Osteoporosis - Wikipedia
The National Osteoporosis Foundation's position statement on peak bone may not) influence the development of peak bone mass. (Table 1). relationships as well as other factors for which a systematic .. struct bone images. Cortical and. Learn about bone loss and osteoporosis, what causes it, how it's detected, and how it can be prevented. Super Foods for Your Bones Slideshow Pictures Bone formation continues until the peak bone mass (maximum solidness and strength) is reached. This is related to both poor nutrition and increased risk of falling. By our early twenties, peak bone mass (maximum bone density) is achieved – this is when our bones are at their strongest. Building a higher peak bone mass.
The independent mechanical contribution can be measured by the differential effect observed according to the skeletal sites solicited. However, the best evidence of the distinct effect of mechanical loading from concomitant increase in nutritional intakes is provided by studies on the use of rackets, as determined by measuring the difference between loaded and unloaded arms.
It has been suggested that the exercise-induced gain in bone mass, size and strength essentially results from an adaptation secondary to the increase in muscle mass and strength. Impaired bone mass acquisition can occur when intensive physical activity leads to hypogonadism and low body mass. Intake of energy, protein and calcium may be inadequate as athletes go on diets to maintain an idealized physique for their sport.
Intensive training during childhood may contribute to a later onset and completion of puberty. Hypogonadism, as expressed by the occurrence of oligomenorrhea or amenorrhea, can lead to bone loss in females who begin training intensively after menarche. The differential impact of calcium The extent to which variations in the intake of certain nutrients by healthy, apparently well-nourished, children and adolescents affect bone mass accumulation, particularly at sites susceptible to osteoporotic fractures, has received increasing attention over the last 15 years.
Most studies have focused on the intake of calcium. However, other nutrients such as proteins, which are not discussed in this review, should also be considered. In most regions of the world, the supply of calcium is sufficient to avoid the occurrence of clinically manifest bone disorders during growth.
Nevertheless, by securing adequate calcium intake, provided the skin and food supply of vitamin D is adequate, it is expected that bone mass gain can be increased during infancy, childhood and adolescence and thereby optimal PBM can be achieved. The prevention of adult osteoporotic fractures is the main reason for this widespread preoccupation.
International and national agencies have adopted recommendations for calcium intake from infancy to the last decades of life. Decisions from these recommending bodies can be based on either calcium balance, allowing estimations to be made regarding maximal retention, or on a factorial method that calculates from available data on calcium accretion and endogenous losses modified by fractional absorption.
Observational and interventional studies are also taken into consideration. The recommendations vary widely among regional agencies56 table I. Thus, for children aged years, the recommended daily calcium intakes are set at,and up to mg, in the United Kingdom, the Nordic European countries, France and the United States of America, respectively.
Variability in calcium intake recommendations can be explained partly by the discrepant results obtained in observational and interventional studies. Retrospective epidemiological data obtained in women aged years, indicated that milk consumption during childhood and adolescence can be positively correlated to bone mineral mass.
Several calcium intervention studies have been carried out in children and adolescents. Nevertheless, the response appears to vary markedly according to several factors including the skeletal sites examined, the stage of pubertal maturation, the basal nutritional conditions, i.
The benefit of supplemental calcium was usually greater in the appendicular that in the axial skeleton. In agreement with our longitudinal observation in healthy subjects aged 8 to 19 years figure 6the skeleton appears to be more responsive to calcium supplementation before the onset of pubertal maturation than during the peripubertal period.
Two co-twin studies strongly suggest that increasing calcium intake after the onset of pubertal maturation above a daily spontaneous intake of about mg does not exert a significant positive effect on bone mineral mass acquisition. This contrasts to the widespread intuitive belief that the period of pubertal maturation with its acceleration of bone mineral mass accrual would be the most attractive time for enhancing calcium intake well above the prepubertal requirements.
