Journal of the Spinal Research Foundation Fall 2013 by Carrie Califano

JOURNAL OF THE SPINAL RESEARCH FOUNDATION

Thank You! The Board of Directors of the Spinal Research Foundation is grateful for the continued investment of our donors and

Research

extends its appreciation to all who have contributed. Through the generous support of our donors, the Spinal Research Foundation has been able to significantly expand the scope of our scientific research and educational programs. These gifts have been utilized to embark on projects geared toward understanding the mechanisms of spinal diseases and developing new treatments for these

Patient Advocacy

support of our donors.

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conditions. This work would not be possible without the

Education

Volume 8, Number 2

JOURNAL OF THE SPINAL RESEARCH FOUNDATION

To make a donation in order to improve the quality of spinal health care in America, please visit:

www.SpineRF.org or contact us at:

Innovation

The Bare Bones of Spinal Disease

Spinal Research Foundation 1831 Wiehle Ave, Ste 100 Reston, VA 20190 Phone: 703-766-5404 Fax: 703-709-1397

VOLUME 8 NUMBER 2

Fall 2013

SPINAL RESEARCH FOUNDATION

Thank you,

DOUGLAS G. ORNDORFF, M.D.

THE JOURNAL OF THE SPINAL RESEARCH FOUNDATION A multidisciplinary journal for patients and spine specialists

Thomas C. Schuler, M.D., F.A.C.S. President

Brian R. Subach, M.D., F.A.C.S. Director of Research

Michael H. Howland Vice Chairman

Andrew T. Greene Treasurer

Raymond F. Pugsley National Race Liaison

Kevin M. Burke, Jr. Member

William H. Evers, Jr., Ph.D. Member

Brian D. Nault Member Najeeb M. Thomas, M.D. Member

THE JOURNAL OF THE SPINAL RESEARCH FOUNDATION EDITORIAL BOARD

Regis W. Haid, Jr., M.D. Atlanta, GA

Christopher H. Comey, M.D. Springfield, MA

Larry T. Khoo, M.D. Los Angeles, CA

Aleksandar Curcin, M.D., M.B.A. Coos Bay, OR George A. Frey, M.D. Englewood, CO Gerard J. Girasole, M.D. Trumbull, CT

Noshir A. Langrana, Ph.D. Piscataway, NJ Mark R. McLaughlin, M.D., F.A.C.S. Langhorne, PA

Matthew F. Gornet, M.D. Chesterfield, MO Journal of The Spinal Research Foundation

Patrick T. Oâ&#x20AC;&#x2122;Leary, M.D. Peoria, IL David P. Rouben, M.D. Louisville, KY

Guy E. Beatty Chairman

J. Kenneth Burkus, M.D. Columbus, GA

SPINAL HERO

SPINAL RESEARCH FOUNDATION (SRF) BOARD OF DIRECTORS

Robert J. Hacker, M.D. & Andrea L. Halliday, M.D. Springfield, OR

Melissa B. Luke and Marcia A. Phillips Editorial Staff

James P. Burke, M.D., Ph.D. Altoona, PA

SPINE COLORADO

Carrie B. Califano and Anne G. Copay, Ph.D. Managing Editors

Paul J. Slosar, Jr., M.D. Member

Spine Surgeon

Brian R. Subach, M.D., F.A.C.S. Editor-in-Chief

Rick C. Sasso, M.D. Indianapolis, IN Thomas C. Schuler, M.D., F.A.C.S. Reston, VA

â&#x20AC;&#x153;

James D. Schwender, M.D. Minneapolis, MN Nirav K. Shah, M.D., F.A.C.S Langhorne, PA Paul J. Slosar, Jr., M.D. Daly City, CA Najeeb M. Thomas, M.D. Metairie, LA Jim A. Youssef, M.D. & Douglas G. Orndorff, M.D. Durango, CO FALL 2013 VOL. 8 No. 2

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Table of Contents Editor’s Note Brian R. Subach, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 President’s Note Thomas C. Schuler, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Ask the Expert Patrick T. O’Leary, M.D. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 We’ve Got Your Back Race for Spinal Health Laura A. Bologna . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Spine Tales: Patients’ Inspirational Stories of Successful Spine Care

Susan Merry— Brian R. Subach, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Joseph Nicolia— Brian R. Subach, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Joseph Mark Ebertz, M.D.—Anthony T. Yeung, M.D. and Susan D. Parker . . . . . . . . . 15 Kristin Greene Skabo—Christopher A. Yeung, M.D. and Susan D. Parker . . . . . . . . . . . . . 18

Public Health The Smoking Spine

Ashley R. Gilchrist, M.P.H, P.A.-C. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

From Your Personal Trainer Weight Training and Bone Density

Melissa Treat, R.N., B.S., C.P.T. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Special Focus: The Bare Bones of Spinal Disease

The Nutritional Aspect of Bone Health

Michael W. Hasz, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

The Genetics of Bone Density

Justin C. Battle, P.A.-C., M.P.A.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28

Bone Physiology and Bone Healing

Brian R. Subach, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

Medications in Bone Health

Michael W. Hasz, M.D., F.A.C.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

The Importance of Bone Health for Spinal Procedures Justin S. Field, M.D. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 FALL 2013 VOL. 8 No. 2

Journal of The Spinal Research Foundation

SPINAL RESEARCH FOUNDATION

From the Editor

Brian R. Subach, M.D., F.A.C.S.

am pleased to introduce the Fall 2013 edition of the Journal of the Spinal Research Foundation. This issue, entitled “The Bare Bones of Spinal Disease,” addresses one of the most important topics pertaining to the structure and function of the spine. Without healthy bones, the ability of the spine to support the body is weakened, placing additional stress on the discs and predisposing one to compression fractures. It may be glamorous to talk about disc herniations, tumors, or sciatic nerves being compressed, but without the strong structural support of the spinal column and the integrity of the vertebral bodies, the spine and its ability to support the entire skeletal system will fail. More than a simple calcium and phosphate mesh, the bones of the spine are a living framework filled with cells constantly remodeling in response to stress. “The Bare Bones of Spinal Disease” is a catchy title; however, bone quality and bone health are both extremely important in the structure and function of the spine, which is why we have gathered together a panel of experts to give their perspectives on bone health in the spine. We have invited Patrick O’Leary, M.D. to give his professional insight into this topic. Ashley Gilchrist, M.P.H, P.A.-C. discusses the public health impact of smoking and osteoporosis, and an overview of bone physiology and healing is also presented in this issue.

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Michael Hasz, M.D., F.A.C.S reviews the effect of diet and medications on bone health, while Justin Battle, P.A.-C., M.P.A.S discusses how one’s inherited genetics may adversely impact bone health. The Spinal Research Foundation’s personal trainer, Melissa Treat, R.N., B.S., C.P.T. gives her perspective on the role of strength training and bone density as well as the positive influence of exercise. Finally, Justin Field, M.D. explains the importance of bone health in regards to surgical intervention. Other updates include a report from Laura Bologna, the Spinal Research Foundation’s National Events and Development Coordinator, on the We’ve Got Your Back races that occurred in 2013 across the country. Additionally, four patients’ stories of their hardships, treatments, and recoveries are recounted in our Spine Tales. These stories provide evidence of successful spine care to inspire hope for all suffering from neck and back pain. Finally, we at the Spinal Research Foundation would like to draw attention to Douglas G. Orndorff, M.D. who is our Spinal Hero for this issue. Dr. Orndorff is not only an outstanding researcher and surgeon, but truly a patient advocate. It is his contributions to the art and science of spinal health care that have earned him this honor.

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From the President

Thomas C. Schuler, M.D., F.A.C.S. A Funny Thing Happened on the Way to Health Care Reform

ur society has a desire to improve the access of quality health care to all Americans. Our great country has recently gone through the initiation of major health care reform. One of the criticisms of this reform is that “death panels” would be established as a means to achieve cost savings, thereby decreasing the quality of care available to Americans. So far, it appears that these “death panels” have not come to fruition. However, what has occurred is the decision to disincentivize physicians to provide care for the elderly and patients with the most complex issues. If doctors are effectively disincentivized, then the “death panels” won’t be needed. The Centers for Medicare and Medicaid Services (CMS) are progressively issuing unilateral decisions that negatively impact patients and physicians. CMS is under the misguided belief that all complications are avoidable, and therefore, if one has a complication it must be the fault of the doctor or the hospital. This is entirely erroneous and does not take into account that the greatest risk factor for many complications is the patient’s health and immune status. Physicians who have complications occur while providing care will have a “black mark” against them and their hospitals. This in turn will affect reimbursements for the hospitals, causing the hospitals to counsel those physicians with high complication rates and ultimately threatening the physician’s ability to practice at those hospitals. The older we get, the poorer our bodies respond to surgical procedures and the greater the chance of complications. The simplest and safest choice for physicians then, is to operate on younger, healthier patients and avoid the high-risk, more sickly patients, which tend to be the elderly. Ultimately, the physicians are forced to ration care, thereby accomplishing the goal of the “death panels” without the government having any visible blood on its hands. To further expedite the rationing of care while directing criticism away from the government, a 15-member committee, known as the Independent Payment Advisory Board (IPAB), was created under the new health care law. IPAB has the authority to determine how much the govFALL 2013 VOL. 8 No. 2

ernment pays physicians for treatments and procedures. In addition, IPAB is responsible for reducing health care spending. They will accomplish this by limiting reimbursements to physicians. Once it costs physicians more to treat a patient than they are being compensated, they will likely stop performing those procedures (or seeing those patients). When you combine punitive threats to one’s reputation, the possible inability to practice at a hospital, and extremely poor reimbursements, it is easy to see how the government has created a system which allows them to accomplish its goal of rationing services and care without having direct ties to their overt policies. Health insurance does not necessarily equal health care. Health insurance is in place to help pay for medical care. However, the treatments or procedures the insurance companies and the government choose to allow will determine what actual health care is available. The more treatments that are denied by insurance companies or by way of government policies, the more this ultimately translates to less care available to any individual. As there is an increase in the number of individuals covered by the same sum of money, there will be less care to distribute amongst all of the insured. Changing our entire health care system to insure 15% of the uninsured population is not logical. We are punishing 85% of Americans who have health insurance to cover the 15% who do not have it. Abraham Lincoln once said, “You cannot make a weak man strong by making a strong man weak.” Why are we punishing the part of the system that is working, to cover the part that is not? This is the equivalent of using a queen sized sheet to cover a king sized bed; in the end, the corners will come up! The health care system cannot be improved by shifting the responsibilities and hiding the shortcomings behind those in the medical field whose intentions and purposes are to treat and heal. As it stands, this new health care system is asking us to do more with less. Ultimately, all that we, as Americans, are going to get is less medical care. Journal of The Spinal Research Foundation 2

SPINAL RESEARCH FOUNDATION

Ask the Expert Patrick T. O’Leary, M.D.

Q: What is bone health anyway, and why is it so important? A: Our bones, aside from being remarkably complex, are remarkably multidimensional. While most people know that bones provide structural support for the human body’s daily functions, e.g., walking, sitting, standing, running, etc., there are other vital functions that bones perform. For instance, they protect our vital organs. The ribs protect the heart, lungs, esophagus, and spleen, while the skull protects the brain. The spine in particular not only allows humans to maintain an erect posture, but it also protects the critical neural elements which allow us to continue to function—the spinal cord and spinal nerves. The inner compartment of some bones (the marrow) is where cells that help make up our blood are formed. There is another critical element provided by our bones; the skeleton is a reservoir for vital minerals. Calcium and phosphorus are vital for helping regulate a number of organs at a cellular level, including heart function, kidney function, muscle function, and to some extent just about every organ in the human body. While most of what we utilize in terms of elemental calcium and phosphorus is derived from diet, complex interactions between the kidneys, thyroid, and skeletal bones allow for calcium and phosphorus to be released from bone when calcium levels in the body are low. In a similar fashion, reversing the process to store calcium and phosphorus together as calcium phosphate, the ultimate element of which our bones are comprised, takes place when system levels of calcium are high. The body’s ability to regulate calcium and phosphorus at appropriate levels for sustaining life is called homeostasis. Bone health entails not only a strong, supportive skeleton to maintain our physical stamina, but also includes providing the body with needed 3 Journal of The Spinal Research Foundation

stores of calcium and phosphorus to a depleted system to maintain appropriate functioning. In the following few paragraphs, I will discuss what is needed to maintain bone health, as well as what happens when bone health starts to diminish.

Q: What activities and behaviors can I adopt to make sure my bones are strong and healthy? A: Current research suggests that maintaining bone health is multifactorial. In other words, there is not one simple solution, such as a single drug, that will fix all bone health ills. Science tells us that exercise is important, and resistance based exercise is of particular importance. Bone is a living material that repeatedly responds to stress or lack of stress. Postural based exercises help to maintain core muscle strength, and simple, resistance based exercises (even lifting just one or two pound weights) can be helpful in maintaining bone mass. Care should be taken in settings of severe osteoporosis, though, as some simple activities of daily living alone can cause bones to fracture. Supplementation of vital minerals is another important aspect of managing bone health. Women of postmenopausal age are at particular risk for calcium depletion, as lower estrogen levels lead to increasing depletion of bone mass. Regular calcium intake is recommended. The National Osteoporosis Foundation recommends 1000 mg of calcium intake per day for adults 50 years and younger. For adults over the age of 50, 1200 mg of calcium per day is recommended. Typically, adults get about half of this through diet alone, highlighting the importance of supplementation. Vitamin D is another element that is critical for maintaining bone health and typically requires suppleFALL 2013 VOL. 8 No. 2

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mentation. Vitamin D is needed for calcium absorption through the gastrointestinal system, and it also plays a pivotal role in signaling other organs that affect bone turnover, namely the thyroid gland. It is recommended that adults less than 70 years of age get at least 600 IU of vitamin D daily. This increases to 800 IU for adults over the age of 70. Current research is only further underscoring the importance of this critical player in maintaining bone health. Additionally, limiting alcohol intake helps to curb the adverse effects of alcohol consumption on bones. Smoking cessation also plays a pivotal role in maintaining and improving bone health. Both excessive alcohol intake and smoking have been shown to have an adverse effect on bone health, typically decreasing bone mineral density.

Q: How is osteoporosis diagnosed? A: The World Health Organization defines osteoporosis based upon scores calculated from a bone mineral density study, commonly known as a DXA scan. Typically, measurements of the bone density at the hip, spine, and/or wrist are taken to determine overall bone mineral density. Because of arthritis in the spine, readings from the spine in individuals greater than 60 years of age are less reliable. In these cases, the hip is best to determine true bone mineral density. These individual scores are then compared to the peak bone mineral density. The number of standard deviations below peak bone density determines the ultimate diagnosis; this is referred to as a T-score. A T-score of 0 to 20.9 is considered within normal range, and a score of 21.0 to 22.5 is considered osteopenia. Osteoporosis is defined as any patient with a T-score below 22.5, and severe osteoporosis occurs in the presence of a fragility fracture and a T-score below 22.5. The FALL 2013 VOL. 8 No. 2

numbers are expressed as negative because it refers to the standard deviations below the mean peak bone mineral density.

