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Osteoporosis translates to “porous bones” in Greek. The World Health Organization (WHO) defines osteoporosis as a bone mineral density (BMD) at the femoral neck, total hip or lumbar spine that is 2.5 standard deviations or more below the young female adult mean, known as the T-score. Osteoporosis is the most common metabolic bone disease, causing more than an estimated 8.9 million fractures annually worldwide.1


Osteoporosis is a disorder characterized by low bone mass and microarchitectural changes in bone tissue that lead to increased bone fragility and fracture risk. It 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).2 Secondary osteoporosis is a result of medical conditions or treatments that alter bone remodeling.Some notable examples include metabolic disease (i.e., parathyroid and thyroid disease, diabetes, hypogonadism), chronic inflammatory conditions (i.e., rheumatoid arthritis, chronic obstructive pulmonary disease, cystic fibrosis), chronic kidney disease, neuromuscular disease (i.e., muscular dystrophy), cerebral palsy, multiple sclerosis, nutritional deficiencies and medication induced bone loss.2

Epidemiology including risk factors and primary prevention

As of 2021, the prevalence of osteoporosis worldwide was estimated at 18.3% in a large scale meta-analysis.2 Older data from 2010 estimated that 75 million people living in Europe, USA, and Japan are affected by osteoporosis and worldwide estimates were approximately 200 million individuals affected.2 Multiple skeletal sites may be affected by osteoporosis with non-hip/non-vertebral representing a much greater incident and overall larger economic costs. Hip fractures almost always require surgical intervention and the incidence increases exponentially after 80 years of age. Vertebral fractures, on the other hand, vary in their presentation and clinical impact; although, these are the most common variety of fragility fracture (a pathologic fracture that results from minimal or no identifiable trauma). The cost of care is expected to rise to $25.3 billion by 2025.4  Geographically, North America and Asia have the highest prevalence and incidence rates of osteoporotic fractures with some variation seen between hip and non-hip related fractures.2 There are multiple risk factors associated with the development of osteoporosis including, but not limited to increased age, female sex, race, low body mass index, hypogonadism or premature ovarian failure, previous history of fractures from low-intensity or minimal trauma and pre-existing medical conditions (i.e., Cushing’s syndrome, diabetes mellitus, multiple myeloma and stroke). 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 and osteoporosis-related fractures.  Lastly, several medications have been shown to negatively impact bone density, including corticosteroids, anticonvulsants, antacids, and heparin.2


Peak bone mass is achieved by age 18-25. Bone remodeling, a process in which old bone is replaced by new bone, occurs daily. This results in the renewal of the skeleton approximately every 10 years. Remodeling occurs when osteoclasts are activated and induce bone resorption and subsequently osteoblasts are recruited to these areas to mineralize new bone resulting in bone formation. Initially, this is a balanced process, but as we age the process starts to favor osteoclastic resorption which is a faster process than osteoblastic formation.5 Remodeling depends upon a balance between bone resorption and bone deposition. Eventually, this can lead to disordered skeletal architecture and an increase in fracture risk. Men and women appear to have slightly different mechanisms as women with osteoporosis appear to have a larger component of osteoclastic resorption leading to bone fragility whereas men predominately experience reduced bone formation and subsequent low bone turnover.5 Genetic factors likely influence BMD as well with INGR3, EPDR1, RANK, RANKL, OPG, and Wnt signaling pathways being implicated in biochemical research studies.2,6

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 and Z-scores.1

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.  It is important to note that T-scores should only be used for postmenopausal women and men over 50 years of age. A Z-score compares the BMD of the individual to the mean of those in their own age and gender group and should be used for children, premenopausal women, and men under 50 years of age. A Z-score >2 SD below the mean may warrant further work-up to investigate secondary causes of bone fragility.7

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.6 Vertebral compression fractures may result in pain, disability, and increased all-cause mortality and overall poor health outcomes. Additionally, wrist or distal radial fractures can interfere with activities of daily living.