As described above efficient adaptive mechanisms secure an adequate bone mineral economy in response to the increased demand of the peripubertal growth spurt. As intuitively expected, the benefit observed at the end of intervention is particularly substantial in children with a relatively low calcium intake. In contrast, the additional gain was minimal in those girls with a relatively high calcium intake. According to the "programming" concept, environmental stimuli during critical periods of early development can provoke long-lasting modifications in structure and function of various biological systems.
The possibility that physical activity could modulate the bone response to dietary calcium supplementation during growth has been considered in infants, children and adolescents. Overall, the results suggest an interaction: At moderately low calcium intake, the effect may not be positive. Thus, in a longitudinal study in infants months of age, i. In young children aged years, either calcium supplement or gross motor activity increased bone mass accrual as compared to either placebo or fine motor activity.
This regional specificity suggests that the effect of physical activity alone or combined with relatively high calcium supply is not merely due to an indirect influence on the energy intake, which in turn would positively affect bone mass acquisition. It has not been established whether the type of calcium salt used to supplement diets may modulate the nature of the bone response. The observation that calcium supplementation can increase bone size, at least transiently, has been observed using either milk extracted calcium-phosphate as well as calcium carbonate salt.
Another uncertainty is the question of whether gains observed by the end of the intervention are maintained or lost after discontinuation of calcium supplementation. A clear answer to this question requires long term follow up, since sustained gain even on bone mass and size may be transient, possibly resulting from some indirect influence of calcium supplementation on the tempo of pubertal and thereby bone maturation.
The observational and interventional studies discussed above illustrate the numerous factors that can modulate the bone response to calcium intake. This foregoing analysis may, at least in part, explain the difficulty to reach a scientifically based worldwide consensus on dietary allowance recommendation for children and adolescents.
Nevertheless, taking into account both the results of all studies as well as our knowledge on the physiology of calcium and bone metabolism, particularly on the adaptive mechanisms operating during the peripubertal period,61 it appears reasonable and safe to recommend food intake that would provide about mg of calcium per day from prepuberty to the end of adolescence.
Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO study group. Briot K, Roux C. Best Pract Res Clin Rheumatol ;19 6: Specker BL, Schoenau E.
Quantitative bone analysis in children: J Pediatr ; 6: Osteoporos Int ;4 Suppl 1: Familial resemblance for bone mineral mass is expressed before puberty. J Clin Endocrinol Metab ;83 2: Differential effect of race on the axial and appendicular skeletons of children. J Clin Endocrinol Metab ;83 5: Pathogenesis of bone fragility in women and men.
Longitudinal monitoring of bone mass accumulation in healthy adolescents: Evidence for a marked reduction after 16 years of age at the levels of lumbar spine and femoral neck in female subjects.
J Clin Endocrinol Metab ;75 4: Relative contribution of vertebral body and posterior arch in female and male lumbar spine peak bone mass. Osteoporos Int ;4 5: Vertebral size in elderly women with osteoporosis. Mechanical implications and relationship to fractures. J Clin Invest ;95 5: Naganathan V, Sambrook P. Gender differences in volumetric bone density: Osteoporos Int ;14 7: Asynchrony between the rates of standing height gain and bone mass accumulation during puberty.
Osteoporos Int ;7 6: Fracture patterns in children. Analysis of 8, fractures with special reference to incidence, etiology and secular changes in a Swedish urban population Acta Orthop Scand Suppl ; Epidemiology of fractures of the distal end of the radius in children as associated with growth. J Bone Joint Surg ;71 8: Childhood fractures are associated with decreased bone mass gain during puberty: An early marker of persistent bone fragility? J Bone Miner Res ;21 4: Bonjour JP, Chevalley T. Pubertal timing, peak bone mass and fragility fracture risk.
