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Osteoporosis: HELP
Articles by Bart L. Clarke
Based on 25 articles published since 2010
(Why 25 articles?)
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Between 2010 and 2020, B. L. Clarke wrote the following 25 articles about Osteoporosis.
 
+ Citations + Abstracts
1 Guideline AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS - 2016. 2016

Camacho, Pauline M / Petak, Steven M / Binkley, Neil / Clarke, Bart L / Harris, Steven T / Hurley, Daniel L / Kleerekoper, Michael / Lewiecki, E Michael / Miller, Paul D / Narula, Harmeet S / Pessah-Pollack, Rachel / Tangpricha, Vin / Wimalawansa, Sunil J / Watts, Nelson B. · ·Endocr Pract · Pubmed #27662240.

ABSTRACT: ABBREVIATIONS: AACE = American Association of Clinical Endocrinologists AFF = atypical femur fracture ASBMR = American Society for Bone and Mineral Research BEL = best evidence level BMD = bone mineral density BTM = bone turnover marker CBC = complete blood count CI = confidence interval DXA = dual-energy X-ray absorptiometry EL = evidence level FDA = U.S. Food and Drug Administration FLEX = Fracture Intervention Trial (FIT) Long-term Extension FRAX

2 Guideline AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS - 2016--EXECUTIVE SUMMARY. 2016

Camacho, Pauline M / Petak, Steven M / Binkley, Neil / Clarke, Bart L / Harris, Steven T / Hurley, Daniel L / Kleerekoper, Michael / Lewiecki, E Michael / Miller, Paul D / Narula, Harmeet S / Pessah-Pollack, Rachel / Tangpricha, Vin / Wimalawansa, Sunil J / Watts, Nelson B. · ·Endocr Pract · Pubmed #27643923.

ABSTRACT: ABBREVIATIONS: AACE = American Association of Clinical Endocrinologists AFF = atypical femur fracture ASBMR = American Society for Bone and Mineral Research BEL = best evidence level BMD = bone mineral density BTM = bone turnover marker CBC = complete blood count CI = confidence interval DXA = dual-energy X-ray absorptiometry EL = evidence level FDA = U.S. Food and Drug Administration FLEX = Fracture Intervention Trial (FIT) Long-term Extension FRAX(®) = Fracture Risk Assessment Tool GFR = glomerular filtration rate GI = gastrointestinal HORIZON = Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly IOF = International Osteoporosis Foundation ISCD = International Society for Clinical Densitometry IU = international units IV = intravenous LSC = least significant change NBHA = National Bone Health Alliance NOF = National Osteoporosis Foundation 25(OH)D = 25-hydroxy vitamin D ONJ = osteonecrosis of the jaw PINP = serum carboxy-terminal propeptide of type I collagen PTH = parathyroid hormone R = recommendation RANK = receptor activator of nuclear factor kappa-B RANKL = receptor activator of nuclear factor kappa-B ligand RCT = randomized controlled trial RR = relative risk S-CTX = serum C-terminal telopeptide SQ = subcutaneous VFA = vertebral fracture assessment WHO = World Health Organization.

3 Editorial Denosumab and atypical femur fractures. 2013

Cating-Cabral, Monica Therese / Clarke, Bart L. · ·Maturitas · Pubmed #23835004.

ABSTRACT: -- No abstract --

4 Review Biomechanical Computed Tomography analysis (BCT) for clinical assessment of osteoporosis. 2020

Keaveny, T M / Clarke, B L / Cosman, F / Orwoll, E S / Siris, E S / Khosla, S / Bouxsein, M L. ·Departments of Mechanical Engineering and Bioengineering, University of California, Berkeley, CA, USA. tonykeaveny@berkeley.edu. · Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic, Rochester, MN, USA. · Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA. · Bone and Mineral Unit, Oregon Health and Science University, Portland, OR, USA. · Toni Stabile Osteoporosis Center, Department of Medicine, Columbia University Medical Center, New York, NY, USA. · Orthopedic Biomechanics Laboratory, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. ·Osteoporos Int · Pubmed #32335687.

ABSTRACT: The surgeon general of the USA defines osteoporosis as "a skeletal disorder characterized by compromised bone strength, predisposing to an increased risk of fracture." Measuring bone strength, Biomechanical Computed Tomography analysis (BCT), namely, finite element analysis of a patient's clinical-resolution computed tomography (CT) scan, is now available in the USA as a Medicare screening benefit for osteoporosis diagnostic testing. Helping to address under-diagnosis of osteoporosis, BCT can be applied "opportunistically" to most existing CT scans that include the spine or hip regions and were previously obtained for an unrelated medical indication. For the BCT test, no modifications are required to standard clinical CT imaging protocols. The analysis provides measurements of bone strength as well as a dual-energy X-ray absorptiometry (DXA)-equivalent bone mineral density (BMD) T-score at the hip and a volumetric BMD of trabecular bone at the spine. Based on both the bone strength and BMD measurements, a physician can identify osteoporosis and assess fracture risk (high, increased, not increased), without needing confirmation by DXA. To help introduce BCT to clinicians and health care professionals, we describe in this review the currently available clinical implementation of the test (VirtuOst), its application for managing patients, and the underlying supporting evidence; we also discuss its main limitations and how its results can be interpreted clinically. Together, this body of evidence supports BCT as an accurate and convenient diagnostic test for osteoporosis in both sexes, particularly when used opportunistically for patients already with CT. Biomechanical Computed Tomography analysis (BCT) uses a patient's CT scan to measure both bone strength and bone mineral density at the hip or spine. Performing at least as well as DXA for both diagnosing osteoporosis and assessing fracture risk, BCT is particularly well-suited to "opportunistic" use for the patient without a recent DXA who is undergoing or has previously undergone CT testing (including hip or spine regions) for an unrelated medical condition.

5 Review Transgender bone health. 2019

Davidge-Pitts, Caroline / Clarke, Bart L. ·Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905, United States. · Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905, United States. Electronic address: clarke.bart@mayo.edu. ·Maturitas · Pubmed #31351518.

