Risk Assessment For Osteoporosis

John A. Grisnik, M.D., and Audrey M. Hodge, M.D.
John A. Grisnik, M.D., is a Clinical Assistant Professor, Department of Community
Health and Family Medicine, University of Florida Health Science Center / Jacksonville.
Audrey M. Hodge, M.D., is a Third Year Family Practice Resident, Department of Community
Health and Family Medicine, University of Florida Health Science Center / Jacksonville.

Introduction And Overview

Osteoporosis is a systemic disease characterized by low bone mass and microarchitectural deterioration of bone tissue that renders bone more susceptible to fracture.1 The risk of developing osteoporosis depends on the magnitude of peak bone mass, overall bone strength, and the rate of bone loss.2 Normal bone tissue exists in a state of constant turnover, called "remodeling". This process involves the resorption of small portions of bone at many sites in the skeleton by bone cells called osteoclasts. Activation of another set of bone cells called osteoblasts results in the replacement of the resorbed portions of bone by new bone formation.1 Remodeling is controlled by local chemical mediators whose production is influenced by systemic hormones, estrogen, and vitamin D.3 New bone formation does not exactly match resorption, resulting in a slight annual bone loss after peak bone mass is obtained. This bone loss begins at about twenty-five (25) years of age and progresses at an annual rate of 0.3% - 0.5% for women and 0.2% - 0.5% for men. This results in a lifetime loss of 30 to 40% of skeletal bone mass for women and 20 to 30% for men.4

The lifetime risk of osteoporotic fracture in fifty-year-old women and men is estimated to be 39.7% and 13.1% respectively. Twenty-five percent of patients who fracture their hip require some degree of long-term care, and 50,000 deaths annually are attributed to hip fracture in our country. Although men are less susceptible to osteoporotic hip fracture than women, the mortality rate for men is 21% vs. 8% for women. In the United States, the annual cost of hip fracture alone is estimated to be 10 billion dollars.1

Risk Assessment

Osteoporosis can be considered a "silent" risk factor for fracture, just as hypertension is for stroke. Osteoporosis is preventable and treatable, but there may be no warning signs until fracture occurs. The challenge to physicians is to recognize patients at risk for the development of osteoporosis, to diagnose the condition, and to proceed with treatment in order to prevent fracture. Numerous, well-recognized risk factors exist for osteoporosis that aid the physician in early recognition of this disease.

The "typical" osteoporosis profile is well known: a small-boned, petite woman of northern European ancestry who is post-menopausal, and relatively inactive with a low calcium containing diet. Unfortunately, this profile only identifies 30 to 40% of patients with osteoporosis.3 Physicians must expand their perception of the "typical" osteoporotic patient in order to effectively detect osteoporosis early.

Risk factors for osteoporosis may be classified as nonmodifiable and modifiable (Table 1).5 Please note that "poor health, frailty" is on both lists, since these factors may or may not be modifiable. A brief discussion of some of the nonmodifiable risk factors follows.

Table 1. Risk Factors For Osteoporotic Fracture

Nonmodifiable

Potentially modifiable

  • Personal history of fracture as an adult
  • History of fracture in first-degree relative
  • Caucasian race
  • Advanced age
  • Gender
  • Dementia
  • Poor health/frailty
  • Current cigarette smoking
  • Low body weight (<127 lbs.)
  • Estrogen deficiency:
  • Early menopause (<age 45) or bilateral ovariectomy
  • Prolonged premenopausal amenorrhea (>1 year)

 

  • Low calcium intake (lifelong)
  • Alcoholism
  • Caffeine
  • Impaired eyesight despite adequate correction
  • Recurrent falls
  • Inadequate physical activity
  • Poor health/frailty

Nonmodifiable Risk Factors For Osteoporosis

Personal History of Fracture

The finding of one compression fracture on x-ray increases the relative risk of another fracture by 4.1 to 5.3 times. The presence of two or more compression fractures increases the risk of fracture by 11.8 times.6

History of Fracture in First Degree Relative

Bone mineral density has been proven to be lower in daughters of osteoporotic mothers than in women without such a family history.7 Additionally, data shows that children develop a bone mass that is the average of their parents' bone masses.8

Advanced Age

Since bone loss accumulates over time, it is intuitive that the older a person gets the greater the risk of osteoporosis. Additionally, the extended life expectancy of our elderly population is anticipated to result in a two-fold increase in osteoporosis _ related fractures in the next fifty (50) years.

