OSTEOPOROSIS
What is osteoporosis?
The word ‘osteoporosis’ means ‘porous bone.’ Itis a disease that weakens
bones, and if you have it, you are at a greater risk for sudden and unexpected
bone fractures. Osteoporosismeans thatyou haveless bone mass and
strength.
The disease often develops without any symptoms or pain, and it is usually not
discovered until the weakened bones causepainful fractures. Mostof these
are fractures of the hip, wristand spine.
Definition
Osteoporosis has been operationally defined on the basis of bone mineral
density (BMD) assessment. According to the WHO criteria, osteoporosis is
defined as a BMD that lies 2.5 standarddeviations or more below the
average value for young healthy women (a T-scoreof <-2.5 SD) (1,6).
Osteopenia
A condition that occurs when the body doesn't make new bone as quickly as it
reabsorbs old bone.
Osteopenia, as defined by the World Health Organization (WHO), is a t-score
between -1 to -2.5, while values less than -2.5 are diagnostic for osteoporosis.
Causes
The endocrine system
Several hormones areassociated with triggering activity in osteoblastor
osteoclastcells, resulting in either reduced bone formation or increased bone
destruction:
Thyroxine: Hyperthyroidism(theoverproduction of thyroid hormone)
increases the activity of osteoclasts, speeding up the rate at which bone cells
are destroyed. This occurs when the level of thyroxine in the body is elevated
for a long period, or when thyroid-stimulating hormone(TSH) levels remain
low for a long period.
Estrogen: Estrogen levels are strongly associated with osteoporosis in
postmenopausalwomen and elderly men. Itis associated with large levels of
bone reabsorption due to increased osteoclasts. Estrogen deficiency affects
the number of osteoclasts both by stimulating their production and decreasing
apoptosis.
Testosterone: Themostimportant predictor of osteoporosis in elderly men is
age-related deficiencies in testosterone. Androgens (an umbrella term for
testosteroneand its precursors) both stimulate the production of osteoblasts
and decreasetheir apoptosis. Androgens also regulatethe formation and
survivalof osteoclastcells.
Cortisol: Produced by the adrenal glands, the overproduction of cortisol can
have powerfuleffects on bone density. In patients with Cushing’s syndrome, a
term used to describea constellation of symptoms caused by an excess of
cortisol, a dramatic reduction in bone density can be observed. In theelderly,
weak correlations between levels of cortisoland bone density, and changes in
cortisoland bone density over time have been observed.
Medications
Drug-induced osteoporosis is a significant health concern as many commonly
prescribed treatments can contribute to bone loss.
Corticosteroids, which arewidely used in the management of many conditions,
are associated with reduced bone density. They are the second most common
causeof secondary osteoporosis with as many as 50% of patients experiencing
an eventual fractureif taken long-term.
Corticosteroids increaseosteoblastapoptosis, increasebone reabsorption and
reduce bone growth factors associated with bone regeneration. Finally, steroid
use also increases calcium deficiency.
Antiepileptics which are used to treat seizuredisorders inducecertain enzymes
that cause the body to rapidly metabolize vitamin D and estrogen.
Anticonvulsants may also inhibit the absorption of calcium and increase bone
loss by inhibiting the production of osteoblasts.
Heparin, an anticoagulant medication used in the treatment of pulmonary
conditions, is associated with loss of bone tissue, especially longer-term use at
higher doses. Although the mechanisms by which this occurs is not yet fully
understood, heparin is thought to stimulate osteoclast production and inhibit
osteoblastproduction.
Malabsorptiondisorders
Gastrointestinaldisorders such as ulcerative bowel diseaseare strongly
associated with secondary osteoporosis. Such disorders interferewith the
absorption of nutrients essential for maintaining the balance between bone
resorption and generation. Furthermore, these conditions are often treated
with corticosteroids.
Lifestyle factors
A poor diet deficient in nutrients such as calcium and vitamin D is a risk factor
for osteoporosis. Peoplewith eating disorders such as anorexia and bulimia
nervosa areparticularly at risk due to a lack of nutrient intake and hormonal
changes associated with low body weight. In males and females, maintaining a
low body weight increases cortisolproduction and decreases growth
hormones. Females may be particularly vulnerable as low weight also inhibits
the production of estrogen.
An inactive lifestyle can increasethe risk of osteoporosis as weight-bearing
exercise stimulates bone development and reduces calcium loss from bones.
Extreme inactivity such as bed rest can causeextreme bone loss, especially in
the firstmonths.
