{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["17(1)"],"submitter":["Wehrhan F"],"funding":["Deutsche Gesellschaft für Zahn-, Mund- und Kieferheilkunde"],"pubmed_abstract":["BACKGROUND:With an increasing indication spectrum of antiresorptive drugs, the medication-related osteonecrosis of the jaw secondary to bisphosphonate therapy [MRONJ (BP)] is continuously gaining clinical relevance. Impaired osteoclast function, accompanied by altered cell morphology and expression of osteoclastic effector proteins, contributes to the pathogenesis of MRONJ (BP). However, the underlying regulatory mechanisms at a transcriptional level are unaddressed so far. These mechanisms are crucial to the development of disease-characteristic osteoclastic anomalies, that contribute to the pathogenesis of MRONJ (BP). NFATc1 is considered a master upstream osteoclastic activator, whereas BCL6 acts as osteoclastic suppressor. The present study aimed to elucidate the NFATc1 and BCL6 mediat"],"journal":["Journal of translational medicine"],"pagination":["69"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6398259"],"repository":["biostudies-literature"],"pubmed_title":["Osteoclastic expression of higher-level regulators NFATc1 and BCL6 in medication-related osteonecrosis of the jaw secondary to bisphosphonate therapy: a comparison with osteoradionecrosis and osteomyelitis."],"pmcid":["PMC6398259"],"pubmed_authors":["Gross C","Weber M","Wehrhan F","Kesting M","Ries J","Geppert CI","Creutzburg K","Amann K"],"additional_accession":[]},"is_claimable":false,"name":"Osteoclastic expression of higher-level regulators NFATc1 and BCL6 in medication-related osteonecrosis of the jaw secondary to bisphosphonate therapy: a comparison with osteoradionecrosis and osteomyelitis.","description":"BACKGROUND:With an increasing indication spectrum of antiresorptive drugs, the medication-related osteonecrosis of the jaw secondary to bisphosphonate therapy [MRONJ (BP)] is continuously gaining clinical relevance. Impaired osteoclast function, accompanied by altered cell morphology and expression of osteoclastic effector proteins, contributes to the pathogenesis of MRONJ (BP). However, the underlying regulatory mechanisms at a transcriptional level are unaddressed so far. These mechanisms are crucial to the development of disease-characteristic osteoclastic anomalies, that contribute to the pathogenesis of MRONJ (BP). NFATc1 is considered a master upstream osteoclastic activator, whereas BCL6 acts as osteoclastic suppressor. The present study aimed to elucidate the NFATc1 and BCL6 mediat","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Mar","modification":"2025-04-19T01:24:19.049Z","creation":"2019-06-06T20:56:46Z"},"accession":"S-EPMC6398259","cross_references":{"pubmed":["30832685"],"doi":["10.1186/s12967-019-1819-1"]}}