Caucasian Race

African Americans have greater bone mineral density (BMD) than do non-Hispanic Caucasians.1 African Americans are not, however, immune from osteoporosis. Preliminary results from a pilot study we are currently conducting indicate that 1 in 4 African American females are at risk for complications associated with osteoporosis.9

Gender

Without hormone replacement, women lose the protection afforded by estrogen against bone loss. Men do not experience this rapid bone loss in their middle years because androgens, the male counterpart to estrogens, are not substantially reduced in men until late in life. Men are further protected from the effects of aging on the skeleton by virtue of the fact that they achieve a peak bone mass that is 7-10% higher than women.2

Although osteoporosis is often viewed as a disease of older women, osteoporosis does occur in men. Men sustain 25-33% of all hip fractures and about 14% of vertebral compression fractures.2 Additionally, as men live longer and are more widely recognized to be at risk for osteoporosis, the incidence of osteoporosis in men will certainly rise.

Potentially Modifiable Risk Factors For Osteoporosis

A review of some of the potentially modifiable risk factors for osteoporosis follows:

Cigarette Smoking

Cigarette smoking negatively affects bone by decreased production and increased degradation of circulating estrogens and by decreasing dietary calcium absorption.1

Low Body Weight

Low body weight has been found to be an independent predictor of osteoporosis. Maintaining appropriate weight and nutritional status is an essential preventive measure against osteoporosis.2

Estrogen Deficiency

Estrogen is the hormone with the most apparent influence on bone mass in women. Because estrogen inhibits the activation of osteoclasts, any reduction in circulating levels will increase osteoclastic activation and bone resorbtion. The menopausal reduction in estrogen levels and the resultant decrease in bone density are well established. Premenopausally, behaviors that create estrogen deficiency, primarily by inducing amenorrhea, have negative consequences for bone. Examples include over exercising and eating disorders, such as anorexia and bulimia.1

Low Calcium Intake

Optimal calcium intake is the amount a person needs to reach maximum peak bone mass, maintain adult bone mass, and minimize bone loss later in life.10 This amount varies throughout a person's lifetime and the National Institutes of Health (NIH) has endorsed new recommendations. (Table 2). Insufficient dietary calcium intake forces hormones such as parathyroid hormone to increase bone resorption. In a normal, healthy diet, dairy products supply about 80% of the daily calcium requirement.3 Other food sources of calcium do not contain nearly as much of this element as dairy products do and calcium supplements may be recommended to compensate for dietary deficiency.

Table 2. Calcium Recommendations (mg/day)

Population NIH RDA *
Infants, children, young adults
0-6 months 
6-12 months  
1-10 years  
11-24 years 

Women

Pregnant/Lactating 
Premenopausal (25-50 years)  
Postmenopausal (50-65), taking estrogen  
Postmenopausal (50-65), not taking estrogen  
> 65 years 

Men

25-65 years 
> 65 years  

*Recommended Daily Allowance

 

400
600
800-1,200
1,200-1,500

 

1,200-1,500
1,000
1,500
1,500
1,500

 

1,000
1,500

 

400
600
800
800

 

1,200
800
800
800
800

 

800
800

Alcoholism

Alcohol abuse is believed to be associated with an increased risk of fracture and this relationship appears to be stronger in men than in women.1 Alcohol directly impedes osteoblastic function and may also increase osteoclastic activities.3

Caffeine

Excessive intake of caffeine increases urinary excretion of calcium and ultimately may decrease bone density. The daily intake of one liter of coffee causes a urinary loss of 1.6 mmol of calcium per day. A lower daily intake of caffeine (2 cups of coffee or 12 ounces of caffeinated soda) has no sufficient effect on skeletal bone density.3

Inadequate Physical Activity

Women who maintain higher levels of physical activity have a lower risk of hip fracture. For middle aged and elderly women, walking regularly for more than thirty minutes a day is associated with a reduced risk of vertebral deformity.2 Chronic extreme reductions in bone loading, such as occurs during immobilization, spinal cord injury and space flight results in substantial bone loss. Reduction in the intensity of an individual's activity, a much less extreme form of skeletal unloading, may contribute to an increased rate of bone loss because of reduced mechanical stimulation of osteoblasts.1

Other Factors

In addition to the risk factors discussed above, numerous other factors, primarily diseases and drugs, are associated with an increased risk of osteoporosis in adults. (Tables 3 and 4).

