Stephen F. Hodgson, MD, FACE

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In this era of constrained health-care resources, a critical need exists for efficient, measurable systems of disease 			management that strike a balance between social responsibility and patient welfare. Clinical guidelines have become 			an important component of these systems because they address those elements of care that have proved to be efficacious 			and reduce the high degree of variability in physicians' approaches to disease management.

 These guidelines address the prevention, diagnosis, and management of postmenopausal osteoporosis, a disorder that 			is recognized as a major public health issue because of its profound physical and socioeconomic effects. Each year, 			approximately 1.3 million fractures which now cost the US health-care system more than $10 billion annually occur 			as the result of osteoporosis.

 With these guidelines, we hope to simplify medical decision making but do not intend to be inclusive or restrictive 			because, ultimately, the physician must assume the responsibility for integrating the needs of the patient with 			those of society. The specific goals of these guidelines are as follows:

 To reduce the incidence of fracture 
 To encourage the highest quality of life possible for individual patients 
 These guidelines address the controversies that exist within the subject of postmenopausal osteoporosis but do 			not debate them. In the absence of concrete cost-effectiveness data, they rely on contemporary consensus whenever 			possible. Physicians are encouraged to assess the recent, relevant reviews and studies listed in the "Recommended 			Reading" section for more detailed information and to continue following the literature.

 The American Association of Clinical Endocrinologists (AACE) also recognizes the physician's prerogative to refer 			the patient for consultation by qualified experts, as a basic principle of medical decision making. Osteoporosis 			is a complex endocrinologic disorder of bone and mineral metabolism, and formal training in the science and management 			of metabolic bone disease is required in the academic realm of endocrinology

. The clinical endocrinologist is a 			reliable source of referral expertise.

 Finally, these guidelines will be continually updated to reflect the latest advances in the prevention, diagnosis, 			and treatment of postmenopausal osteoporosis. Because these changes often exceed the capability of our printed 			medium, these guidelines will be updated first on the AACE home page on the Internet. Please visit our Web site 			at / for the most recent version of these guidelines.


 Co-Chairmen
 Stephen F. Hodgson, M.D., F.A.C.E.
 C. Conrad Johnston, Jr., M.D., F.A.C.E.




 Louis V. Avioli, M.D., F.A.C.E.
 H.Hunter Heath, III, M.D.
 Sundeep Khosla, M.D.
 Michael Kleerekoper, M.D., F.A.C.E.
 Robert Lindsay, M.D., F.A.C.E.
 Edward G. Lufkin, M.D.
 B. Lawrence Riggs, M.D., F.A.C.E.
 Nelson B. Watts, M.D., F.A.C.E. 		


 Postmenopausal osteoporosis is a condition characterized by the following features:

Microarchitectural deterioration of bone tissue leading to bone fragility

In the third or fourth decade of a woman's life, bone mass begins to 			decline in the hip because of an imbalance between the volume of mineral and matrix removed and that reincorporated 			during the remodeling process. When menopause occurs, the rate of bone loss accelerates and is particularly rapid 			in the first postmenopausal decade. This accelerated bone loss is caused by estrogen deficiency, which not only 			induces an enhanced, focal imbalance at remodeling sites but also may increase the overall rate of remodeling. 			Certain nutritional and lifestyle factors, such as inadequate intake of calcium, may contribute to low bone mass 			independent of estrogen level, and this can further increase a woman's risk of developing postmenopausal osteoporosis.

 Postmenopausal osteoporosis affects the entire skeleton. In the early postmenopausal years, bone loss averages 			2% per year but can vary from <1% to >5% (1). In the early phase of postmenopausal bone loss, the rate of 			trabecular (cancellous) bone loss exceeds that of cortical bone, and by the end of the first postmenopausal decade, 			most white women have osteopenia or osteoporosis (2). Postmenopausal osteoporosis is more prevalent in white and 			Asian women than in women of other races.


 Low bone mass is a major feature of postmenopausal osteoporosis and the 			primary determinant of fracture. The relationship between bone mass and fracture risk is more powerful than that 			between serum cholesterol concentration and coronary artery disease (3). Fortunately, bone mass can be readily 			measured, preserved, and increased with therapeutic intervention.




 Fracture is the most clinically significant complication of postmenopausal osteoporosis. The following are some 			of the clinical complications of fracture:

Physical deconditioning due to inactivity

Hip fractures are costly and clinically serious. Among patients with 			hip fracture, 12 to 20% die within 1 year after the fracture, and more than 50% of the survivors are unable to 			return to independent living (4). Spinal injuries, in particular, may also lead to other adverse effects:

Osteoporotic fractures often occur at a site of low bone mass and are 			usually induced by trauma.




 Assessment of risk factors can help the physician:

Identify women who are susceptible to fracture

Develop an osteoporosis prevention program

Several factors associated with osteoporosis are environmental and can 			be altered by the patient. A knowledge of all existing risk factors, when considered in conjunction with the bone 			mineral density (BMD) measurement, may also provide direction for intervention with a therapeutic agent (see "The 			Decision to Intervene").

