Tag Archive | Osteoporosis

Upcoming Own the Bone Events

ownbone_logo-r.pngSpring and Summer 2017 are busy seasons for Own the Bone, the American Orthopaedic Association’s national post-fracture, systems-based, multidisciplinary fragility fracture prevention initiative:

Webinar: Components of a Secondary Fracture Prevention Program – May 4

On Thursday, May 4, at 5:00pm CDT (6:00pm EDT) Paul A. Anderson, MD, FAOA, from the University of Wisconsin, and Karen Cummings, PA-C, from the University of Michigan, will discuss the components of a successful secondary fracture prevention program.

Own the Bone Charlotte SymposiumJune 23: Fragility Fracture Care Coordination and Secondary Fracture Prevention

Join the National Association of Orthopaedic Nurses (NAON) and The American Orthopaedic Association for this full-day event on Friday, June 23. Attendees will receive a Fragility Fracture Symposium Certificate of Completion and continuing education credit.

Fragility Fracture Workshop at PAOS Annual Conference – August 21, Baltimore, MD

Join Physician Assistants in Orthopaedic Surgery (PAOS) and Own the Bone for a full-day fragility fracture and bone health workshop on the first day of the PAOS Annual Conference, Monday, August 21, in Baltimore.

Own the Bone Webinar: Atypical Fractures and Osteo Medications

ownbone_logo-r.pngOn Thursday, February 23, 2017, at 6:00 pm EST, the Own the Bone initiative will offer a webinar titled “Atypical Fractures and Osteoporosis Medication Considerations”

James Goulet, MD, from the University of Michigan, will discuss atypical fractures and other rare outcomes of the use of osteoporosis medication, including what to look for and how to treat these occurrences.  He will also address drug holidays, and how and when to continue treatment on these complex cases.

The American Orthopaedic Association (AOA) developed Own the Bone as a quality improvement program to address the osteoporosis treatment gap and prevent subsequent fragility fractures.

0.75 hour of CME credit is available.

Guest Post: Own the Bone Improves Osteoporosis Care

ownbone_logo-r.pngOrthoBuzz occasionally receives posts from guest bloggers. This guest post comes from Brett A. Freedman, MD.

In the December 21, 2016 edition of the Journal of Bone & Joint Surgery, Bunta, et al. published an analysis of data from the Own the Bone quality improvement program collected between January 1, 2010 and March 31, 2015. Over this period of time, 125 sites prospectively collected detailed osteoporosis and bone health-related data points on men and women over the age of 50 who presented with a fragility fracture.

The Own the Bone initiative is more than a data registry; it’s a quality improvement program intended to provide a paradigm for increasing the diagnostic and therapeutic recognition (i.e. “response rate”) of the osteoporosis underlying fragility fractures among orthopaedic practices that treat these injuries.  With more than 23,000 individual patients enrolled, and almost 10,000 follow-up records, this is the most robust dataset in existence on the topic.

This initiative has more than doubled the response rate among orthopaedic practices treating fragility fractures. The number of institutions implementing Own the Bone grew from 14 sites in 2005-6 to 177 in 2015. According to Bunta et al., 53% of patients enrolled in the Own the Bone quality Improvement program received bone mineral density testing and/or osteoporosis therapy following their fracture.

Own the Bone was a natural progression of rudimentary efforts that came about during the Bone and Joint Decade, and it marks a strategic effort on the part of the American Orthopedic Association to identify and treat the osteoporosis underlying fragility fractures.  Multiple studies have demonstrated that only 1 out of every 4 to 5 patients who present with a fragility fracture will receive a clinical diagnosis of osteoporosis and/or active treatment to prevent secondary fractures related to osteoporosis. Ample Level-1 evidence demonstrates that the initiation of first-line agents like bisphosphonates, or second-line agents when indicated, can reduce the chance of a subsequent fragility fracture by at least 50%.  We know these medicines work.

We also know that osteoporosis is a progressive phenomenon. Therefore, failing to respond to the osteoporosis underlying fragility fractures means we as a medical system fail to treat the root cause in these patients. The fracture is a symptom of an underlying disease that needs to be addressed or it will continue to produce recurrent fractures and progressive decline in overall health.

