The world is facing an osteoporosis epidemic.
Every 30 seconds, someone in the European Community has a fracture as a result of osteoporosis. The number of hip fractures (actually a fracture of the neck of the femur in the thigh) is expected to double in the next 20 years due to increasing population and increased life expectancy. According to Gro Harlem Brundtland, director general of the World Health Organization, the greatest increase in osteoporosis will take place in the developing world.

Obviously osteoporosis is widespread, and as the world's population ages, more and more people will suffer from this debilitating, and sometimes fatal, disease. Therefore it is essential to develop a worldwide strategy for osteoporosis management and prevention. But the general public poorly understands whether osteoporosis can be prevented. One of the best preventive measures to avoid later-in-life osteoporotic fractures is to build up the strongest bones possible during childhood and adolescence. Healthy adults generally reach their peak bone mass by age 20. It is estimated that a 10% increase of peak bone mass reduces the risk of an osteoporotic fracture during adult life by 50%.

Thus, an efficient way of preventing osteoporotic fractures occurring in the second half of life is to build up the strongest bones possible during the juvenile periods when rapid bone growth occurs, thereby achieving maximum bone mass by the end of the teen years.

Is there a key age at which bone development takes place?

Bones are living tissue, and the skeleton grows continually from birth to the end of the teen years, reaching a maximum strength and size around the age of 20. Some ages are particularly important for accelerated growth of the skeleton.

The first period of rapid bone growth occurs from birth to two years. A second period of rapid bone growth corresponds to the years of puberty, when sexual maturation takes place, roughly from age 11 to 14 in girls and 13 to 17 in boys. During puberty, the speed of building up bones in the spine and hip increases by approximately five times.

In girls, the bone tissue accumulated during the ages 11 to 13 approximately equals the amount of bone lost during the 30 years following menopause. However, preventive measures should not be concentrated only on these periods of accelerated bone growth. Indeed the skeleton appears to respond quite well to changes in the intake of calcium or in the degree of physical activity during the years preceeding the period of sexual maturation.

During growth the gain in bone mineral mass is mainly due to an increase in bone size with very little change in bone density, i.e. in the amount of bone tissue within the bones. Just because a child is growing tall does not mean that his or her bone mass is growing at a sufficient rate.

From birth to the onset of the sexual maturation, the bone mineral mass at any given age is the same in girls as in boys. During puberty bone mass increases more in boys than in girls.

This difference appears to mainly due to a more prolonged period of accelerated growth in males than in females, resulting in a larger increase in bone size and thickness of the cortical shell of the bones.

Note that from birth to the end of the growth period there is no gender difference in the density of the spongious bone which is found beneath the harder cortical shell.

Many factors can influence bone mineral mass accumulation from life to the end of the teen years, and thus account for the marked difference of peak bone mass between individuals. At the end of puberty, in healthy individuals of the same sex, same age and having the same height, the difference in the amount of bone contained in the lumbar spine can vary by factor of two. For example, one sexually mature, 165cm tall girl might have 10 grams of bone mineral in one lumbar vertebrae while a physically similar girl of the same age might have 20 grams. Why does this surprisingly large variation exist? Certainly it is due to genetics as well as life style determinants, such as nutrition, physical activity and risk factors, but the relative importance of each variable is unclear.

Comparison either between parents and children or between monozygotic and dizygotic twins suggest that genetics accounts for 60 to 80% of the variability in individual peak bone mass. The hereditary transmission of bone mass is very likely dependent upon several genes which have not been yet identified, but which are being intensively searched for in several research centers throughout the world. However, environmental factors such as nutrition and exercise and exercise may be underestimated when calculating the role of genetics.

Calcium
Calcium is essential for healthy bone development, and increasing the calcium intake in children and adolescents increases bone growth. The benefit of increasing the calcium intake is greater in the shaft of the long bones in arms and legs than in the spine. The skeleton appears to be more responsive to calcium supplementation before the onset of puberty has started. Milk and other dairy products are the most abundant source of calcium. Are children getting enough calcium? Increasingly they are not, and in some countries there is widespread concern about the decrease in the consumption of dairy products.

