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1.
Interleukin-6 (IL-6) is thought to be a major mediator of the host's defense against infection, and it regulates immune responses in inflamed tissue. In this study, we investigated the regulation of IL-6 production in human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPLF). Pro-inflammatory cytokines including interleukin (IL)-lα, IL-1β and tumor necrosis factor (TNF)-α stimulated IL-6 production in HGF and HPLF in a time- and dose-dependent manner. This IL-lα, IL-lβ, or TNF-α-induced IL-6 production was enhanced, but the cAMP accumulation they induced was inhibited by the addition of indomethacin. This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-l or TNF-α-induced IL-6 production, and that the enhancement of IL-6 production by IL-l or TNF-α may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dexamethasone (DEX), a glucocorticoid which is a inhibitor of nuclear factor kappa B (NF-kB) activation, markedly inhibited IL-l (α or β) or TNF-α-induced IL-6 production; so this production may be partially mediated through NF-kB. IL-l (α or β) and TNF-α enhanced IL-6 production synergistically. IL-6 production in HGF or HPLF stimulated with IL-lβ was augmented by the addition of interferon (IFN)-(gama), but was slightly suppressed by the addition of IL-4. Endogenous IL-6 enhanced IL-l (α or β)-induced IL-6 production in the presence of IL-6 soluble receptor (IL-6sR). Accordingly, in inflamed periodontal tissues, gingival fibroblasts and periodontal ligament fibroblasts stimulated with pro-inflammatory cytokines such as IL-l or TNF-α, may produce IL-6, and this production can be differentially modulated by endogenous PGE2, IL-6sR, T cell-derived cytokines such as IFN-(gama) or IL-4, and glucocorticoids.  相似文献   

2.
Interleukin-l (IL-1) molecules, IL-lα and IL-lβ are cytokines involved in the acute-phase response against infection and in the pathogenesis of periodontal destruction. Administration of exogenous IL-1 receptor antagonist (IL-1ra) is effective in reducing the inflammatory reactions mediated by IL-1. However, the relationship between these three naturally occurring IL-1 molecules and periodontal diseases has been poorly characterized. We investigated the correlation of gingival crevicular IL-1 molecules and the clinical status of patients with different severities of periodontitis. IL-lα, IL-1β, IL-1ra and the total IL-1/IL-1ra ratio (IL-1 activity index; IL-1AI) were measured in 75 gingival crevicular fluid (GCF) samples from non-inflamed gingiva sites in 2 healthy subjects and diseased sites in 7 patients with several types of periodontitis. IL-lα, IL-1bT and IL-1ra were measured by specific non-cross-reactive enzyme linked immunosorbent assay. The probing depth, gingival index and alveolar bone loss of each site was recorded at the time of GCF sampling. The total amount of IL-lα, IL-1β and the IL-1AI, but not total IL-1ra, were found to be correlated with alveolar bone loss score. Three IL-1 molecules were also measured in the gingival tissue of patients with periodontitis. A similar progressive decrease of the IL-1AI was detected in gingival tissue with periodontitis. These results suggest that the amounts of both crevicular IL-1 and IL-1AI are closely associated with periodontal disease severity.  相似文献   

3.
The expression of mRNA encoding the inflammatory cytokines interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor α (TNF-α) have been examined in radicular cysts by in situ hybridization. Furthermore, the biological activity of the contents of radicular cysts (RCC) has been assayed by adding extracts of RCC to cultured human gingival fibroblasts (HGFs) and analyzing the culture medium for the release of inflammatory cytokines. In the epithelial layer, keratinocytes expressed all cytokine mRNAs examined at various levels. Basal layer cells expressed mRNA for each cytokine. In the subepithelial granulation tissue of the cysts, fibroblasts and macrophages expressed mRNA for IL-6, IL-8, IL-1β and TNF-α mRNA at varying levels; especially clear expression of TNF-α and IL-1β mRNA was detected on macrophages. The infiltrating lymphoid cells, largely composed of T cells and plasma cells, expressed these cytokine mRNAs, especially those encoding IL-6 and IL-8, at various levels. In vitro analysis indicated dose-dependent release of both IL-6 and IL-8 by HGFs in response to RCC. After heating to 100°C for 10 min, RCC almost completely failed to stimulate IL-6 release from HGFs. Furthermore, anti-IL-1β antibody (neutralization test) did not prevent the stimulation of IL-6 release by RCC. Significant amounts of IL-6 and IL-8 were detected in RCC in two cases, and a trace amount of IL-1β was detected in one case. This study demonstrated the wide expression of mRNA encoding inflammatory cytokines in radicular cyst tissues, and RCC itself was capable of stimulating 1L-6 and 1L-8 production from HGFs.  相似文献   

