Ting Wang

Degenerative meniscus tears (DMTs) are pivotal in knee osteoarthritis progression, yet conventional MRI often fails to capture the subvisual alterations preceding macroscopic failure. We developed a multi‐structural digital risk stratification framework (MSC‐RM) that integrates standardized radiomic signatures from six knee structures (femur, tibia, cartilages, and menisci) derived from 3D double‐echo steady‐state MRI with baseline clinical risk profiles. Utilizing a longitudinal cohort ( n = 674), our framework decoded complex degeneration patterns, achieving superior 4‐year predictive performance (AUC 0.871). Survival analysis revealed that high‐risk individuals had a 6.12‐fold greater hazard of developing DMTs than the low‐risk group. Furthermore, a reader test with five resident surgeons demonstrated that MSC‐RM significantly enhanced diagnostic consistency (Kappa increased from 0.38 to 0.55), effectively bridging the expertise gap. By shifting the paradigm from reactive lesion detection to proactive risk management, this framework provides a scalable strategy for precision preventive medicine and establishes digital biomarkers as critical tools for optimizing musculoskeletal health in aging populations.

Background: Knee osteoarthritis (KOA) worsens both structurally and symptomatically, yet no model predicts KOA progression using Magnetic Resonance Image (MRI) radiomics and biomarkers. This study aimed to develop and test the longitudinal Load-Bearing Tissue Radiomic plus Biochemical biomarker and Clinical variable Model (LBTRBC-M) to predict KOA progression. Methods and findings: Data from the Foundation of the National Institutes of Health Osteoarthritis Biomarkers Consortium were used. We selected 594 participants with Kellgren-Lawrence grades 1–3 and complete biomarker data. The mean age was 61.6 ± 8.9 years, 58.8% were female, and the racial distribution was 79.3% White or White, 18.0% Black or African American, and 2.7% Asian or other non-White. A total of 1,753 knee MRIs were included across the study period, comprising 594 at baseline, 575 at 1-year follow-up, and 584 at 2-year follow-up. Outcomes included (1) both Joint Space Narrowing (JSN) and pain progression (n = 567), (2) only JSN progression (n = 303), (3) only pain progression (n = 295), and (4) non-progression (JSN or pain) (n = 588), corresponding to an approximate ratio of 2:1:1:2. JSN progression was defined as a minimum joint space width (JSW) loss of ≥0.7 mm, and pain progression as a sustained (≥2 time points) increase of ≥9 points on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain subscale (0–100 scale). Using the eXtreme Gradient BOOSTing (XGBOOST) algorithm, the model was developed in the total development cohort (n = 877) and tested in the total test cohort (n = 876). In the total test cohort, the Area Under the receiver operating characteristic Curve (AUC) of LBTRBC-M for predicting JSN and pain progression, JSN progression, pain progression, and non-progression were 0.880 (95% confidence interval (CI) [0.853, 0.903]), 0.913 (95% CI [0.881, 0.937]), 0.886 (95% CI [0.856, 0.910]), and 0.909 (95% CI [0.888, 0.926]), respectively. The overall accuracy of LBTRBC-M was 70.1%. With LBTRBC-M assistance, the prognostic accuracy of resident physicians (n = 7) improved from 44.7%–49.0% to 64.4%–66.5%. The main limitations include the use of a non-routine MRI sequence, the lack of external validation in independent cohorts, and limited incorporation of all knee joint structures in radiomic feature extraction. Conclusions: In this study, we observed that longitudinal MRI radiomic features of load-bearing knee joint tissues provide potentially informative markers for predicting knee osteoarthritis progression. These findings may help guide future efforts toward early risk stratification and personalized management of KOA.

Retinoids have many pharmacological activities, including anti-inflammatory action and antiangiogenesis, effected through the regulation of various gene transcriptions. In this study, we investigated the effect of Am-80, one of the retinoic acid derivatives, on hapten-induced contact hypersensitivity in BALB/c mice. After application of 2,4-dinitrofluorobenzene (DNFB) to the ears of the mice, severe contact hypersensitivity with marked infiltration of inflammatory cells and hypertrophy of the epidermis was caused. The thickness of the ears increased biphasically and reached a peak 3 and 24 h after the DNFB challenge. Am-80 significantly inhibited ear thickness in the late-(24 h), but not the early-phase (3 h) reaction in a dose-dependent manner. In a histopathological study, obvious depression of edema and infiltration of inflammatory cells was observed in the ears of mice treated with Am-80. Am-80 inhibited the levels of expression in mice ears of interferon-γ (IFN-γ) and interleukin-6 (IL-6), but not tumor necrosis factor-α (TNF-α) or interleukin-4 (IL-4). Furthermore, Am-80 inhibited the antigen-induced production of some cytokines, including IFN-γ and IL-6, but not IL-4, in vitro. Therefore, Am-80 inhibited hapten-induced contact hypersensitivity through the direct inhibition of inflammatory cytokines such as IFN-γ and IL-6.