{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T16:50:46Z","timestamp":1790182246142,"version":"4.1.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T00:00:00Z","timestamp":1501804800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,12,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>\u2003<\/jats:title>\n                    <jats:p>Mast cells, important sensor and effector cells of the immune system, may influence bone metabolism as their number is increased in osteoporotic patients. They are also present during bone fracture healing with currently unknown functions. Using a novel c-Kit-independent mouse model of mast cell deficiency, we demonstrated that mast cells did not affect physiological bone turnover. However, they triggered local and systemic inflammation after fracture by inducing release of inflammatory mediators and the recruitment of innate immune cells. In later healing stages, mast cells accumulated and regulated osteoclast activity to remodel the bony fracture callus. Furthermore, they were essential to induce osteoclast formation after ovariectomy. Additional in vitro studies revealed that they promote osteoclastogenesis via granular mediators, mainly histamine. In conclusion, mast cells are redundant in physiologic bone turnover but exert crucial functions after challenging the system, implicating mast cells as a potential target for treating inflammatory bone disorders. \u00a9 2017 American Society for Bone and Mineral Research.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jbmr.3234","type":"journal-article","created":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T09:04:45Z","timestamp":1501837485000},"page":"2431-2444","source":"Crossref","is-referenced-by-count":90,"title":["Mast Cells Are Critical Regulators of Bone Fracture\u2013Induced Inflammation and Osteoclast Formation and Activity"],"prefix":"10.1093","volume":"32","author":[{"given":"Jochen","family":"Kroner","sequence":"first","affiliation":[{"name":"Institute of Orthopedic Research and Biomechanics, Trauma Research Center UlmUlm University Medical 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CenterUlmGermany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Seitz","sequence":"additional","affiliation":[{"name":"Institute of Osteology and BiomechanicsUniversity Medical Center Hamburg-EppendorfHamburgGermany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thorsten","family":"Schinke","sequence":"additional","affiliation":[{"name":"Institute of Osteology and BiomechanicsUniversity Medical Center Hamburg-EppendorfHamburgGermany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Amling","sequence":"additional","affiliation":[{"name":"Institute of Osteology and BiomechanicsUniversity Medical Center Hamburg-EppendorfHamburgGermany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johanna","family":"Kotrba","sequence":"additional","affiliation":[{"name":"Institute for Molecular and Clinical Immunology, Medical FacultyOtto-von-Guericke 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