Biomedical subjects

T Modéer

Publications and source records attributed to T Modéer.

At least 19 recordsLinked to original sources

PubMed2005

Triclosan reduces microsomal prostaglandin E synthase-1 expression in human gingival fibroblasts.

OBJECTIVE: The effect of triclosan (2,4,4'-trichloro-2'-hydroxydiphenyl ether) on the expression of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) and on the translocation of the nuclear factor-kappaB (NF-kappaB) in relation to prostaglandin E2 (PGE2) production was investigated in human gingival fibroblasts challenged with tumor necrosis factor alpha (TNFalpha). METHODS: Fibroblasts were established from gingival biopsies obtained from six children. COX-2 mRNA and protein expression was quantified using mRNA quantitation and enzyme immunometric assay kits. mPGES-1 mRNA was analysed by RT-PCR, mPGES-1 protein and NF-kappaB translocation by immunoblotting. PGE2 was determined by radioimmunoassay. RESULTS: The cytokine TNFalpha enhanced the expression of mRNA as well as the protein levels of both COX-2 and mPGES-1 and subsequently the production of PGE2 in gingival fibroblasts. Treatment of gingival fibroblasts with triclosan (1 microg/ml) significantly reduced the stimulatory effect of TNFalpha (10 ng/ml) on the expression of mPGES-1 at both the mRNA and the protein level by an average of 21% and 43%, respectively, and subsequently the production of PGE2 (p<0.01). Triclosan did not, however, affect the translocation of NF-kappaB or the expression of COX-2 in TNFalpha-stimulated cells. CONCLUSION: The results show that triclosan reduces the augmented biosynthesis of PGE2 by inhibiting the mRNA and the protein expression of mPGES-1 in gingival fibroblasts. This finding may partly explain the anti-inflammatory effect of the agent previously reported in clinical studies.

Alprostadil↗

PubMed2004

Matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 production in human gingival fibroblasts: the role of protein kinase C.

BACKGROUND: Matrix metalloproteinase-1 (MMP-1) plays an important role in tissue remodelling and in the pathology of inflammatory diseases including periodontitis. The activity of MMP-1 is firmly controlled by the endogenous tissue inhibitor of metalloproteinase-1 (TIMP-1). OBJECTIVE: The aim of the study was to investigate the production and regulation of MMP-1 and TIMP-1 with special regards to the enzyme protein kinase C (PKC) in human gingival fibroblasts. METHODS: Gingival fibroblasts were treated with substances related to PKC such as phorbol 12-myristate 13-acetate (PMA), interleukin-1beta, Ca2+ -ionophore A231817 and inhibitors of PKC, p38 mitogen-activated protein kinase (p38 MAPK) and tyrosine kinase. RESULTS: The PKC activator PMA stimulated the production of MMP-1 and TIMP-1 at both the transcriptional and the translational level. The production of MMP-1 and TIMP-1 stimulated by PMA was abolished by the PKC inhibitor bisindolylmaleimide. Treatment of the cells with interleukin-1beta or A23187 synergistically increased the stimulatory effect of PMA on MMP-1 production. In contrast, TIMP-1 production was unaffected by interleukin-1beta and reduced by A23187. Tyrosine kinase inhibitor herbimycin A reduced MMP-1 production induced by PMA, whereas the p38 MAPK-inhibitor SB 203580 synergistically increased the stimulatory effect of PMA on both MMP-1 and TIMP-1 production. CONCLUSION: The present study shows that MMP-1 and TIMP-1 production is regulated differently by interleukin-1beta and calcium in human gingival fibroblasts and that this difference is markedly amplified in the presence of the PKC-activator PMA. Taken together, the discrepancy in the production of MMP-1 and TIMP-1 in gingival fibroblasts may contribute to tissue destruction in periodontal diseases.

Adolescent↗

PubMed2002

Herpes simplex virus type 1 infection and glucocorticoid treatment regulate viral yield, glucocorticoid receptor and NF-kappaB levels.

