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In recent years, deep venous thrombosis (DVT) after spine surgery has received extensive attention, but perioperative prevalence of DVT in patients undergoing percutaneous kyphoplasty (PKP) is lacking. To assess the perioperative prevalence of deep vein thrombosis (DVT) in patients undergoing PKP with routinely applied ultrasonography. We reviewed 1113 consecutive patients undergoing PKP from January 2014 to August 2017. The surgical procedure was bilateral PKP. All patients were routinely examined with ultrasonography when admitted to the hospital and on the first post-operative day. Clinical signs of DVT were checked and recorded before examination. Forty (3.6%) out of 1113 patients were diagnosed with DVT by ultrasonography. Of the 40 detected cases of DVT, only six (0.54%) patients presented with clinical signs of DVT, demonstrating that there were 34 (3.05%) asymptomatic cases. No patient presenting with clinically suspected pulmonary embolism (PE) was observed. Gender, body mass index (BMI), operative time, hypertension, diabetes, heart disease, and lower limb fracture were not significant risk factors for DVT (P > .05). In contrast, patient age, oncologic conditions, DVT history, and paraplegia appeared to be significant risk factors for DVT (P < .01). There was no significant difference in the incidence of DVT found between the three PKP surgical levels (P > .05). The total incidence of perioperative DVT diagnosed with ultrasonography in patients undergoing PKP was 3.6%, of which only 0.54% was symptomatic cases. It is necessary to assess DVT using ultrasonography during the perioperative procedure of PKP, especially for high-risk patients. Level of evidence: Level IV.

Osteoarthritis (OA) involves age‐associated structural and immune changes, yet whether senescence‐associated B‐cell states contribute to cartilage degeneration remains unclear. Integrated single‐cell RNA sequencing and spatial transcriptomics of healthy, aged, and OA mouse joints identify reduced B‐cell abundance but enrichment of a low‐proliferative, inflammatory state with heightened macrophage migration inhibitory factor (MIF) signaling. Cell–cell communication and spatial ligand–receptor analyses identify enhanced predicted MIF–CD74/CD44 interactions in B‐cell‐associated regions adjacent to cartilage. Constitutive MIF deficiency attenuates senescence‐associated B‐cell changes, MMP13 induction, and cartilage damage in vivo. Joint‐derived B cells from aged and OA mice induce chondrocyte senescence, reduce COL2A1 and HMGB1, and increase FN1 and MMP13 through MIF‐dependent paracrine signaling. These effects are suppressed by MIF neutralization and restored by recombinant MIF in MIF‐deficient co‐cultures. A composite hydrogel carrying quercetin and MIF‐siRNA‐loaded PLGA microspheres for local co‐delivery. The microspheres show gradual siRNA release over 96 h in vitro. In DMM‐induced OA, the formulation reduces MIF, P16, and MMP13 signals, restores HMGB1, and preserves cartilage. These findings support a senescence‐associated B cell–MIF signaling axis associated with joint aging and chondrocyte dysfunction and provide proof of concept for a local biomaterial‐based strategy that attenuates OA‐associated changes.