Excessivesmoking and alcohol consumption also increase the risk of bone loss
and fractureby impacting on hormonalsystems associated with bone
production. The risk is increased if they occur in tandem with poor diet and
inactivity.
Pathophysiology
Osteoporosis is a classic example of a multifactorial diseasewith a complex
interplay of genetic, intrinsic, exogenous, and life style factors contributing to
an individual's risk of the disease.
Traditional pathophysiologic models frequently emphasized endocrine
mechanisms, e.g. estrogen deficiency and secondary hyperparathyroidism in
elderly due to estrogen deficiency, reduced dietary intake, and widely
prevalent vitamin D deficiency, as the key determinants of postmenopausal
osteoporosis .
Clinical manifestation
Usually, there are no symptoms of osteoporosis. Thatis why it is sometimes
called a silent disease. However, you should watch out for the following things:
 Loss of height (getting shorter by an inch or more).
 Change in posture(stooping or bending forward).
 Shortness of breath (smaller lung capacity due to compressed disks).
 Bone fractures.
 Pain in the lower back.
Signs and symptoms of early-stage osteoporosis
Early, detectable signs of bone loss are rare. Often people don’t know they
have weak bones until they’vebroken their hip, wrist, or someother bone.
However, somesigns and symptoms can point toward potential bone loss,
such as:
 Receding gums. Your gums can recede if your jaw is losing bone. Ask
your dentist to screen for bone loss in the jaw.
 Weaker gripstrength. postmenopausalwomen and overall bone
mineral density, researchers found that low handgrip strength was
linked to low bone mineral density. In addition, lower grip strength can
increase your risk for falls.
 Weak and brittle fingernails. Nailstrength can signalbone health. But
you should also take other factors into consideration that may affect
your nails, such as exposureto very hot or cold temperatures, regular
use of nail polish remover or acrylic nails, or submersion in water for
long periods of time.
Other than changes in bone density, osteoporosis doesn’tusually causea lot of
initial symptoms. Your best bet for detecting it in the early stages is to talk with
your doctor or healthcare professional, especially if you have a family history
of osteoporosis.
Signs and symptoms of later-stage osteoporosis
Once bone mass has deteriorated further, you may startto experience more
obvious symptoms, such as:
 Loss of height. Compression fracturein the spine can causeyou to
become shorter. This is one of the mostnoticeable symptoms of
osteoporosis.
 Fracture froma fall. A fractureone of the mostcommon signs of fragile
bones. Fractures can occur with a fall or from minor movement such as
stepping off a curb. Some osteoporosis fractures can even be triggered
by a strong sneezeor cough.
 Back or neck pain. Osteoporosis can causecompression fractures of the
spine. These fractures can be very painful becausethe collapsed
vertebrae may pinch the nerves that radiate out from the spinal cord.
The pain symptoms can rangefrom minor tenderness to debilitating
pain.
 Stoopedposture or fracture. The compression of the vertebrae may also
causea slight curving of the upper back. A stooped back is known as
kyphosis, which can causeback and neck pain. Itcan even affect
breathing due to the extra pressureon the airway and limited expansion
of your lungs.
Diagnostic evaluations
BONE DENSITY -A bonemineraldensitytest, sometimesjustcalled a
bonedensity test, examines segmentsof yourbone through X-rays
to detectosteoporosis.
DEXA SCAN -Oneof themostcommonosteoporosistests is dualX-
ray absorptiometry -- alsocalled DXA or DEXA. Itmeasurespeople’s
spine, hip, or total-bodybonedensity to help gaugetheir risk of
fractures.
BONE DENSITOMETRY- is a testlike an X-ray thatquicklyand
accurately measuresthedensity of bone
Laboratory studies. serum calcium,
serum phosphate,
serum alkaline phosphatase,
urine calcium excretion,
hematocrit,
erythrocytesedimentation rate,
x-ray studies are used to exclude other possibledisorders thatcontribute to
bone loss.
MANAGEMENT
 Diet. A diet rich in calcium and vitamin D throughout life, with
an increased calcium intake during adolescence, young
adulthood, and the middle years, protects against skeletal
demineralization.
 Exercise. Regular weight-bearing exercise promotes bone
formation, such as a 20-30-minute aerobic exercise, 3x a week, is
recommended.
