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Understanding Osteoporosis Medications


AUTHOR AND EDITOR INFORMATION

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Author: David Weiss, MD, Medical Director of Physical Medicine and Rehabilitation, Assistant Professor, Internal Medicine, Marianjoy Medical Group

David Weiss is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Editors: Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, University of Medicine and Dentistry of New Jersey, New Jersey Medical School; Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center; Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers, Phoenix

Author and Editor Disclosure

Synonyms and related keywords: spinal cord injury, osteoporosis, osteoporosis and SCI, SCI-induced osteoporosis, functional electrical stimulation, FES, dual-energy radiographic absorptiometry scan, dual-energy X-ray absorptiometry scan, DRA, DXA

INTRODUCTION

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Background

One of the inevitable complications of spinal cord injury (SCI) is the associated osteoporosis that occurs predominantly in the pelvis and the lower extremities. The acute treatment of patients with SCI has always focused on the injury itself and on the immediate complications that subsequently arise. Bone loss as a consequence of SCI has been of secondary concern historically. Osteoporosis in persons with SCI was first studied in relation to calcium metabolism and the associated hypercalcemia and renal calculi that followed.

The differences between SCI-induced osteoporosis and other causes of bone loss (disuse), such as prolonged bed rest, space travel, and lower motor neuron disorders, have since become clearer. New technologies allow monitoring of osteoblastic and osteoclastic activity at the microscopic level, while modern radiographic techniques have allowed more refined studies to be undertaken at the macroscopic level.1, 2

See also the following related Medscape topic:
Resource Center Fracture
Resource Center Osteoporosis

Pathophysiology

The mechanism behind SCI-induced osteoporosis is accepted as being multifactorial in the acute and chronic stages.3 These mechanisms differ from those observed in subjects without SCI after prolonged bed rest and in subjects with other neurologic deficits. SCI causes immediate and, in some regions, permanent gravitational unloading. The result is a disuse structural change with associated metabolic consequences. Hypercalciuria is seen by 10 days following the SCI and reaches a peak 1-6 months postinjury. This level of hypercalciuria is 2-4 times that of persons without SCI who undergo prolonged bed rest. This marked increase in urine calcium is the direct result of an imbalance between bone formation and bone resorption.4, 5

The activity of osteoblasts and osteoclasts is triggered by the SCI; however, markers of osteoblastic activity rise only slightly, while osteoclasts have a significant increase in their activity, peaking at 10 weeks following the SCI with values 10 times the upper limits of normal. In addition, the increased bone resorption precedes the increase in osteoblastic activity. This model at the skeletal level following SCI resembles the high bone turnover rate seen in postmenopausal osteoporosis.

The loss of bone also may be enhanced by lack of muscle traction on bone or by other neural factors associated with SCI. These other factors further separate SCI-induced osteoporosis from other causes of disuse demineralization. Absorption of calcium from the gastrointestinal tract has been found to decrease in the acute period following SCI. Even so, in the past, dietary calcium reduction commonly was recommended as a way to decrease calcium excretion and prevent the complications of hypercalciuria.

The body that has sustained SCI has been considered the model of premature aging, and the role of parathyroid hormone in osteoporosis following SCI illustrates this point. Acutely, the parathyroid gland is relatively inactive, with low parathyroid hormone levels observed up to the 1-year point following injury. Hypercalcemia seen immediately postinjury leads to this low level. A reversal in activity during years 1-9 is noted.6, 7, 8

The parathyroid gland is stimulated to the point that parathyroid hormone levels are above the reference range. The result is an increase in bone re-absorption or osteoporosis related to parathyroid dysfunction in the chronic stages of SCI. This chronic-stage mechanism of osteoporosis is balanced by an increase in bone mineral in regions of the body in which weight bearing is resumed (eg, in the upper extremities, spine) and adds to the demineralization observed in regions that are chronically non–weight-bearing (eg, the pelvis, lower extremities).

Frequency

United States

Bone loss following SCI occurs throughout the skeletal system, with the exception of the skull. These losses are regional; areas rich in trabecular bone are demineralized to the greatest degree. The distal femur and proximal tibia are the bones most affected, followed by the pelvis and arms.9, 10 The amount of demineralization in the skull, pelvis, and lower limbs is independent of the neurologic level.

