Key points

Introduction

Osteoporosis is the most common metabolic bone disorder. The National Osteoporosis Foundation defines osteoporosis as “porous bone … a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures, especially of the hip, spine and wrist, although any bone can be affected.” The National Institutes of Health defines osteoporosis as the “thinning of bone tissue and loss of bone density over time.” Using the young adult mean bone mineral density (BMD) as a reference, the World Health Organization has defined osteoporosis more objectively as having a T score of less than −2.5. This score indicates a BMD less than 2.5 SDs below the BMD of an average 25-year-old adult. According to the National Osteoporosis Foundation, 10 million Americans have been diagnosed with osteoporosis and an additional 34 million Americans are at risk for developing osteoporosis. The economic costs of osteoporosis-related fractures were $19 billion in 2005. These costs are predicted to increase to $25.3 billion by 2025. There were 2 million osteoporosis-related fractures in 2005, of which 547,000 were vertebral fractures.

Similar to diabetes, osteoporosis is often a silent disease, frequently diagnosed after a clinically evident fracture occurs. Osteoporotic spine fractures can manifest as compression fractures, burst fractures, and sacral insufficiency fractures. Osteoporotic patients not only have bone disease, but, because of the skewed advanced age of this population, often have additional comorbid conditions that increase their overall operative risk. In addition to co-morbid conditions, core weakness in this patient population can lead to postoperative problems, hindering recovery and often necessitating inpatient rehabilitation. Understandably, mortality after clinical vertebral fracture is increased. Kado and colleagues looked at 9575 women for more than 8 years and found that 1 vertebral column fracture increased mortality rates 23% to 34%. Given the prevalence, morbidity, and mortality involved with osteoporosis, screening and treatment are paramount.

Knowing the socioeconomic burden of osteoporotic fractures and deformity, spine surgeons must be trained and prepared to treat these patients. It is the aim of this article to remind and inform spine surgeons of osteoporosis and operative techniques that exist to help provide osteoporotic patients excellent and comprehensive care of their disease.

Introduction

Osteoporosis is the most common metabolic bone disorder. The National Osteoporosis Foundation defines osteoporosis as “porous bone … a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and an increased susceptibility to fractures, especially of the hip, spine and wrist, although any bone can be affected.” The National Institutes of Health defines osteoporosis as the “thinning of bone tissue and loss of bone density over time.” Using the young adult mean bone mineral density (BMD) as a reference, the World Health Organization has defined osteoporosis more objectively as having a T score of less than −2.5. This score indicates a BMD less than 2.5 SDs below the BMD of an average 25-year-old adult. According to the National Osteoporosis Foundation, 10 million Americans have been diagnosed with osteoporosis and an additional 34 million Americans are at risk for developing osteoporosis. The economic costs of osteoporosis-related fractures were $19 billion in 2005. These costs are predicted to increase to $25.3 billion by 2025. There were 2 million osteoporosis-related fractures in 2005, of which 547,000 were vertebral fractures.

Similar to diabetes, osteoporosis is often a silent disease, frequently diagnosed after a clinically evident fracture occurs. Osteoporotic spine fractures can manifest as compression fractures, burst fractures, and sacral insufficiency fractures. Osteoporotic patients not only have bone disease, but, because of the skewed advanced age of this population, often have additional comorbid conditions that increase their overall operative risk. In addition to co-morbid conditions, core weakness in this patient population can lead to postoperative problems, hindering recovery and often necessitating inpatient rehabilitation. Understandably, mortality after clinical vertebral fracture is increased. Kado and colleagues looked at 9575 women for more than 8 years and found that 1 vertebral column fracture increased mortality rates 23% to 34%. Given the prevalence, morbidity, and mortality involved with osteoporosis, screening and treatment are paramount.

Knowing the socioeconomic burden of osteoporotic fractures and deformity, spine surgeons must be trained and prepared to treat these patients. It is the aim of this article to remind and inform spine surgeons of osteoporosis and operative techniques that exist to help provide osteoporotic patients excellent and comprehensive care of their disease.

Osteoporosis

There are 3 types of osteoporosis. Type I, or postmenopausal, occurs in women or hypogonadic men. The primary hormonal imbalance is a decrease in estrogen. The fractures involved generally occur between 50 and 60 years of age, predominantly in the wrist and spine. Type II or senile osteoporosis occurs in men and women around 70+ years of age. Type III or secondary osteoporosis occurs because of other medical conditions or treatments, most commonly steroid-induced osteoporosis.

