly greater with 1 ng/mL TGF-beta1 versus 5 ng/mL TGF-beta1 + 5 ng/mL aFGF (P < .05). Osteocalcin mRNA was expressed in all samples. The cells exposed to 1 ng/mL TGF-beta1 were stimulated; however, exposure to growth factors for 8 days was not sufficient for expression of BSP and DSPP mRNA. Cells treated with 1 ng/mL TGF-beta1 exhibited higher activity, whereas 5 ng/mL aFGF-treated cells were inhibited. Although osteocalcin was observed in all cultures, suggestive of the potential for odontoblast formation, under the present conditions, the exposure to TGF-beta1 and aFGF was not sufficient to induce expression of the dentin matrix components BSP and DSPP.     

Analysis of tumor necrosis factor-alpha, interleukin-6, interleukin-1beta, soluble tumor necrosis factor receptors I and II, interleukin-6 soluble receptor, interleukin-1 soluble receptor type II, interleukin-1 receptor antagonist, and protein in the synovial fluid of patients with temporomandibular joint disorders

OBJECTIVE: To measure the levels of various cytokines, cytokine receptors, and cytokine antagonists in the synovial fluid of patients with temporomandibular disorders (TMD) and to determine the correlations among these expression levels. STUDY DESIGN: Synovial fluid was obtained from 55 patients with TMD and from 5 asymptomatic healthy volunteers as controls. The concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1beta, soluble tumor necrosis factor receptors I and II (sTNFR-I and sTNFR-II), IL-6 soluble receptor (IL-6sR), IL-1 soluble receptor type II, and IL-1 receptor antagonist were determined by enzyme-linked immunosorbent assay. RESULTS: The concentrations of TNF-alpha, IL-6, IL-1beta, sTNFR-I, and sTNFR-II were significantly higher in the synovial fluid of patients than in controls (P < .05). TNF-alpha level was positively correlated with those of IL-6, sTNFR-I, and sTNFR-II. In particular, there was a highly significant positive correlation between sTNFR-I and sTNFR-II. CONCLUSION: TNF and sTNFRs in the synovial fluid of patients with TMD may be important in the pathogenesis of these disorders.     

Distribution of interleukin-2, -4, -10, tumour necrosis factor-alpha and transforming growth factor-beta mRNAs in oral lichen planus.

In the present study, MRNA for the cytokines interleukin-2 (IL-2), IL-4, IL-10 tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor beta-1 (TGF-beta-1) were investigated in oral lichen planus (OLP) lesions using in situ hybridization with 35S-labelled oligonucleotide probes on frozen tissue sections. In addition, the expression of interferon-gamma (IFN-gamma), IL-10 and IL-4 mRNAs was analysed in cultured lesional T lymphocytes from oral lichen planus by polymerase chain reaction. Cells expressing mRNA for IL-2, IL-4, IL-10, TNF-alpha and TGF-beta 1 were found in all the biopsies studied. Approximately 1-2% of the total number of infiltrating cells in the lesions were positive for each of the different cytokine mRNAs. Most biopsies contained basement membrane-oriented, mRNA-positive cells. In the cultured T-cell lines, message for IFN-gamma was detected in all the patients, IL-10 in all but one, and IL-4 in just one of the seven patients investigated. The results suggest that mRNA for both pro- and anti-inflammatory cytokines, i.e., mixed T-helper 1 (TH1) and TH2 cytokine profiles, are generated simultaneously by a limited number of cells in chronic lesions of OLP.     

Effect of Porphyromonas gingivalis lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-1beta on calprotectin release in human monocytes

BACKGROUND: Calprotectin is a major cytosolic protein of monocytes, granulocytes, and epithelial cells. It is known that calprotectin is released in inflammatory tissues and detected in gingival crevicular fluid (GCF) of periodontitis patients at high levels. The origin of calprotectin in GCF and its regulation in periodontal disease are unknown. In this study, we investigated the distribution of calprotectin in gingival tissue with inflammation and the induction of calprotectin release from human monocytes by lipopolysaccharide of Porphyromonas gingivalis (P-LPS), tumor necrosis factor-alpha (TNF-alpha), or interleukin-1beta (IL-1beta). METHODS: Gingival tissues were obtained from a healthy donor and a periodontitis patient and calprotectin in gingival tissues was examined by immunohistochemical staining. Monocytes were isolated from the peripheral blood of healthy donors and cultured with P-LPS, TNF-alpha or IL-1beta for 30 minutes to 4 hours. The content of calprotectin in the cell and medium fractions was determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Calprotectin was markedly detected at the epithelial and adjacent connective tissue with many inflammatory cells in the gingival tissue from the periodontitis patient. P-LPS increased calprotectin release from monocytes to the maximum level after 30 minutes of treatment and its level was elevated to about 2- to 3-fold of the control level in a dose-dependent manner (1 to 1,000 ng/ml). When the effect of TNF-alpha and IL-1beta on calprotectin release was investigated, calprotectin release significantly increased to about 2.2- and 1.5-fold that of the control level, respectively. CONCLUSION: These results demonstrate that calprotectin release from monocytes is induced by P-LPS, TNF-alpha, and IL-1beta, which in turn, cause and aggravate periodontal disease.     

Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway

Matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the degradation of extracellular matrix in many inflammatory diseases. Little is known regarding the expression of these mediators in dental pulp fibroblasts. The effects of proinflammatory cytokines (interleukin (IL)-1alpha and tumor necrosis factor-alpha (TNF-alpha)) and prostaglandin E2 (PGE2) on pulp fibroblast MMP-1 and TIMP-1 gene expression were investigated. Northern hybridization showed that IL-1alpha and TNF-alpha induced significant MMP-1 gene expression, with only little effect on TIMP-1 gene. Exogenous PGE2, however, upregulated TIMP-1 mRNA synthesis but not MMP-1. Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. In contrast, PGE2 enhanced the upregulatory effects of TIMP-1 mRNA by IL-1alpha or TNF-alpha. Furthermore, cytokine stimulation of MMP-1 and TIMP-1 gene expressions can be enhanced or blocked by indomethacin, respectively, and reversed by exogenous PGE2. These results suggested that cytokine-stimulated MMP-1 and TIMP-1 gene expression in dental pulp fibroblasts was mediated, at least in part, by a prostaglandin-dependent pathway. The differential regulation of IL-1alpha or TNF-alpha-induced MMP-1 and TIMP-1 mRNA synthesis, as well as the direct upregulation of TIMP-1 gene expression by PGE2, also implied that prostaglandin may serve as a protective mechanism from excessive tissue breakdown during pulpitis.     

The short-term effects of treatment of chronic periodontitis on circulating levels of endotoxin, C-reactive protein, tumor necrosis factor-alpha, and interleukin-6

BACKGROUND: The acute-phase response involves molecules including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and C-reactive protein (CRP). This study aimed to determine whether subgingival scaling resulted in rapid changes in plasma concentrations of these molecules. METHODS: Twenty-three non-smoking adults with chronic periodontitis received subgingival scaling for 60 minutes. Venous blood samples were taken at 0, 15, 30, 60, and 120 minutes. TNF-alpha and IL-6 were assayed from all samples and CRP from the baseline and final samples. Lipopolysaccharide (LPS) was assayed at 0, 15, and 30 minutes using limulus lysate assay (LAL) and EndoCAb Ig assays. RESULTS: LPS assays were suggestive of a transient low-grade bacteremia, but changes in LPS approaching significance (P=0.061) were seen with LAL only. There was a significant increase in circulating TNF-alpha (P=0.0387) and IL-6 (P<0.0001), and the degree of change in TNF-alpha was correlated with the severity of periodontal breakdown (P=0.001). There was also a significant correlation between levels of IL-6 and TNF-alpha (P<0.001). CONCLUSIONS: Chronic periodontitis patients undergoing an episode of subgingival scaling show a significant elevation in circulating TNF-alpha and IL-6. This may account for anecdotal reports of pyrexia following treatment and may be significant in terms of the relationship between periodontal disease, bacteremia, and cardiovascular disease.     

Salivary interleukin-6 and tumor necrosis factor-alpha in patients with burning mouth syndrome

Burning mouth syndrome (BMS) is characterized by burning symptoms on the clinically healthy oral mucosa. To date, etiology of BMS is still unknown. We hypothesized that maybe inflammation which is not clinically apparent might lead to burning symptoms which would then result in altered cytokine profile. In the 28 female patients with BMS (age range 48-80 years, mean 64.05 years) and 28 female controls (age range 40-75 years, mean 63.82 years) by use of enzyme-linked immunosorbent assay, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were determined. Statistical analysis included use of independent sample t-test and P < 0.05 was considered as significant. Our results show no significant differences between patients and controls regarding salivary IL-6 and TNF-alpha.     

