{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T22:32:13Z","timestamp":1792794733714,"version":"4.5.0"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>Inflammation, oxidative stress, and endothelial dysfunction are known to contribute to ischemia-reperfusion injury. Remote ischemic preconditioning (RIPC) protects from endothelial dysfunction and the damage induced by ischemia-reperfusion. Using intensive periodontal treatment (IPT), an established human model of acute systemic inflammation, we investigated whether RIPC prevents endothelial dysfunction and modulates systemic levels of inflammation and oxidative stress.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results:<\/jats:title>\n                    <jats:p>\n                      Forty-nine participants with periodontitis were randomly allocated to receive either 3 cycles of ischemia-reperfusion on the upper limb (N=24, RIPC) or a sham procedure (N=25, control) before IPT. Endothelial function assessed by flow-mediated dilatation of the brachial artery, inflammatory cytokines, markers of vascular injury, and oxidative stress were evaluated at baseline, day 1, and day 7 after IPT. Twenty-four hours post-IPT, the RIPC group had lower levels of IL-10 (interleukin-10) and IL-12 (interleukin-12) compared with the control group (\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.05). RIPC attenuated the IPT-induced increase in IL-1\u03b2 (interleukin-1\u03b2), E-selectin, sICAM-3 (soluble intercellular adhesion molecule 3), and sTM (soluble thrombomodulin) levels between the baseline and day 1 (\n                      <jats:italic>P<\/jats:italic>\n                      for interaction &lt;0.1). Conversely, oxidative stress was differentially increased at day1 in the RIPC group compared with the control group (\n                      <jats:italic>P<\/jats:italic>\n                      for interaction &lt;0.1). This was accompanied by a better flow-mediated dilatation (mean difference 1.75% [95% CI, 0.428\u20133.07],\n                      <jats:italic>P<\/jats:italic>\n                      =0.011). After 7 days from IPT, most of the inflammatory markers, endothelial-dependent and -independent vasodilation, were similar between groups.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>RIPC prevented acute endothelial dysfunction by modulation of inflammation and oxidation processes in patients with periodontitis following exposure to an acute inflammatory stimulus.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Registration:<\/jats:title>\n                    <jats:p>\n                      URL:\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/clinicaltrials.gov\/ct2\/show\/NCT03072342\">https:\/\/clinicaltrials.gov\/ct2\/show\/NCT03072342<\/jats:ext-link>\n                      ; Unique identifier: NCT03072342.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.121.316388","type":"journal-article","created":{"date-parts":[[2021,6,10]],"date-time":"2021-06-10T05:01:02Z","timestamp":1623301262000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":22,"title":["Remote Ischemic Preconditioning Protects Against Endothelial Dysfunction in a Human Model of Systemic Inflammation: A Randomized Clinical Trial"],"prefix":"10.1161","volume":"41","clinical-trial-number":[{"clinical-trial-number":"nct03072342","registry":"10.18810\/clinical-trials-gov"}],"author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1173-3029","authenticated-orcid":true,"given":"Marco","family":"Orlandi","sequence":"first","affiliation":[{"name":"Periodontology Unit, UCL Eastman Dental Institute and Hospital (M.O., Y.L., F.D.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefano","family":"Masi","sequence":"additional","affiliation":[{"name":"National Centre for Cardiovascular Prevention and Outcomes Institute of Cardiovascular Science (S.M., D.B., S.T.C., J.D.), University College London, United Kingdom."},{"name":"Internal Medicine Unit, University of Pisa, Italy (S.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devina","family":"Bhowruth","sequence":"additional","affiliation":[{"name":"National Centre for Cardiovascular Prevention and Outcomes Institute of Cardiovascular Science (S.M., D.B., S.T.C., J.D.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5027-7276","authenticated-orcid":true,"given":"Yago","family":"Leira","sequence":"additional","affiliation":[{"name":"Periodontology Unit, UCL Eastman Dental Institute and Hospital (M.O., Y.L., F.D.), University College London, United Kingdom."},{"name":"Periodontology Unit, Faculty of Odontology, University of Santiago de Compostela and Medical-Surgical Dentistry Research Group (Y.L.), Health Research Institute of Santiago de Compostela, Spain."},{"name":"Clinical Neurosciences Research Laboratory (Y.L.), Health Research Institute of Santiago de Compostela, Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georgios","family":"Georgiopoulos","sequence":"additional","affiliation":[{"name":"School of Biomedical Engineering and Imaging Sciences, King\u2019s College London, St Thomas Hospital, United Kingdom (G.G.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek","family":"Yellon","sequence":"additional","affiliation":[{"name":"The Hatter Cardiovascular Institute (D.Y., D.J.H.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aroon","family":"Hingorani","sequence":"additional","affiliation":[{"name":"Institute of Cardiovascular Science (A.H.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4323-2189","authenticated-orcid":true,"given":"Scott T.","family":"Chiesa","sequence":"additional","affiliation":[{"name":"National Centre for Cardiovascular Prevention and Outcomes Institute of Cardiovascular Science (S.M., D.B., S.T.C., J.D.), University College London, United Kingdom."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek J.","family":"Hausenloy","sequence":"additional","affiliation":[{"name":"The Hatter Cardiovascular Institute (D.Y., D.J.H.), University College London, United Kingdom."},{"name":"Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore 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