ABSTRACT: Gonadal sex steroids play a pivotal role in bone health. Medical and surgical therapies for gender dysphoria in both adolescents and adults can lead to skeletal changes. This review evaluates the literature on transgender bone health, and how the data can be translated into clinical practice.

6 Review Causes of low peak bone mass in women. 2018

Chew, Chee Kian / Clarke, Bart L. ·Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905, USA. · Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905, USA. Electronic address: clarke.bart@mayo.edu. ·Maturitas · Pubmed #29673833.

ABSTRACT: Peak bone mass is the maximum bone mass that accrues during growth and development. Consolidation of peak bone mass normally occurs during early adulthood. Low peak bone mass results from failure to achieve peak bone mass genetic potential, primarily due to bone loss caused by a variety of conditions or processes occurring at younger ages than usual. Recognized causes of low peak bone mass include genetic causes, endocrine disorders, nutritional disorders, chronic diseases of childhood or adolescence, medications, and idiopathic factors.

7 Review Cathepsin K Inhibitors for Osteoporosis: Biology, Potential Clinical Utility, and Lessons Learned. 2017

Drake, Matthew T / Clarke, Bart L / Oursler, Merry Jo / Khosla, Sundeep. ·Division of Endocrinology and Kogod Center on Aging, Mayo Clinic College of Medicine, Rochester, Minnesota 55905. ·Endocr Rev · Pubmed #28651365.

ABSTRACT: Cathepsin K is a cysteine protease member of the cathepsin lysosomal protease family. Although cathepsin K is highly expressed in osteoclasts, lower levels of cathepsin K are also found in a variety of other tissues. Secretion of cathepsin K from the osteoclast into the sealed osteoclast-bone cell interface results in efficient degradation of type I collagen. The absence of cathepsin K activity in humans results in pycnodysostosis, characterized by increased bone mineral density and fractures. Pharmacologic cathepsin K inhibition leads to continuous increases in bone mineral density for ≤5 years of treatment and improves bone strength at the spine and hip. Compared with other antiresorptive agents, cathepsin K inhibition is nearly equally efficacious for reducing biochemical markers of bone resorption but comparatively less active for reducing bone formation markers. Despite multiple efforts to develop cathepsin K inhibitors, potential concerns related to off-target effects of the inhibitors against other cathepsins and cathepsin K inhibition at nonbone sites, including skin and perhaps cardiovascular and cerebrovascular sites, prolonged the regulatory approval process. A large multinational randomized, double-blind phase III study of odanacatib in postmenopausal women with osteoporosis was recently completed. Although that study demonstrated clinically relevant reductions in fractures at multiple sites, odanacatib was ultimately withdrawn from the regulatory approval process after it was found to be associated with an increased risk of cerebrovascular accidents. Nonetheless, the underlying biology and clinical effects of cathepsin K inhibition remain of considerable interest and could guide future therapeutic approaches for osteoporosis.

8 Review Abaloparatide: Recombinant human PTHrP (1-34) anabolic therapy for osteoporosis. 2017

Chew, Chee Kian / Clarke, Bart L. ·Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905 USA. · Mayo Clinic E18-A, 200 1st Street SW, Rochester, MN, 55905 USA. Electronic address: clarke.bart@mayo.edu. ·Maturitas · Pubmed #28159062.

ABSTRACT: The treatment of osteoporosis is generally either by inhibition of bone resorption with antiresorptive agents or by stimulation of bone formation with anabolic agents. Currently, teriparatide (recombinant human parathyroid hormone 1-34 [rhPTH (1-34)]) is the only available approved anabolic agent in the U.S. Other anabolic agents are under investigation however. Abaloparatide is recombinant human parathyroid hormone-related peptide 1-34. This agent is an anabolic agent that appears more potent than teriparatide, and it may have more rapid onset of fracture reduction than teriparatide. It is currently undergoing FDA review, with approval expected in 2017.

9 Review Primary hyperparathyroidism: review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus. 2017

Khan, A A / Hanley, D A / Rizzoli, R / Bollerslev, J / Young, J E M / Rejnmark, L / Thakker, R / D'Amour, P / Paul, T / Van Uum, S / Shrayyef, M Zakaria / Goltzman, D / Kaiser, S / Cusano, N E / Bouillon, R / Mosekilde, L / Kung, A W / Rao, S D / Bhadada, S K / Clarke, B L / Liu, J / Duh, Q / Lewiecki, E Michael / Bandeira, F / Eastell, R / Marcocci, C / Silverberg, S J / Udelsman, R / Davison, K Shawn / Potts, J T / Brandi, M L / Bilezikian, J P. ·McMaster University, Hamilton, Canada. Aliya@mcmaster.ca. · Bone Research and Education Center, 223-3075 Hospital Gate, Oakville, ON, Canada. Aliya@mcmaster.ca. · University of Calgary, Calgary, Canada. · Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland. · University of Oslo, Oslo, Norway. · McMaster University, Hamilton, Canada. · Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. · University of Oxford, Oxford, UK. · CHUM, Montreal, Canada. · Western University, London, ON, Canada. · Division of Endocrinology, University of Toronto, Mississauga, ON, Canada. · McGill University, Montreal, Canada. · Dalhousie University, Halifax, Canada. · Columbia University College of Physicians and Surgeons, New York, NY, USA. · KU, Leuven, Belgium. · University of Aarhus, Aarhus, Denmark. · University of Hong Kong, Hong Kong, China. · Henry Ford Hospital, Detroit, MI, USA. · Postgraduate Institute of Medical Education and Research, Chandigarth, India. · Mayo Clinic, Rochester, MN, USA. · Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. · University of California, San Francisco, CA, USA. · New Mexico Clinical Research and Osteoporosis Center, University of New Mexico School of Medicine, Albuquerque, NM, USA. · Division of Endocrinology, Diabetes and Metabolic Bone Diseases, Agamenon Magalhaes Hospital, Brazilian Ministry of Health, University of Pernambuco Medical School, Recife, Brazil. · Department of Human Metabolism, University of Sheffield, Sheffield, UK. · Department for Clinical and Experimental Medicine, University of Pisa, Endocrine Unit 2, University Hospital of Pisa, Pisa, Italy. · Division of Endocrinology, Columbia University College of Physicians and Surgeons, New York, NY, USA. · Department of Surgery, Yale University School of Medicine, New Haven, CT, USA. · University of Victoria, Victoria, BC, Canada. · Massachusetts General Hospital, Harvard University, Boston, MA, USA. · University of Florence, Florence, Italy. ·Osteoporos Int · Pubmed #27613721.