Peak trabecular vertebral density: Calcif Tissue Int ;43 4: Relationship between bone mass and rates of bone change at appendicular measurement sites. J Bone Miner Res ;7 7: Schweiz Med Wochenschr ;25; Evaluation of a prediction model for long-term fracture risk. J Bone Miner Res. A theoretical analysis of the relative influences of peak BMD, age-related bone loss and menopause on the development of osteoporosis. Osteoporos Int ;14 Structural and biomechanical basis of racial and sex differences in vertebral fragility in Chinese and Caucasians.
Construction of the femoral neck during growth determines its strength in old age. J Bone Miner Res ;22 7: Bone density at various sites for prediction of hip fractures. Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures.
Br Med J ;18; Reduced bone mass in daughters of women with osteoporosis. N Engl J Med ;2; 9: Bone mass in middle-aged osteoporotic men and their relatives: J Bone Miner Res ;13 Endocr Rev ;20 6: Endocr Rev ;23 3: World Rev Nutr Diet ; Gene-environment interactions in the skeletal response to nutrition and exercise during growth. Med Sport Sci ; Endocr Rev ;25 3: Reversing sex steroid deficiency and optimizing skeletal development in the adolescent with gonadal failure.
The earlier gain and later loss of cortical bone: Assessment of the risk of post-menopausal osteoporosis using clinical factors. Clin Endocrinol Oxf ;36 3: The effect of gynecological risk factors on lumbar and femoral bone mineral density in peri- and postmenopausal women.
Epidemiology of spinal osteoporosis. Spine ; 15;22 24 Suppl: Risk factors for hip fracture in European women: J Bone Miner Res ;10 Relation of early menarche to high bone mineral density. Calcif Tissue Int ;57 1: Factors affecting peak bone density in Japanese women.
Calcif Tissue Int ;64 2: Pubertal timing predicts previous fractures and BMD in young adult men: J Bone Miner Res ;21 5: Interaction between calcium intake and menarcheal age on bone mass gain: An eight-year follow-up study from prepuberty to postmenarche.
J Clin Endocrinol Metab ;90 1: Caverzasio J, Bonjour JP. Characteristics and regulation of Pi transport in osteogenic cells for bone metabolism. Kidney Int ;49 4: Biomechanical and molecular regulation of bone remodeling.
Annu Rev Biomed Eng ;8: Mechanical loading reduced osteocyte expression of sclerostin protein. J Bone Miner Res ;21 Suppl 1: Bone mineral density in sclerosteosis; affected individuals and gene carriers.
J Clin Endocrinol Metab Dec;90 Aministration of sclerostin antibodies to female cynomolgus monkeys results in increased bone formation, bone mineral density and bone strength. The effect of mechanical loading on the size and shape of bone in pre- peri- and postpubertal girls: J Bone Miner Res ;17 Exercise during growth and bone mineral density and fractures in old age.
Lancet ; 5; Bone loss and fracture risk after reduced physical activity.
J Bone Miner Res ;20 2: Bone geometry and density in the skeleton of pre-pubertal gymnasts and school children. Schoenau E, Frost HM. The "muscle-bone unit" in children and adolescents. Calcif Tissue Int ;70 5: The relationship between muscle size and bone geometry during growth and in response to exercise.
Bone geometry in response to long-term tennis playing and its relationship with muscle volume: J Endocrinol Invest ;26 9: Prevention and management of osteoporosis. Report of a scientific group. Milk intake during childhood and adolescence, adult bone density, and osteoporotic fractures in US women. Am J Clin Nutr ;77 1: The calculation is made using an algorithm which includes BMD and a series of independent clinical factors which are included in Table 2.
The strongest clinical factors, in addition to the BMD, are age, personal history of fracture, family history, consumption of corticoids and the existence of rheumatoid arthritis. Aetiopathology In the last decade we have seen a revolution in the understanding of bone biology. Osteoporosis is the consequence of an alteration in bone remodelling which consists of an imbalance which favours resorption over formation.