 Fracture management. Osteoporotic compression fractures of
the vertebrae are managed conservatively, pharmacologic and
dietary treatments are aimed at increasing vertebral bone density,
and for patients who do not respond to first-line approaches are
treated with percutaneous vertebroplasty or
kyphoplasty (injection of polymethylmethacrylate bone cement
into the fractured vertebra, followed by inflation of a pressurized
balloon to restore the shape of the affected vertebra).
Pharmacologic Therapy
The first-line medications and other medications used to treat and prevent
osteoporosis include:
 Calcium supplements with vitamin D. To ensure adequate
calcium intake, a calcium supplement with vitamin D may be
prescribed and taken with meals or with a beverage high in
vitamin C to promote absorption, but these supplements should
not be taken at the same day as bisphosphonates.
 Bisphosphonates. Bisphosphonates that include daily or weekly
oral preparations of alendronate or risedronate, monthly oral
preparations of ibandronate, or yearly intravenous infusions
of zoledronic acid increase bone mass and decrease bone loss by
inhibiting osteoclast function.
 Calcitonin. Calcitonin directly inhibits osteoclasts thereby
reducing bone loss adD increasing bone mineral density, and is
administered by nasal spray or
by subcutaneous or intramuscular injection.
 Selective estrogen receptor modulators (SERMs). SERMs such
as raloxifene, reduce the risk of osteporosis by preserving bone
mineral density without estrogenic effects on the uterus.
 Teriparatide is a subcutaneously administered anabolic agent
that is administered once daily, and as a recombinant PTH, it
stimulates osteoblasts to build bone matrix and facilitates overall
calcium absorption.
Surgical Management
Fractures of the hip that occur as a consequence of osteoporosis are managed
surgically through:
 Joint replacement. Joint replacement is a surgery to replace all
or part of a joint with a man-made joint called prosthesis.
 Closed or open reduction with internal fixation. Open
reduction, internal fixation involves the implementation of
implants to guide the healing process of a bone, as well as the
open reduction, or setting, of the bone, while closed reduction is
a procedure to set or reduce a broken bone without surgery.
Discharge and Home Care Guidelines
At the completion of the home care instruction, the patient or caregiver will be
able to implement the following:
 Diet. Identify calciumand vitaminD rich foods and discuss
calcium supplements.
 Exercise. Engagein weight-bearing exercise daily.
 Lifestyle. Modify lifestylechoices: avoid smoking, alcohol,
caffeine, and carbonated beverages.
 Posture. Demonstrategood body mechanics.
 Early detection. Participatein screening for osteoporosis.

0steoporosis

  • 1.
  • 2.
    What is osteoporosis? Theword ‘osteoporosis’ means ‘porous bone.’ Itis a disease that weakens bones, and if you have it, you are at a greater risk for sudden and unexpected bone fractures. Osteoporosismeans thatyou haveless bone mass and strength. The disease often develops without any symptoms or pain, and it is usually not discovered until the weakened bones causepainful fractures. Mostof these are fractures of the hip, wristand spine. Definition Osteoporosis has been operationally defined on the basis of bone mineral density (BMD) assessment. According to the WHO criteria, osteoporosis is defined as a BMD that lies 2.5 standarddeviations or more below the average value for young healthy women (a T-scoreof <-2.5 SD) (1,6).
  • 3.
    Osteopenia A condition thatoccurs when the body doesn't make new bone as quickly as it reabsorbs old bone. Osteopenia, as defined by the World Health Organization (WHO), is a t-score between -1 to -2.5, while values less than -2.5 are diagnostic for osteoporosis. Causes The endocrine system Several hormones areassociated with triggering activity in osteoblastor osteoclastcells, resulting in either reduced bone formation or increased bone destruction: Thyroxine: Hyperthyroidism(theoverproduction of thyroid hormone) increases the activity of osteoclasts, speeding up the rate at which bone cells are destroyed. This occurs when the level of thyroxine in the body is elevated for a long period, or when thyroid-stimulating hormone(TSH) levels remain low for a long period. Estrogen: Estrogen levels are strongly associated with osteoporosis in postmenopausalwomen and elderly men. Itis associated with large levels of bone reabsorption due to increased osteoclasts. Estrogen deficiency affects the number of osteoclasts both by stimulating their production and decreasing apoptosis. Testosterone: Themostimportant predictor of osteoporosis in elderly men is age-related deficiencies in testosterone. Androgens (an umbrella term for testosteroneand its precursors) both stimulate the production of osteoblasts and decreasetheir apoptosis. Androgens also regulatethe formation and survivalof osteoclastcells. Cortisol: Produced by the adrenal glands, the overproduction of cortisol can have powerfuleffects on bone density. In patients with Cushing’s syndrome, a term used to describea constellation of symptoms caused by an excess of cortisol, a dramatic reduction in bone density can be observed. In theelderly,
  • 4.
