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Bone Storage and Release

Frank A. Smith, John B. Hursh

10.1002/cphy.cp090129

Source: Supplement 26: Handbook of Physiology, Reactions to Environmental Agents

Originally published: 1977

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Bone Structure
2 Skeletal Uptake of Foreign Ions: Their Migration and Release
3 Skeletal Metabolism of Selected Airborne Contaminants
3.1 Fluoride
3.2 Lead
4 Summary
Figure 1. Figure 1.

Sequence of cellular events in bone remodeling unit on endosteal bone surface. Initial step (left) is activation of mesenchymal cells (MC) to become osteoprogenitor cells (OP), which by further division become preosteoclasts (PC), which then fuse to become osteoclasts (OC). These eventually undergo modulation to become preosteoblasts (PB), which go on to become osteoblasts (OB), which after completing their synthetic function become osteocytes (O). Once the sequence of events has transpired, osteocytes in a bone metabolic unit function in maintaining mineral homeostasis. In carrying out this function, they recapitulate, in a sense, a similar cell cycle of resorption (osteoclastic osteocyte — OCO) and formation (osteoblastic osteocyte — OBO). In severe hyperparathyroidism the osteoclastic phase of the osteocytic cell cycle may be exaggerated to the point where several adjacent osteocytes (O) remove all the bone between them, and then fuse to become osteoclasts (OC).

From Rasmussen & Bordier 50
Figure 2. Figure 2.

Diagram of cross section of adult cortical bone to indicate arrangement of Haversian canals, resorption cavities, osteocytes with their canaliculi, and the different cells lining bone surfaces. Left, periosteal surface; right, endosteal surface.

From Vaughan 58, p. 3
Figure 3. Figure 3.

Cross‐sectional representation of hydroxyapatite crystal in aqueous suspension.

From Neuman & Neuman 45, p. 63
Figure 4. Figure 4.

Increase in fluoride content (mg F per 100 g dried fat‐free material) in human rib bone up to the 6th decade and its relation to the amount of fluoride in drinking water.

From Jackson & Weidmann 31
Figure 5. Figure 5.

Fluoride concentrations in human bone ash of lifetime residents of a low‐fluoride area.

From Hodge & Smith 23, p. 518
Figure 6. Figure 6.

Concentration of fluoride in postmortem samples of human bone taken from persons resident in the West Riding of Yorkshire (fluoride content of drinking water < 0.1 ppm). (a) Compact cortical bone from femoral diaphysis. (b) Compact cortical bone from rib. (c) Cancellous bone from rib.

From Weatherall 60
Figure 7. Figure 7.

Mobilization of skeletal fluoride in man.

From Hodge, Smith, and Gedalia 25
Figure 8. Figure 8.

Model for lead exchange by man with his environment. See subsection RELEASE OF LEAD FIXED IN BONE for source of assigned values.


Figure 1.

Sequence of cellular events in bone remodeling unit on endosteal bone surface. Initial step (left) is activation of mesenchymal cells (MC) to become osteoprogenitor cells (OP), which by further division become preosteoclasts (PC), which then fuse to become osteoclasts (OC). These eventually undergo modulation to become preosteoblasts (PB), which go on to become osteoblasts (OB), which after completing their synthetic function become osteocytes (O). Once the sequence of events has transpired, osteocytes in a bone metabolic unit function in maintaining mineral homeostasis. In carrying out this function, they recapitulate, in a sense, a similar cell cycle of resorption (osteoclastic osteocyte — OCO) and formation (osteoblastic osteocyte — OBO). In severe hyperparathyroidism the osteoclastic phase of the osteocytic cell cycle may be exaggerated to the point where several adjacent osteocytes (O) remove all the bone between them, and then fuse to become osteoclasts (OC).

From Rasmussen & Bordier 50


Figure 2.

Diagram of cross section of adult cortical bone to indicate arrangement of Haversian canals, resorption cavities, osteocytes with their canaliculi, and the different cells lining bone surfaces. Left, periosteal surface; right, endosteal surface.

From Vaughan 58, p. 3


Figure 3.

Cross‐sectional representation of hydroxyapatite crystal in aqueous suspension.

From Neuman & Neuman 45, p. 63


Figure 4.

Increase in fluoride content (mg F per 100 g dried fat‐free material) in human rib bone up to the 6th decade and its relation to the amount of fluoride in drinking water.

From Jackson & Weidmann 31


Figure 5.

Fluoride concentrations in human bone ash of lifetime residents of a low‐fluoride area.

From Hodge & Smith 23, p. 518


Figure 6.

Concentration of fluoride in postmortem samples of human bone taken from persons resident in the West Riding of Yorkshire (fluoride content of drinking water < 0.1 ppm). (a) Compact cortical bone from femoral diaphysis. (b) Compact cortical bone from rib. (c) Cancellous bone from rib.

From Weatherall 60


Figure 7.

Mobilization of skeletal fluoride in man.

From Hodge, Smith, and Gedalia 25


Figure 8.

Model for lead exchange by man with his environment. See subsection RELEASE OF LEAD FIXED IN BONE for source of assigned values.

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Article Title: Bone Storage and Release
 

How to Cite

Frank A. Smith, John B. Hursh. Bone Storage and Release. Compr Physiol 2011, Supplement 26: Handbook of Physiology, Reactions to Environmental Agents: 469-482. First published in print 1977. doi: 10.1002/cphy.cp090129