A positive correlation exists between the time following the injury and the degree of bone loss. Rapid loss of bone mineral occurs during the first 4 months following SCI. In patients with SCI, less than 1 year following the injury, reduction in bone mineral densities has been noted in the femoral neck (27%), midshaft (25%), and distal femur (43%), as compared with controls.

Bone mineral loss continues, but to a lesser degree, in the pelvis and lower extremities over the next 10 years.11 By 10 years postinjury, over 50% of bone content in these regions has been demineralized. The arms and trunk demonstrate an increase in bone content after the 4-month point. This gain in mineral content over the next 10-year period helps to offset some of the initial losses in the arms. The net effect is an approximate 10-21% loss of bone at the 10-year point. Interestingly, the trunk has a net gain in mineral content by 12 years postinjury.

Significant differences in upper extremity bone density are observed between paraplegic patients and tetraplegic patients. The bone mineral density of the arms of paraplegic patients returns to near normal by the 10-year postinjury point, which is approximately 16% more bone mineral than is found in the arms of tetraplegic patients.

Individuals with complete injuries tend to have less bone mineral density than those with incomplete lesions. With complete lesions, significantly lower lumbar spine bone mineral densities have been noted (z value -1.47) in patients 1-26 years post injury. In addition, individuals with incomplete motor SCI demonstrate greater bone mineral density at the areas of greater lower extremity muscle strength.

Some controversy exists surrounding the protective effect of spasticity on bone mineral content. Studies have found a decrease in losses of bone density in patients exhibiting spasticity, compared with the flaccid group.

Mortality/Morbidity

The most measurable complication of osteoporosis following SCI is pathologic fracture. The historical incidence of fractures in the SCI population has been 1.45-6%; however, this historically low incidence may be deceptive, because most patients with SCI who sustain subsequent traumas and fractures are not treated in SCI centers. In addition, these studies on fractures have come from inpatient charts. The Model Spinal Cord Injury System has produced figures on fracture rates based on time following SCI, with incidences of 14% at 5 years, 28% at 10 years, and 39% at 15 years postinjury. These incidence rates are based on outpatient studies and have been confirmed.

The sites of fractures correspond to the sites of greatest osteoporosis, with fractures most commonly occurring in the supracondylar region and the tibia.12 A bone mineral density fracture threshold of 50% appears to exist for the knee, and this most likely is the bone mineral density fracture threshold for most regions in the body.

Fracture rates in the lower extremities are 10 times greater in patients with complete SCI than in patients with incomplete injuries. Paraplegic patients are at higher risk than are tetraplegic patients, due to the higher level of function that paraplegic individuals have with regard to mobility and participation in physical activities.

The inciting events that lead to fractures frequently are unknown or are associated with relatively minimal traumas. The reason is that less torque is needed to produce failures in bone in persons with SCI than in individuals who have not sustained SCI.

See also the following related eMedicine topic:
Functional Outcomes per Level of Spinal Cord Injury

Race

No studies have examined whether a correlation exists between race and osteoporosis following SCI.

Sex

Limited studies exist on the connection between sex and osteoporosis following SCI. However, it does appear that, as in the population without SCI, women have more bone loss than do males.

Age

In the last few decades, only one study has included age as a risk factor for osteoporosis. For every 1-year increase in age, the rate at which osteoporosis of the knees developed was shown to increase by 3.54%. In another study, rates for femoral (including hip) fractures in patients following SCI were found to be greater than those in the general population by factors of 104 and 24 at age 50 years and 70 years, respectively.


CLINICAL

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History

Osteoporosis by itself is a subclinical condition. Thus, no associated clinical signs or symptoms exist for this entity. The most common way osteoporosis is discovered in SCI patients is when radiographs are taken following fractures; the radiographs reveal the fracture and significant bone loss.

Physical

No overt physical examination findings exist that lead to the diagnosis of osteoporosis. However, patients with SCI may be predisposed to knee effusions due to osteoporosis, heterotopic ossification, trauma, and benign hydrarthrosis.

Causes

Osteoporosis following an SCI is a primary complication of the SCI itself. For more discussion on risk factors, please see Pathophysiology.


