Differentiating benign intra-articular tumors from SAH remains difficult, particularly among younger and female patient populations with acute presentations of TGCT which, as observed in the present study, may be explained by histopathologic evidence of tumor pedicle torsion and resultant necrosis. MRI can be valuable in identifying intra-articular lesions given that clinical and laboratory findings are frequently equivocal. The proposed diagnostic algorithm offers a framework for identifying cases where preoperative MRI may be beneficial, though it requires validation in larger studies.
Ferroptosis, immune, and proliferation markers differ significantly between TGCT subtypes and recurrence status. The ACSL4+CD8 signature shows excellent potential for subtype differentiation, while the Ki-67+CSF1R+tumor diameter index is a strong recurrence predictor. These exploratory findings support targeted biomarker use in TGCT management, though external validation in larger, prospective cohorts is required.
29 days ago
Observational data • Journal
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CD8 (cluster of differentiation 8) • CD163 (CD163 Molecule) • GPX4 (Glutathione Peroxidase 4) • CSF1R (Colony stimulating factor 1 receptor) • ACSL4 (Acyl-CoA Synthetase Long Chain Family Member 4)
An arthroscopic examination revealed numerous white synovial, chondromate-like tissues under the articular capsule, and D-TGCT was diagnosed based on the histopathological results. One year after the surgery, the patient had good functional recovery and no tumor recurrence.
Our case emphasises that intra-articular NF is a rare entity that can mimic more common intra-articular tumours. The detection of USP6 on histopathological analysis allows accurate diagnosis and treatment.
Although representing just 5% of all identified factors, these appeared in 69% of the included studies, highlighting their prominence in the literature. Apart from the well-known osteoclastogenesis factor CSF1, inflammatory cytokines (TNF-α and IL-1β) and monocyte-macrophage lineage makers (CD68, CD163) are signalling pathways key to TGCT disease progression and associated bone destruction.