{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,13]],"date-time":"2026-11-13T10:35:04Z","timestamp":1794566104668,"version":"4.9.1"},"reference-count":44,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[1999,6,1]],"date-time":"1999-06-01T00:00:00Z","timestamp":928195200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Critical Reviews in Oral Biology &amp; Medicine"],"published-print":{"date-parts":[[1999,6]]},"abstract":"<jats:p>Tissue pressure is the hydrostatic pressure in the interstitial fluid which surrounds the pulpal cells. This pressure outside the vessels is normally considerably lower than the blood pressure inside the vessels. The dental pulp has a relatively low interstitial compliance due to its enclosure between rigid dentin walls. Accordingly, even a modest increase in pulpal fluid volume will raise the tissue pressure, which may compress blood vessels, leading to ischemia and necrosis. Inflammation may lead to an increase in both interstitial fluid volume and blood volume in the low-compliant pulp and thereby increase the tissue pressure. However, the increased tissue pressure may, in turn, initiate increased lymph flow and absorption of fluid into capillaries in nearby non-inflamed tissue. Both of these latter factors will transport fluid out of the affected area and subsequently out of the tooth and consequently lower the tissue pressure. Increased tissue pressure, whether caused by increased blood volume or increased capillary filtration, will promote outward flow of fluid through exposed dentin tubules and thereby help to protect the pulp against entry of harmful substances. It seems physiologically beneficial, therefore, for the pulp to have a high tissue pressure, which promptly increases when blood flow increases due to its low compliance.<\/jats:p>","DOI":"10.1177\/10454411990100030501","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T19:40:32Z","timestamp":1231443632000},"page":"328-336","source":"Crossref","is-referenced-by-count":153,"title":["Interstitial Fluid Pressure in Normal and Inflamed Pulp"],"prefix":"10.1177","volume":"10","author":[{"given":"K.J.","family":"Heyeraas","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Bergen, Arstadveien 19, N-5009 Bergen, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Berggreen","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Bergen, Arstadveien 19, N-5009 Bergen, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[1999,6,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1981.61.3.556"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1993.73.1.1"},{"key":"atypb3","doi-asserted-by":"crossref","unstructured":"Aukland K., Wiig H. 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