Osteoporosis in Rehabilitation

Author(s): Linqiu Zhou, MD, Paul Kitei, MD, Chen Zhou, MS-2

Originally published:11/14/2011

Last updated:04/19/2016



Osteoporosis translates to “porous bones” in Greek. The World Health Organization (WHO) defines osteoporosis as a bone mineral density (BMD) at the hip or lumbar spine that is at least 2.5 standard deviations below the mean BMD T-score of a young-adult female reference population.1Osteoporosis is the most common metabolic bone disease.


Osteoporosis results from changes in the bone remodeling process, which occurs during the skeletal life cycle.  Osteoporosis can be either primary or secondary in etiology.  Primary osteoporosis is more common than secondary osteoporosis and can be divided into postmenopausal osteoporosis (Type 1, occurring in women aged 50-65 years with a phase of accelerated bone loss) and age-associated or senile osteoporosis (Type 2, occurring in women and men older than 70 years with bone loss associated with age).  Secondary osteoporosis is a result of medical conditions or treatments that alter bone remodeling.2

Epidemiology including risk factors and primary prevention

There are multiple risk factors for the development of osteoporosis. Age, race (being Caucasian or Asian), body mass index, genetic factors, and pre-existing medical conditions, such as Cushing’s syndrome, diabetes mellitus, multiple myeloma, and stroke, are well-known risk factors. Social risk factors include cigarette smoking, alcohol abuse, and lack of exercise. Diets low in calcium or vitamin D, excess vitamin A, high salt intake, low estrogen levels in women, and low testosterone levels in men all increase the likelihood of developing osteoporosis.  Lastly, a number of medications have been shown to negatively impact bone density, including corticosteroids, anticonvulsants, antacids, and heparin. The National Osteoporosis Foundation (NOF) has estimated that more than 9.9 million Americans have osteoporosis, and an additional 43.1 million have low bone density.3  More than 2 million fractures are attributed to osteoporosis annually.  Hip fractures account for 14% of incident fractures and 72% of fracture costs. The cost of care is expected to rise to $25.3 billion by 2025.3


Peak bone mass is achieved by age 18-25.  As we age, daily bone remodeling occurs. Effective remodeling depends upon a balance between bone resorption and bone deposition. The bone remodeling cycle is such that osteoclasts are activated, resulting in bone resorption. Next, osteoblasts lay down new bone matrix. Osteoblastic activity requires more time than osteoclastic activity, and thus, there is a tendency for overall bone loss when there is an increase in bone resorption. Eventually, this can lead to disordered skeletal architecture and an increase in fracture risk.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The WHO describes 4 stages of progressively worsening BMD: normal bone mass, low bone mass (osteopenia), osteoporosis, and severe/established osteoporosis.  These stages are based on BMD scores, as determined by central dual-energy x-ray absorptiometry (DXA), and their corresponding T-scores.3

Normal bone mass is defined as a BMD within 1 standard deviation of the mean BMD in a young-adult reference population (T-score ≥ -1).  Low bone mass (osteopenia) is defined as a BMD between 1 and 2.5 standard deviations below the mean BMD (T-score between -1 and -2.5).  Osteoporosis is defined as a BMD more than 2.5 standard deviations below the mean (T-score ≤ -2.5). Severe/established osteoporosis is defined as osteoporosis in the setting of at least 1 fracture.3

Specific secondary or associated conditions and complications

The conditions most commonly associated with osteoporosis are vertebral body, hip, and radius fractures. Hip fractures are associated with an 8.4 to 36% excess mortality within 1 year, with a higher mortality in men than in women.3  Vertebral compression fractures may result in pain, disability and mortality.  Additionally, wrist or distal radial fractures can interfere with activities of daily living.3



Osteoporotic patients are generally asymptomatic until a fracture occurs. Taking a careful patient history with a specific focus on risk factors (see above) is crucial.  Assessment of fall risk is also important. The WHO Fracture Risk Algorithm (FRAX) is a validated tool that can help in patient risk stratification.3 FRAX was developed to calculate the 10-year probability of hip fracture and the 10-year probability of a major osteoporotic fracture and is based on a number of risk factors.4

Physical examination

The examiner should take careful note of the patient’s body frame, as well as any signs of anorexia, chronic liver disease, alcoholism, and thyroid disease, in an attempt to identify specific secondary, treatable causes of osteoporosis. Skin and facial examinations will help to evaluate for endocrine disorders. Findings compatible with an osteoporotic fracture should be noted. This may include kyphosis and point tenderness over spinous processes for vertebral fractures. Height should be measured annually, preferably with a wall-mounted stadiometer, in postmenopausal women and men older than 50.3,5

Functional assessment

A thorough functional assessment is an important tool in evaluating a patient’s fall risk. Some of the most important aspects are a history of falls, muscle weakness, and deficits in gait, balance, or visual acuity.

