Julie E Davis1, Robert J Ward2, James W MacKay3, Bing Lu4, Lori Lyn Price5,6, Timothy E McAlindon1, Charles B Eaton7, Mary F Barbe8, Grace H Lo9,10, Matthew S Harkey1, Jeffrey B Driban1. 1. Division of Rheumatology, Tufts Medical Center, Boston, MA, USA. 2. Department of Radiology, Tufts Medical Center, Boston, MA, USA. 3. Department of Radiology, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, UK. 4. Brigham & Women's Hospital and Harvard Medical School, Tufts University, Boston, MA, USA. 5. The Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Tufts University, Boston, MA, USA. 6. Tufts Clinical and Translational Science Institute, Tufts University, Boston, MA, USA. 7. Center for Primary Care and Prevention, Alpert Medical School of Brown University, Pawtucket, RI, USA. 8. Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA, USA. 9. Medical Care Line and Research Care Line, Houston Health Services Research and Development (HSR&D) Center of Excellence Michael E. DeBakey VAMC, Houston, TX, USA. 10. Section of Immunology, Allergy, and Rheumatology, Baylor College of Medicine, Houston, TX, USA.
Abstract
OBJECTIVES: To determine whether greater effusion-synovitis volume and infrapatellar fat pad (IFP) signal intensity alteration differentiate incident accelerated knee OA (KOA) from a gradual onset of KOA or no KOA. METHODS: We classified three sex-matched groups of participants in the Osteoarthritis Initiative who had a knee with no radiographic KOA at baseline (recruited 2004-06; Kellgren-Lawrence <2; n = 125/group): accelerated KOA: ⩾1 knee progressed to Kellgren-Lawrence grade ⩾3 within 48 months; common KOA: ⩾1 knee increased in radiographic scoring within 48 months; and no KOA: both knees had the same Kellgren-Lawrence grade at baseline and 48 months. The observation period included up to 2 years before and after when the group criteria were met. Two musculoskeletal radiologists reported presence of IFP signal intensity alteration and independent readers used a semi-automated method to segment effusion-synovitis volume. We used generalized linear mixed models with group and time as independent variables, as well as testing a group-by-time interaction. RESULTS: Starting at 2 years before disease onset, adults who developed accelerated KOA had greater effusion-synovitis volume than their peers (accelerated KOA: 11.94 ± 0.90 cm3, KOA: 8.29 ± 1.19 cm3, no KOA: 8.14 ± 0.90 cm3) and have greater odds of having IFP signal intensity alteration than those with no KOA (odds ratio = 2.07, 95% CI = 1.14-3.78). Starting at 1 year prior to disease onset, those with accelerated KOA have greater than twice the odds of having IFP signal intensity alteration than those with common KOA. CONCLUSION: People with IFP signal intensity alteration and/or greater effusion-synovitis volume in the absence of radiographic KOA may be at high risk for accelerated KOA, which may be characterized by local inflammation.
OBJECTIVES: To determine whether greater effusion-synovitis volume and infrapatellar fat pad (IFP) signal intensity alteration differentiate incident accelerated knee OA (KOA) from a gradual onset of KOA or no KOA. METHODS: We classified three sex-matched groups of participants in the Osteoarthritis Initiative who had a knee with no radiographic KOA at baseline (recruited 2004-06; Kellgren-Lawrence <2; n = 125/group): accelerated KOA: ⩾1 knee progressed to Kellgren-Lawrence grade ⩾3 within 48 months; common KOA: ⩾1 knee increased in radiographic scoring within 48 months; and no KOA: both knees had the same Kellgren-Lawrence grade at baseline and 48 months. The observation period included up to 2 years before and after when the group criteria were met. Two musculoskeletal radiologists reported presence of IFP signal intensity alteration and independent readers used a semi-automated method to segment effusion-synovitis volume. We used generalized linear mixed models with group and time as independent variables, as well as testing a group-by-time interaction. RESULTS: Starting at 2 years before disease onset, adults who developed accelerated KOA had greater effusion-synovitis volume than their peers (accelerated KOA: 11.94 ± 0.90 cm3, KOA: 8.29 ± 1.19 cm3, no KOA: 8.14 ± 0.90 cm3) and have greater odds of having IFP signal intensity alteration than those with no KOA (odds ratio = 2.07, 95% CI = 1.14-3.78). Starting at 1 year prior to disease onset, those with accelerated KOA have greater than twice the odds of having IFP signal intensity alteration than those with common KOA. CONCLUSION:People with IFP signal intensity alteration and/or greater effusion-synovitis volume in the absence of radiographic KOA may be at high risk for accelerated KOA, which may be characterized by local inflammation.
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