{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T06:48:47Z","timestamp":1791960527281,"version":"4.3.4"},"reference-count":76,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JBJS Rev"],"published-print":{"date-parts":[[2016,6,14]]},"abstract":"<jats:p>\n                    <jats:list list-type=\"plain\">\n                      <jats:list-item>\n                        <jats:p>\u27a2 Fracture nonunion is a failure of the biological processes of fracture-healing.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\u27a2 Critical cellular events in fracture-healing include the inflammatory response, differentiation and proliferation of progenitor cells, formation of fibrocartilage callus, angiogenesis and subsequent mineralization of the callus, vascular union (restoration of normal medullary circulation), and conversion of woven bone to lamellar bone.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\u27a2 All critical events are closely regulated and coordinated by numerous cytokines and growth factors, which are expressed in complex spatial and temporal patterns throughout the repair process.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\u27a2 At all phases of fracture-healing, poor cellular and metabolic capacity (e.g., chronic disease), excessive instability, and poor vascularity inhibit cellular responses and healing.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\u27a2 Many biological treatments to prevent or treat nonunions are emerging in clinical use, including stem-cell and bone-marrow-aspirate preparations, various progenitor cells and growth factors (e.g., recombinant human bone morphogenetic proteins), and gene therapy.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>","DOI":"10.2106\/jbjs.rvw.15.00078","type":"journal-article","created":{"date-parts":[[2016,6,15]],"date-time":"2016-06-15T09:26:32Z","timestamp":1465982792000},"source":"Crossref","is-referenced-by-count":31,"title":["The Biological Basis for Nonunions"],"prefix":"10.2106","volume":"4","author":[{"given":"Mark R.","family":"Brinker","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery, University of Texas Health Science Center at Houston, Houston, Texas"},{"name":"Fondren Orthopedic Group, Texas Orthopedic Hospital, Houston, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel 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