Effects of transforming growth factor-beta and epidermal growth factor on clonal rat pulp cells

These factors influence proliferation and differentiation in various cell types. Their effects on a clonal cell line (RPC-C2A) having high ALPase activity were examined by assay of [3H]-thymidine incorporation and ALPase activity. Neither factor (at a dose of 0.5 ng/ml) altered the shape of the pulp cells. DNA synthesis was not affected by transforming growth factor-beta either in growing cells or in those nearly confluent, but epidermal growth factor, in doses ranging from 0.5 to 10 ng/ml, stimulated the incorporation of [3H]-thymidine in nearly confluent cells. Both factors inhibited ALPase activity in a dose-dependent manner. Indomethacin did not affect this inhibition, suggesting that this effect of growth factors may not be mediated by prostaglandin synthesis. Inhibitory effects of ALPase antagonists (L-phenylalanine, L-homoarginine, levamisole) were not affected by transforming growth factor-beta. Thus epidermal growth factor stimulates DNA synthesis and both transforming growth factor-beta and epidermal growth factor inhibit ALPase activity of clonal rat pulp cells, suggesting that both factors may act as regulators of biological function, including cell differentiation, in pulp cells.     

Interleukin 1 beta, interleukin 6, beta 2-microglobulin, and transforming growth factor-alpha in gingival crevicular fluid from human periodontal disease.

Inflammatory mediators are central to the pathogenesis of periodontal diseases and may be used as markers in diagnosis. The aim of this study was to identify and quantify the various growth factors, apoptosis-related modifiers [soluble form of Fas (sFas) and bcl-2] and cytokines in the gingival crevicular fluid (GCF) of patients with different severities of periodontitis as compared with those of controls. GCF samples were taken from patients with periodontal disease and from controls. The concentrations of epidermal growth factor, transforming growth factor (TGF)-alpha, interleukin (IL)-1 beta, IL-6, interferon-gamma, beta 2-microglobulin (beta 2-MG), and apoptosis-related modifiers sFas and bcl-2 in the samples were determined by enzyme-linked immunosorbent assay. TGF-alpha was significantly lower in patients with periodontal disease than in the controls. In contrast, the concentrations of IL-1 beta, IL-6; and beta 2-MG were significantly higher in the group with severe periodontal disease than in the controls. The amount of total protein in the GCF was considerably higher in the disease group than the controls (p < 0.05). TGF-alpha, IL-1 beta, and beta 2-MG concentrations were associated (Spearman rank correlation, r < 0.05 for all) with clinical measures of disease severity (pocket depth) and inflammation (bleeding when probed). Apoptosis-related modifiers (sFas and bcl-2) could not be detected in any samples. These results suggest that the growth factor TGF-alpha and certain cytokines are associated with the presence of periodontal disease.     

The influence of interleukin gene polymorphism on expression of interleukin-1beta and tumor necrosis factor-alpha in periodontal tissue and gingival crevicular fluid.

BACKGROUND: A specific composite genotype of the polymorphic interleukin-1 (IL-1) gene cluster has recently been associated with severe periodontitis. One polymorphism of the composite periodontitis-associated genotype (PAG) has been functionally linked with expression of high levels of IL-1. The purpose of this study was to test whether gingival crevicular fluid (GCF) levels of IL-1beta and tumor necrosis factor-alpha (TNFalpha), and gingival tissue levels of IL-1alpha, IL-1beta, and TNFalpha correlate with PAG, and to examine the effect of conservative periodontal therapy on these levels. METHODS: Twenty-two adults with moderate to advanced periodontal disease were enrolled. Polymerase chain reaction amplification and restriction enzymes were used to identify specific polymorphisms from peripheral blood samples. GCF samples were collected at baseline and 3 weeks following conservative treatment and analyzed by ELISA for IL-1beta and TNFalpha. An interproximal gingival biopsy was collected at baseline and follow-up and analyzed for IL-1alpha, IL-1beta, and TNFalpha by ELISA. RESULTS: The genotyping identified 7 as PAG(+) and 15 as PAG(-). The 2 groups were comparable in terms of existing periodontitis and age. In shallow sites (<4 mm), total IL-1beta in GCF was 2.5 times higher for PAG(+) patients prior to treatment (P=0.03), and 2.2 times higher after treatment (P=0.04), while differences were less apparent in deeper sites. Following treatment, a reduction in IL-1beta concentration in GCF was seen for PAG(-) but not for PAG(+) patients. While not statistically significant, a trend was observed in mean tissue levels of IL-1beta which were 3.6 times higher in PAG(+) versus PAG(-) patients (P=0.09). CONCLUSIONS: These data suggest that PAG(+) patients may demonstrate phenotypic differences as indicated by elevated levels of IL-1beta in GCF.     

