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Chapter 9
The skeletal system has two main components.
The first consists of the bones, which are the organs of the
system and number approximately 206 in the adult body (Fig.
9.1). Some individuals have a few additional small bones, sometimes in the
skull, which provide additional strength. The second component consists of the joints,
which attach bones to each other and contribute to the proper functioning of
the system (Fig.
9.1).
MAIN FUNCTIONS FOR HOMEOSTASIS
The bones and joints work together to maintain homeostasis
(i.e., continuing good health)
in two main ways. One is by minimizing changes in the body's internal
conditions; this is accomplished by providing support and protection from
traumatic injury. The second way is by helping to restore errant conditions to
proper levels. The skeletal system contributes to this goal by helping the
muscles move, storing minerals and fat, and producing blood cells.
The support provided by the skeletal system is important for
the same reasons mentioned in Chap. 8 about the muscle system. Recall that some
structures of the body are not strong enough to hold themselves up but must be
held in position to work properly. For example, the spinal cord, which extends
down the back from the base of the head to slightly above the waist, is quite
soft and very flexible (Fig.
9.2); it cannot stand on end by itself.
If the spinal cord is bent sharply or excessively, the
resulting injury can inhibit its impulse conduction and result in permanent
paralysis. To prevent such disastrous alterations in the position of the cord,
it is encased within the vertebral column. The vertebral column is composed of a row of ring-shaped
bones that are firmly attached to each other by joints that allow only slight
movement. Therefore, the skeletal system holds the spinal cord in proper
position while allowing it to bend an acceptable amount and in a smooth curve.
Similarly, without support from the skeletal components in
the thoracic region, the lungs would collapse like leaky balloons and a person
would be incapable of breathing. However, the joints among the thoracic bones
permit limited flexibility of the thorax, allowing for breathing (Fig.
9.1).
The weak, delicate nature of many
parts of the body requires that they be protected from injury. Recall that fat
in the subcutaneous layer of the integument contributes to such protection. The
skeletal system also provides protection from trauma.
The soft and delicate nature of the spinal cord requires not
only that it be given support but also that it be protected from pressure and
sharp objects. Even a slight squeezing of the cord could crush its nerve cells:
Nerve impulses would be blocked, and the victim would be paralyzed. However,
the spinal cord is rarely damaged because it is shielded by the vertebrae that
encircle it (Fig.
9.2).
Consider also the brain, lungs, heart, and bone marrow. Each
is essential for life, is easily damaged, and, like the spinal cord, is encased
within bones. Through this arrangement, these organs are kept safe from
crushing, tearing, cutting, and other forces that may be encountered.
Movement is a second homeostatic function shared by the
muscle and skeletal systems. Recall that movement is one key means by which the
body makes adjustments when it detects that a change in conditions is about to
take place or has already taken place. By moving, the body can attain what is
desirable and avoid what is detrimental. Since muscle cells are the only cells
that can furnish motion, one might ask what role the skeletal system plays in
movement. The answer to this question has two parts.
The first part is that the skeletal system provides stable
anchoring points for muscles (Fig.
9.3). These points are needed to make the force generated by muscle
contraction effective. If muscles were not firmly attached to other structures,
they would slide about inside the body when they contracted, and no helpful
actions would be performed.
The second part of the answer is that the skeletal system
acts as a set of levers to modify the motion provided by the muscles (Fig.
9.3). This converts the simple shortening of muscles into the multitude of
varied movements that people perform to maintain themselves. Therefore, people
can perform bending, twisting, turning, and lengthening actions as well as
shortening ones. All these actions can be observed when one watches people
perform ordinary tasks such as household chores. A skeletal lever is also able
to increase or decrease the distance, speed, and force obtained from the
contraction of a muscle so that they better suit the task to be performed. For
example, the muscles of the leg can move only a few inches. However, since
these muscles are attached to the long bones of the leg, a person can quickly
jump far out of the way of an oncoming vehicle.
Besides helping to maintain homeostasis in mechanical ways,
the skeletal system helps in maintaining homeostasis of certain chemicals
through mineral storage.
Minerals are needed so that the body cells can perform
properly. For example, calcium is necessary for muscle contraction and nerve
impulses and is also important in regulating the speed of many cell activities.
Phosphorus is used in the processes that supply energy in all cells, and it is
a main ingredient of cell membranes. Each cell must be supplied with the
correct level of each mineral at all times. An overabundance can injure or
poison cells, and a deficiency can make a cell function abnormally or prevent
it from functioning.
The skeletal system helps maintain homeostasis of minerals
through two activities. First, extra minerals are taken out of the blood by the
bones when their concentration begins to rise above the proper point. This
situation often occurs after one has eaten calcium-rich foods such as dairy
products. Later, the level of minerals in the blood begins to drop below the
proper concentration because they are being used by cells and are being lost in
urine and perspiration. Then the bones put back into the blood just enough of
the minerals they had stored so that the body cells always have enough. The
skeletal system can also store toxic minerals such as lead.
The skeletal system helps prevent changes in the amount of cellular components of the blood (red blood cells,
certain types of white blood cells, platelets) by producing them whenever their
numbers drop too low. Blood cell production is the one function of the skeletal
system that is not performed by the bone material; rather, it is accomplished
by specialized bone marrow tissue within the bones (Fig.
9.4).
Red blood cell production is increased when oxygen in the
blood begins to drop. With more red cells, the oxygen is restored to normal
levels. As long as oxygen levels remain high, red cell production is slow.
