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Since the publication of the Osteoporosis Canada guidelines in 2002, there has been a paradigm shift in the prevention and treatment of osteoporosis and fractures.1,2 The focus now is on preventing fragility fractures and their negative consequences, rather than on treating low bone mineral density, which is viewed as only one of several risk factors for fracture. Given that certain clinical factors increase the risk of fracture independent of bone mineral density, it is important to take an integrated approach and to base treatment decisions on the absolute risk of fracture. Current data suggest that many patients with fractures do not undergo appropriate assessment or treatment.3 To address this care gap for high-risk patients, the 2010 guidelines concentrate on the assessment and management of women and men over age 50 who are at high risk of fragility fractures and the integration of new tools for assessing the 10-year risk of fracture into overall management.
Fragility fractures, the consequence of osteoporosis, are responsible for excess mortality, morbidity, chronic pain, admission to institutions and economic costs.4–6 They represent 80% of all fractures in menopausal women over age 50.3 Those with hip or vertebral fractures have substantially increased risk of death after the fracture.5 Postfracture mortality and institutionalization rates are higher for men than for women.7
Despite the high prevalence of fragility fractures in the Canadian population and the knowledge that fractures predict future fractures,8 fewer than 20% of women3,9 and 10% of men10 receive therapies to prevent further fractures. These statistics contrast sharply with the situation for cardiovascular disease, where 75% of patients who have had myocardial infarction receive β-blockers to prevent another event.11
The target population for these guidelines is women and men over age 50, because of the overall burden of illness in that age group. As a consequence, we focused our systematic literature reviews on this population. The application of these guidelines to children and young adults, as well as high-risk groups such as transplant recipients, was considered, but in-depth reviews of conditions that increase risk were largely beyond the scope of these guidelines.
The development of these guidelines followed the Appraisal of Guidelines, Research and Evaluation (AGREE) framework.12 We surveyed primary care physicians, patients, osteoporosis specialists from various disciplines, radiologists, allied health professionals and health policy-makers to identify priorities for these guidelines. We then conducted systematic reviews of the literature according to these priorities to update our knowledge in two key areas: assessment of risk of fracture and therapies for osteoporosis. Additional topics covered here were identified as important for the management of osteoporosis.
We convened a Best Practice Guidelines Committee consisting of participants from across Canada with methodologic and content expertise. We performed literature searches in seven electronic databases (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.100771/DC1), adapted search strategies from systematic reviews performed by the Cochrane Musculoskeletal Group and followed the PRISMA flow diagram for selection of studies, the PRESS (Peer Reviewed Electronic Search Strategy) checklist and the Cochrane Collaboration Handbook. We identified 35 papers for assessment of fracture risk, published from January 1990 to December 2009. We used the systematic review of osteoporosis therapies of MacLean and colleagues,13 who included 76 randomized trials and 24 meta-analyses, supplemented with data from 30 randomized controlled trials published since 2008. We abstracted all papers, graded them for quality of evidence and assigned a level of evidence using established criteria (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.100771/DC1).1 We then developed and graded initial recommendations. We incorporated relevant data up to Sept. 19, 2010.
An expert panel, consisting of members of the Osteoporosis Canada Scientific Advisory Council, members of stakeholder organizations, family physicians and experts from across Canada, met to discuss the initial recommendations. The group used a modified RAND/University of California, Los Angeles Delphi method for developing consensus to ensure clinical relevance and applicability.14 The Guidelines Committee and the Executive Committee of the Osteoporosis Canada Scientific Advisory Council then reviewed the recommendations. The revised recommendations (presented below with grades in square brackets) are based on the feed-back provided and were endorsed by the expert panel.
Women and men over age 50 should be assessed for risk factors for osteoporosis and fracture to identify those at high risk for fractures.
A detailed history and a focused physical examination are recommended to identify risk factors for low bone mineral density, falls and fractures, as well as undiagnosed vertebral fractures (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.100771/DC1). In selected individuals, bone mineral density should be measured with dual-energy x-ray absorptiometry (Table 1).
