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)

In Brazilian folk medicine, Lippia sidoides (Ls) and Myracrodruon urundeuva (Mu) have gained popularity and reputation as effective antimicrobial and anti-inflammatory agents. This work aimed to evaluate the effect of topical herbal gel from Ls 0.5% (v/w) and Mu 5% (w/w) in experimental periodontal disease (EPD) in rats. Wistar rats were subjected to ligature placement around the second upper left molars. Animals were treated topically with Ls and/or Mu-based gel, immediately after EPD induction and three times/day for 11 days until the rats were sacrificed (11th day). Saline-based gel was utilized as control for all experiments and doxycycline based gel 10% (w/w) was utilized as reference substance. Animals were weighed daily. Alveolar bone loss was measured as the difference (in millimeters) between the cusp tip and the alveolar bone. The periodontum and the surrounding gingivae were examined at histopathology, as well as the neutrophil influx into the gingivae was assayed using myeloperoxidase activity and cytokine production mainly tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) levels by ELISA method. The local bacterial flora was assessed through culture of the gingival tissue in standard aerobic and anaerobic media. Alveolar bone loss was significantly inhibited by Ls and Mu combined treatment compared to the saline control group. Ls and Mu combined treatment reduced tissue lesion at histopathology, with partial preservation of the periodontum, coupled to decreased myeloperoxidase activity as well as significantly inhibited TNF-alpha and IL-1beta production in gingival tissue compared to the saline control group. Ls and Mu combined treatment also prevented the growth of oral microorganisms and the weight loss. Ls and Mu combined based gel treatment preserved alveolar bone resorption and demonstrated anti-inflammatory and antibacterial activities in experimental periodontitis.
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PMID:Lippia sidoides and Myracrodruon urundeuva gel prevents alveolar bone resorption in experimental periodontitis in rats. 1771 97

Generalized aggressive periodontitis (GAP) comprises a group of periodontal diseases characterized by the rapid destruction of periodontal tissues which affect young individuals who generally present no systemic disorders. Polymorphisms in the interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) genes have been associated with an increased severity of chronic periodontitis. The objective of the present study was to evaluate the association between IL-1A (-889) and TNFA (-308) gene polymorphisms and GAP. One hundred nonsmoking subjects were selected, including 30 with GAP and 70 without periodontal disease. Gene polymorphisms were analyzed by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. For IL-1 (-889), the frequency of genotype 1/1 was 54.3% in the control group and 56.7% in the study group. The frequency of genotype 1/2 was 37.1% in the control group and 40% in the study group. Genotype 2/2 was detected at a frequency of 8.6% and 3.3% in the control and study groups, respectively. For TNFA, genotype 1/1 was present in 68.6% of control subjects and in 80.0% of patients with GAP, while the frequency of genotype 1/2 was 27.1% in the control group and 20% in the study group. Genotype 2/2 was present in 4.3% of control subjects and was not detected in the study group. The frequencies of allele 1 and allele 2 of the IL-1A (-889) gene were 72.9% and 27.1%, respectively, in the control group and 76.7% and 23.3% in the GAP group. For the TNFA (-308) gene, the frequency of allele 1 was 82.15% in the control group and 90% in the study group, whereas the frequency of allele 2 was 17.85% in the control group and 10% in the study group. Statistical analysis revealed no significant difference in allele distribution for either gene between the two groups. No association was observed between GAP and IL-1A (-889) and TNFA (-308) gene polymorphisms in Brazilian patients.
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PMID:Analysis of IL-1A(-889) and TNFA(-308) gene polymorphism in Brazilian patients with generalized aggressive periodontitis. 1782 82

Histamine is an important mediator in immune responses, but it is unclear whether periodontal tissues express histamine receptors and are able to respond to histamine. We hypothesized that histamine, inflammatory cytokines, and bacterial components released in inflamed periodontal tissues may be synergistically involved in periodontitis. The present study showed that human gingival fibroblasts mainly express histamine receptor H1R, and responded to histamine to produce interleukin (IL)-8. Stimulation of gingival fibroblasts with tumor necrosis factor-alpha, IL-1alpha, and lipopolysaccharide markedly induced IL-8 production, and the IL-8 production was synergistically augmented in the presence of or pre-treatment with histamine. Selective inhibitors of mitogen-activated protein kinases (MAPKs), nuclear factor (NF)-kappaB, and phospholipase C (PLC) significantly inhibited the synergistic effect. These results indicate that histamine induces IL-8 production from gingival fibroblasts through H1R, and synergistically augments the inflammatory stimuli by amplification of the MAPK and NF-kappaB through H1R-linked PLC. Abbreviations used: HDC, histidine decarboxylase; LPS, lipopolysaccharide; IL, interleukin; TNF, tumor necrosis factor; HR, histamine receptor; PLC, phospholipase C; MAPK, mitogen-activated protein kinase; NF, nuclear factor; ERK, extracellular signal-related kinase; JNK, c-Jun N-terminal kinase; R, receptor; TLR, Toll-like receptor; alpha-MEM, alpha-minimum essential medium; FCS, fetal calf serum; RT-PCR, reverse-transcriptase polymerase chain-reaction; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation; LDH, lactate dehydrogenase.
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PMID:Histamine amplifies immune response of gingival fibroblasts. 1795 1