Thus, the skeletal system helps keep red blood cell numbers and oxygen levels
proper and fairly stable.
White blood cells play a variety of roles, including
defending against infection and controlling the inflammatory response.
Platelets prevent the loss of blood by helping it clot. The mechanisms
controlling the bone marrow so that levels of white blood cells and platelets
remain within a normal range are not clearly understood.
The production of blood cells occurs only in red bone
marrow. In adults, this marrow is found within the bones of the head, the
trunk, the arm bones at the shoulder, and the leg bones at the hip. The rest of
the marrow is yellow bone marrow, which stores fat molecules. Yellow marrow is
converted to active red marrow when the body needs an extra supply of blood
cells and is converted back to yellow marrow once the need has been met.
Though the bones are of many sizes and shapes, they are all
built of the same types of materials. Each component is in the same position
relative to the others, and each contributes to one or more of the five
functions of the skeletal system.
The bony material (bone matrix) in bones
contains three types of cells. Osteoblasts are cells that produce
bone matrix by first secreting fibers made of collagen and then coating the
fibers with mineral materials. In this way, the osteoblasts build bone, repair
damaged or broken bone, and place extra amounts of certain minerals found in
the blood into bones for storage (Fig.
9.5). Osteoblasts also activate osteoclasts (see below) by secreting
signaling materials (e.g., IL-6) (see Chapter 15).
As the osteoblasts work, many of them become surrounded and
entrapped by the mineralized material they produce. These cells become
quiescent and are called osteocytes. They will remain in a
retired state unless a severe condition such as a fracture develops in the
bone.
Osteoclasts
dissolve some minerals in the matrix whenever the concentration of these
minerals in the blood drops too low, restoring blood mineral concentrations to
normal levels. This action is regulated by many factors (e.g., IL-6, hormones).
Osteoclasts also remove unwanted bone material when bones have to be remodeled
or repaired. Osteoblasts often fill the vacated areas with new bone matrix at a
later time.
The activities of the three types of bone cells are
carefully controlled by a variety of hormones and other substances so that
minerals are simultaneously being added to and removed from the bones (see
Chapter 14). Since the speed of these two processes is not always equal, the
bones may gain minerals at one time and lose them at another. These control
mechanisms usually assure preservation of homeostasis in the body.
Since minerals cannot be easily deposited into bone matrix
unless fibers are present, the fibers in bone matrix play a role in mineral
storage. The fibers make up about one-third of the bone matrix in young adults;
the remainder consists of mineral salts. The fibers hold the minerals together
and keep them from cracking. Therefore, the reinforcing fibers contribute to
three other functions of the skeletal system: support, protection from trauma,
and movement.
About 90 percent of the minerals in the matrix consist of
calcium and phosphorus. The presence of minerals provides the means by which
the skeletal system stores minerals. The minerals also make the bone hard and
rigid. These two properties allow the bone to provide good support and
protection from trauma. The hard and rigid bones also provide secure anchoring
points and levers to aid the muscles in performing varied movements.
Cortical Bone Bone cells produce
two types of bone tissue. One type forms the outer layer of the bone (cortical
bone). This bone tissue is made up of many long thick tubes of bone
matrix called osteons (Fig.
9.4 and
Fig. 9.5). The osteons are welded
tightly together with bone matrix; therefore, this type of tissue is also
called compact bone. Old osteons are always being gradually
dissolved and replaced with new osteons.
Trabecular Bone The second type of bone tissue is inside the
bone. It consists of small pieces of bone matrix called trabeculae;
therefore, this type of bone tissue is called trabecular bone.
The trabeculae are of varied shapes, including needles, chips, and flakes,
which are fused together by bone matrix. However, unlike the osteons in
cortical bone, the irregular arrangement of the trabeculae leaves many open
spaces. Since this arrangement provides a structure resembling that of a
sponge, this is also called spongy bone. However, since trabecular
bone is quite hard, rigid, and rough rather than soft and spongy, it might be
better named coral bone.
Bones contain more than just bone tissue. For example, the
hollow shell formed by cortical bone and the arrangement of trabeculae in
spongy bone leave much space inside a bone, which is filled with bone marrow (Fig.
9.4). The outer surface of compact bone is covered by a tough layer of
fibrous material called the periosteum, which serves as a place of attachment
for ligaments and tendons. Additionally, where the surface of a bone meets
another bone to form a joint, the bone may have a coating of cartilage, which
may help join the bones or help them move. Finally, bones have blood vessels
and nerves to serve the parts already mentioned. Therefore, bones are complex,
dynamic, living parts of the body that change continuously. Some alterations
are reversible physiological changes, such as removing and adding minerals,
while others are biological age changes.
The matrix and the cartilage in bones seem to undergo most
age changes; the functional capacity of bone cells and bone marrow seems to
remain largely unchanged regardless of age. Some bone cells may function slower
with age, though this appears to be due to changes in the control signals they
receive. If the bone cells are stimulated, as when a fracture occurs, they
resume rapid functioning. Exceptions are osteoblasts in the endosteum, which
covers the inner surfaces of bones (Fig.
9.4) These osteoblasts have an age-related decrease in sensitivity to
stimulation by vitamin D. Sensitivity may decline by 60 percent by age 50. This
change contributes to age-related thinning of bones.
Age changes in bone matrix are complex and are far from
being understood. This is partly due to the variety of factors that influence
bone matrix. The factors include genes; amount of exercise; nutrition; levels
of hormones; amount of exposure of skin to sunlight; levels of chemicals in the
blood; and the functioning of skin, intestines, and kidneys.