Q: What spinal diseases are directly correlated to the quality of my bones? A: One of the most commonly treated conditions today is the osteoporotic vertebral compression fracture. Approximately 750,000 new compression fractures, and possibly more, are diagnosed each year in the United States. With totals of approximately 1.5 million fragility fractures per year in the United States, vertebral compression fractures are easily the most prevalent fragility fracture. Vertebral compression fractures typically cause back pain and can be associated with minor trauma, such as a fall or twist, but can also be present seemingly without any trauma. Fractures can be managed with a brace and symptomatic treatment of pain. For patients with acute compression fractures and significant pain with ambulating, vertebral augmentation via vertebroplasty or kyphoplasty can be considered. This involves injecting bone cement into the fractured vertebrae to stabilize the fracture, potentially improving alignment of the bone. This procedure allows for less narcotic intake and improved ability to perform activities of daily living. Vertebral compression fractures are potentially a source of substantial morbidity. Loss of vertebral height due to compression can cause local instability and the formation of kyphosis, or rounding of the back. Persistent fractures/new fractures can compound this by increasing kyphosis, making it difficult for an individual to stand up straight. Patients with scoliosis can also experience increases in the magnitude of their scoliosis due to osteoporosis, either Journal of The Spinal Research Foundation 4

SPINAL RESEARCH FOUNDATION

from fracture or vertebral body collapse/erosion due to forces driving the spinal curvature. Lastly, mortality increases with each subsequent diagnosis of a compression fracture.

Q: Are treatment options for my back or neck pain limited by the quality of my bones? A: Weaker, osteoporotic vertebrae make treating spinal conditions with surgery very challenging. Certain conditions such as spondylolisthesis, stenosis, scoliosis, kyphosis, flatback deformity, and degenerative disc disease can be successfully treated with surgery. However, surgery often includes fusion to optimally address spinal instability/deformity. Instrumentation is commonly used to improve correction of instability/deformity and enhance fusion rates. Instrumentation can include pedicle screws, cages, and plates. The quality of the bone is crucial to maintain fixation while the spinal segment fuses. Weaker bone increases risks of screw toggling at the bone-screw interface, potentially reducing fusion rates. Osteoporotic bone also increases cage subsidence and can predispose the adjacent segment to fracture in longer fusion constructs. In order to successfully perform surgery in patients with osteoporosis, preoperative DXA scans should be performed and bone health optimized prior to surgery if the situation permits.

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Q: What if I take supplements, exercise, and still suffer from osteoporosis? A: Today there are many pharmacologic options for treating osteoporosis. These agents have been shown to reduce subsequent risk of some fragility fractures and improve bone health. These agents include bisphosphonates (alendronate, ibandronate, zoledronic acid, risedronate). Bisphosphonates work by inhibiting the activity of osteoclasts-cells which primarily resorb bone. Calcitonin can help to alleviate fracture pain, but it has not been shown alone to reduce the risk of vertebral compression fracture. Other agents include antiresorptive drugs such as estrogen and raloxifene. An anabolic agent, teriparatide, is one of the more potent medications available to treat osteoporosis and is usually reserved for severe osteoporosis that is refractory to bisphosphonate treatment. It is recommended that you discuss these pharmacologic options with your doctor. Patrick T. O’Leary, M.D. Dr. O’Leary is a board certified, fellowship trained orthopedic spine surgeon on staff at all three Peoria, IL hospitals. He earned his medical degree from Loyola University in Chicago, IL. He completed his residency in Orthopedic Surgery and Rehabilitation at Loyola University Medical Center in Maywood, IL. He completed an Adult and Pediatric Spine Fellowship at the Washington University School of Medicine in St. Louis, MO. Dr. O’Leary has authored numerous peer-reviewed articles.

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We’ve Got Your Back Race for Spinal Health Laura A. Bologna

he Spinal Research Foundation is proud to host the only run/walk event in the nation designed to celebrate the accomplishments of Spinal Champions and to raise funds supporting research to improve spinal health care for future generations. Spinal Champions are celebrated on race day with commemorative race shirts and a special tent where they can share their stories of success. A Spinal Champion is defined as someone who has suffered from back and/or neck pain and has overcome it through either nonsurgical or surgical treatment. First Annual WGYB Events Freehold, NJ April 6th, 2013

Although the morning started chilly and foggy for the first annual race in Freehold, NJ, Princeton Brain and Spine Care partnered with Centra State Hospital to put on a successful event at their new location on Centra State’s campus. Many hospital employees came out to support the event in its first year; the hospital’s surgical nurses represented the largest team of the day! Princeton Brain and Spine Care looks forward to continuing to grow this event in the upcoming years,

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welcoming more participants, more volunteers, and most excitingly, more Spinal Champions to celebrate at next year’s event. Gilbert Derry did a great job organizing this inaugural event with Dr. Nirav Shah, and we look forward to their race in 2014. Carmel, IN April 27th, 2013

Indiana Spine Group hosted one of the largest first year events with a great group of both employees and com-

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SPINAL RESEARCH FOUNDATION munity volunteers and attracted an enthusiastic group of participants from the Carmel, IN area. They hosted several other non-profit organizations that were there to support the Spinal Research Foundation’s cause and raise awareness about their own causes—ranging from breast cancer awareness to organ donation. The honorary chair, a local firefighter who came out to walk the race after her spine surgery, spoke to the crowd about her success after surgery and the importance of promoting this cause both locally and nationally. The race announcer was a local newswoman who helped bring media attention to the event and promote it in the years to come. We would like to thank Stacia Matthews who was the organizer of the race and spinal health fair, and we are excited for the continued growth of this event. Coos Bay, OR May 18th, 2013

South Coast Orthopaedic hosted their first We’ve Got Your Back Race for Spinal Health in partnership with Bay Area Hospital to celebrate and raise funds for the newest wing of the hospital. The hilly race course challenged participants on a warm May morning while taking them through Bay Area Hospital’s campus and back to South Coast Orthopaedic’s practice location. The partnership with Bay Area was a huge success and drew participants from all over the South Coast region to come out and support the Spinal Research Foundation’s efforts to improve research and patient advocacy. We look to build on the event’s success next year by partnering again with South Coast Orthopaedic’s Cathy Noel, Dr. Aleksander Curcin, and the rest of his team, as well as Barb Bauder and Dina Laskey from Bay Area Hospital.

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Durango, CO June 15th, 2013

Spine Colorado hosted the Spinal Research Foundation’s first ever WGYB Silent Auction the Friday evening before kicking off their We’ve Got Your Back Race for Spinal Health on Saturday morning. The auction was a huge success and raised over $1,000 for the Foundation with a wide array of items that drew people from both the Spine Colorado practice and the local Durango community. The race was hosted at the Spine Colorado practice in Three Springs, CO with a beautiful terrain and wonderful weather. The event boasted a large group of enthusiastic volunteers on hand to kick off the event and cheer on our participants. We welcomed several college athletes from local universities who came out to compete in their off season and large teams organized from the local community. Erica Gabreski and Morgan Scott planned and executed both the silent auction and the 5K and 1 Mile Fun Run with the help

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of Dr. Jim Youssef and Dr. Doug Orndorff. We would like to extend our appreciation for all their hard work! 6th Annual Reston, VA May 18th, 2013

We’ve Got Your Back Race for Spinal Health was held for the sixth year in Reston, Virginia, hosted by the Virginia Spine Institute. This venue attracted an SRF record-setting 963 registrants and raised $100,000 for the Spinal Research Foundation. “We are proud to team up with the Spinal Research Foundation as a regional sponsor and host for the sixth consecutive year. As the flagship site, our goal is to empower our patients with knowledge and hope, and today celebrated that,” said Dr. Brian R. Subach, Spinal Specialist at the Virginia Spine Institute. Washington Redskins players Reed Doughty, Roy Helu, and former Redskin Lorenzo Alexander, served as honorary chairs and gave powerful testaments to the value of effective spinal treatment. Thomas C. Schuler, M.D., F.A.C.S, founder and president of SRF, spoke about the nine out of ten people who will suffer from severe neck and/or low back pain during their lifetimes and the Spinal Research Foundation’s efforts to improve spinal health care through research. FALL 2013 VOL. 8 No. 2

The race festivities also included live entertainment, refreshments, free giveaways, an inflatable obstacle course, and kids activities. We would like to extend a special thank you to Erin Orr and Heather Buck who continue to grow this event year after year. Upcoming Races We are excited to announce eight upcoming races in 2014. Our first event of 2014 will be held on February 8th by our newest Research Partner, Desert Institute for Spine Care (DISC); it will be their first We’ve Got Your Back Race for Spinal Health in Scottsdale, AZ. The next upcoming race is the 2nd annual event in New Orleans, LA hosted by Southern Brain and Spine on February 15th. To learn more about the We’ve Got Your Back Race for Spinal Health visit SpineRF.org/race. Laura A. Bologna Ms. Bologna is the National Events and Development Coordinator at the Spinal Research Foundation (SRF). She is responsible for coordinating the Foundation’s We’ve Got Your Back Races for Spinal Health, managing the organization’s fundraising activities, and supporting SRF’s social media. She holds B.A. degrees in Public Relations and History from Pennsylvania State University.

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SPINAL RESEARCH FOUNDATION

Spine Tale Susan Merry Brian R. Subach, M.D., F.A.C.S.

me with the most thorough consultation based on xrays, surveys, and examinations. His advice was to offer me the best surgical option that would return me to the active life I’d always been able to enjoy. Dr. Subach recalls evaluating Susan Merry’s pain and recommending a fusion surgery. “Her pain seemed to be worse in the morning, although it would loosen up during the course of the day. The pain was often severe enough to awaken her from sleep at night. Standing seemed to be worse, while sitting and lying on her side were somewhat better. Susan described 90% back pain and 10% lower extremity symptoms, mostly with numbness and weakness into the legs. Essentially all of the things that she enjoyed were difficult to perform secondary to the severity of her pain.” “Her initial imaging studies, including x-rays and an MRI scan, demonstrated spondylolisthesis at both L3/L4 and L4/L5 levels with an obvious scoliosis posture leaning toward her left. The MRI scan showed severe spinal stenosis at the areas of spondylolisthesis, as well as compression of the exiting nerve roots.” “Based upon her scoliosis and her spondylolisthesis, I advocated a three-disc level fusion. By taking out the discs spaces and replacing them with small wedges of donor bone, I thought I would be able to restore her posture, alignment, and decompress the nerve roots

n the winter of 2004, I was skiing off trail on a very steep terrain when I hit ice, which sent me tumbling backwards down the mountain and eventually hitting a small tree. I was airlifted off the mountain and treated for injuries to my chest and a concussion. When I returned home from my ski trip, I resumed all my usual activities—biking, walking, swimming, kayaking, and taking care of the house and my family. Gradually though, my back began feeling very painful, and I was unable to continue certain exercises. I went to a doctor who told me my symptoms were primarily due to arthritis. I had some improvement in my pain after trying anti-inflammatory medication, injections, and physical therapy. Eventually I was able to return to my active lifestyle. In the spring of 2011, I participated in a 62-mile hike in D.C., and around the 22nd mile I had excruciating pain in my back. I had to stop the hike and resumed conservative treatments of medications, physical therapy, and rest; nothing seemed to relieve my discomfort. At this point, I began considering surgical options. I Figure 1. The neutral lateral lumbar view of the sought opinions from three surgeons pre-operative x-ray shows loss of disc height at L2/L3, L3/L4, and L4/L5, as well as sponbefore meeting Dr. Subach from the levels dylolisthesis at level L3/L4 and L4/L5 (indicated Virginia Spine Institute. He provided by arrows). 9 Journal of The Spinal Research Foundation

Figure 2. The anteroposterior (AP) lumbar view of the pre-operative x-ray displays lumbar scoliosis leaning towards the left.

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all at the same time. The other surgical opinions had recommended a five-level fusion, which was more significant than I thought was necessary.” “On June 20, 2012, Susan underwent a transforaminal lumbar interbody fusion at L2/L3, L3/L4, and L4/L5. In the areas of scoliosis, I was able to use an osteotome to cut through the bone that was holding her into a misaligned position. By placing spacers into the disc spaces and then compressing the screws together, I was able to restore both her normal postures as seen on the side view and front view x-rays.” Approaching the date of my sur- Figure 3. The lateral view of the post- Figure 4. The AP lumbar view of the postgery, I was pretty apprehensive about operative x-ray shows restored height operative x-ray shows correction of the of the intervertebral disc spaces at the patient’s scoliosis. the lengthy procedure, but I took Dr. L2/L3, L3/L4, L4/L5 levels following a 3-level Subach’s advice and continued to exer- transforaminal lumbar interbody fusion. cise as much as was possible until the operation. During my recovery in the hospital, I wasn’t in any particuities have been sorely reduced due to pain. Don’t wait larly bad pain. I was able to get up and do laps around too long to consult with an expert. I have now referred the hospital floor almost immediately. Once I was back a number of people to Dr. Subach and the Virginia home, I was able to go out for walks in the neighborSpine Institute. Dr. Subach is amazing, and the whole hood and then go back to my gym at just two weeks office is incredibly efficient; everyone from the reafter surgery. I gained back my lost two inches, skiied this winter, am kayaking on Puget Sound, walking a lot, and back doing boot camps, stretch classes, etc. Dr. Subach is thrilled with Susan’s quick and complete recovery. “Prior to surgery, Susan rated her back pain and leg symptoms as a six on a visual analog scale of zero to ten. At her one-month postoperative visit she had zero leg symptoms and zero back pain. With the size of the intervention and the corrections of both her side view and front view x-rays, it was fairly amazing that she was feeling better rather than worse. She initiated physical therapy and began getting her strength and flexibility back. Her imaging studies demonstrated evidence of progressive healing and excellent correction of her scoliosis.” While I still think surgery or any invasive procedure should be a last resort, it should be an option to consider for anyone in enormous pain or whose activFALL 2013 VOL. 8 No. 2

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SPINAL RESEARCH FOUNDATION Spine Tale: Susan Merry

ceptionist to the billing team, the x-ray technician to the very talented physicians’ assistants—knows what their jobs are and do them well, with helpfulness and “ This surgery friendliness. was nothing It is one year out from surshort of gery, and I have absolutely no miraculous.” pain and don’t even take an occasional Advil. We just moved from the east coast to the west coast, packing up our house of 30 years. For four months, I was lifting boxes (carefully), reaching into the far recesses of the house, etc., and all with no ill effects. This surgery was nothing short of miraculous.

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Brian R. Subach, M.D., F.A.C.S. Dr. Subach is a spine surgeon and the President of the Virginia Spine Institute. He is a nationally recognized expert in the treatment of spinal disorders and an active member of the American Association of Neurological Surgery, the Congress of Neurological Surgeons, and the North American Spine Society. He is a Fellow in the American College of Surgeons. He lectures extensively regarding the management of complex spinal disorders in both national and international forums. He is the Director of Research and Board Member for the non-profit Spinal Research Foundation and Editor-in-Chief of the Journal of the Spinal Research Foundation. He has written 15 book chapters and more than 50 published articles regarding treatment of the spine.