    weak correlations betweenlevels of cortisoland bone density, and changes in cortisoland bone density over time have been observed. Medications Drug-induced osteoporosis is a significant health concern as many commonly prescribed treatments can contribute to bone loss. Corticosteroids, which arewidely used in the management of many conditions, are associated with reduced bone density. They are the second most common causeof secondary osteoporosis with as many as 50% of patients experiencing an eventual fractureif taken long-term. Corticosteroids increaseosteoblastapoptosis, increasebone reabsorption and reduce bone growth factors associated with bone regeneration. Finally, steroid use also increases calcium deficiency. Antiepileptics which are used to treat seizuredisorders inducecertain enzymes that cause the body to rapidly metabolize vitamin D and estrogen. Anticonvulsants may also inhibit the absorption of calcium and increase bone loss by inhibiting the production of osteoblasts. Heparin, an anticoagulant medication used in the treatment of pulmonary conditions, is associated with loss of bone tissue, especially longer-term use at higher doses. Although the mechanisms by which this occurs is not yet fully understood, heparin is thought to stimulate osteoclast production and inhibit osteoblastproduction. Malabsorptiondisorders Gastrointestinaldisorders such as ulcerative bowel diseaseare strongly associated with secondary osteoporosis. Such disorders interferewith the absorption of nutrients essential for maintaining the balance between bone resorption and generation. Furthermore, these conditions are often treated with corticosteroids. Lifestyle factors
  • 5.
    A poor dietdeficient in nutrients such as calcium and vitamin D is a risk factor for osteoporosis. Peoplewith eating disorders such as anorexia and bulimia nervosa areparticularly at risk due to a lack of nutrient intake and hormonal changes associated with low body weight. In males and females, maintaining a low body weight increases cortisolproduction and decreases growth hormones. Females may be particularly vulnerable as low weight also inhibits the production of estrogen. An inactive lifestyle can increasethe risk of osteoporosis as weight-bearing exercise stimulates bone development and reduces calcium loss from bones. Extreme inactivity such as bed rest can causeextreme bone loss, especially in the firstmonths. Excessivesmoking and alcohol consumption also increase the risk of bone loss and fractureby impacting on hormonalsystems associated with bone production. The risk is increased if they occur in tandem with poor diet and inactivity. Pathophysiology Osteoporosis is a classic example of a multifactorial diseasewith a complex interplay of genetic, intrinsic, exogenous, and life style factors contributing to an individual's risk of the disease. Traditional pathophysiologic models frequently emphasized endocrine mechanisms, e.g. estrogen deficiency and secondary hyperparathyroidism in elderly due to estrogen deficiency, reduced dietary intake, and widely prevalent vitamin D deficiency, as the key determinants of postmenopausal osteoporosis .
  • 6.
    Clinical manifestation Usually, thereare no symptoms of osteoporosis. Thatis why it is sometimes called a silent disease. However, you should watch out for the following things:  Loss of height (getting shorter by an inch or more).  Change in posture(stooping or bending forward).  Shortness of breath (smaller lung capacity due to compressed disks).  Bone fractures.  Pain in the lower back. Signs and symptoms of early-stage osteoporosis Early, detectable signs of bone loss are rare. Often people don’t know they have weak bones until they’vebroken their hip, wrist, or someother bone. However, somesigns and symptoms can point toward potential bone loss, such as:
  • 7.
     Receding gums.Your gums can recede if your jaw is losing bone. Ask your dentist to screen for bone loss in the jaw.  Weaker gripstrength. postmenopausalwomen and overall bone mineral density, researchers found that low handgrip strength was linked to low bone mineral density. In addition, lower grip strength can increase your risk for falls.  Weak and brittle fingernails. Nailstrength can signalbone health. But you should also take other factors into consideration that may affect your nails, such as exposureto very hot or cold temperatures, regular use of nail polish remover or acrylic nails, or submersion in water for long periods of time. Other than changes in bone density, osteoporosis doesn’tusually causea lot of initial symptoms. Your best bet for detecting it in the early stages is to talk with your doctor or healthcare professional, especially if you have a family history of osteoporosis. Signs and symptoms of later-stage osteoporosis Once bone mass has deteriorated further, you may startto experience more obvious symptoms, such as:  Loss of height. Compression fracturein the spine can causeyou to become shorter. This is one of the mostnoticeable symptoms of osteoporosis.  Fracture froma fall. A fractureone of the mostcommon signs of fragile bones. Fractures can occur with a fall or from minor movement such as stepping off a curb. Some osteoporosis fractures can even be triggered by a strong sneezeor cough.  Back or neck pain. Osteoporosis can causecompression fractures of the spine. These fractures can be very painful becausethe collapsed vertebrae may pinch the nerves that radiate out from the spinal cord. The pain symptoms can rangefrom minor tenderness to debilitating pain.
