AACE Clinical Practice Guidelines for the Prevention and Treatment of Postmenopausal Osteoporosis

Introduction

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.

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

Committee Members
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.

 

Definition
Postmenopausal osteoporosis is a condition characterized by the following features:

• Low bone mass

• Microarchitectural deterioration of bone tissue leading to bone fragility

• A consequent susceptibility to fracture

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.

 

 

 

Clinical Features and ComplicationsLow Bone Mass
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
Fracture is the most clinically significant complication of postmenopausal osteoporosis. The following are some of the clinical complications of fracture:

• Pain

• Deformity

• Postural changes (spinal fractures)

• Disability

• Physical deconditioning due to inactivity

• Changes in self-image

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:

• Loss of height

• Kyphosis (Dowager's hump)

• Back pain (acute and chronic)

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

Risk Factor Assessment
Assessment of risk factors can help the physician:

• Identify women who are susceptible to fracture

• Formulate clinical suspicion

• 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:

• Age

• Caucasian or Asian race

• Sedentary lifestyle

• Smoking

• Low body weight

• Family history of osteoporosis

• Excessive alcohol intake

• Prolonged calcium-deficient diet

• Nulliparity

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

• Estrogen-deficient states

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:

• Maternal history of hip fracture

• Greater height

• Increased likelihood of falling

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.

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

• To optimize bone mass

• To preserve skeletal integrity

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