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Spine Tale Joseph Nicolia Brian R. Subach, M.D., F.A.C.S.

hile I had some mild neck and shoulder pain for many years, it was tolerable and never caused any real distress until November 2010 when I experienced the onset of severe symptoms. I was awoken in the middle of the night with excruciating shooting pain and intense numbness running down my right arm. Following this episode, the pain improved slightly, but I had intermittent pain for the next several months. Nothing specific seemed to trigger it, and the daily uncertainty that it might come back any time was somewhat terrifying. At the end of 2010, I had started to diet and became much more active, taking up mountain biking on a regular basis. I was losing weight and riding regularly, but slowly the pain made it harder to engage in everyday activities, including riding. Eventually, the pain became so agonizing that I had to decide whether or not I would go to work, how long I could stay, and what I would be able to do aside from lay in bed or sit inactive. The greatest impact of my symptoms was on my mood. I became much more irritable, short-tempered, and impatient due to the constant pain. I would snap at family and friends, interrupt them, or hurry them along. I even remember lamenting that my pain had been affecting me for so long that I was not sure if it would go away, even if I had a successful surgery. I was incredibly worried that this pain had hard-wired something new in me. Thankfully, that was not the case. Despite the various treatments I received before considering surgery, the pain and numbness continued to come and go. During all of that, I was becoming more and more irritable. Knowing that I couldn’t live this way, I started looking seriously for a spinal specialist to help me. In May 2012, I visited Dr. Subach at the Virginia Spine Institute (VSI) to determine the cause of my discomfort and seek a solution. Dr. Subach recalls asFALL 2013 VOL. 8 No. 2

sessing Joseph’s condition. “Joseph presented with one of the most common debilitating sources of pain that we can face-degenerative cervical disc disease. He had a history of neck pain and right upper extremity pain, numbness, and weakness. He had tried the usual medications and physical therapy with little benefit. Upon initial evaluation, I found that he clearly had evidence of degenerative arthritis at the C5/C6 level with evidence of nerve compression involving the right C6 nerve root which extends strength to the biceps and forearm musculature on the right side. The sensation goes down to the thumb and index finger, and he had evidence of both weakness and numbness following this C6 distribution.” “We performed a nerve test called an EMG study which identified acute nerve damage in the C6 nerve root coming from his neck. His x-rays and MRI scan showed evidence of degenerative arthritis at this level with a disc herniation, which was clearly compressing the nerve. When I asked Mr. Nicolia about his symptoms, he said that the neck symptoms had started approximately one and a half years ago and the arm symptoms began at approximately the same time. He worked as an art technology specialist and that involved sitting, working on a computer, and in-

Figure 1. The axial view of the pre-operative MRI shows a herniated disc (indicated by the arrow) compressing the C6 nerve root.

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SPINAL RESEARCH FOUNDATION Spine Tale: Joseph Nicolia

frequently moving heavy equipment. Based on his symptoms of 80% neck pain and 20% right arm pain with numbness and weakness, we discussed the possibility of continued conservative management including medications, injections, and physical therapy versus the possibility of surgery. Since he had an EMG study performed, which demonstrated acute nerve damage in C6, the risk associated with living with this problem and continued conservative management was significant. He was more likely to progressively damage the nerve, resulting in chronic and permanent nerve damage if nothing was done.” “I performed an anterior cervical fusion on Mr. Nicolia in November of 2012. At the level of his arthritis, C5/C6, I removed the lower part of the C5 bone, removed the entire disc between C5 and C6, and removed the cartilage separating the disc from the bone. I spread the disc space apart, took the pressure off of both the right and left-sided nerve roots C6, and then placed a donor bone spacer in the disc space to maintain its new height and alignment. I used a titanium plate across the front of the spine with screws that fixated from bone five to bone six, giving immediate strength and allowing the bones to heal in the correct alignment.” “Prior to surgery, Joseph stated that his pain number was a four on a visual analog scale of zero to ten. When he came back two weeks after his surgery, he still had some neck pain, but the pain was clearly different. He felt that he had been stretched. In reality we had opened up the disc space at C5/C6 and taken the pressure off the nerve roots, and in doing so, we had stretched the surrounding structures, giving him this feeling of muscular tension in the back of his neck. He felt that his arm symptoms were already improving and that he had better sensation in his thumb and index finger as well as better strength.” “At six months out from surgery in May 2013, Joseph returned with zero neck pain and zero symptoms in his upper extremities. He felt that his posture was normal. He had no discomfort whatsoever in his neck or shoulders, and his strength and sensation had returned to normal. Degenerative cervical disc disease 13 Journal of The Spinal Research Foundation

Figure 2. Lateral view of the post-operative x-ray shows the results of the anterior cervical fusion at C5-C6.

can cause pain from the shoulder blade, the shoulder, and all the way down the arm. It is associated with progressive loss of sensation and strength in one or both arms. By restoring his height and realigning his posture, we were able to directly take the pressure off of the nerve roots and leave him with an excellent result.”

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Immediately after waking The relief up from my surgery, the pain “ I felt and in my arm was gone and all still feel has sensations had returned. The allowed me to numbness and pain had set drive my life on so slowly and each day I forward with endured it in a new way, but an incredible following the operation, it was amount of like actually being awake and purpose.” fully aware again. Without the constant pain, my mood stabilized, and my outlook became incredibly positive. The relief I felt and still feel has allowed me to drive my life forward with an incredible amount of purpose. I’m doing all the things I did before, but I’m able to do them more often and with greater intensity. I’ve been riding better than ever before, my work is improving, and all of my hobbies come with an ease that I feel like I didn’t have for years. I would tell people suffering from this kind of pain to trust in medical science. Making sure a doctor can run the right tests to get real, usable information is key.

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Finding a great, dedicated group of people to deliver treatment means everything. Everyone at the Virginia Spine Institute, from the techs and physical therapists to Dr. Subach and Diana DeWolfe, who performed my surgery, was incredibly invested in helping me. Brian R. Subach, M.D., F.A.C.S. Dr. Subach is a spine surgeon and the President of the Virginia Spine Institute. He is a nationally recognized expert in the treatment of spinal disorders and an active member of the American Association of Neurological Surgery, the Congress of Neurological Surgeons, and the North American Spine Society. He is a Fellow in the American College of Surgeons. He lectures extensively regarding the management of complex spinal disorders in both national and international forums. He is the Director of Research and Board Member for the non-profit Spinal Research Foundation and Editor-in-Chief of the Journal of the Spinal Research Foundation. He has written 15 book chapters and more than 50 published articles regarding treatment of the spine.

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SPINAL RESEARCH FOUNDATION

Spine Tale Joseph Mark Ebertz, M.D. Anthony T. Yeung, M.D. and Susan D. Parker

never thought this whole ordeal with my back pain could happen to me. I am a physician and I live a healthy life, but I wasn’t so healthy five years ago. So I actively made lifestyle changes and lost 85 pounds through exercise and diet. I exercised properly and never took risks with my activities or health in general. I felt that finally I was the captain of my ship, and I really thought spinal problems were not in my future; after all, I was doing everything right. However, one Friday afternoon in September 2012, while doing yard work at my home in North Dakota, I bent over to lift a heavy sprayer and was suddenly gripped by excruciating pain. It coursed through my lower back and legs, and I dropped to the ground. I had never before experienced pain so intense that it dropped me to my knees and made me feel like passing out. I contacted my physician who told me that I likely ruptured a disc, and I should rest over the weekend, take pain medications, and see if I improve by Monday. I was given Aleve, oral steroids, a muscle relaxant, and a strong narcotic. I tried ice packs and heating pads. None of these helped at all. Even though my lower back pain was significant, I was amazed to find that the muscles in my leg hurt far worse. The muscles in the front of my right thigh and on the side of my right calf ached beyond belief. Fortunately, Monday morning finally arrived, and my visit to the MRI center confirmed the diagnosis of a severely bulged disc. Over the next two weeks I had three steroid injections. These shots are administered right into the exit point of the affected spinal nerves and are painful to the point of requiring sedation. The good news was that they were truly helpful and finally gave me good temporary relief. Slowly, I returned to work, and about three months after the disc bulged, I was back exercising in full force. I felt that I had conquered my injured disc. 15 Journal of The Spinal Research Foundation

But all it took was a forceful move in a Zumba class three months later and I was on the floor again. However, this time it would take more than conservative treatment to return to “normal.” I was eventually able to partially return to work, but life was empty. The things that had given me the most joy in everyday life, normal interactions with family, exercise, and working pain-free were taken away from me; this was in spite of numerous spinal injections and all kinds of physical therapy. I spent three months dealing with this. When I failed to improve and my right thigh lost considerable strength, a repeat MRI showed a new development; a broken piece of disc had migrated upwards away from the normal disc space and was lodged vertically between the body of a spinal vertebral bone and the ligaments and muscle surrounding it. I consulted two notable local spine surgeons, one of whom felt he could try microsurgery and remove the bulged disc, but he didn’t have any plan for the portion that had broken off and lodged vertically next

Figure 1. The lateral cut of the pre-operative MRI suggests a herniated disc at L4/L5 with a migrated disc fragment (indicated by the arrow).

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to my vertebra. My other orthopedic spine surgeon, who was a friend and colleague, told me his opinion. The bulged portion of the disc might easily be removed but the vertically lodged component was a significant challenge. He didn’t know if he could remove it without making a much larger incision into my back, and as a result I might end up with fusion surgery. Having two fused vertebrae is sometimes the only option to solve numerous back issues, however, it limits the mobility of your back. My colleague told me that he happened to know a physician in Arizona, Dr. Anthony Yeung, who would be best qualified to help me. I didn’t hesitate. I immediately contacted Dr. Yeung’s office and within a week, I heard back from the Desert Institute for Spine Care (DISC) in Phoenix. His staff was warm, welcoming, and confident. He was patient and understanding, and he reassured me that he felt that even though there were risks, there was a 90% chance he could help me with a microsurgery. I signed on immediately, and 24 hours later I was undergoing the procedure that would give my life back to me. Amazingly, I was awake during the entire process, and thanks to a superb anesthesiologist, I experienced no pain whatsoever during the procedure. Dr. Anthony Yeung explained that Joseph’s particular situation required his specific skill set as an endoscopic spine surgeon. “Dr. Ebertz’s MRI indicated a herniated disc that migrated upward with an extraforaminal component. Surgical consensus included fusion recommendation due to a need for a facetectomy to address the extraforaminal herniation as well FALL 2013 VOL. 8 No. 2

as the migrated fragment. But Joseph is so active that the referring physician hesitated to offer the fusion procedure to him. So instead, I performed a transforaminal decompression at L4/L5 and extracted the migrated fragment under endoscopic control. That is why it is crucial to evaluate the patient’s condition as well as the individual’s lifestyle to perform the appropriate operation and find best surgeon for the procedure.” The first night after my surgery, I expected to experience some pain and was given a prescription for narcotic pain pills, but I didn’t even need one pill! My post-op visit went very well and I was given the O.K. to fly home the next day—only two days after surgery. I took two and a half weeks off work to allow healing without interruption, but subsequently my return to work was uneventful, and I was able to work as if I had never had a spinal problem. I returned to a regular course of exercise, and within eight weeks of surgery I was at 90% of my pre-surgical exercise routine and had recovered 80–90% of the strength that I had lost in my right quadriceps muscles. I’m 58 years old and I can do Zumba class as well as any 20 year olds on the floor! Exercise has been a critical part of my life for years now. It kept my weight down and my confidence up. For nearly six months I had lost that part of my life. If I had not met Dr. Yeung and not had this surgery, my quality of life would have been permanently diminished. Everyday activities and work would have continued to be adversely affected. Dr. Yeung has the confidence of decades of experience and he has scientifically proven that spine surgery is effective and life-changing. Journal of The Spinal Research Foundation 16

SPINAL RESEARCH FOUNDATION Spine Tale: Joseph Mark Ebertz, M.D.

Some people have scoffed at the idea of me flying from North Dakota to Phoenix for this surgery. I have no second thoughts. I simply cannot thank him adequately; how do you thank a man that has Anthony T. Yeung, M.D. Dr. Anthony Yeung is a board certified orthopedic spine surgeon at Desert Institute for Spine Care. He specializes in diagnosing and treating back pain and sciatica caused by painful traumatic and degenerative conditions of the lumbar spine. He is an internationally renowned world leader in endoscopic spine surgery and the developer of the FDA-approved Yeung Endoscopic Spine System (YESS™). Dr. Yeung was the first to utilize endoscopically guided radiofrequency probes and lasers for selective endoscopic discectomy and dorsal endoscopic facet rhizotomy procedures in the lumbar spine. Additionally, Dr. Yeung is an international lecturer, the recipient of numerous awards, and a prolific author of over 70 scientific publications on his technique. He is currently the President of the World Congress of Minimally Invasive Spine Surgeons and the Executive Director of the Intradiscal Therapy Society.

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given you your life back? The only thing I can do is to offer my story as testament that spinal surgery is not experimental, but effective. I am living, walking proof! Susan D. Parker Susan Parker is the Director of Marketing at Desert Institute for Spine Care (DISC), a spine surgery practice in Phoenix, Arizona. She specializes in business development, strategic partnerships, sales, and marketing. Susan has spent the majority of her career in biologic and medical device sales, often chosen for national task forces and leadership roles in training and mentoring peers. Her experience includes regional, national, and international sales and marketing for Johnson & Johnson, Sanofi-Synthelabo, Reebok International, and Desert Institute for Spine Care. Named a Marketing Expert in the Worldwide Who’s Who in 2012, Susan is passionate about using her skills and expertise to help patients find pain relief at DISC.

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Spine Tale Kristin Greene Skabo Christopher A. Yeung, M.D., and Susan D. Parker

first injured my lower back seven years ago while playing with my son. I had re-injured my lumbar disc at least twice a year every year since then. However, this past April I began to feel a distinctly different pain. The pain radiated down my leg, which was something I hadn’t experienced before. Within a week, the pain in my leg and lower back were constant and became so debilitating that I was unable to sit. I could not sleep, I couldn’t focus on anything besides the pain, and I could not walk! This time, my disc had herniated and was impinging on a spinal nerve. I immediately went to the emergency room, but the physician simply gave me pain medication and dismissed me. However, when I remained unable to walk, I decided to reconsider back surgery. I had always felt intimidated by spine surgery, but then I realized, “I am having back problems and will for the rest of my life if I don’t seek treatment. What if surgery alleviates the issues in the future?” Beyond the physical limitations, my back pain affected me psychologically as well. I am a fit forty-one year old active mother. I couldn’t understand why my body was breaking down. How had this happened to me? I didn’t know if I would get better this time, and it was frightening. For seven years I experienced back pain, but I never sought treatment. After the rupture, I knew I needed help. Most importantly, I want to be able to always play with my son. He has lived most of his life with my injured back. When the last episode occurred, I told him that I was going to get better soon, and I would be careful so this would never happen again. He looked at me and said, “You say that every time,” and walked away with his head hung. Needless to say, when my disc ruptured, I knew I had to make good on my word to never let this happen again. FALL 2013 VOL. 8 No. 2

One particular event made me reconsider a surgical solution. I had ruptured the disc two days before I had to travel to Washington, DC for meetings. Since I could not walk at all, I had to arrange to use a wheelchair. I had a meeting in the White House and was unable to walk through those halls I admired so much. I was holding back tears from the pain while trying to be coherent in my arguments. A meeting in the White House was such a special opportunity for me, and my damaged disc had ruined the experience. I couldn’t let any more experiences pass me by. Two weeks after the rupture, I met Dr. Chris Yeung. Dr. Yeung recalls meeting Kristin and evaluating her back. “Kristin had managed intermittent back pain exacerbations for years. She likely had partial tears in the outer parts of the intervertebral disc (the annulus) which caused localized back pain. Eventually, the annulus weakened and the softer central part of the disc (the nucleus) herniated through the annulus and into the spinal canal and compressed her nerve.” “Kristin’s images revealed she had a very large disc herniation compressing her S1 spinal nerve. It

Figure 1. The axial view of the pre-operative MRI shows a herniated disc (indicated by the red arrow) at the L5/S1 level.

