Gout Urate Cryst. Depos. Dis., Volume 4, Issue 2 (June 2026) – 4 articles

Basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate (CPPD) crystals drive the degenerative and inflammatory pathways that lead to crystal arthropathy. Although recent classification criteria and imaging recommendations have improved standardisation for CPPD disease, it remains underdiagnosed in practice. In contrast, BCP disease lacks validated classification criteria and standardised diagnostic descriptors, limiting translational research and clinical recognition. Accurate diagnoses are limited by varied reference standards, operator-dependent techniques, and the absence of validated bedside tools. As the population ages and the burden of crystal disease rises, there will be increased demand for reliable diagnostic tools in clinical practice. This review summarises current and emerging diagnostic tools for identifying BCP and CPPD, with emphasis on bridging the diagnostic gap from research to routine care. Polarised light microscopy remains a highly specific test for the diagnosis of CPPD but is limited by inter-observer variability and access to polarising light microscopes. Imaging tools such as ultrasound, conventional radiography, computed tomography (CT) and dual-energy CT can identify CPPD, although performance varies by anatomical site, disease stage and technical parameters. Ultrasound is a useful bedside tool for identifying BCP disease, whereas CT and DECT also have diagnostic utility but lack validation for routine use. Emerging technologies such as computational polarised light microscopy and Raman spectroscopy are promising techniques, but require further research to evidence their use in clinical practice. Development of clear diagnostic reference standards, classification criteria for BCP disease, and evidence-based multimodal diagnostic pathways are essential to bridge the gap between research and routine clinical diagnosis. Full article

The crystal arthropathies gout and calcium pyrophosphate deposition (CPPD) disease represent a significant subset of rheumatic and musculoskeletal diseases, yet their overlap with common entities such as osteoarthritis (OA), rheumatoid arthritis (RA), and psoriatic arthritis (PsA) remains underrecognized. We conducted a structured narrative review of studies published through August 2025, exploring the epidemiology, clinical presentation, imaging characteristics, and treatment implications of these overlapping conditions. We particularly examine how crystal deposition may mimic or complicate the clinical course of OA, RA, and PsA, especially in older adults with multimorbidity. Recognizing these overlaps is critical to avoid misdiagnosis, inappropriate escalation of immunomodulatory therapy, and missed opportunities for targeted crystal-directed treatment. Full article

Prior research suggests a connection between osteoarthritis and gout at sites commonly affected by gouty attacks. Whether this connection exists at sites with known monosodium urate crystal deposition but less commonly affected by gouty attacks, such as the lumbosacral spine, has not been previously investigated. We assessed whether lumbosacral osteoarthritis is more prevalent and more severe in subjects with gout compared with controls, and whether lumbosacral osteoarthritis is associated with higher levels of spinal monosodium urate deposition. Fifty gout subjects and 25 controls underwent dual-energy computed tomography imaging of the lumbosacral spine. We assessed lumbosacral osteoarthritis using a modification of a validated computed tomography scoring system, incorporating grade of intervertebral disc narrowing and facet joint osteoarthritis, and presence of spondylolysis and spondylolisthesis. We quantified spinal monosodium urate deposition using the default post-processing algorithm, plus a maximally specific algorithm to exclude potential artefacts. Forty-six gout subjects and 25 controls, average age 62 years, were included in the final analysis. Both gout and control subjects exhibited high rates of facet joint osteoarthritis and degenerative disc disease, with no difference in prevalence or severity between groups. Gout subjects did not have differing prevalence of spondylolysis and spondylolisthesis vs. controls. Subjects with lumbosacral osteoarthritis did not have higher levels of spinal monosodium urate deposition. Overall, lumbosacral osteoarthritis was not more prevalent or more severe in gout patients compared with controls, and spinal monosodium urate crystal deposition did not differ between patients with and without lumbosacral osteoarthritis. Full article

Hyperuricemia influences several aspects of the immune system. It enhances cytokine production by monocytes and activates neutrophils and natural killer cells. Within the adaptive immune system, hyperuricemia enhances antigen presentation, skews T helper cell differentiation toward the Th17 lineage and may also activate B cells. Beyond its established role in the pathogenesis of gout, hyperuricemia may therefore contribute to other rheumatic diseases. In this review, we summarize current evidence on the role of hyperuricemia in osteoarthritis, psoriatic arthritis, axial spondylarthritis, rheumatoid arthritis, systemic sclerosis, primary Sjögren’s disease and systemic lupus erythematosus. Available data do not support a causal role for hyperuricemia in the disease onset of osteoarthritis or rheumatoid arthritis. In contrast, hyperuricemia is associated with the development of psoriatic arthritis and may be linked to a more severe disease course. Small, predominantly cross-sectional studies further suggest a potentially adverse role of hyperuricemia in systemic sclerosis, Sjögren’s disease, and systemic lupus erythematosus. Across several rheumatic diseases, hyperuricemia is associated with cardiovascular disease, renal dysfunction and interstitial lung disease. However, both mechanistic and causal evidence remain limited, underscoring the need for more studies. Full article