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  NUCLEAR MEDICINE APPLICATIONS FOR BONE METASTASES 

The Quarterly Journal of Nuclear Medicine 2001 March;45(1):2-6

Copyright © 2009 EDIZIONI MINERVA MEDICA

lingua: Inglese

Physiopathological basis of bone turnover

Masi L., Brandi M. L.

From the *Department of Clinical Physiopathology, Endocrine Unit, Department of Internal Medicine, University of Florence, Florence, Italy


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Bone remod­eling ­involves the con­tin­uous ­removal of ­bone (­bone resorp­tion) fol­lowed by syn­thesis of new ­bone ­matrix and sub­se­quent min­er­al­iza­tion (­bone for­ma­tion). The prin­cipal ­cells ­that ­mediate the ­bone-­forming pro­cesses of the ­skeleton are oste­o­blast ­cells. ­They are respon­sible for the pro­duc­tion of the ­matrix con­stit­u­ents and the dif­fe­ren­ti­a­tion of oste­o­blasts ­from ­stromal ­cell pre­cur­sors is stim­u­lated by sev­eral hor­monal and non-hor­monal mole­cules. On the ­other ­hand, the oste­o­clasts are ­giant mul­ti­nu­cle­ated ­cells respon­sible of ­bone resorp­tion. ­They are ­formed in the ­bone ­marrow and ­mature ­cells are stim­u­lated by PTH and ­locally ­acting ­agents ­such as trans­forming ­growth ­factor α (­TGFα), ­tumor ­necrosis ­factor (TNF) inter­leukin 1 (IL-1) and inter­leukin 6 (IL-6). The ­first ­events ­during ­bone remod­eling is oste­o­clast acti­va­tion, fol­lowed by oste­o­clast for­ma­tion, pola­riza­tion con­sti­tu­tion of the ruf­fled ­border, resorp­tion and ulti­mately apop­tosis. Oste­o­clast apop­tosis is fol­lowed by a ­series of sequen­tial ­changes in ­cells in the oste­o­blast lin­eage, ­including oste­o­blast chem­o­taxis, pro­life­ra­tion and dif­fe­ren­ti­a­tion, ­which in ­turn is fol­lowed by for­ma­tion of min­er­al­ized ­bone and ces­sa­tion of oste­o­blast ­activity. The ­final ­phase of the for­ma­tion pro­cess is ces­sa­tion of oste­o­blast ­activity. The resorp­tion ­lacunae are usu­ally ­repaired ­either com­pletely or ­almost com­pletely. Under­standing the ­sequence of cel­lular ­events may be impor­tant to ­better ­know the mech­a­nisms respon­sible for ­bone ­loss ­that ­occurs in age and in sev­eral path­o­log­ical con­di­tions.

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