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THU0456 Infrapatellar Fat Pad Volume and Signal Intensity Alteration Were Associated with Knee Osteoarthritic Changes in Patients with Knee Symptomatic Osteoarthritis
  1. J. Cai1,
  2. K. Wang1,
  3. J. Xu1,
  4. S. Zheng1,
  5. X. Yang1,
  6. C. Ding2
  1. 1Department of Rheumatology and Immunology, Arthritis Research Institute, the First Affiliated Hospital of Anhui Medical University, Hefei, China
  2. 2Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia


Background Osteoarthritis (OA) is the most prevalent form of arthritis, characterised by cartilage damage, osteophytes formation and other joint structural changes. Mechanical and metabolic factors have been played important roles in the development of knee OA. Infrapatellar fat pad (IPFP) is an intracapsular structure that may reduce loading on the joint and play a beneficial role in the progression of knee OA. However, the function of infrapatellar fat pad is still uncertain for knee OA.

Objectives The aim of this study was to investigate the associations between IPFP volume, signal intensity alteration and knee structures, including cartilage volume, cartilage defects, bone marrow lesions (BMLs) and radiographic changes in patients with knee OA. The associations between IPFP volume and signal intensity alteration and serum levels of interleukin 17 and adiponectin were also been studied.

Methods 174 randomly-selected patients with knee symptomatic OA (mean 55.5 years, range 34 to 74, female 85.6%) participated in Anhui Osteoarthritis (AHOA) Study. T1-weighted 3D-SPGR magnetic resonance imaging (MRI) was used to measure the IPFP volume and knee cartilage volume. T2-weighted fat suppressed fast spin echo MRI was utilized to assess knee cartilage defects, bone marrow lesions and IPFP signal intensity changes. Radiographic knee joint space narrowing and osteophytes were assessed using the Osteoarthritis Research Society International atlas. Serum interleukin-17 and adiponectin levels were measured using ELISA.

Results After adjustment for potential confounders, IPFP volume was significantly and positively associated with knee tibial and patellar cartilage volume (all p<0.05). There were apparently negative associations between IPFP volume and cartilage defects at medial tibial, lateral tibial, medial femoral, lateral femoral and patellar sites. Similarly there were significant and negative associations between IPFP volume and bone marrow lesions at lateral tibial and medial femoral sites. IPFP volume was also significantly associated with lateral femoral osteophytes. Furthermore, IL-17 was negatively associated with IPFP volume. IPFP signal intensity alteration was significantly associated with lateral tibiofemoral cartilage defect and bone marrow lesions at lateral and medial tibiofemoral compartment. The associations of IPFP signal intensity alteration with lateral and medial femoral osteophytes were significant. There were distinctly positive associations between IPFP signal intensity alteration and medial tibiofemoral cartilage defects, and lateral and medial tibial osteophytes, but these did not reach statistically significance. Furthermore, there was a negative association between IPFP signal intensity alteration and adiponectin.

Conclusions This study was the first to report that in patients with knee OA, IPFP volume was negatively associated with knee cartilage volume and positively associated with knee cartilage defects, bone marrow lesions and osteophytes; in contrast, IPFP abnormal quality had opposite associations. These suggest potentially a protective role of IPFP volume and a detrimental role of IPFP abnormal quality in knee OA. Furthermore, interleukin 17 was associated with reduced IPFP volume but adiponectin was associated with decreased abnormal changes of IPFP in knee OA.

Disclosure of Interest None declared

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