 Risk factors for osteoporotic fractures can be broadly categorized into two groups: (1) those that increase risk 			by increasing the likelihood of developing low bone mass and (2) those that increase risk independently of low 			bone mass for example, through increasing the risk of falling or by altering bone strength through mechanisms other 			than bone mass.

 Risk factors that increase the likelihood that a patient may have low bone mass have limited utility. Although 			in the absence of bone mass measurements they convey information about risk, these factors offer no additional 			information once a bone mass measurement has been obtained. Moreover, their use as a prescreening device that is, 			to select patients for bone mass measurements and further clinical assessment has been shown to be inefficient 			and to result in failure to identify a substantial proportion of patients with low bone mass.



The following risk factors are in this first group:

Long-term use of certain medications (for example, glucocorticoids, 				phenytoin, excessive thyroxine)

These risk factors may not contribute independently to the risk of having 			low bone mass. Low body weight, cigarette smoking, and excessive alcohol consumption, for example, may be found 			in the same person, but these factors may not separately increase the risk for low bone mass.

 Once bone mass is known, several variables further influence the risk of 			subsequent fractures. Primary among these factors is a history of having suffered a fracture after age 40 years. 			Numerous investigators have observed that those persons with a history of fracture in adulthood have, independent 			of bone mass, roughly a doubled risk of sustaining another fracture. In addition to this risk, the Study of Osteoporotic 			Fractures has identified certain factors that have been shown to increase the risk of hip fractures (5), although 			no data suggest that these factors influence the risk of other osteoporotic fractures. The presence of any of the 			following factors should be considered to indicate an increased susceptibility to hip fracture beyond that attributable 			to low bone mass:

Each of these elements may be thought to reflect more general characteristics 			affecting hip fracture risk. Greater frailty, generalized weakness, poor visual function, and certain medications 			(such as long-acting benzodiazepines) increase the risk of suffering an injurious fall, by both increasing the 			probability of occurrence of a fall and decreasing the patient's ability to use protective reflexes. In fact, other 			studies have shown that both the direction of a fall (toward the side) and the absence of protective reflexes increase 			fracture risk independently of bone mass. Both maternal history of hip fracture and greater height may be associated 			with non-BMD structural characteristics of the proximal femur. Although not yet available in most clinical settings, 			scan data have shown that a longer hip axis confers an increased risk of fracture. Longer hip axes are associated 			with greater height and may be genetically determined; thus, some basis is provided for the observations about 			maternal history of hip fracture and greater height.




 Physicians should emphasize prevention of osteoporosis whenever possible. Any prevention program should have two 			primary goals:

As part of any general osteoporosis prevention program, the physician 			should incorporate the following principles.

 Promote a diet with adequate 			calcium content, particularly for growing children and adolescents. The recommended daily calcium intake for various 			populations is outlined in 

, 			and a guide to calcium-rich foods is provided in 

. 			Adequate calcium intake is a fundamental element of any osteoporosis prevention or treatment program, and calcium 			and vitamin D

 supplementation should be prescribed whenever needed to achieve the recommended daily intake levels 			(see "Intervention Agents").

 Encourage 			good general nutrition, with adequate intake of vitamin D--especially in elderly patients.

 Advocate regular weight-bearing 			exercise. Weight-bearing exercise enhances development of bone in children and adolescents and may slow bone loss 			attributable to disuse in elderly persons. In addition, regular exercise promotes mobility, agility, and muscle 			strength that may help prevent falls.

 Strongly discourage use of 			tobacco. In general in comparison with nonsmokers, cigarette smokers are thinner, have an earlier natural menopause, 			may catabolize exogenous estrogen more rapidly, and have more fractures.

 Consider additional preventive 			measures, including estrogen replacement therapy or estrogen + progestin replacement therapy (hormone replacement 			therapy) with calcium and vitamin D supplementation, for perimenopausal and postmenopausal women at high risk of 			developing osteoporosis. These additional measures, listed in 

, 			should be personalized to the needs of each patient (see "Intervention Estrogen Replacement Therapy").


 When intervention with an agent is being considered whether for prevention or for treatment of postmenopausal osteoporosis

 			and the patient is willing to accept available therapy, a thorough medical evaluation and BMD measurement are indicated. 			



 			
 The medical evaluation includes elicitation of a family and a medical history and performance of a complete physical 			and gynecologic examination. Many patients with osteoporosis take medications or have coexisting diseases that 			cause or aggravate bone loss, and primary postmenopausal osteoporosis cannot be diagnosed or appropriately treated 			until these possibilities are eliminated.



The following laboratory tests are appropriate for excluding 			secondary causes of osteoporosis:

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In this era of constrained health-care resources, a critical need exists for efficient, measurable systems of disease management that strike a balance between social responsibility and patient welfare.

Author | Stephen F. Hodgson, MD, FACE

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