Osteoporosis is a metabolic bone disease characterized by a decrease in bone density and deterioration of the microarchitecture of bones, the consequence of which is greater bone fragility and an increased risk of fractures.

Osteoporosis is a worldwide public health problem. It affects more than 200 million people and it is estimated that between 30 and 50% of postmenopausal women and men over the age of 70 will develop this disease.

The World Health Organization (WHO) defines an osteoporotic fracture (fragility fracture) as that caused by injury and that results from a force or torsion that is exerted on the bone (and that would be insufficient to fracture normal bone).

The fractures characteristically related to osteoporosis are those of the hip, vertebral, and distal forearm (Colles fracture). However, since the decrease in bone mass is a widespread process of the skeleton, almost all fractures that occur in the elderly are due to osteoporosis.

Taking into account that the population over 65 increases by 1% per year, that the mortality rate that follows a hip fracture is 20% higher within the first year, than 10% of women do dependent after a fracture, that 19% require home care, that less than 50% return to their usual activities and that the direct and indirect costs generated by this pathology are extremely high, it is necessary to develop guidelines for diagnosis, prevention and treatment that to mitigate the effects on Public Health that osteoporosis produces from a medical, social and financial point of view.

Determining Bone Strength

Bone strength implies the integrity of two elements: bone density and bone quality. Bone density is expressed in grams of mineral per area or per volume and is determined by the peak bone mass reached and the balance between gain and loss produced.

Quality is determined by architecture, replacement, damage build-up (eg microfracture), and mineralization. Although the methods for evaluating various parameters of bone quality, such as architecture, porosity, size and geometry, are advanced, they are not yet available for mass clinical use, although they are available for clinical research. For this reason, the diagnosis of osteoporosis continues to be made on the basis of low bone mineral density (BMD).

At a consensus meeting organized by the WHO, a classification was made based on the comparison of the patient's BMD values with the mean of the normal young adult population of the same sex and race.

Classification of Bone Mineral Density values, according to the WHO Expert Committee:

Normal up to -1.0
Osteopenia: <-1.0 to -2.5
Osteoporosis: <-2.5
Severe osteoporosis: <-2.5 plus the presence of fracture

How to Prevent Osteoporosis

Effective preventive strategies should be instituted from the early stages of skeletal development (childhood and adolescence) in order to minimize the consequences of osteoporosis. Here are some recommendations to improve bone health and prevent the development of osteoporosis.

Maintain Balanced Nutrition

The main nutritional factors to prevent osteoporosis are calcium, phosphorus, and vitamin D, since they actively participate in bone formation.

The calcium provided by the diet is essential to achieve proper bone mineralization and maintain its quantity and quality; however, calcium has multiple cellular biological functions that are very important for the proper functioning of the organism, so it must always be kept within a range of minimum concentration in the extracellular medium.

In order that dietary calcium insufficiency does not impair cellular biological functions, calcium mobilization mechanisms are put in place from bone deposits to maintain extracellular levels normal, at the cost of the quantity or density of bone mass and the structure or quality of the bone. Therefore, it is recommended to increase calcium consumption through food or if necessary, with supplements, until reaching a total contribution of 1,000-1,200 mg daily.

Vitamin D is essential for the absorption and metabolism of calcium; its deficiency is a decisive factor for the development of osteoporosis.

Vitamin D not only participates in calcium homeostasis, but it also influences the tone and muscle contraction. Vitamin D deficiency produces muscle weakness that increases the predisposition to falls, further increasing the risk of fractures.

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The body gets 90% of vitamin D from sun exposure and less than 10% from the diet. Therefore, it is recommended to sunbathe at least 15 minutes daily.

Virtually all clinical trials with drugs for osteoporosis have routinely included co-administration of calcium and vitamin D supplements. Consumption of dairy, vegetable, and fruit derivatives contributes to adequate calcium and vitamin D intake.

Various studies have shown that salt intake is associated with increased urinary calcium loss. Four weeks on a high sodium diet (> 15-17 grams/day of salt) are sufficient to cause a significant increase in bone resorption in women after menopause. It is very important to decrease sodium intake to <5-6 grams/day in the usual diet, especially limiting prepared foods.

