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OP0144 Infra Patellar Fat Pad Signal Intensity Alterations and Effusion-Synovitis Predict Knee Pain, Cartilage Volume Loss and Total Knee Replacement over 10.7 Years in Older Adults
  1. B.S. Eathakkattu Antony1,
  2. X. Jin1,
  3. X. Wang1,
  4. W. Han1,
  5. F. Cicuttini2,
  6. C. Ding1,
  7. G. Jones1
  1. 1Menzies Institute for Medical Research, University of Tasmania, Hobart
  2. 2Epidemiology, Monash University, Melbourne, Australia

Abstract

Background There are no long-term studies that describe the independent association of infrapatellar fat pad (IPFP) signal intensity alterations and effusion-synovitis with knee osteoarthritis (KOA) severity and progression.

Objectives To describe the associations between baseline IPFP signal intensity alterations and effusion-synovitis and long-term knee pain, knee dysfunction, tibial cartilage volume loss and total knee replacement (TKR) over 10.7 years.

Methods Participants (n=983, mean age 62.8 years, 50% female) were selected randomly from the local community of Tasmania and followed up at 2.6 years, 5.1 years and 10.7 years later. MRI was acquired at baseline and 10.7 year follow-up. Effusion-synovitis was measured on T2-weigthed MRI using a modified WORMS system (grade 0–3) at suprapatellar pouch, central portion, posterior femoral recess and subpopliteal recess. IPFP signal intensity alteration was assessed on T2-weighted MRI and was defined as discrete areas of increased signal within IPFP, and was graded as follows: grade 0 = none; grade 1 = <10% of the region; grade 2 = 10% to 20% of the region; grade 3 = >20% of the region. Cartilage volume at baseline and 10.7 years was measured using manual segmentation of T1-weighted MRI. Clinical symptoms and TKR data were recorded at each follow-up visit. Multivariable analyses were performed using linear mixed-effects models for clinical symptoms, linear regression for cartilage volume loss and cox proportional hazards for TKR.

Results After adjustment for age, sex, BMI, radiographic KOA status, baseline IPFP signal intensity alteration was associated with total WOMAC score (β=2.19, 95% CI = 0.29, 4.09), WOMAC pain and WOMAC function scores (all p<0.01) over 10.7 years. However, these associations became borderline significance after further adjustment for cartilage defects, BMLs or effusion-synovitis. Baseline IPFP signal intensity alteration was independently associated with tibial cartilage volume loss (β=0.08 mm3, 95% CI = 0.14, 0.02) and TKR (HR=1.89, 95% CI = 1.31, 2.74) over 10.7 years.

Baseline total effusion-synovitis and suprapatellar pouch effusion-synovitis were independently associated with total WOMAC score (β=2.08,95%CI=0.16,4.16) and pain and dysfunction scores (all p<0.05) over 10.7 years. However, there was no significant association between effusion-synovitis and cartilage volume loss. Total (HR=1.58,95%CI=1.01,2.49), sub popliteal recess (HR=1.53, 95%CI=1.11,2. 11) and suprapatellar pouch (HR=1.90,95%CI=1.25,2.89) effusion-synovitis was associated with TKR over 10.7 years. However, these associations were dependent of other structural pathologies except grade 3 suprapatellar effusion-synovitis.

Conclusions Signal intensity alterations of IPFP at baseline were significantly associated tibial cartilage volume loss and TKR over 10.7 years independent of other structural pathologies. Effusion-synovitis (especially at suprapatellar pouch) was independently associated with knee pain and TKR. These results suggest that effusion-synovitis was associated with clinical progression and IPFP signal intensity alteration was associated with structural progression and TKR, and can be used as independent markers of progression of KOA.

Acknowledgement National Health and Medical Research Council of Australia funded this study.

Disclosure of Interest None declared

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