The result is low bone mass, and changes in the microarchitecture There are various types of osteoporosis which can be classified into two groups, primary and secondary The most common type of osteoporosis is postmenopausal, which is linked to two conditions, the menopause and aging. In women the ceasing of ovary function, and the consequent reduction in oestrogens, is accompanied by a phase of accelerated bone loss. Treatment by substituting the oestrogens reverses, to a great degree, this situation.
The oestrogens reduce osteoclastogenesis by means of a complex, and not yet completely understood, interaction of cellular signals and bone cells Their deficiency increases resorption and the loss of bone mass and structure, which translates into bone fragility.
Another type of primary osteoporosis is involutive osteoporosis, which affects both men and women, and which is more associated with aging. The existence of a negative calcium balance and a certain degree of secondary hyperparathyroidism have been the pathogenic mechanisms linked to this bone loss.
However, recent studies suggest that oestrogen deficiency may play a significant role in later stages of life, regulating the homeostasis of extraskeletal calcium. The oestrogens may modulate the cacium balance, favouring its intestinal absorption and limiting its renal elimination.
In addition, an active influence of the oestrogens in the metabolism of vitamin D and its capacity to reduce the secretory reserve of parathormone PTHhas been described. These circumstances have allowed the development of a unitary model of involutive osteoporosis, in which the deficiency of oestrogens plays a central role Male osteoporosis is less frequent than postmenopausal osteoporosis. From the point of view of using the BMD, recommended as cut-off points for an indication of postmenopausal osteoporosis are a T-score below The occurrence of primary osteoporosis in males appears to be lower than that for women.
In the first situation the production mechanism is principally of an involutive type. The causes of secondary osteoporosis are those which are produced as a consequence of a disease, or from taking pharmaceutical drugs. The most common is osteoporosis due to glucocorticoids. The risk of fracture is independent of BMD and is both related to the daily dose and the accumulated dose.
Yet, even doses lower than 7. When the treatment with glucocorticoids is withdrawn the risk of fracture goes down, but remains higher in relation to patients who have not taken them In general, we may consider that half those patients treated for 6 months with glucocorticoids will have osteoporosis.
The greatest bone loss is produced during the first 3 months of treatment due to its effect in inhibiting the apoptosis of the osteoclasts This action is by empowered by an increase in the apoptosis of the osteoblasts with a reduction in bone formation. The adverse effects of treatment also reach the muscle, which is atrophied, in turn, losing force and resistance, which presents a risk of falls.
Importance of osteoporosis Osteoporosis has a great impact on the general population. Osteoporotic fractures impose a load of great magnitude from a socioeconomic point of view. It is a very common disease which affects million people in the world. Approximately half of these patients come from the developed countries of North America, Europe and Japan.
Although measures have been proposed to reduce the problem, osteoporosis continues to be under-diagnosed and many patients, even with fractures recognisable as osteoporotic, remain without treatment. The social and political measures are not yet sufficient to address the prevention of this serious socio-health problem. The analysis of these costs carry a high degree of uncertainty. The calculation is difficult and unreliable, since the available information is incomplete The costs, as is logical, are not limited to the pharmacological or surgical interventions.
They are divided into direct and indirect costs. Among the first are those due to hospitalisation, outpatient care and drugs. These may be related to immediate assistive, social and hospital care, both short and long term, and to drugs. The costs of hospitalisation can be seen to be influenced by its duration.
Within the outpatient care are included visits to the traumatologist, visits to other doctors, including the general practitioner, nurse visits, physiotherapy, occupational therapy and telephone assistance.
Counted in the direct non-medical costs are social care and informal care. Services to be taken into account within social care, among others, are adaptations to the home, home health care, general home help and transport.
Finally, among indirect costs, should be considered as key the loss of production of the patient, or of the family who looks after them On the other hand, the reduction in quality of life related to health has a significant social and individual cost.
Clinical manifestations Osteoporosis is an asymptomatic disease. It is a mistake to consider that bone loss is accompanied by musculoskeletal pain, and it is relatively common that patients are referred for this reason with the suspicion of osteoporosis, especially women in the peri- or first years of the menopause. The principle clinical manifestations are due to its complications, fractures.
