[Bone involvement in idiopathic XXXX lithiasis].

@entity1 @entity650 @entity310 @entity3873 @entity604 @entity1421 @entity3528 @entity12233 @entity5886 @entity79 @entity1790 @entity1192 @entity460 @entity2527 @entity5200 @entity2841 @entity461
Bone involvement in idiopathic @entity460 @entity1790 is characterized by the following abnormalities: a) the bone density is decreased, the severity of @entity604 being dependent upon the existence of @entity5200 and upon the pathophysiology of this latter: it is inconsistent in the absence of @entity5200 or when @entity5200 is of the absorptive type I or II, whereas it is almost constant in fasting @entity5200 without @entity3528 and constant and severe in the rare true renal @entity5200 . b) The bone histology (which has been evaluated only in idiopathic @entity12233 @entity1 ) mainly shows a defect in bone formation at the exception of the rare renal @entity5200 . @entity2527 is only seen in this latter type of @entity5200 whereas in the other types of @entity5200 only an increase of the total or inactive resorption surface is observed. This phenomenon is possibly explained only by a delayed refilling of the resorption lacunae secondary to the decreased bone formation. The osteoid thickness is either normal or decreased despite decrease in mineralization apposition rate which seems therefore to be secondary to the decreased bone formation. c) Symptomatic @entity79 in @entity12233 stone formers is exceptional and always related to a severe long term @entity460 restriction. d) The biochemical markers of bone resorption tend to be increased in idiopathic @entity5200 . Hydroxyprolinuria is more often elevated than pyridinolinuria. However pyridinolinuria is negatively correlated to bone density. The contrast between the increase of these bone resorption markers and the usual normality of plasma @entity461 and of the osteoclastic resorptive surfaces, suggest the role of meat induced acid load which may favor inactive resorption by dissolution of bone buffers. A disturbed profile synthesis of cytokines which induce differentiation and proliferation of the osteoclasts and which modulate the osteoblastic proliferation and function ( @entity1192 , @entity650 , @entity310 , @entity2841 ...) may play a role in the @entity604 of @entity460 stone formers but further studies are necessary to precise its transient or permanent involvement in their @entity79 . e) The decrease of bone formation may be explained by the suppressed @entity461 secretion which may be explained by hypercalcitriolemia. This excess of @entity3873 synthesis may be secondary either to monocyte increased synthesis of @entity1192 which stimulates the renal 1 alpha-hydroxylase by the mean of an increased @entity1421 synthesis or to the relative @entity5886 of the @entity460 stone formers comparatively to healthy controls. Hypercalcitriolemia may originate from the activated monocyte itself. The decrease in bone formation may also be secondary to the action of monokines on the osteoblast differentiation and/or function.
