Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium hydroxide is a widely used endodontic medicament for eliminating viable bacteria and inactivating virulence factors. Enterococcus faecalis, a pathogenic gram-positive bacterium, has been associated with refractory apical periodontitis. Because lipoteichoic acid (LTA) is a major virulence factor of gram-positive bacteria, we examined whether calcium hydroxide could detoxify LTA from E. faecalis. An enzyme-linked immunosorbent assay showed that calcium hydroxide-killed E. faecalis was less potent than heat-killed bacteria in stimulating the release of tumor necrosis factor-alpha by a murine macrophage line, RAW 264.7 (P < 0.05). Pretreatment of LTA with calcium hydroxide remarkably abrogated the ability of LTA to induce the release of tumor necrosis factor-alpha (P < 0.05). Furthermore, calcium hydroxide-treated LTA was not able to stimulate Toll-like receptor 2, which recognizes functionally intact LTA. These results suggest that calcium hydroxide could detoxify LTA, resulting in attenuation of the inflammatory responses to E. faecalis and its LTA.
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PMID:Calcium hydroxide inactivates lipoteichoic acid from Enterococcus faecalis. 1892 46

Calcium hydroxide, a widely used intracanal medicament, is known to exert an antimicrobial effect and to degrade bacterial-derived lipopolysaccharides. However, little is known about the effect of Ca(OH)(2) on endogenous inflammatory mediators such as interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), and calcitonin gene-related peptide (CGRP). This is an important gap in knowledge because these inflammatory mediators play an important role in mediating the pathogenesis of periradicular periodontitis. We tested the hypothesis that Ca(OH)(2) denatures IL-1 alpha, TNF-alpha, and CGRP. Human IL-1 alpha (0.125 ng/mL), TNF-alpha (0.2 ng/mL), and CGRP (0.25 ng/mL) were incubated with Ca(OH)(2) (0.035 mg/mL) for 1-7 days. At the end of the incubation period, the pH of the samples was neutralized, and the concentrations of the mediators were measured by immunoassays. Data were analyzed with one-way analysis of variance and Bonferroni multiple comparison tests. The results indicate that Ca(OH)(2) denatures IL-1 alpha, TNF-alpha, and CGRP by 50%-100% during the testing periods (P < .001). We concluded that denaturation of these proinflammatory mediators is a potential mechanism by which Ca(OH)(2) contributes to the resolution of periradicular periodontitis.
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PMID:Effect of calcium hydroxide on proinflammatory cytokines and neuropeptides. 1892 47

The periodontal ligament (PDL) is a fibrous connective tissue that exists in the cementum and the alveolar bone. Periodontitis is a chronic inflammatory disease that is caused by a bacterial infection in the periodontal region. This infection increases the production of inflammatory cytokines and causes the destruction of periodontal tissue. High mobility group box 1 (HMGB1) is a nuclear nonhiston DNA-binding protein that is present in many eukaryotic cells. HMGB1 is released actively from macrophages and monocytes stimulated by lipopolysaccharide or tumor necrosis factor-alpha and passively from damaged cells and necrotic cells. Extracellular HMGB1 signals through a specialized receptor for advanced glycation end products (RAGE), toll-like receptor 2 (TLR2), and toll-like receptor 4 (TLR4). According to a recent report, HMGB1 is of concern in periodontitis. The purpose of this study was to examine the effect of HMGB1 in PDL cells. To investigate RAGE, TLR2 and TLR4 mRNA in PDL cells, reverse transcript-polymerase chain reaction experiments were performed. PDL cells were stimulated with HMGB1, with or without anti-RAGE, TLR2 and TLR4 antibodies. IL-6 and IL-11 production was measured using an enzyme-linked immunosorbent assay, and mRNA expression was quantified by real-time PCR. PDL cells expressed RAGE, TLR2 and TLR4 mRNA. Production and mRNA expression of IL-6 and IL-11 were augmented in PDL cells stimulated with HMGB1. In addition, they were also suppressed by anti-RAGE, TLR2 and TLR4 antibodies. In conclusion, PDL cells produce IL-6 and IL-11 in response to HMGB1 via RAGE, TLR2 and TLR4.
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PMID:[Effect of high mobility group box 1 (HMGB1) in cultured human periodontal ligament cells]. 1904 16