The most frequent fragility fractures are located in the spinal column, the wrist and the hip. They are usually classified in a more general way as vertebral or non-vertebral. Among the non-vertebral fractures are also included those of the humerus, pelvis, ribs and other less frequent types.
Not usually included as osteoporotic fractures are those of the finger, and cranium, but there are some doubts about fracture of the ankle They are produced by a minor trauma, such as a simple fall from a standing position.
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For this reason also, they are known as fragility fractures. They appear principally after the age of 50 years, and that differentiates them from the traumatic fractures which predominate in youth. The clinical manifestations of these fractures are the same as other fractures in the same location, and are accompanied with pain, loss of functional power and deformity The vertebral fracture is the most prevalent.
Its typical clinical presentation form is acute pain, although not infrequently it can be asymptomatic. It can be the consequence of a mechanical effort in carrying or lifting weight, but also can have no apparent cause. The most typical manifestation is acute, intense pain located in the spine, which is exacerbated with movement and reduces with rest. This becomes very incapacitating, impeding sleep. The intensity of the pain usually reduces after the first weeks, before disappearing after months.
The pain may radiate towards the ribs or the legs, according to whether it proceeds from the dorsal or lumbar spine. However, almost two thirds of vertebral fractures are asymptomatic and can only be confirmed by means of radiography of the lumbar or dorsal spine. For this reason these are classified as clinical or morphometric fractures, the latter only evident through imaging techniques30, In some patients, as a consequence of structural changes in the spine there may develop an instability of the spine, with paraspinal muscular contraction, ligamentous tension and incongruity in the articular facets which may be the cause of chronic axial pain The loss of height of the vertebral bodies reduces the distance between the ribcage and the pelvis, which in some patients even results in the establishment of painful contact between the ribs and pelvis costo-pelvic syndrome.
The accumulation of vertebral crushing is translated into a loss of height. Some authors consider that a reduction of more than 3 cm in two years may be a sign of vertebral fractures.
It has been proposed that the span of the higher extremities, a measure equal to the body height in youth, be compared with the height of the patient to detect reductions in height. It is of considerable interest that rarely in osteoporotic vertebral fractures are observed the neurological complications which accompany vertebral fractures of a different origin The appearance of medullary or radicular neurological manifestations should make us think of a non-osteoporotic origin for a fracture These modifications in the spine may cause difficulties in thoracic movement and affect breathing.
The abdomen loses capacityand becomes prominent, with consequent modification the intestinal tract. The most serious fracture is that of the hip, generally triggered by a fall. Although there are no data which support it, it has become common belief that in the presence of significant osteoporosis, the patient fractures their hip standing up, after which they fall.
The highest rate of mortality associated with osteoporosis is related to hip fracture and represents one of its most significant social costs. The causes of death are diverse and in many cases are not directly related to the fracture4. Most cases require surgical intervention. But the repercussions of a hip fracture are not limited to its hospital treatment, but also to the deterioration of the quality of life.
The majority of patients have residual disability and a percentage of cases lose the capacity to live an independent life. For example, only a fifth of those patients who walked unaided before the fracture can do so 6 months after it The Colles fracture has fewer repercussions than the two earlier ones.
Some patients can experience persistent local pain, functional incapacity, neuropathy and posttraumatic arthritis; in addition, it is a significant risk factor for future presentation of vertebral or hip fractures Finally, the psychological and social impact should be taken into account, which may result in osteoporotic fractures.
The development of depression is the psychological disorder most frequently cited. The appearance of anxiety, fear of new fractures, and other emotional reactions are also important, and influence the recuperation of those patients The repercussions on families of patients with hip fracture and often with a great physical and psychological dependency, cannot sensibly be calculated due to their complexity.
Am J Med ; Osteoporosis prevention, diagnosis, and therapy. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis.
Mora S, Gilsanz V.