For most patients with osteoporosis, defined as bone mineral density of 2.5 or more standard deviations below the peak bone mass for young adults (i.e., T-score ≤ −2.5), only limited laboratory investigations are usually required (Box 1). Increased values for bone turnover markers are associated with an approximately two-fold increased risk of fractures, which is largely independent of bone mineral density; however the value of measuring these markers to estimate an individual’s risk of fracture is unclear.15
Assessment for vertebral fractures by dual-energy x-ray absorptiometry is available as an option on some bone densitometers.16 Vertebral fractures unrelated to trauma are best defined (on lateral radiographs or via vertebral fracture assessment) as vertebral height loss of 25% or more with disruption of the end plate. Such fractures are associated with a five-fold increase in the risk of future vertebral fractures relative to those without vertebral fractures.17
Currently, two closely related tools are available in Canada for estimating the 10-year risk of a major osteoporotic fracture (i.e., fracture of the hip, vertebra [clinical], forearm or proximal humerus): the updated tool of the Canadian Association of Radiologists and Osteoporosis Canada (CAROC; see www.osteoporosis.ca)18 and the Fracture Risk Assessment tool (FRAX) of the World Health Organization (WHO), specific for Canada (www.sheffield.ac.uk/FRAX/tool.jsp?country=19).19 Both use the bone mineral density or T-score for the femoral neck only. They have been calibrated using the same Canadian fracture data and have been directly validated in Canadians.20–22 The 2010 version of the Canadian Association of Radiologists and Osteoporosis Canada tool replaces the 2005 version, which used Swedish fracture data.23
The Canadian Association of Radiologists and Osteoporosis Canada tool stratifies women and men over age 50 into three zones of risk for major osteoporotic fracture within 10 years (Figure 1):23 low (< 10%), moderate (10%–20%) and high (> 20%). An initial risk category is obtained from age, sex and T-score for the femoral neck, derived from the reference range for white women of the National Health and Nutrition Examination Survey III.18 Certain clinical factors increase the risk of fracture independent of bone mineral density, the most important being the presence of a prior fragility fracture after age 408 and recent prolonged use of systemic glucocorticoids (i.e., at least three months cumulative use during the preceding year at a prednisone-equivalent dose ≥ 7.5 mg daily).24 The presence of either risk factor raises the individual’s risk to the next risk category (i.e., from low to moderate or from moderate to high). When both are present, the patient is considered to have a high risk of fracture, regardless of bone mineral density.18
The WHO Fracture Risk Assessment tool uses sex, age, body mass index, prior fracture, parental hip fracture, prolonged glucocorticoid use, rheumatoid arthritis (or secondary causes of osteoporosis), current smoking, alcohol intake (three or more units daily) and (optionally) bone mineral density of the femoral neck. Fracture discrimination using the WHO Fracture Risk Assessment tool with bone mineral density is better than the Fracture Risk Assessment tool without bone mineral density or bone mineral density alone.25 Bone mineral density of the lumbar spine is not considered in the initial risk assessment for either of these two tools, and fracture risk is slightly underestimated when the lumbar spine T-score is much lower than the hip T-score.26
Observed fracture rates for women and men are in close agreement to the rates predicted by both of these tools.18 The WHO Fracture Risk Assessment tool is based upon a more complete set of clinical risk factors and can be used even without results for bone mineral density, but the calculations require access to the system’s software, website or paper charts. The 2010 version of the Canadian Association of Radiologists and Osteoporosis Canada tool is less complete but is easier to use. There is high concordance between the two systems (about 90%) in risk categorization.18 Differences, when they occur, usually relate to the presence of one or more risk factors that contribute to the Canadian version of the WHO Fracture Risk Assessment tool but that are not considered in the 2010 version of the Canadian Association of Radiologists and Osteoporosis Canada tool (parental history of hip fracture, smoking, excess alcohol intake, rheumatoid arthritis). The choice of tool is largely a matter of personal preference and convenience.