The basic pathologic condition involves an imbalance between bone formation and resorption whereby the latter is in favor, resulting in a loss in bone mineral density over time. Although adults lose bone mass at 0.5% per year, not every individual develops osteoporosis. Rather, osteoporosis is multifactorial, involving environment, lifestyle, genetic, hormonal, medication, nutrition, and other disease processes. The underlying concepts behind these pathophysiologic causes of osteoporosis are peak bone mass and rate of bone loss. Not only does osteoporosis place a patient at risk of fracture, but also, once a fracture occurs, surgical fixation can be difficult. In addition, osteoporosis can cause progression of deformity by gradual loss of height within the spinal column.

Medical optimization

If possible, before surgical intervention, medical management of osteoporosis and other comorbidities must be optimized. These patients should be aware that they are at increased surgical risk because of their age. Involvement of the primary care physician and an endocrinologist is key in this multidisciplinary approach to spinal care. Treatment begins with calcium and vitamin D supplementation to decrease the rate of bone resorption and to mineralize osteoid. In select patients, hormone replacement therapy with selective estrogen receptor modulators can be beneficial. Bisphosphonates, calcitonin, and parathyroid hormone therapies play key roles in osteoporosis treatment.

Controversy exists with patients actively taking bisphosphonates as they may inhibit or delay spinal fusion. In 2005, Huang and colleagues performed an animal study showing that alendronate, in a dose-dependent fashion, showed increased bone mass area but inhibited actual bone fusion in the spine by nearly 50% at 8 weeks. At the time, they recommended that patients should not take alendronate until bone fusion is achieved. Similarly, in 2004 Lehman and colleagues used an animal study to show alendronate delayed or inhibited bone fusion in the spine. They thought this was the result of uncoupling of the osteoclastic and osteoblastic cells needed for bone healing and also recommended that alendronate should not be given in the acute fusion period.

However, in the osteoporotic spine, bisphosphonate therapy may actually be beneficial. In 2011, Nagahama and colleagues showed that in a prospective randomized control study of 40 osteoporotic patients, 95% of the alendronate patients and 65% of the control patients had achieved bone fusion at 1 year. Although there was a trend toward better clinical outcomes in the alendronate group, there was no statistically significant difference in clinical outcomes. They concluded that osteoporotic patients should take bisphosphonates throughout the postoperative period. In addition, in 2011, Nakao and colleagues assessed spinal fusion in osteoporotic rats and also concluded that alendronate may improve spine fusion healing in the presence of osteoporosis.

A discussion should occur with the endocrinologist as to whether they feel the bisphosphonate patient should switch to another anti-osteoporotic medication in the postoperative period. Future medical therapies on the horizon include antibodies directed against the endogenous inhibitors of bone formation. In addition, physical therapy and Tai Chi improve patient strength, balance, and proprioception, which not only aid in fracture prevention but also help in postoperative rehabilitation.

Surgical techniques in the osteoporotic spine

The indications for surgical intervention are similar to a nonosteoporotic patient population and include radiculopathy, myelopathy, mechanical back pain, progressive spinal deformity with or without fracture, neurogenic claudication, and failure of conservative management. A thorough risk-benefit analysis is required before operating on an osteoporotic patient. Although the risks are higher in this surgical population, once stable fixation and fusion have been achieved, patients’ self-reported health assessments significantly improve with respect to physical function, social function, bodily pain, and perceived health change. In the study by Okuda and colleagues, fusion rates in patients older than 70 were delayed in 10%, had collapsed union in 13%, but had similar fusion rates to patients younger than 70 (100%). Surgical treatment of this patient population is a reasonable and viable option in the appropriately selected patient.

Once conservative management has failed and appropriate time for medical optimization has been met, a spine surgeon must carefully plan their surgical intervention. Less is often more in deformity correction in the osteoporotic spine. Aggressive deformity correction can lead to implant overload and hardware failure. Major corrections should be avoided in favor of limited corrections. For example, when dealing with spinal stenosis, a greater attempt should be made to try to identify the specific level or nerve root of pathologic abnormality or the area of worst compression to have a 1-level or 2-level decompression, rather than large multilevel decompressions. Some surgeons may discuss in situ fusion when a significant concern exists of instrumentation failure because of abnormal bone or where the risk of progressive deformity is low. The specific criteria for in situ fusion remain open for discussion. In 1992, Lenke and colleagues looked at 56 isthmic spondylolisthesis patients and had an in situ fusion rate of about 50% but despite this low fusion rate they had improvement in clinical outcomes in greater than 80% of their patients. In situ fusion is simply 1 tool a spine surgeon can use when needed.

Another option for osteoporotic patients is to increase the extent of surgery by performing combined anterior/posterior intervention. A 360° fusion allows load-sharing and places less strain on the posterior-only fixation, yielding a more stable construct. Caution must be used with anterior interbody devices as they may subside in the weak osteoporotic bone. Given that the cortical bone is usually stronger in osteoporotic spine, anterior implants should have an appropriate size or footprint to engage this stronger cortical bone. The potential benefit of using anterior interbody load-sharing devices must be weighed against the increased risk to this medically fragile patient population from increased operative time, blood loss, and overall surgical risk. In addition, osteotomy may be used to correct deformity and decrease strain on the hardware.

