Osteoporosis; Causes, Symptoms, Diagnosis, Treatment

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Osteoporosis means “porous bone.” Viewed under a microscope, healthy bone looks like a honeycomb. When osteoporosis occurs, the holes and spaces in the honeycomb are much larger than in healthy bone. Osteoporotic bones have lost density or mass and contain abnormal tissue structure. As bones become less dense, they weaken and are more likely to break. If you’re 50 or older and have broken a bone, ask your doctor or healthcare provider about a bone density test.

The components of the word ‘osteoporosis’ literally mean ‘porous bones’ – ‘osteo’ is for bones, and ‘porosis’ means porous – helpfully describing this condition that results in reduced bone density and increased fragility of the bones.

The thinning of the bones in osteoporosis, combined with the formation of weaker bone crystals, puts people at a higher risk of fractures.


Although osteoporosis itself does not directly increase the risk of falls, people who have osteoporosis have a higher risk of breaking a bone if they fall, with common sites of fracture including the hip, spinal vertebrae, and wrist. Osteoporosis results in a loss of bone mineral density and a higher risk of fractures.

Osteoporosis can affect people of any gender, but women make up the majority of cases, and over 40 million people in the US have osteoporosis or are at high risk because of low bone mass, according to the National Institutes othe f Health.

During their lifetime, half of all postmenopausal women will have an osteoporosis-related fracture, says the US Preventive Services Task Force.

  • One estimate put the financial cost of osteoporosis across 27 European countries at 37 billion euros in 2010, in terms of the cost of bone fractures. The researchers found that, around the world, an estimated 1,000 fractures happen every hour because of osteoporosis.

Causes of osteoporosis

A number of risk factors have been identified that raise the likelihood of getting osteoporosis – some of these are modifiable (something you can do something about) while others cannot be avoided.

Non-modifiable risk factors for osteoporosis include

  • Each decade beyond the fourth decade is a 1.5-fold risk
  • Reduction in the absorption of calcium
  • The rise in parathyroid hormone levels
  • Decline in calcitonin
  • White, Asian, Latino, and black (in order of risk potential)
  • Women more than men
  • Familial prevalence
  • High concordance in monozygotic twins
  • Low calcium intake
  • High alcohol
  • High caffeine
  • High sodium
  • High animal protein
  • Cigarette use
  • Low physical activity
  • Menopausal age
  • Obesity
  • Exercise-induced amenorrhea
  • Ethnicity – the risk is higher in white people and Asians
  • Bone structure – the risk is higher in those with small bone structure
  • Genetics – risk is higher if there is osteoporosis in the family, especially if a parent or sibling has the disease, particularly if a parent has incurred a hip fracture
  • Fracture history – risk is higher in people with a previous fracture during a low-level injury, especially if this occurred after the age of 50.

Drug That Causes osteoporosis

  • Thyroid replacement therapy
  • Glucocorticoid drugs
  • Anticoagulants
  • Chronic lithium therapy
  • Chemotherapy (breast cancer or lymphoma)
  • Gonadotropin-releasing hormone
  • Anticonvulsants
  • Chronic phosphate binding antacid use
  • Extended tetracycline use
  • Diuretics producing calciuria
  • Phenothiazine derivatives
  • Cyclosporin A

Secondary causes of osteoporosis (, )

Lifestyle changesGenetic diseasesEndocrine disordersOther
Vitamin D insufficiencyCystic fibrosisCentral obesityAIDS/HIV
High salt intakeGlycogen storage diseasesCushing’s syndromeAmyloidosis
Smoking (active or passive)Menkes steely hair syndromeDiabetes mellitus (types 1 and 2)Chronic obstructive lung disease
Alcohol abuseOsteogenesis imperfectaHyperparathyroidismCongestive heart failure
ImmobilizatıonRiley–Day syndromeThyrotoxicosisChronic metabolic acidosis
Excessive thinnessEhler DanlosHypogonadal states:Depression
Frequent fallingHemochromatosisAndrogen insensitivityEnd-stage renal disease
Low calcium intakeMarfan syndromeAthletic amenorrheaHypercalciuria
Inadequate physical activityParental history of hip fracturePremature menopause (<40 years)Post-transplant bone disease
Excess vitamin AGaucher’s diseaseHyperprolactinemiaIdiopathic scoliosis
HypophosphatasiaAnorexia nervosaWeight loss
PorphyriaTurner’s and Klinefelter’s syndromes
Gastrointestinal disordersHematological disordersNeurological and musculoskeletal factorsRheumatologic and autoimmune diseases
Celiac diseaseHemophiliaEpilepsyAnkylosing spondylitis
Gastric bypassLeukemia and lymphomasMultiple sclerosisSystemic lupus
Gastrointestinal surgerySickle cell diseaseMuscular dystrophyRheumatoid arthritis
MalabsorptionMultiple myelomaParkinson’s diseaseSystemic lupus
Inflammatory bowel diseaseMonoclonal gammopathiesSpinal cord injuryOther rheumatic and autoimmune diseases
Pancreatic diseaseSystemic mastocytosisStroke
Primary biliary cirrhosisThalassemiaProximal myopathy
Endocrinological AbnormalitiesGlucocorticoid excess, hyperthyroidism, hypogonadism (androgen insensitivity, Turner’s and Klinefelter’s Syndrome, hyperprolactinemia, premature menopause), anorexia, athlete triad, vitamin D deficiency, hyperparathyroidism, Diabetes Mellitus (Types 1 and 2)
Cardiovascular, Renal, Pulmonary and Miscellaneous DisordersChronic kidney disease, post-transplant bone disease, congestive heart failure, chronic obstructive lung disease, AIDS/HIV
Connective Tissue DisordersOsteogenesis Imperfecta, Ehlers-Danlos syndrome, Marfan Syndrome, ankylosing spondylitis,
Gastrointestinal DiseasesCeliac sprue, Inflammatory bowel disease, post-gastrectomy, primary biliary cirrhosis, bariatric surgery
Hematological DisordersMultiple myeloma, mastocytosis, leukemia. Hemophilia, sickle cell disease, leukemia, lymphoma, Thalassemia
Other Genetic DisordersHomocystinuria, Cystic fibrosis, Hemochromatosis, Hypophosphatasia
Rheumatological DisordersAnkylosing spondylitis, rheumatoid arthritis
MedicationsAromatase inhibitors, heparin (long-term), anticonvulsants, methotrexate, Cytoxan, gonadotropin-releasing hormone (GnRH) agonists and antagonists, tamoxifen (in premenopausal women), excess thyroid hormone, lithium, cyclosporine A, tacrolimus, glucocorticoids, thiazolidinediones, depo-medroxyprogesterone (premenopausal women) proton-pump inhibitors, selective serotonin reuptake inhibitors (SSRIs), tenofovir

Risk factors for osteoporosis

  • Reduced sex hormones, particularly in women (less estrogen after the menopause, for example)
  • Anorexia nervosa and bulimia (eating disorders), and orthorexia
  • Tobacco smoking
  • Excessive alcohol intake
  • Reduced calcium, magnesium and vitamin D status (caused by low dietary intake, malabsorption, and the use of some medications)
  • Inactivity or immobility (weight-bearing exercise that places a degree of stress on the bones is needed for bone growth).

