T. Yang
Boston University
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Annals of the Rheumatic Diseases | 2015
I.K. Haugen; Devyani Misra; Tuhina Neogi; Jingbo Niu; T. Yang; Yuqing Zhang; David T. Felson
Objectives To study whether hand osteoarthritis (OA) is associated with increased mortality and cardiovascular events in a large community based cohort (Framingham Heart Study) in which OA, mortality and cardiovascular events have been carefully assessed. Methods We examined whether symptomatic (≥1 joint(s) with radiographic OA and pain in the same joint) and radiographic hand OA (≥1 joint(s) with radiographic OA without pain) were associated with mortality and incident cardiovascular events (coronary heart disease, congestive heart failure and/or atherothrombotic brain infarction) using Cox proportional hazards models. In the adjusted models, we included possible confounding factors from baseline (eg, metabolic factors, medication use, smoking/alcohol). We also adjusted for the number of painful joints in the lower limb and physical inactivity. Results We evaluated 1348 participants (53.8% women) with mean (SD) age of 62.2 (8.2) years, of whom 540 (40.1%) and 186 (13.8%) had radiographic and symptomatic hand OA, respectively. There was no association between hand OA and mortality. Although there was no significant relation to incident cardiovascular events overall or a relation of radiographic hand OA with events, we found a significant association between symptomatic hand OA and incident coronary heart disease (myocardial infarction/coronary insufficiency syndrome) (HR 2.26, 95% CI 1.22 to 4.18). The association remained after additional adjustment for pain in the lower limb or physical inactivity. Conclusions Symptomatic hand OA, but not radiographic hand OA, was associated with an increased risk of coronary heart disease events. The results suggest an effect of pain, which may be a possible marker of inflammation.
Seminars in Arthritis and Rheumatism | 2013
Frank W. Roemer; David T. Felson; T. Yang; Jingbo Niu; Michel D. Crema; Martin Englund; Michael C. Nevitt; Yuqing Zhang; J.A. Lynch; George Y. El Khoury; James C. Torner; Cora E. Lewis; Ali Guermazi
OBJECTIVE Synovitis is thought to be a secondary phenomenon in the osteoarthritis (OA) process and the menisci might be triggers of localized synovitis. The aim was to assess the cross-sectional associations of posterior horn meniscal damage with perimeniscal synovitis, and with synovitis posterior to the posterior cruciate ligament (PCL) using contrast enhanced (CE) MRI. DESIGN The Multicenter Osteoarthritis (MOST) Study is a longitudinal observational study of subjects with or at risk for knee OA. Subjects are a subset of MOST who were examined with 1.5T CE MRI and had semiquantitative synovitis (scored from 0 to 2 at 11 locations) and meniscal readings (scored with WORMS from 0 to 4) available. Logistic regression was used to assess the association of posterior meniscal damage and perimeniscal synovitis in the same compartment, and between posterior meniscal damage and synovitis posterior to the PCL. RESULTS Three hundred and seventy seven knees were included (mean age 61.1 years±6.9, mean BMI 29.6±4.9, 44.3% women). The odds for ipsi-compartmental perimeniscal synovitis were increased for knees with medial posterior horn meniscal damage (adjusted odds ratio [aOR] 2.5, 95% confidence intervals [95% CI] 1.3,4.8), but not for lateral damage (aOR 1.7, 95% CI 0.4,6.6). No positive associations were found for meniscal damage and presence of synovitis posterior to the PCL (aOR 0.9, 95% CI 0.6,1.5). CONCLUSIONS Meniscal damage of the posterior horns is associated with ipsi-compartmental perimensical synovitis. No associations were found for posterior horn meniscal damage with synovitis posterior to the PCL, which suggests that synovitis posterior to the PCL is likely to be triggered by different pathomechanisms.
