The story of osteoporosis, a disease that weakens bones and makes them more susceptible to breaks, begins with normal bone. The appearance of bone belies its structural complexity. It is neither as solid nor as static as it seems. It consists of two types of tissue — compact bone and trabecular bone — both of which are beehives of microscopic activity. The origins of these terms say a lot about the structure of bone.

Compact bone was originally known as lamellar or cortical bone. Lamellar derives from lamina, meaning plate; cortical, from cortex (or shell). The basic units of compact bone are tightly packed plates wound into tubular forms, called osteons, which look a little like rolled magazines (see Figure 1). Each osteon has a tiny blood vessel called a capillary running through its central channel. The osteons are arranged in vertical stacks to form a hard, shell-like membrane.

Figure 1: Types of bone Types of bone Most bones in your body are composed of two types of tissue: compact bone and trabecular bone. Often, the compact bone — tightly packed tubes of bone tissue that resemble the rings of a tree trunk — forms the outer casing, while the trabecular bone, which is more porous, is found at the center.

Although the second type of bone tissue is usually referred to as trabecular (meaning little beam), it is sometimes called cancellous (meaning lattice-like) bone. Indeed, this tissue comprises millions of tiny beams that form a lattice-like matrix (see Figure 1).

Most bones contain both compact and trabecular tissue. Compact bone forms the dense outer casing, while trabecular bone spans the interior. However, the proportion of these two tissues varies from bone to bone. Long, regular bones, like those of the arms, legs, and ribs, consist primarily of compact bone. Irregularly shaped bones, such as the ends of the leg or arm bones, the pelvis, and the vertebrae, consist principally of trabecular bone.

Both compact and trabecular bone are made from the same fabric — a meshwork of collagen fibers. This meshwork is inlaid with calcium and phosphate, which are mixed with water to form a hard cement-like substance called hydroxyapatite. Sodium, magnesium, and potassium are also present in smaller amounts.

These materials are surprisingly strong. Ounce for ounce, bone bears as much weight as reinforced concrete. However, unlike concrete, it isn't inert. Bone is a living tissue. It serves as a repository of minerals for use by the body, and these elements are continuously lent out and replaced. Thus, like most other body tissues, bone is in a constant state of flux.

Bone remodeling

Calcium is the principal currency of bone. It carries a lot of weight in the body, both literally and figuratively. Not only is it the major component of the cement-like hydroxyapatite, but it also plays an important role in other body systems.

Buoyed along in the blood, lymph, and other fluids, calcium bustles in and out of cells, transmitting signals to nerves and muscles. It is vital to many physical processes, including heart rate, blood pressure, and the regulation of the internal organs. However, the amount of calcium required to do this is slight — only about 1% of your body's total calcium stores. The rest — about 2.25 to 4.5 pounds' worth — is sequestered in your bones. When the supply of calcium in the blood drops below the critical level, it can be replenished from bone.

Tapping and replenishing calcium stores

The process by which calcium is released from bone is known as resorption. It is executed by osteoclasts — scavenger cells somewhat similar to those in the immune system. However, instead of gobbling up bacteria and cellular debris, osteoclasts go after intact bone. Their saw-toothed membranes enable them to attach to the surface of bone, and they are equipped with acids to dissolve hydroxyapatite and with enzymes to break down collagen and other proteins (see Figure 2). As they eat away at bone, they regurgitate the freed proteins and minerals into the bloodstream for reuse in other parts of the body. This recycling effort leaves tiny tunnels in the bone.

Figure 2: The cycle of bone construction and demolition The cycle of bone construction and demolition Bone is constantly being constructed and demolished. During resorption (A), cells known as osteoclasts break down bone, releasing calcium into the bloodstream. The trenches that are left behind (B) are then filled in by construction cells known as osteoblasts. The osteoblasts release collagen into these troughs and eventually evolve into structural bone cells, or osteocytes (C). Once these osteocytes mix together with calcium, phosphate, and other minerals to form a cement-like substance known as hydroxyapatite, the process of replacing the lost bone is complete (D).

Resorption is coupled with another process known as formation, which is carried out by construction cells called osteoblasts. These cells move into the tunnels left by the osteoclasts and release strands of collagen into the void. Eventually, they become trapped in the web they have woven. Held by these moorings, they evolve into structural bone cells, or osteocytes.

Calcium, phosphate, and other minerals carried in the bloodstream also accumulate in the web. The minerals coalesce into the crystalline hydroxyapatite, and the formation process is complete. The bone that was removed has been fully replaced.

