FIGURE 8.22 • Microradiograph of the cross section of a bone. This 200-m-thick cross section of bone from a healthy 19-year-old male shows various degrees of mineralization in different osteons. Mature compact bone is actively replacing immature bone, which is seen on the periosteal (upper) surface. The degree of mineralization is reflected by the shade of light and dark in the microradiograph. Thus, very light areas represent the highly mineralized tissue that deflects the X-rays and prevents them from striking the photographic film. Conversely, dark areas contain less mineral and, thus, are less effective in deflecting the X-rays. Note that the interstitial lamellae (the older bone) are very light, whereas some of the osteons are very dark (these are the most newly formed). The Haversian canals appear black, as they represent only soft tissue. 157. (Courtesy of Dr. Jenifer Jowsey.)  At this stage of high extracellular Ca2 and PO4 concentration, the osteoblasts release small (50to 200-nm) matrix vesicles into the bony matrix by exocytosis. The matrix vesicles contain ALP and pyrophosphatase that cleave PO 4 ions from other molecules of the matrix.
 The matrix vesicles that accumulate Ca2 and cleave PO4 ions cause the local isoelectric point to increase, which results in crystallization of CaPO4 in the surrounding matrix vesicles.
 The CaPO4 crystals initiate matrix mineralization by the formation and deposition of hydroxyapatite crystals [Ca10(PO4)6(OH)2] in the matrix surrounding the osteoblasts.
The osteoblast-derived matrix vesicles are the essential factors in controlling the initial site of mineral deposition in osteoid. Once the initial crystals of hydroxyapatite have precipitated, they grow rapidly by accretion until they join neighboring crystals produced around other matrix vesicles. In this way, a wave of mineralization sweeps through the osteoid. Other cells that produce osteoid are the ameloblasts and odontoblasts of developing teeth.
Bone serves as a reservoir for body calcium.
The maintenance of normal blood calcium levels is critical to health and life. Calcium may be delivered from the bone matrix to the blood if the circulating blood levels of calcium fall below a critical point (physiologic calcium concentration in the human ranges from 8.9 to 10.1 mg/dL). Conversely, excess blood calcium may be removed from the blood and stored in bone.
These processes are regulated by parathyroid hormone (PTH), secreted by the parathyroid gland, and calcitonin, secreted by the parafollicular cells of the thyroid gland (see Folder 8.4).
 PTH acts on the bone to raise low blood calcium levels to normal.  Calcitonin acts to lower elevated blood calcium levels to normal.
PTH acts by stimulating both osteocytes and osteoclasts to resorb bone, allowing the release of calcium into the blood. As described previously (see page 227), resorption of bone by osteocytes constitutes osteocytic osteolysis. PTH also reduces excretion of calcium by the kidney and stimulates absorption of calcium by the small intestine. PTH further acts to maintain homeostasis by stimulating the kidney to excrete the excess phosphate produced by bone resorption. Calcitonin inhibits bone resorption, specifically inhibiting the effects of PTH on osteoclasts.