<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ramos-Junior ES</submitter><funding>NIDCR NIH HHS</funding><pagination>1308657</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10751373</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Periodontitis is an immune-mediated inflammatory disease affecting almost half of the adult population and is the leading cause of tooth loss in the United States. The role of extracellular nucleotide signaling including nucleotide metabolizing enzyme CD73 adds an important layer of interaction of purine mediators capable of orchestrating inflammatory outcomes. CD73 is able to catabolize 5'-adenosine monophosphate into adenosine at the extracellular level, playing a critical role in regulating many processes under physiological and pathological conditions. Here, we explored the role of CD73 in ligature-induced periodontitis &lt;i>in vivo&lt;/i> comparing wild-type C57Bl/6J and CD73-deficient mice.&lt;h4>Methods&lt;/h4>We assessed gingival levels of inflammatory cytokines &lt;i>in viv</pubmed_abstract><journal>Frontiers in oral health</journal><pubmed_title>The protective role of CD73 in periodontitis: preventing hyper-inflammatory fibroblasts and driving osteoclast energy metabolism.</pubmed_title><pmcid>PMC10751373</pmcid><funding_grant_id>R01 DE019456</funding_grant_id><pubmed_authors>Goncalves Fernandes J</pubmed_authors><pubmed_authors>Morandini AC</pubmed_authors><pubmed_authors>Zhong R</pubmed_authors><pubmed_authors>Clinebell B</pubmed_authors><pubmed_authors>Ramos-Junior ES</pubmed_authors><pubmed_authors>Shaddox LM</pubmed_authors><pubmed_authors>Cutler CW</pubmed_authors><pubmed_authors>Serrano-Lopez R</pubmed_authors><pubmed_authors>Brumbaugh R</pubmed_authors><pubmed_authors>Dawson S</pubmed_authors><pubmed_authors>Ryan W</pubmed_authors><pubmed_authors>Russell M</pubmed_authors></additional><is_claimable>false</is_claimable><name>The protective role of CD73 in periodontitis: preventing hyper-inflammatory fibroblasts and driving osteoclast energy metabolism.</name><description>&lt;h4>Introduction&lt;/h4>Periodontitis is an immune-mediated inflammatory disease affecting almost half of the adult population and is the leading cause of tooth loss in the United States. The role of extracellular nucleotide signaling including nucleotide metabolizing enzyme CD73 adds an important layer of interaction of purine mediators capable of orchestrating inflammatory outcomes. CD73 is able to catabolize 5'-adenosine monophosphate into adenosine at the extracellular level, playing a critical role in regulating many processes under physiological and pathological conditions. Here, we explored the role of CD73 in ligature-induced periodontitis &lt;i>in vivo&lt;/i> comparing wild-type C57Bl/6J and CD73-deficient mice.&lt;h4>Methods&lt;/h4>We assessed gingival levels of inflammatory cytokines &lt;i>in viv</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2026-05-28T20:39:46.549Z</modification><creation>2024-11-20T20:52:58.281Z</creation></dates><accession>S-EPMC10751373</accession><cross_references><pubmed>38152410</pubmed><doi>10.3389/froh.2023.1308657</doi></cross_references></HashMap>