ABSTRACT: The purpose of this review is to assess the most recent evidence in the management of primary hyperparathyroidism (PHPT) and provide updated recommendations for its evaluation, diagnosis and treatment. A Medline search of "Hyperparathyroidism. Primary" was conducted and the literature with the highest levels of evidence were reviewed and used to formulate recommendations. PHPT is a common endocrine disorder usually discovered by routine biochemical screening. PHPT is defined as hypercalcemia with increased or inappropriately normal plasma parathyroid hormone (PTH). It is most commonly seen after the age of 50 years, with women predominating by three to fourfold. In countries with routine multichannel screening, PHPT is identified earlier and may be asymptomatic. Where biochemical testing is not routine, PHPT is more likely to present with skeletal complications, or nephrolithiasis. Parathyroidectomy (PTx) is indicated for those with symptomatic disease. For asymptomatic patients, recent guidelines have recommended criteria for surgery, however PTx can also be considered in those who do not meet criteria, and prefer surgery. Non-surgical therapies are available when surgery is not appropriate. This review presents the current state of the art in the diagnosis and management of PHPT and updates the Canadian Position paper on PHPT. An overview of the impact of PHPT on the skeleton and other target organs is presented with international consensus. Differences in the international presentation of this condition are also summarized.

10 Review Managing Osteoporosis in Patients on Long-Term Bisphosphonate Treatment: Report of a Task Force of the American Society for Bone and Mineral Research. 2016

Adler, Robert A / El-Hajj Fuleihan, Ghada / Bauer, Douglas C / Camacho, Pauline M / Clarke, Bart L / Clines, Gregory A / Compston, Juliet E / Drake, Matthew T / Edwards, Beatrice J / Favus, Murray J / Greenspan, Susan L / McKinney, Ross / Pignolo, Robert J / Sellmeyer, Deborah E. ·McGuire Veterans Affairs Medical Center and Virginia Commonwealth University School of Medicine, Richmond, VA, USA. · American University of Beirut Medical Center, Beirut, Lebanon. · University of California, San Francisco, San Francisco, CA, USA. · Loyola University of Chicago, Maywood, IL, USA. · Mayo Clinic College of Medicine, Rochester, MN, USA. · University of Michigan, Ann Arbor, MI, USA. · University of Cambridge School of Clinical Medicine, Cambridge, UK. · MD Anderson Cancer Center, Houston, TX, USA. · University of Chicago, Chicago, IL, USA. · University of Pittsburgh, Pittsburgh, PA, USA. · Duke University School of Medicine, Durham, NC, USA. · University of Pennsylvania, Philadelphia, PA, USA. · The Johns Hopkins Bayview Medical Center, Baltimore, MD, USA. ·J Bone Miner Res · Pubmed #26350171.

ABSTRACT: Bisphosphonates (BPs) are the most commonly used medications for osteoporosis. This ASBMR report provides guidance on BP therapy duration with a risk-benefit perspective. Two trials provided evidence for long-term BP use. In the Fracture Intervention Trial Long-term Extension (FLEX), postmenopausal women receiving alendronate for 10 years had fewer clinical vertebral fractures than those switched to placebo after 5 years. In the HORIZON extension, women who received 6 annual infusions of zoledronic acid had fewer morphometric vertebral fractures compared with those switched to placebo after 3 years. Low hip T-score, between -2 and -2.5 in FLEX and below -2.5 in HORIZON extension, predicted a beneficial response to continued therapy. Hence, the Task Force suggests that after 5 years of oral BP or 3 years of intravenous BP, reassessment of risk should be considered. In women at high risk, for example, older women, those with a low hip T-score or high fracture risk score, those with previous major osteoporotic fracture, or who fracture on therapy, continuation of treatment for up to 10 years (oral) or 6 years (intravenous), with periodic evaluation, should be considered. The risk of atypical femoral fracture, but not osteonecrosis of the jaw, clearly increases with BP therapy duration, but such rare events are outweighed by vertebral fracture risk reduction in high-risk patients. For women not at high fracture risk after 3 to 5 years of BP treatment, a drug holiday of 2 to 3 years can be considered. The suggested approach for long-term BP use is based on limited evidence, only for vertebral fracture reduction, in mostly white postmenopausal women, and does not replace the need for clinical judgment. It may be applicable to men and patients with glucocorticoid-induced osteoporosis, with some adaptations. It is unlikely that future trials will provide data for formulating definitive recommendations. © 2015 American Society for Bone and Mineral Research.

11 Review Bone biology, signaling pathways, and therapeutic targets for osteoporosis. 2015

Iñiguez-Ariza, Nicole M / Clarke, Bart L. ·Mayo Clinic E18-A, 200 1st Street SW, Rochester, Minnesota 55905, USA. Electronic address: nicmiamd@gmail.com. · Mayo Clinic E18-A, 200 1st Street SW, Rochester, Minnesota 55905, USA. Electronic address: clarke.bart@mayo.edu. ·Maturitas · Pubmed #26255682.

ABSTRACT: Major advances have occurred recently in the treatment of osteoporosis in recent years. Most patients are currently treated with bisphosphonates, denosumab, raloxifene, or teriparatide, and in some countries, strontium ranelate. Strontium ranelate and calcitonin have recently had their use restricted due to cardiovascular concerns and malignancy, respectively. The available agents have generally provided excellent options that effectively reduce fracture risk. New targets are being sought based on appreciation of the bone biology and signaling pathways involved in bone formation and resorption. These agents will directly target these signaling pathways, and further expand the options available for treatment of osteoporosis.