Low body mass index (≤19 kg/m2)
Previous fragility fracture, particularly of the hip, wrist and spine including morphometric vertebral fracture
Secondary causes of osteoporosis including:
Parental history of hip fracture
Current glucocorticoid treatment (any dose, by mouth for three months or more)
Current smoking Alcohol intake of three or more units daily
Rheumatoid arthritis
Untreated hypogonadism in men and women
Prolonged immobility
Organ transplantation
Type I diabetes
Gastrointestinal disease
Chronic liver disease
Chronic obstructive pulmonary disease
Frequent falling

Other factors that increase the risk of osteoporosis include diseases or drugs that cause changes in hormone levels and drugs that reduce bone mass. Diseases that affect hormone levels include hyperthyroidism, hyperparathyroidism and Cushing’s disease.

People who are transgender and who undergo surgery that affects hormone levels, or who take hormones for long periods of time may also face a higher risk of osteoporosis.10 Some autoimmune diseases, such as Rheumatoid arthritis and ankylosing spondylitis, are also associated with an increased risk of osteoporosis.

Medications that increase the risk of osteoporosis include

  • Glucocorticoids and corticosteroids, including prednisone (Deltasone, Orasone, for example) and prednisolone (Prelone) – glucocorticoid-induced osteoporosis is the most common type of drug-induced osteoporosis
  • Excess thyroid hormone replacement
  • Anticoagulants and blood-thinners (including heparin and warfarin)
  • Protein-pump inhibitors and other antacids that adversely affect the mineral status
  • Some antidepressant medications
  • Some vitamin A (retinoid) medications
  • Thiazolidinediones (used to treat type 2 diabetes), which decrease bone formation
  • Some immunosuppressant agents, such as cyclosporine, which increase both bone resorption and formation
  • Aromatase inhibitors and other treatments that deplete sex hormones, such as anastrozole (Arimidex)
  • Some chemotherapeutic agents, including letrozole (Femara), which is used against breast cancer, and leuprorelin (Lupron) for prostate cancer (and other conditions).

Recent developments on causes of osteoporosis


Risk factors

A number of factors can increase the likelihood that you’ll develop osteoporosis — including your age, race, lifestyle choices, and medical conditions and treatments.

  • Your sex – Women are much more likely to develop osteoporosis than are men.
  • Age. The older you get, the greater your risk of osteoporosis.
  • Race. You’re at greatest risk of osteoporosis if you’re white or of Asian descent.
  • Family history. Having a parent or sibling with osteoporosis puts you at greater risk, especially if your mother or father experienced a hip fracture.
  • Body frame size. Men and women who have small body frames tend to have a higher risk because they may have less bone mass to draw from as they age.
  • A 50-year-old current smoker with a body mass index (BMI) less than 21 kg/m 2, daily alcohol use, and parental fracture history
  • A 55-year-old woman with a parental fracture history
  • A 60-year-old woman with a BMI of less than 21 kg/m 2 and daily alcohol use
  • A 60-year-old current smoker with daily alcohol use

Assessment of fracture risk

A thorough history should be obtained to screen for and identify the presence of known risk factors for osteoporosis and osteoporotic fracture. Specifically, history should focus on the following :

  • Age (>50 years), sex (female), and race (white or Asian) the US Preventive Services Task Force (USPSTF) recommendations include screening for osteoporosis in women aged 65 years or older and in younger women with a fracture risk that is the same or greater than that of a 65-year-old white woman who has no additional risk factors
  • The family history of osteoporosis, particularly the maternal history of fractures
  • Reproductive factors, especially regarding early menopause and estrogen replacement therapy: postmenopausal women are at high risk, as are women who have undergone hysterectomy and oophorectomy
  • Hypogonadal states: men with hypogonadism secondary to any genetic or other conditions are at higher risk the USPSTF notes that there is insufficient current evidence to assess the risk versus benefit of screening for osteoporosis in men
  • Smoking: smokers are at higher risk
  • Alcohol consumption
  • Low levels of physical activity: immobility increases the risk of spinal cord injury and stroke cause physical impairment and are common causes of immobility
  • Strenuous exercise that results in amenorrhea (such as that which occurs in marathon runners)
  • Calcium and vitamin D intake
  • History of low-trauma “fragility” fracture in patients aged 40 years or older: a fragility fracture is defined as a fracture due to trauma that would not normally cause fracture (a force equal to or less than that resulting from a fall from standing height)
  • Signs of vertebral fracture (see below)
  • Coexisting medical conditions associated with bone loss
  • Medications associated with bone loss
  • Risk factors for falls in older patients: these include poor balance, orthostatic hypotension, weakness of the lower extremity muscles and deconditioning, use of medications with sedative effects, poor vision or hearing, and cognitive impairment

Although the USPSTF did not find any studies that assessed effects of the use of risk prediction instruments on patient outcomes, either alone or in combination with bone measurement tests, there are many validated instruments for predicting the risk for low bone mineral density (BMD) in postmenopausal women; few of these, however, have been validated for use in men.

White women between the ages of 50 and 64 years with ≥10-year fracture risks based on specific risk factors include the following persons.

Differentiating fracture types by history

  • Patients with acute insufficiency fractures may report a history of minimal or no trauma resulting in pain. They may report a fall from a standing or sitting position. Patients with compression fractures resulting in thoracic kyphosis may report iliocostal friction with an associated abdominal protrusion, decreased tolerance for oral intake, and breathing difficulties. Patients with hip, pelvic, or sacral fractures may report pain that is worsened with weight-bearing.
  • Patients who have sustained a vertebral compression fracture may note progressive kyphosis with loss of height. They may also present with an episode of acute back pain after bending, lifting, or coughing. It should be noted, however, that two-thirds of vertebral fractures are asymptomatic.

