The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of
monosodium urate, characteristic of
gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood
uric acid level. The appearance of crystals also is dependent on time since crystallisation of
monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of
gout without
hyperuricemia or the rapid crystallisation which seems to characterise some types of
drug-induced
gout. Crystal deposits of
calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by
trauma, which could deplete cartilage of crystallisation inhibitors, notably
proteoglycans. High
pyrophosphate levels within cartilage also play an important role. The appearance of these
pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme,
nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some
chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of
calcium pyrophosphate dihydrate by raising the
calcium-pyrophosphate product, or by decreasing the activity of
alkaline phosphatase, an
enzyme responsible for breakdown of extracellular
pyrophosphates. The pathophysiology of
calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within
collagen fibres. Increase in the
calcium-phosphate product can also be a cause, for example, during
renal osteodystrophy or
vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)