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SPINAL RESEARCH FOUNDATION Spine Tale: Kristin Greene Skabo

caused nerve damage with This type of weakness, numbness, and de- “ pain can bilitating pain (sciatica). This turn even the type of pain can turn even the most stoic most stoic person into a cripperson into pled shadow of themself.” a crippled “I treated her with a mishadow of croscopic lumbar discectomy themself.” through a 2.5 centimeter incision to remove the disc herniation and relieve the nerve compression. She had arrived to the surgery center in a wheelchair and was able to walk out two hours later. She had immediate relief of her nerve pain and quickly recovered strength and sensation. This is a very successful procedure and is indicated for disc herniations in patients that have a significant neurologic deficit, debilitating pain, or have failed to get relief with an appropriate trial of non-operative care.” Prior to my operation, I had always feared damaging the disc again. Would it be when I sneezed? How long will I be bedridden this time? How long before I could run around and play with my son? I lived in constant fear of the next injury. I wasn’t ever able to live in the moment and enjoy it. However, after the microdiscectomy with Dr. Yeung, I feel changed in so many ways. I can play football and soccer with my son! I don’t worry about when the next episode will

be. Sneezing, twisting and Don’t let bending don’t worry me. I no “ the fear of longer have to say, ‘I have a the surgery bad back.’ I have banished hinder you; the phrase from my life! the result is For those experiencing remarkable!” back pain, don’t let life pass you by because you are always in pain or waiting for the next painful episode. Don’t let the fear of the surgery hinder you; the result is remarkable! Christopher A. Yeung, M.D. Dr. Christopher Yeung is a board certified, fellowship trained orthopedic spine surgeon at Desert Institute for Spine Care in Phoenix, AZ. He has a special interest in minimally invasive spine surgery techniques with a philosophy of choosing the least invasive yet most effective method to treat spine problems. Dr. Yeung treats the full spectrum of degenerative and traumatic spinal conditions, and he has been the principal investigator in many FDA studies for artificial disc replacement and fusion alternatives. Dr. Yeung speaks nationally and internationally on the latest, most innovative treatment options in minimally invasive spine surgery and has published numerous articles. In addition, Dr. Yeung is the team spine surgeon for the Arizona Diamondbacks, the Los Angeles Dodgers, the Cincinnati Reds, and the Arizona Rattlers. He was recognized by his peers to be one of the top Phoenix spine surgeons in 2009, 2010, 2012 and 2013.

Susan D. Parker Susan Parker is the Director of Marketing at Desert Institute for Spine Care (DISC), a spine surgery practice in Phoenix, Arizona. She specializes in business development, strategic partnerships, sales, and marketing. Susan has spent the majority of her career in biologic and medical device sales, often chosen for national task forces and leadership roles in training and mentoring peers. Her experience includes regional, national, and international sales and marketing for Johnson & Johnson, Sanofi-Synthelabo, Reebok International, and Desert Institute for Spine Care. Named a Marketing Expert in the Worldwide Who’s Who in 2012, Susan is passionate about using her skills and expertise to help patients find pain relief at DISC.

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Public Health The Smoking Spine Ashley R. Gilchrist, M.P.H., P.A.-C.

obacco use remains the leading preventable cause of death, disease, and disability in the United States1 and is a significant public health concern. Roughly one in five American adults are currently smokers, and half will die prematurely from smokingrelated causes.1 Cigarette smoking, or nicotine use, adversely affects nearly all tissues and systems in the body. Many people are well aware that tobacco use increases the risks for cancer, lung diseases, heart disease, stroke, and depression. However, many people are surprised to learn that smoking damages the spine, contributing to intervertebral disc disease and facilitating osteoporosis.

specialized sheets of connective tissue called lamellae, which are layered for strength. The annulus has a high amount of collagen that makes the outer layer extremely stiff. The nucleus pulposus is the soft, jelly-like center. It serves as the main shock absorber and is held in place by the outer annulus. The nucleus consists of a gel-like matrix that provides maximum hydration. It functions to distribute pressures in all directions within each disc under compressive forces. The intervertebral disc is essential for providing spinal stability and proper alignment, withstanding compressive shock forces, and allowing for movement between vertebral bones. Discs in the spine increase in size from the neck to the low back as there are increasing needs for shock absorption due to weight and gravity. The intervertebral disc is an avascular tissue, meaning it does not naturally have a blood supply. Capillaries from the surface of the vertebral bodies supply the disc with nutrients. Thus, the disc is dependent on the blood supply to the vertebral bones. ANNULUS FIBROSUS NUCLEUS PULPOSUS

Anatomy of the Intervertebral Disc An intervertebral disc connects one vertebral bone to the next. The discs are the shock-absorbing cushions between each vertebra of the spine. The disc is made up of three basic structures: the annulus fibrosus, the nucleus pulposus, and the vertebral endplates. All three disc structures are made of different percent compositions of proteoglycan (proteins that bind water), collagen (the main protein in connective tissue), and water. The varying compositions create different functions. All these properties make the disc unique and highly specialized. Each disc has a strong outer ring of fibers called the annulus fibrosus. The annulus is comprised of FALL 2013 VOL. 8â&#x20AC;&#x201A; No. 2

LAMELLAE

Figure 1.â&#x20AC;&#x201A;Structure of an Intervertebral Disc. Image courtesy of Medtronic, Inc.

Nutrients and Nicotine It is important to understand the effects nicotine and cigarette smoke have on the body. Tobacco smoke contains more than 7,000 chemicals with at least 250 known harmful chemicals, many of which are cancer-causing.2 Nicotine is naturally derived from the tobacco plant and attaches to nicotinic receptors in the body found in the central nervous system, autonomic nervous system, and neuromuscular junctions.3 Nicotine is largely responsible for the addictive properties associJournal of The Spinal Research Foundationâ&#x20AC;&#x192; 20

SPINAL RESEARCH FOUNDATION A.R. Gilchrist/Journal of the Spinal Research Foundation 8 (2013) 20–23

• Respiratory diseases • Early menopause • Erectile dysfunction • Stained teeth and bad breath • Gum disease and tooth decay • Premature wrinkles • Dementia and Alzheimer’s disease • Osteoporosis and increased fracture risk Degenerative Disc Disease The association between back pain and smoking in adults is well established by decades of research. Degenerative disc disease is a condition where vertebral discs are weakened; they no longer properly act as cushions between the vertebrae. Instead of remaining strong, the discs become softer. This condition can develop naturally as part of the aging process, but may also result Figure 2. These are some of the harmful chemicals found in a cigarette. Image courfrom injury. Disc degeneration is thought to tesy of ClarkIsIt.com. be largely responsible for back pain.3 Degen3 ated with cigarette smoke. Smoking affects the entire erative discs typically begin with small annular tears. body. Nicotine enters the blood supply and is rapidly Just like other injuries, the tears heal by creating scar distributed to most body tissues. Cigarette smoking is tissue, which is not as strong as the original disc wall. a leading cause of structural and functional changes Over time, the process of tearing and scarring continuin the cardiovascular system. Smoking causes injury ally weakens the disc wall. In addition, as people age, and inflammation to blood vessels, decreasing essenthe hydrated nucleus becomes damaged and loses its tial blood flow to all tissues. This injury promotes the water content. This fluid maintains needed pressures development of dangerous plaque and blood clots. Not to act as a functional shock absorber. The nucleus can only is the body’s major circulation compromised, but collapse and allow the vertebral bones to slide closer so is blood flow to the intervertebral discs. Smoking together with improper alignment. In time, improper also impairs collagen formation, one of the necessary alignment and arthritic changes can create bone spurs, structural proteins of the disc. Smoking literally preherniated discs, pinched nerves, and spinal stenosis, vents proper essential nutrients from reaching the discs all of which lead to pain. and prevents adequate healing. These processes cause Nicotine use may be directly responsible for interdiscs to prematurely degenerate and become diseased. vertebral disc degeneration by causing cell damage in the In addition to damaging the disc, smoking has annulus and nucleus.3 Evidence suggests that nicotine 4 many other ill effects in the body including: may have a direct toxic effect on the nucleus cells.3 This impacts the long-term health of the disc and its functional • Cancer ability. All these detrimental changes mean that smokers • Pregnancy complications including premature damage not only healthy discs, but greatly accelerate disc birth, death and low birth weight degeneration in any already damaged discs. • Heart and blood disease 21 Journal of The Spinal Research Foundation

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Smoking may also increase sensitivity to pain by altering the perception of pain through the neuroendocrine system.5 One study evaluated self-reported health statuses from over 25,000 patients and found smokers who had spinal symptoms for the same amount of time as non-smokers reported symptoms as more severe and present for a greater percentage of time each day.5 A dose-dependent relationship may exist where the risk for developing low back pain increases with the amount smoked.

Normal bone

Osteoporosis Osteoporosis means “porous bone” and is a bone-thinning disease characterized by losing too much bone or not making enough new bone. This loss of bone mass leads to fragile bones that are more susceptible to fractures. The National Osteoporosis Foundation estimates that 9 million Americans have osteoporosis and 48 million have low bone density.6 Because of the widespread prevalence and increased risk for fractures, approximately one in two women and up to one in four men over 50 years old will break a bone due to osteoporosis.6 Spinal fractures are the most common type of osteoporotic fractures. While osteoporosis has many risk factors contributing to its development, there is a strong association between smoking and osteoporosis.7 One study found that women who smoked more than one pack per day throughout adulthood had an average of 5–10% lower bone density than non-smokers in the low back by the time of menopause.7 Even second hand smoke has been shown to negatively affect bone mineral density.7 Smoking clearly plays a role in increasing the loss of bone density in all bones, and the rate of loss is related to the daily number of cigarettes smoked and years of exposure. This is an independent risk factor from other factors that contribute to bone health such as sex, age, weight, BMI, and unhealthy lifestyle habits. For smoking alone, the lifetime risk of developing a spinal fracture is increased by 32% in men and 13% in women.7 Smoking also delays fracture healing. This is likely due to the fact that the toxic activity of FALL 2013 VOL. 8 No. 2

Osteoporosis Figure 3. Microarchitecture of Cancellous Bone in a Healthy Person (left) and in an Older Person with Osteoporosis (right). Healthwise illustration provided courtesy of Healthwise, Incorporated.

nicotine stops the growth of cells essential for healing and reduces needed blood and oxygen supply.7 This is important not only for fracture healing, but for any healing after a surgery. Nicotine Use and Spinal Surgery Smoking negatively affects bone healing and the success rates in spinal surgery.3 Decades of research show that smokers have significantly poorer spinal surgery outcomes than non-smokers.5 Smokers experience higher rates of delayed wound healing, postoperative infections, and decreased successful spinal fusions than non-smokers.5 Smokers stay in the hospital longer and consume more hospital resources.7 One study looked at nearly 300 spinal fusion patients and found smokers were almost three times as likely to have a nonunion (failure to completely fuse) than non-smokers.5 The incidence of delayed wound and fusion healing is so significant that many surgeons feel proceeding with an elective fusion surgery would not be worth the risk while the patient is still smoking.7 Journal of The Spinal Research Foundation 22

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Quit Today Smoking cessation is strongly advised. Positive and immediate improvements can be seen. Complete cessation can improve the healing process, reduce postoperative complications, and decrease the hospital stay. Even stopping five to seven days before surgery favorably increases wound healing.7 From just days to decades after quitting, your body continues to become healthier. Quitting smoking is hard. The National Cancer Institute recommends these five steps be the START of every successful plan to quit smoking.8

• Set a quit date. • Tell family, friends and co-workers you plan to quit. • Anticipate and plan for the challenges you will face while quitting. • Remove cigarettes and other tobacco products from your home, car, and workplace. • Talk to your doctor about getting help to quit. If you are someone who has back pain or disc disease, quit now and improve your life. Your spine will thank you. References 1. Centers for Disease Control and Prevention. Smoking and Tobacco Use: Fast Facts. Updated June 2013. Available from: http://www.cdc.gov/tobacco/data_statistics/fact_sheets/fast_ facts/index.htm 2. National Cancer Institute. Harms of Smoking and Health Benefits of Quitting. Available from: http://www.cancer.gov/cancer topics/factsheet/Tobacco/cessation 3. Akmal M, Kesani, A, Anand B, et al. Effect of Nicotine on Spinal Disc Cells: A Cellular Mechanism for Disc Degeneration. Spine. Mar 2004;29(5):568–75. 4. National Cancer Institute. Harms of Smoking and Health Benefits of Quitting. Reviewed 2011. Available from: http://www. cancer.gov/cancertopics/factsheet/Tobacco/cessation 5. Vogt MT, Hanscom B, Lauerman WC, Kang JD. Influence of smoking on the health status of spinal patients: the National Spine Network database. Spine. Feb 2002;27(3):313–9. 6. National Osteoporosis Foundation. What is Osteoporosis? National Osteoporosis Foundation Website. Available from: http://www.nof. org/articles/7 7. Abate M, Vanni D, Pantalone A, Salini V. Cigarette smoking and musculoskeletal disorders. Muscles Ligaments Tendons J. Apr–Jun 2013;3(2):63–69. Published online 2013 July 9. doi: 10.11138/mltj/2013.3.2.063 8. 5 Steps to START. NIH MedlinePlus: the magazine [Internet]. 2011 Winter [cited 2013Aug 26];5(4):5.Available from: http://www.nlm. nih.gov/medlineplus/magazine/issues/winter11/articles/winter 11pg5.html

Ashley R. Gilchrist, M.P.H, P.A.-C. Ashley Gilchrist is a skilled physician assistant at the Virginia Spine Institute. She studied in a unique joint masters program at George Washington University in Washington, DC to ultimately receive a Master of Sciences in Health Sciences in Physician Assistant Studies and a Master of Public Health. Figure 4. Image courtesy of BeTobaccoFree.gov.