The members of the Own the Bone initiative must be commended for their admirable work. We as an orthopedic community need to attempt to incorporate lessons learned through the Own the Bone experience into our practice to ensure that we provide complete care to those with a fragility fracture. The report from Bunta et al. represents a large—but single—step forward on the journey toward universal recognition and treatment of the diminished bone quality underlying fragility fractures. I look forward to additional reports from this group detailing their continued success in raising the bar of understanding and intervention.

Brett A. Freedman, MD is an orthopaedic surgeon specializing in spine trauma and degenerative spinal diseases at the Mayo Clinic in Rochester, MN.

JBJS Editor’s Choice: Improving Function After Fragility Fractures

hip_fracture_drugs_11_16_16In the past several years, the orthopaedic community has become highly engaged in improving the follow-up management of patients presenting with fragility fractures. We have realized that orthopaedic surgeons are central to the ongoing health and welfare of these patients and that the episode of care surrounding a fragility fracture represents a unique opportunity to get patients’ attention. Using programs such as the AOA’s “Own the Bone” registry, increasing numbers of orthopaedic practices and care centers are leading efforts to deliver evidenced-based care to fragility-fracture patients.

In the November 16, 2016 edition of The Journal, Aspenberg et al. carefully examine the impact of the anabolic agent teriparatide versus the bisphosphonate risedronate on the 26-week outcomes of more than 170 randomized patients (mean age 77 ±8 years) who were treated surgically for a low-trauma hip fracture. This investigation is timely and appropriate because our systems of care are evolving so that increasing numbers of patients are receiving pharmacologic intervention for low bone density both before and after a fragility fracture.

The secondary outcomes of the timed up and go (TUG) test and post-TUG test pain were better in the teriparatide group, but there were no differences in radiographic fracture healing or patient-reported health status.

Although this study was designed primarily to measure the effects of the two drugs on spinal bone mineral density at 78 weeks, these secondary-outcome findings confirm the value of initiating pharmacologic intervention early on after a fragility fracture, whether it’s a bisphosphonate or anabolic agent. The orthopaedic community needs to continue leading multipronged efforts to deal with the public health issues of osteoporosis and fragility fractures.

Click here for additional OrthoBuzz posts related to osteoporosis and fragility fractures.

Marc Swiontkowski, MD
JBJS Editor-in-Chief

Guest Post: Osteoporosis Treatment Still Lacking

OrthoBuzz occasionally receives posts from guest bloggers. This guest post comes from Brett A. Freedman, MD, in response to a study published in JAMA about a new agent to prevent fractures in postmenopausal women with osteoporosis.

The August 16, 2016 issue of JAMA published the results of the ACTIVE (Abaloparatide Comparator Trial In Vertebral Endpoints) trial.  This 28-site randomized trial allocated postmenopausal women with low bone mineral density (BMD) and/or a prior fragility fracture into one of three arms:  abaloparatide (80 µg subcutaneously, daily ) vs. daily placebo injection vs. teriparatide (20 µg subcutaneously, daily).  The primary end point was new vertebral fracture over the 18-month trial.

As expected, both anabolic agents significantly outperformed placebo, with incident vertebral fractures occurring in only 4 subjects in the abaloparatide arm (0.6%) and 6 in the teriparatide arm (0.8%), while there were 30 in the placebo arm (4.2%).  Although the study was not powered to evaluate differences between the two anabolic agents, the results suggest that abaloparatide and teriparatide performed essentially the same over the 18-month period.

In an accompanying commentary,1 Cappola and Shoback note that institutional review boards (IRBs) approved a prospective clinical trial protocol in which patients with known osteoporosis and/or a prior fragility fracture were allowed to be randomized to a non-treatment arm for 18 months.  Subjects whose BMD dropped more than 7% from baseline and those who experienced an incident fracture during the trial “were offered an option to discontinue and receive alternative treatment,” but in some sense IRB approval of this protocol implicitly acknowledged that osteoporosis is undertreated.