With respect to those vertebral fractures that are painful, typical subjective information may include the following

  • The episode of acute pain may follow a fall or minor trauma
  • Pain is localized to a specific, identifiable, vertebral level in the midthoracic to lower thoracic or upper lumbar spine
  • The pain is described variably as sharp, nagging, or dull; movement may exacerbate pain; in some cases, pain radiates to the abdomen
  • Pain is often accompanied by paravertebral muscle spasms exacerbated by activity and decreased by lying supine
  • Patients often remain motionless in bed because of fear of causing an exacerbation of pain
  • Acute pain usually resolves after 4-6 weeks; in the setting of multiple fractures with severe kyphosis, the pain may become chronic

Patients who have sustained a hip fracture may experience the following:

  • Pain in the groin, posterior buttock, anterior thigh, medial thigh, and/or medial knee during weight-bearing or attempted weight-bearing of the involved extremity
  • Diminished hip range of motion (ROM), particularly internal rotation and flexion
  • External rotation of the involved hip while in the resting position

Symptoms of osteoporosis

Osteoporosis generally does not become clinically apparent until a fracture occurs. Two-thirds of vertebral fractures are painless. Typical findings in patients with painful vertebral fractures may include the following:

  • The episode of acute pain may follow a fall or minor trauma
  • Pain is localized to a specific, identifiable, vertebral level in the midthoracic to lower thoracic or upper lumbar spine
  • The pain is described variably as sharp, nagging, or dull; movement may exacerbate pain; in some cases, pain radiates to the abdomen
  • Pain is often accompanied by paravertebral muscle spasms exacerbated by activity and decreased by lying supine
  • Patients often remain motionless in bed because of fear of causing an exacerbation of pain
  • Acute pain usually resolves after 4-6 weeks; in the setting of multiple fractures with severe kyphosis, the pain may become chronic

Patients who have sustained a hip fracture may experience the following:

  • Pain in the groin, posterior buttock, anterior thigh, medial thigh, and/or medial knee during weight-bearing or attempted weight-bearing of the involved extremity
  • Diminished hip range of motion (ROM), particularly internal rotation and flexion
  • External rotation of the involved hip while in the resting position

On physical examination, patients with vertebral compression fractures may demonstrate the following:

  • With acute vertebral fractures, point tenderness over the involved vertebra
  • Thoracic kyphosis with an exaggerated cervical lordosis (dowager hump)
  • The subsequent loss of lumbar lordosis
  • A decrease in height of 2-3 cm after each vertebral compression fracture and progressive kyphosis

Patients with hip fractures may demonstrate the following:

  • Limited ROM with end-range pain on a FABER (flexion in the abduction and external rotation) hip joint test
  • Decreased weight-bearing on the fractured side or an antalgic gait pattern

Patients with Colles fractures may have the following:

  • Pain on movement of the wrist
  • Dinner fork (bayonet) deformity

Patients with pubic and sacral fractures may have the following

  • Marked pain with ambulation
  • Tenderness to palpation, percussion, or both
  • With sacral fractures, pain with physical examination techniques used to assess the sacroiliac joint (eg, FABER, Gaenslen, or squish test)

Balance difficulties may be evident, especially in patients with an altered center of gravity from severe kyphosis. Patients may have difficulty performing tandem gait and performing single limb stance.

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Tests and Diagnosis of Osteoporosis

Laboratory Tests

  • Complete blood cell count
  • Sedimentation rate
  • Electrolytes
  • Creatinine
  • Blood urea nitrogen
  • Calcium
  • Phosphorus
  • Protein
  • Albumin
  • Alkaline phosphatase
  • Liver enzymes
  • 24-hour urine calcium
  • Serum protein electrophoresis
Biochemical Markers of Bone Formation and Resorption
Bone Formation
  • Osteocalcin
  • Bone-specific alkaline phosphatase
  • Procollagen extension peptides
Bone Resorption
  • Tartrate-resistant acid phosphatase
  • Urinary calcium
  • Urinary hydroxyproline
  • Urinary hydroxyproline/creatinine ratio
  • Urinary pyridinoline/deoxypyridinoline
  • Urinary N-telopeptide

Osteoporosis may be diagnosed directly through the use of a bone scan that measures bone mineral density (BMD).

  • X-ray technology is used for bone density scanning, also known as a bone mineral density test, dual-energy X-ray absorptiometry (DXA for short) and bone densitometry.
  • In combination with the determination of a patient’s risk factors, DXA offers an indication of the likelihood of fractures occurring due to osteoporosis. This test is also used to monitor response to treatment.
  • International Osteoporosis Foundation (IOF) and International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) Working Group evaluated BTMs in the prediction of fracture risk and for monitoring treatment; it was recommended that bone formation markers (s-PINP) and bone resorption markers (s-CTX) should be used as reference markers and measured by standardized assays in observational and intervention studies [.

Following studies are necessary to rule out secondary osteoporosis [

  • Complete blood count (CBC)
  • Serum creatinine, calcium, phosphorus, and magnesium
  • Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (AP)
  • Thyroid-stimulating hormone (TSH) and free T4
  • Vitamin D (V-D) (25 (OH) D)
  • Parathyroid hormone (PTH)
  • Total testosterone and gonadotropin in younger men
  • BTMs

Considered in select patients

Serum protein electrophoresis (SPEP), serum immunofixation, and serum-free light chains

  • Tissue transglutaminase antibodies (IgA and IgG)
  • Iron and ferritin levels
  • Homocysteine
  • Prolactin
  • Tryptase
  • 24-h urinary calcium
  • Urinary protein electrophoresis (UPEP)
  • Urinary-free cortisol level
  • Urinary histamine

Two types of device are available for a DXA scan

  • Central device – a hospital-based scan that measures hip and spine bone mineral density while the patient lies on a table
  • Peripheral device – a mobile machine to test bone in the wrist, heel or finger.
  • Two X-ray readings are taken to ascertain bone density – one to detect peak energy absorbed by the bone and another for the energy absorbed by soft tissue – the difference between the two gives a measurement of bone density. The risk of side-effects from this low-dose X-ray radiation is small.
  • The results of the bone mineral density test are given as a DXA T-score; -1.0 or above is considered normal, while a DXA T-score between -1.0 and -2.5 represents a mild bone loss.

Osteoporosis is diagnosed when the T-score is -2.5 or below.

After DXA, the second most common testing option in the US does not involve radiation: quantitative ultrasonography of the calcaneus (heel bone) uses ultrasound and can be carried out in the primary care setting. It is not as widely used as DXA, however, and the measurements cannot be compared against DXA T-scores.

Treatment and prevention of osteoporosis

The risk of developing osteoporosis and/or incurring a fracture can be lowered by preventive lifestyle measures and drug treatments that protect against bone loss and encourage healthy bone mineralization.

Food and Drug Administration-Approved Indications for Osteoporosis Treatments,,,,,,,,,

Drug (Brand, Manufacturer)Treatment of PMOPrevention of PMOTreatment (men)Treatment of GIOPrevention of GIO
Alendronate (Fosamax, Merck)xxxxx
Alendronate/cholecalciferol (Fosamax Plus D, Merck)xx
Alendronate effervescent (Binosto, Mission Pharmacal)xx
Risedronate IR (Actonel, Warner Chilcott)xxxxx
Risedronate DR (Atelvia, Warner Chilcott)x
Ibandronate injection (Boniva, Genentech)x
Ibandronate tablets (Boniva, Genentech)xx
Zoledronic acid (Reclast, Novartis)xxxxx
Denosumab (Prolia, Amgen)axx
Raloxifene (Evista, Lilly USA)xx
Conjugated estrogens/bazedoxifene (Duavee, Pfizer)x
Teriparatide (Forteo, Lilly USA)bxcx
Abaloparatide (Tymlos, Radius Health)x
a Also indicated to increase bone mass in women and men at high risk of fracture without osteoporosis.
b Treatment only for those at high risk of fracture.
c Increases bone mass in men with primary or hypogonadal osteoporosis at high risk of fracture.
d Miacalcin injection (Novartis) is indicated for the treatment of PMO in women more than five years postmenopause when alternative treatments are not suitable.

