The classical concept of PTH action related to the regulation of serum calcium levels and bone resorption is more complex. For some time now, it has been known that PTH can also stimulate bone formation. In other words, it has an anabolic action (increases bone formation) in contrast to its catabolic action to cause bone resorption. In fact, clinical trials in which PTH hormone was administered to post-menopausal women with osteoporosis have shown significant increases in bone formation and bone mineral density. Increases in the amount of cancellous (trabecular) bone due to PTH treatment were shown in the ilium, vertebral bodies, and the shafts of radial and femoral bones (see Folder 8.2). The possible mechanisms behind this counterintuitive anabolic action of PTH are largely unknown. It is speculated that activation of different PTH-regulated genes might be responsible for each of the hormone’s contrasting effects.
Bone can repair itself after injury.
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 and producing a soft callus (Fig. 8.23). 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.
 FOLDER 8.4 Functional Considerations: Hormonal Regulation of Bone Growth
Hormones other than PTH and calcitonin have major ef-fects 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. It acts directly on osteopro-genitor cells, stimulating them to divide and differentiate. Chondrocytes in epiphyseal growth plates are regulated by insulinlike growth factor I (IGF-I), which is primarily pro-duced by the liver in response to GH. In addition to IGF-I, insulin and thyroid hormones also stimulate chondrocyte activity. Oversecretion in childhood, caused by a defect in the mechanism regulating GH secretion or a GH-secreting tumor in the pituitary gland, leads to gigantism, an abnormal increase in the length of bones. Absence or hy-posecretion of GH in childhood leads to failure of growth of the long bones, resulting in pituitary dwarfism. Absence or severe hyposecretion of thyroid hormone dur-ing development and infancy leads to failure of bone growth and dwarfism, a condition known as congenital hypothyroidism. When oversecretion of GH occurs in an adult, bones do not grow in length as a result of epiphy-seal closure. Instead, abnormal thickening and selective overgrowth of hands, feet, mandible, nose, and intramem-branous bones of the skull occurs. This condition, known as acromegaly, is caused by increased activity of osteoblasts on bone surfaces.