Osteoporosis

MEDICAL APPLICATION
 DEFINITION
Osteoporosis – a chronic, progressive disease characterized by low bone mass, impaired bone quality, decreased bone strength, and
enhanced risk of fractures

 EPIDEMIOLOGY
 the most common metabolic bone disease
Race: non-Hispanic white women and Asian women are at higher risk
Age: (F > 50 y.o.) (M > 70 y.o.)
Gender: F > M (especially postmenopausal women who are estrogen deficient)

 ETIOLOGY
PRIMARY OSTEOPOROSIS SECONDARY OSTEOPOROSIS
 mild but prolonged negative calcium balance  prolonged therapy with corticosteroids, heparin,
 declining gonadal and adrenal function anticonvulsants, and other medications
 relative or progressive estrogen deficiency  alcoholism, malnutrition, malabsorption, or lactose intolerance
 sedentary lifestyle  endocrine disorders

Primary osteoporosis has no known definite cause, but Secondary osteoporosis is caused by prolonged use of medications or
there are many contributing factors associated with the secondary to another disease or condition which inhibits the absorption of
disorder. These include prolonged negative calcium calcium or impedes the body's ability to produce bone.
balance, impaired gonadal and adrenal function,
oestrogen deficiency, or sedentary lifestyle.

RISK FACTORS
 Women: estrogen status, heredity, and ethnicity
 Men: alcoholism, cigarette smoking, steroid therapy, and hypogonadism or androgen withdrawal therapy for prostate cancer

 BMS
SKELETAL SYSTEM
TYPES OF BONE: There are 4 types of bone based on their shape.
 Long Bone – longer than they are wide, enhances function in movement in appendages; arms & legs
 Short Bone – as wide as they are long, help transfer force between long bones; wrist & ankle
 Flat Bone – thin & flat, provides strong barrier around soft organs such as the brain & heart; skull, ribs, scapulae, sternum
 Irregular Bone – have specialized functions (provides protection while allowing bending & flexing); spine
STRUCTURE OF A LONG BONE
A long bone consists of a central shaft called DIAPHYSIS and 2 ends, each called EPIPHYSIS. The epiphysis is where the bone
articulates with other bones & it is covered with a thin layer of articular cartilage.
In this picture, we could see the difference between a young bone and an adult bone. A long bone that is still growing has an
epiphyseal plate which is composed of cartilage. This is the part where the bone grows in length. This is why it is sometimes called as
the growth plate. When the bone growth stops, the cartilage of each epiphyseal plate is replaced by bone and becomes an
epiphyseal line.
Bones contain cavities, such as the large medullary cavity in the diaphysis and the smaller cavities in the epiphysis. These spaces are
filled with soft tissue called MARROW. YELLOW MARROW consists mostly of adipose tissue. RED MARROW consists of blood-forming
cells and is the only site of blood formation in adults. Children’s bones have proportionately more red marrow than do adult bones
because, as a person ages, red marrow is mostly replaced by yellow marrow.
Most of the outer surface of bone is covered by dense connective tissue called PERIOSTEUM. Peri = around. The surface of the
medullary cavity is lined with a thinner connective tissue membrane called ENDOSTEUM. Endo = inside.
BONE HISTOLOGY
TYPES OF CELLS PRESENT IN BONE TISSUE: (from Tortora)
1. Osteoprogenitor cells - unspecialized bone stem cells derived from mesenchyme, the tissue from which almost all connective
tissues are formed. They are the only bone cells to undergo cell division; the resulting cells develop into osteoblasts.
Osteoprogenitor cells are found along the inner portion of the periosteum, in the endosteum, and in the canals within bone
that contain blood vessels.
2. Osteoblasts - bone-building cells. They synthesize and secrete collagen fibers and other organic components needed to build
the extracellular matrix of bone tissue, and they initiate calcification. As osteoblasts surround themselves with extracellular
matrix, they become trapped in their secretions and become osteocytes.
3. Osteocytes - mature bone cells, are the main cells in bone tissue and maintain its daily metabolism, such as the exchange of
nutrients and wastes with the blood. Like osteoblasts, osteocytes do not undergo cell division.
4. Osteoclasts - huge cells derived from the fusion of as many as 50 monocytes (a type of white blood cell) and are concentrated in
the endosteum. On the side of the cell that faces the bone surface, the osteoclast’s plasma membrane is deeply folded into a
ruffled border. Here the cell releases powerful lysosomal enzymes and acids that digest the protein and mineral components of

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 the underlying extracellular bone matrix. This breakdown of bone extracellular matrix, termed bone resorption is part of the
normal development, maintenance, and repair of bone.