Calcium
Calcium is essential for healthy bone development, and increasing the calcium intake in children and adolescents increases bone growth. The benefit of increasing the calcium intake is greater in the shaft of the long bones in arms and legs than in the spine. The skeleton appears to be more responsive to calcium supplementation before the onset of puberty has started. Milk and other dairy products are the most abundant source of calcium. Are children getting enough calcium? Increasingly they are not, and in some countries there is widespread concern about the decrease in the consumption of dairy products.

This trend may be related to the fact that many children do not have a proper breakfast, with its traditional variety of calcium-rich foods. The reasons are an increasingly fast-paced life and the independent life styles of different people in a family. Also, children increasingly drink soft drinks during meals and snacks instead of milk products. Another factor is that many children, particularly teenage girls, believe that diary products are high in fat content and that eating too many dairy products will lead to obesity. Of course this is related to a perception, particularly among girls, that skinny is beautiful. Besides being of debatable aesthetics, an obsession with thinness can lead to eating disorders, such an anorexia, which can in turn damage a girl's skeleton. Eating disorders often are associated with cessation of menstrual periods, with a corresponding decrease in estrogen levels. Since estrogen in girls is essential in growing bone tissue, a girl who suffers amenorrhea (an unnatural cessation of menstruation not due pregnancy) is likely to suffer reduced bone growth. For those who refuse or cannot consume dairy products there are available alternatives such as calcium-enriched foods which can be prescribed by dieticians or pediatricians.

Vitamin D
Vitamin D is essential for bone growth and health at all ages, because vitamin D helps the body absorb ingested calcium and to deposit the calcium, with phosphate, into the skeleton. One natural source of vitamin D is exposure to sunlight.

When exposure to natural sunlight is insufficient (for example, when babies are kept indoors), it is essential to supplement infants with approximately 400 I.U.of vitamin D per day. A failure to ensure a normal supply of vitamin D, either by sunshine exposure or by oral supplementation, may jeopardize the building up of strong bones.

Proteins
In addition to calcium, protein plays a key role in bone mass acquisition. During growth, under-nutrition, including insufficient caloric intake and protein, can severely impair bone development. Low protein intake can be detrimental for skeletal integrity by lowering both the production and action of a growth factor, IGF 1, which enhances bone formation. In addition this growth factor stimulates both the intestinal absorption of the bone mineral elements, calcium and phosphate, via an increase in the renal production of calcitriol, the hormonal form of vitamin D. Therefore, during growth and pubertal maturation, an impaired production and/or action of IGF-1 due to a low protein intake may result in reduced bone development. This is why we find a positive correlation between protein intake and bone mass gain in children.

Young bones respond more to exercise than do adult bones.

The most effective exercise is weight-bearing exercise-walking, gymnastics, aerobics, ball games, competitive sports, dancing and children and adolescents who exercise regularly show significant increase in bone mass.

Interestingly, the increased bone mass that results from intense physical activity, training for competitive sports, during childhood and adolescence is maintained in young adults even after training slows down or ceases completely.

Too much exercise, particularly among girls, can harm bone growth, particularly when intensive physical activity is accompanied by loss of body weight and reduced sexual hormone production that leads to the cessation of menstruation. Obviously, most young people do not engage in intense physical activity at a high competitive level. So how much exercise is enough?

Moderate exercise programs in schools increase the bone mass gain of children. It is still not clear which moderate exercises are most effective for developing bone at different sites of the skeleton.

On the one hand it is certain that bone, like muscle, can become stronger in response to more or less moderate physical stress. On the other hand, the increasing attraction of television. video games or surfing on the internet promotes a sedentary life style which does not favor the optimal development of bone mass and strength during childhood and adolescence.

