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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histological and clinical studies have found that periodontal ligament fibroblasts can produce connective attachment,while gingival fibroblasts cannot yet.The mechanism for gingival fibroblasts losing their ability of new attachment is unknown.We investigated the function of colagen synthesis by gingival fibroblasts from periodontitis sites,and normal sites and their response to TGF-beta,and Nicotinamide and Lactate,the inhibitors of poly(ADP-ribosyl)ation.We found that gingival fibroblasts from diseased sites produce much less collagen than from control sites (73.6+/-8.8vs.107.1+/-12.3,P<0.01),and these cells show unresponsive to TGF-beta,Nicotinamide and Lactate on collagen synthesis.These results may partly explain why gingival fibroblasts from periodontitis site lose their ability of new attachment.
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PMID:[The biologic character of gingival fibroblasts from normal and periodontitis sites] 1515 80

The use of topical NSAIDs to complement periodontal therapy could help resolve the inflammatory process and clinical signs of the disease more rapidly. A randomized clinical trial was performed on 59 patients, of whom 33 had chronic periodontitis and 26 were healthy controls. All diseased patients underwent scaling and root planing in one quadrant per week with subgingival application of gel 48 hours after each session. Gel was applied to healthy patients with the same frequency. Four types of gel were used, containing respectively placebo, acetylsalicylic acid (ASA) 1%, Ketoprofene (KTP) 1% and Ketoprofene 2%. The following clinical variables were studied: probing depth, attachment level, dental mobility, plaque index, gingival index and bleeding on probing; as well as the biochemical variables: bleeding time (Ivy), platelet count in whole blood and platelet-rich plasma, and platelet aggregation induced by different agonists. Regarding clinical results, ASA was the most effective in reducing probing depth, gingival index and bleeding on probing (p < 0.05). KTP 1% and 2% behaved similarly to each other and less effectively than ASA but differed significantly from placebo (p < 0.05). Regarding biochemical tests, ASA had a highly significant inhibitory effect on platelet aggregation for all the agonists used. KTP 2% produced similar though weaker responses. KTP 1% only showed alteration in the first aggregation phase at maximum ADP concentration of and none at the minimum concentration (p < 0.05).
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PMID:Alteration of hemostasis in patients treated with subgingival NSAIDs during periodontal therapy. 2292 89

Porphyromonas gingivalis is a gram-negative anaerobic bacterium and an etiologic agent of adult periodontitis. By inducing a dysbiotic state within the host microbiota it contributes to a chronic inflammatory environment in the oral cavity. Under some circumstances, the oral bacteria may gain access to systemic circulation. While the most widely recognized function of platelets is to reduce hemorrhage in case of vascular damage, it is known that platelets are also involved in the hematologic responses to bacterial infections. Some pathogenic bacteria can interact with platelets, triggering their activation and aggregation. The aim of this study was to assess platelet responses to the presence of P. gingivalis in whole blood. Human whole blood was pretreated with P. gingivalis and then platelet plug formation was measured under high shear conditions using the PFA-100. In the presence of P. gingivalis, time for a platelet plug to occlude the aperture in the collagen/ADP cartridge was shortened in a manner dependent on bacterial concentration and the duration of bacterial preincubation of blood. P. gingivalis enhances thrombus forming potential of platelets in whole blood.
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PMID:Platelet plug formation in whole blood is enhanced in the presence of Porphyromonas gingivalis. 3294 12