Proteins and Minerals With aging, the balance between the amount
of protein and the amount of minerals in bone matrix shifts in favor of the
minerals. Therefore, bones become more rigid, brittle, and likely to fracture.
Quantity The quantity of bone matrix decreases with
aging because matrix formation becomes slower than matrix removal. This decline
may begin in some individuals at age 20, and by age 30 most people are losing
bone matrix. It seems that by age 35 everyone has begun to lose bone at a
substantial rate (Fig.
9.12).
Structure At first, only trabecular bone is removed.
In this type of bone, all the trabeculae become thinner and weaker (Fig.
9.6a). Trabeculae can become thicker and stronger again if osteoblasts are
stimulated to replace the missing matrix. This often occurs when a person who
has been sedentary begins to exercise. However during
aging, some trabeculae disappear completely and cannot be replaced. The
weakening of the bone at that spot is permanent. Also, as the matrix joining
trabeculae dissolves, some trabeculae become disconnected from the others and
can no longer contribute significantly to bone strength.
The decline in cortical bone is not detected until about age
40, and the loss is quite slow until age 45. The rate of loss then begins to
increase significantly, though it remains approximately half the rate of
trabecular bone loss. The loss of cortical bone takes place on the inside of
the bone only, and the process proceeds outward toward the surface. Therefore,
the layer of cortical bone becomes thinner while the overall width and length
of the bone remain the same.
During the removal and replacement of cortical bone matrix,
old mature osteons are gradually dissolved and shrink while new osteons are formed
next to them (Fig.
9.6b) Small portions of the old osteons often remain behind. As years pass,
the number of osteon remnants and the number of new osteons increase. As a
result, the number of points of fusion among the osteons increases, causing the
matrix to become weaker.
At first the new osteons that form fill all the space left
by the old ones. However, as a person gets older, the new osteons fail to fill
these spaces completely and the number of gaps between the osteons increases.
This change in structure also weakens the matrix.
Effects of Menopause Most experts agree that the rates of loss of
trabecular and cortical bone matrix in women are increased by menopause, the
time when menstrual cycles cease. Menopause usually takes place between ages 45
and 55. As it occurs, the production of the hormone estrogen by the ovaries is
greatly reduced. Actually, since estrogen production probably drops gradually
in the years just before menopause, the effects of declining estrogen begin
before menopause.
The combined effects of aging and menopause result in a loss
of 15 percent to 20 percent of trabecular bone in the 10 years after menopause.
This is two times to three times faster than the rate of loss in women before
menopause or the rate of loss in men. As a result, very old women may have only
half the amount of trabecular bone they had at age 25. Men have lost only
two-thirds as much trabecular bone during the same period.
Cortical bone loss also accelerates because of menopause,
with a loss of 10 percent to 15 percent of the cortical bone in the decade
after menopause. This is a threefold to fourfold increase over the rate of loss
before menopause. The rate of loss eventually slows down so that by age 70 it
has dropped to the same rate found in men of that age. As with trabecular bone,
a very elderly woman probably has less than half the amount of cortical bone
she had during her twenties. Again, bone loss in a man of the same age is
one-third less.
Therefore, because of menopause, a very elderly woman can
expect to have considerably less bone material than does a man of the same age.
This difference in the amount of bone material is usually made greater because
men generally have more bone matrix than do women when bone loss begins.
Variability in Loss Trabecular bone loss begins earlier and occurs
faster than does cortical bone loss. Since some parts of the skeleton have a
higher proportion of trabecular bone, different regions have different rates of
decreases in matrix. We will examine two important examples.
First, vertebrae are composed mostly of trabecular bone.
Therefore, they begin to lose bone sooner and lose more bone than do bones in
the arms and legs, which contain mostly cortical bone. Because of this, there
is a higher incidence of vertebral fractures among the elderly, especially
elderly women.
The second example involves the bone in the thigh called the
femur (Fig.
9.1). The upper part of the femur, which joins with the pelvis at the hip,
contains a high percentage of trabecular bone, while the long central shaft is
made up almost entirely of cortical bone. Therefore, the upper end loses bone
earlier and faster than does the shaft. This contributes to the higher rate of
hip fractures as age increases.
Consequences Although age-related alterations in the
composition, quantity, and structure of bone matrix result in weakening of the
bones, the degree of weakening normally is not great enough to reduce
substantially the reserve capacity of the bone matrix. Unless a very heavy load
or strong force is applied, the bones are able to provide support and
protection for the body as long as a person lives. Of course, large forces from
accidents and severe falls cause fractures more frequently as a person ages. Since women end up with less bone matrix than men do,
they are at higher risk for fractures.
Fractures are painful, hinder or prevent normal activities,
and can lead to serious complications such as infection. Treatment of fractures
is often quite expensive. Though elderly individuals who develop a fracture
face the same problems, the adverse effects multiply with increasing age
because healing of a fracture proceeds slower as one gets older. Slower healing
can mean prolonged immobility, which increases the risk of complications, such
as bedsores, blood clots, and pneumonia. Prolonged immobility also leads to
faster loss of matrix, which in turn increases the risk of developing another
fracture.
To assure that a normal skeleton serves a person well, it is
important to compensate for the weakened condition of the aging skeleton. One
way to do this is to avoid abusing the skeleton. Since falling is among the
most common causes of skeletal abuse resulting in fractures among older people,
reducing falls is of prime importance. A second way to assist the skeleton is
to reduce the loss of bone matrix.