Laboratory studies

Essential laboratory tests for the initial evaluation of all patients with osteoporosis include a complete blood count, CHEM-7, serum calcium and phosphorus levels, liver function tests, thyroid-stimulating hormone (TSH) level, serum 25-hydroxyvitamin D (25(OH)D) level, 24-hour urinary calcium. In younger men, total testosterone and gonadotropin levels should be ordered as well. Based on initial lab work results, a number of other tests may be warranted.


The American Medical Association (AMA) and the NOF recommend a DXA for definitive diagnosis of osteoporosis and for monitoring the effects of therapy.3 Current NOF recommendations suggest that the following groups have a DXA scan: all women aged 65 and older and all men aged 70 or older, menopausal and postmenopausal women with risk factors (regardless of age), men aged 50-69 with risk factors, and both men and women who have had broken bones after the age of 50.  DXA scan may also be indicated based on significant height loss and abnormal X-rays of the spine. Vertebral imaging should be considered if a patient has a significant decrease in height.3

Additional imaging studies include quantitative computer tomography (QCT), peripheral dual-energy X-ray absorptiometry (pDXA), and quantitative ultrasound densitometry (QUS).3  Quantitative ultrasound (QUS) is a safe and powerful screening tool for osteoporosis, and it is particularly useful in areas that do not have access to DXA machines.  Currently, it is recommended that only the calcaneus be used with QUS for assessment of bone health status.  This is in part due to the large amount of research conducted on the calcaneus relative to other bones.  Importantly, QUS devices have not been standardized, and thus, measurements obtained using a particular QUS device should not be compared to those found using a different device.6

Supplemental assessment tools

In addition to the initial diagnostic workup for osteoporosis (outlined above), a number of other tests may be useful.  Causes of secondary osteoporosis may be identified by obtaining parathyroid hormone levels, celiac antibodies levels, serum/urine protein electrophoresis, 24-hour urinary free cortisol, and an overnight dexamethasone suppression test. Biomarkers are a useful tool in detecting bone remodeling.  Resorption biomarkers include serum C-terminal telopeptide (CTx) and urinary N-terminal telopeptide (NTx).  Formation biomarkers include serum bone-specific alkaline phosphatase (BSAP), osteocalcin (OC), and aminoterminal propeptide of type 1 procollagen (PINP).7

Early predictions of outcomes

The development of osteoporosis in anorexic females is best predicted by body weight history.  Hip fractures have higher mortality rates than other bony fractures, though the risk of mortality significantly decreases with time.  Interestingly, patients with vertebral fractures have an increased risk of mortality even after 1 year has elapsed from time of injury. Serum albumin (a measure of protein intake) has strong prognostic value for survival in patients who have suffered a hip fracture.


Evaluating a patient’s home environment and discussing ways to safely maneuver around the home can decrease the risk of falls.  Potential environmental hazards should be discussed with the patient with a focus on practical ways to remove such hazards from the home.

Social role and social support system

Patient, family, and clinician knowledge and awareness of osteoporosis can lead to early detection and diagnosis. Community and family support allows for better access to health care, thus decreasing the risk of fractures and complications.

Professional Issues

The physiatrist must always consider osteoporosis as a differential diagnoses for the underlying causes of musculoskeletal conditions, in female and senior patients. Information should be given to a patient diagnosed with osteoporosis regarding prevention of fractures, prevention of falls, and treatment options.


Available or current treatment guidelines

NOF [National Osteoporosis Foundation] revised the Clinician’s Guide to Prevention and Treatment of Osteoporosis in 2014, though internationally, many countries or regional medical societies have set up their own protocols.3 The NOF guidelines are described below. The International Osteoporosis Foundation (IOF) has not endorsed specific guidelines, as emphasis of primary prevention varies across regions.3

At different disease stages

Osteoporosis is considered a “silent thief” that is typically asymptomatic until a fracture occurs. During the acute phase of fracture, relieving pain, appropriately stabilizing the fracture, and treating other comorbidities are essential.

