Osteoporosis-related fractures: What they are and how they occur following spinal cord injury

Abbreviations

25(OH)D

25 hydroxyvitamin D

aBMD

areal bone mineral density

AIS

ASIA Impairment Scale

BMD

bone mineral density

BMI

Bone Mass Index

BWSTT

body-weight exercises supported treadmill training

CTX-I

type I collagen C-telopeptide

DEXA

dual-energy X-ray absorptiometry

EMS

electromyostimulation

ES

electrical stimulation

FAO

bone-specific alkaline phosphatase

FES

functional electrical stimulation

FRAX

fracture risk assessment tool

pQCT

quantitative computed tomography

PTH

parathyroid hormone

SCI

spinal cord injury

WHO

World Health Organization

Introduction

In 2017, approximately 22 million people around the world were living with a spinal cord injury (SCI), a rate increase of 14.21% in the last 10 years ( ). The better access to medical care resources such as emergency medical services and rehabilitation departments led to longer survival for this population ( ). Henceforth, many consequences were related to SCI such as neurogenic bladder, neurogenic bowel, neuropathic pain, spasticity, and osteoporosis ( ; ).

Osteoporosis affects the health of individuals with SCI because it increases the risk of fragility fractures with consequences related to fractures such as ulcers, immobility, depression and even death ( ; ; ). Osteoporosis after SCI is defined as an excessive bone resorption after SCI and bone fragility fractures are defined as fractures caused by a trauma that would be insufficient for a normal bone to fracture ( ; ) or by minimally loaded situations ( ; ).

The impact of fractures on the lives of individuals with SCI suggests that most patients will be hospitalized after the fracture and undergone to surgery, and complications as worse performance in activities of daily living and ambulation after the fracture are mostly described. These issues mean increased disability and costs for the health system ( ).

Special attention should be paid to the prevention of fractures, and appropriate treatments should be instigated to prevent excessive bone loss and futher investigations should be performed. Most of the physicians are not educated to measure risk factors for bone fragility fractures. Dual-energy X-ray absorptiometry (DEXA) should be performed in patients with SCI, likely before the occurrence of fractures. Bone remodeling markers could give us a clue of the resorption rate and treatments to prevent further loss should be consider.

Physiopathology

Bone demineralization after SCI occurs in a rate loss of approximately 4% per month in the first year ( ; ; ), primarily in the knees. Demineralization begins in the early days, peaks around the 10th to 16th weeks and stabilizes around the 16th to 24th months ( ; ; ). Recent studies suggest that the bone loss extends 3 to 8 years after SCI ( ). Previous studies demonstrated bone demineralization greater than 20% in the hip, 37% to 52% in the distal femur and 36% to 70% in proximal tibia after 1 to 3 years after SCI ( ; ; ).

Bone loss associated with SCI is related to immobility and metabolic changes ( ; ; ). Individuals with SCI exhibit primarily hypercalcemia, hypercalciuria, hyperparathyroidism, decreased levels of osteocalcin, and higher levels of sclerotin. The loss of bone mineral density is 2 to 4 times greater than the loss that occurs in an immobilized individual without SCI ( ).

Other related factors may contribute to this bone loss, such as vitamin D deficiency and the use of methylprednisolone, anti-convulsant drugs, and psychotropic substances. Previous studies discovered that 14% to 32% of individuals with SCI were deficient in vitamin D ( ; ). Even in tropical countries, vitamin D deficiency is a common health problem ( ).

Fractures

The consequence of osteoporosis in individuals with SCI is fracture due to bone fragility. It usually occurs in transfers and activities with minimal or no trauma, such as low-speed falls, torsional stress ( ; ). Studies ( ; ; ) detected a specific time between SCI and fracture was 9 to 10 years, average age of first fracture for women 50 + and for men 40 + years-old ( ). Fractures may occur in 25% to 46% of these individuals over their lifetimes ( ; ; ). Fractures are primarily related to torsional forces during transfer, passive mobilization, compressive forces, and falls ( ; ; ). It seems the most frequent fracture cause is due to falls from a wheelchair or even their own height while walking or standing ( ). This result is not surprising because falls are a common health problem in individuals with SCI, and the prevention of falls should be a priority. Another study found transfer as the main cause of fracture ( ).