DIFFERENTIALS

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Osteoporosis (Primary)
Osteoporosis (Secondary)
Spinal Cord Injury and Aging

WORKUP

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Lab Studies

  • The biomechanical markers that have been measured in studies of SCI-induced osteoporosis include serum calcium, phosphorous, alkaline phosphatase, 1,25–dihydroxyvitamin D and calcitonin, and urinary calcium and hydroxyproline. These markers may not be followed routinely in the ongoing care of the person with SCI. However, their sensitivity and early response indicate that these markers would be useful in the early identification of patients with SCI who are at risk of developing severe osteoporosis.5, 13, 14

Imaging Studies

  • Advances in technology have resulted in the ability to precisely quantify bone density. Quantitative computed tomography (QCT) scans can isolate densitometric and geometric changes in cortical and trabecular components of bone.15 This kind of testing allows for volumetric measurements, grams per cubic centimeter, which is the most precise measurement of bone density. The most commonly used method for clinical studies, dual-energy radiographic absorptiometry scan, records absolute bone mineral densities in various regions of the body.14, 16 This allows for comparison of bone mineral densities in patients with SCI with measurements from uninjured individuals of similar age, race, and sex. These imaging studies are not used commonly in the standard of care of patients with SCI.


TREATMENT

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Rehabilitation Program

Physical Therapy

The effect of remobilization on SCI-induced osteoporosis has been fairly well studied. Weight-bearing exercises with standing frames and bikes, using forms of functional electrical stimulation (FES), have been shown to be effective when started within 6 weeks of injury. These same programs in the population with chronic SCI, however, are ineffective in preventing osteoporosis or restoring bone mineral.17, 18, 19, 20, 21, 22

Medical Issues/Complications

For more discussion on complications of osteoporosis following SCI see Mortality/Morbidity.

Surgical Intervention

Typically, conservative treatment is pursued, with healing reported in 3-4 weeks. Soft splints may be required. Hard splints and materials should not be used. With deformity of the extremity from fracture (eg, displacement of bones), surgical intervention of open reduction and internal fixation may be required.

Consultations

An orthopedic consultation may be warranted in cases of the above-described deformities.

Other Treatment

FES-induced lower extremity cycling has not been shown to increase bone density in the hip parameters of patients with chronic SCI.17, 18, 19, 22


MEDICATION

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Changes occur rapidly in the skeleton of a patient with SCI, and interventions must be undertaken quickly. The fact that there are no effective treatments to restore bone mineral once it has been lost makes early treatment even more imperative. Thus, early prevention is the main focus in treating SCI-induced osteoporosis.8, 23, 24, 25, 26, 27, 28

See also the following related Medscape topic:
CME Advances in Osteoporosis Management: Clinical Insights

Drug Category: Bisphosphonate derivatives

To date, the bisphosphonates are the most well-studied class of medications to prevent demineralization following SCI. They are potent inhibitors of osteoclastic bone resorption and have been found to have a positive effect in preventing SCI-induced osteoporosis. The studies on bisphosphonates in persons with SCI, however, are preliminary, and there is no consensus on drug of choice or a dosing regimen. In addition, the effectiveness and side effects of other drug therapies oriented to the more common forms of osteoporosis have not been studied well in this population.

Drug NamePamidronate (Aredia)
DescriptionInhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.
Adult DoseModerate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; hypocalcemia
InteractionsNone reported
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMonitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women

Drug NameEtidronate disodium (Didronel)
DescriptionInhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.
Adult DoseModerate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; hypocalcemia
InteractionsNone reported
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMonitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women

Drug NameClodronate (Bonefos)
DescriptionInhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.
Adult DoseModerate hypercalcemia: 60 mg dose as initial IV dose infusion over 4 h; alternatively, 90 mg dose as initial single IV dose infusion over 24 h
Severe hypercalcemia: 90 mg as initial IV dose infusion over 24 h
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; hypocalcemia
InteractionsNone reported
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMonitor hypercalcemia-related parameters, such as serum levels of calcium, phosphate, magnesium, and potassium, once treatment begins; adequate intake of calcium and vitamin D is necessary to prevent severe hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not co-administer with alendronate for osteoporosis in postmenopausal women

