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National Institutes of Health
Consensus Development Conference Statement
April 2-4, 1984

Conference artwork depicting a series of pelvis and femur bones, each one with a little less density.

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus, keep in mind that new knowledge is inevitably accumulating through medical research.

This statement was originally published as: Osteoporosis. NIH Consens Dev Conf Consens Statement 1984 Apr 2-4; 5(3):1-6.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Osteoporosis. NIH Consens Dev Conf Consens Statement Online 1984 Apr 2-4 [cited year month day]; 5(3):1-6.


Osteoporosis is a major underlying cause of bone fractures in postmenopausal women and older persons in general. It is a condition in which bone mass decreases, causing bones to be more susceptible to fracture. A fall, blow, or lifting action that would not bruise or strain the average person can easily cause one or more bones to break in a person with severe osteoporosis.

Medical practitioners and patients alike are concerned with the optimum approach to the treatment and prevention of osteoporosis. The appropriate timing and proper use of agents, such as calcium, vitamin D, estrogens, and fluorides, as well as the role of exercise are issues that have generated major research efforts and considerable controversy.

In an effort to resolve some of the questions surrounding these issues, the National Institutes of Health convened a Consensus Development Conference on Osteoporosis on April 2-4, 1984. After a day and a half of presentations by experts in the field, a consensus panel including representatives of orthopaedics, endocrinology, gynecology, rheumatology, epidemiology, nutrition, biochemistry, family medicine, and the general public considered the evidence and agreed on answers to the following key questions:

  • What is osteoporosis?
  • What are the clinical features of osteoporosis, and how is it detected?
  • Who is at risk for developing osteoporosis?
  • What are the possible causes of osteoporosis?
  • How can osteoporosis be prevented and treated?
  • What are the directions for future research?


Panel's Conclusions

Osteoporosis is a major public health problem. Although all bones are affected, fractures of the spine, wrist, and hip are typical and most common. The risk of developing osteoporosis increases with age and is higher in women than in men and in whites than in blacks. Its cause appears to reside in the mechanisms underlying an accentuation of the normal loss of bone, which follows the menopause in women and occurs in all individuals with advancing age. There are no laboratory tests for defining individuals at risk or those with mild osteoporosis. The diagnosis of primary osteoporosis is established by documentation of reduced bone density or mass in a patient with a typical fracture syndrome after exclusion of known causes of excessive bone loss. Prevention of fracture in susceptible patients is the primary goal of intervention. Strategies include assuring estrogen replacement in postmenopausal women, adequate nutrition including an elemental calcium intake of 1,000-1,500 mg a day, and a program of modest weight-bearing exercise. There is great need for additional research on understanding the biology of human bone, defining individuals at special risk, and developing safe, effective, low-cost strategies for fracture prevention.

What Is Osteoporosis?

Primary osteoporosis is an age-related disorder characterized by decreased bone mass and by increased susceptibility to fractures in the absence of other recognizable causes of bone loss.

Osteoporosis is a common condition affecting as many as 15-20 million individuals in the United States. About 1.3 million fractures attributable to osteoporosis occur annually in people age 45 and older. Among those who live to be age 90, 32 percent of women and 17 percent of men will suffer a hip fracture, most due to osteoporosis. The cost of osteoporosis in the United States has been estimated at $3.8 billion annually.

Bone is composed of a collagen-rich organic matrix impregnated with mineral--largely calcium and phosphate. Two major forms of bone exist. Compact cortical bone forms the external envelopes of the skeleton; trabecular or medullary bone forms plates that traverse the internal cavities of the skeleton. The proportions of cortical and trabecular bone vary at different sites. Vertebral bodies contain predominantly trabecular bone, while the proximal femur contains predominantly cortical bone. The responses of the two forms of bone to metabolic influences and their susceptibility to fracture differ.

Bone undergoes continuous remodeling (turnover) throughout life. Osteoclasts resorb bone in microscopic cavities; osteoblasts then reform the bone surfaces, filling the cavities. Normally, bone resorption and formation are linked closely in space, time, and degree. Mechanical and electrical forces, hormones, and local regulatory factors influence remodeling.

Peak bone mass is achieved at about 35 years of age for cortical bone and earlier for trabecular bone. Sex, race, nutrition, exercise, and overall health influence peak mass. Bone mass is approximately 30 percent higher in men than in women and approximately 10 percent higher in blacks than in whites. In each group, bone mass varies among individuals.