The risk of fracture after SCI is different from the risk of osteoporosis ( ; ), individuals with tetraplegia have more osteoporosis than those with paraplegia, however, individuals with paraplegia have a higher frequency of fractures due to exposure to falls ( ; ; ). Most places of fractures are in the tibia and/or distal fibula, distal femur, or hip/proximal femur and proximal tibia ( ; ; ). It seems hip/proximal femur and distal tibia/fibula are as common as the distal femur ( ). However, individuals who are ambulatory and wheelchair dependent may have different areas of fractures. Ambulatory individuals fracture more often the distal tibia/fibula, and wheelchair-bound patients fractured the distal and proximal femur ( ). A second (15%) and third (2%) fracture are experienced by patients ( ).

The impact of fractures on the lives of people with SCI suggests that most of the patients are hospitalized after the fracture, and some had complications. Almost one-third of the participants reported worse performance in activities of daily living and ambulation after the fracture had healed. Individuals with osteoporosis-related fractures after SCI had several complications. Most individuals were hospitalized, and half of them underwent surgery ( ). These issues mean increased disability and costs for the health system.

Risk factors

Previous studies showed risk factors ( ; ; ) and the following ones were described associated with increased fracture criteria: AIS (ASIA Impairment Scale) A or B; age 40 + years old; SCI longer than 3 years; age at SCI of 16 years or less; three servings of coffee per day; smoking; women; family history of osteoporotic fractures; low bone mineral density; low weight Bone Mass Index (BMI) < 19 kg/cm ² ; alcohol intake greater than 30 g/day; paraplegia, and the use of corticosteroids ( ). Studies by Craven developed protocols conducive to treatment based on these risk factors. Other aspects related to fractures are 25 hydroxyvitamin D [25(OH)D] levels less than 20 ng/mL ( ).

Diagnosis

Laboratory

Bone formation markers are useful in the management of SCI patients. Procollagen type I N-propeptide reflects osteoblastic activity, bone-specific alkaline phosphatase, which is a bone formation marker, is elevated on the first year after injury. Osteocalcin, another bone remodeling marker is reduced in the first year others ( ; Uebelhart et al., 1995).

Bone resorption markers such as deoxypyridinoline, pyridinoline, sclerostin, and type I collagen C-telopeptide (CTX-I) can be used. CTX-I is increased in the second week after SCI and peaks between 2 and 4 months, and its levels can remain increased for up to 5 years ( ; ).

The immobilization resulting from acute SCI stimulates osteoclastic bone resorption and calcium homeostasis markers as parathyroid hormone (PTH) is reduced in the first year after injury, urinary calcium is elevated, serum calcium is increased, while ionized calcium is generally normal. These alterations peak from the 3rd to the 10rd month after SCI ( ; ).

Dual-energy X-ray absorptiometry

Dual-energy X-ray absorptiometry (DEXA) for patients with SCI is a confirmatory test to predict the future risk of fracture and also serves for ongoing monitoring of bone health and to access bone loss ( ) by the bone mineral density (BMD) measurements. It is precise and safe ( ) since there were strong associations among different observers and it emits a very low level of radiation (0.1 mSV), that is, 1/10–1/30 less radiation than a chest X-ray. DEXA calculates the measurement of bone mineral density in g/cm ² and protocols for calculating bone mineral density for patients with SCI already exist. Some studies suggested that low BMD in the hip predicted fracture in individuals with SCI ( ) and other authors suggested that DEXA measurement of the distal femur and proximal tibia, with specific protocols for the evaluation of these sites ( ; ; ) and for knee fracture thresholds of 0.78 g/cm ² which a fracture may start to occur and fracture breakpoint of 0.49 g/cm ² ( ; Fig. 1 ).

The measurement of BMD of the knees is extremely important for monitoring bone loss, as the hip and spine do not show the highest losses of BMD after SCI and because osteoporosis is most severe below the level of the injury ( ; ). It can be even more useful in those patients where assessing the spine and hip is not possible, such as cases with spine surgeries or hip heterotopic ossifications. The limitations for measuring BMD in the knees are fractures and orthopedic surgeries. In cases of flexion deformities, the assessment of bone mineral density can be performed in the lateral scans ( Fig. 2 ).