Essentials of Assessment


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; see Figure 1. FRAX was developed to calculate the 10-year probability of hip fracture and the 10-year probability of a major osteoporotic fracture.  The Osteoporosis Self-Assessment Tool (OST), a simple calculation using age and weight to identify individuals at higher risk of low BMD is filled out in advance by the patient. Other screening tools of use by the investigating physician include the Osteoporosis Risk Assessment Instrument, Osteoporosis Index of Risk and the Simple Calculated Osteoporosis Risk Estimation. These tests all have similar strengths and are moderately accurate at identifying patients with osteoporosis.8 The US Preventative Services Task Force recommends BMD measurement be conducted on all women aged 65 years and older, as well as young postmenopausal women whose 10-year fracture probability on FRAX is the same or greater than that of a 65-year-old white woman without additional risk factors.7

Physical examination

The examiner should take careful note of the patient’s body habitus, 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. An antalgic gait and true leg length discrepancy may suggest femoral fractures. Height should be measured annually, preferably with a wall-mounted stadiometer, in postmenopausal women and men older than 50.5

Functional assessment

A thorough functional assessment is essential 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. The Timed Up and Go Test (TUG) is a validated instrument that can be used to assess mobility, balance, walking ability and fall risk in older adults.9

Laboratory studies

Essential laboratory tests for the initial evaluation of all patients with osteoporosis include a complete blood count, basic metabolic panel, serum calcium and phosphorus levels, liver function tests, thyroid-stimulating hormone (TSH) level, serum 25-hydroxyvitamin D (25(OH)D) level, and 24-hour urinary calcium. In younger men, total testosterone and gonadotropin levels should be ordered as well.3,5 Based on initial lab work results, several other tests may be warranted.


Multiple different medical societies recommend a DXA for definitive diagnosis of osteoporosis and for monitoring the effects of therapy.   General 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 50.10 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 to look for compression fractures.

Additional imaging studies include quantitative computer tomography (QCT), peripheral dual-energy X-ray absorptiometry (pDXA), and quantitative ultrasound densitometry (QUS). 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. Studies have shown calcaneus QUS is a low-cost and readily available alternative that is as effective as axial DXA at predicting osteoporosis-related fractures in elderly women; it can be a useful initial screening tool while minimizing exposure to ionizing radiation.11 However, 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.

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.5 Biomarkers are a potentially 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).12,13 Widespread clinical use of biomarkers is still not a reality with many experts having difficulty agreeing on their clinical utility.2,5

Early predictions of outcomes

The development of osteoporosis in anorexic females is best predicted by body weight history. Hip fractures have initial higher mortality rates than other bony fractures, though the risk of mortality significantly decreases with time.5 Interestingly, patients with vertebral fractures have an increased risk of mortality even after 1 year has elapsed from time of injury. In women who have had a vertebral fracture, 19% will have another fracture in the next year.3 Additionally, studies indicate that baseline T-scores at initial assessment are important in determining how often older adults should be screened, with higher scores being associated with a much smaller risk of transitioning to fragility fractures in the immediate future.5


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. A home inspection to evaluate walkway obstacles, uneven surfaces, areas of poor illumination, icy sidewalks, and potential slippery floors will minimize fall risk. Clothing modifications such as supportive orthopaedic footwear and avoidance of baggy/obstructive clothing is helpful. The addition of grab bars, shower chairs, and brighter lighting are just some of the modifications that can be done with the help of social work and occupational therapists.14

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 and resources for physical activities, thus decreasing the risk of fractures and complications.

Professional issues

The physiatrist must always consider osteoporosis as a differential diagnosis for the underlying causes of musculoskeletal conditions in female and elderly patients. Information should be given to a patient diagnosed with osteoporosis regarding prevention of fractures, prevention of falls, and treatment options. Osteoporosis can be treated best with a multidisciplinary team approach including the physiatrist, primary care provider, endocrinologist, physical therapists, or personal trainers, as well as the patient’s family and friends.

