{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T13:39:28Z","timestamp":1793194768001,"version":"4.5.0"},"reference-count":37,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,12,28]],"date-time":"2013-12-28T00:00:00Z","timestamp":1388188800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001807","name":"State of S\u00e3o Paulo Research Foundation","doi-asserted-by":"crossref","award":["2010\/10715-9"],"award-info":[{"award-number":["2010\/10715-9"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100003593","name":"National Council for Scientific and Technological Development","doi-asserted-by":"crossref","award":["2010\/10715-9"],"award-info":[{"award-number":["2010\/10715-9"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2014,12]]},"abstract":"<jats:sec><jats:title>Background and Objective<\/jats:title><jats:p>After activation, platelets express mediators that modulate inflammation. We hypothesized that drug\u2010induced platelet inactivation may interfere in the inflammatory process in experimental periodontal disease by suppressing the release of biological mediators to the injury site.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>To evaluate the effects of antiplatelet drugs on experimental <jats:styled-content style=\"fixed-case\">periodontal disease<\/jats:styled-content>, 60 rats were randomly assigned to six groups (<jats:italic>n<\/jats:italic>\u00a0=\u00a010) and ligatures were placed around lower first molars in three groups. The other three groups were not subjected to the induction of <jats:styled-content style=\"fixed-case\">periodontal disease<\/jats:styled-content> and were used as negative controls. During the experimental period, animals were given aspirin (30\u00a0mg\/kg) or clopidogrel (75\u00a0mg\/kg) intragastrically once daily for 3\u00a0d. On day 3, they were killed and gingival tissue were used to evaluate myeloperoxidase activity and the expression of the chemokine <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>4. Hemi\u2010mandibles were used for microscopic evaluation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Clopidogrel significantly reduced the inflammatory infiltrate and increased the amount of collagen fibers. Histometric analysis showed that clopidogrel impaired alveolar bone loss. Expression of <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>4 was significantly increased (<jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.001) in rats subjected to <jats:styled-content style=\"fixed-case\">periodontal disease<\/jats:styled-content>. Systemic administration of aspirin and clopidogrel induced a significant decrease ( <jats:italic>p<\/jats:italic>\u00a0&lt;\u00a00.05) in the expression of <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>4. Treatment with antiplatelet drugs resulted in a significant reduction of <jats:styled-content style=\"fixed-case\">myeloperoxidase<\/jats:styled-content> activity when compared to saline\u2010treated animals with <jats:styled-content style=\"fixed-case\">periodontal disease<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Clopidogrel but not aspirin showed the ability of preventing bone loss in experimental periodontitis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12155","type":"journal-article","created":{"date-parts":[[2013,12,28]],"date-time":"2013-12-28T08:00:44Z","timestamp":1388217644000},"page":"729-735","source":"Crossref","is-referenced-by-count":11,"title":["Antiplatelet drugs reduce the immunoinflammatory response in a rat model of periodontal disease"],"prefix":"10.1111","volume":"49","author":[{"given":"L. 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