Minimizing Loss of Matrix Though the cause of bone matrix loss with aging
is not known, much has been discovered about factors that modify the rate of
loss. Many of these factors are easily regulated; therefore, much can be done
to reduce the loss of bone matrix. In so doing, individuals can make
significant contributions to the strength of the skeleton and its ability to
serve them.
The condition of a person's bone matrix depends on how well
it is treated throughout life. Much more benefit can be derived from taking
steps to assist in building and maintaining bone matrix through early and late
adulthood rather than just in old age, after a considerable amount of matrix
has been lost. While the loss of bone matrix can be slowed at any age, little
of the bone matrix and bone strength that are lost early in adulthood can be replaced
later in life.
Numerous steps can be taken to build a large reserve of bone
matrix before age 35 and minimize decreases in bone matrix at any age (Table
9.1). Each of the steps in the table contributes to one or more of the
following: (1) maintaining high calcium levels, (2) stimulating matrix
production, and (3) inhibiting matrix removal. Of course, elderly individuals
and persons with known diseases should seek qualified professional advice
before changing their normal activities.
Though normal bone matrix retains much of its strength
throughout life, many individuals develop a disease called osteoporosis,
which causes substantial reductions in the quantity and strength of bone
matrix. Affected individuals develop bone fractures quite easily even when
carrying out ordinary daily activities or simply walking or sitting.
Osteoporosis
means "bones with pores." This name is appropriate since osteoporosis
causes matrix production to be much slower than matrix removal, leaving bones
full of holes. Affected bones become thin, hollow, and fragile.
Type I, or
Postmenopausal, Osteoporosis
There are two types of osteoporosis. Type I
osteoporosis is also called postmenopausal osteoporosis
because it usually affects women after menopause. This occurs because the
lowered estrogen levels after menopause seem to be the main factor in bone
deterioration. Type I osteoporosis rarely occurs in men since the level of the
hormone testosterone in men does not decline dramatically with aging.
Postmenopausal osteoporosis affects trabecular bone more
than it affects cortical bone and thus leads to fractures in regions of the
skeleton that consist largely of trabecular bone. These regions include the
vertebrae, the neck of the femur near the hip, the radius near the wrist, and
the humerus near the shoulder (Fig.
9.1).
Type II, or Senile,
Osteoporosis
Type II osteoporosis
is also called senile osteoporosis because it usually affects
people of advanced age, especially those over age 60. The late appearance
occurs because senile osteoporosis affects cortical bone more that trabecular
bone. Type II osteoporosis occurs twice as frequently in women as in men.
Though senile osteoporosis affects many areas of the body,
most of the resulting fractures occur in the neck of the femur. Other fractures
occur in the radius near the wrist, the humerus near the shoulder, the tibia
(shin bone) near the knee, and the pelvis (Fig.
9.1).
Osteoporosis affects more than 24 million Americans, and
this number is rising as the number of elderly people increases. Approximately
80 percent of those with osteoporosis are women, and as many as 60 percent of
all women over age 60 have osteoporosis. In the three decades following age 50
and based on World Health Organization standards, the incidences of
osteoporosis among women are 15 percent, 25 percent, and 40 percent
respectively. A substantial percentage of women classified as not having
osteoporosis have serious thinning of bone. The incidences among men are 33
percent less.
Each year osteoporosis causes more than 1.5 million
fractures. Almost half are fractures of vertebrae, while about 20 percent are
hip fractures.
Vertebral Fractures Seven of eight vertebral fractures occur in
women. The incidence of these fractures in women rises quickly and
continuously, beginning soon after menopause. Vertebral fractures occur in
about two-thirds of all women over age 65.
Vertebral fractures caused by osteoporosis are usually crush
fractures, or fractures in which the supporting part of a vertebra,
called the body, becomes so weak that it collapses (Fig.
9.8b). When this happens, the upper part of the vertebral column settles
down on the part below the fracture. These fractures often happen spontaneously
or when a person is lifting a heavy object.
Crush fractures produce serious problems. Extreme pain often
occurs because the nerves extending out from the spinal cord become pinched
where they pass between the collapsed vertebrae. The misalignment of the
vertebrae limits mobility, and the settling down of the vertebrae results in a
decrease in height and a hunched-over or humpbacked posture. These people may
have a drastically altered appearance, and their clothing often does not fit properly.
The poor posture also produces complications in other systems, such as
difficulty breathing and poor circulation. All these changes have an impact on
the ability of affected individuals to care for themselves. Their social
interactions change, they frequently have lower self-esteem and suffer from
depression, and they may encounter problems in performing occupational tasks.
These effects also affect the people in their families and communities.
Hip Fractures The incidence of hip fractures is low until about age 60,
after which the rate of occurrence increases gradually each year until about
age 70. Then the rate of occurrence rises much more quickly each year.
One-third of all women and one-sixth of all men who reach age 90 will have had
a hip fracture due to osteoporosis.
Like vertebral crush fractures, many hip fractures occur
spontaneously. Others often result from falling. It is sometimes difficult to
tell whether a person fell because a hip fractured or fractured a hip because
of a fall.
Fractures of the hip caused by osteoporosis lead to
significant problems that are different from those resulting from vertebral
fractures. Over half the individuals who suffer a hip fracture lose the ability
to walk without assistance. Many people with hip fractures no longer can
perform normal daily activities such as bathing and dressing without help.
