201
CHAPTER SEVEN
Skeletal System
Both male and female sex hormones (called testoster-
one and estrogens, respectively) from the testes and ovaries
promote formation of bone tissue. Beginning at puberty,
these hormones are abundant, causing the long bones to
grow considerably (see chapter 22, pp. 846, 857). However,
sex hormones also stimulate ossiF
cation of the epiphyseal
plates, and consequently they stop bone lengthening at a
relatively early age. The effect of estrogens on the epiphy-
seal plates is somewhat stronger than that of testosterone.
±or this reason, females typically reach their maximum
heights earlier than males.
Physical stress also stimulates bone growth. ±or exam-
ple, when skeletal muscles contract, they pull at their attach-
ments 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 ath-
letes are usually stronger and heavier than those of nonath-
letes
(f
g. 7.12)
. It is also why fractured bones immobilized
in casts may shorten. Clinical Application 7.1 describes what
happens when a bone breaks.
Astronauts experience a 1% loss of bone mass per month in space.
Under microgravity conditions, osteoblast activity decreases and
osteoclast activity increases, with greater loss in spongy compared to
compact bone. Researchers predict that a 50% bone loss could occur
on a several-year-long space F
ight, such as a mission to Mars.
PRACTICE
9
Explain how nutritional factors a±
ect bone development.
10
What e±
ects do hormones have on bone growth?
11
How does physical exercise a±
ect bone structure?
About 90 % of the protein that is part of bone is collagen. Less abun-
dant bone proteins are important too.
Osteocalcin is activated by vitamin K to bind calcium, which in
bone is part of the compound hydroxyapatite the main compo-
nent of bone matrix.
Osteonectin binds hydroxyapatite and collagen and stimulates
mineral crystal deposition in bone.
Osteopontin speeds bone remodeling.
Bone morphogenetic proteins include growth factors that
induce bone and cartilage formation. They are used in spinal
fusion procedures.
Hormones secreted by the pituitary gland, thyroid gland,
parathyroid glands, and ovaries or testes affect bone growth
and development. The pituitary gland secretes
growth hor-
mone,
which stimulates division of cartilage cells in the
epiphyseal plates. In the absence of this hormone, the long
bones of the limbs fail to develop normally, and the child
has
pituitary dwarf
sm.
He or she is very short but has nor-
mal body proportions. If excess growth hormone is released
before the epiphyseal plates ossify, height may exceed 8 feet—
a condition called
pituitary gigantism.
In an adult, secretion
of excess growth hormone causes
acromegaly,
in which the
hands, feet, and jaw enlarge (see chapter 13, pp. 494–495).
The thyroid hormone thyroxine stimulates replacement
of cartilage in the epiphyseal plates of long bones with
bone tissue. This hormone increases cellular metabolism,
including stimulating osteoblast activity. In contrast to the
bone-forming activity of thyroid hormone, parathyroid
hormone stimulates an increase in the number and activ-
ity of osteoclasts, which break down bone (see chapter 13,
pp. 501–503).
FIGURE 7.11
Radiograph showing epiphyseal plates (arrows) in a
child’s bones indicates that the bones are still lengthening.
Sites of
muscle
attachments
FIGURE 7.12
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 forces resulting from muscle contraction.
previous page 231 David Shier Hole's Human Anatomy and Physiology 2010 read online next page 233 David Shier Hole's Human Anatomy and Physiology 2010 read online Home Toggle text on/off