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SAT0347 Cartilaginous Uric Acid Deposition in Advanced Osteoarthritis: Innocent Bystander or Promotor of Cartilage Destruction?
  1. T. Bongartz1,
  2. O. M. Andre2,
  3. R. J. Sierra2,
  4. H. D. Arlen2,
  5. T. J. Michael2
  1. 1Rheumatology
  2. 2MAYO CLINIC, Rochester, United States


Objectives Recent studies have suggested that synovial fluid uric acid could contribute to tissue inflammation, disease severity and progression of osteoarthritis (OA). Intraarticular uric acid has been associated with OA disease severity and may promote cartilage destruction through inflammasome activation (1).

We aimed to explore if intraarticular uric acid deposition does indeed occur in patients with OA of the knee who have never experienced an episode of gout.

Methods We recruited patients with advanced OA of the knee and no history of gout who were scheduled to undergo knee replacement surgery.

All subjects underwent dual-energy computed tomography (DECT) scanning of the target joint. DECT images were screened for areas of monosodium urate (MSU) deposition.

During knee replacement surgery, samples of tibial and femoral condyle cartilage, menisci and synovium were obtained. Areas of possible MSU deposition as identified through DECT were particularly targeted for sample collection.

A musculoskeletal pathologist performed bright field (DeGalantha and H&E stains) and polarizing microscopy and recorded the presence of MSU crystals in a descriptive manner.

Results 5 patients with advanced OA of the knee underwent DECT. In all subjects, DECT indicated areas of MSU deposition within the joint cartilage and the menisci.

In 4 of these 5 patients, histopathology examination confirmed presence of MSU crystal clusters in the cartilage and/or menisci. In 2 patients, MSU deposition also involved the synovium. Of note, synovial fluid in all patients was negative for MSU crystals as detected by polarizing microscopy. The mean serum uric acid level was 5.7mg/dl, range 5.0-6.4 mg/dl.

Conclusions This small pilot study revealed evidence of cartilaginous uric acid deposition in the majority of patients with advanced osteoarthritis.

Future studies will have to confirm this finding in a larger patient cohort and clarify if intracartilaginous urate crystals accelerate cartilage damage or are deposited simply a result of matrix exposure and subsequent monosodium urate crystallization without significant effects on disease progression.

Disclosure of Interest None Declared

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