SPONGY BONE & COMPACT BONE:

 COMPACT BONE OR CORTICAL BONE – forms the perimeter of the diaphysis of a long bone and the thinner surfaces of all other
bones. It has more matrix and is denser. It has a predictable pattern of repeating units called OSTEONS. Each osteon consists of
concentric rings of lamellae surrounding a central canal called HAVERSIAN CANAL. Blood vessels that run parallel to the long
axis of the bone are located in the central canal. Osteocytes are located in lacunae between the lamellae of each osteon.
Osteocytes are connected to one another by cell processes in canaliculi. That canaliculi give the osteon the appearance of
having tiny cracks within the lamellae.
 SPONGY BONE – very porous, located in the epiphyses of long bones, lines the medullary cavity of long bones. It has less bone
matrix and more open space than compact bones. It consists of delicate interconnecting rods or plates of bone called
TRABECULAE (resemble the beams or scaffolding of a building). Like scaffolding, the trabeculae add strength to a bone without
the added weight that would be present if the bone were solid mineralized matrix. The spaces between the trabeculae are filled
with marrow.
BONE FORMATION/OSSIFICATION
[from Seeleys]
Ossification is the formation of bone by osteoblasts
Intramembranous Ossification – bone formation that occurs within connective tissue membranes; occurs in a 12-week-old fetus at
ossification centers in the flat bones of the skull
Endochondral Ossification – bone formation that occurs inside hyaline cartilage; occurs at bones at the base of the skull & most of
the remaining bones.
Primary Ossification Center – center part of the diaphysis where bone first begins to appear
Secondary Ossification Center – forms in the epiphysis
[from Tortora]
The process by which bone forms is called ossification or osteogenesis. Bone formation occurs in 4 principal situations: (1) the initial
formation of bones in an embryo and fetus, (2) the growth of bones during infancy, childhood, and adolescence until their adult sizes
are reached, (3) the remodeling of bone (replacement of old bone by new bone tissue throughout life), and (4) the repair of fracture
(breaks in bones) throughout life.
[photo] The activity of the epiphyseal plate is the only way that the diaphysis can increase in length. As a bone grows, chondrocytes
proliferate on the epiphyseal side of the plate. New chondrocytes replace older ones, which are destroyed by calcification. Thus, the
cartilage is replaced by bone on the diaphyseal side of the plate. In this way the thickness of the epiphyseal plate remains relatively
constant, but the bone on the diaphyseal side increases in length.

 PATHO
[ninja nerd]

EFFECTS OF PTH IN BONE TISSUE

Causes osteoclastic activity while inhibiting osteoblastic activity

Result: Blood calcium levels are increased. Blood phosphate levels are
increased.

There are 2 different types of cells that are very important in regulating bone
remodeling processes:

 Osteoclast - bone resorption (breaks down bone and resorbs out/pulls out
the calcium, phosphates, breakdown collagen out of the bone into the
blood plasma)
 Osteoblast - bone deposition (takes calcium, phosphates, amino acids from the blood and deposits it into the bone tissue)

PTH is stimulated by low blood calcium levels. So its goal is to INCREASE blood calcium levels. So what it does is it stimulates the Osteoclasts.

1. There are receptors for PTH on the osteoblasts. When PTH binds to these receptors, it stimulates the osteoblasts to secrete a specific
chemical, called RANK ligand (Receptor Activator of Nuclear factor Kappa-B ligand).

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 2. There are RANK receptors on the osteoclasts. When RANK ligands bind to the RANK receptors, it triggers the osteoclast to be very active.
When the osteoclast becomes active, it will start to secrete chemicals like Cathepsin K (a protein digesting enzyme), acid phosphotases,
etc. These chemicals will start breaking down some of the chemicals within the bone. It will start to resorb and breaking away the bone.
Lots of calcium and phosphate are accumulated from this breakdown. These will go to the blood.
3. Blood calcium level is increased.

