Abstract

Hemophilic arthropathy is a progressive, disabling condition with poorly understood pathobiology. Since there is an emerging interest to study the role of intra-articular fat pad size and biology in arthritic conditions, we explored fat pad volume changes in hemophilic arthropathy and to what extent they differed from osteoarthritis. We matched a cohort of 13 adult patients with hemophilic arthropathy of the knee with age- and gender-matched cohorts without osteoarthritis (“control cohort”) and with the same degree of radiographic osteoarthritis (“OA cohort”) in 1 : 2 fashion. Infrapatellar fat pad (IPFP) and suprapatellar fat pad (SPFP) volumes were calculated based on magnetic resonance imaging and differences in fat pad volumes, demographics, height, weight, and osteoarthritis scores were evaluated. Fat pad volumes were positively associated with body size parameters in all three cohorts but were unaffected by the degree of osteoarthritis. While IPFP volumes did not differ between cohorts, SPFP volumes expanded disproportionally with weight in hemophilia patients. Our observations indicate that IPFPs and SPFPs behave biologically differently in response to different arthritic stimuli. The exaggerated expansion of the SPFP in hemophilia patients highlights the importance of further studying the implications of fat pad biology for progression of hemophilic arthropathy.

Highlights

  • IntroductionAt times fat pads in the knees extended into the medial and lateral recesses (Figure 1)

  • Hemophilia is an X-linked bleeding disorder due to a partial or complete deficiency of clotting factor VIII or IX

  • Hemophilic arthropathy is characterized by joint effusions, synovial inflammation, soft tissue hypertrophy, cartilage destruction, subchondral bone irregularities, and changes in vascularity caused by recurrent hemarthroses [2,3,4]

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Summary

Introduction

At times fat pads in the knees extended into the medial and lateral recesses (Figure 1). These are potential spaces, but in pathologic settings may become occupied by fluid, hypertrophied synovial structures, or intra-articular bodies. Since fat pad extension into these spaces has not been previously described to the best of our knowledge, we became interested to study to what extent fat pad volume changes occur in hemophilic joints. We were interested in exploring whether fat pad alterations play a role in the pathobiology of hemophilic arthropathy. This line of investigation seemed pertinent because of a new movement to elucidate the biological role of Arthritis (a)

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