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Bone Density Tests: A Weapon Against Osteoporosis
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Osteoporosis vs. Osteoarthritis: How Can You Tell The Difference?
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When is Back Pain Osteoporosis?
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Are You at Risk for Osteoporosis?
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Treating Osteoporosis: What are Your Options?
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Vanishing Bones: Understanding Osteoporosis
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When Bones Break: The Consequences of Osteoporosis
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Exercise for Bone Health
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Bone Density: Should You Be Tested?
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The Hidden Causes of Osteoporosis
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Living With Osteoporosis: A Patient's Perspective
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Psychological Issues in Osteoporosis
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What is Osteoporosis?
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Milk and More: Eating Right for Your Bones
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Preventing Osteoporosis Fractures
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Should You Get a Bone Density Test?
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Osteoporosis is a disease characterized by low bone mass and deterioration of bone tissues, leading to bone fragility and, consequently, an increase in fracture risk.
The term osteoporosis comes from the Greek word osteon, meaning bone, and porus, meaning pore or passage. Osteoporosis literally makes bones porous. The amount of calcium stored in bones decreases over time causing the skeleton to weaken.
In the body of early adults, both the mineral portion and the framework of bone is in constant flux. Old tissue is broken down and reabsorbed and new bone is created at approximately the same rate. In later years, this rate of renewal begins to slow behind the rate of removal. This slowing is what leaves the bones thinner and more fragile. The most typical sites of fractures related to osteoporosis are the hip, spine, wrist, and ribs, although the disease can affect any bone in the body.
The average woman acquires 98% of her skeletal mass by approximately age 20. Building strong bones during childhood and adolescence is a key defense against developing osteoporosis later. There are four main steps to preventing osteoporosis: consuming a balanced diet rich in calcium and vitamin D; participating in weight-bearing exercise; following a healthy lifestyle, including no smoking and limited alcohol intake; and testing bone density and taking medication when appropriate.
Type I, postmenopausal osteoporosis, is the most common. It is usually a consequence of reproductive hormone deficiency, and afflicts mostly women over age 50. The disorder typically appears within the first ten or twenty years after menopause. Men may also develop the disorder, usually around 50-60 years of age, as a result of:
Type II, senile osteoporosis, affects both men and women over the age of 70, although women are twice as likely to develop the disorder.
In some cases, osteoporosis is secondary to another cause. It can accompany endocrine disorders such as acromegaly and Cushing syndrome. It results from excessive use of drugs such as corticosteroids. In these cases, the treatment is directed at curing the principal ailment or at not using the offending drug. Blood or urine tests will diagnose other causes of bone loss or bone density.
Osteoporosis results from a complex interaction between genetic and environmental factors throughout life. Evidence suggests that peak bone mass is inherited, but current genetic markers are only able to explain a small proportion of the variation in individual bone mass or fracture risk. At this time, no specific mode of inheritance has been identified. Heritability of bone mass has been estimated to account for 60-90% of its variance. Studies have shown reduced bone mass in daughters of osteoporotic women when compared with controls; in men and women who have first-degree relatives with osteoporosis; and in perimenopausal women who have a family history of hip fracture. Body weight in infancy may be a determinant of adult bone mineral area.
Some scientists think that environmental influences during early life interact with the genome to establish the functional level of a variety of metabolic processes involved in skeletal growth.
Many candidate genes exist for osteoporosis, however relatively few have been studied. The first candidate gene to be identified was the vitamin D receptor (VDR) gene, and studies are ongoing as to how much this gene accounts for variance in bone mass. The response of bone mass to dietary supplementation with vitamin D and calcium is known to be dependent, in part, on VDR polymorphisms. Other genes may aid in establishing who would benefit from treatments like hormone replacement therapy, bisphosophonates, or exercise. Associations between bone mass and polymorphisms have also been found in the estrogen receptor gene, the interleukin-6 genes, the transforming growth factor beta, and a binding site of the collagen type I alpha1 (COLIA1) gene.
The risk of osteoporosis is greatly determined by peak bone mass, and any gene linked to fractures in the elderly may possibly be associated with low bone mass in children as well.
Environmental influences such as diet, climate, and physical exercise may have significant impact on gene expression, as well. In particular, malnutrition early in life is likely to have permanent effects resulting in lowered bone mass.
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Author Info: Jennifer F. Wilson MS, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Genetic Disorders Part I, 2002 |