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Osteoporosis and the orthopedist: Are we relinquishing diagnosis and medicinal treatment?
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In the last century, the orthopedist was easily involved in the medical management of osteoporosis. Diagnosis was made by radiographic “guesstimate” and/or fragility fracture. Treatment consisted of calcium, vitamin D and estrogens, although the majority of orthopedists refrained from prescribing estrogens for a variety of reasons.
The 1990s saw the advent of dual energy X-ray absorptiometry (DXA); the World Health Organization (WHO) classification for the diagnosis of osteoporosis using bone mineral density (BMD) measurements; and the approval of bisphosphonates for treatment. These ensured that the orthopedist could easily remain involved in the medicinal treatment.
The WHO classification of osteoporosis via a BMD T -score was simple: normal, -1 or higher; osteopenia, between -1 and -2.5; and osteoporosis,-2.5 or lower. Bisphosphonates were easy to prescribe; a single dosage fits all, they had high efficacy for most patients and few side effects.
However, the 21st century began an unraveling of this simplicity. The majority of fractures were occurring in the T-score range of -1 to -2.5. Bone strength reflects more than BMD — the amount of calcium hydroxyapatite per cm2 of bone. It also includes bone quality-damage accumulation (microfracture), turnover, architecture and mineralization. Perhaps the BMD was not enough. Furthermore, a low BMD was not enough to cause fracture, it required other risk factors, such as a fall.
Finally complications of medicinal treatment with bisphosphonates, such as osteonecrosis of the jaw, spontaneous femur fractures and even decreased fracture healing, were noted.
Guidelines for treatment have been evolving as well. The primary reference for managing osteoporosis is the National Osteoporosis Foundation’s “Clinician’s Guide to Prevention and Treatment of Osteoporosis.” This was first published in 1999 and updated in 2003 and 2008. These new guidelines were complemented by the release of the WHO fracture risk assessment tool (FRAX). This tool integrates the BMD measures with the clinical risk factors for fragility fractures. An algorithm provides a 10-year probability of osteoporotic fracture at various sites.).
The diagnosis and treatment of osteoporosis is becoming more specific and perhaps more complicated. For part 1 of this two-part discussion, I have gathered a panel of orthopedic and endocrine physicians to discuss if this is causing orthopedists to alter their roles in the diagnosis and medicinal management of this disease.
Douglas E. Garland, MD
Moderator
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Douglas E. Garland, MD
Richard M. Dell, MD
Aasis Unnanuntana, MD 
Nelson Watts, MD Douglas E. Garland, MD: Is the orthopedist’s role evolving in the management of osteoporosis?
Richard M. Dell, MD: Orthopedic surgeons play a key role in osteoporosis disease management. When a patient has a fragility fracture the orthopedic surgeon should initiate screening by ordering a DXA scan to access bone density/fracture risk and initiate or refer for treatment. The diagnosis and treatment of osteoporosis is crucial to help prevent future fragility fractures including hip fractures. They should also take a more active role in primary screening for osteoporosis by ordering DXA scans on all women older than 65 years and all men older than 70 years. The problem is orthopedic surgeons, for the most part, are not taking this active role in osteoporosis disease management
Aasis Unnanuntana, MD: Orthopedic surgeons are often the first to encounter osteoporotic patients presenting with fragility fractures. Although osteoporosis remains the most common cause of fragility fracture, it still remains unrecognized and untreated in more than 70% of patients who present with fracture complications. Therefore, it is crucial to recognize and perform a comprehensive evaluation to prevent subsequent fractures in this vulnerable population. Once diagnosed with a fragility fracture, a complete medical history and physical examination should be performed with particular attention to the risk factors for osteoporosis and other causes of fragility fractures such as osteogenesis imperfecta or other endocrine disorders. Generally, laboratory investigations other than BMD measurement are not required for the diagnosis of osteoporosis. Some routine tests, however, should be performed to obtain baseline values as part of the initial work up. These include complete blood count with differential, urinalysis, complete metabolic profiles, serum 25-hydroxy vitamin D, intact PTH levels and bone markers.
In addition to medical management, a clinical pathway should be established in each institution with goals to develop a multidisciplinary team; promote appropriate use of diagnostic tools and therapeutic approaches without compromising the quality of care; and educate patients about the management of osteoporosis.
Henry Van den Berg, MD: The role is changing too slow. Orthopedic surgeons need to become more proactive in preventing further fractures in patients who they see with fractures. They need to leverage more of their opportunity to stop future fractures, because it is becoming more and more apparent that having a (nontraumatic) fracture is by far the strongest risk of getting a future fracture.