After reaching its peak, bone mass declines throughout life due to an imbalance in remodeling. Bones lose both mineral and organic matrix but retain their basic organization. In women, bone mass decreases rapidly for 3 to 7 years after menopause. Bone loss also is enhanced in a variety of diseases.

Women have more fractures than men, and whites have more fractures than blacks. Three factors determine the likelihood of fractures: first, the magnitude, direction, and duration of the applied force; second, the dissipation of that force by muscle contraction and soft tissue absorption; and finally, bone strength. Injuries are more frequent and energy dissipation diminishes with advancing age. Reduction in bone mass is the most important reason for the increased frequency of bone fractures in postmenopausal women and in the elderly.

Classifying primary osteoporosis into clinical, histological, or biochemical subsets may be useful from the standpoints of etiology, prevention, and treatment. There is clinical and histological evidence for different subsets. Vertebral fractures occur most frequently in women aged 55 to 75 with accelerated loss of trabecular bone. Hip fractures occur most frequently in older men and women who slowly have lost both cortical and trabecular mass. Bone biopsies from some individuals with primary osteoporosis show high turnover rates; biopsies from others show low or intermediate rates of turnover.

What Are the Clinical Features of Osteoporosis, and How Is It Detected?

The clinical manifestations of osteoporosis include fractures and their vertebral bodies, the neck and intertrochanteric regions of the femur, and the distal radius. Osteoporotic individuals may fracture any bone more easily than their nonosteoporotic counterparts.

Vertebral compression fractures occur more frequently in women than in men, and typically affect T8-L3. These fractures may develop during routine activities, such as bending, lifting, or rising from a chair or bed. Immediate, severe, local back pain often results. Pain usually subsides within several months. Some individuals experience persistent pain due to altered spinal mechanics. In contrast, some vertebral fractures do not cause pain. Gradual asymptomatic vertebral compression may be detected only upon radiographic examination. Loss of body height and/or the development of kyphosis may be the only signs of multiple vertebral fractures. Discomfort, debility, and, rarely, pulmonary dysfunction may accompany thoracic shortening. Abdominal symptoms may include early satiety, bloating, and constipation.

Hip fractures are another important manifestation of osteoporosis. The affected population tends to be older and the sex distribution more even than is the case in vertebral fracture. Acute complications--hospitalization, depression, and mechanical failure of the surgical procedure--are common. Most patients fail to recover normal activity, and mortality within 1 year approaches 20 percent. Distal radial fractures limit use of the extremity for 4 to 8 weeks, although long-term disability is uncommon. These fractures promote fear of loss of independent living, fear of additional falls and fractures, and depression.

Detection of low skeletal mass and/or a fracture after minor trauma should alert the physician to the presence of metabolic bone disease. The physician should evaluate further to exclude osteomalacia, hyperparathyroidism, hyperthyroidism, multiple myeloma, metastatic disease, syndromes of glucocorticoid excess, and other causes of secondary osteoporosis. No blood or urine test establishes specifically the diagnosis of primary osteoporosis, but such tests may exclude secondary causes.

Several noninvasive methods are available to evaluate bone density. These vary widely in cost, availability, and radiation dose. Standard radiographs of the spine are most widely available. Roentgenograms are, however, insensitive indicators of bone loss, since bone density must be decreased by at least 20 to 30 percent before the reduction can be appreciated. Characteristic abnormalities on standard roentgenograms are sufficient for establishing the diagnosis of osteoporosis if secondary causes are excluded clinically or radiographically. If the spine film is not diagnostic but clinical suspicion is high, a variety of other procedures may be indicated. These include radiogrammetry for measurement of cortical thickness, photodensitometry, the Singh Index of femoral trabecular pattern, single and dual photon absorptiometry, neutron activation, Compton scattering, and single and dual energy computed tomography. Use of these techniques will depend on their availability, cost, and further studies of their discriminatory capabilities and sensitivity.

With histomorphometry, usually performed on a bone biopsy from the iliac crest, bone mass can be evaluated and osteomalacia and certain forms of secondary osteoporosis excluded. Bone biopsy is safe but requires specialized equipment and expert analysis that are not widely available.

Who Is At Risk for Developing Osteoporosis?

The correlation of osteoporosis with the following factors is well documented. Bone mass declines with age in all people and is related to sex, race, menopause, and body weight-for-height.

Women are at higher risk than men in that they have less bone mass and, for several years following natural or induced menopause, the rate of bone mass decline is accelerated. Early menopause is one of the strongest predictors for the development of osteoporosis. White women are at much higher risk than black women, and white men are at higher risk than black men. Women who are underweight also have osteoporosis more often than overweight women. Cigarette smoking may be an additional predictor of risk. Calcium deficiency has been implicated in the pathogenesis of this disease.

