Covering, Support, and Movement of the Body
that something as simple as a hearty sneeze or stepping off a
curb can cause them to break. Te composition of the matrix
remains normal but bone mass declines, and the bones become
porous and light
(Figure 6.16)
Even though osteoporosis affects the entire skeleton, the
spongy bone of the spine is most vulnerable, and compression
fractures of the vertebrae are common. Te femur, particularly
its neck, is also very susceptible to fracture (a
broken hip
) in
people with osteoporosis.
Risk Factors for Osteoporosis
Osteoporosis occurs most oFen in the aged, particularly in
postmenopausal women. Although men develop it to a lesser
degree, 30% of American women between the ages of 60 and 70
have osteoporosis, and 70% have it by age 80. Moreover, 30% of
all Caucasian women (the most susceptible group) will experi-
ence a bone fracture due to osteoporosis.
Sex hormones—androgens in males and estrogens in
females—help maintain the health and normal density of the
skeleton by restraining osteoclasts and promoting deposit of
new bone. AFer menopause, however, estrogen secretion wanes,
compact bone is laid down to reconstruct the shaF walls.
Te final structure of the remodeled area resembles the
original unbroken bony region because it responds to the
same set of mechanical stressors.
Check Your Understanding
If osteoclasts in a long bone are more active than osteoblasts,
how will bone mass change?
Which stimulus—PTH (a hormone) or mechanical forces
acting on the skeleton—is more important in maintaining
homeostatic blood calcium levels?
How does an open fracture differ from a closed fracture?
How do bone growth and bone remodeling differ?
For answers, see Appendix H.
Homeostatic Imbalances
of Bone
Contrast the disorders of bone remodeling seen in
osteoporosis, osteomalacia, and Paget’s disease.
Imbalances between bone deposit and bone resorption underlie
nearly every disease that affects the human skeleton.
Osteomalacia and Rickets
she-ah; “soF bones”) includes a
number of disorders in which the bones are poorly mineralized.
Osteoid is produced, but calcium salts are not adequately de-
posited, so bones are soF and weak. Te main symptom is pain
when weight is put on the affected bones.
is the analogous disease in children. Because young
bones are still growing rapidly, rickets is much more severe than
adult osteomalacia. Bowed legs and deformities of the pelvis,
skull, and rib cage are common. Because the epiphyseal plates
cannot calcify, they continue to widen, and the ends of long
bones become visibly enlarged and abnormally long.
Osteomalacia and rickets are caused by insufficient calcium
in the diet or by a vitamin D deficiency. Drinking vitamin D–
fortified milk and exposing the skin to sunlight (which spurs
the body to form vitamin D) usually cure these disorders. Al-
though the seeming elimination of rickets in the United States
has been heralded as a public health success, rickets still rears
its head in isolated situations. ±or example, if a mother who
breast-feeds her infant becomes vitamin D deficient because of
sun-deprivation or dreary winter weather, the infant too will be
vitamin D deficient and will develop rickets.
±or most of us, the phrase “bone problems of the elderly” brings
to mind the stereotype of a victim of osteoporosis—a hunched-
over old woman shuffling behind her walker.
sis) refers to a group of diseases in which bone
resorption outpaces bone deposit. Te bones become so fragile
(b) Osteoporotic bone
(a) Normal bone
Figure 6.16
The contrasting architecture of normal versus
osteoporotic bone.
Scanning electron micrographs, 300
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