12 Review The Pathophysiology and Treatment of Osteoporosis. 2015

Drake, Matthew T / Clarke, Bart L / Lewiecki, E Michael. ·Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota. · New Mexico Clinical Research & Osteoporosis Center, University of New Mexico School of Medicine, Albuquerque, New Mexico. Electronic address: mlewiecki@gmail.com. ·Clin Ther · Pubmed #26163201.

ABSTRACT: PURPOSE: The objectives of this article are to review the pathophysiology of bone loss associated with aging and to review current pharmacologic approaches for the treatment of osteoporosis. METHODS: A literature search with PubMed was performed with the terms osteoporosis and pathophysiology and osteoporosis and treatment and limited to studies written in English that were published within the preceding 10 years. Given the large number of studies identified, we selectively reviewed those studies that contained primary data related to osteoporosis pathophysiology or osteoporosis pharmacologic treatments and references included within selected studies identified from abstract review. FINDINGS: Published studies have consistently reported that osteoporosis in older adults is caused by an imbalance of bone resorption in excess of bone formation. The dominant factor leading to bone loss in older adults appears to be gonadal sex steroid deficiency, with multiple genetic and biochemical factors, such as vitamin D deficiency or hyperparathyroidism, that may accelerate bone loss. Conditions that adversely affect growth and development may limit development of peak bone mass and accelerate subsequent bone loss. Studies of bone microarchitecture have shown that trabecular bone loss begins in the third decade of life, before gonadal sex steroid deficiency develops, whereas cortical loss typically begins in the sixth decade, about the time of menopause in women and about the same age in men. Antiresorptive agents for the treatment of osteoporosis act primarily by limiting osteoclast activity, whereas osteoanabolic agents, such as teriparatide, act primarily by stimulating osteoblastic bone formation. Clinical investigation of new compounds for the treatment of osteoporosis is mainly directed to those that stimulate bone formation or differentially decrease bone resorption more than bone formation. Therapies for osteoporosis are associated with adverse effects, but in patients at high risk of fracture, the benefits generally far outweigh the risks. IMPLICATIONS: Current osteoporosis therapies mitigate or reverse the loss of bone associated with age-related decreases of gonadal sex steroids, increase bone strength, and reduce fracture risk. With improved knowledge of the pathophysiology of osteoporosis, new targets for therapeutic intervention have been identified. Clinical investigations of potential new treatments for osteoporosis are primarily directed to stimulating osteoblastic bone formation or to modulating the balance of bone resorption and formation in ways that improve bone strength.

13 Review Anti-sclerostin antibodies: utility in treatment of osteoporosis. 2014

Clarke, Bart L. ·Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Department of Medicine, College of Medicine, Mayo Clinic, Rochester, MN, United States. Electronic address: Clarke.Bart@mayo.edu. ·Maturitas · Pubmed #24842796.

ABSTRACT: Monoclonal antibodies to molecular targets important for bone formation and bone resorption are being investigated for treatment of postmenopausal osteoporosis. Postmenopausal osteoporosis is characterized by increased bone turnover, with bone resorption typically exceeding bone formation. These pathophysiological changes cause decreased bone mineral density and disruption of bone microarchitecture which lead to low-trauma fractures. Sclerostin is a glycoprotein inhibitor of osteoblast Wnt signaling produced by osteocytes that has been recognized as a new target for therapeutic intervention in patients with osteoporosis. Sclerostin was first recognized when disorders with inactivating mutations of the sclerostin gene SOST were found to be associated with high bone mass. These observations suggested that inhibitors of sclerostin might be used to increase bone mineral density. Romosozumab (AMG 785) is the first humanized anti-sclerostin monoclonal antibody that has been demonstrated to increase bone formation. This investigational monoclonal antibody, and blosozumab, another investigational anti-sclerostin antibody, have osteoanabolic properties with the potential to improve clinical outcomes in patients with osteoporosis. Similar to preclinical animal studies with sclerostin antibodies, initial clinical studies have shown that romosozumab increases bone formation and BMD. Further evaluation of the efficacy and safety of this agent in a large phase III controlled study is awaited. Phase I clinical trial data have recently been published with blosozumab. These novel interventions appear to be promising agents for the treatment of osteoporosis.

14 Review Osteoporosis prevention, screening, and treatment: a review. 2014

Kling, Juliana M / Clarke, Bart L / Sandhu, Nicole P. ·1 Department of Internal Medicine, Mayo Clinic Hospital , Phoenix, Arizona. ·J Womens Health (Larchmt) · Pubmed #24766381.

ABSTRACT: Osteoporosis, defined as low bone mass leading to increased fracture risk, is a major health problem that affects approximately 10 million Americans. The aging U.S. population is predicted to contribute to as much as a 50% increase in prevalence by 2025. Although common, osteoporosis can be clinically silent, and without prevention and screening, the costs of osteoporotic fracture-related morbidity and mortality will burden the U.S. healthcare system. This is a particularly relevant concern in the context of diminishing health care resources. Dual-energy X-ray absorptiometry is the most widely used, validated technique for measuring bone mineral density (BMD) and diagnosing osteoporosis. Cost-effectiveness analyses support early detection and treatment of high-risk patients with antiresorptive medications such as bisphosphonates. Moreover, optimization of bone health throughout life can help prevent osteoporosis. Current guidelines recommend screening women by age 65 years, but because no guidelines for screening intervals exist, decisions are made on the basis of clinical judgment alone. Although the recent literature provides some guidance, this review further explores current recommendations in light of newer evidence to provide more clarity on prevention, screening, and management strategies for patients with osteoporosis in the primary care setting.

15 Review Chronic Kidney Disease-Mineral and Bone Disorders (CKD-MBDs): What the Endocrinologist Needs to Know. 2014

Zangeneh, Farhad / Clarke, Bart L / Hurley, Daniel L / Watts, Nelson B / Miller, Paul D. ·Endocrine, Diabetes & Osteoporosis Clinic (EDOC), Sterling, VA. · Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota. · Mercy Health Osteoporosis and Bone Health Services, Cincinnati, Ohio. · Colorado Center for Bone Research, University of Colorado Health Sciences Center. ·Endocr Pract · Pubmed #24325991.

