Calcium Deficient Bone Radiograph

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Third month of prenatal development

Ossification in long bones begins.

15 to 18 years (females) 17 to 20 years (males)

Bones of the upper limbs and scapulae completely ossify.

Fourth month of prenatal development

Most primary ossification centers have appeared in the diaphyses of bones.

16 to 21 years (females) 18 to 23 years (males)

Bones of the lower limbs and coxal bones completely ossify.

Birth to 5 years

Secondary ossification centers appear in the epiphyses.

21 to 23 years (females) 23 to 25 years (males)

Bones of the sternum, clavicles, and vertebrae completely ossify.

5 to 12 years in females, or 5 to 14 years in males

Ossification rapidly spreads from the ossification centers, and certain bones are ossifying.

By 23 years (females) By 25 years (males)

Nearly all bones completely ossify.

Space Outside Blood Vessels


Micrograph of a bone-resorbing osteoclast (800x).


Micrograph of a bone-resorbing osteoclast (800x).

epiphyses meet and the epiphyseal plates ossify, lengthening is no longer possible in that end of the bone.

A developing bone thickens as compact bone is deposited on the outside, just beneath the periosteum. As this compact bone forms on the surface, osteoclasts erode other bone tissue on the inside (fig. 7.10). The resulting space becomes the medullary cavity of the diaphysis, which later fills with marrow.

The bone in the central regions of the epiphyses and diaphysis remains spongy, and hyaline cartilage on the ends of the epiphyses persists throughout life as articular cartilage. Table 7.2 lists the ages at which various bones ossify.

Homeostasis of Bone Tissue

After the intramembranous and endochondral bones form, the actions of osteoclasts and osteoblasts continually remodel them. Thus, throughout life, osteoclasts resorb bone tissue, and osteoblasts replace the bone. These opposing processes of resorption and deposition are well regulated so that the total mass of bone tissue within an adult skeleton normally remains nearly constant, even though 3% to 5% of bone calcium is exchanged each year.

Failure Bone Exchange Calcium For


Radiograph showing the presence of epiphyseal plates (arrows) in a child's bones indicates that the bones are still lengthening.


Radiograph showing the presence of epiphyseal plates (arrows) in a child's bones indicates that the bones are still lengthening.

A child's long bones are still growing if a radiograph shows epiphyseal plates (fig. 7.11). If a plate is damaged as a result of a fracture before it ossifies, elongation of that long bone may prematurely cease, or if growth continues, it may be uneven. For this reason, injuries to the epiphyses of a young person's bones are of special concern. On the other hand, an epiphysis is sometimes altered surgically in order to equalize growth of bones that are developing at very different rates.

In bone cancers, abnormally active osteoclasts destroy bone tissue. Interestingly, cancer of the prostate gland can have the opposite effect. If such cancer cells reach the bone marrow, as they do in most cases of advanced prostatic cancer, they stimulate osteoblast activity. This promotes formation of new bone on the surfaces of the bony trabeculae.

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 os-teoblast 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 in 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 condition called pituitary gigantism. In an adult, secretion of excess growth hormone causes a condition called acromegaly, in which the hands, feet, and jaw enlarge (see chapter 13, page 517).

Pituitary dwarfism is treated with human growth hormone (HGH). Today, HGH is plentiful and pure, thanks to recombinant DNA technology. Bacteria given the human gene for HGH secrete the hormone. Previously, HGH was pooled from donors or cadavers. This introduced the risk of transmitting infection. A controversial use of HGH is to give it to children who are of short stature, but not abnormally so, or to use it to enhance height with the goal of improving athletic ability.

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 andro-gens 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 (fig. 7.12). It is also why fractured bones immobilized in casts may shorten. Clinical Application 7.1 describes what happens when a bone breaks.

O Describe the development of an intramembranous bone.

Explain how an endochondral bone develops.

Sites of muscle attachments


Note the increased amount of bone at the sites of muscle attachments in the femur on the left. The thickened bone is better able to withstand the force resulting from muscle contraction.

Sites of muscle attachments

Thickened Bone

Note the increased amount of bone at the sites of muscle attachments in the femur on the left. The thickened bone is better able to withstand the force resulting from muscle contraction.

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  • Anthony
    What conditions causes bones to ostefy?
    7 years ago

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