Immobilization and prolonged bed rest produce rapid bone loss, while exercise involving weight bearing has been shown both to reduce bone loss and to increase bone mass. The optimal type and amount of physical activity that will prevent osteoporosis have not been established. Exercise sufficient to induce amenorrhea in young women may lead to decreased bone mass.

The relationship of osteoporosis to hereditary and dietary factors, such as alcohol, vitamins A and C, magnesium, and protein, is less firmly established. Some of these factors may act indirectly through their effect on calcium metabolism or body weight.

What Are the Possible Causes of Osteoporosis?

Because primary osteoporosis is characterized by decreased bone mass, the causes of the disorder must be sought among the factors that determine the quantity and quality of bone, including the magnitude of maximum bone mass at maturity and the rate of bone loss with aging.

Complex cellular, physiologic, and metabolic factors may underlie the pathogenesis of osteoporosis. Discrete cell types, anatomically and functionally connected, are continually renewed and maintain the complex skeletal tissue. Several systemic hormones and an increasingly recognized number of local (paracrine) factors regulate bone cell activity. Diet, as well as intestinal and renal function, influences mineral ion homeostasis needed to maintain the skeleton. The formation and resorption of bone and their coupling also are modified by external physical forces such as those generated by body weight and exercise.

Osteoporosis is histologically, biochemically, and kinetically heterogeneous; rapid bone turnover or reduced rates of bone formation have been documented in patients with primary osteoporosis. Multiple etiologies would not be surprising, considering the complex factors regulating normal bone metabolism. Among the many possible etiologies of primary osteoporosis, current data point to two probable causes: deficiency of estrogen and deficiency of calcium. Rapid bone loss often accompanies menopause, and premature osteoporosis follows bilateral oophorectomy. Estrogen replacement prevents bone loss in both conditions. The following observations support a causal relationship between calcium deficiency and osteoporosis: Calcium deficiency in experimental animals causes osteoporosis; a low calcium intake is common among the elderly in the United States; and calcium supplementation reduces bone loss.

How Can Osteoporosis Be Prevented and Treated?

Physicians must emphasize measures that retard or halt the progress of osteoporosis before irreversible structural defects occur. The mainstays of prevention and management of osteoporosis are estrogen and calcium; exercise and nutrition may be important adjuncts.

Estrogen replacement therapy is highly effective for preventing osteoporosis in women. Estrogen reduces bone resorption and retards or halts postmenopausal bone loss. Case-controlled studies have shown a substantial reduction in hip and wrist fractures in women whose estrogen replacement was begun within a few years of menopause. Studies also suggest that estrogen reduces the rate of vertebral fractures. Even when started as late as 6 years after menopause, estrogen prevents further loss of bone mass but does not restore it to premenopausal levels. Oral estrogen protects at low doses, such as 0.625 mg of conjugated equine estrogen, (25 micrograms of mestranol and 2 mg of estradiol valcrate daily exemplify other protective regimens reviewed by the panel).

All of the above data on efficacy are based almost exclusively on studies in white women. Therefore, the following recommendations on therapy for osteoporosis pertain to that group. Cyclic estrogen therapy should be given to women whose ovaries are removed before age 50 in whom there are no specific contraindications. Women who have had a natural menopause also should be considered for cyclic estrogen replacement if they have no contraindications and if they understand the risks and agree to regular medical evaluations. The duration of estrogen therapy need not be limited. There is no convincing evidence that initiating estrogen therapy in elderly women will prevent osteoporosis. The decision to treat women of other racial backgrounds should be determined on a case-by-case basis.

Estrogen-associated endometrial cancer is usually manifested at an early stage and is rarely fatal when managed appropriately. The bulk of evidence indicates that estrogen use is not associated with an increased risk of breast cancer. Adding a progestogen probably reduces the risk of endometrial cancer, but there is little information about the safety of long-term combined estrogen and progestogen treatment in postmenopausal women. Younger patients receiving progestogens in oral contraceptives experienced an increased risk of hypertension and cardiovascular disease. Some progestogens may blunt or eliminate the favorable effects of estrogen on lipoproteins.

Until more data on risks and benefits are available, physicians and patients may prefer to reserve estrogen (with or without progestogen) therapy for conditions that confer a high risk of osteoporosis, such as the occurrence of premature menopause.