ABSTRACT: OBJECTIVE: Chronic kidney disease-mineral and bone disorders (CKD-MBDs) are a spectrum of abnormalities involving skeletal hormones, minerals, and bone turnover and mineralization. This paper focuses on what the endocrinologist should know about the assessment and management of skeletal and metabolic disorders in CKD-MBDs. METHODS: Relevant literature was reviewed to (1) define disturbances of minerals and hormones in the course of CKD; (2) identify the variable radiographic and histomorphometric changes of CKD-MBDs; (3) review the association among CKD-MBDs, vascular calcification, cardiovascular disease (CVD), and mortality; and (4) clarify issues in CKD-MBDs therapy. RESULTS: Assessment and treatment of CKD-MBDs is complicated by progressive changes in bone minerals and skeletal regulatory hormones as kidney function declines. CKD-MBDs are associated with fracture risk, and studies demonstrate that bone mineral density can be used to assess bone loss and fracture risk in these patients. Treatment of CKD-MBDs continues to evolve. Use of calcium, phosphate binders, vitamin D, vitamin D-receptor analogs, and drugs for osteoporosis and CKD-MBDs treatment are discussed in the context of safety and efficacy for patients with CKD. CONCLUSION: The association of CKD with bone disease, vascular calcification, CVD, and mortality mandates earlier recognition and treatment of CKD-MBDs. Osteoporosis as a distinct entity can be diagnosed and managed in CKD, although assessment of osteoporosis becomes challenging in late (stage 4 to 5) CKD. Diabetes is common in early (stage 1 to 3) CKD. In addition, 96% of all individuals identified as having CKD have early CKD. The endocrinologist is uniquely positioned to address and treat both diabetes and many of the metabolic and skeletal disorders associated with early CKD-MBDs, including osteoporosis.

16 Review New therapeutic targets for osteoporosis: beyond denosumab. 2012

Lim, Vivien / Clarke, Bart L. ·Mayo Clinic, 200 1st Street SW, Rochester, MN 55905, USA. ·Maturitas · Pubmed #22925430.

ABSTRACT: Treatments for osteoporosis over the last few decades have largely focused on antiresorptive agents that effectively prevent bone loss. Beginning with hormone therapy, a variety of new potent antiresorptive agents were developed, including oral and intravenous bisphosphonates, raloxifene and other selective estrogen receptor modulators, nasal spray calcitonin, and denosumab. Teriparatide and PTH 1-84 are the only approved anabolic agents to date that primarily build new bone density. A variety of new biologic agents that focus on molecular targets important for the stimulation of new bone formation are being developed. Cathepsin K inhibitors appear to have mixed antiresorptive and anabolic actions because they inhibit one of the major osteoclast digestive enzymes without suppressing bone formation, thereby leading to anabolic effects on bone. New biologic agents in clinical trials include anti-sclerostin and anti-dickkopf antibodies that stimulate the Wnt/β-catenin pathway in osteoblasts, leading to new bone formation. These new agents will effectively stimulate new bone formation by different mechanisms, leading to improved bone mineral density and reduced fractures.

17 Review Corticosteroid-induced osteoporosis: an update for dermatologists. 2012

Clarke, Bart L. ·Mayo Clinic School of Medicine, Rochester, MN, USA. Clarke.Bart@Mayo.edu ·Am J Clin Dermatol · Pubmed #22393910.

ABSTRACT: Long-term corticosteroid treatment is the most common secondary cause of bone loss. Patients treated with long-term corticosteroid therapy may develop osteopenia or osteoporosis, and many have fractures. It is difficult to predict which corticosteroid-treated patients will develop significant skeletal complications because of variability in the underlying diseases treated with corticosteroids, and because of variation in corticosteroid dose over time. Corticosteroid therapy causes an alteration in the ratio between osteoprotegerin (OPG) and receptor activator of nuclear factor κ B (RANK) ligand (RANKL), which leads to early increased bone resorption for the first 3-6 months, with long-term treatment leading primarily to suppression of bone formation. Recently published recommendations advise the use of bisphosphonates or teriparatide in high-risk patients, depending on fracture risk assessed by bone mineral density testing. This article gives an update of current knowledge regarding the pathophysiology, clinical presentation and evaluation, and prevention and treatment of patients with corticosteroid-induced osteoporosis.

18 Review Modulators of androgen and estrogen receptor activity. 2010

Clarke, Bart L / Khosla, Sundeep. ·Mayo Clinic, Rochester, MN, USA. ·Crit Rev Eukaryot Gene Expr · Pubmed #21395502.

ABSTRACT: This review focuses on significant recent findings regarding modulators of androgen and estrogen receptor activity. Selective androgen receptor modulators (SARMs) interact with androgen receptors (ARs), and selective estrogen receptor modulators (SERMs) interact with estrogen receptors (ERs), with variable tissue selectivity. SERMs, which interact with both ERб and ERв in a tissue-specific manner to produce diverse outcomes in multiple tissues, continue to generate significant interest for clinical application. Development of SARMs for clinical application has been slower to date because of potential adverse effects, but these diverse compounds continue to be investigated for use in disorders in which modulation of the AR is important. SARMs have been investigated mostly at the basic and preclinical level to date, with few human clinical trials published. These compounds have been evaluated mostly for application in different stages of prostate cancer to date, but they hold promise for multiple other applications. Publication of the large STAR and RUTH clinical trials demonstrated that the SERMs tamoxifen and raloxifene have interesting similarities and differences in tissues that contain ERs. Lasofoxifene, bazedoxifene, and arzoxifene are newer SERMs that have been demonstrated in clinical trials to more potently increase bone mineral density and lower serum cholesterol values than tamoxifen or raloxifene. Both SARMs and SERMs hold great promise for therapeutic use in multiple disorders in which tissue-specific effects are mediated by their respective receptors.