  • 8.
     Stoopedposture orfracture. The compression of the vertebrae may also causea slight curving of the upper back. A stooped back is known as kyphosis, which can causeback and neck pain. Itcan even affect breathing due to the extra pressureon the airway and limited expansion of your lungs. Diagnostic evaluations BONE DENSITY -A bonemineraldensitytest, sometimesjustcalled a bonedensity test, examines segmentsof yourbone through X-rays to detectosteoporosis. DEXA SCAN -Oneof themostcommonosteoporosistests is dualX- ray absorptiometry -- alsocalled DXA or DEXA. Itmeasurespeople’s spine, hip, or total-bodybonedensity to help gaugetheir risk of fractures. BONE DENSITOMETRY- is a testlike an X-ray thatquicklyand accurately measuresthedensity of bone Laboratory studies. serum calcium, serum phosphate, serum alkaline phosphatase, urine calcium excretion, hematocrit, erythrocytesedimentation rate, x-ray studies are used to exclude other possibledisorders thatcontribute to bone loss. MANAGEMENT  Diet. A diet rich in calcium and vitamin D throughout life, with an increased calcium intake during adolescence, young adulthood, and the middle years, protects against skeletal demineralization.
  • 9.
     Exercise. Regularweight-bearing exercise promotes bone formation, such as a 20-30-minute aerobic exercise, 3x a week, is recommended.  Fracture management. Osteoporotic compression fractures of the vertebrae are managed conservatively, pharmacologic and dietary treatments are aimed at increasing vertebral bone density, and for patients who do not respond to first-line approaches are treated with percutaneous vertebroplasty or kyphoplasty (injection of polymethylmethacrylate bone cement into the fractured vertebra, followed by inflation of a pressurized balloon to restore the shape of the affected vertebra). Pharmacologic Therapy The first-line medications and other medications used to treat and prevent osteoporosis include:  Calcium supplements with vitamin D. To ensure adequate calcium intake, a calcium supplement with vitamin D may be prescribed and taken with meals or with a beverage high in vitamin C to promote absorption, but these supplements should not be taken at the same day as bisphosphonates.  Bisphosphonates. Bisphosphonates that include daily or weekly oral preparations of alendronate or risedronate, monthly oral preparations of ibandronate, or yearly intravenous infusions of zoledronic acid increase bone mass and decrease bone loss by inhibiting osteoclast function.  Calcitonin. Calcitonin directly inhibits osteoclasts thereby reducing bone loss adD increasing bone mineral density, and is administered by nasal spray or by subcutaneous or intramuscular injection.  Selective estrogen receptor modulators (SERMs). SERMs such as raloxifene, reduce the risk of osteporosis by preserving bone mineral density without estrogenic effects on the uterus.  Teriparatide is a subcutaneously administered anabolic agent that is administered once daily, and as a recombinant PTH, it stimulates osteoblasts to build bone matrix and facilitates overall calcium absorption.
  • 10.
    Surgical Management Fractures ofthe hip that occur as a consequence of osteoporosis are managed surgically through:  Joint replacement. Joint replacement is a surgery to replace all or part of a joint with a man-made joint called prosthesis.  Closed or open reduction with internal fixation. Open reduction, internal fixation involves the implementation of implants to guide the healing process of a bone, as well as the open reduction, or setting, of the bone, while closed reduction is a procedure to set or reduce a broken bone without surgery. Discharge and Home Care Guidelines At the completion of the home care instruction, the patient or caregiver will be able to implement the following:  Diet. Identify calciumand vitaminD rich foods and discuss calcium supplements.  Exercise. Engagein weight-bearing exercise daily.  Lifestyle. Modify lifestylechoices: avoid smoking, alcohol, caffeine, and carbonated beverages.  Posture. Demonstrategood body mechanics.  Early detection. Participatein screening for osteoporosis.