Tobacco
Over the last ten years tobacco use among adolescents has increased substantially in several countries, particularly in female teenagers. Smoking may affect the attainment of peak bone mass, particularly when it is associated with other health risk behavior such as inadequate nutrition and low physical activity. However, the greatest concern is the fact that cigarette use during adolescence increases the risk of continued and heavy smoking during adulthood. In adult female smokers bone mineral mass is reduced and the risk of hip fractures is increased. The same increased risk also exists in men. Therefore, avoiding tobacco use during adolescence is an efficient way of reducing the risk of osteoporotic fractures as well as preventing other health problems in later life.

Alcohol
There is little information on the influence of alcohol on peak bone mass attainment in young people. In adult men and women excessive alcohol consumption is associated with a decrease in bone formation. Hence, it can be predicted that alcohol will also exert a negative effect on bone mass development during adolescence.

Coffee
There is no evidence that caffeine consumed in a reasonable amount impairs bone mass acquisition during adolescence.

Soft drinks
It has been suggested that low peak bone mass results from the excessive consumption of soft drinks because of the high phosphate content of carbonated cola beverages. There is no scientific evidence that supports this claim. However, soft drinks are not necessarily good for bone health, and any negative influence of soft drinks on the acquisition of peak bone mass is probably related to the associated low consumption of calcium-rich beverages, the so-called “milk-displacement effect”.

Body weight and bone health
Excessive leanness in adolescence leads to a low peak bone mass. It is not clear whether obesity during childhood and adolescence either impairs or favors bone mass gain.

In order to establish scientifically based recommendations, additional research is needed on the impacts of nutrition and physical activity on peak bone mass and strength. Particularly it will be important to determine, by well designed studies carried out at various ages during childhood and adolescence with a follow up period till the end of skeletal development, the most efficient ways to increase peak bone mass and strength.

The prevention of osteoporosis begins with optimal bone mass acquisition during growth. Factors which limit this acquisition result in a reduced peak bone mass, which in turn is an important determinant of the risk of osteoporotic fracture in later life. Several non-genetic factors, particularly nutrition, physical activity, and sun exposure can influence substantially the gain of bone mass during childhood and adolescence. Despite a certain number of uncertainties which need more research, there is enough evidence from studies on bone development in children and adolescents so that the following recommendations for bone growth in children and adolescents can be made:

1. Ensure an adequate calcium intake which meets the relevant dietary recommendations in the country or region concerned
2. Avoid under nutrition and protein malnutrition
3. Maintain an adequate supply of vitamin D through sufficient exposure to the sun or oral supplementation
4. Increase the general level of physical activity
5. Avoid smoking
6. Educate adolescents about the risk of high alcohol consumption

Each country or region should develop its own strategy in order to translate these general recommendations into specific adapted to the local cultural and economic conditions.

The Silent Epidemic
Osteoporosis is a disease in which the bone structure has been eroded so that the mass of bone is reduced and the architecture is disrupted, predisposing to fragility or a susceptibility to fracture with minimal trauma, particularly, of the spine, hip, wrist, pelvis and upper arm. Osteoporosis and associated fractures are an important cause of mortality and morbidity.

In many affected people, bone loss, which occurs in women and men of all races, is gradual and without symptoms or warning signs until the disease is advanced. Osteoporosis is a global problem which is increasing in significance as the population of the world both grow and ages. For these reasons, osteoporosis is often referred to as the “silent epidemic”.

The loss of bone occurs throughout life and becomes more severe after menopause in women when lack of estrogen, the female hormone, results in an increase in bone remodeling or renewal on the inner surface. We do not understand why bone remodeling occurs so intensely after estrogen withdrawal after menopause but when this is prevented from occurring fine structural arrangement of bone and its mass are maintained.

After menopause, osteoclasts erode the honeycomb structure of trabecular bone. As a result the spine loses its flexibility, its ability to act as a shock absorber or spring moving in its elastic range. With the erosion of the trabecular network, loading, even daily walking, can result in the loss of flexibility in the vertebrae of the spine and may produce microfractures. In the long bones, which are weight-bearing pillars, the cortical shell is placed around the perimeter with a marrow cavity between to confer bending rigidity so necessary in ambulant persons. As we age the cortical shell becomes porous and liable to fracture as the mass of bone is compromised. The result is that these structures can no longer support the loads and may crack.