Annals of the Rheumatic Diseases | 2014
Ali Guermazi; F. Eckstein; Daichi Hayashi; Frank W. Roemer; W. Wirth; T. Yang; Jingbo Niu; Leena Sharma; M. Nevitt; Cora E. Lewis; J. Torner; David T. Felson
Background Studies have shown associations of structural progression of knee OA with several MRI-assessed pathologic features such as bone marrow lesions (BMLs) cartilage damage and meniscal lesions1,2. However previous studies commonly evaluated one risk factor at a time and not in a combination simultaneously, though these features are known to partly coexist. Objectives To determine which radiographic and semiquantitative MRI-based OA features predict cartilage thickness loss in the same femorotibial compartment (FTC). Methods One knee of each subject of a subcohort of Multicenter OA Study (MOST) was evaluated. The subcohort comprised persons who volunteered for a longitudinal study, in which quantitative MRI-based cartilage thickness was done. These subjects also had MRI for semiquantitative Whole Organ MRI Score based evaluation of BMLs, cartilage damage, meniscal damage and extrusion, Hoffa-synovitis and effusion-synovitis, at baseline and at 30-month. Progression in medial or lateral FTC (MFTC/LFTC) was defined as cartilage thinning exceeding the change observed in OAI control cohort knees (mean ± 2xSD, MFTC/LFTC: -162μm/-145μm). All MRI predictors were dichotomized into present/absent. Differences in baseline scores of predictor variables in the same FTC were compared between progressor and nonprogressor knees using multivariable logistic regression adjusting for age, sex, BMI and alignment axis. We combined MFTC and LFTC to calculate adjusted odds ratio (aOR) and 95% CI of cartilage thickness loss across compartments (ie. medial cartilage thinning with medial risk factors and lateral cartilage thinning with lateral risk factors) using GEE. ORs and 95%CIs were also calculated for MFTC and LFTC cartilage thickness loss, individually. Results 196 persons with mean age 59.8±6.3 years, mean BMI 29.5±4.6 and 62% women were included. 46 knees had baseline radiographic knee OA (KL grade≥2). In the MFTC/LFTC, 35/29 progressors and 161/167 nonprogressors were observed, respectively. Change in MFTC cartilage thickness was -63.0μm and that in LFTC cartilage thickness -25.1μm. For combined MFTC+LFTC analysis, predictors of cartilage thinning were baseline BML (aOR 1.9 95%CI [1.1-3.3]), cartilage damage (2.6 [1.4-5.0]), meniscal damages (4.5 [2.4-8.4]) and meniscal extrusion (3.3 [1.9-5.8]), all in the same FTC. Hoffa- and effusion-synovitis did not predict cartilage thinning. In MFTC-only analysis MFTC progressors showed higher aOR for having baseline meniscal damage (2.4 [1.1-5.6]) and meniscal extrusion (2.6 [1.1-5.8]). In LFTC-only analysis baseline cartilage damage (3.4 [1.3-9.3]), meniscal damage (13.9 [3.3-9.0]) and meniscal extrusion (5.0 [1.4-18.0]) predicted LFTC progression. Conclusions The presence of semiquantitatively assessed BMLs, cartilage damage, meniscal damage and extrusion in the same FTC predict cartilage thickness loss over 30-months. References Roemer et al. Arthritis Rheum 2012;64:1888-98. Crema et al. Osteoarthritis Cartilage 2010;18:336-43. Disclosure of Interest : A. Guermazi Shareholder of: Boston Imaging Core Lab, LLC, Consultant for: Merck Serono, TissueGene, Sanofi Aventis, F. Eckstein Shareholder of: Chondrometrics GmbH, Consultant for: MerckSerono and Abbvie, D. Hayashi: None declared, F. Roemer Shareholder of: Boston Imaging Core Lab, LLC, Consultant for: Merck Serono and the NIH, W. Wirth Shareholder of: Chondrometrics, GmbH, T. Yang: None declared, J. Niu: None declared, L. Sharma: None declared, M. Nevitt: None declared, C. Lewis: None declared, J. Torner: None declared, D. Felson: None declared DOI 10.1136/annrheumdis-2014-eular.2558
Osteoarthritis and Cartilage | 2013
Natalie A. Glass; J. Torner; L.A. Frey Law; Ke Wang; T. Yang; Michael C. Nevitt; David T. Felson; Cora E. Lewis; Neil A. Segal
Osteoarthritis and Cartilage | 2013
David T. Felson; Jingbo Niu; T. Yang; J. Torner; Cora E. Lewis; Piran Aliabadi; Burton Sack; Leena Sharma; Ali Guermazi; Joyce Goggins; Michael C. Nevitt
Osteoarthritis and Cartilage | 2015
Ali Guermazi; F. Eckstein; Daichi Hayashi; Frank W. Roemer; W. Wirth; T. Yang; Jingbo Niu; Leena Sharma; Michael C. Nevitt; Cora E. Lewis; James C. Torner; David T. Felson
Osteoarthritis and Cartilage | 2014
Ali Guermazi; F. Eckstein; Daichi Hayashi; Frank W. Roemer; W. Wirth; T. Yang; Jingbo Niu; Leena Sharma; Michael C. Nevitt; Cora E. Lewis; J. Torner; David T. Felson
Osteoarthritis and Cartilage | 2013
I.K. Haugen; Devyani Misra; Tuhina Neogi; Jingbo Niu; T. Yang; Yuqing Zhang; David T. Felson
Annals of the Rheumatic Diseases | 2013
I.K. Haugen; Devyani Misra; Tuhina Neogi; Jingbo Niu; T. Yang; Yuqing Zhang; David T. Felson
Annals of the Rheumatic Diseases | 2013
Frank W. Roemer; David T. Felson; T. Yang; Jingbo Niu; Michel D. Crema; Martin Englund; Michael C. Nevitt; Yuqing Zhang; J.A. Lynch; G.Y. El Khoury; Cora E. Lewis; Ali Guermazi