Neither of these models should be applied to individuals younger than age 50. For individuals younger than age 50 with medical conditions that may have adverse skeletal consequences, risk assessment and treatment considerations are complex and often benefit from consultation with a specialist. In addition, the results obtained with these risk assessment tools reflect the theoretical risk of a patient who is treatment-naive; they do not reflect any reduction in risk associated with therapy.
The software for the Canadian version of the WHO Fracture Risk Assessment tool is not yet widely available on bone mineral density machines; therefore, for purposes of reporting bone mineral density, the 2010 version of the Canadian Association of Radiologists and Osteoporosis Canada tool is the only system that can be applied on a national basis at the present time. This situation may change as the WHO Fracture Risk Assessment software becomes more widely available. Clinical practitioners need to be aware of the WHO Fracture Risk Assessment tool, given its international importance as the 10-year risk assessment system developed and recommended by the WHO and given that many patients will have access to the tool’s website. Some clinical practitioners may also prefer the versatility of the WHO Fracture Risk Assessment tool, which allows assessment of risk in the absence of a bone mineral density measurement and is more accurate for patients with one or more of the additional risk factors listed above.
Exercise improves quality of life for those with osteoporosis, particularly in the domains of physical function and pain, and improves muscle strength and balance.27 Although there is limited evidence that exercise programs reduce fractures, one study showed that a program of moderate to vigorous walking reduced the risk of hip fractures.28 Home safety assessment was effective only for those with severe visual impairment and others at high risk for falls.29 Removal of an individual’s first cataract reduced the frequency of falls,29 but interventions to reduce falls did not reduce fractures.30 Hip protectors have been cost-effective in reducing hip fractures among residents of Canadian long-term care facilities but not for those residing in the community, probably because of poor compliance.31
There is controversy about both the efficacy of calcium supplementation for reducing fractures32,33 and the potential adverse effects of high-dose supplementation.34 Another group within Osteoporosis Canada (of which some of the current authors were members) recently developed guidelines on vitamin D.35 Here, we highlight the major changes in vitamin D recommendations from the 2002 guidelines of Osteoporosis Canada.
A growing number of therapeutic options are available in Canada, both antiresorptive agents (bisphosphonates, receptor activator for nuclear factor κ B [RANK] ligand inhibitor, selective estrogen receptor modulator, hormone therapy, calcitonin) and a bone-forming agent (teriparatide), with a range of dosing frequencies and routes of administration. There is consistent evidence from randomized clinical trials that all therapies currently available in Canada reduce the risk of vertebral fractures for menopausal women with osteoporosis (as defined by a T-score ≤ −2.5).13 There is also evidence that some interventions prevent nonvertebral and/or hip fractures36 and may reduce the mortality rate among individuals at high risk for fractures37,38 (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.100771/DC1). Women with prior fragility fractures affecting the vertebra or hip also benefit from pharmacologic intervention. In general, pharmacotherapy reduces the risk of vertebral fracture by 30% to 70%, depending on the agent and level of adherence. The effect on nonvertebral fractures is lower and varies by fracture site. There is inconsistent evidence regarding the benefits of pharmacologic therapy for those who have sustained a fracture at a site other than the hip or the spine (e.g., the wrist), unless they also have an osteoporotic T-score. Both calcitonin and teriparatide may decrease the pain associated with vertebral fractures.39,40
Few studies of men have assessed the reduction of fracture rate as a primary outcome.13 Systematic reviews and meta-analyses have found reductions in vertebral fractures with bis-phosphonates,13,41 but there is no evidence that testosterone reduces fractures.13 In fact, hypogonadal and eugonadal men respond similarly to bisphosphonate therapy.41
In this section, we highlight issues that are common or that have surfaced in postmarketing surveillance. Some of these issues remain unresolved.