4.
To examine the effects of interleukin-lβ (IL-1β) on collagenase production by human periodontal ligament fibroblasts (PLF) and gingival fibroblasts (GF) in Culture, collagenase activity in conditioned media was determined using a novel procedure that circumvented interference by enzyme inhibitors. Fibroblasts obtained from five paired periodontal ligament and gingival tissues were cultured for two weeks, and then incubated for a further 72 h in α-MEM supplemented with various concentrations of IL-1β (0 to 1250 pg/ml). The conditioned media from individual cultures were harvested and treated with dithiothreitol to inactivate TIMPs, and then with APMA, to activate the latent collagenase. Collagenase activity was measured fluorometrically using FITC-collagen as a substrate. IL-lβ induced a ∼2.4 to 5.2-fold increase in collagenase activity in PLF compared to a ∼1.4 to 2.2-fold increase in GF. These results are in contrast to previous studies in which collagenase activity was measured in the presence of TIMPs, and indicate that PLF are more sensitive to IL-1β than GF. Since both PLF and GF are present in periodontal lesions, it is possible that collagenase secretion stimulated by exposure to inflammatory cell products such as IL-lβ may participate in the destruction of collagen fibers involved in periodontal attachment.  相似文献   

5.
Cytokine generation by tissue-infiltrating mononuclear cells (TIMC) and by keratinocytes (KC) was investigated in material obtained from the oral mucosal tissues of patients with oral lichen planus (OLP). Peripheral blood mononuclear cells (PBMC) and chronically inflamed and noninflamed gingival KC (CIG-KC, NOR-KC, respectively) were used as the controls. Compared to NOR-KC and CIG-KC, KC from OLP patients (OLP-KC) produced much more interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and granulocyte-macrophage colony-stimulating factor (GM-CSF). The OLP-KC superiority in the production of these cytokines was more prominent when the KC were cultured in the presence of interleukin-l beta (IL-1β), lipopolysaccharide and phorbol myristate acetate. OLP-KC also produced more monocyte-chemotactic factor(s) which were not inactivated by the antibodies against GM-CSF, macrophage colony-stimulating factor and monocyte chemoattractant protein-1. TIMC in OLP tissues (OLP-TIMC) were superior to PBMC in the generation of IL-6 and GM-CSF. OLP-TIMC were stimulated to produce more TNF-a by IL-1β, IL-6 and GM-CSF, more IL-6 by IL-1β and GM-CSF, and more GM-CSF by IL-1β and IL-6 than PBMC. When compared to cytokine generation in TIMC from the chronically inflamed gingivae, more interferon-gamma, IL-6 and TNF-α were generated by OLP-TIMC. These results indicate that KC play a critical role in OLP, producing cytokines including monocyte-chemotactic factor(s), and that the cytokines produced by TIMC and OLP-KC through autocrine and paracrine processes enhance the local inflammatory response.  相似文献   