Nelson Watts, MD: My father was an orthopedist. After I became an internist/endocrinologist, I realized that orthopedists have “cases” — the “back” in room 632, the “hip” at 8:00 — and internists have “patients.” I don’t think people go into surgical specialties with the idea of diagnosing and treating chronic diseases such as osteoporosis. However, a fracture should set off alarm bells about the possibility of osteoporosis and the orthopedist is usually the one who treats the fracture. I believe there is a responsibility, and liability, there. What could you say to a patient who has her second hip fracture because nothing was done to test or treat for osteoporosis after her first one?
I’m on the advisory board for the American Orthopaedic Association’s Own the Bone program which provides the tools and structure for a robust postfracture care program. I don’t believe orthopedists want to or should “own the bone,” but they are key to getting fracture patients plugged in to a local bone specialist.
Garland: Are there clinical re-interpretations of the T- and Z- scores regarding fracture risk?
Dell: The T-score is one of many factors important in calculating absolute risk for future fragility fractures. Other risk factors used to calculate the FRAX score include age, sex, race, prior fragility fractures, family history of hip fractures etc. The FRAX score helps to calculate a 10-year absolute hip fracture rate and can then to be used to help determine if treatment is needed. The Z-score (a measure of your current bone density compared to a bone density of an age-matched group) can be used to assess if a secondary cause of osteoporosis may be present. If the Z-score is -2.0 or worse, a complete secondary osteoporosis work-up should be considered by an endocrinologist.
Unnanuntana: Young women with BMD Z-scores greater than -2.0 should be classified as having BMD that is “within the expected range for age” and those with Z-scores less than -2.0 should be categorized as having BMD that is “below expected range for age” which needs further investigation for possible underlying causes. Not only is BMD testing by DXA a useful clinical tool to assess fracture risk, it is also used to monitor responses after pharmacologic treatment.
In calculating change over time, the absolute BMD values should be provided to obtain “the least significant change” for each site. An adequate time interval, usually 18 to 24 months, between measures is required to show significant change. In general, the least significant change is approximately 5.3% in the spine, 5% in the hip and 6.9% in the femoral neck area. Although measurement of BMD from DXA is the so-called gold standard for diagnosis of osteoporosis, it cannot be used as the sole predictor of fracture risk. In addition, the majority of patients who experience fragility fractures have BMD T-scores above -2.5 (in the osteopenic range). This information suggests that factors other than BMD contribute to a patient’s risk of fracture.
Watts: I have been on a personal crusade for years to stamp out the use of the term “osteopenia” because the risk for fracture varies so widely from the top to the bottom of that category that a single label just doesn’t work. A T-score of -2.5 or below is still “osteoporosis.” Although that is a high-risk group, it is a relatively small group. Most of the fractures due to osteoporosis occur in patients with T-scores higher than -2.5 – a much larger population, with a lower risk of fractures, but just a lot of them. The Fracture Risk Assessment Tool (FRAX) provides a tool to identify patients with osteopenia who would be candidates for treatment and to reassure those who don’t need treatment.
Garland: What does the orthopedist need to know about FRAX?
Unnanuntana: Fracture Risk Assessment tool (FRAX) is used to evaluate fracture risk in patients who have BMD within the osteopenic range. It has been developed by adding 12 clinical risk factors to the calculation, and offers a better assessment of fracture risk than BMD measurement alone. According to guidelines established by the NOF, patients with a 10-year fracture risk of 3% or greater at the hip or 20% or greater of a major osteoporotic fracture should be considered for pharmacologic treatment.
Although FRAX helps with clinical decision-making, it must be emphasized that the calculated 10-year fracture probability is only a guideline for treatment decision. Specific treatment decisions should be individualized. The limitations of FRAX include not incorporating data on serum vitamin D, fall risks of the patient, and biochemical markers of bone turnover. In addition, FRAX does not consider BMD at the spine. Nevertheless, it provides the surgeon a cost-effective approach to determine which patients will benefit from treatment.
Watts: FRAX is a major step forward but has significant limitations. It has only been available on the Internet which may be a barrier to its use. It only considers femoral neck BMD, so patients who are low at the spine may not be assessed correctly. It does not incorporate known risk factors such as falling, drugs such as aromatase inhibitors or androgen deprivation therapy, and assigns an average risk for all the risk factors included — for example, a prior wrist fracture raises fracture risk to the same degree as a prior hip fracture. FRAX can also be used without BMD. It is certainly something that might be useful to the orthopedist, but I think its main role is to help the clinician decide whom to treat. The orthopedist doesn’t need FRAX to start the ball rolling in the post-fracture period.