Periodontitis is an inflammatory process that ultimately results in tooth loss. Although the primary etiologic agent for periodontitis is bacteria, the majority of periodontal tissue destruction is thought to be caused by an inappropriate host response. Reactive oxygen species (ROS) have been known to be involved in periodontal tissue destruction. We treated human gingival fibroblasts with lipopolysaccharide (LPS) obtained from E. coli and the periodontopathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis, and examined their inflammatory responses in the presence and absence of the antioxidant N-acetylcysteine (NAC). LPS enhanced ROS production, as well as, expression of pro-inflammatory cytokines such as interleukin-1beta, interleukin-6, interleukin-8 and tumor necrosis factor-alpha, and the production and activation of MMP2. NAC suppressed all LPS-induced inflammatory responses examined, suggesting that LPS-induced ROS may play a major regulatory role in these responses in gingival fibroblasts. In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB. These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation. Furthermore, this work suggests that antioxidants may be useful in adjunctive therapies that complement conventional periodontal treatments.
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PMID:N-acetylcysteine prevents LPS-induced pro-inflammatory cytokines and MMP2 production in gingival fibroblasts. 1803 7

Periodontal disease, for which smoking is a known risk factor, is infectious, and is associated with oral biofilm. Cytokines mediate and regulate immune and inflammatory responses. Lipopolysaccharide produced by periodontopathic bacteria plays a role in the progression of periodontitis. The effect of nicotine on cytokine production in mice was evaluated in this study. Nicotine (10 or 200 microg mouse(-1)) was administered intraperitoneally to 4-week-old female BALB/c mice, once a day, for 49 days. Control mice received injections of phosphate-buffered saline. Blood was collected from all mice and serum IL-6, IL-10, tumor necrosis factor (TNF)-alpha and IFN-gamma levels were measured by an enzyme-linked immunosorbent assay on the 42nd day. IL-6, IL-10 and IFN-gamma levels in the nicotine-treated mice were higher than those in the control mice. However, no differences were found in TNF-alpha levels between nicotine-treated and control mice. Lipopolysaccharide (20 microg mouse(-1)) purified from Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans) Y4 was administered intraperitoneally on the 49th day. A rapid increase in TNF-alpha was observed in the control mice at 2 h after administration of lipopolysaccharide. In contrast, no increase was noted in the nicotine-treated groups. Significantly higher levels of IFN-gamma were seen in the 200 microg nicotine-treated mice at 2 h after administration of lipopolysaccharide (P<0.05). The results showed that cytokine levels were influenced by nicotine in mice.
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PMID:Nicotine involved in periodontal disease through influence on cytokine levels. 1820 5

Osteoporosis represents a major healthcare burden, affecting approximately 10 million people aged over 50 years in the United States and with another 30 million or more at risk. One of the major contributing factors to osteoporosis is withdrawal of estrogen during menopause in women. Human and animal experiments have implicated pro-inflammatory cytokines as primary mediators of the accelerated bone loss at menopause including interleukin-1, tumor necrosis factor-alpha, and interleukin-6. Increased production of pro-inflammatory cytokines is associated with osteoclastic bone resorption in a number of disease states including rheumatoid arthritis, periodontitis, and multiple myeloma; estrogen withdrawal is associated with increased production of pro-inflammatory cytokines, and exposure of bone cultures to supernatants from activated leukocytes is associated with increased bone resorption. A major advance has been the discovery of RANKL, its receptor RANK, and the endogenous inhibitor osteoprotegerin. The binding of RANKL to RANK is essential for the differentiation and activation of osteoclasts and mediates the actions of essentially all known stimulators of osteoclastic bone resorption. RANKL expression is heightened in post- compared with pre-menopausal women, and this effect is attenuated by estrogen replacement therapy. RANKL is also a therapeutic target; a human antibody with high specificity and affinity to RANKL is currently under clinical evaluation for the treatment of osteoporosis in post-menopausal women and of metastatic bone disease in cancer patients with bone metastasis. Early data are promising.
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PMID:Osteoporosis and inflammation. 1824 May 39

Studies suggest a correlation between ethanol consumption and periodontal disease. We hypothesized that elevated levels of blood reactive oxygen species following ethanol consumption may increase inflammation in periodontal tissue. Rats were divided into 4 groups (6-7 rats/group). Two groups were fed an ethanol-containing liquid diet, and 2 groups were fed a pair-fed control diet. In one of each dietary group, periodontitis was ligature-induced, while the other group was left unligated. Chronic ethanol feeding alone decreased the ratio of reduced/oxidized glutathione and increased 8-hydroxydeoxy-guanosine and tumor necrosis factor (TNF)-alpha levels in the gingiva. Blood hydroperoxides were also increased. In ligature-induced periodontitis lesions, ethanol feeding enhanced polymorpho-nuclear leukocyte infiltration and TNF-alpha expression. The results suggest that chronic alcohol consumption increased periodontal inflammation, oxidative damage, and TNF-alpha production and had an additive effect on polymorphonuclear leukocyte infiltration and gingival oxidative damage, increasing the severity of periodontal inflammation in the ligature model.
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PMID:Effects of ethanol consumption on periodontal inflammation in rats. 1843 76