Turning back to the study itself, I noted with interest that subjects who had regularly used bisphosphonates in the last 5 years or denosumab in the last year were excluded.  So, none of the 2463 subjects who were randomized had received any active treatment for osteoporosis in the 1 to 5 years prior to enrollment, despite the fact that the average T-score in the lumbar spine (-2.9 for all 3 arms) was in the osteoporotic range and that almost one-third of subjects had had at least one prior fragility fracture.

This is a sad commentary on “our” (meaning all providers involved in bone health) continued inability to diagnose and treat osteoporosis effectively.  Despite the “National Bone and Joint Health Decade” (2002-2011) and our continued attempts to “Own the Bone,” we have made little progress in recognizing and treating the osteoporosis underlying the fragility fractures that we so frequently treat.  Colleagues of mine and I published that only 38% of patients in 2002 with clinically diagnosed vertebral compression fragility fractures were receiving active treatment for osteoporosis.2  Over the ensuing decade, Solomon et al. showed that that figure actually decreased to 20%.3

This JAMA study provides empiric Level-I support for the efficacy of another anabolic agent to treat osteoporosis.  Cost, subcutaneous delivery, and osteosarcoma concerns have limited the only FDA-approved anabolic osteoporosis medication, teriparatide, to second-line status, behind bisphosphonates.  If and when approved, abaloparatide will probably bump up against the same limitations.  Still, the parathyroid hormone receptor agonists are particularly pertinent to orthopaedic surgeons, because they are the most effective secondary fracture prevention agents—and the only ones that show meaningful improvement in bone mineral density.  This bone-building property has also led to progressive acceptance of teriparatide as an important perioperative adjunct for instrumented spinal fusion surgery in patients with known osteoporosis.

However, as has been repeatedly shown, parathyroid receptor agonists only work when they are prescribed, and they are only prescribed when osteoporosis is diagnosed.2,3  Patients with incident clinical fragility fractures need to be effectively educated about osteoporosis, its treatment, and the impact of failing to treat it.  Orthopaedic surgeons need to continue to set the signal flares and advocate for our patients to receive effective treatment for all their chronic musculoskeletal illnesses, not the least of which is osteoporosis.

References:

  1. Cappola AR, Shoback DM. Osteoporosis Therapy in Postmenopausal Women With High Risk of Fracture. JAMA. 2016 Aug 16;316(7):715-6.
  1. Freedman BA, Potter BK, Nesti LJ, Giuliani JR, Hampton C, Kuklo TR. Osteoporosis and vertebral compression fractures-continued missed opportunities.Spine J. 2008 Sep-Oct;8(5):756-62.
  1. Solomon DH, Johnston SS, Boytsov NN, McMorrow D, Lane JM, Krohn KD. Osteoporosis medication use after hip fracture in U.S. patients between 2002 and 2011. J Bone Miner Res. 2014 Sep;29(9):1929-37.

JBJS Editor’s Choice: The Harder They Fall

Balance_7_20_16.gifIn the July 20, 2016 issue of The Journal, Louer et al. detail the association between distal radial fractures and poor balance. We have long understood that inherently poor balance was a major contributor to fall risk, and now we have more hard evidence thanks to this research team.

In this case-control evaluation comparing 23 patients ≥65 years of age who had sustained a low-energy distal radial fracture with 23 age- and sex-matched control patients, the authors found that those in the fracture cohort:

  • Demonstrated poorer balance based on dynamic motion analysis (DMA) scores
  • Were able to perform the balance test for significantly less time
  • Rated themselves as having worse mobility

Among both cohorts, only 3 patients had completed an evaluation of or treatment for balance deficiencies.

The orthopaedic community has begun to pay attention to fragility fracture risk reduction through programs such as the AOA’s “Own the Bone” initiative, which focuses on identifying patients with fragility fracture and applying evidence-based treatment and prevention guidelines. Fragility fracture programs led by nurse practitioners or physician assistants have gained traction in many centers and have been proven effective in identifying at-risk patients and providing appropriate follow-up care.