High-dose calcium supplementation may increase the risk of renal calculi and cardiovascular events.33,34 Bisphosphonates may cause self-limited flu-like symptoms, especially after the first dose of zoledronic acid by infusion (reported in up to 10% of patients).42 Denosumab may increase the risk of cellulitis.43 Raloxifene and hormone therapy increase the risk of thromboembolic events, including pulmonary embolism.13 Teriparatide can cause hypercalciuria and hypercalcemia, both generally mild and both resolving spontaneously or with discontinuation of calcium supplementation.13
Whether bisphosphonate therapy for osteoporosis increases the risk of osteonecrosis of the jaw, atypical fractures of the femur, esophageal cancer or atrial fibrillation remains controversial. Osteonecrosis of the jaw is defined as an area of exposed alveolar bone in the mandible or maxilla that does not heal after eight weeks.44 It is extremely rare (< 1 case per 10 000 patient-years among patients with primary osteoporosis).45 The risk is higher for those with malignancy, those undergoing radiation and chemotherapy, those receiving high-dose bisphosphonates for bone metastases or glucocorticoids, those with diabetes or poor dental hygiene, and those undergoing invasive dental procedures such as tooth extractions or implants.
Atypical fractures of the femur are those occurring in the subtrochanteric or diaphyseal regions. Although extremely rare, they may be more common among those undergoing long-term bisphosphonate therapy; however, a link has not been definitively established. Such fractures tend to appear as clean transverse or oblique “chalk-like” breaks. Some patients have prodromal thigh or groin pain. Radiographic findings may include cortical thickening with beaking. Nuclear bone scans often reveal increased uptake in the area, which suggests a stress fracture with increased remodelling. Radiography or bone scanning (or both) should be considered for individuals who have been on long-term bisphosphonate therapy and who experience new thigh pain.46
Esophageal cancer occurred in 23 patients who had been receiving bisphosphonate therapy from October 1995 to mid-May 2008, as described in a case series prepared by the US Food and Drug Administration; however, the number of patients not on this type of therapy who had esophageal cancer during the same period was not reported.47 Analysis of a national register found similar rates of this type of cancer in bisphosphonate-treated and untreated patients.48 Two recent large retrospective cohort studies reported conflicting results.49,50
In general, for patients at high 10-year fracture risk, the benefits of pharmacologic therapy far outweigh the potential risks. These risks must be placed in perspective during discussion of these issues with patients.
Bone loss associated with glucocorticoid therapy develops quickly, within three to six months, and the risk of fracture increases with doses as low as 2.5–7.5 mg/day.51 Long-term use of glucocorticoids (three months or more) has resulted in a 30%–50% incidence of fractures, particularly among those over the age of 40 and those using high doses.13,51 Osteoporosis therapies, including alendronate, risedronate and teriparatide, reduce the risk of vertebral fractures and maintain bone mineral density in those taking glucocorticoids.13,52,53 Similarly, etidronate, zoledronic acid and calcitonin maintain bone mineral density in those taking glucocorticoids.53,54 For patients undergoing long-term glucocorticoid therapy, the appropriate duration of osteoporosis treatment is unknown. Bisphosphonates and denosumab maintain bone mineral density in women who are taking aromatase inhibitors and men undergoing androgen-deprivation therapy.55–58
An integrated approach is important for the management of patients with a risk of fracture (Figure 2). For all patients, regular weight-bearing, balance and strengthening exercises, smoking cessation, and optimization of total (dietary and supplements) calcium and vitamin D intake are recommended. For patients at risk of falls, fall-prevention strategies should be implemented.
Within the integrated management strategy, categories of low, moderate and high fracture risk are used to guide decisions on particular therapies. The clinician should consider the ratio of benefit to harm, particularly for patients who are not at high risk. When choosing among therapies, the patient’s individual risk profile, comorbid conditions, preferences and lifestyle should be considered.
Many individuals designated as being at moderate risk for fracture should be considered for pharmacologic treatment. More osteoporotic fractures occur in the moderate-risk group than the high-risk group (because there are more individuals in the moderate-risk group), even though the individual risk of fracture is higher in the high-risk group.18 Therefore, patients who are at moderate risk should undergo a careful clinical evaluation to identify additional risk factors that are not considered in the risk assessment system, and certain of these individuals should be offered pharmacologic therapy.