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FALL 2013

From Your Personal Trainer Weight Training and Bone Density Melissa Treat, R.N., B.S., C.P.T.

ur modern society has experienced a rising awareness of overall health and fitness, and health care providers are focusing on the importance of preventing medical issues through lifestyle changes. One of the hallmark features of aging is loss of bone strength and muscle mass, which can potentially lead to decreased functional ability and an increased risk of injury. Today’s aging population is faced with an increase of spine, hip, shoulder, and wrist fractures due to weakened bones, or osteoporosis. Current studies Figure 1. Osteoporotic bone (right) is at a much higher risk to fracture show that one in two women and one in four men over than healthy bone (left). the age of fifty will sustain an osteoporotic fracture.1 lifestyle reduces the constant forces that bone needs in The cost of osteoporosis to Americans is increasing. A order to continue its normal process of remodeling.1 ccording to the National Osteoporosis Foundation of Exercise is vital at any age for improving bone health America, more than 38 million dollars are spent daily and preventing weakened bone density. A regular exon osteoporotic and associated fractures. Osteoporoercise program that includes resistance training will sis is not considered a normal aspect of aging, as it allow us to maintain bone and muscle strength, coordiis highly preventable, and early treatment can greatly nation, and balance, which will help prevent falls and reduce the risks of chronic skeletal issues. related fractures. It is important to understand that osteoporosis is Research has shown that resistance training and not a disease in the clinical sense, but a condition. Osimpact loading exercises can restore bone mineral teoporosis is a multi-faceted ailment caused by numerdensity in men and women of all ages. In response ous interrelated factors, and it must be treated as such to loading of the bone, created by repetitive muscufor optimal prevention and treatment. Until about age 30–35, our bones are in a constant state of building. After that time, we begin to lose bone density. Bone strength can be affected by heredity, diet, sex hormones, physical activity, lifestyle choices, and the use of certain medications.1 For the prevention and management of osteoporosis, it is necessary to use an interactive approach that integrates lifestyle interventions in order to maintain bone health. Bone is a living tissue, constantly undergoing demolition and renewal as it responds to changing forces in the environment. Like muscle, bone responds to exercise by becoming stronger. Lack of weightbearing exercise is considered one of the earliest contributing risk factors to Figure 2. Image courtesy of OpenStax College. Exercise, Nutrition, Hormones, and Bone decreased bone density, as a sedentary Tissue [Connexions Web site]. June 3, 2013. Available at: http://cnx.org/content/m46305/1.4/. FALL 2013 VOL. 8 No. 2

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lar contractions or mechanical forces, the bone begins the process of remodeling.2 This important process involves the manufacturing of protein molecules that are deposited into the spaces between bone cells, creating a bony matrix that gives bone its rigid structure and strength. In order to create long-lasting improved bone health, there needs to be systematic administration of sufficient stimulus, followed by adaptation of the tissue, and then the introduction of a new, increasingly greater stimulus. Implementing a consistent and progressive resistance training program can greatly reduce the risk of developing osteoporosis or any bone demineralization. Activities that stimulate bone growth need to include progressive overload, variation of load, and specificity of loading.2 Utilizing progressive overload allows the bone and associated connective tissue to develop necessary strength without being asked to exceed the critical level of safety. Specificity of loading refers to exercises that directly place a load on a certain region of the skeleton. With osteoporosis, the sites of fracture that are most devastating are in the axial skeleton (the spine and hip). Multi-joint motions (such as squats, lunges, and deadlifts) direct forces through the axial skeleton and allow greater loads to be utilized. Progressive and specific loading of the muscles, bones, and joints through safe and effective ranges of motion will improve bone health, strength, and total body functioning. For any resistance training program, it is essential to use proper form and technique for each exercise. Utilizing proper body mechanics will en-

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sure maximal bone strengthening benefit without compromising the tissues or putting the body at risk for injury. It is important for the individual to feel competent and safe while performing each exercise. Today, both sexes are embracing weight training, resistance training, and plyometric exercises. When performed with proper technique, weight lifting can not only help you lose weight and build lean mass, but can also help you work towards a healthier and stronger future. References 1. Humphries, B. D. (2009). Strength training for bone, muscle, and hormones. American College of Sports Medicine. Retrieved from www.acsm.org/docs/current-comments/strengthtrainingforbmh. pdf 2. Kravitz, L. (2006). Resistance training: Adaptations and health implications. IDEA Today, 14(9):38–46.

Melissa Treat, R.N., B.S., C.P.T. Melissa Treat has been in the fitness industry for 6 years, working as a personal trainer and group fitness instructor at Tyson’s Sport and Health in McLean, VA. She has a degree in Kinesiology from University of Maryland and is certified with ACE, NASM Corrective Exercise, Crossfit Level One, Crossfit Mobility, and TRX Suspension Training. She works with her clients on total health and wellness, overall fitness, disease and injury prevention, mobility and flexibility, total body restoration, performance enhancement, and rehabilitation from various injuries and surgeries. She is passionate for health and fitness and enjoys helping people bring exercise and nutrition into their lives.

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FALL 2013

The Nutritional Aspect of Bone Health Michael W. Hasz, M.D., F.A.C.S.

ating a well-balanced and complete diet is an essential part of maintaining strong, healthy bones. It is not enough to merely include adequate calcium in one’s diet; other minerals such as magnesium, phosphorus, and sodium can also affect bone health. In addition, sugar, refined grains and flour, caffeine, and alcohol can all significantly impact bone health. Therefore, it is important to embrace exercise and overall good health in accordance with a well-balanced diet to maintain healthy bones.

This refined sugar displaces other nutrient-rich foods, which would help with bone health. By eating as much sugar as we do, we get less calcium, magnesium, and other vitamins including zinc, copper, vitamin B, and other nutrients that are essential for overall health. Eating this excessive amount of sugar can also directly deplete our bodies of calcium. The increased intake of sugar has been shown to increase the excretion of urinary calcium. It has also been associated with increased kidney stones. Other studies have demonstrated that patients with kidney stones have an increased risk of osteoporosis. It appears that with this increased excretion of calcium, the calcium is no longer available for use elsewhere in the body and can lead toward weakening of the bones. Furthermore, eating so much sugar has led to other diseases resulting from the stress of excess insulin production, as well as excess inflammation in the body. Elevated sugar in one’s diet increases the release of cortisol level by the adrenal gland, and increased cortisol levels over the long term have been shown to be associated with osteoporosis.

Calcium and Magnesium

Refined Foods such as Grains and Flour

Both calcium and magnesium are very important minerals for building strong bones and teeth and for supporting many essential body functions, such as contracting and relaxing muscles, sending and receiving nerve signals, regulating blood pressure and heart health, and releasing hormones. Green leafy vegetables such as broccoli, kale, and cabbage, are all good sources of calcium and magnesium. Additionally, salmon and sardines, some nuts such as almonds, Brazil nuts, and sunflower seeds are also good sources for these minerals. Of course, vitamin D is important to help these minerals in building good, strong bones. Sources of vitamin D include dietary supplements as well as getting adequate sunlight every day.

Refined foods, particularly grains from which the outer hull has been removed, have fewer nutrients than their wholegrain counterparts. This refining process results in a significant loss of vitamins and minerals, such as calcium, magnesium, copper, zinc, vitamin B, and folic acid. The lack of vitamins and minerals, can not only lead toward osteoporosis, but also can lead toward other diseases associated with poor nutrition. Additionally, many people discovered they have gluten sensitivities. Gluten sensitivities to grains in particular have led toward inflammation along the gastrointestinal (GI) tract and poor absorption of minerals and other nutrients. This poor absorption of minerals as well as inflammation has been associated with increased osteoporosis and poor bone health.

Sugar

Caffeine

Today, the average American consumes approximately one hundred fifty pounds of refined sugar every year.1

Caffeine is found in many products including coffee, tea, many sodas, and other beverages. Caffeine

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drink often needs to be buffered. A source of the buffer of the acid is the bicarbonate available in the bones. Proteins A diet very high in proteins has been shown to increase calcium excretion in the urine. In addition to calcium being excreted in the urine, proteins cause calcium loss because calcium is mobilized to buffer the acidic breakdown products of proteins. Hence, consuming high levels of proteins may negatively affect bone health since there is less calcium available for bones. Smoking

Figure 2. Anatomy of a Whole Grain Kernel. The process of refining grains by removing the outer shell causes the loss of essential nutrients. Image courtesy of the US Department of Agriculture.

has various effects on the human body, including an increased susceptibility to some diseases in some individuals. Some diseases attributed to or associated with caffeine include diarrhea, constipation, abdominal pain, fibrocystic disease, elevated cholesterol and blood sugar, hypertension, and headaches. Caffeine has effects throughout the body and has been associated with bone loss. Studies have demonstrated that drinking caffeinated coffee has increased the excretion of calcium in the urine within a few hours after drinking the coffee. The increase of calcium excretion could mean that there is less calcium available for the bones which could lead to osteoporosis. Sodas The chronic drinking of sodas has been associated with osteoporosis. This may be due to the sugar content of the sodas, and it may also be due to the relatively acidic composition of sodas. The acid within the

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The nicotine and other many compounds present in tobacco lead to osteoporosis as well. Not only does smoking increase cortisol levels, but smoking can also damage small vessels, leading to poor blood supply and fewer nutrients reaching the bones. In conclusion, many dietary factors contribute to bone health. Favoring the consumption of the positive factors and avoiding the over-consumption of the negative dietary items, one has the opportunity to increase bone heath and help avoid the onset of osteoporosis. Reference 1. How much sugar do you eat?. (2007, July). Retrieved from http:// www.dhhs.state.nh.us/dphs/nhp/adults/documents/sugar.pdf

Dr. Hasz is a spine surgeon at the Virginia Spine Institute. He is board certified by the American Board of Spine Surgery, a Fellow in the American Academy of Orthopaedic Surgeons, and a member of both the American Association of Orthopaedic Surgeons and the North American Spine Society. He was Chairman of the Department of Orthopaedic Surgery and Director of Spinal Surgery at the Andrews Air Force Base/Malcolm Grow Medical Center in Maryland. He currently holds an appointment as Clinical Instructor of Orthopaedic Surgery and Assistant Professor of Surgery at the Uniformed Services Health Science University in Bethesda, Maryland.

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The Genetics of Bone Density Justin C. Battle, P.A.-C., M.P.A.S.

ecently, a study was published in the medical journal, Nature Genetics, which linked 32 novel genetic regions to bone mineral density.1 The findings may help researchers understand why some people are more susceptible to bone fractures based upon factors inherited from their parents. The research also points to potential targets for medications which may help potentially treat or prevent osteoporosis. Bones are made of a mineral and protein scaffold filled with living cells. In a nearly continuous remodeling process, cells known as osteoblasts build new bone, while osteoclast cells dissolve or resorb bone. Essentially each of our bones is continually broken down and replaced. When the rate of bone loss exceeds the rate of replacement, bones weaken, eventually leading to osteopenia (mild weakening), followed by osteoporosis and an associated higher risk of fracture. Nearly 50 million people in the United States have either osteoporosis or are at increased risk for broken bones because of low bone mineral density (osteopenia). Prior studies suggest that genetic differences may account for more than half the variance in bone mineral density among people. Previous genome-wide association studies identified 24 genetic regions that influence bone mineral density. However, these genetic variants explained only a small fraction of the variation in bone density, and none were shown to influence the risk of fracture in a definitive way. A worldwide consortium with multiple research groups set out to do the largest search to date for variants related to bone mineral density. The effort was funded by many sources, including the European Commission and several National Institute of Health (NIH) components such as the National Institute on Aging (NIA) and the National Institute for Arthritis, Musculoskeletal, and Skin Diseases (NIAMS). The extensive research team—led by a group at Erasmus Medical Center in Rotterdam, The Netherlands—also included scientists from the NIA. The study2 appeared online in Nature Genetics on April 15, 2012. The researchers first combined data from 17 different studies involving more than 80,000 people across North America, Europe, East Asia, and Australia. They looked across the genome for genetic FALL 2013 VOL. 8 No. 2

variants associated with bone mineral density of the femoral neck (a part of the thigh bone) and the lumbar spine. The researchers found 96 independent variations from 87 genomic regions. The scientists next tested these associations in over 50,000 more people from 34 other studies. They confirmed the association with bone mineral density in 56 regions, 32 of which hadn’t been previously tied to bone density. The team also examined whether the 96 variants were associated with bone fractures. They analyzed data from 50 studies with fracture information. Combined, the studies involved over 31,000 people with fractures and over 102,000 controls. Fourteen of the regions, the researchers found, were also associated with bone fracture risk. Although these findings reinforce the relationship between genetic factors and the risk of osteoporosis, the ability to predict osteoporosis is significantly improved when one combines the genetic predisposition

Figure 1. Compressive Facture. Image courtesy of joelgarrismd.com.

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osteoporosis when possible, in addition to identifying patients at risk for the disease long before it becomes symptomatic,” says Dr. Mark McLaughlin of Princeton Brain and Spine Care in Langhorne, PA. References 1. Struan F. A. Grant, David M. Reid, Glen Blake, Ruth Herd, Ignac Fogelman & Stuart H. Ralston. Reduced bone density and osteoporosis associated with a polymorphic Sp1 binding site in the collagen type I a 1 gene. Nature Genetics 1996;14:203–205. 2. Karol Estrada, Unnur Styrkarsdottir, Evangelos Evangelou, YiHsiang Hsu, Emma L Duncan, et al. Genome-wide meta-analysis identifies 56 bone mineral density loci and reveals 14 loci associated with risk of fracture. Nature Genetics 2012;44:491–501. doi:10.1038/ng.2249

Justin C. Battle, P.A.-C., M.P.A.S. Figure 2. Compressive forces combined with osteopenia can lead to painful fractures in the spine. Image adapted from joelgarrismd.com.

with clinical risk factors such as age, tobacco use, and body weight. “The ultimate goal of genetic studies like these is to develop personalized, gene-based treatments for

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Justin Battle is a talented physician assistant at the Virginia Spine Institute where he completed a one year residency and one year fellowship in medical and surgical management of spinal disorders. Justin has a Master of Physician Assistant Studies from Marietta College, OH and is also certified by NCCPA and Athletic Training Certified (ATC).

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Bone Physiology and Bone Healing Brian R. Subach, M.D., F.A.C.S.

one is living tissue composed of metabolically active cells that are integrated into a rigid mineral framework. When injury occurs or surgical bony fusion is attempted, there is a continuous process of bone deposition, resorption, and remodeling which eventually results in healing. The success of many spine operations depends on the restoration of long-term spinal stability. The hardware, or spinal instrumentation, provides a temporary support, but a solid bony union must be achieved to provide permanent stability. If the bones fail to fuse, it often causes the failure of the supporting instrumentation and a recurrence of symptoms. Understanding the basic biological and physiological principles of bone transplantation and healing aids the spine surgeon in selecting the most effective techniques to achieve successful fusion and patient satisfaction. This article reviews the anatomy and physiology of bone, its metabolism, and the healing process of surgical fusion.

Bone Anatomy and Histology The cellular components of bone consist of osteoprogenitor cells, osteoblasts, osteoclasts, osteocytes, and the stem cells in the bone marrow. Osteoprogenitor cells are present on all bone surfaces and are found in the deep layer of the periosteum and in the endosteum, which lines the internal medullary surfaces. The periosteum is a tough, vascular layer of connective tissue that covers the bone, but not the joint surfaces. Osteoblasts are immature, metabolically active, bone-forming cells. They secrete osteoid, the nonmineralized organic matrix which eventually undergoes mineralization, giving the bone its strength. Over time, some osteoblasts are converted into osteocytes (mature cells). Osteocytes are mature osteoblasts trapped within the bone matrix. Each osteocyte is essentially connected to other osteocytes and local blood vessels to help control plasma levels of calcium and phosphorus and to maintain the integrity of the bone.

Figure 1. Bone Remodeling Osteoblasts and Osteoclasts Differentiation. Figure was produced using Servier Medical Art from Ewa Ste ˛ pien (2011). Acceleration of New Biomarkers Development and Discovery in Synergistic Diagnostics of Coronary Artery Disease, Coronary Angiography— Advances in Noninvasive Imaging Approach for Evaluation of Coronary Artery Disease, Prof. Baskot Branislav (Ed.), ISBN: 978-953-307-675-1, InTech, DOI: 10.5772/18940. Available from: http://www.intechopen.com/books/coronary-angiography-advances-in-noninvasive-imaging-approach-forevaluation-of-coronary-artery-disease/acceleration-of-new-biomarkers-development-and-discovery-in-synergistic-diagnostics-of-coronary-arte.

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Osteoclasts, on the other hand, are multinucleated, bone-resorbing cells controlled by hormonal and cellular mechanisms. These cells attach to bony surfaces and through certain enzymes, they are able to dissolve bone and calcified cartilage. This process results in the formation of shallow grooves or valleys on the bone surface called Howship’s lacunae. There are three primary types of bone: woven bone, cortical bone, and cancellous bone. Woven bone is typically seen during embryonic development, during fracture healing (callus formation), and in some pathological states such as hyperparathyroidism and Paget’s disease. It is comprised of disorganized collagen bundles and irregularly shaped vascular spaces lined with osteoblasts. Woven bone is a precursor and is generally

replaced with cortical or cancellous bone. Cortical bone, also known as compact bone, is remodeled by means of vascular channels that invade the woven bone from its outer surfaces. Cortical bone is important in providing the strength and weight-bearing potential of bone. The primary structural unit of cortical bone is an osteon. Osteons consist of bone that surrounds vertically-oriented blood vessel channels called Haversian canals. Adjacent osteons are connected by horizontally-oriented Volkmann canals. The mechanical strength of cortical bone comes from the close packing of the osteons. Cancellous bone, also known as trabecular bone, lies between cortical bone surfaces and contains the cells responsible for producing the cellular components of circulating blood.