Drug NameIbandronate (BONIVA)
DescriptionInhibits osteoclast-mediated bone resorption. In postmenopausal women, reduces bone turnover rate, leading to a net gain in bone mass.
Adult Dose2.5 mg PO qd; administer with water at least 1 h prior to first food or beverages (other than water) of the day
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; uncorrected hypocalcemia; inability to stand or sit upright for at least 60 min following drug administration
InteractionsMultivalent cations (eg, calcium, aluminum, magnesium, iron) decrease absorption, administer ibandronate at least 1 h prior to vitamin and mineral supplements; NSAIDs may aggravate GI irritation
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMay cause upper GI disorders (eg, dysphagia, esophagitis, ulceration), minimize GI risk by standing or sitting upright 1 h following dose; calcium and vitamin D supplementation required; not recommended with severe renal impairment (ie, CrCl <30 mL/min)

Drug Category: Parathyroid hormone

Promotes new bone formation, leading to increased bone mineral density. Teriparatide is a biological product containing a portion of human parathyroid hormone, which primarily regulates calcium and phosphate metabolism in bones. Teriparatide is approved for patients at high risk of fracture due to primary osteoporosis, hypogonadal osteoporosis (men), or postmenopausal osteoporosis (women).

See also the following related eMedicine topic:
CME Teriparatide Effective for Osteoporosis Following Prior Antiresorptive Therapy

Drug NameTeriparatide (Forteo)
DescriptionRecombinant human parathyroid hormone rh-PTH (1-34), which has identical sequence to 34 N-terminal amino acids (biologically active region) of 84–amino acid human parathyroid hormone (PTH). Acts as endogenous PTH, thus regulating calcium and phosphate metabolism in bone and kidney. Works primarily to stimulate new bone by increasing number and activity of osteoblasts (bone-forming cells). Additional physiological actions include regulation of bone metabolism, renal tubular re-absorption of calcium and phosphate, and intestinal calcium absorption. When administered with calcium and vitamin D, teriparatide increases bone mineral density and decreases risk of fractures in patients with osteoporosis.
Adult Dose20 mcg SC qd
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; increased risk for osteosarcoma (including patients with Paget disease of bone or with unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving the skeleton); children or growing adults; patients with bone metastases or history of skeletal malignancies, and persons with metabolic bone disease other than osteoporosis
InteractionsNone reported
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsMonitor for hypercalcemia; may cause orthostatic hypotension (particularly following first several doses), dizziness, or leg cramps


FOLLOW-UP

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Further Inpatient Care

  • No standards exist for follow-up care after the diagnosis of osteoporosis in persons with SCI.

Deterrence

  • In the acute and chronic stages of SCI, appropriate nutritional intake of calcium and vitamin D, as well as proper precautions in transfers and wheelchair sports, can help in prevention of osteoporosis and, later, in the prevention of fractures.
  • Appropriate amounts of calcium intake and early mobilization are the main means of limiting mineral loss; however, there is no known way to completely prevent osteoporosis in this population.

See also the following related eMedicine topic:
Sports Participation by Paraplegics

Complications

  • Fractures are the only complication that arises as a result of osteoporosis. For more details on fractures and osteoporosis in persons with SCI, see Mortality/Morbidity.

Patient Education

  • Patients should be educated in their nutritional needs and in the benefits of early mobilization. Transfer techniques and wheelchair sport safety also are important educational areas that can help to limit the amount of osteoporosis and prevent the fractures that may result.
  • For excellent patient education resources, visit eMedicine's Osteoporosis and Bone Health Center. Also, see eMedicine's patient education articles Osteoporosis and Understanding Osteoporosis Medications.


MISCELLANEOUS

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Medical/Legal Pitfalls

  • To date, no standard of care exists for follow-up in persons with SCI when it comes to osteoporosis.


MULTIMEDIA

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Media file 1:  Fracture of an osteoporotic bone in a patient with a spinal cord injury.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  X-RAY

Media file 2:  Fracture of an osteoporotic bone in a patient with a spinal cord injury.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  X-RAY

Media file 3:  Osteoporotic femur in a patient with a spinal cord injury.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  X-RAY

Media file 4:  Osteoporotic femur in a patient with a spinal cord injury.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  X-RAY


REFERENCES

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Osteoporosis and Spinal Cord Injury excerpt

Article Last Updated: Apr 1, 2008