Cannabidiol (CBD) is a cannabinoid component from Cannabis sativa that does not induce psychotomimetic effects and possess anti-inflammatory properties. In the present study we tested the effects of CBD in a periodontitis experimental model in rats. We also investigated possible mechanisms underlying these effects. Periodontal disease was induced by a ligature placed around the mandible first molars of each animal. Male Wistar rats were divided into 3 groups: control animals; ligature-induced animals treated with vehicle and ligature-induced animals treated with CBD (5 mg/kg, daily). Thirty days after the induction of periodontal disease the animals were sacrificed and mandibles and gingival tissues removed for further analysis. Morphometrical analysis of alveolar bone loss demonstrated that CBD-treated animals presented a decreased alveolar bone loss and a lower expression of the activator of nuclear factor-kappaB ligand RANKL/RANK. Moreover, gingival tissues from the CBD-treated group showed decreased neutrophil migration (MPO assay) associated with lower interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha production. These results indicate that CBD may be useful to control bone resorption during progression of experimental periodontitis in rats.
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PMID:Cannabidiol decreases bone resorption by inhibiting RANK/RANKL expression and pro-inflammatory cytokines during experimental periodontitis in rats. 1907 Jun 83

Periodontal disease is a chronic inflammatory condition induced by tooth-associated microbial biofilms that induce a host immune response. Therapeutic control of progressive tissue destruction in high-risk patients is a significant challenge in therapy. Soluble protein delivery of antagonists to tumor necrosis factor-alpha (TNF-alpha) inhibits alveolar bone resorption due to periodontitis. However, protein therapy raises several concerns, such as recurrence of disease activity after treatment cessation and repeated dosing regimens. In this study, we used pseudotyped adeno-associated virus vector based on serotype 1 (AAV2/1) to deliver the TNF receptor-immunoglobulin Fc (TNFR:Fc) fusion gene to rats subjected to experimental Porphyromonas gingivalis (Pg)-lipopolysaccharide (LPS)-mediated bone loss. Animals received Pg-LPS delivered to the gingivae thrice weekly for 8 weeks, vehicle alone, Pg-LPS and intramuscular delivery of pseudotyped AAV2/1-TNFR:Fc vector (1 x 10(11) DNase I-resistant particles) or AAV2/1-TNFR:Fc vector delivered to naive animals. AAV2/1-TNFR:Fc therapy led to sustained therapeutic levels of serum TNFR protein and protected against Pg-LPS-mediated loss of bone volume and density. Furthermore, AAV2/1-TNFR:Fc administration reduced local levels of multiple proinflammatory cytokines and osteoclast-like cells at the periodontal lesions. These findings suggest that delivery of AAV2/1-TNFR:Fc may be a viable approach to modulate periodontal disease progression.
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PMID:AAV2/1-TNFR:Fc gene delivery prevents periodontal disease progression. 1907 94

This study evaluated the frequency of the tumor necrosis factor-alpha (TNF-alpha) -308 G/A polymorphism in Brazilians with periodontal health (PH = 51), chronic periodontitis (CP = 74) and generalized aggressive periodontitis (GAgP = 38). Human DNA was obtained from mouthwash samples and TNF-alpha genotyping was performed by PCR and RFLP analyses. Differences in clinical and genetic parameters among groups were sought by Kruskal-Wallis, chi(2) and Fisher's exact tests. The allele -308G was detected in 91.7%, whereas the allele -308A was found in 35.4% of all subjects. No significant differences were observed in the frequency of these alleles (chi(2) = 2.610, p > 0.05) and the genotypes G/G, G/A, and A/A (chi(2) = 2.547, p = 0.636) among groups. The data suggest that the TNF-alpha -308 G/A polymorphism is not associated with periodontitis in this Brazilian population.
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PMID:Lack of association between the TNF-alpha -308 (G/A) genetic polymorphism and periodontal disease in Brazilians. 1914 87

Periodontitis is a chronic disease associated with inflammation of the tooth-supporting tissues. The inflammation is initiated by a group of gram-negative anaerobic bacteria. These express a number of irritating factors including a lipopolysaccharide (LPS), which plays a key role in periodontal disease development. Plant extracts with anti-inflammatory and anti-microbial properties have been shown to inhibit bacterial plaque formation and thus prevent chronic gingivitis. In this study we tested effects of Prunella vulgaris L. extract (PVE; 5, 10, 25microg/ml) and its component rosmarinic acid (RA; 1microg/ml) on LPS-induced oxidative damage and inflammation in human gingival fibroblasts. PVE and RA reduced reactive oxygen species (ROS) production, intracellular glutathione (GSH) depletion as well as lipid peroxidation in LPS-treated cells. Treatment with PVE and RA also inhibited LPS-induced up-regulation of interleukin 1beta (IL-1beta), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and suppressed expression of inducible nitric oxide synthase (iNOS). The results indicate that PVE and RA are able to suppress LPS-induced biological changes in gingival fibroblasts. The effects of PVE and RA are presumably linked to their anti-inflammatory activities and thus use of PVE and RA may be relevant in modulating the inflammation process, including periodontal disease.
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PMID:Prunella vulgaris extract and rosmarinic acid suppress lipopolysaccharide-induced alteration in human gingival fibroblasts. 1915 70

