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Life sciences · Journal article
Cureus · October 31, 2026
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Knee osteoarthritis (OA) is now recognized as a disease of the whole joint with disease processes affecting the cartilage, synovium, subchondral bone, and periarticular soft tissues.In particular, the infrapatellar fat pad (IPFP), also known as Hoffa's fat pad, has received growing interest as an active tissue within the knee joint, rather than a passive mechanical pad.This narrative review critically evaluates the immunometabolic role of the IPFP, its molecular interactions with synovial tissues, cartilage, subchondral bone and menisci, links with knee pain and structural progression, and its potential as a biomarker and therapeutic target in knee OA.PubMed/MEDLINE and Scopus were searched from inception to 30 September 2026, supplemented by reference-list screening, and reporting followed the Scale for the Assessment of Narrative Review Articles (SANRA).In human explant, histological and imaging studies, the osteoarthritic IPFP produces the adipokines (leptin, adiponectin, resistin and visfatin), cytokines (IL-1β, IL-6, TNF-α) and chemokines (CCL2) with a different immune infiltrate profile, where macrophages and T lymphocytes are the predominant cells.Cartilage and synoviocyte cultures are stimulated by IPFP-conditioned medium to show catabolic and inflammatory effects, which provide some biological plausibility for a pathogenic effect; however, the data are mostly correlative and cross-sectional.MRI-detected Hoffa synovitis was associated with pain in multiple, but not all, cohorts, and its association with histologically proven inflammation is not perfect.Fibrotic and angiogenic remodelling are documented in end-stage OA IPFP tissue; IPFP-derived stromal cells show in vitro chondrogenic capacity without proven superiority over other cell sources, and the independent contribution of metabolic syndrome, as distinct from obesity-related loading, remains unresolved.The IPFP is much more than a mere structural filler; it is, more likely than not, an active member of the immunometabolic microenvironment of the osteoarthritic knee.The causal role in the primary driver, amplifier, or mostly a consequence of joint disease has yet to be determined, and human evidence is still limited.Its capacity to damage as well as repair suggests that it should not be indiscriminately suppressed by therapy or excised by surgery and should continue to be investigated in a phenotype-specific manner.