[osmosis]
BONE REMODELING STEPS
 Bone Resorption - osteoclasts break down bone
 Bone Formation - osteoblasts form new bone

Bone Remodeling is highly dependent on blood calcium levels which are kept in a normal range a balance between PTH, calcitonin, &
vitamin D
 PTH is produced by the parathyroid glands in response to low blood calcium level. It increases bone resorption to release calcium
into the bloodstream
 Calcitonin is produced by the Thyroid gland in response to high blood calcium level. It opposes the action of PTH. Therefore,
promoting bone formation and decreasing bone resorption.
 Vitamin D promotes calcium absorption in the GUT. It increases blood calcium level - promoting bone formation and decreasing
bone resorption.

The balance between these regulatory factors results in a peak bone mass, usually by age 20-29. This occurs earlier in F > M
FACTORS THAT DETERMINE THE PEAK BONE MASS:
 genetics (African people have greater bone mass)
 nutrition (adequate vitamin D intake increases peak bone mass)
 strength training (increases peak bone mass)
 hormones (estrogen & androgen inhibit bone resorption).

When osteoclasts break down bone faster than the osteoblasts can rebuild it, it results to a decreased bone mass and eventually
OSTEOPOROSIS.
WITH OSTEOPOROSIS, ABNORMAL FINDINGS include:
 fewer trabeculae in the spongy bone
 thinning of the cortical bone,
 widening of the haversian canals
These bone changes increase the risk of fracture (Fragility/Pathologic Fracture). Some bones like the vertebrae, scapula, & ribs consist
mainly of spongy bone, so they are in great risk of fragility fractures.

FACTORS THAT ACCELERATE BONE MASS LOSS AND INCREASE RISK OF OSTEOPOROSIS:
 low estrogen levels (after menopause)
 low blood calcium level
 alcohol consumption
 driving
 drugs (glucocorticoids which decreases calcium absorption from the gut through antagonism of vitamin D, heparin, & L-thyroxine)
 physical inactivity (bone deposition decreases due to a lack of stress while resorption increases)
 diseases (Turner syndorme, Cushing syndrome, DM)

2 TYPES OF CELLS IMPORTANT IN REGULATING BONE REMODELING PROCESSES:

Osteoclast - bone resorption
Osteoblast - bone deposition

PTH has effects in regulating blood calcium level.

Stimulated by: low blood calcium levels
Goal: increase blood calcium. How?
1. PTH binds to PTH receptors on osteoblasts
2. Osteoblasts secrete a chemical: RANK ligand
3. RANK ligand binds to RANK receptors on osteoclasts
4. Osteoclasts become very active and secrete chemicals that will resorb and break down the bone
5. Calcium and phosphate are accumulated from this breakdown and will go to the blood.

In osteoporosis, osteoclasts break down bone faster than the osteoblasts can rebuild it --> decreased bone mass

 S/SX
Most Common Presenting Features Of Osteoporosis:
1. Loss of height

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 2. Postural changes
 lax abdominal musculature
 protuberant abdomen
 forward head
 kyphosis
 dowager’s hump
 loss of lumbar lordosis
 posterior pelvic tilt
 knee hyperextension
 shoulder internal rotation
 scapular forward rotation
 palms facing backward
3. Back pain
4. Fracture
most common fracture sites (in order): 1) vertebral bodies, 2) hip, 3) ribs, 4) radius, and 5) femur
 A first fracture is a risk factor for a second fracture, which, in turn, increases the risk of death
 Vertebral compression fractures (VCFs) are the most common osteoporosis-related spinal fractures presenting with clinical
symptoms of back pain, posture change, loss of height, functional impairment, disability, and diminished quality of life. These
can occur without injury or fall when the bone becomes so porous or weak and it begins to compress.
 Pain associated with VCFs is usually severe and localized to the site of fracture, typically midthoracic, lower thoracic, and
lumbar spine.
 Tenderness to palpation over the fracture is common in both symptomatic and otherwise asymptomatic cases.
 Pain may radiate to the abdomen or flanks and is aggravated by prolonged sitting or standing, bending, or performing a Valsalva
maneuver. Side lying with hips and knees flexed may alleviate the pain.
 Muscular pain and spasm can occur in the lower back paravertebral muscles, as can burning pain in the midthoracic region
lateral to the spine because of excess stretch placed on the rhomboid muscles from the compensatory forward rotation of the
scapulae