The interplay between the endocrine and immune systems has come into focus in recent years with the insight that endocrine parameters may affect susceptibility to both auto-immune and infectious diseases. Our interest in immunoendocrine regulation led us to investigate the effects of glucocorticoids on Herpes simplex virus type 1 (HSV-1) infections. Glucocorticoids used to treat inflammatory conditions are not yet recommended for HSV-1 therapy, since they have been reported to prolong viral shedding both in vivo and in vitro. Here we report that glucocorticoids did not alter the viral yield in human gingival fibroblast (HGF) cell culture when glucocorticoid treatment and viral infection occured simultaneously, but the viral yield increased when cells were treated with the glucocorticoid dexamethasone (dex) prior to viral infection. We found that viral infection in our primary cell system increased NF-kappaB levels and DNA binding. In addition, the amount of glucocorticoid receptor (GR) increased following viral infection, and HSV-1 infection as such could induce glucocorticoid-driven transcription of a reporter gene in human embryo kidney (HEK) 293 cells stably transfected with GR. Dex treatment did not affect HSV-1-induced binding of p65 to an NF-kappaB element in an electrophoretic mobility shift assay, and acyclovir was still efficient as an anti-viral drug in the presence of dex. Further studies of the observed effects of HSV-1 infection and glucocorticoid treatment on GR and NF-kappaB regulation could give insights into the immunoendocrine mechanisms important for defence and therapy against viral infections.

Acyclovir↗

PubMed2001

Production of Rantes/CCL5 in human gingival fibroblasts challenged with tumor necrosis factor alpha.

Chemokines are small-secreted proteins that stimulate the directional migration of leukocytes and thereby mediate the inflammatory process. The present study investigates the capacity of human gingival fibroblasts to produce the beta chemokine Rantes/CCL5. In situ hybridization, immunohistochemistry and ELISA were used to measure the induction of Rantes/CCL5 at the mRNA and protein levels, both in unstimulated gingival fibroblasts as well as in fibroblasts treated with the proinflammatory cytokines tumor necrosis factor (TNF)alpha or interleukin (IL)-1beta. TNFalpha in different concentrations (0.1-10 ng/ml) induced Rantes/CCL5 mRNA expression and protein production in 24-h cultures of human gingival fibroblasts. The expression of Rantes/CCL5-mRNA and protein production, induced by TNFalpha, was evident at 6 h and thereafter increased continuously during the study period (24 h). IL-1beta (3-300 pg/ml) also enhanced the production of Rantes/CCL5 in gingival fibroblasts. The amount of Rantes/CCL5 induced by IL-1beta (300 pg/ml), however, was less than that induced by TNFalpha (10 ng/ml). The study suggests that human gingival fibroblasts, by producing the chemokine Rantes/CCL5, participate in the regulation of the host response during the inflammatory process in the periodontal tissue.

Cells, Cultured↗

PubMed2001

Enhanced cyclooxygenase-2 mRNA expression in human gingival fibroblasts induced by cell contact with human lymphocytes.

Prostaglandins, especially prostaglandin E2 (PGE2), play a crucial role in the pathogenesis of periodontal disease. We have previously reported that inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) increase the production of PGE2 in human gingival fibroblasts. In this study, we investigated the effect of cell-to-cell interactions between gingival fibroblasts and lymphocytes on PGE2 production by using co-culture technique. Cell-to-cell contact between gingival fibroblasts and lymphocytes synergistically enhanced the production of PGE2 in co-cultures. In contrast to lymphocytes, the cyclooxygenase-2 (COX-2) mRNA expression in gingival fibroblasts was strongly enhanced following cell contact between gingival fibroblasts and lymphocytes. The level of COX-1 mRNA expression, however, was not affected either in gingival fibroblasts or in lymphocytes by the interactions between fibroblasts and lymphocytes. The study demonstrates that cell contact between gingival fibroblasts and lymphocytes strongly stimulates PGE2 production partly due to enhanced COX-2 mRNA expression in gingival fibroblasts. The cell-to-cell contact between gingival fibroblasts and lymphocytes should be considered as an important regulatory aspect for the enhancement of PGE2 in periodontal disease.

Cell Communication↗

PubMed2001

Oral health in liver transplant children administered cyclosporin A or tacrolimus.