Rehabilitation Management and Treatments

Available or current treatment guidelines

There are several osteoporosis treatment guidelines currently available. Some notable examples include: The Endocrine Society (Updated in 2019), The American Association of Clinical Endocrinologists (Updated in 2020), International Osteoporosis Foundation (Compendium released in 2020), and the UK National Osteoporosis Guideline Group (Updated in 2022). Non-osteoporosis specific organizations such as The American College of Physicians and the American College of Obstetrics and Gynecology have additionally made treatment guidelines with recent updates in 2023 and 2022, respectively. While treatment recommendations are similar among all these groups, there are some key differences with suggestions about screening criteria, medication choices, and follow up imaging timelines.5,8,10

At different disease stages

Osteoporosis is often clinically silent and asymptomatic until a fracture occurs. During the acute phase of fracture, relieving pain, appropriately stabilizing the fracture, and treating other comorbidities are essential.

The National Osteoporosis Foundation  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 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% based on FRAX.Other organizations such as the UK based National Osteoporosis Guidelines Group further sub-stratify these recommendations based upon age (>50, >65, and >70 years of age getting separate recommendations) and utilization of age normalized scores for FRAX scores. There is much agreement between the various societies but no consensus.5,8,10

The Endocrine Society has recently updated their clinical practice guidelines regarding medication management. In postmenopausal women at high risk of fractures, initial treatment with bisphosphonates (i.e., alendronate, risedronate, zoledronic acid, and ibandronate) or denosumab are appropriate to reduce fracture risk. In postmenopausal women with known osteoporosis at high risk of fracture (or with known severe or multiple vertebral fractures), teriparatide for up to 2 years is recommended. In postmenopausal women with severe osteoporosis (T score < -2.5) or multiple vertebral fractures, romosozumab for up to 1 year is recommended. Multiple clinical trials have revealed the superiority of bone forming agents (teriparatide/romosozumab) over anti-resorptives (bisphosphonates).16 Bone forming agents should always be followed by an anti-resorptive agent to prevent rapid loss of BMD after treatment is stopped.15-17

The effectiveness of treatments should be closely monitored.  Although no standard guidelines exist for monitoring response to treatment, some organizations suggest measuring height annually, obtaining bone turnover markers pre-treatment and, thereafter, every three to six months, as well as DXA testing every two years. The duration of medication therapy needs to be individualized based on each patient’s osteoporosis risk assessment; although, there has been a movement for longer duration of treatment after long term outcome research has revealed that significant side effects from medication are uncommon. The incidence of osteonecrosis of the jaw with bisphosphonates is ~0.001-0.15% which is only slightly higher than the general population. Atypical subtrochanteric/diaphyseal femur fractures in denosumab/bisphosphonate treated patients remains low with incident rates of 1.8 per 100,000 cases in 2-year exposure and 113.1 per 100,000 in 8-10 years of treatment exposure.15-17

In addition to this, dietary supplementation with calcium and vitamin D can also aid in decreased risk of osteoporosis-related fractures. The recommended dietary allowance (RDA) for calcium is 1000 mg/day for women ages 19-50 years and increases to 1200 mg/day for those 50 years and older; for men, the RDA is 1000 mg/day for those ages 19-70 years and increases to 1200 mg/day in those 70 years and older.18 The preferred sources are calcium-rich foods and beverages. Calcium supplementation at doses higher than this may predispose to cardiovascular morbidity and renal stones and is thus not recommended. The RDA for vitamin D is 600 IU/day for men and women ages 19-70 years and increases to 800 IU/day for those 70 years and older. These calculations correspond to a serum 25-hydroxyvitamin D level of 20 ng/ml.19 Vitamin D supplementation should also be tailored to address any persistent deficiencies that are not corrected with traditional doses/dietary intake.