Between 15 and 25 percent of individuals with a hip fracture need to enter an
institution for extended care. Most of these patients will never be able to return
to living in the community. As with vertebral fractures, all-encompassing
shifts in lifestyle are imposed on people who suffer hip fractures due to
osteoporosis, and hip fractures have an impact on people associated with hip
fracture patients. Finally, 20 percent to 30 percent of those who have
osteoporosis-related hip fractures die within one year as a result of
complications such as pneumonia and blood clots.
The cause of osteoporosis remains unknown, but the changes
in bone matrix brought about by Type I osteoporosis in women result primarily
from drastic reductions in estrogen. Low levels of estrogen result in profound
changes because estrogen helps build and maintain bone matrix through numerous
complex mechanisms. Type I osteoporosis occurs relatively infrequently in men,
but when it does occur, it seems to follow abnormally large decreases in
testosterone.
Type II osteoporosis is primarily due to an age-related
decrease in vitamin D activation by the kidneys. In addition, the aging
intestines seem to become less sensitive to vitamin D and less able to respond
to bodily needs for calcium. The result is a declining supply of calcium to
body cells, leading to breakdown of bone matrix. Since the intestines do not
absorb enough calcium, the matrix that is destroyed is not replaced.
Diagnosing osteoporosis is very difficult, and in almost all
cases individuals do not find out that they have osteoporosis until they have
suffered a fracture. The diagnosis is difficult because the appropriate tests
are dangerous (e.g., radiation, surgery), time-consuming, expensive, and
difficult to interpret. In addition, to truly determine that a person has
osteoporosis, that person should be tested regularly every few years to track
the rate of loss of bone matrix.
The best way to protect oneself from the effects of
osteoporosis is to build as much bone matrix as possible before age 35 and keep
the deterioration of matrix as slow as possible thereafter (Table 9.1). The
first four items in the table seem to be the most important. Following these
recommendations will minimize the modifiable risk factors for osteoporosis and
diminish the incidence of fractures and the destructive immobility that usually
follows.
Lifelong involvement in weight-bearing activities such as
walking and running is one of the best ways to minimize the effects of normal
bone demineralization and decrease the chances of developing osteoporosis.
However, any increase in weight-bearing exercise by sedentary older individuals
will be helpful. Any strenuous activity will slow the demineralization process.
While all people should take the appropriate steps to
protect themselves from osteoporosis, this is especially important for those
who are intrinsically at high risk. These high-risk categories include being
female; having early menopause; having the ovaries removed; being white or
Asian; having fair skin; having relatives with osteoporosis; being very thin;
having kidney disease; having thyroid or parathyroid gland disease; having an
intestinal disease that inhibits calcium absorption; and having chronic
bronchitis or emphysema. Of course, belonging to more than one category places
a person at even greater risk. Individuals at very high risk may benefit from
diagnostic testing by qualified professionals.
Though prevention is the key to success in battling
osteoporosis, individuals who have already lost much bone matrix because of
this disease can be helped to some degree.
Strengthening Bone Many treatments have been shown to slow the
loss of bone matrix in at least some individuals. Often these treatments are
based on the recommendations in Table 9.1.
For some individuals, such as very sedentary older women,
vigorous exercise can reverse the process of demineralization and increase the
amount of minerals in bones subjected to heavy loads. The length of time over
which more minerals will be added to the bones depends on the nature of the
exercise regimen. Regardless of the nature or duration of the activity,
however, demineralization of the bones will eventually resume. If a high level
of physical activity is continued, demineralization occurs at a slow rate. If
the exercise is stopped, demineralization soon recurs at a rapid rate.
Many researchers believe that the exercise-induced addition
of minerals to bones or the slowing of bone demineralization decreases the risk
of fractures among the elderly. Exercise such as walking a mile three times a
week has been shown to reduce the risk of fractures in many older individuals.
Though exercise alone may be beneficial, the most successful treatment plans
incorporate several recommendations. For example, an exercise program may be
combined with dietary supplements of calcium and vitamin D.
Since changes in bone matrix occur slowly, treatment
programs should be continued for many years. Because of the heterogeneity and
the higher incidence of diseases among the elderly, a complete assessment of an
older person should be performed before a treatment program is initiated.
The most successful treatment programs for postmenopausal
women usually include estrogen replacement therapy, and most women can be
helped by such therapy. However, there is a small risk from complications such
as the formation of blood clots and the development of uterine or breast
cancer. Women at high risk for these complications probably should avoid
estrogen therapy. For other women, the risks are very small when estrogen is
administered with certain types of progesteronelike hormones.
Women receiving such treatments have much higher life expectancies than do
women who do not receive them. Not only are the effects of osteoporosis
reduced, but, with the proper progesterone, the risk of other diseases such as
atherosclerosis is reduced. To be most effective, estrogen therapy should begin
at menopause and continue for up to 10 years afterward.
The use of other substances for treating osteoporosis is
increasing. Biphosphonates (e.g., alendronate, etridonate) reduce the risk of vertebral fractures, and are
most effective when combined with estrogen. Biphosphonates
can cause inflammation of the esophagus and stomach. Fluoride has little effect on the femur and
results in brittle matrix. Calcitonin is expensive and causes painful calcium
deposits.
Avoiding Injury A second aspect in
treating osteoporosis patients involves minimizing traumatic injuries that may
make weakened bones fracture. One way of doing this is to refrain from putting
strain on the skeleton by, for example, lifting heavy objects. Perhaps an even
more important factor is reducing the risk of falling, one of the most common
causes of such injury among the elderly. Falling causes so many fractures that
it has become an area of specialized research.