BACKGROUND: Immunosuppression by cyclosporin A (CsA) is associated with adverse side-effects, including nephrotoxicity, neurotoxicity and gingival overgrowth. Tacrolimus (TAC/FK506) is a new immunosuppressive agent, recently approved for use in solid-organ transplants. The mode of action of TAC is similar to that of CsA and the toxicity profile of CsA is duplicated by TAC. The effect of TAC on the gingival tissue is not yet conclusive. SAMPLE: Gingival overgrowth was assessed in 30 liver transplant children, 20 boys and 10 girls, aged 2-19 years. Seventeen children (10 boys, seven girls) were on a CsA-based immunosuppressive regimen whereas 13 children (10 boys, three girls) were on TAC for at least 1 year (mean 4.3 +/- 2.7). RESULTS: In the CsA group, 35% of children exhibited gingival overgrowth characterized by one or more units with increased sulcus probing depth (> or = 4 mm), i.e. pseudopockets. In contrast to the CsA group, none of the children in the TAC group exhibited gingival overgrowth. The occurrence of enamel hypoplasia was observed in 11 children (36%) and enamel opacities were found in 23 children (76%). Six of the 12 children (50%) with hyperbilirubinaemia biliary atresia exhibited a marked greenish discoloration of the teeth. Caries experience (dmft/DMFT) among these children was 2.0 +/- 2.8. CONCLUSION: No difference in caries experience or enamel defect was observed between the CsA and TAC group.

Adolescent↗

PubMed2001

Bradykinin induces a rapid cyclooxygenase-2 mRNA expression via Ca2+ mobilization in human gingival fibroblasts primed with interleukin-1 beta.

We have previously demonstrated that bradykinin potentiates prostaglandin E(2)release in human gingival fibroblasts pretreated with interleukin-1 beta (priming). In this study, we demonstrate a potentiating effect of bradykinin on cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts. Interleukin-1 beta (200 pg/ml) induced cyclooxygenase-2 mRNA expression, but not bradykinin (1 microM). However, bradykinin rapidly and markedly increased the cyclooxygenase-2 mRNA expression in the fibroblasts primed with interleukin-1 beta. In the primed fibroblasts, ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on the cyclooxygenase-2 mRNA expression. Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin. These results suggest that bradykinin-induced prostaglandin E2 synthesis is regulated at the level of the transcription of cyclooxygenase-2 mRNA via Ca2+ mobilization in the interleukin-1 beta-primed human gingival fibroblasts.

Bradykinin↗

PubMed2000

Bradykinin potentiates prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta via Ca(2+) mobilization.

Interleukin-1beta, a proinflammatory cytokine, causes a slow increase in prostaglandin E(2) release. On the other hand, bradykinin, a chemical mediator for inflammation, induces a rapid prostaglandin E(2) release. Simultaneous stimulation with interleukin-1beta (200 pg/ml) and bradykinin (1 microM) evoked a moderately synergistic increase in prostaglandin E(2) release in human gingival fibroblasts. However, in the human gingival fibroblasts pretreated with interleukin-1beta, bradykinin drastically enhanced prostaglandin E(2) release. NS-398, a specific inhibitor of cyclooxygenase-2, inhibited not only interleukin-1beta-induced prostaglandin E(2) release but also bradykinin-induced prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta. Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts. In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release. These results suggest that interleukin-1beta- and bradykinin-induced prostaglandin E(2) release is dependent on cyclooxygenase-2 and the potentiated effect of bradykinin in the human gingival fibroblasts primed with interleukin-1beta is caused by Ca(2+) mobilization.

Bradykinin↗

PubMed2000

Induction of interferon gamma in human gingival fibroblasts challenged with phytohaemagglutinin.

Interferon gamma (IFN-gamma) is a potential immunoregulatory cytokine, which is secreted mainly by cells of immune origin. In this study, we examined the capacity of human gingival fibroblasts as non-professional immune cells to express IFN-gamma messenger RNA (mRNA) and to produce the protein. Cultures of fibroblast cells were established from gingival biopsies from three children. The expression of mRNA for IFN-gamma was studied by in situ hybridization, and the level of IFN-gamma was determined by cell-released capturing ELISA. Treatment of the cells with phytohaemagglutinin (PHA) (2.5, 5.0, and 10 microg/ml) increased the number of IFN-gamma mRNA expressing cells and the protein production at 1, 6, and 24 h. Non-stimulated cells did not reveal measurable levels of IFN-gamma mRNA or the protein. The inflammatory cytokines interleukin 1beta (IL-1beta) (100 microg/ml) and tumour necrosis factor alpha (TNFalpha) (10 ng/ml) did not affect IFN-gamma mRNA expression or protein production. Treatment of the cells with 1 microM phorbol 12-myristate-13-acetate (PMA) stimulated IFN-gamma mRNA expression but had no effect on IFN-gamma protein production. We conclude that human gingival fibroblasts not only transcribe IFN-gamma mRNA but also produce the IFN-gamma protein in response to PHA. The finding that human gingival fibroblasts, produce the cytokine IFN-gamma, further support the concept that these cells take an active part in the modulation of the inflammatory and immune response in the periodontal tissue.