Quantitative computed tomography

Quantitative computed tomography (pQCT) is also a safe method and evaluates density, volume and geometry, differentiates cortical bone and trabecular bone, but it is difficult to establish prediction, and have plus radiation, and aBMD < 114 mg/cm ³ in the femur and aBMD < 72 mg/cm ³ in the tibia are described as fracture thresholds ( ; ).

Treatment

It is still under debate the best way to prevent fragility fractures after SCI ( ; ). A diet rich in fruits and vegetables, daily doses of calcium of 1000 to 1200 mg vitamin D, 200 to 1000 iU/day aiming a serum level of 30 ng/dL, physical exercises, stop smoking and drinking alcoholic beverages and avoid over doses of coffee are contributive recommendations ( ; ; ; ).

Pharmacologic therapy

Studies showed the efficacy of bisphosphonates in daily doses of alendronate 10 mg (orally) and calcium 500 mg to decrease bone turnover in people with SCI ( ). Bisphosphonates were more effective if 25-OH > 33 ng/mL and vitamin D deficiency should be investigated because of osteomalacia risk ( ; ). However, it is a medication with around 50% adherence despite being generally well-tolerated ( ; ). The association of calcium 500 mg, alendronate, 70 mg weekly and vitamin D 400 U starting 10 days after SCI and use for twelve months to 24 months prevented the decrease of BMD in the distal tibial epiphysis in patients with SCI ( ; ). In contrast, the isolated use of 500 mg of calcium daily for the same period didn’t prevent it ( ).

Pamidronate 60 mg usage, intravenously 4 times a year associated with dietary calcium (700 mg/day) and vitamin D, didn’t prevent bone loss in the long term, in patients with spinal cord injury with complete motor injury ( ; ). Zoledronic acid administered once a year, intravenously, showed a significant reduction in bone loss of lumbar spine, hip and trochanter with some side effects as myalgia, fever and nasal congestion ( ). Another study described zoledronic acid administration failed to prevent bone loss at the knee in persons with acute spinal cord injury ( ).

Many complications are associated with bisphosphonates as hypocalcemia, gastrointestinal effects, osteomalacia, osteonecrosis of the jaw (1/10,000 patients) after more than 4 years of use, atrial fibrillation, hepatotoxicity, teratogenicity for women of childbearing age and it cannot be used in chronic renal failure.

Vitamin D is also effective ( ; ). Vitamin D treatment determined significant reduction of urinary bone resorption markers despite neutral effects on bone formation markers ( ; ).

Teriparatide reduced the risk of vertebral fractures at a dose of 20 μg daily, subcutaneously, when associated with robotic treatment. Teriparatide alone, did not improve BMD either on the spine or on the hip for patients with SCI ( ).

Denosumab inhibits osteoclast formation, prevents bone resorption, and reduces risk of spine fractures. A study by treated 14 patients with SCI with denosumab, calcium, and vitamin D with improvement of bone mineral density in 12 months. Despite that, there are still poor evidence for people with SCI.

There is no consensus on the follow-up after staring pharmacologic therapy. It is recommended to repeat DEXA after 1 to 2 years after start of treatment ( ).

Treatment with bisphosphonate has been done for 4 to 5 years and should be consider drug holiday after 3 to 5 years of use, because of its prolonged effect ( ; ).

Rehabilitation/non-pharmacological therapy

One of the possible causes of osteoporosis after SCI is the inability to perform weight bearing activities and loss of the strengthening effects of bone stress related to muscular contraction and gravity. In this way, rehabilitation is an option for osteoporosis prevention and treatment after SCI focus on stimulation muscle contraction and weight bearing in order to stimulate the mechanical stress, to which bone is exposed to daily activities among healthy people ( ; ).

The mechanostat theory, based on Wolff’s law, states that mechanical loading influences bone structure by changing its mass (amount of bone) and architecture (its arrangement) to provide a structure that resists to habitual loads. There are strains within bone that are kept within certain limits by adding and removing bone tissue that could promote bone strengthening, depending on the applied forces. The paralysis secondary SCI causes a decrease in the mechanical load and results in bone tissue loss ( ; ).

Standing and walking

Supported standing with standing frames, tilt tables, long leg braces, wheelchair standing have long been used as a treatment for reducing and or delaying osteoporosis after SCI. It is traditionally incorporated in rehabilitation programs, even without proof of its effectiveness ( ).

