Osteoporosis

History

The term osteoporosis—Greek for porous bone—was first coined in the 1830s by French pathologist Georges Chretien Frederic Martin Lobstein in describing the larger than normal holes he noticed in some bones. At the time of the observation, no further significance was associated with the condition. A century later, in 1934, Yale anatomists discovered estrogen's role in bone formation while studying factors causing increased bone mass in female pigeons as compared with males. With the pigeon study in mind, six years later, Fuller Albright, a Massachusetts General Hospital physician, proposed estrogen to be important in controlling calcium concentrations in human bone and suggested that estrogen-related bone loss was responsible for the fractures afflicting his older women patients.

Etiology

Primary, age-related osteoporosis is the most common form of the disease, resulting largely from ageand hormone-related decreases in bone quality. Risk factors for osteoporosis and related fractures include physical inactivity, previous fractures, smoking, low body weight, low exposure to sunlight (in people above 50), tendency to fall, alcohol consumption, and impaired vision. Preliminary research also suggests an important role for genetic predisposition in the development of osteoporosis. Reduced bone quality due to diseases, disorders, medication use, and/or toxin exposure is referred to as secondary osteoporosis. Many who are diagnosed with osteoporosis have had exposures to secondary causes occurring earlier in life.

Pathogenesis

Bone is a living matrix comprised largely of crystals of calcium and phosphate, or hydroxyapatite, and the protein collagen. Throughout life, bones change in shape, size, and position through the processes of modeling and remodeling. Modeling allows bones to grow and shift in space by forming new bone at one site while removing it from another within the same [Page 768]bone. Remodeling is the removal and replacement of bone at the same site. Remodeling, which becomes the dominant process in both sexes around 20 years of age, is important in the repair of microdamage resulting from stresses on the skeleton, in the replacement of older bone tissue, and in the bioavailability of calcium and phosphate stored in bone for use in other bodily functions. Estrogen influences bone quality by directly and indirectly affecting the activity of osteoclasts, cells that break bone down, and osteoblasts, cells that build bone.

During menopause, a drastic reduction in estrogen production by the ovaries leads to remodeling imbalance and subsequent loss of bone mineral density (BMD). The sudden decrease in estrogen triggers an increase in osteoclast formation and recruitment, inhibits osteoclast apoptosis, and promotes osteoblast apoptosis. This acute phase of rapid bone loss lasts for 4 to 8 years.

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