Child↗

PubMed2000

Fluoride concentration in plaque in adolescents after topical application of different fluoride varnishes.

The aim of the study was to measure the fluoride (F) concentration in plaque after a single topical application of different fluoride varnishes with contrasting levels of F. Thirty adolescents (12-17 years) with fixed orthodontic appliances were randomly assigned to one of three groups: Bifluoride (6% F), Duraphat (2.23% F) and Fluor Protector (0.1% F). The varnishes were applied after professional cleaning in one upper quadrant, leaving the opposite quadrant untreated according to the split-mouth technique. Pooled plaque samples from each quadrant were collected at baseline and 3 days, 7 days and 30 days after the varnish treatment, and fluoride was analysed by microdiffusion. All fluoride varnishes increased the fluoride concentration in plaque compared with baseline, and the mean values varied between 23 and 138 ng F/mg after 3 days, depending on varnish F concentration. Compared with the control quadrant, statistically significant elevations were recorded for Bifluoride after 3 days and 7 days and Duraphat after 3 days, while no significant differences were revealed in the Fluor Protector group. The fluoride concentration in plaque was back to baseline levels for all participants in the Duraphat group after 7 days, while some individuals in the Bifluoride and Fluor Protector groups still registered slightly increased levels after 30 days. The results suggest that fluoride varnish treatments resulted in elevated fluoride levels in plaque adjacent to fixed orthodontic appliances for a period of up to 1 week, although different patterns was disclosed for the various brands.

Adolescent↗

PubMed2000

Effect of triclosan on interferon-gamma production and major histocompatibility complex class II expression in human gingival fibroblasts.

BACKGROUND, AIMS: The effect of triclosan (2,4,4'-trichloro-2'-hydroxyl-diphenyl ether) on the production of interferon-gamma (IFN-gamma) and the expression of major histocompatibility complex (MHC) class II antigen was studied in human gingival fibroblasts isolated from 4 individuals. METHODS/RESULTS: All cell lines demonstrated high IFN-gamma production in 24-h cultures of human gingival fibroblasts stimulated by phytohemagglutinin (PHA) (5 microg/ml). Human gingival fibroblasts showed a high expression of MHC class II when stimulated with 500 and 1,000 pg/ml rIFN-gamma in 7-day cultures. Treatment of the cells with triclosan (0.5 microg/ml) reduced both IFN-gamma production and MHC class II expression in human gingival fibroblast cultures. Similar inhibitory effects on IFN-gamma production and MHC class II expression were observed when the anti-inflammatory agent dexamethazone (1 microM) was used. CONCLUSION: The present study further supports the view that the agent has an anti-inflammatory effect in addition to its antibacterial capacity.

Anti-Infective Agents, Local↗

PubMed2000

Effect of phenytoin on the production of interleukin-6 and interleukin-8 in human gingival fibroblasts.

The in vitro effect of phenytoin (PHT) on the production of interleukin-6 (IL-6) and interleukin-8 (IL-8) in human gingival fibroblasts, challenged with or without interleukin-1beta (IL-1beta), was studied. PHT (20 microg/ml) alone increased the mRNA level for both IL-6 and IL-8, as well as synergistically enhancing the production of IL-6 and IL-8, at both transcriptional and translational level in fibroblasts challenged with IL-1beta (30 pg/ml). The stimulatory effect of PHT on IL-1beta-induced IL-6 production was strongly reduced by the specific cyclooxygenase-2 inhibitor NS-398 (1 microM). The anti-inflammatory drug, dexamethasone (1 microM), abolished the production of both IL-6 and IL-8 in gingival fibroblasts challenged with PHT in the presence or absence of IL-1beta. The ability of PHT, alone as well as in combination with IL-1, to upregulate the production of IL-6 and IL-8 in human gingival fibroblasts may contribute to enhanced recruitment and activation of inflammatory cells. This effect of PHT may thereby give a prerequisite for the establishment of an interaction between cytokines and connective tissue cells in the periodontal tissue, which is suggested to lead to gingival overgrowth.