19 Review Physiology of bone loss. 2010

Clarke, Bart L / Khosla, Sundeep. ·Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, 200 1st Street Southwest, Rochester, MN 55905, USA. Clarke.Bart@Mayo.edu ·Radiol Clin North Am · Pubmed #20609887.

ABSTRACT: The physiology of bone loss in aging women and men is largely explained by the effects of gonadal sex steroid deficiency on the skeleton. In women, estrogen deficiency is the main cause of early rapid postmenopausal bone loss, whereas hyperparathyroidism and vitamin D deficiency are thought to explain age-related bone loss later in life. Surprisingly, estrogen deficiency also plays a dominant role in the physiology of bone loss in aging men. Many other factors contribute to bone loss in aging women and men, including defective bone formation by aging osteoblasts, impairment of the growth hormone/insulin-like growth factor axis, reduced peak bone mass, age-associated sarcopenia, leptin secreted by adipocytes, serotonin secreted by the intestine, and a long list of sporadic secondary causes. Further elucidation of the relative importance of each of these factors will lead to improved preventive and therapeutic approaches for osteoporosis.

20 Article Osteoporosis Management in the Era of COVID-19. 2020

Yu, Elaine W / Tsourdi, Elena / Clarke, Bart L / Bauer, Douglas C / Drake, Matthew T. ·Endocrine Unit, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA. · Department of Medicine III, Universitätsklinikum Dresden, Dresden, Germany. · Center for Healthy Aging, Universitätsklinikum Dresden, Dresden, Germany. · Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, MN, USA. · Department of Medicine, University of California, San Francisco, San Francisco, CA, USA. · Department of Epidemiology & Biostatistics, University of California, San Francisco, San Francisco, CA, USA. · Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA. ·J Bone Miner Res · Pubmed #32406536.

ABSTRACT: Osteoporosis is a chronic condition which reflects reduced bone strength and an associated increased risk for fracture. As a chronic condition, osteoporosis generally requires sustained medical intervention(s) to limit the risks for additional bone loss, compromise of skeletal integrity, and fracture occurrence. Further complicating this issue is the fact that the abrupt cessation of some therapies can be associated with an increased risk for harm. It is in this context that the COVID-19 pandemic has brought unprecedented disruption to the provision of healthcare globally, including near universal requirements for social distancing. In this Perspective, we provide evidence, where available, regarding the general care of patients with osteoporosis in the COVID-19 era, and provide clinical recommendations based primarily on expert opinion when data is absent. Particular emphasis is placed on the transition from parenteral osteoporosis therapies. It is hoped that these recommendations can be used to safely guide care for patients with osteoporosis until a return to routine clinical care standards is available.

21 Article Secondary Fracture Prevention: Consensus Clinical Recommendations from a Multistakeholder Coalition. 2020

Conley, Robert B / Adib, Gemma / Adler, Robert A / Åkesson, Kristina E / Alexander, Ivy M / Amenta, Kelly C / Blank, Robert D / Brox, William Timothy / Carmody, Emily E / Chapman-Novakofski, Karen / Clarke, Bart L / Cody, Kathleen M / Cooper, Cyrus / Crandall, Carolyn J / Dirschl, Douglas R / Eagen, Thomas J / Elderkin, Ann L / Fujita, Masaki / Greenspan, Susan L / Halbout, Philippe / Hochberg, Marc C / Javaid, Muhammad / Jeray, Kyle J / Kearns, Ann E / King, Toby / Koinis, Thomas F / Koontz, Jennifer Scott / Kužma, Martin / Lindsey, Carleen / Lorentzon, Mattias / Lyritis, George P / Michaud, Laura Boehnke / Miciano, Armando / Morin, Suzanne N / Mujahid, Nadia / Napoli, Nicola / Olenginski, Thomas P / Puzas, J Edward / Rizou, Stavroula / Rosen, Clifford J / Saag, Kenneth / Thompson, Elizabeth / Tosi, Laura L / Tracer, Howard / Khosla, Sundeep / Kiel, Douglas P. ·Center for Medical Technology Policy, Baltimore, MD, USA. · Osteoporosis Centre, Damascus, Syria. · McGuire VA Medical Center, Richmond, VA, USA. · Lund University and Skåne University Hospital, Lund, Scania, Sweden. · UConn School of Nursing, University of Connecticut, Storrs, CT, USA. · Department of Physician Assistant Studies, Mercyhurst University, Erie, PA, USA. · Department of Endocrinology, Metabolism and Clinical Nutrition, Medical College of Wisconsin, Milwaukee, WI, USA. · Garvan Institute of Medical Research, Darlinghurst, NSW, Australia. · UCSF Fresno, Fresno, CA, USA. · Department of Orthopaedics and Rehabilitation, University of Rochester Medical Center, Rochester, NY, USA. · Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA. · Division of Endocrinology, Diabetes, Metabolism, Nutrition, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA. · American Bone Health, Raleigh, NC, USA. · University of Southampton, Southampton, UK. · Department of Medicine, University of California, Los Angeles, CA, USA. · Department of Orthopaedic Surgery and Rehabilitation Medicine, University of Chicago Medicine, Chicago, IL, USA. · National Council on Aging, New York, NY, USA. · American Society for Bone and Mineral Research, Washington, DC, USA. · Science Department, International Osteoporosis Foundation, Nyon, Switzerland. · Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. · International Osteoporosis Foundation, Nyon, Switzerland. · Division of Rheumatology, University of Maryland School of Medicine and VA Maryland Health Care System, Baltimore, MD, USA. · Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, USA. · Prisma Health - Upstate (formerly Greenville Health System), Greenville, SC, USA. · US Bone and Joint Initiative, Rosemont, IL, USA. · Duke Primary Care Oxford, Oxford, NC, USA. · Orthopedics & Sports Medicine, Newton Medical Center, Newton, KS, USA. · Department of Family and Community Medicine, University of Kansas School of Medicine, Wichita, KS, USA. · 5th Department of Internal Medicine, University Hospital, Comenius University, Bratislava, Slovakia. · Bones, Backs and Balance, LLC, Bristol Physical Therapy, LLC, Bristol, CT, USA. · Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, Victoria, Australia. · Department of Geriatric Medicine, Sahlgrenska University Hospital, Mölndal, Sweden. · Geriatric Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · Hellenic Osteoporosis Foundation, Athens, Greece. · The University of Texas MD Anderson Cancer Center, Houston, TX, USA. · Nevada Rehabilitation Institute, Las Vegas, NV, USA. · Department of Medicine, McGill University, Montreal, Canada. · Department of Medicine, Warren Alpert Medical School, Brown University, Providence, RI, USA. · Department of Nutrition and Metabolic Disorders, Campus Bio-Medico University of Rome, Rome, Italy. · Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA. · HiROC Program/Rheumatology, Geisinger Health System, Danville, PA, USA. · Tufts University School of Medicine, Boston, MA, USA. · Maine Medical Center Research Institute, Portland, ME, USA. · Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, USA. · National Osteoporosis Foundation, Arlington, VA, USA. · Department of Orthopaedic Surgery and Sports Medicine, Children's National Hospital, Washington, DC, USA. · Center for Evidence and Practice Improvement, Agency for Healthcare Research and Quality, Rockville, MD, USA. · Harvard Medical School, Musculoskeletal Research Center, Marcus Institute for Aging Research, Hebrew SeniorLife, Boston, MA, USA. ·J Bone Miner Res · Pubmed #31538675.