The diet rich in animal protein produces an increase in organic acids and metabolic acidosis, which leads to an outflow of calcium from the bone, loss of bone mass and an increase in the calcium load excreted by the kidney. In general, it is recommended to decrease the intake of animal proteins and increase the consumption of fish, dairy products, vegetable proteins, soy, fruits, and vegetables.

Moderating caffeine consumption can have a beneficial effect because the diuretic effect of caffeine enhances the excretion of calcium through the urine. It is advised not to consume more than 4 cups of coffee daily.

Avoid Harmful Habits that Affect the Health of Your Bones

It has been observed that people with high alcohol consumption have a lower bone density that usually improves when they stop drinking. Excess alcohol also increases the risk of falls.

There is evidence that shows the unfavorable effects of smoking on the integrity of bone tissue. Smoking has been found to appear to decrease calcium absorption and accelerate urinary excretion.

Furthermore, smokers tend to be thinner, have menopause at younger ages, have increased catabolism of endogenous estrogens, and experience a higher incidence of fractures.

Exercising Regularly Prevents Bone Degeneration

Physical activity has numerous beneficial effects on the health of individuals of all ages. The specific effects of physical exercise on bone structure have been evaluated in observational studies and randomized clinical trials. There is strong evidence that physical activity at an early age of life contributes to achieving a higher peak of bone mass, as well as data indicating that resistance and impact exercises would be the most favorable.

Exercising during mid-life stages has numerous benefits, but there are few studies of its effects on bone tissue. On the other hand, it seems clear that physical activity from the sixth decade of life does not have a relevant impact on the rate of bone loss; however, it produces increases in muscle mass, coordination and muscular resistance, which is beneficial for bone microarchitecture and the prevention of falls, helping to improve self-sufficiency and quality of life at advanced ages. Some trials have shown a 25% reduction in the risk of falls.

Gonadal Steroids and Growth Factors

During puberty, gonadal steroids increase mineral density and peak bone mass and influence the maintenance of bone tissue throughout life in both sexes. The age of onset of menarche, the presence of oligo or amenorrheic cycles, and the age of menopause have a definite influence on the values and maintenance of bone mineralization. Similarly, the production of testosterone in adolescents and adult men is important in achieving and maintaining adequate bone mass.

On the other hand, estrogens have also been implicated in the growth and maturation of the skeleton in males. Thus, the alterations resulting in pubertal delay and various forms of hypogonadism must be corrected to avoid deleterious effects on bone mineral density.

Furthermore, growth hormone and certain growth factors (especially insulin-like growth factor type I [IGF-1]) that are primarily secreted during puberty continue to exert a significant influence on the maintenance of bone integrity. in the adult stage.

Pharmacological Interventions for Osteoporosis

In addition to the administration of calcium and vitamin D supplements, different pharmacological interventions have been evaluated in subjects with risk factors for osteoporosis. In this sense, postmenopausal women with risk factors and densitometric criteria for osteopenia are eligible for preventive treatment. Thus, estrogens, etidronate, alendronate, and raloxifene have been shown to be effective in preventing bone loss. However, considering its possible side effects and the large number of patients that need to be treated to prevent a fracture, its use should be limited to specific cases, except if the treatment is justified by factors other than osteoporosis prevention.

Independent consideration is deserved by patients who require glucocorticoid treatment for prolonged periods (7.5 mg prednisone or equivalent for more than three weeks). In these cases, pharmacological intervention with bisphosphonates (alendronate or risedronate) has been shown to be effective.

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Sources

1.       NIH. Consensus Development Panel on Osteoporosis Prevention. Diagnosis and Therapy. JAMA 2001; 285: 785-95.
2.       Quesada Gómez JM, y col. Low calcium intake and insufficient serum vitamin D status in treated and non-treated postmenopausal osteoporotic women in Spain. J Bone Miner Metab 2007; 22: S309
3.       AACE Osteoporosis Task Force. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract 2003; 9:544-64.
4.       Schurman L, Bagur A, Claus-Hermberg H, Messina D, Negri A, Sánchez A. Guidelines for diagnosis, prevention and osteoporosis treatment. Rev Arg Osteología 2004; 3 (3): 4-15.

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