This activity is intended for primary care physicians, orthopaedists, endocrinologists, rheumatologists, and other physicians who care for patients with Paget's disease.
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CME Released: 8/4/2009
Valid for credit through: 8/4/2010, 11:59 PM EST
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Paget disease of bone is a focal disorder of the skeleton that can affect one or more bones. Many patients are discovered accidentally because of elevated serum alkaline phosphatase activity or an abnormal skeletal radiograph intended to evaluate an unrelated condition. Patients are often asymptomatic, but a subset experience considerable morbidity that can include bone pain and skeletal deformity, as well as a variety of regional complications, such as hearing loss associated with cranial involvement, degenerative arthritis of the hip or knee, fractures of the lower extremities and, rarely, sarcoma or giant cell tumors. Bisphosphonates have proven to be effective in controlling disease activity because they inhibit osteoclast function. Administration of these agents can relieve bone pain, decrease biochemical markers of bone resorption and bone formation, and retard or reverse the early osteolytic phase of the disease. Future studies are needed to determine whether these drugs, if used in an early stage of the disease, can prevent complications in asymptomatic patients.
In 1877 sir James Paget published his classic study of patients he had seen with focal enlargement and de formity of the skeleton.[1] Later, with the advent of radiologic evaluation of the skeleton,[2] it was appreciated that the earliest phase of Paget disease was characterized by one or more focal osteolytic lesions, which developed over many years into sclerotic lesions that could then be detected on physical examination (Figure 1).
Cortical changes in an untreated patient with Paget disease. Evolution of cortical changes in the left tibia on the lateral view of an untreated woman with Paget disease from age 45 to 68 years, as assessed by radiography. The arrows indicate the area of marked cortical thickening. The distal tibia appeared normal in 1964, but sclerotic changes progressively increased by 1987. Anterior bowing, which was mild in 1964, became progressively worse by 1987. Reproduced with permission from the American society for Bone and Mineral research © J. Bone Miner. Res. 12, 691–692 (1997).