There are three good quality studies that evaluate the influence of weight bearing activities in the acute phase of SCI, with controversial results ( ). It was observed that an early mobilized subject showed no or insignificant loss of trabecular bone when compared with non-interventional groups ( ). In the same other way, two studies has found that patients who performed daily standing or walking exercises for more than 1 h, 5 times per week had significantly higher BMD in the lower extremities after 2 years, in comparison to those who did not perform standing movements ( ).

For the chronic phase, the results seemed more uniform, with very little evidence of any gain in BMD when the first year after injury had passed ( ). Goktepe et al. found no significant effect on BMD in chronic patients after daily standing for less or more than 1 h for a period of 4 years ( ). In the same way, a study by did not detect changes in fracture risk at femoral neck after standing in a frame program for 45 min twice a day for 5 months. Dudley-Javoroski et al. compared the effect of bone compressive loads using 0% body weight (no standing), 40% body weight (passive standing—“low dose”), and 150% body weight (quadriceps stimulation in supported stance—“high dose”). After a 3 year training protocol, 3 times a week, the high dos group had an attenuated BMD decline when compared to passive standing or no standing individuals. There were no differences between low-dose and no standing group, suggesting that BMD for participants doing passive stance is the same as those who performed no standing ( ).

Gait training with walking frame, orthosis, body-weight exercises supported treadmill training (BWSTT), and exoskeleton is among the activities of a rehabilitation program with the main purpose to facilitate ambulation SCI persons. Besides that, there are some studies investigating its benefits on bone loss after SCI, but up to now, there is no good quality evidence in favor of this kind of intervention. showed that a BWSTT (30%–50% weight relief) with neuromuscular electrical stimulation, twice a week, for 20 min, for 6 months, in tetraplegic individuals led to elevate bone formation and reduce bone resorption markers, although the BMD did not enough. Another study with 12 months of BWSTT training did not increase bone density in individuals with chronic incomplete SCI, but BMD did not decrease at fracture-prone sites ( ). Other studies involving ambulatory orthosis also observed that walking did not improve BMD ( ; ).

Karelis et al., in a case report, noticed little benefits on locomotor training using a robotic exoskeleton 3 times/week, for 6 weeks. A previous case report study did not find BMD benefits after robotic-assisted BWSTT (Lokomat) for 1 h activity, 3 times a week, in a period of 3 months, in an acute SCI. It is important to be careful about fractures occurring during this activity as cited by Zleik et al. Some studies suggested that low BMD may be a relative contraindication for the use of these devices ( ).

The bone loss prevention/treatment needs intensive body loading and for a long period in order to maintain body mass. Although there is no BMD cut-off value to preclude patients from participating in rehab interventions, an assessment of fracture risk is indicated before activities such as standing and walking to ensure its safety ( ; ). It is recommended to avoid exercises that result in torsion of the distal lower extremity or that have a risk of falling ( ).

Although practices for increased mobility and weight-bearing are clearly important to skeletal health in SCI, there is not sufficient evidence in their capability to maintain BMD of the lower extremity ( ). In summary, there is low evidence that more than 5 h per week standing exercises could preserve tibial BMD in acute (less than 1 year) SCI cases ( ).

Electrical stimulation

Electrical stimulation (ES) and Functional Electrical Stimulation (FES) involve the use of surface or implanted electrodes to stimulate muscular activity. Whereas both methods typically employ cyclical patterns of electrical stimulation that simulate natural muscular activity, FES is directed toward the attainment of purposeful movement such as cycling or walking.

FES is the most extensively investigated approach since it combines the benefits from electrical stimulation and mechanical loading of the lower extremity long bones. Although FES intervention has been demonstrated to improve muscle atrophy, solid evidence from a large-scale study is still lacking regarding its influence on sub-lesional BMD attenuation.