For patients with a low risk of fracture, pharmacologic therapy is not usually required. In general, lifestyle measures such as exercise, prevention of falls, optimization of calcium and vitamin D intake, and smoking cessation are sufficient for individuals with a low risk of fracture, provided they do not have any risk factors for rapid loss of bone mineral density.
No randomized trials have directly assessed the value of repeat bone mineral density testing on persistence with treatment or reduction of fractures;59 however, if used correctly, serial testing can be a helpful clinical tool.23 Measurement error must be considered when interpreting serial assessments of bone mineral density to determine whether any changes are real and not simply random fluctuation or artifact.60 For patients who are undergoing treatment, repeat measurement of bone mineral density should initially be performed after one to three years; the testing interval can be increased once therapy is shown to be effective. If bone mineral density has improved or remains unchanged, the patient is considered to have had a good response to therapy. Continued loss of bone mineral density or a new fracture may reflect poor adherence with therapy, failure to respond to therapy or previously unrecognized secondary causes of osteoporosis. For moderate-risk individuals, including those with a T-score of −2.5 or below, a repeat measurement of bone mineral density should be obtained after one to three years to monitor for rapid bone loss. If bone mineral density is stable, then less frequent monitoring can be considered. For individuals with low risk of fracture and without additional risk factors for rapid loss of bone mineral density, a testing interval of 5–10 years may be sufficient.61
There is little evidence to support any recommendation regarding duration of therapy or the use of drug holidays. Rates of clinical vertebral fracture decreased by 55% among those who continued alendronate therapy after five years of initial treatment (for a total of 10 years) relative to those who stopped after five years, but there were no differences in rates of nonvertebral fractures or radiographic vertebral fractures.62 Discontinuation of risedronate or hormone therapy (estrogen) may result in loss of bone mineral density.63,64 Combinations of hormone therapy or raloxifene with a bisphosphonate have yielded improvement in bone mineral density,65,66 but proof of additional reduction in fracture rate is lacking.
Patients with any of the following factors may benefit from referral to a physician with expertise in osteoporosis: fracture or significant ongoing loss of bone mineral density despite good adherence while on first-line therapy; intolerance of first- and second-line therapies; any secondary cause of osteoporosis that is outside the expertise of the primary care physician; and extremely low bone mineral density.
Both the US National Osteoporosis Foundation and the UK National Osteoporosis Guideline Group use absolute 10-year risk of fracture to guide interventions. The National Osteoporosis Foundation recommends treating menopausal women and men over age 50 with T-score ≤ −2.5 at the hip or spine or with a prior hip or spine fracture. In addition, patients with low bone mass (T-score between −1.0 and −2.5) should be treated when the 10-year risk of hip fracture is ≥ 3% or the 10-year risk of major osteoporosis-related fracture is ≥ 20%.67 The National Osteoporosis Guideline Group recommends an age-dependent intervention threshold, which ranges from 7.5% risk of major osteoporotic fracture at age 50 to 30% at age 80.68 These two approaches are different: the National Osteoporosis Foundation guidelines are driven by cost-effectiveness, whereas the National Osteoporosis Guideline Group uses a translational approach to determine treatment thresholds. A much smaller proportion of the population would be treated under the approach of the National Osteoporosis Guideline Group than that of the National Osteoporosis Foundation. It is unclear which approach is better suited to the Canadian context.
