Factors affecting bone development, growth, and repair.

A number of factors influence bone development, growth, and repair. These include nutrition, exposure to sunlight, hormonal secretions, and physical exercise. For example, vitamin D is necessary for proper absorption of calcium in the small intestine. In the absence of this vitamin, calcium is poorly absorbed, and the inorganic salt portion of bone matrix lacks calcium, softening and thereby deforming bones. In children, this condition is called rickets, and in adults, it is called osteomalacia.

Vitamin D is relatively uncommon in natural foods, except for eggs. But it is readily available in milk and other dairy products fortified with vitamin D. Vitamin D also forms from a substance (dehydrocholesterol) produced by cells in the digestive tract or obtained in the diet. Dehydrocholesterol is carried by the blood to the skin, and when exposed to ultraviolet light from the sun, it is converted to a compound that becomes vitamin D.

Vitamins A and C are also required for normal bone development and growth. Vitamin A is necessary for osteoblast and osteoclast activity during normal development. Thus, deficiency of vitamin A may retard bone development. Vitamin C is required for collagen synthesis, so its lack also may inhibit bone development. In this case, osteoblasts produce less collagen n the intercellular material of the bone tissue, and the resulting bones are abnormally slender and fragile.

Hormones secreted by the pituitary gland, thyroid gland, parathyroid glands, and ovaries or testes affect bone growth and development. The pituitary gland, for instance, secretes growth hormone, which stimulates division of cartilage cells in the epiphyseal disks. In the absence of this hormone, the long bones of the limbs fail to develop normally, and the child has pituitary dwarfism. Such a person is very short, but has normal body proportions. If excess growth hormone is released before the epiphyseal disks ossify, height may exceed 8 feet-a conduction called pituitary gigantism. In an adult, secretion of excess growth hormone causes a condition called acromegaly, in which the hands, feet, and jaw enlarge.

Thyroid hormone stimulates replacement of cartilage in the epiphyseal disks of long bones with bone tissue. Thyroid hormone can halt bone growth by causing premature ossification of the disks. Deficiency of thyroid hormone also may stunt growth, because without its stimulation, the pituitary gland does not secrete enough growth hormone. In contrast to the bone-forming activity of thyroid hormone, parathyroid hormone stimulates an increase in the number and activity of osteoclasts.

Both male and female sex hormones (called androgens and estrogens, respectively) from the testes, ovaries, and adrenal glands promote formation of bone tissue. Beginning at puberty, these hormones are abundant, causing the long bones to grow considerably. However, sex hormones also stimulate ossification of the epiphyseal disks, and consequently they stop bone lengthening at a relatively early age. The effect of estrogens on the disks is somewhat stronger than that of androgens. For this reason, females typically reach their maximum heights earlier than males.

Physical stress also stimulates bone growth. For example, when skeletal muscles contract, they pull at their attachments on bones, and the resulting stress stimulates the bone tissue to thicken and strengthen (hypertrophy). Conversely, with lack of exercise, the same bone tissue wastes, becoming thinner and weaker (atrophy). This is why the bones of athletes are usually stronger and heavier than those of nonathletes. It is also why fractured bones immobilized in casts may shorten.


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