|
|
|
Osteoporosis
April 2-4, 1984
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?
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.
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.
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.
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.
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.
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.
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:
- 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.
- Clinical studies to determine whether the observed age, sex, and skeletal distribution
differences in osteoporosis reflect different mechanisms and predict different responses
to intervention.
- 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.
- 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.
- Studies to determine the optimal regimen of gonadal hormones for prevention of bone loss
and fracture.
- Studies to elucidate further the mechanisms of bone growth and remodeling, their local
and systemic regulation, and their alteration in osteoporosis.
- 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.
- William A. Peck, M.D. (Chairman)
- Simon Professor and Co-Chairman
- Department of Medicine
- Washington University School of Medicine
- Physician-in-Chief
- 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"
- Chairman
- 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
- Lyon FRANCE
- 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
- Lawrence E. Shulman, M.D., Ph.D. (Chairman)
- Director
- 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.
- Director
- 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
- Physician-in-Chief
- 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
- 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
|