Knowledge translation for these guidelines was developed through the knowledge-to-action framework. A systematic review has shown that disease management tools for osteoporosis that targeted both the physician and patient and that were multifaceted (such as having reminders, education and risk assessment tools in either paper or electronic format) improved appropriate use of both bone mineral density testing and treatment.69 Several Canadian randomized controlled trials have demonstrated the effectiveness and cost-effectiveness of multifaceted approaches in which case managers coordinate care.70,71 Therefore, we developed a toolkit and a dissemination strategy after widespread national consultation with primary care physicians, patients, allied health professionals, specialists, radiologists and health policy-makers. A group of Canadian knowledge translation and osteoporosis specialists has been convened to develop and evaluate novel tools that will enhance the implementation of these guidelines. In addition, more than 10 professional organizations have endorsed these guidelines and will assist in its dissemination (Appendix 1, available at www.cmaj.ca/cgi/content/full/cmaj.100771/DC1). Tools and resources can be found at www.osteoporosis.ca.
Many gaps exist in our current knowledge about how to best prevent fractures and their negative consequences. Future research should examine the risk of fractures in special populations (including younger patients who have already had a frature and younger patients who are taking glucocorticoids), the value of bone turnover markers in assessing individuals’ fracture risk and monitoring their treatment, whether exercise or fall-prevention programs reduce fractures and the optimal daily dose of vitamin D for musculoskeletal and other health benefits.
The authors thank their support team for their dedication to the guidelines project and acknowledge their contributions: Best Practices Project Coordinator Elke Henneberg of ebmed Inc. (www.ebmed.ca); researchers Loretta Hillier MA, Christina Lacchetti MHSc, Tamara Rader MLIS and Hajera Khaja MSc; and consumer representative Marg Mac-Donell. We also acknowledge the support of Famida Jiwa DC MHSc, Farah Samji DC MHSc and Donna Spafford RN BA of Osteoporosis Canada. We thank the members of the expert panel for their contributions to the guidelines: Brian Lentle MD (moderator), Jacques Levesque MD, Sumit R. Majumdar MD, Heather Frame MD, Lynn Nash MD, Michel Fortier MD, Earl Bogoch MD, David Goltzman MD, Robert Josse MBBS, Colleen Metge BSc(Pharm) PhD, Louis-Georges Ste-Marie MD, Diane Theriault MD and Anne Marie Whelan PharmD. In addition, we gratefully acknowledge Gillian Hawker MD, Jonathan D. Adachi MD, Heather McDonald-Blumer MD and Irene Polidoulis MD for reviewing materials related to the manuscript.
Competing interests: All authors received consulting fees and travel support from Osteoporosis Canada during the preparation of this article. In addition, Alexandra Papaioannou has been an advisory board member for Amgen, Eli Lilly, Merck Frosst, Novartis and Procter & Gamble; has served as a consultant to Amgen, Aventis Pharma, Eli Lilly, Lundbeck Canada Inc., Merck Frosst, Novartis, Procter & Gamble, Servier, Warner Chillcott and Wyeth-Ayerst; has received unrestricted research grants from Amgen, Eli Lilly, Merck Frosst, Procter & Gamble and Sanofi-Aventis; has received clinical trial grants from Novartis and Pfizer; has received a research grant from the Ontario Ministry of Health and Long-Term Care; and has served as a member of the Continuing Medical Education Steering Committee of the Ontario College of Family Physicians. Suzanne Morin has been an advisory board member for Amgen, Eli Lilly, Novartis and Warner-Chilcott and has received speaker’s honoraria from Amgen, Novartis and Merck. Angela M. Cheung has been an advisory board member for Amgen and Eli Lilly; has served as a consultant for Merck; and has received speaker’s honoraria from Amgen, Eli Lilly, Merck, Novartis and Warner Chilcott. Stephanie Atkinson has served as a consultant to Pfizer and Wyeth Nutritionals and has participated in a multisite clinical trial funded by Novartis. Jacques P. Brown has been an advisory board member for Amgen, Eli Lilly, Merck, Novartis and Warner Chilcott; has served as a