Introduction & Objectives
Growing evidence suggests a link exists between cartilage damage in osteoarthritis and monosodium urate (MSU) crystal formation in gout. MSU crystal deposition and gout flares frequently affect joints that have been damaged or are affected by osteoarthritis. Imaging and histologic studies have shown that MSU crystals are deposited on cartilage surfaces, and MSU crystals align to collagen fibers in vivo. In addition, various cartilage factors, including bovine nasal homogenates and proteoglycans, have been shown to affect urate solubility in vitro. Given these observations, it’s plausible that tissue factors released by osteoarthritic or damaged cartilage can influence MSU crystallization. This study was undertaken to examine the effects of human cartilage homogenates on MSU crystallization and MSU crystal-induced inflammation.
Human cartilage homogenates were prepared from macroscopically healthy and macroscopically diseased knee joint samples. Crystallization assays were used to test the effects of cartilage homogenates or individual cartilage factors on MSU crystallization. Changes in urate solubility, crystal nucleation, crystal growth, and total crystal mass were determined. THP-1 cell assays were used to assess cytokine release following culture with MSU crystals grown in the presence or absence of cartilage homogenates or individual proteins.
The addition of either 5% or 10% healthy cartilage homogenate to the crystallization assays increased the total mass of MSU crystals formed and resulted in formation of shorter MSU crystals compared with controls without cartilage homogenate. MSU crystal bows were observed in both the presence and absence of cartilage homogenate; however, bows formed in the presence of cartilage homogenates were significantly shorter than bows formed in their absence. There were no effect differences between macroscopically healthy and macroscopically diseased cartilage homogenates in all assessments. Addition of either type II collagen or albumin also led to the formation of shorter MSU crystals. In THP-1 cell assays, MSU crystals grown with healthy cartilage homogenate increased the release of interleukin 8, whereas MSU crystals grown with type II collagen or albumin had no effect on inflammatory cytokine release.
In the presence of elevated urate levels, human cartilage homogenates increase MSU crystal formation and promote the formation of smaller crystals, which have greater inflammatory potential. These processes may contribute to the predilection of osteoarthritic joints to develop gout.
Refer to the full study for all source material.
Excerpted and adapted from:
Chhana A, Pool B, Wei Y, et al. Human cartilage homogenates influence the crystallization of monosodium urate and inflammatory response to monosodium urate crystals: A potential link between osteoarthritis and gout. Arthritis Rheumatol. 2019 Dec;71(12):2090–2099.