The bone thinning process during ageing can be likened to a block of ice that disappears particularly rapidly in the last stages melting. Bones become more fragile, more quickly during ole age. One in every two women and one in every four men will sustain an osteoporotic fracture in their lifetime. Spine fractures result in increased risk of death, physical deformity, dependence and severe pain. One fracture occurs every seven minutes and the burden of fractures is increasing because more and more persons are living into old age.

Virtually all aspects of the problem of fractures and bone fragility are to be discussed at the Congress. The importance of vertebral fractures is underestimated. Vertebral fractures cost €329 million annually in direct costs alone; this is just 25% less than hip fractures which are much more frequently reported. Patients with vertebral fractures have a lower quality of life than patients with hip fractures. Many spine fractures result in severe pain that produces long-term disability, curvature of the spine, and respiratory problems because of the collapse of the vertebral column.

Hip fractures have a profound impact on quality of life. Twenty percent of patients with hip fractures die within the first six months of fracture, and are likely to be unable to live at home, and require nursing homes or assistance from family members of health professionals and many require assistance in daily activities. It costs twice as much to treat a hip fracture patient (€6000 per patient) than it does to treat obstructive lung disease or myocardial infraction, and a hip fracture is three times more costly to treat than alcoholic liver disease.

Despite the devastating impact on quality of life and costs to health care systems throughout the world, doctors, patients and governments do not recognize how serious osteoporosis is To put this lack of knowledge in context, it would be totally unacceptable if a doctor failed to treat high blood pressure and the patient then had a stroke. Similarly, if a doctor failed to lower cholesterol in a patient who later suffered a myocardial infarction, this would be regarded as negligence. Yet doctors are not diagnosing patients at risk of osteoporosis, nor are they treating patients who have already fractured a bone, despite the fact that easy diagnostic techniques exists and any fracture is predictor of future fractures.

The reasons doctors do not diagnose osteoporosis partly relate to the mistaken belief that brittle bones reflect a ‘natural' ageing process and that nothing can be done.

We now have safe and effective ways of measuring bone density using densitometry, ultrasound and quantitative computed tomography, techniques that identify women and men at greatest risk for fracture due to low bone density. The loss of bone during ageing can be prevented. The thinning of trabeculae, which form the naturally spongy honeycomb network of bone, can rebuild the decayed structure of bone. Drug therapy is cost effective yet doctors are not investigating or treating women or men with fractures.

This situation is unacceptable and efforts are being made to increase the awareness that this disease is preventable and treatable.

Fractures are a serious problem in men as well as women. One third of hip fractures occur in men. By the year 2025 the numbers of hip fractures in men will be equal to that seen in women now, and the burden on health care systems will be compounded by the increasing numbers of hip fractures in women. The numbers of hip fractures is increasing because more and more women and men are living into old age. In addition, it appears that the age-specific risk of hip fracture is increasing as well. In other words, more elderly men and women suffer hip fractures today than the same number a generation ago. The reason for this is uncertain. Perhaps young people today produce a weaker skeleton than their elders because of changes of diet, environment and life styles. Perhaps elderly people loose more bone as they age.

Although spine and hip fractures are less common in men, men suffer greater disability, morbidity and mortality than women for reasons that are incompletely understood. One possible explanation: Men have more illnesses than women in general because men are more reluctant than women to seek medical care. The prevalence of spine fractures is similar in men and women about 15-25% after the age of 50.

Tobacco use, excess alcohol and male hormone (testosterone) deficiency contribute to the risk of osteoporosis in men but new data suggests that estrogen deficiency is important in men as well as women, and may be more important than testosterone deficiency as a cause of bone loss. Should we treat men with estrogen? The answer to this is not known but new estrogen drugs with specific benefits for the skeleton without feminizing effects may be an option in men. Testosterone regulates bone size in males and may be important in making the bone wider in men. Smoking interferes with production of estrogen and increases the degradation of estrogens and produces bone fragility in men as well as women.