FES studies enrolled participants with both acute and chronic injuries and are therefore difficult to classify as pure prevention or treatment interventions. In one review study, described that FES training administered at the time of acute injury appears to markedly reduced bone loss at the site applied or, if administered to those with chronic SCI, was also efficacious, albeit with a reduced magnitude of effect, at the place to which the load was applied. investigated in a literature review the prevention- and evidence-based treatments for osteoporosis related to SCI. They discovered low-quality evidence indicating that ES provided no significant effects. Very low-quality evidence did not show any benefit for low-intensity (3 days per week) cycling with FES in chronic SCI.

carried out a meta-analysis study to investigate whether bisphosphonate administration or functional electrical stimulation (FES) training could effectively decrease bone mineral. They noticed that FES cycling did not significantly decrease BMD loss in acute SCI individuals. Whereas, for people with a chronic SCI, BMD demonstrated a significant increase near the site of maximal mechanical loading. Furthermore, the studies employing FES ≥ 5 days per week were likely to have better effectiveness than studies using FES ≤ 3 days per week ( ).

In the acute phase, there is a non-randomized trial reporting that FES cycling provided 1 to 3 months after SCI can partially reduce BMD loss in distal femur ( ). In addition, the effect on the attenuation of bone loss in the distal femur diminished once FES cycling was discontinued ( ). measured the effect of an FES cycling intervention on bone mineral density (BMD) of the tibia in recently injured SCI people in a non-randomized clinical trial. The intervention consisted of 30-min FES cycling three times a week for 6 months. They concluded that FES cycling was not effective for improving bone mass at the tibial mid shaft during the first year after injury.

For the chronic phase, the studies are conflicting, but the investigations that show improvement seem to be those with a longer period of training, which is 12 months or more, 5 times/week ( ; ). It is also evident that all these studies measured their improvement corresponding to the trabecular bone, in particular in the distal femur or the proximal tibia.

FES cycling studies that reported a positive effect on bone parameters used protocols of at least 3 sessions per week for 6 months in duration. The increase in bone parameters was in areas directly affected by the stimulated muscles. Although a study showed that the FES cycling intervention needed to be maintained or bone gains were lost ( ). found that BMD was preserved in the distal locations of some participants in 12 months. They concluded that the high-volume FES-induced cycle training had clinical relevance as it could partially reverse bone loss and thus may reduce fracture risk at this fracture-prone site.

The use of ES to clinical care has been fraught with difficulties due to the labor intensive nature of the present approaches and the appreciation that any effect on bone is rapidly lost, when the ES training is either reduced in frequency or terminated ( ; ; ). Considerations for FES efficacy in osteoporosis in SCI should consider attention to the duration, frequency, and power of the output ( ). Guidelines include intensities with loads of 1–1.5 times body weight, sessions of 3 or more per week for several months to 1 or more years, and safety considerations to prevent fractures ( ). considered that ES and FES should be used with caution in patients with combined hip and knee flexion contractures of > 30, a prior lower extremity fracture, severe lower extremity spasticity, and/or significant ankle plantar flexion contractures.

Finally, although the use of FES cycling looks promising, the limited availability of cycle ergometry for home or longitudinal use may limit its generalization, if therapy cannot be maintained outside a clinical trial environment. The quality of evidence available in this field is poor. Some results suggest physical activity could attenuate bone loss ( ; ). Studies reported benefits on arm bone mass maintenance but did not prevent demineralization in the lower body ( ). The type of activity and training intensity were not well-described, and many studies used a self-reported physical activity as a reference.

Physical activity

The quality of evidence available in this field is poor. Some results suggest physical activity could attenuate bone loss ( ; ). Two of them reported benefits on arm bone mass maintenance but did not prevent demineralization in the lower body ( ). The type of activity and training intensity were not well-described, and many studies used a self-reported physical activity as a reference. Miyahara et al. found that the earlier the athlete started sports after injury, the higher the BMD of the legs. Further, a longer period of athletic career after restarting was significantly related to higher leg BMD.

Vibration

The mechanical vibration used to prevent and/or treat the loss of BMD mixed results ( ; ). Similar to FES, the specifications of the chosen full-body vibration platform, including intensity and frequency of vibration, signal transmission, and joint position and angle, could play a role in effectiveness ( ; ).

Ultrasound

Ultrasound does not seem to play a role in preventing or treating osteoporosis. The only randomized study by did not indicate any benefit of low-intensity pulsed ultrasound to prevent decreased BMD. Therapeutic pulsed ultrasound was applied to the heel of individuals with spinal cord injury for 20 min a day, 5 times a week for a period of 6 consecutive weeks. The contralateral heel was simultaneously treated with inactive United States. No improvement was observed in any of the parameters evaluated ( P > .05). According to the authors, this finding may be related mainly to the inability of the US to effectively penetrate the external cortex of the bone due to its acoustic properties.

