Osteoporosis: The silent disease, part 1

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Osteoporosis: The silent disease, part 1

ABSTRACT: Osteoporosis threatens 28 million Americans, 80% of whom are women. Each year osteoporosis causes 1.5 million fractures of the hip, spine, wrist, ribs, and other bones. With 10 million people in the United States diagnosed with osteoporosis and another 18 million with low bone mass, chances are very good that every chiropractic physician has at least one patient with this disease.

Chiropractors, by the very nature of their profession, may be the first health care providers to recognize symptoms of osteoporosis in their patients. Because of their hands-on approach, chiropractors must be alert to the dangers of osteoporosis, and should have a broad knowledge of the mechanism of osteoporosis, its clinical and radiological features, and its prevention and treatment.

DESCRIPTION

The word osteoporosis literally means "increased porosity of bone." Osteoporosis is an absolute and exaggerated decrease in bone tissue mass. The remaining bone is morphologically normal or of poor quality, a condition that leads to reduced bone strength and an increased risk of fractures, even to the point where a simple cough can fracture a rib. Osteoporosis is the most common cause of hip fracture, a very serious disorder that may result in permanent disability, disfigurement, pain, loss of independence, and even death.

Many older people who complain of falling and breaking a hip actually have the sequence of events wrong. Their osteoporotic hip fractures under load, and then they fall. One of six people who have hip fractures caused by osteoporosis die from complications within 3 months.

LIVING BONE

Contrary to many patients' beliefs, bones are not inert structures that muscles and organs hang upon. Bones are living tissue that continuously regenerate throughout life by a process called remodeling. Old bone is removed by osteoclasts and replaced with new bone by osteoblasts. Osteoporosis occurs when not enough new bone is formed, when too much bone is removed, or both.

Osteoclasts, normally active on less than 1% of bone surfaces and cavities, continually absorb bone minerals and matrix. Acting as phagocytes, the osteoclasts secrete proteolytic enzymes and acids that digest the matrix and dissolve the bone salts. Meanwhile osteoblasts, found on about 4% of bone surfaces and cavities, continually deposit new bone. With the exception of growing bones, the rates of bone deposition and consumption are normally equal to each other so that the total mass of bone remains constant.

Osteoclasts tend to clump in small, concentrated masses and usually absorb bone for about 3 wk. Each mass may create a void in the bone reaching 1 mm in diameter and several millimeters long. At the end of 3 wk, the osteoclasts disappear and the osteoblasts arrive.

Osteoblasts deposit new bone for several months until the void is filled. Production of new bone ceases when the bone encroaches on blood vessels supplying the area, leaving only cavities called haversian canals for the blood vessels.

The continual remodeling of bone has at least three important functions: bone adjusts its strength in proportion to the stress placed on it, the shape of bone alters in response to mechanical forces placed on it, and new, strong bone replaces degenerated, old bone matrix that is relatively weak and brittle. By these processes, the normal strength of bone is maintained.

Peak bone mass is reached around 30 years of age. After this age, bone mass and density may remain stable, or bone loss may occur at a rate as high as 90 mg/day, or up to 1% total loss per year.

RISK FACTORS

Several factors can increase a person's chance of developing osteoporosis:

- Race (Caucasian or Asian are more prone).

- Gender (women are more prone).

- Heredity (older family members have osteoporosis).

- A thin, small-boned frame.

- Tallness (a woman taller than 5'6".

- Estrogen deficiency from early menopause.

- Estrogen deficiency from amenorrhea.

- Postmenopausal.

- Advanced age.

- Low calcium intake.

- Malabsorption problems.

- Anorexia nervosa or bulimia.

- Inactive lifestyle.

- Cigarette smoking.

- Excessive alcohol use.

- Prolonged use of certain medications.

- Chronic diseases that affect kidneys, lungs, stomach, and intestines, or alter hormone levels.

- Low testosterone (in men).

DETECTING OSTEOPOROSIS

Osteoporosis is called the "silent disease" because there are no early warning signs or symptoms and few outward indications of the disease until a fracture occurs. Major radiographic signs of osteoporosis consist of increased radiolucency, cortical thinning, and altered trabecular patterns. Additional superimposed changes, such as fractures or degenerative arthritis, also may be evident.

Increased radiolucency. Unfortunately, ordinary X-rays cannot detect osteoporosis until there is about 50% loss of bone mass, at which time osteopenic signs are evident, but are not differentiated from other disease states, such as osteomalacia, hyperparathyroidism, and rickets (Fig. 1).

Cortical thinning. Cortices show a general thinning, described as "pencil-thin." Endosteal scalloping may be demonstrated, particularly in the early phases (Fig. 1).

Altered trabecular patterns. Trabecular patterns are often visible even though there is a loss of bone mass. Those that are most visible are the trabeculae that lie along the lines of greatest stress. As osteoporosis progresses, even those trabeculae may be lost, giving the bone a "washed-out" appearance.

Changes in shape. Radiographic views of the spine may reveal any number of changes in vertebral shape (Fig. 2).

Vertebra Plana ("pancake" vertebra, compression fracture). Both anterior and posterior portions of the vertebra are reduced in height. Vertebra plana is an unusual presentation for osteoporosis and must be differentiated from other, malignant diseases.
Wedged Vertebra is a compression fracture exhibiting anterior loss of height with a preservation of the posterior height. Wedged vertebrae may also be seen in traumatic compression fractures.
Biconcave Deformities ("fish," "codfish," or "hourglass" vertebrae) are central depressions in the vertebral end plates, which may be found in multiple, contiguous sites. The deformity arises from pressure exerted by the nucleous pulposa on the weakened end plates This sign may also be found in osteomalacia, Paget's disease, and hyperparathryoidism.
Isolated End Plate Deformities consist of altered end plate orientation, a sharp break in continuity, and increased density bordering the acute fracture site.
Schmorl's Nodes are localized intrabody discal herniations superimposed on the osteoporotic spine, usually in the thoracic and upper lumbar regions. They are smaller, with more irregular borders than the nodes of juvenile onset.