consultant for Amgen, Eli Lilly, Merck, Novartis and Warner Chilcott; has received grants from Abbott, Amgen, Eli Lilly, GlaxoSmithKline, Merck, Novartis, Pfizer, Roche, Sanofi-Aventis, Servier and Warner Chilcott; and has received speaker’s honoraria from Amgen, Eli Lilly, Merck, Novartis and Warner Chilcott. David A. Hanley has served as an advisory board member for Amgen Canada, Eli Lilly Canada, Novartis Canada, NPS Pharmaceuticals, Servier Canada and Warner Chilcott; has participated in clinical trials funded by Amgen, Eli Lilly, Novartis, NPS Pharmaceuticals, Pfizer, Servier and Wyeth Ayerst; and has received speaker’s honoraria from Amgen Canada, Eli Lilly Canada, Novartis Canada, NPS Pharmaceuticals and Servier Canada. Anthony Hodsman has been an advisory board member for Amgen Canada, Novartis Canada, Procter & Gamble Canada, Shire Pharmaceuticals Canada and Warner-Chilcott Canada; has served as a consultant to Cytochroma Canada; and has received speaker’s honoraria from McGill University and Novartis Canada. Stephanie M. Kaiser has served as an advisory board member for Amgen, AstaZeneca, Bristol Myers Squibb, Eli Lilly Canada, Merck Frosst/Schering, Novartis and Servier; has received speaker’s honoraria from Amgen, AstraZeneca, Eli Lilly, Merck Frosst/Schering Plough, Novartis, Procter and Gamble (now Warner Chilcott/Aventis), and Servier Canada; has received payment for development of educational presentations from Eli Lilly Canada Inc.; and has received travel funds for activities unrelated to this paper from Amgen Canada. Brent Kvern has been an advisory board member for the Alliance for Better Bone Health (sponsored by SanofiAventis and Warner) and for Amgen Canada; has served as a consultant for Servier Canada; has received honoraria from the Alliance for Better Bone Health, Amgen Canada, Eli Lilly, Merck Frosst Canada and Servier Canada; and has received payment for development of educational presentations from the Alliance for Better Bone Health, Amgen Canada, Eli Lilly, Merck Frosst Canada and Servier Canada. William D. Leslie has been an advisory board member for Amgen, Genzyme and Novartis; has received unrestricted research grants from Amgen, Genzyme, Merck Frosst, Procter & Gamble and Sanofi-Aventis; has received speaker’s fees from Amgen and Merck Frosst; and has received travel funds for activities unrelated to this paper from Genzyme. No additional competing interests declared for Sidney Feldman, Sophie Jamal and Kerry Siminoski.
Funding: Alexandra Papaioanou is supported by a Canadian Institutes of Health Research (CIHR)/Eli Lilly Chair in Women’s Health, Angela M. Cheung by a CIHR/Institute of Gender and Health Senior Scientist Award and Sophie A. Jamal by a CIHR New Investigator Award. Osteoporosis Canada provided financial support for the face-to-face meetings and for the project coordinator and research assistants who worked under the direction of the guidelines cochairs.
Previously published at www.cmaj.ca
Contributors: The Clinical Practice Guidelines for the Diagnosis and Management of Osteoporosis in Canada were created with input from more than 30 experts and stakeholders in the field of osteoporosis. Dr. Papaioannou, chair of the Therapies Working Group, and Dr. Leslie, chair of the Risk Assessment Working Group, were the overall project leaders. The members of the two working groups (Alexandra Papaioannou, Suzanne Morin, Angela M. Cheung, Stephanie Atkinson, Sophie A. Jamal, Stephanie M. Kaiser and Brent Kvern for the Therapies Working Group and William D. Leslie, Angela M. Cheung, Jacques P. Brown, Sidney Feldman, David A. Hanley, Anthony Hodsman and Kerry Siminoski for the Risk Assessment Working Group) participated in the design and development of the guidelines, including analysis and interpretation of data and writing and editing of the various sections in the full guidelines document. A smaller writing group (Alexandra Papaionnou, Suzanne Morin, Angela M. Cheung and William D. Leslie) was responsible for developing the current summary version of the guidelines, which was reviewed and approved by all members of the two working groups.
*Should be measured after three to four months of adequate supplementation and should not be repeated if an optimal level (at least 75 nmol/L) is achieved.
This article was peer reviewed.