[Crystal arthropathies].

Area of Science:

• Rheumatology
• Immunology
• Crystal Arthropathies

Background:

• Crystal-induced arthropathies, primarily gout (monosodium urate, MSU) and calcium pyrophosphate deposition disease (CPPD), are frequent causes of acute joint inflammation.
• Microscopic identification of crystals in synovial fluid remains the gold standard for diagnosis, though imaging techniques like ultrasound and dual-energy-computed tomography (DECT) can aid in visualizing MSU crystal-induced changes.
• These crystals act as danger signals, activating the innate immune system and leading to inflammatory flares, positioning crystal arthropathies as autoinflammatory conditions.

Purpose of the Study:

• To summarize current knowledge on crystal arthropathies, focusing on recent advancements in gout and CPPD.
• To highlight diagnostic approaches and therapeutic strategies for crystal-induced joint inflammation.
• To underscore the autoinflammatory nature of crystal arthropathies.

Main Methods:

• Review of current literature and guidelines on crystal arthropathies.
• Discussion of diagnostic methods including synovial fluid analysis, ultrasound, and DECT.
• Analysis of inflammatory pathways involving neutrophils, monocytes, macrophages, and Interleukin-1β.

Main Results:

• MSU and CPP crystals are key triggers of acute inflammatory arthritis.
• Diagnosis relies on crystal identification, with imaging as an alternative when arthrocentesis is not feasible.
• Neutrophils, monocytes, macrophages, and IL-1β play crucial roles in the inflammatory response.

Conclusions:

• Crystal arthropathies are autoinflammatory conditions driven by MSU and CPP crystals.
• Colchicine and IL-1β inhibition are effective anti-inflammatory treatments.
• While urate-lowering therapy offers causal treatment for gout, no such therapy currently exists for CPPD.