par Brauman, Julie;Verbanck, Michel 
Référence Journal belge de radiologie, 56, 4, page (271-282)
Publication Publié, 1973
Référence Journal belge de radiologie, 56, 4, page (271-282)
Publication Publié, 1973
Article révisé par les pairs
| Résumé : | Ectopic calcifications are engendered by the same factors as bone mineralization, the study of which can serve as a means of approach to the understanding of the physiopathology of cerebral calcifications. The calcification processus consists of the deposit of a mineral phase in the form of hydroxyapatite crystal 3 Ca2 (PO4)3 Ca (OH)2 in a matrix formed of fibrous protein ground substance. The study of bone mineralization shows that the bone cells effect the synthesis of the matrix and play a part in the regulation of the mineral deposit. Collagen is a fibrous protein, the structure of which is characterized by the repetition of certain chemical sequences that are the captation centers for the mineral phase. The mechanism by which phosphate and calcium are precipitated and then crystallize at this site brings several factors into play. The fibrous protein acquires properties that promote mineral accretion at the site (lyotrope). The localized increase of P and Ca concentration has a bearing on the induction of precipitation on the matrix that has become calcifiable. The concentration of the mineral phase at the sites of calcification takes place through osteoblasts. This electrolytic movement is controlled by parathormone, vitamin D, phosphate ion and calcitonin. The role of mineralization inhibitors such as pyrophosphates, and of activators such as some enzymes, is discussed. Cerebral calcifications can be classified into two groups; dystrophic calcifications and those which have a symmetrical effect on the basal ganglions. The dystrophic calcifications are found in the affected tissues in patients with normal biology. Collagen changes probably play a part in the genesis of thse calcifications. Symmetrical calcifications of the basal ganglions are found more especially in conditions characterized by a rise in the blood phosphorus rate, as in hypoparathyroidism. The similarity between bone and ectopic calcification processes is recalled. The etiopathogenesis of the cerebral calcifications must be sought in the modification of one or another of the calcification mechanisms. |