Other key players

This remodeling process not only liberates calcium, but also maintains the skeleton by replacing old bone with new. This important task in the body's housekeeping scheme requires more than osteoclasts and osteoblasts; a host of hormones work quietly behind the scenes to influence the behavior of cells.

Parathyroid hormone (PTH), which is secreted by small islands of tissue near the thyroid gland, is a primary force in resorption. Parathyroid hormone is secreted when the level of calcium in the blood falls below the amount needed by the body's cells. This hormone helps restore the appropriate levels of calcium in the blood in several ways. It promotes the absorption of calcium by the digestive system and slows the excretion of calcium into the urine. It also stimulates osteoclasts to break down bone to release calcium into the blood. When the calcium level in the blood is adequate, the production of parathyroid hormone falls.

It takes a sizeable squad of other hormones and substances to carry out bone formation. For example, vitamin D, which is actually a hormone, plays a pivotal role, limiting withdrawals of calcium from bone by promoting calcium absorption from the intestines.

A delicate balance

Although formation and resorption go hand in hand, the processes occur at different rates. As with any remodeling project, demolition is always speedier than reconstruction. So to preserve the skeleton, it's necessary to have more building sites than demolition projects. For most adults in their 30s, when bone mass is at its peak but no longer increasing, about 1% of bone is undergoing resorption and about 4% is under formation at any given moment.

Peak bone mass

During the first 20 years of life, new bone is built more quickly than old bone is removed. By the late teens, most bone formation has already occurred. By age 20, most women have already built 98% of their skeletal mass, and by age 30 most men and women reach their peak bone mass.

Subsequently, among women, bone mass remains level until the onset of menopause, when bone is lost rapidly. While the pace of bone loss slows after the first few years of menopause, women continue to lose bone. In the five to seven years after menopause, women can lose up to one-fifth of their bone mass. Bone loss usually begins later for men — most often, when they are in their 50s — and it progresses more slowly. But by ages 65–70, most men and women lose bone at the same rate.

Peak bone mass varies from person to person. Heredity, lifestyle, state of health, and estrogen levels all play important roles in determining how much bone you'll have in the bank when heavy withdrawals begin. It's important to begin growing this "rainy day fund" early, when you have the most opportunity to influence your bone mass. Building up your bones in your teens pays hefty dividends later in life.

Here are some of the factors that can influence your peak bone mass:

Inherited traits. Sex, race, and genetics help determine peak bone density. As a rule, bone density is 30% higher in men than in women and 10% higher in blacks than in whites. Even so, there is a wide variation within these groups. The difference may be due to the work of several genes that determine bone mass, bone turnover, and bone loss.

Diet. What you eat early in life has a lot to do with the state of your bones later on. Research indicates that women whose diets contain the greatest amounts of calcium and vitamin D during childhood and adolescence have denser bones during adulthood. Consuming enough calories is also vital: When girls and women have too little body fat to support menstruation because of anorexia or bulimia, their bones suffer and they are in greater jeopardy of developing osteoporosis.

Exercise. Regular weight-bearing exercise during your early years contributes to peak bone density. This includes any activities that involve overcoming gravity's pull — not just weightlifting, but also running, walking, aerobics, soccer, basketball, gymnastics, tennis, golf, or comparable forms of exercise. Exercise puts stress on bone, and bones respond by toughening up — in this case, by adding tissue through formation. However, exercising to the extreme, which is increasingly common among young dancers, long-distance runners, and gymnasts, can result in declining estrogen levels, amenorrhea (abnormal absence of menstrual periods), and eventually bone loss.

Medical conditions. Certain chronic disorders that result in excessive resorption can reduce peak bone mass (see "Possible causes of secondary osteoporosis"). Some common culprits include hyperthyroidism, certain cancers, chronic liver disease, rheumatoid arthritis, and malabsorptive disorders (conditions that develop because nutrients from food aren't being absorbed into the bloodstream properly).

Certain medications. Some drugs can also lead to bone loss (see "Possible causes of secondary osteoporosis"). One is too much thyroid hormone taken as therapy for an underactive thyroid gland. Others include glucocorticoids, which are taken to control asthma, immune disorders, and other diseases (see "Six ways glucocorticoids hinder bone formation"). Also, because several drugs that speed bone loss are commonly given after organ transplants, people who have had these operations are at considerable risk of developing osteoporosis.