GIO = glucocorticoid-induced osteoporosis; PMO = postmenopausal osteoporosis.

Calcium is available from certain foods – we need a higher intake in old age.
  • Ensuring adequate calcium intake (about 1,000-1,200 mg a day, with a higher amount needed by women over 50 and everyone over 70). Calcium is available in the diet or through supplements
  • Ensuring adequate vitamin D status (doctors can help monitor this, and supplements may be necessary for anyone who is housebound, has very dark skin, little sun exposure, or who lives at a more northerly latitude; vitamin D is synthesized through the action of sunlight on skin, and is available in the diet through fortified foods, egg yolks, saltwater fish, and liver; the daily recommended amount is 600 international units, and 800 IU in men and women over 70)
  • Stop smoking if applicable (this affects a number of factors, including reducing the growth of new bone and decreasing women’s estrogen levels)
  • Drink alcohol only in moderation (elevated alcohol intake is also associated with other risk factors, such as poor nutrition and an increased risk of falls)

For people who already have osteoporosis, nutrition, exercise, and fall prevention play a key role in reducing risks and bone loss.

Drugs that are currently available to prevent and treat osteoporosis include

  • Bisphosphonates – antiresorptive drugs that slow down bone loss and reduce fracture risk
  • Estrogen agonists/antagonists (also known as selective estrogen receptor modulators, SERMS) – for example, raloxifene (Evista) is approved for use in postmenopausal women, for whom it can cut the risk of spine fractures
  • Calcitonin (Calcimar, Miacalcin) – also used to prevent spinal fracture in postmenopausal women, as well as to manage pain if a fracture occurs
  • Parathyroid hormone – for example, teriparatide (Forteo), approved for people with a high risk of fracture as it stimulates bone formation
  • Estrogen therapy
  • Hormone therapy
  • Currently, no treatment can completely reverse established osteoporosis. Early intervention can prevent osteoporosis in most people. For patients with established osteoporosis, medical intervention can halt its progression. If secondary osteoporosis is present, treatment for the primary disorder should be provided.
  • Therapy should be individualized based on each patient’s clinical scenario, with the risks and benefits of treatment discussed between the clinician and the patient.
  • Patients identified as at risk for osteoporosis (including children and adolescents) should undergo preventive measures, including adequate calcium intake, vitamin D intake, and exercise. It is recommended to counsel patients to avoid tobacco and excessive alcohol use.
  • Protective measures should be taken in patients who must take glucocorticoids for other medical conditions. These include using the minimum effective dose, discontinuing the drug as soon as possible, and supplementing with calcium and vitamin D.

Calcium Metabolism Modifiers

  • Calcium metabolism modifiers such as bisphosphonates are stable analogs of inorganic pyrophosphate. Bisphosphonates have a high affinity for hydroxyapatite crystals, and by binding at sites of active bone resorption, these agents can inhibit osteoclastic resorption. All oral bisphosphonates have poor absorption and have a bioavailability of less than 5%. Bone uptake is 20-80%, with the remainder being rapidly excreted through the kidneys.
  • Bisphosphonates are approved in the United States for the prevention and treatment of postmenopausal osteoporosis, osteoporosis in males, and glucocorticoid-induced osteoporosis. Their major pharmacologic action is the inhibition of bone resorption.

Alendronate (Fosamax); alendronate sodium/cholecalciferol (Fosamax Plus D)

  • Alendronate inhibits osteoclast activity and bone resorption. By binding to calcium salts, alendronate blocks the transformation of calcium phosphate into hydroxyapatite and inhibits the formation, aggregation, and dissolution of hydroxyapatite crystals in bone. Alendronate increases bone mineral density (BMD) at the spine by 8% and the hip by 3.5%. It reduces the incidence of vertebral fractures by 47% and nonvertebral fractures by 50% over 3 years. Alendronate is approved for the treatment and prevention of postmenopausal osteoporosis, male osteoporosis, and glucocorticoid-induced osteoporosis.

Risedronate (Actonel, Atelvia)

  • Risedronate is a potent antiresorptive agent that does not affect bone mineralization. The inclusion of an amino group within the heterocyclic ring makes risedronate one of the most potent antiresorptive bisphosphonates. As with other bisphosphonates, risedronate inhibits osteoclast formation and activity. Risedronate increases BMD at the spine by 5.4% and the hip by 1.6%. It reduces vertebral fractures by 41% and nonvertebral fractures by 39% over 3 years. It is approved for the treatment and prevention of postmenopausal osteoporosis, male osteoporosis, and glucocorticoid-induced osteoporosis.

Calcitonin salmon (Miacalcin, Fortical)

  • Calcitonin is used for the treatment of postmenopausal osteoporosis in women more than 5 years post menopause with low bone mass relative to healthy premenopausal females. The calcitonin-salmon injection should be reserved for patients who refuse or cannot tolerate estrogens or in whom estrogens are contraindicated. Use of calcitonin-salmon injection is recommended in conjunction with adequate calcium and vitamin D intake to prevent the progressive loss of bone mass. It inhibits osteoclastic bone resorption and has some analgesic effects in patients with fractures.
  • Although no research data support the idea that the use of intranasal calcitonin reduces the incidence of fractures, studies do show an increase in BMD with the use of calcitonin. Calcitonin increases BMD at the lumbar spine by 1-1.5%. It reduces the incidence of spine fracture by 33% in groups receiving 200 IU/day. It is available in parenteral and intranasal forms; however, the intranasal form is more convenient and better tolerated.

Ibandronate (Boniva)

  • Ibandronate increases BMD and reduces the incidence of vertebral fractures. Ibandronate increases BMD at the spine by 5.7-6.5% and the hip by 2.4-2.8%. It reduces vertebral fractures by 50% with intermittent (nondaily) dosing over 3 years; it has no effects on reduction of nonvertebral fractures. Ibandronate is approved for the treatment and prevention of postmenopausal osteoporosis. It is available as a 150-mg oral tablet and intravenous solution.


  • Bisphosphonates – are the most commonly used agents for osteoporosis. They have been employed for both treatment and prevention. Oral and intravenous options are available.
  • Alendronate (Fosamax) – is approved for the treatment of osteoporosis in men, in postmenopausal women, and in patients with glucocorticoid-induced osteoporosis. It has been shown to increase spinal and hip mineral density in postmenopausal women. Well-conducted controlled clinical trials indicate that alendronate reduces the rate of fracture at the spine, hip, and wrist by 50% in patients with osteoporosis. The treatment dose of alendronate is 70 mg/wk, to be taken sitting upright with a large glass of water at least 30 minutes before eating in the morning. Alendronate is also available in combination with cholecalciferol (vitamin D3). The combination of alendronate/vitamin D3 (Fosamax Plus D) is indicated for the treatment of osteoporosis in men to increase bone mass.
  • Other oral bisphosphonates include risedronate (Actonel) – or risedronate delayed-release (Atelvia), given daily, weekly, or monthly. It is also available as a combination product with calcium as risedronate/calcium carbonate (Actonel with Calcium). Risedronate reduced vertebral fractures by 41% and nonvertebral fractures by 39% over 3 years.
  • Ibandronate (Boniva) – is another bisphosphonate that can be given orally once a month. Intravenous bisphosphonates are excellent choices for patients intolerant of oral bisphosphonates or for those in whom adherence is an issue. Ibandronate is also available as an intravenous formulation that is given every 3 months. Ibandronate has not shown efficacy in nonvertebral fractures in clinical trials.