Garland: The FDA stated that bisphosphonates were not associated with femur fractures —. Thoughts?
Dell: There are several studies and multiple case reports that show atypical femur fractures can occur in patients on long term bisphosphonates. Our own study at Kaiser also suggests that there is an association between oral bisphosphonates and these atypical femur fractures, and that bisphosphonates help prevent hip fractures and the benefit of bisphosphonates exceeds the risk of these atypical femur fractures. The risk of these atypical femur fractures appear to increase after being on a bisphosphonate longer than 3 to 5 years.
Unnanuntana: Many recent studies reported the possible association between long-term treatment of bisphosphonates and low-energy femoral fractures, so-called “atypical fractures.” However, most of the literature on this subject is case reports, case series or case-control studies. It is important to recognize that associations in these studies can be due to chance, biases, confounding factors or may be true indicative of causality. Since the mechanism of these fractures remains unknown, a concern for patients with these unusual atypical femoral fractures should not preclude the rationale for use of bisphosphonates in the treatment of osteoporosis. However, these drugs should be used with caution and closely monitored by the clinicians.
The optimal management of patients with these fractures is controversial and many questions remain unanswered. Until these issues are resolved, orthopedic surgeons must be aware of the occurrence of this atypical femoral fracture in the setting of prolonged bisphosphonate therapy. Patients with thigh pain who are currently being treated with bisphosphonates should undergo imaging studies such as plain radiographs. If complications are still suspected, bone scan or MRI should be considered. For all patients with atypical fractures, serum calcium and vitamin D levels should be corrected, bisphosphonates should be stopped, and the use of an anabolic agent should be considered. Prophylactic internal fixation may be considered in patients with stress fractures if they fail from conservative treatment or the pain worsens.
Van den berg: There are not enough data to support whether this is true or false. What is true is that overall more fractures (including femur) are being prevented by bisphosphonates then are caused. It is also true that not all bisphosphonates are the same. Bisphosphonates like zoledronate and alendronate will have a much greater risk to over suppress bone over time vs. risedronate, clodronate and etidronate.
Excluding fixation, what else should we do when we evaluate an atypical fracture? Accurate diagnosis including medical history to help to build up the knowledge of these atypical femur fractures. If the patient took zoledronate or alendronate, then stop treatment.
Watts: You mean “atypical” femur fractures – those in the shaft or subtrochanteric region. The fractures in question have a stereotypical appearance on X-ray: going straight across, like breaking a piece of chalk, usually with a “spike” or “beak” on the medial side. The femoral cortex is extremely thick, which is not something that bisphosphonates will cause. I don’t think the FDA said that bisphosphonates were not associated with these fractures, just that there was not enough information at the present time to know about the relationship. For such a rare event, these fractures have gotten a lot of attention and have frightened many people who have stopped treatment. For most patients with osteoporosis, the benefits of treatment far outweigh the risks.
Garland: Excluding fixation, what else should we do when we evaluate an atypical femur fracture?
Dell: There are often bilateral changes and the clinician should get X-rays of both femurs to evaluate if cortical thickening or stress fractures on the other femur are present. These changes in the other femur may be present in half of patients with an atypical femur fracture even if pain is not present in the other extremity.
Watts: Commonly, patients with these “atypical” fractures have prodromal pain, frequently bilateral. So, if the patient has an “atypical” fracture on one side, it may be worth looking at the other side with radiographs, MRI or bone scan. It may make sense to fix an impending fracture prophylactically, or at least limit weight bearing until the symptoms resolve.
Garland: What are the current recommendations for a drug holiday from bisphosphonates?
Dell: The 2006 FLEX study by Black and colleagues suggests that a drug holiday can be done after 5 years of bisphosphonate treatment. During the drug holiday, it is important to continue calcium/vitamin D and to re-assess bone quality in 2 years with a follow-up DXA scan. Further work is needed to better address who should initiate treatment; at what age treatment should begin; what medication is best to use; how long should we continue medication.
