{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T08:03:22Z","timestamp":1789459402954,"version":"build-2803163510"},"reference-count":140,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:00:00Z","timestamp":1789430400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:00:00Z","timestamp":1789430400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>O\u2010GlcNAcylation is a dynamic and reversible post\u2010translational modification of serine\/threonine residues on cytoplasmic and nuclear proteins. Although it has been implicated as a \u201cdifferentiation switch and functional regulator\u201d in osteoclast biology, a systematic synthesis of its role across the macrophage\u2013osteoclast axis and its contribution to bone remodeling disorders has not been elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The present study examines evidence on O\u2010GlcNAc cycling in macrophage polarization, RANKL signaling amplification, and the maintenance of the osteoclast transcriptional program. The analysis integrates findings from cellular and molecular studies with clinical evidence from diseases such as osteoporosis, inflammatory bone destruction, and tumor bone metastasis to provide a comprehensive overview of the underlying mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>O\u2010GlcNAcylation is emerging as a pivotal regulator that disrupts bone remodeling equilibrium through multiple interconnected mechanisms along the macrophage\u2013osteoclast axis. It promotes polarization of pro\u2010inflammatory macrophages, amplifies RANKL\u2010mediated signaling cascades, and stabilizes the transcriptional programs that drive osteoclast differentiation and function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>O\u2010GlcNAc glycosylation may provide a novel approach for restoring bone homeostasis in skeletal diseases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/odi.70498","type":"journal-article","created":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T07:12:41Z","timestamp":1789456361000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["O\u2010\n                    <scp>GlcNAcylation<\/scp>\n                    : A Metabolic\u2010Immune Hub Regulating Macrophage Fate and Osteoclast 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