Adiponectin is an adipokine with potent anti-inflammatory properties. We previously reported that a globular adiponectin (gAd) suppresses Aggregatibacter actinomycetemcomitans lipopolysaccharide-induced nuclear factor-kappaB activity, suggesting an anti-inflammatory effect of gAd. In this study, we investigated whether gAd is able to modulate the effect of A. actinomycetemcomitans lipopolysaccharide on cytokine induction in a murine macrophage cell line (RAW 264). The phosphorylation of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, extracellular signal-regulated kinase, and IkappaB kinase alpha/beta and the degradation of IkappaB, which were induced by A. actinomycetemcomitans lipopolysaccharide intoxication, were clearly reduced in gAd-pretreated RAW 264 cells compared with the untreated cells. Expression levels of tumor necrosis factor (TNF)-alpha and interleukin-10 (IL-10) mRNA were assessed by real-time PCR. Cell-free supernatants were collected after 12 h of stimulation and analyzed by enzyme-linked immunosorbent assay for TNF-alpha and IL-10. Pretreatment with gAd significantly inhibited the A. actinomycetemcomitans lipopolysaccharide-induced TNF-alpha mRNA expression and protein secretion. In contrast, pretreatment with gAd significantly enhanced the A. actinomycetemcomitans lipopolysaccharide-induced IL-10 mRNA expression and protein secretion. These data suggest a mechanism for the anti-inflammatory activity of gAd in local inflammatory lesions, such as periodontitis.
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PMID:Anti-inflammatory activity of a globular adiponectin function on RAW 264 cells stimulated by lipopolysaccharide from Aggregatibacter actinomycetemcomitans. 1955 15

The Japanese apricot, known as Ume in Japanese, has been a traditional Japanese medicine for centuries, and is a familiar and commonly consumed food. The health benefits of Ume are now being widely recognized and have been strengthened by recent studies showing that MK615, an extract of compounds from Ume, has strong anticancer and anti-inflammatory effects. However, the potential role of MK615 in the periodontal field remains unknown. Here, we found that MK615 significantly reduced the production of pro-inflammatory mediators (tumor necrosis factor-alpha and interleukin-6) induced by Porphyromonas gingivalis lipopolysaccharide (LPS), a major etiological agent in localized chronic periodontitis, in murine macrophage-like RAW264.7 cells. MK615 markedly inhibited the phosphorylation of ERK1/2, p38MAPK, and JNK, which is associated with pro-inflammatory mediator release pathways. Moreover, MK615 completely blocked LPS-triggered NF-kappaB activation. The present results suggest that MK615 has potential as a therapeutic agent for treating inflammatory diseases such as periodontitis.
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PMID:MK615 attenuates Porphyromonas gingivalis lipopolysaccharide-induced pro-inflammatory cytokine release via MAPK inactivation in murine macrophage-like RAW264.7 cells. 1970 86

Bone metabolism results from a balance between osteoclast-driven bone resorption and osteoblast-mediated bone formation. Diseases such as periodontitis and rheumatoid arthritis are characterized by increased bone destruction due to enhanced osteoclastogenesis. Here we report that interferon regulatory factor-8 (IRF-8), a transcription factor expressed in immune cells, is a key regulatory molecule for osteoclastogenesis. IRF-8 expression in osteoclast precursors was downregulated during the initial phase of osteoclast differentiation induced by receptor activator of nuclear factor-kappaB ligand (RANKL), which is encoded by the Tnfsf11 gene. Mice deficient in Irf8 showed severe osteoporosis, owing to increased numbers of osteoclasts, and also showed enhanced bone destruction after lipopolysaccharide (LPS) administration. Irf8-/- osteoclast precursors underwent increased osteoclastogenesis in response to RANKL and tumor necrosis factor-alpha (TNF-alpha). IRF-8 suppressed osteoclastogenesis by inhibiting the function and expression of nuclear factor of activated T cells c1 (NFATc1). Our results show that IRF-8 inhibits osteoclast formation under physiological and pathological conditions and suggest a model where downregulation of inhibitory factors such as IRF-8 contributes to RANKL-mediated osteoclastogenesis.
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PMID:Interferon regulatory factor-8 regulates bone metabolism by suppressing osteoclastogenesis. 1971 38


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