Any intervention for patients presenting with the first fragility fracture must include assessing fall risk. Home evaluations addressing hazards such as loose carpets, poor lighting, and poorly designed stairway transitions are critical. We also know that activities such as tai chi, low-impact aerobics, and yoga, when regularly practiced, can help preserve balance. Now, developing programs that actually improve postural balance must be part of our collective research agenda as we attempt to address the major public health issue of fall-related fragility fractures.

Marc Swiontkowski, MD
JBJS Editor-in-Chief

AOA Symposium: Secondary Fracture Prevention

ownbone_logo-r.pngOn Thursday, June 23, 2016, the American Orthopaedic Association and the National Association of Orthopaedic Nurses will host a full-day symposium focused on how to establish and run a fracture liaison service.

  • When: Thursday, June 23, 2016, 9:00 am to 5:30 pm
  • Where: The Westin Seattle, Seattle, WA

Learn from national and local experts and network with other clinicians interested in secondary fracture prevention programs. JBJS Editor-in-Chief Marc Swiontkowski, MD will be one of the presenters.

Register before June 1 to receive reduced pricing.

Vitamin D Controversy Is Focus of Free Webinar

On Thursday, December 10, 2015, from 6:00 to 6:30pm EDT, the Own the Bone initiative will offer a free webinar titled “Vitamin D in Chaos: A Common Sense Approach for Orthopaedics.”

OwnBone_Logo-RNeil C. Binkley, MD, from the University of Wisconsin will review the physiology of vitamin D, current approaches to 25(OH)D testing, and recommendations for treatment of those whose levels are low. Defining “low” vitamin D status remains extremely controversial, but many fracture patients have vitamin D inadequacy that may contribute to low bone mass and fragility fracture risk.

The American Orthopaedic Association (AOA) developed Own the Bone as a quality improvement program to address the osteoporosis treatment gap and prevent subsequent fragility fractures.

Lumbar Spine Surgery Helps Parkinson Patients

Despite a higher rate of complications than in the general population, overall outcomes of lumbar spine surgery in patients with mild to moderate Parkinson disease are favorable, with significant improvements in spine-related pain and function. So concludes a study by Schroeder et al. in the October 21, 2015 Journal of Bone & Joint Surgery. Improvements were seen in surgeries with and without instrumentation over an average follow-up of more than two years.

Among the 20 of 96 patients in the study who required revision surgery, risk factors for revision included a Parkinson disease severity of ≥3 on the modified Hoehn and Yahr scale, a history of diabetes mellitus, treatment for osteoporosis, and a combined anterior/posterior surgical approach (which was used in 22 of 63 patients who underwent instrumented fusions).

In light of these findings, Schroeder et al. recommend that, among patients who have Parkinson severity ≥3 and in those with non-insulin-dependent diabetes or severe osteoporosis, lumbar spine surgery should be done only in cases with concomitant myelopathy. They also remind surgeons that if the patient’s spine pathology is severe enough to mandate a combined anterior and posterior approach, “the risk of surgery is high.”

Increased Calcium Intake Neither Boosts BMD nor Reduces Fracture Risk

In two separate studies published recently in the BMJ, New Zealand researchers concluded that increased calcium intake, through diet or supplements, is unlikely to have clinically meaningful effects on bone density or fracture prevention. The findings call into question recommendations from most health care professionals for daily calcium intake of at least 1,000 to 1,200 mg in older adults.

The first study reviewed 59 randomized controlled trials (nearly 14,000 patients total) that examined the association between bone mineral density (BMD) and either dietary or supplemental sources of calcium. Increases in BMD ranged from only 0.6% to 1.8% with increased calcium intake, regardless of the source and whether calcium was taken with vitamin D. The authors concluded that these small BMD effects were “unlikely to translate into clinically meaningful reductions in fractures.”

The second study reviewed 28 randomized trials and 44 observational studies (more than 58.000 patients total) that examined the relationship between increased calcium intake and fracture prevention among people older than 50 years. The analysis found that calcium supplements have “small inconsistent benefits on fracture prevention” but that overall “there is currently no evidence that increasing calcium intake prevents fractures.”

What do you make of these findings? Please comment by clicking on the “Leave a comment” button in the box next to the title.