The usual daily intake of elemental calcium in the United States, 450 mg to 550 mg, falls well below the National Research Council's (NRC) recommended dietary allowance (RDA) of 800 mg; the RDA is designed to meet the needs of approximately 95 percent or more of the population. Calcium metabolic balance studies indicate a daily requirement of about 1,000 mg of calcium for premenopausal and estrogen-treated women. Postmenopausal women who are not treated with estrogen require about 1,500 mg daily for calcium balance. Therefore, the RDA for calcium is evidently too low, particularly for postmenopausal women and may well be too low in elderly men. In some studies, high dietary calcium suppresses age-related bone loss and reduces the fracture rate in patients with osteoporosis. It seems likely that an increase in calcium intake to 1,000 to 1,500 mg a day beginning well before the menopause will reduce the incidence of osteoporosis in postmenopausal women. Increased calcium intake may prevent age-related bone loss in men as well.

The major sources of calcium in the U.S. diet are milk and dairy products. Each 8 ounce glass (240 ml) of milk contains 275-300 mg calcium. Skim or low fat milk is preferred to minimize fat intake. For those unable to take 1,000 to 1,500 mg calcium by diet, supplementation with calcium tablets is recommended, with special attention to their elemental calcium content.

Levels of calcium intake greater than those recommended herein could cause urinary tract stones in susceptible people. Anyone with a history of kidney stones should only undertake calcium supplementation with the guidance of a physician.

Normal levels of vitamin D are required for optimal calcium absorption. The requirement for vitamin D increases with age. Persons who do not receive adequate daily sunlight exposure, such as those confined to home or to a nursing facility, are at special risk for vitamin D deficiency. Vitamin D has dangerous effects at high doses. Although the toxic dose varies among individuals, toxicity has occurred at levels as low as 2,000-5,000 international units [I.U.] daily. No one should consume more than 15 to 20 micrograms (600 to 800 units, twice the daily RDA) without a doctor's recommendation.

Inactivity leads to bone loss. Some recent studies suggest that weightbearing exercise may reduce bone loss. Modest weight-bearing exercise, such as walking, is recommended.

Several agents and modalities of treatment are currently under investigation, but their efficacy and/or safety have not been established. These include sodium fluoride, calcitriol, calcitonin, weakly androgenic anabolic steroids, thiazides, bisphosphonates, the 1-34 fragment of parathyroid, and "ADFR", a complex system of several drugs. Sodium fluoride, in association with a high calcium intake, may have a role to play in patients afflicted with severe osteoporosis, but its efficacy and safety are unproven; prospective studies are now under way.

Strategies to prevent falls are important in elderly patients who may fall frequently for a variety of reasons, such as from effects of drugs. Specific environmental interventions can minimize home hazards that increase the chances of falling.

Physicians treating fractures in osteoporotic patients should recognize the benefits of rapid return to function and avoidance of prolonged immobilization.

What Are the Directions for Future Research?

Future research in osteoporosis should approach the currently unanswered basic research questions concerning the development and maintenance of bone as a tissue. At the same time, there is great need for clinical and epidemiological research to further explore and extend the current potential for practical prevention and treatment of the disease. A deeper knowledge of factors controlling bone cell activity and regulation of bone mineral and matrix formation and remodeling should contribute ultimately to our understanding of the etiology of osteoporosis. This understanding will permit a more rational choice and evaluation of therapies, even as current treatments are evaluated clinically.

The panel recommends:

  1. Observational and epidemiological studies to determine the impact of multiple demographic and behavioral factors on bone mass and fracture frequency. Such studies could be conducted by appropriate additions to existing population-based studies.
  2. Clinical studies to determine whether the observed age, sex, and skeletal distribution differences in osteoporosis reflect different mechanisms and predict different responses to intervention.
  3. Studies to develop accurate, safe, inexpensive methods for determining the level of risk for osteoporosis in an individual, to establish early diagnosis, and to assess the clinical course of the disease.
  4. Studies to develop safe, effective, low-cost strategies which might be applicable to populations at large for maximizing peak bone mass, minimizing bone loss, and preventing fractures.
  5. Studies to determine the optimal regimen of gonadal hormones for prevention of bone loss and fracture.
  6. Studies to elucidate further the mechanisms of bone growth and remodeling, their local and systemic regulation, and their alteration in osteoporosis.
  7. Studies to understand alterations in the structure and biomechanical properties of bone in osteoporosis and the relationship of these alterations to the mechanisms and management of fractures.