6.
The present study demonstrates that interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) induce and synergistically stimulate monocyte chemoattractant protein-1 (MCP-1) expression in fibroblasts from human periodontal ligament. IL-1β and TNF-α induced in a dose-dependent manner the expression of the MCP-1 gene in the fibroblasts from the human periodontal ligament. However, such an inducing effect was not observed with IL-6 and interferon-γ. The peak expression of the MCP-1 gene by IL-1β or TNF-α was observed at 3 h after initiation of their treatment. Furthermore, IL-1β in combination with TNF-α synergistically stimulated the MCP-1 gene expression in the cells. We also observed significant chemotactic activity for human monocytes in conditioned medium of fibroblasts from the human periodontal ligament treated with both cytokines. The stimulated chemotactic activity induced by these cytokines depended on both dose and treatment time. The chemotactic activity in conditioned medium of IL-1β-treated fibroblasts from the human periodontal ligament was neutralized by antiserum specific for MCP-1 protein. The MCP-1 gene product in conditioned medium of IL-1β-treated fibroblasts from the human periodontal ligament was shown to have a molecular mass of 11,000 Da by immunoprecipitation with the specific antiserum, and IL-1β also stimulated synergistically MCP-1 protein expression in combination with TNF-α. These results suggest that IL-1β and TNF-α may contribute to the infiltration of monocytes into inflammatory sites of periodontal ligament tissues via the MCP-1 gene product produced by fibroblasts from the human periodontal ligament.  相似文献   

7.
Cytokines are believed to play an important role in the pathogenesis of periodontal diseases. In the present study, gingival crevicular fluid (GCF) levels of two important cytokines, interleukin 1-/3 (IL-1β) and tumour necrosis factor-α (TNF-α) and, in addition, serum IL-1β levels, were determined in patients with severe and rapid periodontal breakdown by use of ELISA. While IL-1β was detected in all of the GCF samples studied, TNF-α could only be detected in about half the samples. The mean GCF IL-1β level was 38.45 ± 13.99 pg/mL, and the mean TNF-α level was 3.20 ± 1.39 pg/mL, respectively. The GCF IL-1β levels also presented a strong positive correlation with the mean pocket depths. Although weak, both of the cytokines also presented correlations with the presence of bleeding on probing. Additionally GCF samples contained increased IL-1β levels when compared with the serum samples suggesting local production mechanisms. The findings of the present study suggest that these cytokines may be involved in the pathogenesis of periodontal diseases (IL-1β being more significant), and also may help in defining the active phase of periodontal breakdown.  相似文献   

8.
Background:  The role of cytokines in pathogenesis of periapical lesions is not well understood. The aim of this study was to study the correlation between proinflammatory and immunoregulatory cytokines in periapical lesions and their relationship with cellular composition and clinical presentation.
Methods:  Inflammatory cells were isolated from 67 human periapical lesions and cultivated for 24 h. The levels of proinflammatory cytokines: interleukin-1 beta (IL-1β), IL-6, IL-8 and tumour necrosis factor alpha (TNF-α) and immunoregulatory cytokines: transforming growth factor-beta (TGF-β) and IL-10 were determined in culture supernatants using a fluorescent bead immunoassay or ELISA. The phenotype of cells was analysed by immunocytochemistry.
Results:  Inflammatory cells from symptomatic lesions which contained higher proportion of granulocytes, secreted higher levels of IL-1, IL-6 and IL-8 compared with asymptomatic lesions. Large-size lesions contained lower percentages of mononuclear phagocytes, higher percentages of CD8+ T cells and produced higher levels of TNF-α, IL-6 and IL-10 compared with small-size lesions. There were negative correlations between the concentrations of TGF-β and proinflammatory cytokines. TGF-β, added to cultures, downregulated the levels of proinflammatory cytokines more strongly than IL-10, independently of clinical presentation of the lesions. By contrast, exogenous IL-10 was mainly immunosuppressive in cultures of asymptomatic lesions.
Conclusion:  Symptomatic lesions are characterized by higher production of proinflammatory cytokines. Immunoregulatory cytokines are more important for suppression of inflammation in asymptomatic lesions and in this context the effect of TGF-β is more potent and different from IL-10.  相似文献   