Patient & family education

Osteoporosis is a preventable disease. The NOF recommends that postmenopausal women and men aged 50 and older be counseled on the risk of osteoporosis and osteoporosis-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 is helpful to prevent morbidity related to the condition.

Exercise is essential to prevent and treat the loss of bone mass, help postural stability and the prevention of falls. Exercise intervention should apply the principle of specificity by tailoring the exercise to the affected area. Individuals with poor BMD at the femoral neck appear to benefit from progressive resistance strength training in the lower extremities or a high impact jumping exercise program.20 The patient should be instructed to periodically increase the rate of exercise and frequency of mechanical load based upon tolerance of exercise. The lumbar spine is better treated with back extension strengthening programs with the use of a weighted backpack and other core strengthening such as Pilates.20 Vibration platforms may be helpful as adjunctive treatment for bone health and aerobic conditioning.21 More generally, weight bearing aerobic exercises (i.e., walking, stair climbing, jogging, and Tai Chi) and strength/resistance exercises (i.e., body weight lifting, free weights, machines, or resistance bands) utilized in combination for 30-60 minutes, 3-5 times weekly, is recommended for all osteoporosis patients.22  

Emerging/unique interventions

Serial central DXA BMD testing is the gold standard for monitoring response to pharmacologic therapy. BMD should be measured approximately 12 to 24 months after initiating or changing therapy and periodically thereafter; although, no clear consensus currently exists.10

Serially testing bone turnover markers can also be used for evaluating the efficacy of drug therapy. PINP levels may be obtained at 3 to 6 months after the initiation of medical management to gauge therapeutic response.13

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

Early identification of patients with osteoporosis to assess the risks of fracture can reverse bony deterioration thereby preventing future fractures. Screening for risk factors and ordering tests for low BMD is crucial for preventing negative outcomes. There is still an estimated 11% of postmenopausal women who have never been screened or never had follow-up counseling and treatment for low BMD.3 A 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:

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

Special populations

Male adults

Osteoporosis in men remains an underrecognized and undertreated condition.  Loss of bone mass increases in men after age 70 and may be either primary or secondary in nature. Simple age-related bone loss is the predominant form of primary osteoporosis, but testosterone related depletion directly affects both cortical and trabecular bone mass, as well. Elderly men will often present with hip fracture as the first sign of osteoporosis which places them at high risk for developing future fractures   if left untreated.  Additionally, men who sustain hip fracture have a higher post-fracture complication and mortality rate.23

Secondary causes of osteoporosis should be considered and corrected, if possible. The most common causes of secondary osteoporosis include chronic glucocorticoid use, hypogonadism, alcohol abuse, smoking, hypercalciuria, gastrointestinal disease, and prolonged immobilization.24 Bone mineral density is less helpful in this population, and FRAX should be used to determine whether a specific patient requires treatment.  Treatment options include lifestyle modification, stopping causative agents, and the previously mentioned medication options. Testosterone replacement therapy is typically not indicated.23


Pediatric osteoporosis is defined as having a Z-score < -2, in the presence of clinically significant fracture history. Z-scores of the lumbar spine, hip, and total body are available. Clinically significant fracture is defined as at least one long bone fracture in the lower extremity, at least 2 long bone fractures in the upper extremity, or a vertebral compression fracture.25 The potential etiologies of pediatric osteoporosis are numerous and may be related to genetic disorders, metabolic abnormalities, medications, calcium or vitamin D deficiency, excessive exercise leading to amenorrhea, or other behavioral factors (i.e., smoking, alcohol, etc.). As with other groups, the prevention and treatment of pediatric osteoporosis should be tailored to the cause of the osteoporosis.

