Objective: Knee-adjacent subcutaneous fat (kaSCF) has emerged as a potential biomarker and risk factor for osteoarthritis (OA) progression. This study aims to develop an artificial intelligence-based tool for the automatic segmentation of kaSCF thickness and evaluate the cross-sectional associations between kaSCF, cartilage thickness, magnetic resonance imaging-based cartilage T2 relaxation time, knee pain, and muscle strength independent of body mass index (BMI).
Design: Baseline 3.0T MR images of the right knee from the entire Osteoarthritis Initiative cohort (n=4796) were used to quantify average values of kaSCF, cartilage thickness, and T2 using deep learning algorithms. Regression models (adjusted for age, gender, BMI, and race) were used to evaluate the associations between standardized kaSCF and outcomes of cartilage thickness, T2, pain, and knee extension strength.
Results: Model prediction CVs for kaSCF thickness ranged from 3.57% to 9.87% across femoral and tibial regions. Greater average kaSCF was associated with thinner cartilage in men (std. β= -0.029, 95% CI: -0.050 to -0.007, p=0.010) and higher T2 in women (std. β=0.169, 95% CI: 0.072 to 0.265, p=0.001). Greater kaSCF was also associated with lower knee extension force (std. β= -15.36, 95% CI: -20.39 to -10.33, p<0.001) and higher odds of frequent knee pain (std. odds ratio=1.156, 95% CI: 1.046 to 1.278, p=0.005) across all participants.
Conclusions: Greater kaSCF was associated with thinner cartilage in men, higher T2 in women, reduced knee strength, and greater knee pain, independent of BMI. These findings suggest a potential role of kaSCF as a predictor for knee osteoarthrits-related structural, functional, and clinical outcomes independent of the effects of BMI.
Objective: People with osteoarthritis (OA) commonly experience flares. Whether COVID-19 vaccination triggers OA flares is unknown.
Design: Adults with OA enrolled in a COVID-19 Rheumatology Registry were invited to participate in a case-crossover study. Vaccine data were ascertained from self-report and electronic health records (EHR). OA was identified using coding algorithms and validated via EHR. Participants reported flare and non-flare periods. Vaccine exposures in the 2-, 7-, and 14-day "lookback windows" prior to OA flares were compared to vaccine exposures during similar non-flare ("control") periods.
Results: 279 participants had validated OA, and 136 (49%) contributed at least one flare and one control period. Mean age was 68 years [SD ±8], 82% female, 87% White, 62% knee OA, 56% hip OA, 37% hand/wrist OA and 60% had >= one anatomic location of OA. 525 COVID-19 vaccine doses were recorded, and participants reported 374 OA flares: 30% were mild, 55% were moderate, and 14% were severe. OA flares were not associated with COVID-19 vaccination 2 or 7 days prior (odds ratios [OR] 0.69 [95% confidence interval (CI): 0.28, 1.66], OR 0.54 [95% CI: 0.27, 1.07], respectively). In the 14-day lookback window, fewer flares occurred after vaccination (OR 0.57 [95% CI: 0.34, 0.97], p=0.039). Analyses stratified on sex, age, knee or hand OA, vaccine brand, and dose showed no increased association between COVID-19 vaccination and OA flares.
Conclusion: The lack of positive association between COVID-19 vaccination and OA flare in any primary or secondary analysis provides reassurance regarding the use of COVID-19 vaccines in people with OA.