February 07, 2012
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The Detection and Management of Osteoporosis Author's Note: I would like to thank Dr. Catherine Hammett-Stabler, Associate Professor, Department of Pathology and Laboratory Medicine, University of North Carolina-Chapel Hill, and Associate Director of Core Laboratory (Director: Clinical Toxicology, Clinical Pharmacology, Endocrinology, Pediatric Metabolism, Special Chemistry) McLendon Laboratories, UNC Hospitals, Chapel Hill, NC, for her helpful information and advice for this article.
The two most devastating effects of osteoporosis (OP), hip fracture and vertebral fracture, are the result of people living longer and the altered lifestyle of our modern age. In the United States, poor nutrition, or wrong nutrition, and inadequate activity make the genetic predisposition that many have for fragile bones much worse. Though extra weight some carry strengthens bones, obesity is a false cure for it will also lead to arthritis and obesity related illnesses. Some Definitions
Primary osteoporosis is age-related bone loss, resulting in fragile bones at increased risk for fracture. Secondary osteoporosis is bone loss caused by medication, cancer, hormone, kidney or other systemic diseases. Although we now identify osteoporosis with a lab result measuring bone density, it is probably more useful to think of the disease as a sign of bone fragility, as an imbalance between bone formation and normal bone loss (resorption) during the lifetimes of men and women.(1) Bone is an active metabolic tissue and is constantly being formed by cells called osteoblasts and broken down by cells called osteoclasts. About 10% of bone is replaced each year, so that your entire skeleton turns over every 10 years.
Bone Formation and Bone Resorption
There are many sites for formation and breakdown of bone. And these sites vary in their sensitivity to hormones responsible for bone activity. Androgens, the male hormones, build up the outer, or periosteal, layer of bones; Estrogens, the female hormones stimulate growth of the inner, or endosteal, layers of cortical or compact bone (see http://darkwing.uoregon.edu/~louiso/BNSTRUC.GIF). In the long (arm and leg) bones, the thickness may be the same in men and women but because of their greater diameter, bones in males are stronger in resisting stress. These hormones add to the thickness of the bone pillars (trabeculae) in cancellous, or spongy bone that is present inside the vertebrae and at the ends of the long bones (see figure linked above.) Estrogens are active in bone formation in men as well as women, and the net thickness of trabeculae in cancellous bone will be greater in men. Because of the larger diameter of cortical bones and thicker trabeculae of cancellous bones, men have a larger bone mass than women.
Estrogens not only increase bone formation, they inhibit bone resorption by decreasing the activity of osteoclasts. When estrogen is withdrawn, bone resorption increases. The actual mechanism is a decrease in the inhibition of osteoclast formation. The increase in the multicellular osteoclasts, and the larger number of resorptive sites they occupy, creates an imbalance between formation and breakdown of bone, resulting in net bone loss. In women this is accelerated at the time of menopause with the steep drop in estrogen. In the first 5-8 years of menopause, 1%-2% of bone is lost per year in addition to the 0.4% of bone lost per year after peak bone density is achieved at age 30.(23) In women at menopause, the decline in estrogen levels leads to an increase in the lifespan of osteoclasts which break down bone and a decrease in the lifespan of the bone-forming osteoblasts. Among men, age-related decreases in estrogen also result in increased bone breakdown. Measuring Bone Mass
The term "bone mass" simply means the amount of bone in the whole body or in a specified area of bone. We currently measure bone mineral density (BMD) as a way to estimate bone mass. From BMD measurements we have developed standards to determine the presence of osteoporosis. The techniques used include single and dual-energy x-ray absorptiometry (SXA & DXA), quantitative computed tomography (QCT) and quantitative ultrasound.
In SXA and DXA, bone mineral density is expressed as the mineral content divided by a given area of bone in two dimensions. The sites usually measured are the hip and lumbar vertebrae. DXA is currently the test used most commonly for diagnosis and treatment decisions for osteoporosis. QCT measures density in three dimensions and can give a more accurate picture of bone density. The radiation exposure is much higher than DXA and its value in clinical practice has not been determined. Ultrasound can determine bone density based on the transmission of sound waves through bone. This has been used on the heel bone as a screening test. DXA and SXA can also measure BMD at the heel. These peripheral measurements are less expensive than hip and spine DXA, but there is more variation in the results compared to the hip and spine measurements.
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