 Consensus Development Panel
William A. Peck, M.D. (Chairman)
Simon Professor and Co-Chairman
Department of Medicine
Washington University School of Medicine
The Jewish Hospital of St. Louis
St. Louis, Missouri
Elizabeth Barrett-Connor, M.D.
Professor and Chair
Department of Community and Family Medicine
University of California, San Diego
San Diego, California
Joseph A. Buckwalter, M.D.
Associate Professor
Department of Orthopaedic Surgery
University of Iowa Hospitals and Clinics
Iowa City, Iowa
R. Don Gambrell, Jr., M.D.
Clinical Professor of Endocrinology and Obstetrics and Gynecology
Department of Endocrinology
Medical College of Georgia
Augusta, Georgia
Bevra H. Hahn, M.D.
Professor of Medicine
Chief, Division of Rheumatology
Department of Medicine
UCLA-Center for Health Sciences
Los Angeles, California
Ralph S. Paffenbarger, Jr., M.D., Dr. P.H.
Visiting Professor of Epidemiology
Harvard School of Public Health
Boston, Massachusetts
John T. Potts, Jr., M.D.
Chief of the General Medical Services
Massachusetts General Hospital
Jackson Professor of Clinical Medicine
Richard S. Rivlin, M.D.
Chief, Nutrition Service
Memorial Sloan-Kettering Cancer Center
Professor of Medicine and Chief Nutrition Division
New York Hospital-Cornell Medical Center
New York, New York
Gideon A. Rodan, M.D., Ph.D.
Professor and Head
Department of Oral Biology
University of Connecticut Health Center
Farmington, Connecticut
Paula H. Stern, Ph.D.
Professor of Pharmacology
Northwestern University Medical and Dental Schools
Chicago, Illinois
Barbara Warden
Executive Director
National Consumers League
Washington, D.C.
Barbara N. W. Weissman, M.D.
Associate Professor of Radiology
Harvard Medical School
Director of Skeletal Radiology
Brigham and Women's Hospital
Boston, Massachusetts
G. Donald Whedon, M.D.
Adjunct Professor of Medicine (Endocrinology)
Department of Medicine
UCLA-Center for Health Sciences
Los Angeles, California
J. Jerome Wildgen, M.D.
Department of Family Medicine
University of Washington
Kalispell, Montana


Louis V. Avioli, M.D.
"Bone Metabolism and Calcium"
Shoenberg Professor of Medicine
Washington University School of Medicine
Jewish Hospital of St. Louis
St. Louis, Missouri
Ernesto Canalis, M.D.
"Local Skeletal Factors in Osteoporosis"
Associate Professor of Medicine
University of Connecticut School of Medicine
Director of Research Laboratory
St. Francis Hospital and Medical Center
Hartford, Connecticut
Charles H. Chesnut III, M.D.
"Noninvasive Techniques in the Diagnosis of Osteoporosis"
Associate Professor of Medicine and Radiology
Division of Nuclear Medicine
University of Washington School of Medicine
Seattle, Washington
Claus Christiansen, M.D.
"Estrogen/Progestogen as a Prophylactic Treatment of Postmenopausal Osteoporosis"
Department of Clinical Chemistry
University of Copenhagen
Glostrup Hospital
Glostrup DENMARK
Leonard Deftos, M.D.
"Calcitonin and Parathyroid Hormone in Osteoporosis"
Professor of Medicine
University of California, San Diego
Chief, Endocrine Section
San Diego Veterans Administration Medical Center
La Jolla, California
J. Chris Gallagher, M.D.
"The Effect of Calcitoriol on Patients with Postmenopausal Osteoporosis with Special Reference to Fracture Frequency"
Associate Professor of Medicine
Creighton University School of Medicine
St. Joseph Hospital
Omaha, Nebraska
Ralph S. Goldsmith, M.D.
"Vitamin D and Osteoporosis"
Chief of Staff
Veterans Administration Medical Center, San Francisco
Professor of Medicine and Associate Dean
University of California, San Francisco
San Francisco, California
Robert P. Heaney, M.D.
"Role of Calcium in Pathogenesis, Prophylaxis, and Treatment of Osteoporosis"
Vice President for Health Sciences
Creighton University
Omaha, Nebraska
Patrick Irvine, M.D.
"Osteoporosis: A Geriatric Perspective"
Director, Program on Geriatric Medicine
Department of Medicine
St. Paul-Ramsey Medical Center
University of Minnesota
Minneapolis, Minnesota
C. Conrad Johnston, Jr., M.D.
"Identification of Population Susceptible to Osteoporosis"
Professor of Medicine
Director, Division of Endocrinology and Metabolism
Indiana University School of Medicine
Indianapolis, Indiana
Jennifer L. Kelsey, Ph.D.
"Osteoporosis: Prevalence and Incidence"
Professor of Public Health (Epidemiology)
Columbia University
New York, New York
Joseph M. Lane, M.D.
"Osteoporosis: Orthopaedic Perspectives"
Professor of Surgery
Cornell Medical School
Chief, Metabolic Bone Disease Unit
The Hospital for Special Surgery
New York, New York
Ronald E. LaPorte, Ph.D.
"Physical Activity and Osteoporosis"
Associate Professor
Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Robert Lindsay, M.B.Ch.B., Ph.D., M.R.C.P.
"The Role of Estrogen in the Development of Osteoporosis"
Professor of Clinical Medicine
College of Physicians and Surgeons
Columbia University
Director of Research Helen Hayes Hospital
West Haverstraw, New York
Pierre J. Meunier, M.D.
"Diagnosis Value of Bone Histomorphometry and Biochemistry in Osteoporosis"
Professor of Medicine
INSERM -- Unit 234 Faculty A. Carrel
A. Michael Parfitt, M.D., M.B., B.Chir.
"Definition of Osteoporosis: Age-Related Loss of Bone and Its Relationship to Increased Fracture Risk"
Director, Bone and Mineral Research Laboratory
Henry Ford Hospital
Detroit, Michigan
Lawrence G. Raisz, M.D.
"Management of Osteoporsis: Endocrinologic Perspective"
Professor of Medicine
University of Connecticut Health Center
Farmington, Connecticut
B. Lawrence Riggs, M.D.
"Treatment of Osteoporosis with Sodium Fluoride and by Other Regimens That Increase Bone Mass"
Professor of Medicine
Mayo Medical School
Chairman Division of Endocrinology and Metabolism
Mayo Clinic and Foundation
Rochester, Minnesota
William W. Scott, Jr., M.D.
"Osteoporosis-Related Fracture Syndromes"
Assistant Professor of Radiology
Chief, Section of Bone Radiology
The Johns Hopkins Hospital
Baltimore, Maryland