9.
10.
Background/aim:  Periodontitis begins as the result of perturbation of the gingival epithelial cells caused by subgingival bacteria interacting with the epithelial cells via pattern recognition receptors. Toll-like receptors (TLRs) have been shown to play an important role in the recognition of periodontal pathogens so we have studied the interaction of TLR ligands with TLR2 and TLR5 for cytokine production in the cultures of gingival epithelial cells.
Methods:  Immunohistochemistry was used for the localization of TLR2 and TLR5 in tissue specimens. Enzyme-linked immunosorbent assays were performed to detect the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), released from gingival epithelial cell cultures following stimulation with TLR ligand alone or in combination with IL-17.
Results:  Both TLR2 and TLR5 were increased in periodontitis (2128 ± 159 vs. 449 ± 59 and 2456 ± 297 vs. 679 ± 103, respectively, P  < 0.001) including gingival epithelial cells that stained strongly. Cultured gingival epithelial cells stimulated with their respective ligands (HKLM, a TLR2 ligand that is also found in Porphyromonas gingivalis , and flagellin, a TLR5 ligand that is also found in Treponema denticola ) produced both IL-1β and TNF-α. To mimic T-cell help, IL-17 was added. This further greatly enhanced TLR ligand-induced IL-1β ( P  < 0.001) and TNF-α ( P  < 0.01) production.
Conclusions:  These findings show how pathogen-associated molecular patterns, shared by many different periodontopathogenic bacteria, stimulate the resident gingival epithelial cells to inflammatory responses in a TLR-dependent manner. This stimulation may be particularly strong in periodontitis and when T helper type 17 cells provide T-cell help in intercellular cooperation.  相似文献   

11.
Differences in expression of intercellular adhesion molecule-1 (ICAM-1) and ICAM-1 mRNA levels were studied in cultured skin and oral keratinocytes before and after stimulation with different pro-inflammatory cytokines. Basal expression of ICAM-1 was undetectable on skin keratinocytes but oral keratinocytes expressed ICAM-1 at high levels. Interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) increased ICAM-1 expression on both cell types, although TNF-α had a greater effect on oral than skin keratinocytes ( P < 0.05) and IFN-γ was more effective than TNF-α on both cell types ( P < 0.01). In combination, TNF-α and IFN-γ synergistically increased ICAM-1 expression on skin keratinocytes only, although ICAM-1 mRNA was synergistically increased in both cell types. IL-lα and IL-1β induced a small increase in ICAM-1 expression on oral keratinocytes but had no effect on skin keratinocytes.  相似文献   

12.
13.
Inflammatory mediators released as a result of smokeless tobacco (ST)-induced irritation may play a role in the development of oral mucosal lesions at habitual tobacco placement sites in ST users. The present study examined levels of interleukin-1 (IL-1) and prostaglandin E2 (PGE2) in ST-induced mucosal lesions and compared these to mediator levels in clinically normal mucosa. Soft tissue biopsies were obtained from white mucosal lesions at habitual placement sites and normal alveolar mucosal tissue at non-placement sites in 18 ST users. Fifteen non-tobacco using subjects also provided normal alveolar mucosal biopsies. IL-1 and PGE2 were recovered from the specimens, and mediator levels were determined by enzyme immunoassay. Prostaglandin E2 levels (pg/mg) were lower in both regions in the ST subjects, but values did not vary significantly between the regions with 2.77±0.72 and 2.86±0.99 at placement and non-placement sites, respectively, in ST users and 7.31±3.84 in non-tobacco users. Both IL-1α and IL-lβ (pg/mg) were significantly (p < 0.0I) elevated in ST lesions (IL-lã=25.56±4.00; IL-1β=7.76±1.68) compared to either non-placement sites in ST users (IL-lα=14.64±2.65; IL-lβ=1.63±0.72) or non-tobacco users (IL-lα=12.84±2.60; IL-lβ=2.04±0.75). In view of IL-l's role in keratinocyte proliferation and its inflammatory effects, this cytokine may contribute to mucosal and gingival alterations observed in ST users.  相似文献   