 DIAGNOSTIC TOOLS & IMAGING STUDIES

 Bone Mineral Density Testing. A BMD test is the simplest way to assess
for osteoporosis. Without this test, most people are unaware they have
osteoporosis until a fracture occurs, although some fractures can be
painless or the pain may be mistaken for arthritis, delaying diagnosis.
BMD is a measurement of the mineral content of bone in grams per
square centimeter (g/cm2) for the area of the body that has been
scanned.

 Dual X-ray Absorptiometry (DXA). DXA is an enhanced form of x-ray technology that is used to measure bone loss. DXA is today's
established standard for measuring bone mineral density (BMD).
 Peripheral Computed Tomography (Pct). pCT is a type of quantitative computed tomography (QCT), used for making measurements
of the bone mineral density (BMD) in a peripheral part of the body, such as the forearms or legs

 D/DX
R/I R/O
Low bone density BMD Testing
OSTEOPENIA Pain 2° fracture Osteopenia: -1.0 to -2.5
Osteoporosis: -2.5 or lower
Pain in bones & joints Softening of the bones caused by Vitamin D deficiency
OSTEOMALACIA Risk of fractures Osteomalacia: ratio of bone mineral to bone matrix is low
Osteoporosis: ratio of bone mineral to bone matrix is normal
Pain in bones & joints Paget's Disease: localized, affects one or few bones
PAGET’S DISEASE
Osteoporosis: affects all bones
PRIMARY Bone weakness Primary hyperparathyroidism: parathyroid glands become
HYPERPARATHYROIDIS Risk of fractures overactive 2° a benign tumor (adenoma)
M

https://www.msdmanuals.com/professional/multimedia/table/v7821336

Paget's disease of bone is a chronic disease of the skeleton. In healthy bone, a process called remodeling removes old pieces of bone and replaces
them with new, fresh bone. Paget's disease causes this process to shift out of balance, resulting in new bone that is abnormally shaped, weak, and
brittle.

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Primary hyperparathyroidism is a condition in which one or more of the parathyroid glands makes too much PTH. This can lead to the loss of bone
tissue. This condition is more common in women than in men. A job of PTH is to keep blood calcium levels from going too low.
 COURSE & PROGNOSIS
[Medscape]
The prognosis for osteoporosis is good if bone loss is detected in the early phases and proper intervention is undertaken. Patients can
increase bone mineral density (BMD) and decrease fracture risk with exercise, a diet rich in calcium, and the appropriate anti-
osteoporotic medication.

[Goodman]
Osteoporosis, once thought to be a natural part of aging among women, is no longer considered age- or gender-dependent. Although
osteoporosis is one of the greatest deterrents to women’s health and accounts for significant morbidity and mortality, it is largely
preventable because of the remarkable progress in the scientific understanding of its causes, diagnosis, and treatment. Even so, at the
present time, 24% of women over the age of 50 years die from complications (e.g., pneumonia, infections, and fracture emboli) in the
first year after an osteoporotic-associated hip fracture.

Osteoporosis is not curable, but intervention can stop the progression of bone loss and prevent further morbidity . Secondary
osteoporosis intervention begins with treatment of the underlying cause. Management of primary and secondary osteoporosis in the
adult should include lifestyle measures to reduce bone loss such as a high calcium intake, smoking cessation, reducing alcohol intake, and
physical activity and exercise. Besides eliminating factors, such as chronic alcohol abuse and cigarette smoking, a key to prevention is
developing as great a peak bone mass as possible through adequate calcium intake and regular exercise. Calcium is required for bone
mineralization and also suppresses bone turnover, slowing the remodeling process. Fall prevention is an important intervention for
anyone with low bone mass and high risk factors.