Adolescent↗

PubMed2000

Periodontal diseases in children and adolescents.

The predominant form of periodontal disease in children and adolescents is gingivitis, which is a nonspecific inflammatory reaction of the marginal gingiva. The inflammatory reaction in the tissue, initiated by dental plaque accumulation, starts early during infancy and reflects the bacterial challenge to the host. In most children, the process of gingival inflammation remains superficial. In some cases, however, the balance between the microbial challenge and the host response is disrupted, leading to an inflammatory process that may result in loss of attachment. Genetic factors that modify the host response to the bacterial challenge are major determinants of susceptibility to the development of EOP, and many systemic diseases have been reported to predispose children and adolescents to periodontal disease. It is important to take a complete medical history of the patient and assess if there is a hereditary trend for periodontitis within the family. Dental professionals should rely on clinical and radiographic criteria of the disease for early identification of children at risk, with special focus on the presence of subgingival calculus. Children with overt gingival inflammation, subgingival calculus, or early signs of alveolar bone loss should be considered as periodontitis-risk patients and should be included in a preventive program as early as possible.

Adolescent↗

PubMed1999

Involvement of tyrosine kinases on cyclooxygenase expression and prostaglandin E2 production in human gingival fibroblasts stimulated with interleukin-1beta and epidermal growth factor.

The purpose of the present study was to investigate the involvement of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and tyrosine kinase on prostaglandin E2 (PGE2) production in human gingival fibroblasts stimulated by interleukin-1beta (IL-1beta) and/or epidermal growth factor (EGF). The cytokine IL-1beta and to a lesser extent EGF, enhanced COX-2 mRNA levels in gingival fibroblasts. Simultaneous treatment with EGF and IL-1beta resulted in enhanced COX-2 mRNA levels accompanied by a synergistic stimulation of PGE2 biosynthesis compared to the cells treated with IL-1beta or EGF alone. Neither IL-1beta EGF nor the combination of IL-1beta and EGF enhanced COX-1 mRNA levels in gingival fibroblasts. The tyrosine kinase inhibitors, Herbimycin A and PD 153035 hydrochloride, reduced COX-2 mRNA levels as well as PGE2 production induced by IL-1beta or the combination of IL-1beta and EGF whereas COX-1 mRNA levels were not affected. Furthermore, the COX-2 specific inhibitor, NS-398, abolished the PGE2 production induced by IL-1beta, EGF, or the combination. These results indicate that the synergy between IL-1beta and EGF on PGE2 production is due to an enhanced gene expression of COX-2 and that tyrosine kinase(s) are involved in the signal transduction of COX-2 in gingival fibroblasts.

Benzoquinones↗

PubMed1999

Changes of periodontal status in patients with Down syndrome during a 7-year period.

The development of periodontal disease in Down syndrome adolescents (n = 34) was studied clinically and on intraoral radiographs during a 7-yr period. The occurrence of gingival inflammation (GBI), pathological periodontal pockets (>4 mm), sub- and supragingival calculus, alveolar bone height, alveolar bone loss, and the occurrence of the periodontal pathogens Actinobacillus actinomycetemcomitans, Capnocytophaga, and Porphyromonas gingivalis in subgingival plaque were determined. Of the subjects, 41% had one or more pathological periodontal pockets at baseline compared to 65% at follow-up. At the baseline examination, 35% of the individuals exhibited alveolar bone loss compared to 74% at the follow-up. The median value of sites with alveolar bone loss increased from 0 to 1, the new lesions mainly being located in the incisor region. The estimated annual reduction of alveolar bone height in each subject was 0.04 mm on average. The occurrence of the periodontal pathogens A. actinomycetemcomitans, Capnocytophaga, and P. gingivalis in subgingival plaque did not differ between baseline and follow-up. The results of the present study indicate that the frequency of periodontitis, mainly located on the lower incisors, markedly increased during a 7-yr period in Down syndrome individuals, although the severity and progression was limited compared to what has previously been described.

Adolescent↗

PubMed1999

Fluoride concentration in whole saliva and separate gland secretions after topical treatment with three different fluoride varnishes.