NOF suggests pharmacologic treatment in the following groups: patients with a hip or vertebral fracture, patients with a BMD with an associated T-score ≤ -2.5 (as measured by DXA) at either the femoral neck, total hip, or lumbar spine, postmenopausal women and men age 50 and older with low bone mass (T-score between -1.0 and -2.5), and patients with a 10-year major osteoporosis-related fracture probability of ≥ 20% or a 10-year hip fracture probability of ≥ 3%.3

The American Association of Clinical Endocrinologists (AACE) recommends adequate calcium and vitamin D intake (via foods or supplements). Recommended calcium intake is 1000 mg/day for men aged 50-70 and 1200 mg/day for both women over 50 and men over 70.8 NOF recommends vitamin D intake of 800-1000 IU/day, though other experts recommend up to 2000 IU/day.

Additional AACE pharmacologic guidelines are as follows: First-line agents include alendronate, risedronate, zoledronic acid, and denosumab. Second-line agents include ibandronate and raloxifene (though raloxifene is sometimes considered a third-line agent). The last-line agent is calcitonin. Treatment with teriparatide (an anabolic agent similar to PTH) may also be considered in patients with very high fracture risks or in those who have failed bisphosphonate therapy previously.8

The effectiveness of treatments should be closely monitored.  Height should be measured yearly, biochemical markers of bone turnover should be examined every three to six months, and DXA testing should be ordered every two years.3 The duration of medication therapy needs to be individualized based on a given patient’s osteoporosis risk assessment.  Typically, bisphosphonate therapy is three to five years in duration, and teriparatide therapy does not exceed 18 to 24 months.3

Patient & family education

Osteoporosis is a preventable disease. The NOF recommends that postmenopausal women and men age 50 and older be counseled on the risk of osteoporosis and related fractures.  Recommendations for the general population should include adequate intake of calcium, vitamin D, and vitamin K.  Smoking and heavy drinking should be avoided, and risk factors for falls should be reduced. Early identification and treatment of patients with osteoporosis are essential.3  Exercise is approved to prevent and treat the loss of bone mass, help postural stability and the prevention of falls.9Exercises can also maximize peak bone mass in children.10

Emerging/unique Interventions

Serial central DXA BMD testing is the gold standard for monitoring response to pharmacologic therapy. BMD should be measured 12 to 24 months after initiating or changing therapy and periodically thereafter.3

Serially testing bone turnover markers can also be used for evaluating the efficacy of drug therapy. PINP levels should be obtained prior to and 3 to 6 months after the initiation of osteoporosis treatment in order to gauge therapeutic response.11

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Early identification of patients with osteoporosis and assessing the risks of fracture can reverse bony deterioration and prevent fracture. Multidisciplinary approach and effective communication between the physician and the patient/family lead to better outcomes. Referral to specialists should be strongly considered if the patient has any of the following:

  1. Uncontrolled pain (pain medicine specialist)
  2. Primary osteoporosis or failure to respond to conventional treatment for osteoporosis (endocrinologist, rheumatologist)
  3. Fractures (orthopedist, neurosurgeon)3

Special populations

Male adults

Though more prevalent in women, osteoporosis is a major health concern in elderly men.  In fact, 1 in 8 men older than 50 have osteoporosis-related fractures during their lifetime.  Importantly, mortality rates during the 1-year period following hip and acetabular fractures is actually higher in men than in women.  It is thought that the decrease in bone mineral density seen in men as they age is more closely related to less bioavailable estradiol rather than diminished testosterone levels.12

Secondary causes of osteoporosis should be considered and corrected for, if possible.  Bone mineral density is less helpful in this population, and FRAX (see above) should be used to determine whether a specific patient requires treatment.  Treatment options include a number of bisphosphonates, denosumab (a monoclonal antibody), and teriparatide. Testosterone is not indicated.12


Pediatric osteoporosis is defined as having a bone density Z score below -2, in the setting of a fracture. Z scores of the lumbar spine, hip, and total body are available. Pediatric osteoporosis may be related to genetic predisposition, calcium or vitamin D deficiency, or a number of other medical conditions (chronic liver disease, burn injuries, malignancies). As with other groups, the prevention and treatment of pediatric osteoporosis should be tailored to the cause of the osteoporosis.10

Adequate calcium intake and weight-bearing exercises can maximize peak bone mass. The NIH Consensus Conference on Osteoporosis recommends a calcium intake of 800 mg/d until age 10, 1200 mg/d during adolescence, and 1000 mg/d after adolescence. Additional management with bisphosphonates can be helpful, while hormone replacement therapy is not appropriate in this population.1