Macrophage tolerance response to Aggregatibacter actinomycetemcomitans lipopolysaccharide induces differential regulation of tumor necrosis factor-alpha, interleukin-1 beta and matrix metalloproteinase 9 secretion

Background and Objective: The lipopolysaccharide of Aggregatibacter actinomycetemcomitans, a potent stimulator of the immune system, induces the secretion of inflammatory mediators that modulate periodontal tissue destruction. In this study, we investigated the tolerance response of human macrophages to stimulation with A. actinomycetemcomitans lipopolysaccharide. Material and Methods: U937 monocytes were differentiated into adherent macrophage‐like cells by treatment with phorbol myristic acid. Macrophage‐like cells were then pretreated for 24 h with either 0.01 or 0.1 μg/mL LPS A. actinomycetemcomitans. Culture medium supernatants were removed and cells were restimulated with LPS at 1 μg/mL. Cell‐free supernatants were collected after 24 h of stimulation and analyzed by ELISA for TNF‐α, IL‐1β, IL‐6, IL‐8, PGE₂ and MMP‐9. Results: Phorbol myristic acid‐differentiated U937 macrophages treated with low doses of lipopolysaccharide developed tolerance to subsequent lipopolysaccharide treatments, resulting in significantly reduced secretion of tumor necrosis factor‐α. However, this tolerance response was associated with increased secretion of interleukin‐1β and matrix metalloproteinase 9, whereas the secretion of interleukin‐6, interleukin‐8 and prostaglandin E₂ was unaffected. Phosphatidylinositol‐3′‐kinase inhibitors added during the tolerance‐induction period markedly attenuated the increase in interleukin‐1β secretion but had no effect on tumor necrosis factor‐α. Conclusion: This study showed that A. actinomycetemcomitans lipopolysaccharide can induce a tolerance response in macrophages that alters the secretion of two important inflammatory mediators as well as of the tissue‐degrading enzyme matrix metalloproteinase‐9. This phenomenon may play a role in modulating the host inflammatory response and the progression of periodontitis.     

Interleukin-1beta,tumor necrosis factor-alpha levels and neutrophil elastase activity in peri-implant crevicular fluid

The aim of this study was to determine interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) levels and neutrophil elastase (NE) activity in peri-implant crevicular fluid (PICF) of smoker and nonsmoker patients, and to investigate their relationships with clinical parameters. A total of 42 endosseous root-form dental implants of 14 patients were clinically examined by modified Plaque index (PI), modified Gingival index (GI) and probing depth (PD). Smoking habits of the patients were recorded. PICF of implants were collected by Periopaper strips and IL-1beta, TNF-alpha levels were determined by enzyme-linked immunosorbent assay (ELISA). NE was analyzed with a neutrophil specific chromogenic substrate, N-methoxysuccinyl-Ala-Ala-Pro-Val-p-nitroanilide. The cytokine and enzyme levels in PICF were expressed as total amount/activity and as concentrations. NE activity in PICF significantly correlated with GI and PD, and IL-1beta levels with GI and PICF volume (P < 0.05). The correlations were stronger when the PICF levels were expressed as total IL-1beta amount and as total NE activity. The implants with inflamed gingiva (GI > 1) had higher levels of IL-1beta and NE activity than implants with noninflamed or slightly inflamed gingiva (GI 3 mm) was greater than the implants with shallow pockets (PD 相似文献   

Different roles of dexamethasone on transforming growth factor-beta1-induced fibronectin and nerve growth factor expression in dental pulp cells

During pulp injury, it has been hypothesized that transforming growth factor-beta1 (TGF-beta1) is released from dentin into pulp tissue and promotes pulp tissue healing. Dexamethasone is a glucocorticoid that has been used to treat pulp injury and shown to induce differentiation of hard tissue forming cells. However, the interaction between dexamethasone and TGF-beta1 is still unknown. This study aimed to examine the effects of dexamethasone on human pulp cells in the presence of TGF-beta1. TGF-beta1 increased expression and synthesis of both fibronectin and nerve growth factor (NGF), whereas dexamethasone stimulated fibronectin synthesis but inhibited NGF expression. The application of both TGF-beta1 and dexamethasone resulted in an additional effect on fibronectin; however, dexamethasone inhibited the TGF-beta1-induced NGF expression. Dexamethasone promotes fibronectin synthesis and suppresses NGF secretion, suggesting that this reagent could be used clinically to reduce pain and promote dental pulp tissue healing.