What causes osteoporosis?

Bone loss occurs when the cells that form bone (osteoblasts) cannot keep pace with the cells that are eating away at bone (osteoclasts). If you were to view a microscopic movie taken over time, you would see the osteoclasts going about business as usual, while the osteoblasts' efforts fall short. Although the tunnels dug by the osteoclasts aren't getting any deeper, neither are they being refilled completely (see Figure 3). As tunnels accumulate, the bone becomes thinner, more porous, and weaker than it once was.

Figure 3: When bone is lost When bone is lost Bone is constantly being demolished and rebuilt. If reconstruction lags behind demolition, then bone is lost. Osteoclasts gnaw at bone, releasing calcium and other minerals into the bloodstream and leaving troughs behind (A). If the osteoblasts that build bone cannot keep pace, these tunnels will not be completely refilled (B). The result is bone that is weaker and more susceptible to breaks.

There are no symptoms associated with such bone loss. But if it continues indefinitely, bones will eventually become too weak to bear the load they were designed to carry. The result is usually a fracture of the wrist, hip, or spine.

There are a variety of underlying reasons for osteoporosis. Experts use the following classifications to distinguish among the different causes.

Primary osteoporosis

The result of a normal physiological process, such as menopause or aging, primary osteoporosis is the most common form of the disease.

Type 1 primary osteoporosis

Type 1 primary osteoporosis, also known as postmenopausal osteoporosis, is the result of a rapid loss of bone associated with the decline in estrogen levels in women during the three to five years preceding menopause, at menopause, and following menopause. Typically, bone loss accelerates in the first few years after menopause, and then begins to level off. The effects are most prominent in the trabecular bone, which isn't as dense as compact bone. Several factors may contribute to this process. A number of researchers are examining the roles of chemical regulators, such as interleukin-1, interleukin-6, prostaglandin E2, and tumor necrosis factor, which appear to speed up bone resorption by spurring on osteoclasts as estrogen levels decline.

Type 2 primary osteoporosis

This condition results from the cumulative effects of the gradual loss of both trabecular and compact bone that occurs with aging. Type 2 primary osteoporosis develops more slowly than type 1 and is usually not apparent until age 75 or later. As with all age-related changes, it is probably due to several factors.

One is the general slowdown in bone formation as you age (see "Peak bone mass"). Another is a decline in the availability of minerals. With age, the intestines gradually absorb less calcium from the diet, and the kidneys seem to be less efficient at conserving calcium. Thus, more calcium is lost in the stool and urine, and less reaches the bloodstream, making it more likely that the bones' calcium stores will be tapped.

To make matters worse, most people consume less dietary calcium as they age, further straining the bones' calcium supplies. Many people shy away from dairy products, often because of lactose intolerance (the reduced ability to digest milk sugar), which can produce gas and abdominal discomfort. Others may shun calcium-containing foods and supplements because they have constipating effects.

The body's production of vitamin D frequently drops as well. Your skin cells use sunlight to produce a precursor of vitamin D; the liver and kidneys then convert this precursor into active vitamin D. Vitamin D plays a central role in the body's absorption of calcium and in the process of turning calcium into bone. If you don't have enough vitamin D to signal your intestines to absorb calcium, your body will break down bone to get the calcium it needs — no matter how much calcium you're getting from food or supplements. Many people don't get enough vitamin D — a problem that is particularly common among older adults. One reason is that people often spend less time in the sunlight as they grow older; thus, they are unable to produce an adequate supply of vitamin D. In addition, many older adults consume fewer vitamin D–fortified dairy products.

Secondary osteoporosis

The term secondary osteoporosis is used to describe osteoporosis resulting from a medical condition or the use of certain medications. (For a list of disorders and drugs that lead to secondary osteoporosis, see "Possible causes of secondary osteoporosis.") If you have one of these conditions or if you're taking any of these medications, talk to your doctor about what you can do to keep your bones healthy.

The most common cause of drug-related secondary osteoporosis is the use of glucocorticoids (also known as corticosteroids) like prednisone, which are often prescribed to treat conditions such as asthma, rheumatoid arthritis, and chronic obstructive pulmonary disease. Some medications that are commonly used after organ transplants can also further bone loss. People using any of these medications should be even more vigilant about protecting their bones.

Source: from Harvard Health Publications, Copyright © 2008 Harvard University. All rights reserved. Harvard Medical School does not endorse products.
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