ABSTRACT: Osteoporosis-related fractures are undertreated, due in part to misinformation about recommended approaches to patient care and discrepancies among treatment guidelines. To help bridge this gap and improve patient outcomes, the American Society for Bone and Mineral Research assembled a multistakeholder coalition to develop clinical recommendations for the optimal prevention of secondary fracture among people aged 65 years and older with a hip or vertebral fracture. The coalition developed 13 recommendations (7 primary and 6 secondary) strongly supported by the empirical literature. The coalition recommends increased communication with patients regarding fracture risk, mortality and morbidity outcomes, and fracture risk reduction. Risk assessment (including fall history) should occur at regular intervals with referral to physical and/or occupational therapy as appropriate. Oral, intravenous, and subcutaneous pharmacotherapies are efficacious and can reduce risk of future fracture. Patients need education, however, about the benefits and risks of both treatment and not receiving treatment. Oral bisphosphonates alendronate and risedronate are first-line options and are generally well tolerated; otherwise, intravenous zoledronic acid and subcutaneous denosumab can be considered. Anabolic agents are expensive but may be beneficial for selected patients at high risk. Optimal duration of pharmacotherapy is unknown but because the risk for second fractures is highest in the early post-fracture period, prompt treatment is recommended. Adequate dietary or supplemental vitamin D and calcium intake should be assured. Individuals being treated for osteoporosis should be reevaluated for fracture risk routinely, including via patient education about osteoporosis and fractures and monitoring for adverse treatment effects. Patients should be strongly encouraged to avoid tobacco, consume alcohol in moderation at most, and engage in regular exercise and fall prevention strategies. Finally, referral to endocrinologists or other osteoporosis specialists may be warranted for individuals who experience repeated fracture or bone loss and those with complicating comorbidities (eg, hyperparathyroidism, chronic kidney disease). © 2019 American Society for Bone and Mineral Research.

22 Article A Lot of Progress, With More to Be Done: A Response to NIH Pathways to Prevention Report "Research Gaps for Long-Term Drug Therapies for Osteoporotic Fracture Prevention". 2019

Leder, Benjamin Z / Clarke, Bart L / Shane, Elizabeth / Khosla, Sundeep / Kiel, Douglas P. ·Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. · Mayo Clinic College of Medicine, Rochester, MN, USA. · Columbia University College of Physicians and Surgeons, New York, NY, USA. · Harvard Medical School, Musculoskeletal Research Center, Marcus Institute for Aging Research, Hebrew SeniorLife, Boston, MA, USA. ·J Bone Miner Res · Pubmed #31237962.

ABSTRACT: The public health implications of osteoporosis are enormous but the disease remains underdiagnosed and undertreated. In October 2018, the National Institutes of Health (NIH) convened a Pathways to Prevention (P2P) Workshop entitled "Appropriate Use of Drug Therapies for Osteoporotic Fracture Prevention" designed to identify research gaps, suggest future research opportunities, and advance the field through an evidence-based assessment. By design, the P2P report focused on "gaps" in our knowledge base. Unfortunately, however, the report did not sufficiently acknowledge the current evidence that unequivocally demonstrates the therapeutic efficacy of existing pharmacologic therapies for osteoporosis, which has the potential to exacerbate the current crises in osteoporosis diagnosis and treatment. © 2019 American Society for Bone and Mineral Research.

23 Article Comprehensive Assessment of Osteoporosis and Bone Fragility with CT Colonography. 2016

Fidler, Jeff L / Murthy, Naveen S / Khosla, Sundeep / Clarke, Bart L / Bruining, David H / Kopperdahl, David L / Lee, David C / Keaveny, Tony M. ·From the Department of Radiology (J.L.F., N.S.M.), Division of Endocrinology (S.K., B.L.C.), and Division of Gastroenterology and Hepatology (D.H.B.), Mayo Clinic, 200 1st Ave SW, Rochester, MN 55902 · O.N. Diagnostics, Berkeley, Calif (D.L.K., D.C.L., T.M.K.) · and Departments of Mechanical Engineering and Bioengineering, University of California-Berkeley, Berkeley, Calif (T.M.K.). ·Radiology · Pubmed #26200602.