In general, skeletal sites other than the spine exhibit similar manifestations of radiolucency, trabecular changes, cortical thinning, and fracture deformities.

Low bone mass is a major cause of fractures. Bone mineral density (BMD) tests, which are more sensitive than ordinary X-rays in measuring bone mass, can confirm suspected osteoporosis and are useful in establishing a baseline measurement for high-risk women at menopause. BMD measurements are not stand-alone tests; they are best used as one component of a complete clinical assessment. Other blood and urine tests may be used to determine osteoclastic and osteoblastic activity and to identify possible causes of bone loss.

BMD tests are simple, painless tests that use small amounts of radiation (usually less than 10% of a chest X-ray) to determine the density of bones in the hip, spine, and wrist. One technique uses computer-analyzed X-rays of the hand taken at different settings to determine bone density at various sites throughout the body (Table 1).

Bone density tests are useful in: detecting low bone density before a fracture occurs, predicting chances of future fractures, confirming a diagnosis of osteoporosis after a fracture, distinguishing spinal osteoporosis from other spinal abnormalities, determining rates of bone loss if tested at intervals of one year or more, monitoring treatment if tested at intervals of one year or more. Patients who should have bone density tests include: allopathic patients deciding whether to start long-term estrogen replacement therapy; allopathic patients taking steroid medications like prednisone, for diseases such as asthma, arthritis, lupus, Addison's disease, or Crohn's disease; those who have primary hyperparathyroidism; those who have a recent fracture from suspected osteoporosis; those monitoring progress of osteoporosis treatment; and those who have multiple risk factors.

INTERPRETING BMD RESULTS

A BMD test measures bone mass and density. The test is compared with two norms: "agematched," which compares the patient's BMD with what is expected in someone of like age and body size, and "young-normal," which compares the BMD with the peak density of a healthy young adult.

The difference between the results of a BMD and that of a healthy young adult is defined as a "standard deviation (SD)." One SD equals 10-12% decrease in bone density. The World Health Organization (WHO) developed the following diagnostic categories of bone loss:

- Normal: BMD within 1 SD of young normal.

- Low Bone Mass: BMD falls between 1 and 2.5 SD below young normal.

- Osteoporosis: BMD equals or exceeds 2.5 SD below young normal.

BIBLIOGRAPHY AND SUGGESTED READING

Berkow R, ed. The merck manual of diagnosis and therapy, 14th ed. Rahway, NJ: Merck & Co., Inc.; 1982.
Dempster DW, Johnston CC Jr, Raisz LG, Stern PH. Medications and bone loss. Washington: National Osteoporosis Foundation; 1997.
Gottlieb W, Bricklin M, eds. Aging slowly. Emmaus, PA: Rodale Press; 1984.
Gottlieb W, Bricklin M, eds. Fighting disease. Emmaus, PA: Rodale Press; 1984.
Gottlieb W, Bricklin M, eds. Pain free. Emmaus, PA: Rodale Press; 1984.
Gottlieb W, Bricklin M, eds. Understanding vitamins and minerals. Emmaus, PA: Rodale Press; 1984.
Gottlieb W, Keough C, Feltman J, Bricklin M, editors. Intensive healing diets. Emmaus, PA: Rodale Press; 1988.
Guyton AC. Textbook of medical physiology, 6th ed. Philadelphia: WB Saunders Company; 1981.
Krause MV, Mahan LK. Food, nutrition, and diet therapy, 7th ed. Philadelphia: WB Saunders Company; 1984.
National Dairy Council. Thinking about calcium? Rosemont, IL. The Council; 1997.
National Osteoporosis Foundation. Act against osteoporosis! Washington. The Foundation; n.d.
National Osteoporosis Foundation. Facts about osteoporosis, arthritis, and osteoarthritis. Washington: The Foundation; 1991.
National Osteoporosis Foundation. How strong are your bones? Washington. The Foundation; 1997.
National Osteoporosis Foundation. Osteoprosis: a woman's guide. Washington: The Foundation; 1997.
National Osteoporosis Foundation. Osteoporosis -- can it happen to you? Washington: The Foundation; 1996.
National Osteoporosis Foundation. Menopause and osteoporosis. Washington: The Foundation; n.d.
National Osteoporosis Foundation. Men with osteoporosis. Washington: The Foundation; 1997.
National Osteoporosis Foundation. Osteoporosis & women. Washington: The Foundation; 1995.
National Osteoporosis Foundation. Stand up to osteoporosis. Washington: The Foundation; 1997.
National Osteoporosis Foundation. Talking with your doctor about osteoporosis. Washington: The Foundation; 1997.
National Osteoporosis Foundation. The older person's guide to osteoporosis. Washington: The Foundation; 1991.
National Osteoporosis Foundation. What people with arthritis need to know about osteoporosis. Washington: The Foundation; 1997.
Nutrition masters course, session #5. Prevention and treatment of bone loss. Maple Plain, MN: Nutrition Dynamics; n.d.
Pennington JAT, Church HN. Bowes and church's food values of portions commonly used, 13th ed. New York: Harper & Row; 1980.
Tortora GJ, Anaguostakos NP. Principles of anatomy and physiology, 4th ed. New York: Harper & Row, Publishers; 1984.
Yochum TR, Rowe LJ. Essentials of skeletal radiology, vol 2. Baltimore, MD: Williams & Wilkins; 1987.

The National College of Chiropractic.

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By Larry W. Greenly

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