The risk of fractures and other injury from a fall increases
with age. Reasons beyond the decreased strength of bones include weaker muscles
and slower reflexes to break the fall, and reduced subcutaneous fat and muscle
mass to absorb the shock.
Falls are more common as age increases, partly because of
the increased occurrence of diseases such as atherosclerosis, stroke, and
parkinsonism. Other contributing factors include poor vision, age changes in
the ears, muscle weakness, joint stiffness, altered gait, slow reflexes, and
certain medications.
Much can be done to reduce the incidence of falls, including
providing adequate lighting and grab bars, avoiding slippery surfaces such as
wet or highly waxed floors, removing obstacles such as throw rugs, and wearing
well-fitted shoes.
After a Fracture Various combinations of
approaches are
employed to help people who have sustained a fracture. Surgery may be performed
to quickly mobilize the individual because surgical repair compensates for the
slow healing of bones in older people. Rapid mobilization reduces further bone
and muscle deterioration and the risk of blood clots, pneumonia, and
psychological problems such as depression. Physical therapy and the use of
support devices such as a back brace or cane can also help restore a person to
activities. Medications are often prescribed to reduce pain.
In summary, four weapons are used to treat osteoporosis:
reducing the loss of matrix; replacing matrix to strengthen bones; preventing
injury; and assisting in the recovery from fractures. Currently, all except
replacing bone matrix can be successfully employed.
The bones that constitute the skeletal system are held
together by special structures called joints. By furnishing
strong attachments, joints contribute to the support provided by the skeletal
system. They also protect the body from traumatic injury by absorbing shock and
vibration in two ways. One way is by allowing the bones to move somewhat, which
permits the skeletal system to yield to sudden physical forces. The other way
derives from the cushioning provided by the fluids and resilient cartilage
found in many joints. Because of these two features, joints can prevent much of
the damage to delicate parts of the body caused by jolting forces from
activities such as running and jumping. Assistance with movement derives, of
course, from the various movements of bones permitted by the joints. The joints
do not help the skeleton store minerals or produce blood cells.
There are three main types of joints in the body. An immovable
joint consists of tough collagen fibers that bind bones tightly
together. The unyielding strength of the collagen, together with the tight fit
of the bones, essentially eliminates shifting of the bones. Among the immovable
joints are the suture joints between skull bones (Fig.
9.1). These joints keep the shieldlike skull bones in place to support and
protect the brain.
Age Changes As people age, the collagen fibers between the
bones at immovable joints are coated with bone matrix, and so the space between
the bones gets narrower. Eventually the bones may fuse together. Thus,
immovable joints improve with aging because they get stronger.
The second type of joint is the slightly movable joint.
There is a layer of cartilage between the bones joined by these structures.
Some of these joints have ligaments, which help hold the bones together.
Ligaments are cablelike structures consisting primarily of collagen fibers.
There are two kinds of slightly movable joints. One kind
contains hyaline cartilage, which is a smooth, slippery white
substance with the consistency of hard rubber. Slightly movable joints with
hyaline cartilage join the ribs to the sternum (Fig.
9.1). The limitation of movement in these joints allows the ribs to support
and protect the lungs, the heart, and other organs in the chest cavity while
permitting enough movement of the ribs to allow breathing.
In the other kind of slightly movable joints, symphysis
joints, the bones are separated by a pad of fibrocartilage.
This type of cartilage is also smooth, slippery, and resilient. It is stronger
than hyaline cartilage because it contains many more thick collagen fibers. The
fibers add toughness by binding the rubbery cartilage matrix together.
Symphysis joints are located where greater strength is
needed, such as between the bodies of the vertebrae (Fig.
9.8a), where the intervertebral disks of fibrocartilage
permit limited and smooth bending of the vertebral column. Together with the
vertebrae, the disks support the weight of the body. Each disk contains a soft
center called the nucleus pulposus. The nucleus pulposus helps
with support and is important in shock absorption. The intervertebral joints
also contain strong ligaments to hold the vertebrae together while allowing a
limited amount of bending and twisting of the spine.
Age Changes With aging, the hyaline cartilage in slightly
movable joints becomes stiffer because of a decrease in water and an increase
in hard and rigid calcium salts within the cartilage. The fibers in the
ligaments develop more cross-links with age, causing the ligaments to become
stiffer and less elastic. The combination of these age changes reduces the
movement allowed. For example, such stiffening in the chest area makes
breathing more difficult.
Aging causes the fibrocartilage disks in symphysis joints to
lose water and gain calcium. These changes may contribute to age-related
stiffening of the joints and a decrease in the movement permitted by the
vertebral column. The nucleus pulposus becomes weaker and somewhat crumbly,
decreasing its ability to provide support for the body and cushioning for the
spinal cord and head.
The center region of each vertebral body weakens with aging
(Fig.
9.8c). The weight of the body then forces the central part of each
intervertebral disk to expand into the body of the vertebra, forming a concave
region. This alteration in structure seems to place more of the weight of the
body onto the outer edge of the intervertebral disk, compressing it somewhat.
The net result is a decrease in the height of the body with aging.
Decreasing height with age also has other causes. There is a
thinning of the cartilage in other joints, such as the knees and hips. The
weakening of muscles and a decrease in muscle tone often lead
to poorer posture, further reducing overall height. The rate of loss of height
is slow at first and becomes more rapid with age.