Zoledronic acid

  • Zoledronic acid (Reclast) – is the most potent bisphosphonate available. It increases BMD at the spine by 4.3-5.1% and the hip by 3.1-3.5%, as compared with placebo. Over 3 years, it reduces the incidence of spine fractures by 70%, hip fractures by 41%, and nonvertebral fractures by 25%. A similar effect on vertebral fractures has been shown in men. A 2012 randomized, 2-year trial of men with osteoporosis found that once-yearly zoledronic acid infusions significantly decreased the risk of new morphometric vertebral fractures by 67%.
  • Zoledronic acid – is a once-yearly intravenous infusion approved for the treatment of osteoporosis in men, in postmenopausal women, and in patients with glucocorticoid-induced osteoporosis.A randomized, placebo-controlled, double-blind trial suggested that a once-yearly 5-mg dose of IV zoledronic acid increases bone mass in men within 90 days of hip fracture repair; similar increases were noted in women.
Bisphosphonates and bone turnover
  • Over time, bisphosphonate therapy decreases bone turnover and, at very high levels in animals, decreases bone strength and resilience. Some limited reports, including that by Odvina et al, describe patients on long-term bisphosphonate therapy developing transverse stress fractures; biopsy specimens of these individuals have suggested extremely low turnover states in some of them.
  • Alendronate and risedronate inhibit bone resorption at doses 10-fold lower than those reducing osteoclast number. Thus, suppression of bone resorption with these agents is independent of their effects on apoptosis.
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Treatment interval and complications with bisphosphonate therapy

  • The limited trial data available regarding long-term treatment with bisphosphonates has raised questions about the optimal length of treatment with these medications. This issue has become more important, given newly recognized complications of bisphosphonate use, including osteonecrosis of the jaw and atypical (subtrochanteric or femoral shaft) femur fractures (see the images below).
Diagrams Of Leg Bones Anatomy Of Human Leg Bone Femur On Healthfavo Com Skeletal System – The Anatomy Body
Normal femoral anatomy.

The AACE recommends that if osteoporosis is mild, clinicians should consider a drug holiday after 4-5 years of bisphosphonate treatment; if fracture risk is high, a drug holiday of 1-2 years may be considered after 10 years of treatment. BMD and bone turnover markers should be monitored during the drug holiday, and treatment should be restarted if density declines substantially, bone turnover markers increase, or a fracture occurs.

In 2016, the American Society for Bone and Mineral Research published guidelines on long-term bisphosphonate treatment that included the following recommendations:

  • After 5 years of oral bisphosphonates or 3 years of intravenous bisphosphonates, reassessment of risk should be considered.
  • In women at high risk (eg, older women, those with a low hip T-score or high fracture risk score, those with previous major osteoporotic fracture, or those who fracture on therapy), continuation of treatment for up to 10 years (oral) or 6 years (intravenous), with periodic evaluation, should be considered.
  • The risk of atypical femoral fracture, but not osteonecrosis of the jaw, clearly increases with the duration of bisphosphonate therapy, but such rare events are outweighed by vertebral fracture risk reduction in high-risk patients.
  • For women not at high fracture risk, a drug holiday of 2 to 3 years can be considered after 3 to 5 years of BP treatment.

    RANK ligand (RANKL) inhibitor – denosumab (Xgeva) is an immune therapy and a new type of osteoporosis treatment.

Pharmacologic Therapy

There are 8 common types of Calcium

  • Calcium Carbonate – A common form of calcium supplement, calcium carbonate is an alkaline-based compound found in rocks, limestone, shells of marine animals, pearls, eggshells, and snails. It holds one of the highest concentrations of elemental calcium (35-40%), but is not high in bioavailability and requires the production of extra stomach acid to be absorbed. Bioavailability refers to the amount of calcium in the supplement that can be assimilated by the digestive system and ultimately used for cellular activity and health benefits. Calcium Carbonate is currently one of the cheapest and most prevalent forms of calcium supplements sold today. Be sure to avoid this form and check all of your multivitamin/mineral supplement labels.
  • Calcium Citrate – Differing from the alkaline qualities of calcium carbonate, calcium citrate has an acidic base. This acidity requires less production of natural stomach acids, allowing this type of calcium to be better absorbed than the carbonate form. It does, however, have less elemental calcium concentration (20%), and again, low bioavailability.
  • Oyster Shell Calcium – While it may seem like a more natural form of calcium, and thus higher in absorbable content, oyster shell calcium, as well as dolomite and bone meal, are difficult to quality-control and have been found to show levels of lead toxins. In general, these “natural forms” of calcium should be avoided.
  • Calcium Gluconate – A form of calcium with very low levels of actual calcium concentration. You would need to take very large amounts of the supplement to reach calcium requirements, and the bioavailability is still not certain.
  • Calcium Lactate – The form of calcium found in foods such as aged cheese and baking powder. It has a medium bioavailability in the body because it can be absorbed in various pHs.
  • Calcium Phosphate – The main form of calcium coming from cow’s milk. Tooth enamel and bones are very high in calcium phosphate, although supplemental forms have not shown to be readily bioavailable.
  • Calcium Citrate Malate – A water-soluble form of calcium. It is created by mixing the calcium salt found in citric acid with malic acid. This combination has higher levels of bioavailability than other forms, as it is water-soluble and does show some evidence of being dissolved into cell membranes. More bioavailable than the other forms listed above.
  • Calcium Orotate The most effective form of calcium supplement, created through the use of the mineral salts of orotic acid. Calcium orotates are found in small amounts in all living beings. It is a primary mineral for the creation of bones and teeth and fosters cellular communications. In my experience, this is by far the best calcium supplement to use for supporting calcium levels, and the one product I recommend is IntraCal.

Both plants and animals use orotates to create DNA and RNA. Extensive scientific research done by by Hans A. Nieper, M.D. has found that orotates can penetrate cell membranes, enabling the effective delivery of the calcium ion to the inner-most layers of the cellular mitochondria and nucleus.

Calcium Orotate supplements have been found to be beneficial in

  • Preventing osteoporosis
  • Reduction of muscle cramps
  • Reduction in pain associated with spinal problems
  • Maintaining bone health
  • Maintaining teeth health
  • Alleviation of sleep disorders like insomnia
  • Increasing the body’s ability to metabolize iron
  • Overall stress reduction and mental alertness

Calcium orotates contain many properties that can help protect you and your health while offering your cells the most readily absorbable form of calcium on the market today.