Fluoride concentration in whole saliva and in separate gland secretions was determined after a single application of each of 3 different fluoride varnishes with contrasting levels of fluoride in a randomized crossover design. The study group comprised 8 healthy schoolchildren aged 10-12 years treated with A: Bifluorid 12 (6% F); B: Duraphat (2.26% F); and C: Fluor Protector (0.1% F). Unstimulated and stimulated whole saliva, as well as stimulated parotid and submandibular-sublingual saliva, were collected at baseline and 1, 6, 12, and 24h after the varnish treatments. The fluoride concentrations were determined with an ion-selective electrode. Time- and dose-dependent concentration curves were obtained in all the collected secretions, A > B > C. In whole saliva, the fluoride levels were significantly elevated (P<0.01) 1 h after the A and B varnish applications compared with baseline, while the increase was insignificant for varnish C. Similar patterns were unveiled in the parotid and submandibular-sublingual secretions, although the increase in fluoride concentration was modest. The elevated levels did not exceed 6 h for any of the varnish tested. The results of this study suggest a correlation between the concentration of fluoride of the varnish and fluoride levels obtained in saliva after application.

Calcium Fluoride↗

PubMed1999

Effect of an antibacterial dental varnish on the levels of prostanoids, leukotriene B4, and interleukin-1 beta in gingival crevicular fluid.

The aim of this study was to investigate the effects of a chlorhexidine/thymol-containing dental varnish on the levels of prostaglandin E2 (PGE2), prostaglandin I2 (PGI2), leukotriene B4 (LTB4), and interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF). The material consisted of 15 adolescents undergoing treatment with fixed orthodontic appliances. Four buccal sites adjacent to bands or brackets and exhibiting a mild chronic gingival inflammation were selected in the upper quadrants of each patient. According to a split-mouth technique, the first and second quadrants were randomly treated with either a varnish (Cervitec) containing 1% chlorhexidine diacetate and thymol (CHX/thymol) or a placebo varnish without active ingredients. The varnishes were applied immediately after the baseline registration, and follow-up examinations were carried out after 3, 8, and 30 days. GCF was sampled with the aid of a paper strip and the volume was determined using a Periotron 8000. The concentrations of PGE2, PGI2, LTB4, and IL-1 beta in GCF were assessed using radioimmunoassay and ELISA techniques. The results unveiled statistically significant reductions of PGE2, PGI2, and LTB4 levels in GCF following the active varnish treatment when compared to baseline values. A slight drop in IL-1 beta levels was registered after both active and placebo varnish applications, but the differences were not significant. The results suggest that treatment with an antibacterial varnish decreases the levels of inflammatory mediators PGE2, PGI2, and LTB4 in gingival crevicular fluid and further support the concept that topical application of a CHX/thymol-containing varnish is beneficial in patients with chronic gingival inflammation.

Adolescent↗

PubMed1999

Benzydamine reduces prostaglandin production in human gingival fibroblasts challenged with interleukin-1 beta or tumor necrosis factor alpha.

Benzydamine [1-benzyl-3-(3-dimethylamino)propoxy-1H-indazole] is a drug with analgesic, anesthetic, antimicrobial and anti-inflammatory activity. The purpose of the present study was to investigate the effect of benzydamine on prostaglandin production in human gingival fibroblasts. Benzydamine significantly reduced the basal production of both prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha, the stable breakdown product of prostaglandin I2 (PGI2), in unstimulated human gingival fibroblasts. When the cells were treated simultaneously with benzydamine and the cytokines IL-1 beta or TNF alpha, the agent benzydamine reduced (P < 0.05) the stimulatory effect of IL-1 beta and TNF alpha respectively, on PGE2 and PGI2 production in human gingival fibroblasts. Furthermore, benzydamine reduced (P < 0.05) both the basal level and the cytokine-induced 3H-arachidonic acid release 3H-(AA) in gingival fibroblasts. The addition of exogenous arachidonic acid to the cells resulted in enhanced PGE2 production, which was reduced (P < 0.05) in the presence of benzydamine. The study indicates that benzydamine reduces the prostaglandin synthesis in gingival fibroblasts, partly at the level of phospholipase A2, by diminishing the liberation of arachidonic acid (AA) from phospholipids, and partly at the level of cyclooxygenase. The inhibitory effect of benzydamine on prostaglandin production may explain the anti-inflammatory effect of the drug in the management of patients with oral inflammatory conditions.

Adolescent↗