Combined treatments

There are few evaluated studies that combined interventions for the treatment of bone loss in chronic SCI. These studies assess the concomitant administration of pharmacological therapy with non-pharmacological rehabilitation interventions ( ; ; ). and investigated the combination of zoledronate (ZA) with FES-rowing. The results demonstrated that the osteogenic response to FES-rowing was dose-dependent and combination therapy with ZA and FES-row training had therapeutic potential to improve bone quality, and perhaps reduced fracture risk at the most common fracture site following SCI. evaluated the response of bone to recombinant parathyroid hormone in combination with weight bearing. The results did not show a statistically significant increase in BMD of the lumbar spine ( ).

Conclusion

Special attention should be paid to prevent fractures, and appropriate treatment for preventing excessive bone loss and investigations should be performed in rehabilitation hospitals for patients with SCI. Most of the physicians are not educated to measure these risk factors. DEXA should be performed, mainly after an osteoporotic fracture and in fact DEXA should be performed before the occurrence of fracture to prevent such event. Bone remodeling markers (like CTX-I) could give us a clue of the resorption rate and treatment could prevent further loss. Consider identifying risk factors and establishing prevention programs and appropriate treatment. Campaigns to prevent falls and stimulate the appropriate identification and treatment of osteoporosis in individuals with SCI must be promoted.

The analysis of literature for treatments still show mixed results, although there is no guideline, treatment with pharmacological therapy should be considered for patients with SCI, risk factors for fractures and DEXA criteria for osteoporosis. Use of oral bisphosphonates as alendronate or intravenous zoledronic acid, have showen efficacy but further studies should be performed.

The studies suggest standardization of the osteometabolic evaluation of patients with SCI, it is recommended undergo to laboratory evaluation before treatment, 6 months after beginning pharmacological therapy and repeated on annual basis. DEXA should be performed before treatment, 1 year after and every 2 years. Discussions with patients about side effects of these medications are recommended. It is important to emphasize that the protection of typical fractures is greater than the side effects when used for the appropriate length of time.

The effects of non-pharmacological measures are insufficient as a sole modality for osteoporosis prevention and treatment. Several literature reviews were conducted along the time and realized that studies on the use of physical therapies to prevent bone demineralization were inconclusive. The detection of an effective clinical intervention in this study area will require rigorous minimization of bias through a randomized controlled clinical trial design and likely require the involvement of multiple centers. It will also be dependent on appropriate measurement, with adequate intensity and duration of the intervention to detect a treatment effect. However, given the difficulty in conducting large-scale randomized controlled trials to address these issues, many of these gaps can best be addressed by using a multi-faceted approach including a combination of literature synthesis, large longitudinal observational studies and an expert opinion. Any prospective intervention is likely to benefit from early timing after acute SCI.

Before a treatment prescription, it is important to take into consideration timing since SCI, type, frequency, intensity and duration of intervention and the patient’s possibilities to follow-up with a long-term treatment. Exercise and pharmacological prescriptions have to be safe. The patient has to be informed about the treatment evidence, risks, benefits and burdens of each alternative (including no intervention) and, together, make a shared decision, depending on their goals, preferences and concerns.

Applications to other areas of neuroscience

In this chapter, we have reviewed the effects of osteoporosis after spinal cord injury and related fractures.

Osteoporosis after SCI is defined as an excessive bone resorption after SCI and bone fragility fractures caused by a trauma that would be insufficient for a normal bone to fracture ( ; ) or by minimally loaded situations ( ; ).

Osteoporosis is the most common silent disease in humans whose complication is fragility fractures. Osteoporosis is a treatable disease before fracture occurrence, and even if the first fracture occurred, there is benefit to prevent a new event.

Osteoporosis investigations should be performed for spinal cord injury, traumatic brain injury, neuromuscular disorders, and others because osteoporosis-related fractures in patients with chronic disabilities are a complication with consequences in activities of daily living and rehabilitation ( ).

Dual-energy X-ray absorptiometry is an important method for diagnosis and should be performed in all patients with chronic disabilities ( ).