Planning Committee

Lawrence E. Shulman, M.D., Ph.D. (Chairman)
Division of Arthritis, Musculoskeletal and Skin Diseases
National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Michael J. Bernstein
Director of Communications
Office of Medical Applications of Research
Office of the Director
National Institutes of Health
Bethesda, Maryland
Jacob A. Brody, M.D.
Associate Director
Epidemiology, Demography, and Biometry Program
National Institute on Aging
National Institutes of Health
Bethesda, Maryland
Stephen L. Gordon, Ph.D.
Musculoskeletal Diseases Program
Division of Arthritis, Musculoskeletal and Skin Diseases
National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland
Patrick J. Kelly, M.D.
Professor of Orthopaedic Surgery
Mayo Clinic
Rochester, Minnesota
Stephen M. Krane, M.D.
Chief, Arthritis Unit
Massachusetts General Hospital
Boston, Massachusetts
Fitzhugh Mullan, M.D.
Chief Medical Officer
Office of Medical Applications of Research
Office of the Director
National Institutes of Health
Bethesda, Maryland
William A. Peck, M.D.
Simon Professor and Co-Chairman
Department of Medicine
Washington University School of Medicine
The Jewish Hospital of St. Louis
St. Louis, Missouri
Lawrence G. Raisz, M.D.
Professor of Medicine
University of Connecticut Health Center
Farmington, Connecticut
Barbara A. Weldon
Information Specialist/Writer
Office of Health Research Reports
National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases
National Institutes of Health
Bethesda, Maryland

Conference Sponsors

National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases
Lester B. Salans, M.D. Director
Office of Medical Applications of Research
J. Richard Crout, M.D. Director

Supplemental Information for NIH Consensus Statement on Osteoporosis

Since the NIH Consensus Statement on Osteoporosis was issued, additional information has become available that supplements the original statement. This supplemental information may be obtained from the following sources:

  • Report from a consensus development conference held in Hong Kong April 1-2, 1993, in conjunction with the Fourth International Symposium on Osteoporosis, NIH Consensus Development Program Information Center, 1-888-NIH-CONSENSUS
  • Assorted publications on osteporosis, National Institute of Arthritis and Musculoskeletal and Skin Diseases Clearinghouse, Box AMS, 9000 Rockville Pike, Bethesda, MD 20892

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