Bone fragility in old age has its origin in youth, if not during intrauterine growth. We know that the basic plan of the skeleton is hidden in the genetic code and passed down from generation to generation. Abnormalities in structure or variation in size and density probably originate in the genes but are modifiable through environmental factors acting throughout life. Maternal leptin levels may affect bone mass in the fetus, while vitamin D deficiency, protein malnutrition, and sex hormone deficiency in growth influence peak bone size and density. Exercise is probably most important during the early years of growth at which time the skeleton is extremely responsive to loading and will grow larger and denser as a result. It is possible that children's current passive life styles, with hours spent in front of computers and TV, causes lower peak skeletal development, which then sets up the situation for bone fragility in old age.

Similarly, adults face numerous life style factors that contribute to low bone density- lack of exercise, little calcium (because of the fear dairy products contain and fat), insufficient protein, tobacco use in younger adults, and avoidance of sunlight in a skin cancer-fearing world. As well, geography plays a role.

Just as we need ways of identifying persons at risk for osteoporosis and fractures we need tools that are easy to use and that can monitor who may be at risk for fracture, who may be taking treatment properly, and whether the patient is responding to treatment . New evidence suggests that measurement of circulating biochemical markers of remodeling predicts bone loss, fracture risk and response to drug therapy. A blood sample or urine sample in the doctor's office can be used to help the doctor determine whether the patient is at risk for osteoporosis, whether the patient is complying with treatment and whether the patient is responding to treatment. These tests, not yet in common use, are important in monitoring treatment and may encourage patients to comply with treatment.

Perhaps the most exciting data concerns a wealth of evidence supporting the efficacy and safety of new therapies for prevention of bone loss, and restoration of bone mass, structure and strength using bone building agents such as intermittent subcutaneous injection of parathyroid hormone and oral strontium ranelate.

PTH is a hormone which in large doses causes bone thinning but in low intermittent doses is ‘anabolic' or bone building. For reasons that are still not understood, low dose administration stimulates the bone forming cells to make new bone so that the bone mass increases. The drug rebuilds the skeleton by increasing cortical and trabecular thickness and perhaps even trabecular connectivity- the connection between the honeycomb structure needed for the spine bones, the vertebra, to act as sponges or springs to be shock absorbers. Strontium ranelate, a new orally active drug, has been reported to increase bone formation and reduces bone resorption.

The new antiresorptive drug ibandronate reduces spine and non-spine fractures. Risedronate maintains trabecular architecture, reduces spine and non-spine fractures within 12 months, and halves intertrochanteric hip fracture risk in people over 80 years old . Alendronate reduces spine fracture risk in women with osteopenia as well as osteoporosis and increases bone density in women and men with primary and secondary osteoporosis. Raloxifene is likely to have benefits outside the skeleton such as reducing the risk of breast cancer and ischemic cardiac events and may protect the skeleton in men as well as women. Newer drugs such as minodronate , bisphosphonate, and bazedoxifene acetate which is a third generation selective estrogen receptor modulator. (SERM) expand the therapeutic alternatives in the field.

The ease, safety and efficacy of new regimens like once weekly alendronate, risedronate and oral ibandronate, three monthly intravenous ibandronate, neridronate or pamidronate, and once yearly zolendronate reduce the inconvenience, adverse events and improve compliance to current treatments. There are many other advances, including confirmatory work regarding antifracture efficacy of vitamin D and calcium, alendronate in women and men with primary and secondary osteoporosis, the combination of monofluorophosphate and raloxifene, and reanalyses of the calcitonin PROOF study.

The epidemic proportions of osteoporotic fracture will continue as people live longer, particularly in densely populated Asian countries. Will osteoporosis become a major 21 st century epidemic? The osteoporosis epidemic parallels that seen in the 19 th century with ischemic heart disease, diabetes, tobacco use and other diseases. The concerted efforts of scientists and governments throughout the world are needed to reduce the burden of fractures that ruin the lives of millions of people and will drain health care resources