Figure 2. Schematic overview of bone that is depicting gross overview, and cellular distribution. Figure was produced using Servier Medical Art and found at Chao Le Meng Bao, Erin Y. Teo, Mark S.K. Chong, Yuchun Liu, Mahesh Choolani and Jerry K.Y. Chan (2013). Advances in Bone Tissue Engineering, Regenerative Medicine and Tissue Engineering, Prof. Jose A. Andrades (Ed.), ISBN: 978-953-51-1108-5, InTech, DOI: 10.5772/55916. Available from: http://www.intechopen.com/books/regenerative-medicine-and-tissue-engineering/advances-in-bone-tissue-engineering.

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FALL 2013 The Bare Bones of Spinal Disease Bone Biochemistry Bone is composed of organic and inorganic elements. By weight, bone is approximately 20% water. Dry bone is made up of calcium phosphate/calcium carbonate (70%) and collagen (30%). Osteoid is the non-mineralized organic matrix secreted by osteoblasts. It is composed of 90% type I collagen and 10% ground substance, which consists of glycoproteins, proteoglycans, peptides, carbohydrates, and lipids. The calcification of osteoid provides bone with its strength. The inorganic content of bone consists primarily of calcium phosphate and calcium carbonate, with small quantities of magnesium, fluoride, and sodium. The initial calcification of osteoid typically starts within a few days of secretion, but may take months to complete. Regulators of Bone Metabolism Bone metabolism is influenced by hormonal and local factors. Three such hormones that may affect bone metabolism are parathyroid hormone, vitamin D, and calcitonin. Parathyroid hormone causes bone to lose calcium to maintain the bodyâ&#x20AC;&#x2122;s normal calcium levels. Osteoblasts are the only bone cells that have parathyroid hormone receptors. Vitamin D stimulates intestinal and kidney calcium-binding proteins and facilitates active calcium transport. Calcitonin is secreted by the cells of the thyroid gland in response to an acute rise in plasma calcium. Bone metabolism is also affected by a series of proteins, or growth factors, released from platelets, macrophages, and fibroblasts. These proteins cause healing bone to vascularize, solidify, incorporate, and function mechanically. They can induce mesenchymal-derived cells, such as monocytes and fibroblasts, to migrate, proliferate, and differentiate into bone cells. The proteins that enhance bone healing include the bone morphogenetic proteins (BMPs), insulin-like growth factors, transforming growth factors, plateletderived growth factor, and fibroblast growth factor among others. The best known of these proteins are the BMPs, a family of glycoproteins derived from bone matrix. Bone morphogenetic proteins induce FALL 2013 VOL. 8â&#x20AC;&#x201A; No. 2

mesenchymal cells to differentiate into bone cells. Although typically present in only minute quantities in the body, several BMPs have been synthesized using recombinant DNA technology and have been found to facilitate bone fusion in humans. Other proteins influence bone healing in different ways. Transforming growth factor regulates angiogenesis, bone formation, extracellular matrix synthesis, and controls cell-mediated activities. Osteonectin, fibronectin, and osteocalcin promote cell attachment, facilitate cell migration, and activate cells. Physiology of Bone Repair The use of a bone graft for purposes of achieving arthrodesis (fusion) is affected by each of the aforementioned anatomical, histological, and biochemical principles. Additionally, several physiological properties of bone grafts directly affect the success or failure of graft incorporation. These properties are osteogenesis, osteoinduction, and osteoconduction. Osteogenesis is the ability of the graft to produce new bone, and this process is dependent on the presence of live bone cells in the graft. Osteogenic graft materials contain viable cells with the ability to form bone (osteoprogenitor cells) or the potential to differentiate into bone-forming cells (inducible osteogenic precursor cells). These cells, which participate in the early stages of the healing process to unite the graft with the host bone, must be protected during the grafting procedure to ensure viability. Osteogenesis is a property found only in fresh autogenous bone and in bone marrow cells, although the authors of radiolabeling studies of graft cells have shown that very few of these transplanted cells survive. Osteoconduction is the physical property of the graft to serve as a scaffold for viable bone healing. Osteoconduction allows for the ingrowth of neovasculature and the infiltration of osteogenic precursor cells into the graft site. Osteoconductive properties are found in cancellous autografts and allografts, demineralized bone matrix, hydroxyapatite, collagen, and calcium phosphate. Osteoinduction is the ability of graft material to induce stem cells to differentiate into mature bone cells. Journal of The Spinal Research Foundationâ&#x20AC;&#x192; 32

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This process is typically associated with the presence of bone growth factors within the graft material or as a supplement to the bone graft. Bone morphogenetic proteins and demineralized bone matrix are the principal osteoinductive materials. To a much lesser degree, autograft and allograft bone also have some osteoinductive properties. The Healing Process The process of bone graft incorporation or healing in a spinal fusion is similar to the bone healing that occurs in fractured long bones. Fracture healing restores the tissue to its original physical and mechanical properties and is influenced by a variety of systemic and local factors. Healing occurs in three distinct, but overlapping stages: the early inflammatory stage, the repair stage, and the remodeling stage. In the inflammatory stage, a hematoma develops at the fracture site during the first few hours after injury. Inflammatory cells (macrophages, monocytes, lymphocytes, polymorphonuclear cells) and fibroblasts infiltrate the bone under the influence of prostaglandins. This results in the formation of granula-

Figure 2. The Process of Bone Healing.

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tion tissue, ingrowth of blood vessels, and migration of mesenchymal cells. The primary source of nutrients and oxygen for this initial process is provided by the exposed cancellous bone and muscle. The use of anti-inflammatory (NSAID) or cytotoxic medications during this first week may alter the inflammatory response and inhibit bone healing. During the repair stage, fibroblasts begin to lay down a collagen framework that helps support blood vessel ingrowth. It is during this stage that the presence of nicotine in the system can inhibit this capillary ingrowth. A significantly decreased rate of healing has been consistently demonstrated in tobacco users. As vascular ingrowth progresses, a collagen matrix is laid down as a scaffold while osteoid is secreted by osteoblasts and subsequently mineralized, leading to the formation of a soft callus around the site of injury. In terms of resistance to movement, this callus is very weak in the first 4 to 6 weeks of the healing process and requires adequate protection in the form of bracing (cast) or internal fixation (hardware). Eventually, the callus ossifies, forming a bridge of woven bone between the fracture fragments. Alternatively, if proper immobilization is not used, ossification of the callus may not occur, and an unstable fibrous union may develop instead. Fracture healing is completed during the remodeling stage in which the healing bone is restored to its prior structure and mechanical strength. Remodeling of the bone occurs slowly over months to years and is facilitated by mechanical stress placed on the bone. As the fracture site is exposed to an axial loading force, bone is generally laid down where it is needed and resorbed from where it is not needed. Adequate strength is typically achieved in three to six months. FALL 2013 VOL. 8 No. 2

FALL 2013 The Bare Bones of Spinal Disease Although the stages of bone repair in spinal fusion are similar to those that occur in long bone fractures, there are some important differences. Unlike long bone fractures, bone grafts are used in spinal fusion procedures. During the spinal fusion healing process, bone grafts are incorporated by a process in which old devitalized bone is slowly resorbed and simultaneously replaced with new viable bone. This process is termed “creeping substitution”. Primitive mesenchymal cells differentiate into osteoblasts that deposit osteoid around cores of necrotic bone. This process of bone deposition and remodeling eventually results in the replacement of necrotic bone within the graft. The most critical period of bone healing is the first two weeks in which inflammation and revascularization occur. The incorporation and remodeling of a bone graft require that mesenchymal cells have vascular access to the graft to differentiate into osteoblasts and osteoclasts. A variety of systemic factors can inhibit bone healing, including cigarette smoking, malnutrition, diabetes, rheumatoid arthritis, and osteoporosis. In particular, during the first week of bone healing, steroid medications, cytotoxic agents, and nonsteroidal anti-inflammatory medications (NSAID) can have harmful effects. Irradiation of the fusion site within the first two to three weeks can inhibit cell proliferation and induce an acute vasculitis that significantly compromises bone healing. Bone grafts are also strongly influenced by local mechanical forces during the remodeling stage. The density, geometry, thickness, and trabecular orientation of bone can change depending on the mechanical demands of the graft. In 1892, Wolff first popularized the concept of structural adaptation of bone, noting that bone placed under compressive or tensile stress is remodeled. Bone is formed where stresses require its presence and resorbed where stresses do not require it. This serves to optimize the structural integrity of the graft. Conversely, if the graft is significantly shielded from mechanical stresses (stress shielding), as in the case of rigid spinal implants, excessive resorption can potentially occur resulting in a weakening of the graft and, ultimately, failure of the fusion. This potential disadvantage of instrumentation needs to be balanced with FALL 2013 VOL. 8 No. 2

the beneficial effects that spinal fixation has on the fusion process. In general, loading the graft or placing it under stress, prior to instrumentation placement, addresses this issue. References 1. Aurori BF, Weierman RJ, Lowell HA, et al: Pseudoarthrosis after spinal fusion for scoliosis. A comparison of autogenic and allogenic bone grafts. Clin Orthop 1985;199:153–158. 2. Bishop RC, Moore KA, Hadley MN: Anterior cervical interbody fusion using autogeneic and allogeneic bone graft substrate: a prospective comparative analysis. J Neurosurg. 1996;85:206– 210. 3. Brown CW, Orme TJ, Richardson HD: The rate of pseudarthrosis (surgical nonunion) in patients who are smokers and patients who are nonsmokers: a comparison study. Spine 1986;11:942– 943. 4. Habal MB: Different forms of bone grafts, in Habal MB, Reddi AH (eds): Bone Grafts and Bone Substitutes. Philadelphia: WB Saunders, 1992, pp. 6–8. 5. Kalfas, Iain H. Principles of Bone Healing. Neurosurg Focus 10 (4): Article 1, 2001. 6. Kaufman HH, Jones E: The principles of bony spinal fusion. Neurosurgery 1989;24:264–270. 7. Urist MR: Bone transplants and implants, in Urist MR (ed): Fundamentals and Clinical Bone Physiology. Philadelphia: JB Lippincott, 1980, pp. 331–368. 8. Wolff J: The Law of Bone Remodelling. Translated by Maquet P, Furlong R. Berlin: Springer-Verlag, 1986. 9. Zdeblick TA, Ducker TB: The use of freeze-dried allograft bone for anterior cervical fusions. Spine 1991;16:726–729.

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SPINAL RESEARCH FOUNDATION

Medications in Bone Health Michael W. Hasz, M.D., F.A.C.S.

steoporosis and other bone diseases are becoming more and more prevalent in our society. These diseases have a serious impact on oneâ&#x20AC;&#x2122;s health and also create an economic burden on society. Over two million fractures related to osteoporosis were reported in a study in 2005, which led to a cost of greater than $17 billion dollars for treatment of these fractures. Not only is the aging of the United States population leading towards a greater incidence of osteoporosis, but decreased activity levels also contribute to these numbers. Additionally, certain medications can influence the incidence of osteoporosis. There are many medications that are being appropriately used for the treatment of various diseases, but they can also have detrimental effects on bone quality. Some medications, which are commonly used to treat symptoms related to heartburn, depression, diabetes, and even anticancer drugs, can lead toward a greater incidence of osteoporosis, while other drugs can help improve bone quality. Often, the benefits of the drug being used can outweigh the risks associated with it. However, the risks associated with osteoporosis should be considered when using some of the following medications.

diabetes is often significantly less than patients without. Additionally, many diabetics often take other medications as well, which can lead toward decreasing bone strength.

Steroid Drugs

Antidepressant Drugs

Steroids are very useful for treating inflammation and are often used to treat arthritis, for example. These medications, such as prednisone or cortisone, can inhibit bone formation and increase bone resorption by osteoclasts, which can make osteoporosis more likely. Increased osteoporosis is the same as having less strong bones, which can lead to an increased risk of having a fracture. Some medications used for the treatment of diabetes are also associated with osteoporosis. Diabetes itself is correlated with osteoporosis due to the change in metabolism associated with the disease. Although researchers do not quite know why there is a link with diabetes, the bone density in patients with

Selective serotonin reuptake inhibitors (SSRI) medications, such as Celexa, Prozac, Paxil, and Zoloft are common drugs used to relieve symptoms of depression that may also affect your bone density. Research suggests a correlation between the use of SSRI and decreased bone integrity. One study found that patients taking SSRI antidepressants were more than twice as likely to have a fracture of their spine as those not taking these medications. When weighing the risks and benefits of taking medications, it is very important to note the potential side effects of medication. It is also noted that patients with a diagnosis of depression have been linked to poor bone density.

35â&#x20AC;&#x192; Journal of The Spinal Research Foundation

Anticancer Drugs Approximately 15% of men will be diagnosed with prostate cancer during their lives, and about 12% of women will be diagnosed with breast cancer during their lives. Often, treatment of these cancers will include hormone blocking medications. In the case of breast cancer, aromatase inhibitors, such as Arimidex, lead to lower estrogen levels which can slow the growth of estrogen-induced cancers. While this is good for the treatment of cancers, lowering estrogen levels can lead to an increase of osteoporosis since estrogen is very helpful maintaining and growing bone density. Men diagnosed with prostate cancer are often treated with antiandrogen therapy such as Casodex. Again, while this is a useful treatment for the prostate cancer by lowering testosterone levels, bone density can also be negatively affected. Overall, by decreasing bone density, there is increased fracture risk. This increased risk of fracture needs to be considered during the treatment of these cancers.

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FALL 2013 The Bare Bones of Spinal Disease Gastric Reflux Disease Drugs Common medications used to treat gastroesophageal reflux disease (GERD), including H2 blockers such as Tagamet and Zantac and proton pump inhibitors (PPI) like Nexium and Prevacid, work by decreasing the production of stomach acid. While inhibiting the secretion of gastric acid for the short-term may help

ulcers heal and reduce symptoms related to gastric reflux, decreased acidity in the stomach is associated with a decreased absorption of nutrients. Calcium and magnesium, which are required minerals for bone health, are absorbed much less with low acid levels. This leads toward weaker bones and osteoporosis. Conclusion Many medications are useful in the treatment of a variety of diseases. However, there is rarely the perfect medication, and several are associated with affecting bone health and may lead to osteoporosis. It is crucial to use a multifaceted approach, considering the benefits and potential harms of each medication, to help mitigate the risk of osteoporotic fractures.

Michael W. Hasz, M.D., F.A.C.S.

Figure 2. Stomach acidity (low pH) is required for the proper absorption of calcium (Ca2+) and is, therefore, essential to maintain normal levels of serum calcium. Serum calcium, in turn, negatively regulates secretion from the parathyroid gland of PTH, a hormone that stimulates osteoclast differentiation and bone resorption. Bone resorption by osteoclasts also occurs at low pH and contributes to the maintenance of serum calcium. Peripheral serotonin is produced by the duodenum and inhibits bone formation by osteoblasts, whereas dietary intake of amino acids (proteins) favors collagen synthesis by osteoblasts. Image courtesy of Karsenty, G. and Ferron, M. The Contribution of bone to whole-organism physiology. Nature. 481, 314–230. (2012).