ABSTRACT: PURPOSE: To evaluate the ability of additional analysis of computed tomographic (CT) colonography images to provide a comprehensive osteoporosis assessment. MATERIALS AND METHODS: This Health Insurance Portability and Accountability Act-compliant study was approved by our institutional review board with a waiver of informed consent. Diagnosis of osteoporosis and assessment of fracture risk were compared between biomechanical CT analysis and dual-energy x-ray absorptiometry (DXA) in 136 women (age range, 43-92 years), each of whom underwent CT colonography and DXA within a 6-month period (between January 2008 and April 2010). Blinded to the DXA data, biomechanical CT analysis was retrospectively applied to CT images by using phantomless calibration and finite element analysis to measure bone mineral density and bone strength at the hip and spine. Regression, Bland-Altman, and reclassification analyses and paired t tests were used to compare results. RESULTS: For bone mineral density T scores at the femoral neck, biomechanical CT analysis was highly correlated (R(2) = 0.84) with DXA, did not differ from DXA (P = .15, paired t test), and was able to identify osteoporosis (as defined by DXA), with 100% sensitivity in eight of eight patients (95% confidence interval [CI]: 67.6%, 100%) and 98.4% specificity in 126 of 128 patients (95% CI: 94.5%, 99.6%). Considering both the hip and spine, the classification of patients at high risk for fracture by biomechanical CT analysis--those with osteoporosis or "fragile bone strength"--agreed well against classifications for clinical osteoporosis by DXA (T score ≤-2.5 at the hip or spine), with 82.8% sensitivity in 24 of 29 patients (95% CI: 65.4%, 92.4%) and 85.7% specificity in 66 of 77 patients (95% CI: 76.2%, 91.8%). CONCLUSION: Retrospective biomechanical CT analysis of CT colonography for colorectal cancer screening provides a comprehensive osteoporosis assessment without requiring changes in imaging protocols.

24 Article Validation of a CT-derived method for osteoporosis screening in IBD patients undergoing contrast-enhanced CT enterography. 2014

Weber, Nicholas K / Fidler, Jeff L / Keaveny, Tony M / Clarke, Bart L / Khosla, Sundeep / Fletcher, Joel G / Lee, David C / Pardi, Darrell S / Loftus, Edward V / Kane, Sunanda V / Barlow, John M / Murthy, Naveen S / Becker, Brenda D / Bruining, David H. ·Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. · Department of Radiology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. · 1] O.N. Diagnostics, Berkeley, California, USA [2] Departments of Mechanical Engineering and Bioengineering, UC Berkeley, California, USA. · Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota, USA. · O.N. Diagnostics, Berkeley, California, USA. ·Am J Gastroenterol · Pubmed #24445572.

ABSTRACT: OBJECTIVES: Osteoporosis and bone fractures are of particular concern in patients with inflammatory bowel disease (IBD). Biomechanical computed tomography (BCT) is an image-analysis technique that can measure bone strength and dual-energy X-ray absorptiometry (DXA)-equivalent bone mineral density (BMD) from noncontrast CT images. This study seeks to determine whether this advanced technology can be applied to patients with IBD undergoing CT enterography (CTE) with IV contrast. METHODS: Patients with IBD who underwent a CTE and DXA scan between 2007 and 2011 were retrospectively identified. Femoral neck BMD (g/cm(2)) and T-scores were measured and compared between DXA and BCT analysis of the CTE images. Femoral strength (Newtons) was also determined from BCT analysis. RESULTS: DXA- and CTE-generated BMD T-score values were highly correlated (R(2)=0.84, P<0.0001) in this patient cohort (n=136). CTE identified patients with both osteoporosis (sensitivity, 85.7%; 95% confidence interval (CI), 48.7-97.4 and specificity, 98.5%; 95% CI, 94.5-99.6) and osteopenia (sensitivity, 85.1%; 95% CI, 72.3-92.6 and specificity, 85.4%; 95% CI, 76.6-91.3). Of the 16 patients who had "fragile" bone strength by BCT (placing them at the equivalent high risk of fracture as for osteoporosis), 6 had osteoporosis and 10 had osteopenia by DXA. CONCLUSIONS: CTE scans can provide hip BMD, T-scores, and clinical classifications that are comparable to those obtained from DXA; when combined with BCT analysis, CTE can identify a subset of patients with osteopenia who have clinically relevant fragile bone strength. This technique could markedly increase bone health assessments in IBD patients already undergoing CTE to evaluate small bowel disease.

25 Unspecified Proceedings of the 2016 Santa Fe Bone Symposium: New Concepts in the Management of Osteoporosis and Metabolic Bone Diseases. 2017

Lewiecki, E Michael / Bilezikian, John P / Bukata, Susan V / Camacho, Pauline / Clarke, Bart L / McClung, Michael R / Miller, Paul D / Shepherd, John. ·New Mexico Clinical Research & Osteoporosis Center, Albuquerque, NM, USA. Electronic address: mlewiecki@gmail.com. · Columbia University College of Physicians and Surgeons, New York, NY, USA. · UCLA Orthopaedic Center, Santa Monica, CA, USA. · Loyola University Chicago Stritch School of Medicine, Maywood, IL, USA. · Mayo Clinic College of Medicine, Rochester, MN, USA. · Oregon Osteoporosis Center, Portland, OR, USA. · Colorado Center for Bone Research at Centura Health, Lakewood, CO, USA. · Department of Radiology and Biochemical Imaging, University of California, San Francisco, CA, USA. ·J Clin Densitom · Pubmed #28185765.

ABSTRACT: The Santa Fe Bone Symposium is an annual meeting of healthcare professionals and clinical researchers that details the clinical relevance of advances in knowledge of skeletal diseases. The 17th Santa Fe Bone Symposium was held in Santa Fe, New Mexico, USA, on August 5-6, 2016. The program included plenary lectures, oral presentations by endocrinology fellows, meet-the-professor sessions, and panel discussions, all aimed to provide ample opportunity for interactive discussions among all participants. Symposium topics included recent developments in the translation of basic bone science to patient care, new clinical practice guidelines for postmenopausal osteoporosis, management of patients with disorders of phosphate metabolism, new and emerging treatments for rare bone diseases, strategies to enhance fracture healing, and an update on Bone Health Extension for Community Healthcare Outcomes, using a teleconferencing platform to elevate the level of knowledge of healthcare professionals in underserved communities to deliver best practice care for skeletal diseases. The highlights and important clinical messages of the 2016 Santa Fe Bone Symposium are provided herein by each of the faculty presenters.