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Functional Considerations: Hormonal Regulation of Bone Growth

Hormones other than PTH and calcitonin have major effects on bone growth. One such hormone is pituitary growth hormone (GH, somatotropin). This hormone stimulates growth in general and, especially, growth of epiphyseal cartilage and bone. Oversecretion in childhood leads to gigantism, an abnormal increase in the length of bones; absence or hypose-cretion of somatotropin in childhood leads to failure of growth of the long bones, resulting in pituitary dwarfism. Absence or severe hyposecretion of thyroid hormone during development and infancy leads to failure of bone growth and dwarfism, a condition known as congenital hypothyroidism. Oversecretion of somatotropin in an adult leads to acromegaly, an abnormal thickening and selective overgrowth of hands, feet, mandible, nose, and intramembranous bones of the skull.

• 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 above (see page 190), 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.

v fractures and bone repair

The initial response to a fracture is similar to the response to any injury that produces tissue destruction and hemorrhage. Neutrophils are the first cells to arrive on the scene, followed by macrophages that begin to clean up the site of injury. Fibroblasts and capillaries then proliferate and grow into the site of injury. New loose connective tissue, granulation tissue, is formed, and as this tissue becomes denser, cartilage forms in parts of it. Both fibroblasts and periosteal cells participate in this phase of the healing process. The dense connective tissue and newly formed cartilage grow, covering the bone at the fracture site, producing a callus (Fig. 8.20). A callus will form whether or not the fractured parts of the bone are in immediate apposition to each other. The callus helps stabilize and bind together the fractured bone.

While the callus is forming, osteoprogenitor cells of the periosteum divide and differentiate into osteoblasts. The newly formed osteoblasts begin to deposit new bone on the outer surface of the bone at some distance from the fracture. This new formation of bone progresses toward the fracture site until new bone forms a bony sheath over the fibrocartilaginous callus. Osteogenic buds from the new bone invade the callus and begin to deposit new bone within the callus, gradually replacing the original fibrous and cartilaginous callus with a bony callus. The cartilage in the original callus calcifies and is replaced by bone as in endochondral ossification.

Endosteal proliferation and differentiation also occur in the marrow cavity, and medullary bone grows from both ends of the fracture toward the center. When this bone unites, the bony union of the fractured bone produced by the osteoblasts derived from both the periosteum and endosteum consists of spongy bone. As in normal bone formation, the spongy bone is gradually replaced by compact bone. While compact bone is being formed, the bony callus is removed by the action of os-

202 CHAPTER 8 I Bone teoclasts, and gradual remodeling restores the bone to its original shape.

In healthy individuals, this process usually takes from 6 to 12 weeks, depending on the severity of the break and the particular bone that is broken. Setting the bone, i.e.,

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