Abstract
The deposition of monosodium urate (MSU) crystals in synovial fluid and tissue leads to gouty arthritis frequently associated with synovial inflammation and bone erosions. The cellular mechanism that links MSU crystals to an increased number of osteoclasts has not yet been fully understood. In a recent issue of Arthritis Research & Therapy Lee and colleagues proposed that bone destruction in chronic gouty arthritis is at least in part dependent on expression by T cells of receptor activator of NF-κB ligand (RANKL). The authors showed that pro-resorptive cytokines such as IL-1β, IL-6, and TNFα are expressed within tophi and stromal infiltrates. In vitro stimulation with MSU crystals revealed monocytes as a source for these cytokines, whereas T cells produce RANKL, the major trigger of osteoclastogenesis.
Highlights
The deposition of monosodium urate (MSU) crystals in synovial fluid and tissue leads to gouty arthritis frequently associated with synovial inflammation and bone erosions
The differentiation of monocytes into osteoclasts depends on the presence of the receptor activator of nuclear factor (NF)-κB ligand (RANKL) and is antagonized by osteoprotegerin
Stromal tissue was infiltrated with inflammatory T cells, B cells, and mast cells, whereas the tophi themselves were surrounded by tartrate-resistant acid phosphatase-positive multinucleated osteoclasts
Summary
The deposition of monosodium urate (MSU) crystals in synovial fluid and tissue leads to gouty arthritis frequently associated with synovial inflammation and bone erosions. Gouty arthritis is a chronic disease, characterized by hyperuricemia, precipitating the deposition of inflammatory monosodium urate (MSU) crystals in various tissues. The differentiation of monocytes into osteoclasts depends on the presence of the receptor activator of NF-κB ligand (RANKL) and is antagonized by osteoprotegerin. In samples of gouty tissue Lee and colleagues observed osteolytic lesions close to the tophi [1].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
