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)

The aim of this study was to test the effect of a high dose (6 mg/kg/d) of indomethacin, a PG-synthesis inhibitor, on hamster periodontitis and to verify a possible systemic skeletal action. Thirty animals were separated into three groups: control, untreated periodontitis-affected, and indomethacin treated groups. Compared to affected untreated animals, indomethacin reduced the number of osteoclasts (p less than 0.001) to the control level, and accordingly the extent of resorption (p less than 0.01). A partial decrease in reversal (p less than 0.05) was also obtained; the persistence of aborted reversal lacunae was the scar of the pretreatment period. The extent of formation was markedly increased by indomethacin (p less than 0.01). Bacterial plaque accumulation was not modified but PMNLs investing plaque were dramatically decreased (p less than 0.02). Indomethacin had no influence on the femoral periosteal remodeling, nor on metaphyseal and epiphyseal trabecular density, nor on growth plate thickness. These results confirm the positive effect of indomethacin on hamster periodontitis and emphasize the role of PGs on periodontitic bone disturbances, particularly on the uncoupling of the remodeling sequence. The reduction in PMNL migration is an important feature, which possibly participates in the improvement of the bone status. The lack of femoral changes indicates that a mid-term treatment with indomethacin has no detrimental action on ordered skeletal growth and bone mass.
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PMID:Periodontal and femoral bone status in periodontitis-affected hamsters receiving a high dose indomethacin treatment. 276 31

Studies were designed to assess factors other than pathologic status of the cell donor which affect the blastogenic responsiveness in vitro of peripheral blood mononuclear cells (PBMs) from normal donors and patients with periodontitis. Cultures were established and activated using phytohemagglutinin-P (PHA) or homogenates of Actinomyces viscosus (AVIS), a gram-positive plaque microorganism, and Fusobacterium nucleatum (FUSO), a gram-negative plaque microorganism. Activation was assessed by measuring the incorporation of labeled precursor into DNA. The effects of incubation time, vessel shape, cell concentration, prostaglandin E2 and indomethacin on blastogenic responsiveness were studied. Blastogenic responsiveness became maximal after 5 to 8 days' activation with the bacterial substances, and after 3 days' activation with PHA. Radioactivity incorporated by cultures in microtest wells with flat, round and conical bottoms was 5.9, 7.8 and 10.6 X 10(3) cpm, respectively. Cultures of cells from all of the patients and normal subjects were activated by PHA, AVIS and FUSO, and cell concentration was a major determinant of the magnitude of the blastogenic response. Responsiveness of cultures from all patients and control subjects activated with AVIS and FUSO was inhibited significantly by prostaglandin E-2 (PGE2) at a concentration of 10 microM. Inhibition was generally 50% or greater. Indomethacin, an inhibitor of prostaglandin production, at a concentration of 0.5 micrograms/ml significantly enhanced responsiveness of AVIS- and FUSO-activated cultures from control donors and patients, indicating that prostaglandins are produced endogenously, and that they affect cell responsiveness. The effect of PGE2 and indomethacin on PHA-activated cultures was more variable and, where present, of a lesser magnitude than that observed for cultures activated with bacterial homogenates. In most cultures the effects were not statistically significant. Our data show that in studies of lymphocyte activation, the incubation time, culture-vessel shape, cell concentration and presence of endogenous inhibitors need to be taken into account.
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PMID:Effect of factors other than pathologic status on responsiveness of peripheral blood mononuclear cells from patients with chronic periodontitis. 657 78

In a previous study we showed that the involvement of EP4 subtype of the prostaglandin E (PGE) receptor is crucial for lipopolysaccharide (LPS)-induced osteoclast formation in vitro. The present study was undertaken to test whether EP4 is actually associated with LPS-induced bone resorption in vivo. In wild-type (WT) mice, osteoclast formation in vertebrae and tibiae increased 5 days after systemic LPS injection, and urinary excretion of deoxypyridinoline, a sensitive marker for bone resorption, statistically increased 10 days after injection. In EP4 knockout (KO) mice, however, LPS injection caused no significant changes in these parameters throughout the experiment. LPS exposure for 4 h strongly induced osteoclast differentiation factor (ODF) mRNA expression in primary osteoblastic cells (POB) both from WT and EP4 KO mice, and this expression was not inhibited by indomethacin, suggesting prostaglandin (PG) independence. LPS exposure for 24 h further induced ODF expression in WT POB, but not in EP4 KO POB. Indomethacin partially inhibited ODF expression in WT POB, but not in EP4 KO POB. These data suggest that ODF is induced both PG dependently and PG independently. LPS exposure for 24 h induced slightly greater osteoclastgenesis inhibitory factor (OCIF) mRNA expression in EP4 KO than in WT POB. These findings suggest that the reduced ODF expression and apparently increased OCIF expression also are responsible for the markedly reduced LPS-induced osteoclast formation in EP4 KO mice. Our results show that the EP4 subtype of the PGE receptor is involved in LPS-induced bone resorption in vivo also. Since LPS is considered to be largely involved in bacterially induced bone loss, such as in periodontitis and osteomyelitis, our study is expected to help broaden our understanding of the pathophysiology of these conditions.
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PMID:Impaired bone resorption by lipopolysaccharide in vivo in mice deficient in the prostaglandin E receptor EP4 subtype. 1108

Prostaglandin E(2) (PGE(2)) plays important roles in the bone resorption of inflammatory diseases such as rheumatoid arthritis and periodontitis via specific prostaglandin receptors (i.e., EP1-EP4). In this study, the authors examined whether Prevotella intermedia regulates PGE(2) production and EP expression in human periodontal ligament fibroblasts (hPDLs); they also explored the potential signaling pathways involved in PGE(2) production. P. intermedia induced PGE(2) production and cyclooxygenase-2 (COX-2) expression in a dose- and time-dependent manner. Indomethacin and NS-398 completely abrogated the P. intermedia-induced PGE(2) production without modulating COX-2 expression. Specific inhibitors of extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38, phosphatidylinositol 3-kinase, and protein kinase C--but not c-AMP and protein kinase A--significantly attenuated the P. intermedia-induced COX-2 and PGE(2) expression. P. intermedia reduced EP1 expression in a concentration- and time-dependent manner. The results indicate that the COX-2-dependent induction of PGE(2) by P. intermedia in hPDLs is mediated by multiple signaling pathways.
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PMID:Prevotella intermedia induces prostaglandin E2 via multiple signaling pathways. 2105 37