Selective estrogen receptor modulators

Selective estrogen receptor modulators (SERMs) are considered to provide the beneficial effects of estrogen without the potentially adverse outcomes. Raloxifene (Evista) is a SERM indicated for the treatment and prevention of osteoporosis in postmenopausal women. The usual dose is 60 mg given orally daily. It can also be given in combination with calcium and vitamin D. It is the first SERM studied for breast cancer prevention, and it decreases bone resorption through actions on estrogen receptors.

  • Raloxifene has been shown to prevent bone loss, and data in females with osteoporosis have demonstrated that this agent causes a 35% reduction in the risk of vertebral fractures. It has also been shown to reduce the prevalence of invasive breast cancer.
  • Raloxifene may be most useful in younger postmenopausal women without severe osteoporosis. It has been shown to increase the incidence of deep vein thrombosis, stroke, and hot flashes. In 601 postmenopausal women who had daily therapy with raloxifene, BMD was increased, serum concentrations of total low-density lipoprotein cholesterol were lowered, and the endometrium was not stimulated.
  • Pooled mortality data from large clinical trials of raloxifene (60 mg/day) were analyzed by Grady et al in 2010. When compared with placebo, all-cause mortality was 10% lower in older postmenopausal women receiving raloxifene. The primary reduction was in noncardiovascular, noncancer deaths.

The combination product of bazedoxifene, a SERM, and conjugated estrogens (CE) was approved by the FDA in October 2013 for the prevention of osteoporosis and treatment of vasomotor symptoms in postmenopausal women. Combining a SERM with CEs lowers the risk of uterine hyperplasia caused by estrogens. This eliminates the need for a progestin and its associated risks (eg, breast cancer, myocardial infarction, venous thromboembolism).

In clinical trials, this combination decreased bone turnover and bone loss in postmenopausal women at risk for osteoporosis. Bone mineral density increased significantly more with all bazedoxifene/CE doses compared with placebo at the lumbar spine and total hip and with most bazedoxifene/CE doses compared with raloxifene at the lumbar spine.

Parathyroid hormone

Image result for osteoporosis

  • Teriparatide (Forteo) – is a recombinant human parathyroid hormone and is the only available anabolic agent for the treatment of osteoporosis. It is indicated for the treatment of women with postmenopausal osteoporosis who are at high risk of fracture, who have been intolerant of previous osteoporosis therapy, or in whom osteoporosis treatment has failed to increase bone mass. It is indicated in men with idiopathic or hypogonadal osteoporosis who are at high risk of fracture, who have been intolerant of previous osteoporosis therapy, or in whom osteoporosis therapy has failed. Teriparatide is also approved for the treatment of patients with glucocorticoid-induced osteoporosis. Before treatment with teriparatide, levels of serum calcium, PTH, and 25(OH)D need to be monitored.
  • Teriparatide – cannot be given for more than 2 years. It is contraindicated in patients with pre-existing hypercalcemia, severe renal impairment, pregnancy, breast-feeding mothers, history of bone metastases or skeletal malignancies, and patients who are at an increased baseline risk for osteosarcoma including those with Paget disease, unexplained elevated alkaline phosphatase, children and young adults with open epiphyses or prior radiotherapy of the skeleton. Patients with monoclonal gammopathies of uncertain significance (MGUS) should also not be given teriparatide.
  • When PTH is given continuously – it is associated with increased osteoclastic and osteoblastic turnover, leading to a net loss of bone. However, in an intermittent subcutaneous administration of 20 mcg/day, PTH has been demonstrated to lead to a very active anabolic phase, with bone mass increasing up to 13% over 2 years in the spine and to a lesser degree in the hip.
  • Indications for PTH – in men and women are a bone density decline while on bisphosphonate therapy, bone density stabilization while on extremely low-level bisphosphonate therapy, a fracture occurring while on bisphosphonate therapy, or a very low initial bone turnover rate for which an anabolic effect is clearly warranted. Teriparatide should be considered in younger and older postmenopausal women with severe osteoporosis.

Most studies with PTH have been performed on women. The medication decreases the risk of vertebral and nonvertebral fractures to the same extent as bisphosphonates. Teriparatide is given for a maximum of 2 years, after which time the gains in BMD achieved with PTH are secure and can even be augmented with bisphosphonate therapy; otherwise, the BMD slowly deteriorates to pretreatment levels.


  • Calcitonin-salmon (Fortical, Miacalcin) – is a hormone that decreases osteoclast activity, thereby impeding postmenopausal bone loss. It is indicated for the treatment of women who are more than 5 years post menopause and have low bone mass relative to healthy premenopausal women.
  • Calcitonin-salmon should be reserved – for patients who refuse or cannot tolerate estrogens or in whom estrogens are contraindicated. It is recommended in conjunction with adequate calcium and vitamin D intake to prevent the progressive loss of bone mass. It is available as an injection and as an intranasal spray. The intranasal spray is delivered as a single daily spray that provides 200 IU of the drug. The drug can be delivered subcutaneously, but this route is rarely used.
  • Results from a single controlled clinical trial indicate that – calcitonin may decrease osteoporotic vertebral fractures by approximately 30%. In the first 2 years, calcitonin has been found to increase spinal bone mineral density (BMD) by approximately 2%. Calcitonin also has an analgesic property that makes it ideally suited for the treatment of acute vertebral fractures.
  • Calcitonin is an option for patients who – are not candidates for other available osteoporosis treatments. Common side effects of nasally administered calcitonin include nasal discomfort, rhinitis, irritation of nasal mucosa, and occasional epistaxis. Nausea, local inflammatory reactions at the injection site, sweating, and flushing are side effects noted with parenteral use.


  • Denosumab (Prolia) – is a humanized monoclonal antibody directed against the receptor activator of the nuclear factor-kappa B ligand (RANKL), which is a key mediator of the resorptive phase of bone remodeling. It decreases bone resorption by inhibiting osteoclast activity. Denosumab was approved by the US Food and Drug Administration in June 2010. It has been studied in cancer patients and in patients with postmenopausal osteoporosis.
  • It is indicated to increase bone mass in men and postmenopausal women with osteoporosis who are at high risk of fracture (defined as a history of osteoporotic fracture), have multiple risk factors for fracture, are intolerant to other available osteoporosis therapies, or in whom osteoporosis therapies have failed. In postmenopausal women with osteoporosis, denosumab reduces the incidence of vertebral, nonvertebral, and hip fractures. Denosumab may be considered in certain patients with renal insufficiency, as the impaired renal function does not significantly affect the metabolism or excretion of the drug.
  • Denosumab also increases bone mass in men at high risk for fracture who are receiving androgen deprivation therapy for nonmetastatic prostate cancer. In these patients, denosumab also reduces the incidence of vertebral fractures. It is also used to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. Approved dosage is 60 mg given subcutaneously every 6 months.
  • In patients with multiple myeloma or bone metastases from breast cancer, a single subcutaneous dose of denosumab decreases bone turnover markers within 1 day, and this effect is sustained through 84 days at higher doses. Denosumab has been shown to increase BMD and decrease bone resorption in postmenopausal women with osteoporosis over a 12-month period.

