Crystals are an important cause of inflammatory rheumatic diseases and provide relatively simple paradigms for modelling inflammatory responses in general. Thus, in the case of gout, we know that hyperuricemia leads to precipitation of monosodium urate (MSU) crystals in joints, which are taken up by leukocytes, and then an acute attack of arthritis is triggered. However, fundamental questions remain unanswered. Why are only certain hyperuricemic individuals, and then only certain joints, affected? What factors maintain joints in a quiescent state, what prompts the resolution of an inflammatory attack, and are these related? This article draws on developments during the past year to support the idea that the mononuclear phagocyte may play a key role within the synovial compartment, tipping the balance from the asymptomatic state to acute inflammation, or vice versa, depending on their state of monocyte to macrophage differentiation.