Localized aggressive periodontitis (LAgP) is a complex multifactorial periodontal disease to which genetic factors are thought to predispose individuals. Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are potent immunomodulators and proinflammatory cytokines that have been implicated in the pathogenesis of autoimmune and infectious diseases and proposed to be risk factors for LAgP. Our aim was to investigate IL-1 alpha (+4845), IL-1 beta (+3954), and TNF-alpha (-308) gene polymorphisms in Turkish LAgP patients. We genotyped 31 LAgP patients and 31 healthy controls for IL-1alpha(+4845), IL-1beta(+3954), and TNF-alpha(-308) using standard PCR amplification followed by restriction enzyme digestion and gel electrophoresis. Higher prevalence of heterozygosity for IL-1alpha(+4845) was found in cases (65%) when compared to controls (35%) (P < 0.05). While homozygous allele 1 of IL-1beta(+3954) was the most frequent genotype in cases (62%), no controls were homozygous for this allele (P < 0.001). Homozygous allele 1 was the most common TNF-alpha genotype in both groups, however no significant difference in TNF-alpha genotypes was found between groups. In conclusion, in this Turkish population, susceptibility to LAgP is increased by heterozygosity for allele 1 of IL-1alpha(+4845) or homozygosity for allele 1 of IL-1beta(R+3954). Moreover, IL-1 gene polymorphisms appear to have a role in susceptibility to LAgP, and the above-mentioned genotypes could be an important risk factor for LAgP in the Turkish population.
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PMID:Interleukin-1 and tumor necrosis factor-alpha gene polymorphisms in Turkish patients with localized aggressive periodontitis. 1858 4

Enterococcus faecalis, a pathogenic gram-positive bacterium, is closely related to refractory apical periodontitis. Because lipoteichoic acid (LTA) is considered a major virulence factor of gram-positive bacteria, in the present study, highly pure LTA from E. faecalis was prepared, and its ability to stimulate murine macrophages was investigated in comparison with those of the killed whole cells. Upon exposure to E. faecalis LTA, RAW 264.7 (a murine macrophage cell line) produced a significantly (p < 0.05) high level of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in a concentration-dependent manner. It is to note that the LTA was able to stimulate Toll-like receptor 2 (TLR2) but not TLR4. Concomitantly, LTA enhanced the DNA-binding activity of a transcription factor, nuclear factor-kappa B (NF-kappaB), which plays an important role in the transcriptional activation of genes encoding inflammatory mediators. In contrast, heat-killed E. faecalis stimulated both TLR2 and TLR4, whereas the killed E. faecalis whole cells induced significant (p < 0.05) levels of TNF-alpha and NO in RAW 264.7 cells as their LTA did. These results suggest that LTA partially contributes to E. faecalis-induced inflammatory responses.
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PMID:Lipoteichoic acid partially contributes to the inflammatory responses to Enterococcus faecalis. 1863 30

Inflammation and bone loss are hallmarks of periodontal disease (PD). The question is how the former leads to the latter. Accumulated evidence demonstrates that PD involves bacterially derived factors and antigens that stimulate a local inflammatory reaction and activation of the innate immune system. Proinflammatory molecules and cytokine networks play essential roles in this process. Interleukin-1 and tumor necrosis factor-alpha seem to be primary molecules that, in turn, influence cells in the lesion. Antigen-stimulated lymphocytes (B and T cells) also seem to be important. Eventually, a cascade of events leads to osteoclastogenesis and subsequent bone loss via the receptor activator of nuclear factor-kappa B (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) axis. This axis and its regulation are not unique to PD but rather are critical for pathologic lesions involving chronic inflammation. Multiple lines of evidence in models of PD clearly indicate that increases in RANKL mRNA expression and protein production increase the RANKL/OPG ratio and stimulate the differentiation of macrophage precursor cells into osteoclasts. They also stimulate the maturation and survival of the osteoclast, leading to bone loss. OPG mRNA expression and protein production do not generally seem to be increased in the periodontitis lesion. Studies of RANKL and OPG transgenic and knockout animals provide further support for the involvement of these molecules in the tissue loss observed in PD. Ironically, periodontal practitioners have focused on the bacterial etiology of PD and believed that plaque removal was aimed at eliminating specific bacteria or bacterial complexes. However, it seems that the reduction of inflammation and attenuation of the host's immune reaction to the microbial plaque, eventually leading to a decrease in the ratio of RANKL/OPG and a decrease in associated bone loss, are the actual and desired outcomes of periodontal therapy. Future therapeutic options are likely to have regulation of the RANK-RANKL-OPG axis as their goal.
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PMID:Inflammation and bone loss in periodontal disease. 1867 12


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