Diseases

Diabetes, hyperparathyroidism, and hyperthyroidism impair bone health. Hyperglycemia can lead to excessive loss of phosphate in the urine, an element essential in the bone matrix. Hyperparathyroidism and hyperthyroidism create conditions of high bone turnover due to excessive secretion of their respective hormones.6 The resulting increased bone resorption and bone formation lead to a generalized bone loss.

Abnormalities of the hepatogastrointestinal tract that impair the absorption of calcium, phosphate, and vitamin D from the gut can also cause bone disease. Examples include inflammatory bowel disease, gastrectomy, celiac disease, Crohn's disease, jejunoileal bypass, and pancreatic insufficiency.1 Cushing's disease and depression are associated with elevated levels of endogenous cortisol that may lead to bone loss.1




Table 3. Diseases Associated With An Increased
Risk Of Generalized Osteoporosis In Adults

Acromegaly
Adrenal atrophy and Addison's disease
Amyloidosis
Ankylosing spondylitis
Chronic obstructive pulmonary disease
Congenital porphyria
Cushing's syndrome
Endometriosis
Epidermolysis bullosa
Gastrectomy
Gonadal insufficiency (primary and secondary)
Hemochromatosis
Hemophilia
Hyperparathyroidism
Hypophosphatasia
Idiopathic scoliosis
Insulin-dependent diabetes mellitus
Lymphoma and leukemia
Malabsorption syndromes
Mastocytosis
Multiple myeloma
Multiple sclerosis
Nutritional disorders
Osteogenesis imperfecta
Parenteral nutrition
Pernicious anemia
Rheumatoid arthritis
Sarcoidosis
Severe liver disease, especially primary biliary cirrhosis
Thalassemia
Thyrotoxicosis
Tumor secretion of parathyroid hormone-related peptide

Medications

Many medications, including corticostoids, anticonvulsants, and heparin are known to decrease bone density. Prolonged corticosteroid therapy, especially in a dose of prednisone greater than 7.5 mg per day, is known to triple the risk of fracture and is the most common cause of drug-induced osteoporosis.1 A very recent report links accelerated bone loss to the antiretroviral class of drugs.11

Table 4. Drugs Associated With An Increased
Risk Of Generalized Osteoporosis In Adults

Aluminum
Anticonvulsants
Cigarette smoking
Cytotoxic drugs
Excessive alcohol
Excessive thyroxine
Glococorticosteroids and adrenocorticotropin
Gonadotropin-releasing hormone agonists
Heparin
Lithium
Tamoxifen (premenopausal use)

Summary

Osteoporosis is an insidious, progressive disease that frequently results in significant morbidity, mortality and cost. Early detection may result from consideration of the numerous known risk factors associated with this disease. Confirmation with bone mineral density testing and treatment, when indicated, can significantly impact the health and lives of a significant portion of our population.

REFERENCES

  1. Beck BR, Shoemaker MR. Osteoporosis: Understanding key risk factors and therapeutic options. The Physician and Sports Medicine. February 2000.
  2. Nattiv A. Osteoporosis: Its prevention, recognition, and management. Family Practice Recertification, February 1998.
  3. Licata AA. Update on osteoporosis: Strategies for prevention and treatment. Women's Health in Primary Care. March 1999.
  4. Consensus Development Conference: Diagnosis, prophylaxis and treatment of osteoporosis. Am J Med. 1993.
  5. Physicians guide to prevention and treatment of osteoporosis. National Osteoporosis Foundation, 1999.
  6. Deal CL. Osteoporosis: Prevention, diagnosis and management. Am J Med. 1997:102.
  7. Evans RA, Marel GM, Lancaster EK, et al. Bone mass is low in relatives of osteoporotic patients. Ann Intern Med. 1988:109.
  8. Lonzer MD, Imrie R, Rogers D, et al. Effects of heredity, age, weight, puberty, activity, and calcium intake on bone mineral density in children. Clin Poediatri. 1996:35.
  9. Grisnik JA, Hodge A. Study in progress.
  10. NIH Consensus Development Panel on Optimal Calcium Intake. NIH Consensus Conference: Optimal calcium intake. JAMA. 1994;272:1942-1948.
  11. Accelerated bone loss linked to antiretrovirals. Family Practice News. March 15, 2000.
Jacksonville Medicine / May, 2000 (Supplement)

 

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