Like all collagen, the collagen in the ligaments of the
intervertebral joints becomes shorter, stiffer, and less elastic. These changes
further reduce the mobility of the vertebral column.
Overall, age changes in symphysis joints reduce the ease and
range of motion that these joints provide. This hampers
bending and twisting of the vertebral column and makes performing activities
such as tying shoes, picking up objects, and dancing more difficult or less
enjoyable. The loss is not great enough to be a serious threat to homeostasis
(i.e., to continuing good health).
Moreover, as will be discussed below, the decline in movement of symphysis
joints can be minimized and even reversed by exercise.
The third type of joint is the freely movable joint,
which is the most common type. These joints make up virtually all the joints in
the arms, legs, shoulders, and hips; the joints between the ribs and the
vertebrae; and the joints between the vertebrae except the joints between
vertebral bodies. The joint between the lower jaw and the skull, the
temporomandibular joint (TMJ), is the only freely movable joint in the head.
The bones joined by freely movable joints are separated from
each other by a narrow space called the synovial cavity (Fig.
9.9). This cavity is surrounded by a thin synovial membrane,
which constantly secretes a fluid (synovial fluid) into the
cavity. At the same time, the membrane removes the old fluid. Synovial fluid
contains water and protein molecules. This mixture is somewhat thick and very
slippery, allowing the bones to slide over each other easily. It also absorbs
some shock sustained by the joint.
The end of each bone is covered by a layer of hyaline
cartilage that is very smooth and somewhat resilient. Since the cartilage is
lubricated by the synovial fluid, it is very slippery. The synovial fluid also
supplies nutrients to the cartilage. The slippery cartilage permits easy
movement and cushions the bones and the parts of the body they support.
Surrounding the synovial membrane is the thick sleevelike joint capsule, which consists
mostly of flexible strong collagen fibers. The joint capsule helps bind the
bones together and encases the synovial membrane for support. The flexibility
and slight elasticity of the capsule allow the bones to move freely, though
over a limited range.
Outside the joint capsule and extending from one bone to the
other are cablelike ligaments, which also consist mostly of
collagen fibers. Like joint capsules, ligaments bind the bones together and
allow limited movement of the joint.
Motion allowed at a joint is also limited by the shapes of
the bones and by muscles and tendons. While the joints must allow the bones to
move easily and over enough distance to meet the needs of the body, limiting
motion is important in preventing injury to muscles, nerves, and blood vessels.
Excessive joint motion (e.g., joint dislocation) stretches, twists, and pinches
these soft structures.
Age Changes With aging, there is an increase in the
amount of fibrous material in the synovial membrane, and pieces of cartilage
may form in it. These changes make the membrane stiffer and less elastic. The
membrane also loses some of its blood vessels so that it is less able to
produce and remove synovial fluid. Though there is disagreement about which age
changes take place in the synovial fluid and the cartilage on the ends of the
bones, it is generally agreed that these changes are slight and have little
effect on the functioning of the joint.
More important than these age changes are changes in the
joint capsule and ligaments. Because of an increased formation of cross-links
among their fibers, these structures become shorter, stiffer, and less able to
stretch. These changes make it more difficult to move and reduce the range of
movement of the joint. Both changes cause the initiation of movement and the
speed of movement to occur more slowly. This results in a reduction of the
ability to maintain balance and take action to minimize the force of impact
from a fall or another traumatic event. Thus, the aging of freely movable
joints substantially reduces the ability of the skeletal system to provide
cushioning and movement, resulting in increased injuries and diminished
performance of activities.
The functioning of freely movable joints begins to decline
at age 20. The joints move less easily and over less of a range as time passes.
The decrease in blood vessels in joint structures results in slower healing of
injured joints.
All these changes occur very gradually but unremittingly. It
seems that only part of the reduction in functioning is due to age changes.
Some change may be due to the accumulated effects of the small but repeated
injuries sustained by joints during ordinary activities. Distinguishing true
age changes from these other changes is difficult.
The progressive decrease in mobility caused by aging in both
freely movable and slightly movable joints can be slowed by keeping physically
active. Exercises that involve bending, stretching, and turning minimize the
restraining effects caused by shortening of the collagen fibers. Some mobility
that has been lost over time because of inactivity can be regained by
initiating exercises that stretch and increase the flexibility of restrictive
joint components such as ligaments. Exercise also seems to increase circulation
to the joints. Such exercises reduce the risk of fractures and contribute to
better balance, greater independence, and improved psychological well-being.
However, when people of advanced age engage in new exercises, care should be
taken to avoid injuring the joints.
The problems caused by age changes in the joints are often
compounded by a disease called arthritis, which means "joint
inflammation." The name was chosen because arthritis results in injury and
pain in the joints.
The incidence of arthritis increases with age. More than
half the cases occur in people over age 65. In fact, arthritis is the most
common disease among the elderly and is second only to heart disease in causing
older people to visit a physician.
Different cases of arthritis vary greatly in severity. In
some individuals the symptoms are so mild as to be barely noticed. At the other
extreme, arthritis can cause excruciating and unremitting pain as well as
deformity and crippling incapacitation. This disease results in more limitation
in activity and more disability than does any other chronic illness. Only heart
disease causes people to spend more days in bed.
There are more than 100 types of arthritis, and different
forms are prevalent at different stages of life. A person may have two or more
forms at the same time. The two types discussed below are the forms most
frequently encountered in the elderly.