Unnanuntana: Once administered, bisphosphonates accumulate in the bone and continue to be released for months or years after treatment is stopped. There is a concern that long-term suppression of bone turnover from bisphosphonates therapy leads to microdamage accumulation and decreased bone mechanical properties, resulting in an atypical femoral fracture. Therefore, it is recommended that osteoporosis treatment with bisphosphonates may be stopped for a drug holiday after a course of some years.
Although there is a lack of scientific evidence to answer how long to treat with bisphosphonates and how long the drug holiday should be, most of the experts in this field suggest that bisphosphonates should be stopped after 5 years of treatment. Since there is continued presence of bisphosphonate in bone and continued release of the agent, the anti-fracture efficacy may still remain even after treatment is stopped. The duration of drug holiday depends on fracture risk and pharmacokinetics of the bisphosphonates used. Generally, a drug holiday should be ended if there is a decline in BMD or increase in bone turnover markers. For patients at high risk for fragility fractures, an alternative medication such as raloxifene may be given during the holiday from bisphosphonates. An anabolic agent should be reserved in the settings of fracture or declining BMD despite bisphosphonates therapy.
Van den berg: There are no data to support drug holidays or the duration of drug holidays. What we know is that for zoledronate, one IV keeps your bone shut down for at least 3 years, but probably much longer. For alendronate, treatment of 5 years keeps your bone shut down for at least another 5 years, but could be much longer. For risedronate, after 3 or 5 years treatment, bone turnover normalizes within the year, so no drug holidays are advised.
Watts: There is not much data to inform us on this. We know that bisphosphonates accumulate in bone and are released for months or even years after treatment is stopped, possibly with a lingering therapeutic benefit. We saw this in the risedronate VERT-North America study where patients stopped their study drug after 3 years (placebo or risedronate 5 mg daily). In year 4, BMD decreased and turnover markers increased in the former risedronate subjects, but the risk of new vertebral fractures was reduced by 46%. The FLEX study with alendronate suggests that patients at moderate risk might be adequately treated after 5 years, but higher risk patients seemed to do better with 10 years of treatment. My colleague and I recently published our approach to “drug holidays.”
Editor’s note: Part 2 of this two-part discussion on osteoporosis will appear in the July Issue of Orthopedics Today. In that installment, Douglas E. Garland, MD, will ask surgeons specializing in trauma, hip and spine surgery about their specific diagnosis and treatment preferences.
Reference:
- Black DM, Schwartz AV, Ensrud KE, et al. Effects of continuing or stopping alendronate after 5 years of treatment: the Fracture Intervention Trial Long-term Extension (FLEX): a randomized trial. JAMA. 2006;296(24):2927-2938.
- Watts NB. What is osteopenia and what should be done about it? Cleve Clin J. Med. 2006;73(3):29-32
- Siris ES, Chen Y-T, Abbott TA, et al. Bone mineral density thresholds for pharmacological intervention to prevent fractures. Arch Intern. Med. 2004. 164:1108-1112
- Watts NB, Lewiecki EM, Miller PD, et al. National Osteoporosis Foundation 2008 Clinician’s Guide to Prevention and Treatment of Osteoporosis and the World Health Organization Fracture Risk Assessment Tool (FRAX): What they mean to the bone densitometrist and bone technologist. J Clin Densitom. 2008;11:473-477
- Watts NB, Ettinger B, LeBoff MS. FRAX Facts. J Bone Miner Res. 2009;24:975-979.
- Schwartz AV, Bauer DC, Cummings SR, et al. Efficacy of Continued Alendronate for Fractures in Women with and without prevalent vertebral fractures: The FLEX trial. J Bone Miner Res. 2010. DOI 10.1002/jbmr.11:
- Watts NB, Diab DL. Long-term use of bisphosphonates in osteoporosis. J Clin Endocrinol Metab. 2010;95:1555-1565
- FRAXX can be accessed at www.nof.org
- Richard M. Dell, MD, can be reached in the Department of Orthopedics, Kaiser Permanente Downey Medical Center, 9353 E. Imperial Highway, Downey, CA 90242; 562-657-4125; e-mail: Richard.M.Dell@kp.org.
- Douglas E. Garland, MD, can be reached at 2760 Atlantic Ave., Long Beach, CA 90806; e-mail: dougarland@msn.com.
- Aasis Unnanuntana, MD, can be reached at Department of Orthopaedic Surgery, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021; e-mail: unnanuntanaa@hss.edu.
- Henry J. Van den berg, MD, can be reached at Henry.VanDenBerg@wcrx.com.
- Nelson Watts, MD, can be reached at nelson.watts@uc.edu.