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Dr. Hasz is a spine surgeon at the Virginia Spine Institute. He is board certified by the American Board of Spine Surgery, a Fellow in the American Academy of Orthopaedic Surgeons and a member of both the American Association of Orthopaedic Surgeons and the North American Spine Society. He was Chairman of the Department of Orthopaedic Surgery and Director of Spinal Surgery at the Andrews Air Force Base/Malcolm Grow Medical Center in Maryland. He currently holds an appointment as Clinical Instructor of Orthopaedic Surgery and Assistant Professor of Surgery at the Uniformed Services Health Science University in Bethesda, Maryland.

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SPINAL RESEARCH FOUNDATION

The Importance of Bone Health for Spinal Procedures Justin S. Field, M.D.

aving healthy bones is very important to prevent fractures. Common areas where people sustain broken bones due to fragility are in the spine, hips, and wrists. It is also very important to have healthy bone quality as it pertains to being able to undergo and recuperate from spine surgery. Whether considering a smaller surgery, such as micro-decompression, or a larger reconstruction, such as a bone fusion or disc replacement, adequate bone support and bone healing is necessary for stability of the spine. Vitamin D Deficiency Vitamin D deficiency, osteoporosis, and other nutritional and metabolic disorders can contribute to inadequate bone health and prohibit successful healing. Preoperative evaluation should include an assessment of bone health and a screen for problems in calcium metabolism. While inadequate calcium intake has been long known to be an important factor in bone health, vitamin D deficiency is more common than previously recognized and has the potential to result in poor spine health and poor response to treatment.

Vitamin D is a fat-soluble vitamin that is naturally present in very few foods, added to others, and available as a dietary supplement. It is also produced endogenously when ultraviolet rays from sunlight strike the skin and trigger vitamin D synthesis. Vitamin D is necessary for many bodily functions. Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone. It is also needed for bone growth and bone remodeling by bone formation and remodeling cells. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis. It is very difficult to get adequate vitamin D solely through the diet. If deficient, your vitamin D level can be normalized with the use of prescription strength vitamin D, however this can take several months. Maintaining a proper Vitamin D level is an important step to ensure that fusion occurs. This is important to help with pain relief from surgery and quicker return of function.

Releases calcium and phosphorus

Sense low serum calcium and increase PTH secretion

(1,25(OH)2D)

(25-OH-D)

(1,25(OH)2D)

• Increases calcitriol formation • Decreases excretion of calcium

Increases absorption of dietary calcium

37 Journal of The Spinal Research Foundation

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FALL 2013 The Bare Bones of Spinal Disease Nicotine It is also well known that nicotine decreases spine fusion rates and, thus, must be discontinued before bone fusion operations. Fortunately, there are newer, more successful ways to control the smoking urge, and preoperative counseling may help to find the best suited method to quit the tobacco habit and get through the healing process. Second-hand smoke is also harmful to the healing in spine fusion and must be avoided. Obesity

be able to strengthen their core muscles and increase activity. Osteoporosis Osteoporosis is a result of negative bone remodeling from enhanced function of the osteoclasts. Because bone formation is the result of coupling between osteoblasts and osteoclasts, anti-resorptive agents that induce osteoclast apoptosis (cell death) may not be effective in spinal fusion surgery, necessitating new bone formation. Therefore, anabolic agents may be more suitable for osteoporotic patients who undergo spinal fusion surgery. The instrumentation and techniques, along with increased pullout strength, may increase fusion rate through rigid fixation. Studies on new osteoinductive materials, methods to increase osteogenic cells, and strengthened and biocompatible osteoconductive scaffolds are necessary to enable osteoporotic patients to undergo spinal fusion. When osteoporotic patients undergo spinal fusion, sur-

Obesity has become a major health issue; in fact, it is a national problem. Many disease processes can be dramatically improved or completely reversed with weight loss. More specifically in the orthopedic realm, back pain and knee pain, for example, respond positively to weight reduction. Just losing 10 to 15 pounds can make a huge difference in the reduction of back, hip, and knee pain. Changing eating habits and exercise have been shown to be the most successful strategy for long-term weight reduction and maintenance. Surgical intervention in the spine for obese patients can be fraught with wound complications. Many of these patients are actually nutritionally starved and lack the important nutritional reserves to properly heal. In addition, spine surgery is more difficult on larger patients from the surgeon’s perspective because of more difficult access to the pathology, as well as visual- Figure 2. This schematic outlines the bone remodeling cycle and the balance of bone resorption and ization. It is very important bone formation. (a) In bone tissue, the osteoblasts are involved in new bone formation, while osteoclasts a major role in bone resorption. The first step in the bone remodeling cycle is the resorption of existing to stress weight reduction play bone by osteoclasts, followed by formation of the cement line in resorption lacunae and osteoblasts. Each and change in eating habits cell type seems to be regulated by a variety of hormones and by local factors. (b) If the balance between to overweight patients. This bone formation and resorption is lost by the uncontrolled production of regulators, bone structure would be strikingly damaged, and the subject would be susceptible to osteoporosis and osteopetrosis. Image will also help in their post- courtesy of Eijiro Jimi, et. al. The Current and Future Therapies of Bone Regeneration to Repair Bone Defects. operative recovery period to International Journal of Dentistry. 2012, 1–7. (2012). FALL 2013 VOL. 8 No. 2

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geons should consider appropriate osteoporosis medication, instrumentation, and technique. There are degenerative changes in the intervertebral discs and spinal facet joint capsules in people over 50 years of age that are associated with spinal instability. With increased life expectancy, the elderly desire to be more physically active and have an improved quality of life. Surgical indications for degenerative spinal conditions in elderly patients have increased.2,17,23,27,31 The surgical outcomes and perioperative complications of spinal fusions in elderly patients can be negatively affected by co-morbidities such as cardiopulmonary disease, renal disease, diabetes mellitus, nutritional disorders, and osteoporosis.14 Because osteoporosis is strongly associated with poor fusion rate and bone stability, it is crucial to understand the pathophysiology of osteoporosis and its treatment in order to enhance spinal fusion and preserve bone stability. Spinal surgeons must be informed of the appropriate treatment plan for osteoporosis and formulate appropriate strategies for osteoporotic patients who need to undergo spinal fusion surgery. Osteoporosis is a major global problem because over 10 million people are currently diagnosed with osteoporosis.28 Although 80% of osteoporotic patients are women, a considerable number of men are also affected.15,21 The age matched prevalence of osteoporosis is 17–20% of women over 50 years old, 26% over 65 years old and 50% over 85 years old in the United States. In addition, the prevalence of osteoporosis in male and female patients over 50 years old who underwent spinal surgery were 14.5% and 51.3%, respectively.17 Due to increasing life expectancy, the number of elderly patients with osteoporosis will continue to increase even further. Due to an increasingly aged population, degenerative spinal stenosis and spondylolisthesis have become more frequently diagnosed.48,53 Up to 10% of women over 60 years may be affected by degenerative spondylolisthesis and one study presented the rates of male and female patients with spondylolisthesis (degenerative or spondylolytic types) at 14.8% and 66.1%, respectively.17,40 In elderly patients, iatrogenic cause of instability following spinal surgery may occur because of pre-existing degenerative changes in 39 Journal of The Spinal Research Foundation

the facet joints and intervertebral disc. If instability of the spine at the index level is confirmed by preoperative radiological evaluations or when iatrogenic instability occurs, fusion operation should be considered in elderly patients.34,48,53 Several reports claim that decompression and additional fusions in elderly patients who experienced spinal stenosis and instability, such as spondylolisthesis, produce satisfactory outcome in elderly patients.16,26,34,46,53 Many studies demonstrated fusion failure which negatively impacted clinical outcomes; fusion rates ranged from 56% to 100%.11,40,52 Reports on the outcome of lumbar arthrodesis following instrumentation in patients over 60 years of age indicated the prevalence of delayed and collapsed fusion in elderly patients to be higher than that in younger patients. The fusion rates of elderly patients reported were over 90%, and in elderly osteoporotic patients who underwent lumbar arthrodesis with instrumentation, the fusion rates were 89.7% to 95.8%.16,26,35,41 In other words, old age and osteoporosis are not contraindications in spinal arthrodesis. The number of elderly patients who need spinal surgery will increase, and the prevalence of osteoporosis in elderly patients is high. The existence and severity of osteoporosis should be preoperatively assessed in elderly patients, and an appropriate strategy to facilitate spinal fusion should be formulated. Biology of Spinal Fusion Although instrumentation and technique have been improving, non-union still occurs in 5 to 35% of patients who undergo spinal fusion.8,12 Non-union in spinal surgery frequently leads to unsatisfactory clinical outcomes.19,25 Therefore, understanding the histological and biologic events in spinal fusion is crucial to spinal surgeons who treat patients with and without osteoporosis. Clinically relevant lumbar fusion animal models are analyzed in several articles to provide information on the methods that facilitate fusion. These articles report that non-decortication of the transverse process did not result in arthrodesis (fusion of the joint), and the primary vascular supply to the fusion mass originated from decorticated bone, not from the adjacent muscle.9,50 Decortication is the removal of the superfiFALL 2013 VOL. 8 No. 2

FALL 2013 The Bare Bones of Spinal Disease cial portion of cortical bone of the vertebra’s posterior elements (spinous process, lamina, and articular facets) to expose the inner vertebral cancellous bone. Decortication can increase tissue metabolism in the interface between bone graft and recipient bed by increasing the vascular supply to this region, accelerating integration between bone graft with the recipient bed, and triggering greater bone neoformation.55 Intra-membranous bone formation occurs in the area near the transverse processes, and endochondral bone formation, which involves bone formation through a cartilage intermediate, occurs centrally at the interface between the upper and lower halves of the bridging bone.54

bone graft should be assessed by the surgeon. Although no publication discusses the histological difference between osteoporosis and non-osteoporosis animal models with spinal fusion, reduced osteoblast ability, poor vascularity, and lower bone marrow quality in the host bed may contribute to non-union in elderly osteoporotic patients. Therefore, surgeons must consider bone graft quality, proper osteoinductive materials, increasing the ability of osteoblasts, and preventing factors that may hinder fusion, including long-term use of non-steroidal anti-inflammatory agents and smoking before performing spinal fusion on elderly osteoporotic patients. Strategies for Osteoporotic Patients with Spinal Fusion Osteoporosis reduces bone quality through negative bone remodeling. Low bone quality can reduce the pull-out strength of pedicle screws, and negative bone remodeling can cause delayed bone fusion.3,18 Therefore, before performing spinal fusion surgery on osteoporotic patients, we should pursue effective strategies to increase the pull-out strength and facilitate positive bone remodeling. Pharmacotherapeutic Strategies

Figure 3. Anatomy of a Lumbar Vertebra. Image courtesy of Medtronic, Inc.

Cartilage formed through endochondral ossification has poor vascular supply and low oxygen saturation. However, in the mid and late stages of bone formation, extension of bone formation towards the central zone occurs, and disappearance of cartilage and bone formation occurs in the central area.9,10,50 The transient cartilaginous area may explain why many non-unions are found to occur in the central zone of a fusion mass. Considering the previous description and three factors for bone formation—osteoconductive scaffold, osteogenic cell, and osteoinductive materials—the characteristics of host beds such as vascularity and quality of bone marrow, the distance of fusion site, and the quality of FALL 2013 VOL. 8 No. 2

Osteoporosis, secondary to loss of estrogen, is the cause of negative bone remodeling through reduced function and life span of osteoblasts and the reverse for osteoclasts. In addition, bone remodeling depends on communication between the osteoblast lineage (including lining cells, preosteoblasts, and osteocytes) and the osteoclast lineage. Thus, in order to obtain good fusion rate in osteoporotic patients, we should be aware of the anti-resorptive and anabolic agents. Bisphophonates Biphosphonates are typical anti-resorptive agents that include alendronate, ibandronate, etidronate, and pamidronate. The mechanism of bisphosphonate is to promote apoptosis of mature osteoclasts and result in a slow rate of bone remodeling.32,38,43 Many animal studies present the effects of bisphosphonates on the skelJournal of The Spinal Research Foundation 40

SPINAL RESEARCH FOUNDATION J.S. Field/Journal of the Spinal Research Foundation 8 (2013) 37–43

etal system. In animal studies that investigated fracture healing and pull-out strength of implants, bisphosphonates did not adversely affect the skeletal system.39,44 However, according to recent studies, bisphosphonates inhibit or delay spinal fusion through reduced incorporation between grafted bone and host bone.31,37,49 In other words, the anti-fracture effect of bisphosphonates is not proportional to their efficacy on bone fusion. Therefore, when osteoporotic patients are scheduled to undergo spinal fusion, surgeons must consider the need of using other anti-resorptive or anabolic agents postoperatively.

of tapping the hole can affect the pullout strength in osteoporotic bone, and although the anatomical constraints vary with patients, bigger and longer screws may provide a good solution for fragile bones.20 The angulation of two screws and screw positioning in areas of higher BMD in the vertebrate may also increase pullout strength.45,50 Also, to improve the fixation and fatigue strength of instrumentation, screw augmentation with polymethyl methacrylate has yielded favorable outcomes.5,13 These techniques may enhance bone fusion through stabilization of fusion segments.

Recombinant Human Parathyroid Hormone

Other Strategies

Only one drug acts as an anabolic agent to osteoporosis—recombinant human parathyroid hormone (PTH). Although high levels of PTH cause decreased bone mineral density (BMD) through increased bone resorption, low and intermittent PTH elevation increases bone formation secondary to its anti-apoptotic effect on osteoblasts.29,32,33,45 Prior studies concluded that PTH treatment did not increase the incidence of bone tumors such as osteosacroma.30,42,51 It must be emphasized that the experience of PTH use is so far limited in the United States and Europe to 2 years and 18 months, respectively. If PTH treatment is not followed by anti-resorptive therapy, the increased BMD would be lost.6,22 Therefore, additional anabolic agents need to be developed to be continuously used in osteoporotic patients. The results of animal studies suggested that PTH enhanced the healing of bone fracture and increased BMD, mechanical strength, and arthrodesis of the spine.1,4 As concurrent use of alendronate for increasing positive remodeling reduced the anabolic effect of PTH, the use of PTH on osteoporotic patients taking bisphosphonates may be refrained after spine arthrodesis.7

Mesenchymal cells differentiated to osteoblasts are critical for increasing fusion rate. Although the fusion rate achieved by using bone marrow aspirate (BMA) with collagen was inferior to that of using autologous iliac crest bone for posterior lumbar interbody fusion, the fusion rate of posterolateral lumbar fusion with BMA and collagen was comparable to that of autologous bone.36 However, since there is a low concentration of osteogenic cells in the BMA, it is ineffective as a bone

Implant Based Strategies Cancellous bone is more affected by osteoporosis than cortical bone. Therefore, lower BMD has been a major factor in poor screw fixation, screw loosening, and fixation failure.18 Many techniques have been employed to enhance the pullout strength of the pedicle screw.24 The preparation for the screw hole or the minimization 41 Journal of The Spinal Research Foundation

Figure 4. Bone Marrow Aspiration. Image courtesy of Medtronic, Inc.

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FALL 2013 The Bare Bones of Spinal Disease graft substitute. Therefore, investigations for methods of stimulating osteoblast differentiation, expanding the number of osteoblast, and finding new osteoconductive scaffolds with structural strength are needed. Conclusion Osteoporosis results in fragile bone through negative bone remodeling. As such, prior to performing spinal fusion on osteoporotic patients, surgeons should consider multidisciplinary strategies including the use of the anti-resorptive and anabolic agents, proper instrumentations, and BMA. Perioperative strategies in osteoporotic patients may affect the radiological and clinical outcomes. Justin S. Field, M.D. Dr. Field is a board certified, fellowship trained orthopedic spine surgeon at Desert Institute for Spine Care. Dr. Field has specialized training in minimally invasive spine surgery and motion sparing technologies, such as cervical and lumbar artificial disc replacement and non-fusion stabilization. In addition, he has extensive training in adult deformity correction and treatment. Dr. Field earned his medical degree at Tulane University, where he finished in the top 1% of his class. He completed both his surgical internship and orthopedic surgery residency at Duke University and completed a spine surgery fellowship at The Spine Institute in Santa Monica (CA). Dr. Field was recognized by his peers to be one of the top Phoenix spine surgeons in 2009, 2011, 2012 and 2013. He was also recognized as one of America’s Most Compassionate Doctors.