Spinal cord injuries

Osteoporosis in spinal cord injury (SCI) occurs predominantly in the lower extremities and pelvis as a result of gravitational unloading and an imbalance between bone formation and resorption.  Bone loss may be enhanced by the lack of muscle traction on bone or by other neural factors associated with SCI. Prevention is key. To date, bisphosphonates are the best-studied medications for the prevention of demineralization following SCI, and alendronate has been shown to prevent total body and hip bone loss at 1-year post-injury. Weight-bearing exercises with standing frames and bikes, as well as functional electrical stimulation (FES) have been shown to be effective when started within 6 weeks of injury.13


Osteoporosis after stroke is most often seen in the paretic side, especially in the upper extremities. Bone loss is most significant during the first three to four months following stroke.  The mechanism of post-stroke osteoporosis is thought to be due to a combination of paresis, reduced mobility, side-effects from medications, and nutritional deficits, to name a few.  Importantly, stroke patients are at higher risk for fractures due to both an increase in osteoporosis and fall risks. Post-stroke osteoporosis treatments include behavioral/rehabilitative therapy, dietary supplementation, and drugs (bisphosphonates).14


Cutting edge concepts and practice

Many of the current treatments for osteoporosis have the potential to cause significant adverse effects. Estrogen and serum estrogen receptor modulators (SERMs) have been linked to endometrial cancer, PTH carries a risk of osteosarcoma, and bisphosphonates can cause osteonecrosis of the jaw (ONJ) and subtrochanteric femoral fractures.3

Available treatments have focused on decreasing osteoclast activity, and thus, bone resorption and turnover. Unfortunately, this strategy can affect bone strength and cause a myriad of other side effects after long-term use, some of which have been outlined above.  Future treatments will need to focus on anabolic agents or combined therapy with both anabolic and anti-catabolic agents.


Gaps in the evidence-based knowledge

A number of questions regarding osteoporosis are still unanswered: What is the best tool to assess bone strength?  How can we maximize our peak bone mass when we are young?  What are the best exercise programs to prevent and treat osteoporosis?  How can one best identify and modify risk factors for falling?  How long should patients take antiresorptive therapies, and what are the long-term side effects of these medications?  Further research is needed to answer these questions.


  1. http://www.who.int/chp/topics/Osteoporosis.pdf
  2. http://www.iofbonehealth.org/secondary-osteoporosis
  3. 2014 Clinician’s guide to prevention and treatment of osteoporosis
  4. http://www.rheumatology.org/I-Am-A/Rheumatologist/Research/Clinician-Researchers/Fracture-Risk-Assessment-Tool-FRAX.
  5. Coles RJ,Clements DG, Evans WD. Measurement of height: practical considerations for the study of osteoporosis. Osteoporos In 1994 Nov; 4(6):353-6.
  6. Chin KY, Ima-Nirwana S. Calcaneal Quantitative Ultrasound as a Determinant of Bone Health Status: What Properties of Bone Does It Reflect? Int J Med Sci 2013; 10(12):1778-1783.
  7. Gillian Wheater, Elshahaly M, Tuck SP, Datta HK, and Laar JM. The clinical utility of bone marker measurements in osteoporosis. J Transl Med. 2013; 11: 201
  8. Watts NB, Bilezikian JP, Camacho PM.American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the diagnosis and treatment of postmenopausal osteoporosis. Endocr Pract. 2010 Nov-Dec; 16 Suppl 3:1-37.
  9. Diaz-Curie Effects of Exercise on Osteoporosis. J Osteopor Phys Act 2013.
  10. DiMeglio LA, Bhatia J. Pediatric Osteoporosis. http://emedicine.medscape.com/article/985221-overview
  11. http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/61695. Accessed February 3, 2016
  12. Patrizia D’Amelio and Giovanni Carlo Isaia, “Male Osteoporosis in the Elderly,” International Journal of Endocrinology, vol. 2015, Article ID 907689, 8 pages, 2015. doi:10.1155/2015/907689
  13. Weiss D, Kishner S.  Osteoporosis and Spinal Cord Injury    http://emedicine.medscape.com/article/322204-overview
  14. Carda S, Cisari C, Invernizzi M, Bevilacqua M. Osteoporosis after Stroke: A Review of the Causes and Potential Treatments. Cerebrovasc Dis 2009; 28:191–200

Original Version of the Topic:

Linqiu Zhou, MD, Anthony Lee, MD. Osteoporosis in Rehabilitation. Publication Date: 2011/11/14.

Author Disclosure

Linqiu Zhou, MD
Nothing to Disclose

Paul Kitei, MD
Nothing to Disclose

Chen Zhou, MS-2
Nothing to Disclose


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