Denosumab in combination with teriparatide has been shown to increase BMD more than either drug alone.

Anabolic steroids and growth hormones

  • These act to improve the formation of the protein matrix and stimulate osteoblasts. Because of their adverse effects, they are little used. In cases of secondary osteoporosis due to male hypogonadism, urologists frequently use methyltestosterone with efficient results.

Teriparatide and PTH

  • Parathormone is formed by 84 amino acids arranged in a linear chain. Teriparatide is its homolog, with amino acids 1 to 34 only, obtained by means of the recombinant DNA technique. Together, when administered continuously, they increase the binding of RANK to preosteoclasts, thereby stimulating replication of the latter, and to osteoclasts, thereby stimulating their bone tissue reabsorption action.
  • Thus, PTH and teriparatide have a great capacity for bone reabsorption (cystic fibrous osteitis). However, when used daily in small doses, they inhibit the RANK system and increase OPG levels, thus inhibiting bone reabsorption. In this case, they also stimulate the replication and activity of endosteal and periosteal osteoblasts. Through this, they increase the thickness of the cortical bone, the cross-sectional area of the bone and the thickness and connection of the trabeculae[.


  • AACE/ACE, ACR, NAMS, and the Endocrine Society recommend bisphosphonates, excluding ibandronate, as a first-line option for the prevention and/or treatment of osteoporosis in postmenopausal women, men, and/or GIO patients.,,, Bisphosphonates bind with high affinity to the mineral matrix of the bone and inhibit osteoclast resorption of the bone, leading to a decrease in bone turnover and a net gain in bone mass. Alendronate, risedronate, and zoledronic acid (intravenous IV) have demonstrated an increase in BMD and a decrease in risk of fractures due to osteoporosis in men, postmenopausal women, and GIO patients. Ibandronate is not a first-line recommendation even though high-quality evidence indicates that it reduces vertebral fractures in both men and women; there is insufficient evidence to determine its effect on hip fractures. In addition, there is strong evidence that it has no effect on nonvertebral fracture risk.,


  • The AACE/ACE recommends denosumab as first-line therapy for patients at high risk of fracture and for patients who are unable to use oral therapy. Denosumab was the first biologic agent available for the treatment of osteoporosis. It is a fully human monoclonal antibody that inhibits RANKL to decrease bone resorption. RANKL is a transmembrane protein required for the formation, function, and survival of osteoclasts.
  • Denosumab is FDA approved for the treatment of PMO with high risk for fracture, as well as for women with breast cancer receiving adjuvant aromatase inhibitor therapy. It has also been approved for the treatment of bone loss in men with osteoporosis and with prostate cancer receiving ADT.

Hormone Replacement Therapy


  • Raloxifene, which is characterized as an EAA, exhibits dual agonistic and antagonistic properties in estrogenic pathways. Raloxifene acts as an estrogenic agonist on the bone by decreasing bone resorption and bone turnover, thus increasing BMD. It also has estrogen antagonistic activity on breast and uterine tissue.
  • The AACE/ACE recommends raloxifene as an appropriate first-line therapy for patients requiring the reduced risk of spine fracture only. Due to its selective antagonistic effects on breast tissue, raloxifene may be considered in women with an increased risk of vertebral fractures who may be at risk for developing breast cancer. Raloxifene can also be used as a weaker antiresorptive therapy for higher-risk patients during a bisphosphonate holiday.

Conjugated Estrogens/Bazedoxifen

  • A combination of conjugated estrogens with bazedoxifene (Duavee, Pfizer) received FDA approval in 2013 for use in postmenopausal women with an intact uterus for the prevention of osteoporosis and for the treatment of moderate-to-severe vasomotor symptoms. Duavee is sometimes referred to as a tissue-selective estrogen complex. Bazedoxifene acts as an EAA to reduce the risk of endometrial hyperplasia associated with the estrogen component.

Estrogen-Progestin Therapy

  • In terms of osteoporotic management, estrogen therapy is FDA approved solely for the prevention of osteoporosis in high-risk postmenopausal women and should be used only after all nonestrogenic osteoporotic treatments have been considered inappropriate.
  • The Women’s Health Initiative (WHI) was a randomized controlled trial of 16,608 postmenopausal patients that demonstrated a statistically significant reduction in fractures with estrogen-progestin combination therapy; however, the WHI study data also reported an increase in the risk of cardiovascular events, stroke, VTE, and invasive breast cancer associated with the estrogen-progestin groups. Due to the overall health risks exceeding benefits, hormonal replacement therapy is no longer recommended as first-line for the treatment and prevention of osteoporosis in postmenopausal and premenopausal women.

Testosterone Therapy

  • Despite limited studies involving the use of such combinations, the Endocrine Society recommends combination use of anti-fracture treatment with testosterone therapy for men at high risk of fracture. Testosterone monotherapy is recommended either for those in whom antiosteoporotic therapy is contraindicated and whose testosterone levels are less than 200 ng/dL, or for those at borderline high risk for fracture who have serum testosterone levels less than 200 ng/dL and have signs or symptoms of androgen deficiency or hypogonadism.


  • Calcitonin is a synthetic polypeptide hormone with properties similar to natural calcitonin found in mammals, birds, and fish. The effects of calcitonin on normal human bone physiology are unclear; however, calcitonin receptors have been discovered on osteoclasts and osteoblasts.,
  • Calcitonin is FDA approved for the treatment of osteoporosis in women who have been postmenopausal for more than five years when alternative treatments are not feasible. Results for a five-year, double-blind, randomized, placebo-controlled study of 1,255 postmenopausal women with established osteoporosis indicated that 200 IU of calcitonin daily reduced the risk of new vertebral fractures by 33%. Unlike bisphosphonates and denosumab, calcitonin lacks data showing a reduction in nonvertebral fractures, thus it is not considered first-line treatment for osteoporosis.

Parathyroid Hormone Analogues


  • Teriparatide, a recombinant human PTH (1–34) analog, is the first anabolic treatment approved for osteoporosis. It mimics the physiological actions of PTH in stimulating new bone formation on the surface of bone by stimulating osteoblastic activity when given intermittently at small doses. The AACE/ACE suggests the use of teriparatide for initial PMO treatment in those with prior fragility fractures or with high fracture risk and for those who are unable to take oral therapy. It is also listed as an option for higher-risk patients on bisphosphonate holiday.


  • Abaloparatide (Tymlos, Radius Health), the second recombinant human PTH (1–34) analog to reach the market, received FDA approval in April 2017. It is indicated for the treatment of PMO in women at high risk for fracture, defined as a history of osteoporotic fracture or multiple risk factors for fracture, and in patients who have failed or are intolerant to other available osteoporosis therapy.
  • In phase 3 clinical trial, abaloparatide reduced the incidence of new vertebral fracture by 86% over an 18-month period. The drug also reduced the risk of nonvertebral fracture by 43%.