References 1. Abe Y, Takahata M, Ito M, Irie K, Abumi K, Minami A. Enhancement of graft bone healing by intermittent administration of human parathyroid hormone (1-34) in a rat spinal arthrodesis model. Bone. 2007;41:775–785. 2. Aebi M. The scoliosis. Eur Spine J. 2005;14:925–948. 3. Aldini NN, Fini M, Giavaresi G, Giardino R, Greggi T, Parisini P. Pedicular fixation in the osteoporotic spine: a pilot in vivo study on long-term ovariectomized sheep. J Orthop Res. 2002;20:1217–1224. 4. Alkhiary YM, Gerstenfeld LC, Krall E, Westmore M, Sato M, Mitlak BH, et al. Enhancement of experimental fracture-healing by systemic administration of recombinant human parathyroid hormone (PTH 1-34) J Bone Joint Surg Am. 2005;87:731–734.

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5. Aydogan M, Ozturk C, Karatoprak O, Tezer M, Aksu N, Hamzaoglu A. The pedicle screw fixation with vertebroplasty augmentation in the surgical treatment of the severe osteoporotic spines. J Spinal Disord Tech. 2009;22:444–447. 6. Black DM, Bilezikian JP, Ensrud KE, Greenspan SL, Palermo L, Hue T, et al. PaTH Study Investigators. One year of alendronate after one year of parathyroid hormone (1-84) for osteoporosis. N Engl J Med. 2005;353:555–565. 7. Black DM, Greenspan SL, Ensrud KE, Palermo L, McGowan JA, Lang TF, et al. PaTH Study Investigators. The effects of parathyroid hormone and alendronate alone or in combination in postmenopausal osteoporosis. N Engl J Med. 2003;349:1207–1215. 8. Boden SD. Overview of the biology of lumbar spine fusion and principles for selecting a bone graft substitute. Spine (Phila Pa 1976) 2002;15:S26–S31. 9. Boden SD. The biology of posterolateral lumbar spinal fusion. Orthop Clin North Am. 1998;29:603–619. 10. Boden SD, Schimandle JH, Hutton WC, Chen MI. The use of an osteoinductive growth factor for lumbar spinal fusion. Part I: Biology of spine fusion. Spine (Phila Pa 1976) 1995;20:2626–2632. 11. Brantigan JW, Steffee AD. A carbon fiber implant to aid interbody lumbar fusion. Two-year clinical results in the first 26 patients. Spine (Phila Pa 1976) 1991;18:2106–2107. 12. Bridwell KH, Sedgewick TA, O‘Brien MF, Lenke LG, Baldus C. The role of fusion and instrumentation in the treatment of degenerative spondylolisthesis with spinal stenosis. J Spinal Disord. 1993;6:461–472. 13. Burval DJ, McLain RF, Milks R, Inceoglu S. Primary pedicle screw augmentation in osteoporotic lumbar vertebrae: biomechanical analysis of pedicle fixation strength. Spine (Phila Pa 1976) 2007;32:1077–1083. 14. Carreon LY, Puno RM, Dimar JR, 2nd, Glassman SD, Johnson JR. Perioperative complications of posterior lumbar decompression and arthrodesis in older adults. J Bone Joint Surg Am. 2003;85:2089–2092. 15. Cauley JA, Fullman RL, Stone KL, Zmuda JM, Bauer DC, Barrett-Connor E, et al. Factors associated with the lumbar spine and proximal femur bone mineral density in older men. Osteoporos Int. 2005;16:1525–1537. 16. Cavagna R, Tournier C, Aunoble S, Bouler JM, Antonietti P, Ronai M, et al. Lumbar decompression and fusion in elderly osteoporotic patients: a prospective study using less rigid titanium rod fixation. J Spinal Disord Tech. 2008;21:86–91. 17. Chin DK, Park JY, Yoon YS, Kuh SU, Jin BH, Kim KS, et al. Prevalence of osteoporosis in patients requiring spine surgery: incidence and significance of osteoporosis in spine disease. Osteoporos Int. 2007;18:1219–1224. 18. Coe JD, Warden KE, Herzig MA, McAfee PC. Influence of bone mineral density on the fixation of thoracolumbar implants. A comparative study of transpedicular screws, laminar hooks, and spinous process wires. Spine (Phila Pa 1976) 1990;15:902–907. 19. Conaty JP, Mongan ES. Cervical fusion in rheumatoid arthritis. J Bone Joint Surg Am. 1981;63:1218–1227. 20. Cook SD, Barbera J, Rubi M, Salkeld SL, Whitecloud TS., 3rd Lumbosacral fixation using expandable pedicle screws: an alternative in reoperation and osteoporosis. Spine J. 2001;1:109–114.

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21. Cummings SR, Melton LJ. Epidemiology and outcomes of osteoporotic fractures. Lancet. 2002;359:1761–1767. 22. Deal C. Future therapeutic targets in osteoporosis. Curr Opin Rheumatol. 2009;21:380–385. 23. Fraizer DD, Lipson SJ, Fossel AH, Katz JN. Associations between spinal deformity and outcomes after decompression for spinal stenosis. Spine (Phila Pa 1976) 1997;22:2025–2029. 24. Ferguson SJ, Winkler F, Nolte LP. Anterior fixation in the osteoporotic spine: cut-out and pullout characteristics of implant. Eur Spine J. 2002;11:527–534. 25. Farey ID, McAfee PC, Gurr KR, Randolph MA. Quantitative histologic study of the influence of spinal instrumentation on lumbar fusions: a canine model. J Orthop Res. 1989;7:709–722. 26. Glassman SD, Polly DW, Bono CM, Burkus K, Dimar JR. Outcome of lumbar arthrodesis in patients sixty-five years of age or older. J Bone Joint Surg Am. 2009;91:783–790. 27. Greenfield RT, 3rd, Capen DA, Thomas JC, Jr, Nelson R, Nagelberg S, Rimoldi RL, et al. Pedicle screw fixation for arthrodesis of the lumbosacral spine in the elderly: an outcome study. Spine (Phila Pa 1976) 1998;23:1470–1475. 28. Hart RA, Prendergast MA. Spine surgery for lumbar degenerative disease in elderly and osteoporotic patients. Instr Course Lect. 2007;56:257–272. 29. Hodsman AB, Bauer DC, Dempster DW, Dian L, Hanley DA, Harris ST, et al. Parathyroid hormone and teriparatide for the treatment of osteoporosis: a review of the evidence and suggested guidelines for its use. Endocr Rev. 2005;26:688–703. 30. Horwitz M, Stewart A, Greenspan SL. Sequential parathyroid hormone/alendronate therapy for osteoporosis-robbing Peter to pay Paul? J Clin Endocrinol Metab. 2000;85:2127–2128. 31. Huang RC, Khan SN, Sandhu HS, Metzl JA, Cammisa FP, Jr, Zheng F, et al. Alendronate inhibits spine fusion in a rat model. Spine (Phila Pa 1976) 2005;30:2516–2522. 32. Hughes DE, Wright KR, Uy HL, Sasaki A, Yoneda T, Roodman GD, et al. Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo. J Bone Miner Res. 1995;10:1478–1487. 33. Jilka RL, Weinstein RS, Bellido T, Roberson P, Parfitt AM, Manolagas SC. Increased bone formation by prevention of osteoblast apoptosis with PTH. J Clin Invest. 1999;104:439– 446. [PMC free article] 34. Johnsson KE, Willner S, Johnsson K. Postoperative instability after decompression for lumbar spinal stenosis. Spine (Phila Pa 1976) 1986;11:107–110. 35. Kim KH, Lee SH, Lee DY, Shim CS, Maeng DH. Anterior bone cement augmentation in anterior lumbar interbody fusion and percutaneous pedicle screw fixation in patients with osteoporosis. J Neurosurg Spine. 2010;12:525–532. 36. Kitchel SH. A preliminary comparative study of radiographic results using mineralized collagen and bone marrow aspirate versus autologous bone in the same patients undergoing posterior lumbar interbody fusion with instrumented posterolateral lumbar fusion. Spine J. 2006;6:405–411. 37. Lehman RA, Jr, Kuklo TR, Freedman BA, Cowart JR, Mense MG, Riew KD. The effect of alendronate sodium on spinal fusion: a rabbit model. Spine J. 2004;4:36–43.

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Spinal Research Foundation Research Partners The Spinal Research Foundation has named 26 Research Partners across the country that share one core mission: improving spinal health care through research, education, and patient advocacy. These centers offer the best quality spinal health care while focusing on research programs designed to advance spinal treatments and techniques.

★ ★

★

★ We are excited to welcome our newest Research Partner, Desert Institute for Spine Care!

Allegheny Brain and Spine Surgeon James P. Burke, MD, PhD Altoona, PA centralpabrainandspinesurgeons.com

Atlanta Brain and Spine Care Regis W. Haid, Jr., MD Atlanta, GA atlantabrainandspine.com

Desert Institute for Spine Care Christopher A. Yeung, MD Anthony T. Yeung, MD Justin S. Field, MD Nima Salari, MD Phoenix, AZ sciatica.com

The Hughston Clinic J. Kenneth Burkus, MD Columbus, GA hughston.com

Inova Research Center Zobair M. Younossi, MD, MPH Falls Church, VA inova.org/clinical-education-andresearch/research/index.jsp

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Colorado Comprehensive Spine Institute George A. Frey, MD Englewood, CO coloradospineinstitute.com

Indiana Spine Group Rick C. Sasso, MD Carmel, IN indianaspinegroup.com

Midwest Orthopaedic Center Patrick T. O’Leary, MD Daniel S. Mulconrey, MD Peoria, IL midwest-ortho.com

MUSC Darby Children’s Research Institute Inderjit Singh, PhD Charleston, SC clinicaldepartments.musc.edu/ pediatrics2/research/

Journal of The Spinal Research Foundation 44

SPINAL RESEARCH FOUNDATION

New England Neurosurgical Associates, LLC Christopher H. Comey, MD Springfield, MA

The Orthopedic Center of St. Louis Matthew F. Gornet, MD Chesterfield, MO toc-stl.com

Oregon Neurosurgery Specialists Robert J. Hacker, MD Andrea Halliday, MD Springfield, OR oregonneurosurgery.com

Princeton Brain and Spine Care Mark R. McLaughlin, MD, FACS Langhorne, PA princetonbrainandspine.com

Rutgers University Department of Biomedical Engineering Noshir A. Langrana, PhD, PE Piscataway, NJ South Coast Orthopaedic Associates Aleksandar Curcin, MD, MBA Coos Bay, OR scoastortho.com Spine Colorado Jim A. Youssef, MD Douglas G. Orndorff, MD Durango, CO spinecolorado.com

The Spine Clinic of Los Angeles Larry T. Khoo, MD Los Angeles, CA spineclinicla.com

University of Minnesota Medical Center, Fairview David W. Polly, Jr., MD Minneapolis, MN

The Orthopaedic and Sports Medicine Center Gerard J. Girasole, MD Trumbull, CT osmcenter.com

River City Orthopaedic Surgeons David P. Rouben, MD Louisville, KY rivercityortho.com

Southern Brain and Spine Najeeb M. Thomas, MD Metairie, LA sbsdocs.net

Menlo Medical Clinic Allan Mishra, MD Menlo Park, CA menloclinic.com SpineCare Medical Group Paul J. Slosar, Jr., MD San Francisco Spine Institute Daly City, CA spinecare.com Twin Cities Spine Center James D. Schwender, MD Minneapolis, MN tcspine.com

The Virginia Spine Institute Thomas C. Schuler, MD, FACS Brian R. Subach, MD, FACS Reston, VA spinemd.com

45 Journal of The Spinal Research Foundation

Virginia Therapy & Fitness Center Richard A. Banton, PT, DPT, ATC E. Larry Grine, PT, MSPT, ATC, CSCS Reston, VA vtfc.com

FALL 2013 VOL. 8 No. 2

SPINAL RESEARCH FOUNDATION

Thank you,

DOUGLAS G. ORNDORFF, M.D.

THE JOURNAL OF THE SPINAL RESEARCH FOUNDATION A multidisciplinary journal for patients and spine specialists

Thomas C. Schuler, M.D., F.A.C.S. President

Brian R. Subach, M.D., F.A.C.S. Director of Research

Michael H. Howland Vice Chairman

Andrew T. Greene Treasurer

Raymond F. Pugsley National Race Liaison

Kevin M. Burke, Jr. Member

William H. Evers, Jr., Ph.D. Member

Brian D. Nault Member Najeeb M. Thomas, M.D. Member

THE JOURNAL OF THE SPINAL RESEARCH FOUNDATION EDITORIAL BOARD

Regis W. Haid, Jr., M.D. Atlanta, GA

Christopher H. Comey, M.D. Springfield, MA

Larry T. Khoo, M.D. Los Angeles, CA

Aleksandar Curcin, M.D., M.B.A. Coos Bay, OR George A. Frey, M.D. Englewood, CO Gerard J. Girasole, M.D. Trumbull, CT

Noshir A. Langrana, Ph.D. Piscataway, NJ Mark R. McLaughlin, M.D., F.A.C.S. Langhorne, PA

Matthew F. Gornet, M.D. Chesterfield, MO Journal of The Spinal Research Foundation

Patrick T. Oâ&#x20AC;&#x2122;Leary, M.D. Peoria, IL David P. Rouben, M.D. Louisville, KY

Guy E. Beatty Chairman

J. Kenneth Burkus, M.D. Columbus, GA

SPINAL HERO

SPINAL RESEARCH FOUNDATION (SRF) BOARD OF DIRECTORS

Robert J. Hacker, M.D. & Andrea L. Halliday, M.D. Springfield, OR

Melissa B. Luke and Marcia A. Phillips Editorial Staff

James P. Burke, M.D., Ph.D. Altoona, PA

SPINE COLORADO

Carrie B. Califano and Anne G. Copay, Ph.D. Managing Editors

Paul J. Slosar, Jr., M.D. Member

Spine Surgeon

Brian R. Subach, M.D., F.A.C.S. Editor-in-Chief

Rick C. Sasso, M.D. Indianapolis, IN Thomas C. Schuler, M.D., F.A.C.S. Reston, VA

â&#x20AC;&#x153;

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JOURNAL OF THE SPINAL RESEARCH FOUNDATION

Thank You! The Board of Directors of the Spinal Research Foundation is grateful for the continued investment of our donors and

Research

Patient Advocacy

support of our donors.

FALL 2013

conditions. This work would not be possible without the

Education

Volume 8, Number 2

JOURNAL OF THE SPINAL RESEARCH FOUNDATION

To make a donation in order to improve the quality of spinal health care in America, please visit:

www.SpineRF.org or contact us at:

Innovation

The Bare Bones of Spinal Disease

Spinal Research Foundation 1831 Wiehle Ave, Ste 100 Reston, VA 20190 Phone: 703-766-5404 Fax: 703-709-1397

VOLUME 8 NUMBER 2

Fall 2013