 SURGICAL INTERVENTIONS
VERTEBRAL AUGMENTATION, which includes vertebroplasty and kyphoplasty, are similar spinal procedures in which bone cement is
injected through a small hole in the skin into a fractured vertebra to try to relieve back pain caused by a vertebral compression fractures.
 For a Vertebroplasty, physicians use image guidance, typically fluoroscopy, to inject a cement mixture into the fractured bone
through a hollow needle.
 During Kyphoplasty, a balloon is first inserted into the fractured bone through the hollow needle to create a cavity or space.

 PHARMACOLOGICAL INTERVENTIONS
 Selective Estrogen Receptor Modulators (SERMS) – maximize the beneficial effect of estrogen on bone and minimize or antagonize
the deleterious effects on the breast and endometrium
Raloxifene (Evista) is the only SERM approved by the Food and Drug Administration (FDA) for the treatment and prevention of
osteoporosis. It is the first compound with selective estrogen agonist activity in bone but with estrogen antagonist activity or no
activity in reproductive tissues and breast.
 Antiresorptive Agents – help prevent bone loss.
Example: bisphosphonate. Bisphosphonates are a family of drugs that inhibit bone resorption and actually reverse bone loss. These
drugs are currently being used in various bone conditions involving increased levels of bone resorption
 Calcitonin – not approved for prevention, but approved for treatment because it acts directly on osteoclasts, suppressing activity

SERMs and bisphosphonates have been shown to increase BMD and decrease fracture risk.

PT APPLICATION
 STANDARIZED ASSESSMENT & EVALUATIVE TOOLS
 Pain Ax
 Postural Ax
 Bal/Tol
 ROM
 MMT

 GENERAL FUNCTIONAL PROBLEM LIST

1. Back pain
2. Poor posture
3. Impaired bal/tol

 PT GOALS
1. Relieve pain
2. Improve posture
3. Improve bal/tl

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To improve quality of life of patients
To prevent falls which decreases risk of fractures
To increase bone mineral density though mechanical loading

 APPROPRIATE PHYSICAL AGENTS AND MODALITIES WITH PRECAUTIONS AND CONTRAINDICATIONS

 APPROPRIATE MANUAL THERAPY AND EXERCISES WITH PRECAUTIONS AND CONTRAINDICATIONS

 Axial or Mechanical Loading - increases osteogenic activity which increases Bone Mineral Density
 Non-straining exercise – walking for 45mins, 30 times a week or 30mins daily (for patients with advanced osteoporosis
 Aquatic exercises – for patients who are unable to perform antigravity exercises doe to pain or weakness
 Spine Extension exercises – to reduce lumbar lordosis
 Progressive resistive back-strengthening exercise – improves back strength
 Isometric Abdominal muscle strengthening exercise – to address weakness of abdominal muscles which adds to the problem posture
 Fitness programs such as swimming or short periods of stationary biking – to improve cardiovascular fitness without straining the
osteoporotic frame
 Spine Proprioceptive Extension Exercise Dynamic (SPEED) Program – reeducates back extensors and proprioceptors of the spine
 Posture Training Programs – decrease kyphosis and reduce iliocostal friction syndrome
o Application of weighted kypho-orthosis for 20mins two to three times a day for cases of severe kyphosis
 Rigid Thoracolumbar orthosis – to promote extension of the spine

[Physiopedia]
 Exercises such as walking help to maintain or improve bone density in an osteoporotic population.
 Strengthening exercises, using weights or resistance bands help maintain or improve bone density at the location of the targeted muscle
attachments. Maintaining bone health is extremely important, especially in the elderly as there typically is a decline in bone mass with
age.
 Strengthening and flexibility exercises improve overall physical function and postural control (important to reduce risk for falls).
 Combined balance and progressive strength training programme produced the best results in terms of maintaining leg strength,
balance, bone mineral density and physical function compared to balance or strength training alone.
 Spinal extensor strengthening programme and a dynamic proprioceptive programme increase bone density and reduced the risk of
VCFs.
 Back extensor exercises improve muscle strength, providing a better dynamic-static posture and reduction of the kyphotic deformity.
Correction of the kyphosis also results in pain relief, increased mobility and an improvement in the quality of life.

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