  • Odanacatib is a selective inhibitor of CatK, a protease that is released by osteoclasts to promote the degradation of collagen in bones. Inhibiting CatK is theorized to decrease bone resorption without decreasing bone formation. In 2016, Merck discontinued development of odanacatib due to an increased risk of stroke.


  • Lasofoxifene (Sermonix) is a third-generation SERM. The PEARL trial studied the effects of lasofoxifene in an international, randomized, placebo-controlled trial of 8,556 women between 59 and 80 years of age who had a BMD T-score of 2.5 or less at the femoral neck or spine.
  • Participants received either 0.25 mg or 0.5 mg lasofoxifene daily versus placebo for five years. The group that received the clinically approved dose of lasofoxifene 0.5 mg per day demonstrated a relative risk reduction of 42% and 24% in vertebral fractures and nonvertebral fractures, respectively. Researchers also found that therapy was associated with reductions in breast cancer, coronary heart disease, and stroke. Lasofoxifene is approved for osteoporosis treatment in Europe, but approval is pending in the U.S.

Physical and Occupational Therapy

Physical Therapy

  • Physical therapy focuses on improving a patient’s strength, flexibility, posture, and balance to prevent falls and maximize physical function. Postural retraining is key in this population. Spinal bone mineral density (BMD) is directly correlated with the strength of the back extensors; therefore, maintaining and strengthening the back extensors should be emphasized. In studies by Sinaki and colleagues, strengthening the back extensor muscles reduced kyphosis and decreased the risk of sustaining vertebral compression fractures.
  • As soon as the course of therapy allows, weight-bearing exercises should be initiated. Regular weight-bearing exercises are essential for the maintenance of bone mass and should be encouraged in all patients, including children and adolescents (to strengthen the skeleton during the maturation process). Exercise also improves agility and balance, thereby reducing the risk of falls.

Occupational Therapy

  • Training in the performance of activities of daily living (ADLs) and in the proper use of adaptive equipment are essential to the prevention of future falls. Home modification focuses on reducing the risk of falling by installing handrails and grab bars in hallways, stairs, and bathrooms. The use of a shower chair, tub bench, and adaptive bathing devices also can be beneficial. The application of non-skid tape to steps (indoors and outdoors), as well as the removal of throw rugs, greatly improves home safety.


  • Aerobic low-impact exercises – such as walking and bicycling, generally are recommended. During these activities, ensure that the patient maintains an upright spinal alignment. Sinaki and Mikkelsen showed that exercises that place flexion forces on the vertebrae tend to cause an increase in the number of vertebral fractures in patients.
  • Proper therapy for osteoporosis – includes 3-5 sessions per week of weight-bearing exercises, such as walking or jogging, with each session lasting 45-60 minutes. The patient should be instructed in a home-exercise program that incorporates the necessary elements for improving posture and overall physical fitness.
  • In postmenopausal women – impact exercises can increase BMD in the hip and spine. Chien et al examined the efficacy of a 24-week aerobic exercise program consisting of treadmill walking followed by stepping exercises in osteopenic postmenopausal women aged 48-65 years. Women who exercised had increased bone mineral density in L2-L4 and the femoral neck, as well as improved quadriceps strength, muscular endurance, and peak exercise oxygen consumption (VO2 max), whereas values in the control group declined.
  • Romosozumab – is an investigational monoclonal antibody that binds with and inhibits sclerostin, and thus both increases bone formation and decreases bone resorption. It has been shown to reduce vertebral fracture rates in postmenopausal women with osteoporosis.
  • In the Fracture Study in – Postmenopausal Women With Osteoporosis (FRAME), a phase 3 randomized trial, 7180 postmenopausal women who had a T score of -2.5 to -3.5 at the total hip or femoral neck, 1 year of treatment with romosozumab reduced vertebral fracture rates by 73% compared with placebo. A further reduction in vertebral fracture risk occurred in the second year following the transition to the denosumab.
  • Strontium ranelate – is approved for the treatment of osteoporosis in some countries in Europe. It reduces the risk of both the spine and nonvertebral fractures. Strontium is not approved for the treatment of osteoporosis in the United States.
  • Based on preliminary data – that suggest women on nitrates have higher BMD and lower fracture risk, Jamal et al conducted a randomized placebo-controlled trial of women who applied daily nitroglycerin ointment for 24 months. The nitroglycerin ointment increased BMD and decreased bone resorption, although headaches were a limiting factor for many patients. Other nitrate preparations may be better tolerated and could show efficacy for fracture risk reduction.

Hormone Levels

Osteoporosis is more common in people who have too much or too little of certain hormones in their bodies. Examples include:

  • Sex hormones – Lowered sex hormone levels tend to weaken bone. The reduction of estrogen levels in women at menopause is one of the strongest risk factors for developing osteoporosis. Men experience a gradual reduction in testosterone levels as they age. Treatments for prostate cancer that reduce testosterone levels in men and treatments for breast cancer that reduce estrogen levels in women are likely to accelerate bone loss.
  • Thyroid problems – Too much thyroid hormone can cause bone loss. This can occur if your thyroid is overactive or if you take too much thyroid hormone medication to treat an underactive thyroid.
  • Other glands – Osteoporosis has also been associated with overactive parathyroid and adrenal glands.

Dietary Factors

Osteoporosis is more likely to occur in people who have:

  • Low calcium intake – A lifelong lack of calcium plays a role in the development of osteoporosis. Low calcium intake contributes to diminished bone density, early bone loss and an increased risk of fractures.
  • Eating disorders – Severely restricting food intake and being underweight weakens bone in both men and women.
  • Gastrointestinal surgery – Surgery to reduce the size of your stomach or to remove part of the intestine limits the amount of surface area available to absorb nutrients, including calcium.

Steroids and other medications

Long-term use of oral or injected corticosteroid medications, such as prednisone and cortisone, interferes with the bone-rebuilding process. Osteoporosis has also been associated with medications used to combat or prevent:

  • Seizures
  • Gastric reflux
  • Cancer
  • Transplant rejection

Medical conditions

The risk of osteoporosis is higher in people who have certain medical problems, including:

  • Celiac disease
  • Inflammatory bowel disease
  • Kidney or liver disease
  • Cancer
  • Lupus
  • Multiple myelomas
  • Rheumatoid arthritis

Lifestyle choices


Some bad habits can increase your risk of osteoporosis. Examples include

  • Sedentary lifestyle – People who spend a lot of time sitting have a higher risk of osteoporosis than do those who are more active. Any weight-bearing exercise and activities that promote balance and good posture are beneficial for your bones, but walking, running, jumping, dancing and weightlifting seem particularly helpful.
  • Excessive alcohol consumption – Regular consumption of more than two alcoholic drinks a day increases your risk of osteoporosis.
  • Tobacco use – The exact role tobacco plays in osteoporosis isn’t clearly understood, but it has been shown that tobacco use contributes to weak bones.


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