14.
OBJECTIVE: Langerhans cells are believed to originate from the monocyte lineage and have been reported to increase in number with plaque accumulation and gingival inflammation. The aim of this study was to investigate the effects of local gingival epithelial factors on the induction of CDla, a Langerhans cell phenotype, on monocyte rich populations.
MATERIALS AND METHODS: Peripheral blood monocyte rich populations from healthy subjects were cultured for 24 h with either healthy gingival or periodontally diseased gingival epithelial supernatants. Additionally, the monocyte rich populations were cultured with cytokines IL-Iα, IL-Iβ, IL-6 and TNF-α which are known to be produced by epithelial cells or co-cultured with autologous epithelial cells. The percent CDIa positive cells was determined using FACS analysis.
RESULTS: Healthy gingival supernatants did not induce CDIa expression in monocyte rich populations, however, a significant increase in per cent CDla+ cells for monocyte rich populations cultured with five (P < 0.01) of six periodontal gingival epithelial supernatants was found. IL-lα or TNF-α (10ng/well) resulted in a significant increase in the per cent CDla+ cells (P < 0.01). Depletion of CDla+ Langerhans cells from healthy gingival epithelium did not enhance induction of CDIa expression in monocyte rich populations. Monocyte rich populations cultured together with non-depleted epithelial cultures resulted in a decreased percent of CDla+ cells.
CONCLUSION: These findings indicated that epithelial factor/s associated with periodontally involved epithelia, may be involved in inducing a Langerhans cell phenotype in monocyte rich populations. The data also provide indirect evidence for a role of Langerhans cells in inhibiting induction of CDIa in healthy epithelium.  相似文献   

15.
Background/aims:  Clinical studies indicate that primary proinflammatory cytokines, such as interleukin-1β (IL-1β) are elevated in the gingival crevice around teeth with periodontitis but the secondary cytokines and chemokines, IL-6 and IL-8, are not. The human gingival epithelial cells (HGECs) lining the gingival sulcus respond to perturbation by microbes of dental plaque by releasing a wide range of cytokines. Porphyromonas gingivalis , a putative periodontal pathogen, possesses numerous virulence factors some of which directly impact on the host response. In the present study, we sought to determine how P. gingivalis influences the inflammatory cytokine responses.
Methods:  HGECs were challenged with P. gingivalis and other putative periodontal pathogens, and the resultant production of IL-1β, IL-6, and IL-8 was assayed by enzyme-linked immunosorbent assay (ELISA). Culture supernatants and recombinant human cytokines were challenged with live P. gingivalis wild-type and gingipain-deficient strains and the resultant cytokine profile was assessed by ELISA and Western blot.
Results:  We show here that primary HGECs challenged with live P. gingivalis result in high levels of IL-1β but not the related secondary cytokines IL-6 and IL-8. We further demonstrate that cytokine response differences are the result of the action of P. gingivalis proteases, with lysine gingipain being the most effective.
Conclusion:  We conclude that P. gingivalis , through lysine gingipain, can subvert the protective host proinflammatory response by direct cytokine degradation. Changes in the crevicular cytokine profile have consequences in periodontal disease pathogenesis that should be considered in the development of diagnostic and therapeutic modalities.  相似文献   

16.
Ameloblastomas produce interleukin-1-like activity that could explain some part of their osteolytic capability. However, the cellular source of this osteolytic activity is unknown. In the present study, cytokines with known inflammatory and osteolytic activity, i.e., interleukin-1 (IL-1), tumour necrosis factor (TNF), and interleukin-6 (IL-6), have been localised by immunocytochemistry and in situ hybridisation. The cellular adhesion receptors ICAM-1, E-selectin and VCAM-1 have also been immunolocalised. Immunocytochemistry demonstrated that all seven specimens showed positive staining for IL-1α and IL-6 with these cytokines being located in the stellate reticulum-like cells and vascular endothelium. Very faint staining for IL-1β was seen in four of seven specimens. No reaction was seen for TNF-α. All specimens demonstrated E-selectin staining in the vascular endothelium and ICAM-1 and VCAM-1 staining in the stellate reticulum-like cells and the endothelium. In situ hybridisation for the cytokines showed the presence of mRNA of both IL-1α and IL-6 in the stellate reticulum-like cells. Faint staining for IL-1β was also seen. No staining was seen for TNF. These findings show that ameloblastomas synthesize two bone-modulating cytokines, IL-1α and IL-6, and that these are synthesized mainly by the stellate reticulum-like cells. These tumours also contain a proportion of activated blood vessels in which endothelial cells express the cellular adhesion receptors ICAM-1, E-selectin and VCAM-1.  相似文献   