The effects of non-pharmacological treatments are under debate, and studies showed the efficacy of bisphosphonates and Vitamin D to prevent fragility fractures ( ; ; ; ).

Campaigns to prevent falls are needed because falls are the first event related to fragility fractures ( ).

Mini-dictionary of terms

Osteoporosis: According to the WHO, osteoporosis is defined as a low bone mass and micro-architectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture.
Fragility fractures: These are fractures caused by a force that usually doesn’t cause a fracture as torsional forces during transfer, compressive forces, unknown, fall from wheelchair, self-passive mobilization, exercises, findings on X-ray, orthostatism or walking training, and others. Fractures because of fall from greater than standing height, sports injuries, and motor vehicle/motor cycle accidents are excluded.
Spinal cord injury: Damage of the spinal cord can be traumatic because of motor vehicle/motor cycle accidents, falls, and others or can be non-traumatic because of virus, tumors or demyelinating disorders, and others.
Dual-energy X-ray absorptiometry (DEXA): It calculates the measurement of bone mineral density in g/cm ², is a confirmatory test to predict the future risk of fracture, and also serves for ongoing monitoring of bone health and to access bone loss by the bone mineral density (BMD) measurements.
Bisphosphonates: These are drugs capable to inhibit bone resorption.

Key facts of osteoporosis after spinal cord injury

•

Bone demineralization after SCI occurs in a rate loss of approximately 4% per month in the first year, and bone loss can be extended 3 to 8 years after SCI.
•

Bone loss associated with SCI is related to immobility and metabolic changes.
•

Other related factors may contribute to this bone loss, such as vitamin D deficiency and the use of methylprednisolone, anti-convulsant drugs, and psychotropic substances.
•

Studies demonstrated bone demineralization greater than 20% to 70% in lower limbs after SCI.

Key facts of fragility fractures after spinal cord injury

•

The consequence of osteoporosis in individuals with SCI is fracture due to bone fragility.
•

It usually occurs in transfers, falls and activities with minimal or no trauma.
•

Fractures may occur in 25% to 46% of these people with SCI over their lifetimes.
•

Most places of fractures are in the tibia and/or distal fibula, distal femur, or hip/proximal femur and proximal tibia.

Key facts of diagnosis of osteoporosis after spinal cord injury

•

Osteometabolic evaluation of patients with SCI is recommended for evaluation before treatment, 6 months after beginning pharmacological therapy and repeated on annual basis.
•

DEXA should be performed before treatment, 1 year after and every 2 years.
•

DEXA measurement of the distal femur and proximal tibia, with specific protocols for the evaluation of these sites, is recommended.

Key facts of treatment for osteoporosis-related fractures after spinal cord injury

•

Treatment with pharmacological therapy should be considered for patients with SCI and risk factors plus DEXA criteria for osteoporosis.
•

The effects of non-pharmacological measures are insufficient as a sole modality for osteoporosis prevention and treatment.
•

Discussions with patients about side effects of these medications are recommended.
•

The patient has to be informed by a healthcare professional about the treatment evidence, risks, benefits, and burdens of each alternative (including no intervention), and together make a shared decision, depending on their goals, preferences, and concerns.

Summary points

•

Osteoporosis affects the health of individuals with SCI because it increases the risk of fragility fractures with consequences.
•

Most sites of fractures are in the tibia and/or distal fibula, distal femur, or hip/proximal femur and proximal tibia.
•

Fractures are primarily related to torsional forces during transfer, passive mobilization, compressive forces, and falls.
•

Special attention should be paid to the prevention of fractures, appropriate treatments should be instigated to prevent excessive bone loss, and investigations should be performed.
•

Campaigns to prevent falls and stimulate the appropriate identification and treatment of osteoporosis in individuals with SCI must be promoted.
•

Dual-energy X-ray absorptiometry (DEXA) is an important method for diagnosis.
•

Treatment with pharmacological therapy for people with SCI with risk factors for SCI population should be considered.
•

The patient has to be informed about the diagnosis and treatment options and make a shared decision for treatment, depending on their goals, preferences, and concerns.

References

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Tags: Diagnosis and Treatment of Spinal Cord Injury

Nov 9, 2024 | Posted by drzezo in NEUROLOGY | Comments Off

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