INTERNAL REMODELING OF COMPACT BONE 379 



of these cells upon both the mineral and the matrix of bone; it 

 occurs mainly on the surfaces of bone and in the formation of re- 

 sorption cavities; there is also some indication that osteocvtes mav 

 contribute to the mobilization cf bone mineral. The diffuse com- 

 ponent, visualized bv administration of tracer elements, is regarded 

 by Marshall et al. (1959) as representing the portion of the mineral 

 undergoing long-term exchange. 



It has been stated above that there is a rapid turnover of the 

 calcium in the lilood; this i> so rapid that in adult man one out of 

 four calcium ions leaves the blood everv minute ( Bauer et al., 1961 ) . 

 The calcium can go cnly into the skeleton, and is replaced by other 

 ions from the bones. For the minute-to-minute equilibrium betv^een 

 blood and bone, it is believed that this transfer occurs bv ion ex- 

 change; neither osteoclastic resorption nor long-term exchange is 

 sufficiently rapid to account for it. The source of the calcium trans- 

 ferred from bone to blood, by ion exchange, has not been definitelv 

 localized, although the opinion is held that it comes from the re- 

 centlv deposited mineral in the osteons undergoing mineralization. 

 These osteons constitute the reactive or metabolic bone; in contrast, 

 the fullv mineralized bone, in which deposition of new mineral oc- 

 curs only as the diffuse component, is designated as structural bone 

 (Vincent and Haumont, 1960). There is a pronounced difference 

 between the amounts of stable and of labile, reactive, or exchange- 

 able bone mineral; less than 1 per cent of the mineral is described 

 as exchangeable (Neuman and Neuman, 1958). 



McLean and Urist ( 1961 ) have proposed a dual mechanism to 

 account for homeostatic control of the calcium ion concentration in 

 the body fluids, including the blood plasma. The function of the 

 parathyroid glands is to monitor this concentration. This function 

 is illustrated, in cybernetic terms, in Fig. 4. The parathyroid glands 

 respond to changes in the Ca++ concentration in the plasma by 

 altering the output of parathyroid hormone; the net result is that 

 this concentration is held, in normal man, at approximately 10 mg 

 per 100 cc. It seems certain that the effect of the parathyroid hor- 

 mone on release of calcium from the bones is mediated through the 

 cells of bone, although the mechanisms by which this is accomplished 

 are not fully understood. The three cell tvpes — osteoblasts, osteo- 



