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Traumatic joint injury and the onset of osteoarthritis (OA) dramatically remodel the intra-articular adipose niche, marked by infiltration of fibrotic tissue postulated to underpin OA-associated joint stiffness and pain, yet we know very little about the disease-associated dynamics of joint adipose remodeling nor the mechanisms driving these phenomena. Here, we employed 2D histomorphometry and spatial transcriptomics, alongside 3D osmium tetroxide-enhanced micro-computed tomography to comprehensively define the spatiotemporal, structural, and transcriptional rewiring of joint adipose tissue in a non-invasive mouse model of post-traumatic osteoarthritis (PTOA). These revealed marked loss of intra-articular adiposity accompanied by expansion of fibroblast-rich, collagen-dense tissue with pro-fibrotic hallmarks and Wnt\/\u03b2-catenin-enriched gene programs. Joint adipose exhibited a distinct transcriptional signature compared to subcutaneous white adipose tissue, pointing to unique, depot-specific functions. Stromal cells isolated from PTOA joints had heightened baseline expression of fibrotic and Wnt pathway genes and exhibited impaired\n                  <jats:italic>de novo<\/jats:italic>\n                  adipogenesis, in contrast to cells derived from healthy joints. In accordance with the destabilized biomechanics of PTOA joints,\n                  <jats:italic>in vitro<\/jats:italic>\n                  modeling demonstrated that prolonged, injurious loading and perturbed Wnt\/\u03b2-catenin signaling were convergent anti-adipogenic cues that suppressed lipid droplet formation and adipogenic gene induction, while promoting markers of fibrosis in joint-derived stromal cells. Complementary gain-of-function studies using\n                  <jats:italic>ex vivo<\/jats:italic>\n                  joint adipose explants and\n                  <jats:italic>in vivo<\/jats:italic>\n                  joint injections demonstrated that chronic Wnt\/\u03b2-catenin activation, as seen in OA joints, is sufficient to diminish the intra-articular adipogenic program and shift adipose to a more fibrotic phenotype, independent of joint injury. Collectively, these findings establish a multi-modal framework for quantifying joint adipose atrophy and implicate aberrant Wnt\/\u03b2-catenin signaling and pathological mechanical loading as key factors impairing\n                  <jats:italic>de novo<\/jats:italic>\n                  adipogenesis and driving fibrotic remodeling of intra-articular adipose tissue in PTOA.\n                <\/jats:p>","DOI":"10.64898\/2026.06.08.730865","type":"posted-content","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T01:45:18Z","timestamp":1781142318000},"source":"Crossref","is-referenced-by-count":1,"title":["Wnt\/\u03b2-catenin signaling regulates fibrotic atrophy of intra-articular adipose tissue in post-traumatic osteoarthritis"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8402-2212","authenticated-orcid":false,"given":"Alexander J.","family":"Knights","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery, University of 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