17.
Bacteria can indirectly affect the course of periodontal diseases by activating host cells to produce and release inflammatory mediators and cytokines. These mediators and cytokines, manifest potent proinflammatory and catabolic activity and may play key roles in local amplification of the immune response as well as in periodontal tissue breakdown. This study tested the effect of Actinobacillus actinomycetemecomitans (Aa) and Campylobacter rectus (Cr) challenge on PGE2, IL-1β, IL-6 and IL-8 production by human gingival fibroblasts (HGF). Contact-inhibited HGF were prepared and formalin-killed bacterial cells ( Aa JP2, ATCC 29523 & 33384 and Cr ATCC 33238) at 106-109 were added to the HGF. Culture supernatants were collected at varying time intervals and analyzed for cytokine and mediator content. All concentrations of Aa JP2 and Cr ATCC 33238 suppressed IL-1β production up to approximately 50% during the initial 3-12-h period. No bacterial concentration tested was able to increase IL-1β production above the maximum basal levels. Both bacterial species stimulated production of IL-6 and IL-8. Aa JP2 did not affect PGE2 levels significantly, whereas Cr ATCC 33238 was stimulatory only at the highest concentration tested (109). There were no significant differences among the three Aa strains with respect to IL-1β production. However, Aa ATCC 29523 and ATCC 33384 were less capable of stimulating IL-6 secretion and more efficient in stimulating. IL-8 production than Aa JP2. In general. Cr was the most potent enhancer of cyto-kine and mediator production by HGF. In conclusion, Aa and Cr are capable of amplifying the local immune response and promoting periodontal tissue inflammation by stimulating HGF to secrete mainly IL-6 and IL-8.  相似文献   

18.
19.
The effect of recombinant interleukin-1β (IL-lβ) on hyaluronic acid synthesis by human gingival fibroblasts was studied. IL-1bT caused a dose-dependent increase in the incorporation of (3lucosamine into hyaluronic acid. The 35S/35H ratios of labeled macromolecules did not change regardless of the presence or absence of TL-lβ and indicates stimulation of hyaluronic acid synthesis. Inhibition of cell proliferation by hydroxyurea caused an increase in hyaluronic acid synthesis. The effect of IL-1β on hyaluronic acid synthesis in the presence of hydroxyurea was increased over untreated and IL-lβ-treated controls, but equivalent to the hydroxyurea-treated controls. Thus the effect of IL-1β on hyaluronic acid synthesis may be independent of cell proliferation. Furthermore, inhibition of prostaglandin E2 synthesis by indomethacin abolished the effect of IL-1β on hyaluronic acid synthesis. Inhibition of new protein synthesis by cycloheximide negated the effect of IL-β on hyaluronic acid synthesis. This may be related to inhibition of new hyaluronate synthetase synthesis, since IL-1β stimulated the level of hyaluronate synthetase activity. Sepharose CL-2B chromatography revealed that most of the newly synthesized hyaluronic acid was of large molecular size. The cells exposed to IL-1β retained more large molecular size hyaluronic acid in their cell layer environment than did the control cells. These responses by fibroblasts to IL-1β may be indicative of early tissue repair.  相似文献   

20.
The bone-resorptive cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have been implicated in the pathogenesis of many chronic inflammatory diseases, including pulpitis and apical periodontitis. To further elucidate their role in these disorders, we have identified cells that express IL-1α and TNFα in infected pulps and in developing rat periapical lesions after surgical pulp exposure. As detected by immunohistochemistry, IL-1α- and TNFα-positive cells were present as early as 2 days after pulp exposure in both the pulp and periapical region. The numbers of cytokine-expressing cells increased up to day 4 in the pulp and up to day 30 in the periapex. In contrast, cells expressing IL-1β and TNFβ the homologous forms of these mediators, were not found in pulp or periapical lesions during this period. Cells expressing IL-1α and TNFα were identified primarily as macrophages and fibroblasts, with occasional staining of polymorphonuclear leukocytes. Osteoblasts and osteoclasts were also positive, whereas lymphocytes were negative. In general, cytokine-expressing cells were located proximal to abscesses and the root apex. These findings demonstrate that cells that express bone-resorptive cytokines IL-1α and TNFα are present immediately after pulp exposure in this model, which supports the hypothesis that these mediators play a key role in pulpal and periapical pathogenesis, including the concomitant bone destruction. They also indicate that both resident connective tissue cells as well as infiltrating cells express bone-resorptive cytokines in response to infection in these lesions.  相似文献   

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