The level at which to end the construct is critical in all spine patients. However, in the osteoporotic patient with poor bone mineral density and weaker bone it is even more important to take into account the junctional strain placed at the end levels of a construct. Increased strain at spinal transition zones should be avoided. Ending the cephalad portion of lumbar constructs at L1 should be avoided. Rather, T10 should be used to avoid kyphotic collapse at the thoracolumbar transition zone. The caudal aspect of cervical constructs should extend into T2 rather than ending at C7 to again avoid junctional kyphosis at the cervicothoracic transition point.

Given that insertional torque, pullout strength, and fatigue failure are linearly related to bone mineral density, the weakest link in fixation of the osteoporotic spine is the bone-implant interface. The most common mechanism of bone-implant failure in the osteoporotic spine is screw pullout or cutout. Many techniques have been described to augment fixation, including cement augmentation with polymethylmethacrylate (PMMA) into pedicle screw tracks, hydroxyapatite-coated screws, sublaminar hooks and wiring, cross-linking, and expandable screws and screw design.

In most cases, better screw fixation is achieved with greater outer screw diameter. In addition, the tactile screw purchase achieved may be a reasonable indication of fixation. Screw placement with an insertional screw torque of less than 4 inch-pounds is likely to fail. Some literature suggests that insertional screw torque may not be completely reliable to assess fixation as screw design may alter insertional torque such that certain screws may have higher insertional torques with a decreased pullout strength compared with other screws.

Given the risk of bicortical purchase in pedicle screw placement, surgeons should aim for 80% vertebral body pedicle screw length. Medially angulated pedicle screws in a triangular configuration with a transverse connector increases the allowable length of a pedicle screw and improves pullout strength. Also, diverging the screws in the sagittal plane increases axial load-bearing capacity. Furthermore, screws should be aimed toward the stronger subchondral bone near the endplate.

The type of pedicle screw itself can alter fixation. For example, conical screws may be used over conventional cylindrical screws to improve fixation strength. However, there is controversy regarding whether backing out the conical screw by 180° or 360° may potentially decrease overall pullout strength. Ideally, pedicle screws should be placed at the appropriate depth and should not have to be backed out or reinserted because this decreases insertional torque and pullout strength with any screw. Also, expandable pedicle screws can decrease the risk of screw loosening compared with conventional pedicle screws. Hooks and wires are another fixation option and rely on relatively spared cortical laminar bone and can be used to enhance fixation. One option to use this technique involves using hooks at the cephalad and caudal aspects of the construct.

In the anterior spine, Huang and colleagues analyzed various configurations of double-screw fixation and reported that triangulation of 2 anterior vertebral screws (22° intersection angle) without penetration of the cortex achieved pullout strengths similar to that of 2 parallel double-cortical screws. Although tapping has been shown to improve screw trajectory, undertapping or no tapping with maximization of pedicle screw diameter increases pullout strength and decreases the risk of failure. There was a 47% increase in pullout strength by undertapping by 1 mm compared with undertapping by 0.5 mm. Adding PMMA or calcium phosphate to the screw tract or vertebral body can significantly increase pullout strength. The addition of PMMA gives immediate restoration of strength and stiffness and increases pullout strength by 149%. Placement of the pedicle screw while the PMMA is soft increased pullout strength more than placement of the pedicle screw while the PMMA has hardened. Hydroxyapatite-coated pedicle screws also increase fixation and pullout strength. Some surgeons advise vertebroplasty or kyphoplasty at the adjacent levels of a construct to help decrease the risk of fracture. Another technique that can be used is bone marrow aspirate from the vertebral body through the pedicle screw pilot hole to augment the fusion mass; however, bone marrow aspirate used from an osteoporotic spine may not be as beneficial. Meticulous surgical technique involves avoiding in situ correction to seat the rod in the pedicle screw head. This preloading of the screw can weaken the bone-implant interface and cause early fixation failure.

Multiple points of fixation should be used in the osteoporotic spine above and below the apex of any deformity, to achieve a balanced and stable construct. Often, iliac and sacral fixation is recommended to increase fixation strength. In the pelvis, large-diameter screws with bicortical purchase should be used to increase pullout strength. Leong and colleagues showed that divergent S1 screws with use of a Chopin plate (Colorado II sacral plate) increased pullout 20% to 26%. Iliac bar fixation can also be used to augment the distal construct. Fixation techniques simultaneously involving zone 1, 2, and 3 of the sacrum are possible. McCord and colleagues showed an increased maximum stiffness at failure with screw fixation successively from zone 1, 2, and 3. The disadvantage of pelvic fixation is an increased rate of pseudoarthrosis of up to 26% depending on the specific method used.