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.18,19 Increasing physical activity as adjunctive therapy to appropriate dietary mineral intake is recommended. Additional management with bisphosphonates for refractory cases has been documented.25 Juvenile osteoporosis should be distinguished from osteoporosis due to osteogenesis imperfecta to help with patient/family expectation management given the lifelong nature of the illness, genetic counseling opportunities, and more specific treatment recommendations.25

Spinal cord injuries

Osteoporosis after spinal cord injury (SCI) is extremely common with ~50% of  complete SCI patients developing osteoporosis at 1 year post injury with longer term follow up increasing the rate to greater than 80%.26 Bone loss occurs predominantly in the lower extremities and pelvis as a result of gravitational unloading and an imbalance between bone formation and resorption.26  Bone loss may be enhanced by the lack of muscle traction on bone or by other neural factors associated with SCI. Bone loss begins as early as the first 2 weeks after injury, being accelerated in the first six months post-injury, and finally stabilizing 3-5 years after injury although some researchers have demonstrated chronic steady decremental loss in BMD.26 Fragility fractures can occur from low-impact forces that normally would not cause fractures. Prevention is key. Weight-bearing exercises with standing frames and bikes, as well as functional electrical stimulation (FES) have been shown to be effective when started within six weeks of injury.26 Similar to the non-SCI population, dietary mineral supplementation, vibration therapy, teriparatide, and denosumab have also been shown to be beneficial. The evidence for bisphosphonates is not nearly as strong for SCI patients as it is for the general osteoporosis population.26


Osteoporosis after stroke is most often seen in the paretic side, especially in the upper extremities and the lumbar spine. Bone loss is most significant during the first three to four months following stroke.27 Both hemorrhagic and ischemic stroke survivors have an increased osteoporosis risk at 2.06-fold and 1.77-fold, respectively.28 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.27,28Stroke 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 medications like bisphosphonates, teriparatide, and denosumab.27,28

Cutting Edge/Emerging and Unique Concepts and Practice

The number of patients living with osteoporosis worldwide is projected to increase dramatically over the next 10 years.29 DXA screening remains a vital screening technology but there is currently a movement to fine tune the use of DXA scanning. The addition of trabecular bone score (TBS) grading to traditional DXA has been shown to be a significant predictor of fracture, independent of FRAX calculation.29 TBS is still proprietary software and has not been applied to all DXA machines at this time, but the movement is underway.

Other emerging imaging technologies including radiofrequency echographic multi spectrometry, hip-axis length, hip-strength analysis, and finite element analysis have been proposed to add to DXA scans but these have not been adopted to widespread clinical use at this time. It is believed that these technologies will assist with identifying more focal areas of bone weakness in a given patient.29

Several biomarkers have been proposed as possible screening methods for osteoporosis, including micro RNA and long-non-coding RNA. miRNA-103a, in particular, may represent both a screening method as well as potential treatment method as targeting this region with antagomir-103a can overcome bone formation inhibition. In vitro and animal studies are currently underway.29

Gaps in the Evidence-Based Knowledge

A number of questions regarding osteoporosis are still unanswered: What is the best universally accepted tool to assess bone strength? Should individuals with family history of osteoporosis be tested earlier than the currently identified timeframes? How can we maximize our peak bone mass when we are young? Does calcium and vitamin D supplementation truly alter bone quality? How can one best identify and modify risk factors for falling? What are the long-term adverse effects of the pharmacologic therapies available now?  Unfortunately, despite significant advances in the knowledge of the biochemical basis of osteoporosis, most of these questions are still clinically relevant today. Further research is needed to address these issues and optimize patient outcomes.

Figure 1

FRAX Clinical Risk Factors
Previous fracture
Parental history of hip fracture
Smoking status
Glucocorticoid use
Rheumatoid arthritis
Secondary osteoporosis≥3 units of alcohol/day
Femoral neck BMD


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Original Version of the Topic

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

Previous Revision(s) of the Topic

Linqiu Zhou, MD, Paul Kitei, MD, Chen Zhou, MS-2. Osteoporosis in Rehabilitation. 4/19/2016

Nadia Zaman, DO, Richard G. Chang, MD, MPH. Osteoporosis in Rehabilitation. 7/24/2020

Author Disclosure

Travis Coats, MD
Nothing to Disclose