Osteoarthritis (OA) is by far the most common type of arthritis in adults. It
causes more than half of all cases of arthritis. Approximately 75 percent of
people reaching age 75 will have OA in at least one joint. Most cases of
osteoarthritis occur in women.
The cause of osteoarthritis is still unknown, there is no
method of prevention, and there is no cure. It usually progresses continuously,
though the rate of progress differs among individuals. Main risk factors for OA
include injury to joints, inadequate treatment of injured joints, and extreme
overuse of joints.
Osteoarthritis often affects weight-bearing joints,
including the knees, the hips, and the intervertebral joints in the lower
(lumbar) region of the vertebral column. The joints in the cervical vertebrae
and those in the fingers are also frequent sites of this disease.
Effects When osteoarthritis attacks freely movable
joints, it causes breakdown of the cartilage between bones, and the cartilage
becomes rougher and softer and cracks. The cartilage becomes weaker and thinner
because its cells are removing cartilage faster than they are replacing it.
Because of these changes, the cartilage loses the ability to cushion and
lubricate the ends of the bones, diminishing the operation of the joints (Fig.
9.10).
So much cartilage may be removed that the hard ends of the
bones bump and rub against each other. This contact can sometimes be heard and
felt when a person moves. The bones respond to the resulting abuse by producing
extra bone matrix at the joint. When this buildup occurs in arthritic finger
joints, it may be observed as enlargements of the joints.
The new bone matrix produced is rough and sometimes jagged,
and it abrades the softer tissues in the area, causing pain. As the bone matrix
grows, it protrudes farther, making movement of the joint more difficult and
reducing its range of motion because the edges of the bones bump against each
other.
Other changes from osteoarthritis often reduce the action of
the joint even further. The injured synovial membrane becomes more irregular,
thick, and stiff. It may bind the bones abnormally by adhering more tightly to
them. Pieces of cartilage and bony spurs sometimes break off from the bones and
become lodged within the joint.
Osteoarthritis of the symphysis joints in the vertebral
column causes the same type of extra bone formation that occurs in freely movable
joints (Fig.
9.8d). This extra bone may cause pain by irritating surrounding tissues or
pressing on nerves attached to the spinal cord, reduce ease of movement, and
reduce the range of motion permitted by the joints.
Treatments Treatment of osteoarthritis is aimed at
slowing its progress and reducing the pain and disability it causes. Affected
individuals can be taught how to perform activities in ways that minimize abuse
of diseased joints. The use of canes and other devices that support some body
weight helps in this regards. Mild exercise reduces
stiffness and loss of range of motion, and a variety of medications relieve
pain.
Severely diseased joints may be repaired surgically. Often
the diseased joint is removed and replaced with an artificial one. Total hip
replacement is a common example. Since replacement of intervertebral joints is
impossible, surgeons may eliminate the joint by fusing the vertebrae above and
below the joint. Though this procedure prevents further motion at the joint
site, it relieves the pain and deformity that usually accompany osteoarthritis
of the spine.
Rheumatoid arthritis (RA) has a much lower frequency of occurrence
than does osteoarthritis. Only about 1 percent of all adults have RA. Two of
every three RA patients are women. Most cases begin between the ages of 30 and
40, and the number of cases increases with age.
Effects Rheumatoid arthritis usually attacks the
freely movable joints of the wrists and hands as well as those in the ankles
and feet; the joints closest to the ends of the fingers are spared. It
sometimes affects other joints, including the shoulders, elbows, and knees.
Like osteoarthritis, RA causes pain and loss of joint mobility. Unlike
osteoarthritis, it often produces many other effects, including weakness,
fatigue, and damage to organs such as the heart, blood vessels, lungs, nerves,
skin, and eyes. This widespread damage occurs because RA can attack fibrous
materials everywhere in the body. Another peculiarity of RA is that it goes
into temporary remission in some individuals.
Though the cause of RA is unknown, the method by which it
destroys joints is understood. The root of the problem lies in the immune
system, which mistakenly identifies normal connective tissues as being foreign
to the body. The immune system then reacts in its usual manner by trying to
eliminate the "foreign" substances. In so doing, it kills and removes
these normal connective tissue materials. This reaction is called autoimmunity
since the body is attacking itself.
In joints, the immune system kills and removes cartilage,
which is replaced with a unique type of scar tissue, called a pannus
(Fig.
9.11). The pannus releases enzymes that destroy more of the cartilage. The
immune system also removes bone material and the synovial membrane. As more
normal tissues are eliminated, the pannus enlarges and spreads into the joint,
substituting for normal components. All these activities cause considerable
pain and joint swelling, and proper functioning of the joint becomes
impossible.
As the joint weakens, the bones shift out of position.
Sometimes, the pannus becomes calcified and stiff. Progressive calcification
sometimes results in fusion of the bones. In addition, the ordinary scar tissue
produced at the joint shrinks as time passes, pulling the bones farther out of
alignment and locking them into abnormal positions. Thus, the joint becomes
distorted and immovable. The result is crippling deformity, a condition most
easily seen in the hands and feet.
Treatments There is no way to prevent or cure RA. The
goals of treatment are the same as those for osteoarthritis: slowing the
progress of the disease and minimizing pain and disability. Various medications
may be prescribed to inhibit the immune system and relieve pain. Mild exercise
helps maintain joint mobility. A variety of other treatment modalities may be
initiated. Unfortunately, not all individuals respond well to these treatments.
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Copyright 2020: Augustine G. DiGiovanna, Ph.D.,
Salisbury University, Maryland
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