Figure 817

Diagram of external remodeling of a long bone. This diagram shows two periods during the growth of the bone. The younger bone profile (before remodeling) is shown on the right; the older (after remodeling), on the left. Superimposed on the left side of the figure is the shape of the bone (left half only) as it appeared at an earlier time.

The bone is now longer, but it has retained its general shape. To grow in length and retain the general shape of the particular bone, bone resorption occurs on some surfaces, and bone deposition occurs on other surfaces, as indicated in the diagram. (Based on Ham AW. J Bone Joint Surg Am 1952;34:701.)

Development of the Osteonal (Haversian) System

Osteons typically develop in preexisting compact bone

Compact bone can take several different forms. Compact bone may be formed from fetal spongy bone by continued deposition of bone on the spongy bone spicules; it may be deposited directly as adult compact bone (e.g., the circumferential lamellae of an adult bone); or it might be older compact bone consisting of osteons and interstitial lamellae. The process in which new osteons are formed is referred to as internal remodeling.

In the development of new osteons, a tunnel is bored through compact bone by osteoclasts

Formation of a new osteon in compact bone involves initially the creation of a tunnel-like space, the resorption cavity, by osteoclast activity. This resorption cavity will have the dimensions of the new osteon. When osteoclasts have produced an appropriately sized cylindrical tunnel by resorption of compact bone, blood vessels and their surrounding connective tissue occupy the tunnel. As the tunnel is occupied, new bone deposition on its wall begins almost immediately. These two aspects of cellular activity, namely, osteoclast resorption and osteoblast synthesis, constitute a bone-remodeling unit. A bone-remodeling unit consists of two distinct parts: an advancing cutting cone (also called a resorption canal) and a closing cone (Fig. 8.18). The cutting cone consists of active osteoclasts followed by an advancing capillary loop and pericytes. It also contains numerous dividing cells that give rise to osteoblasts, additional pericytes, and endothelial cells. (Recall that osteoclasts are derived from blood-borne monocytes.) The osteoclasts cut a canal about 200 /xm in diameter. This canal establishes the diameter of the future

Both nutritional and hormonal factors affect the degree of bone mineralization. Calcium deficiency during growth causes rickets, a condition in which the bone matrix does not calcify normally. Rickets may be due to insufficient amounts of dietary calcium or to insufficient vitamin D (a steroid prohormone), which is needed for absorption of calcium by the intestines. In the adult, the same nutritional or vitamin deficiency leads to osteomalacia.

Although rickets and osteomalacia are no longer major problems where nutrition is adequate, another form of insufficient bone mineralization is regularly seen In the condition known as osteoporosis. In this condition, bone tissue (both mineral and matrix) is diminished, presumably because resorption by osteoclasts exceeds deposition by osteoblasts. Osteoporosis develops as a conse quence of immobilization (as in a bedridden patient) and in postmenopausal women. The factors that cause the imbalance in cellular activity are not known, although some relief appears to result from maintaining hormonal (estrogen) levels and dietary fluoride levels.

In addition to its influence on intestinal absorption of calcium, vitamin D is also needed for normal calcification. Other vitamins known to affect bone are A and C. Vitamin A deficiency suppresses endochondral growth of bone; vitamin A excess leads to fragility and subsequent fractures of long bones. Vitamin C is essential for synthesis of collagen, and its deficiency leads to scurvy. The matrix produced in scurvy is not calcifiable.

cutting cone closing cone growth reversal lines

osteoblasts osteoid

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