Peak bone mass and its relationship to osteoporosis pain

Peak bone mass and osteoporosis prevention.

Therefore the logical approach to osteoporosis treatment is preventive. Risk of fracture is determined largely by bone density, which is the end result of peak value at skeletal maturity and subsequent age- and menopause-related bone loss. Osteoporosis-related fractures most commonly occur in the hip, wrist or spine. Back pain, caused by a fractured or collapsed vertebra; Loss of height over time Most people reach their peak bone mass by their early 20s. Over time, a person with osteoporosis will lose bone density. Related link: Bouncing back from accidental falls provider if you experience prolonged back pain, loss of height, and a change in posture. A 10 percent increase in peak bone mass reduces the risk of a fracture due to osteoporosis as an.

This is an antibody that helps stop the development of bone-removing cells before they cause bone loss. Patients taking Prolia might be at greater risk for infection How can I prevent osteoporosis? There are many ways you can protect yourself against osteoporosis, including: Exercise on a regular basis. Exercise makes bones and muscles stronger and helps prevent bone loss. It also helps you stay active and mobile.

Weight-bearing exercises, done three to four times a week, are best for preventing osteoporosis. Walking, jogging, playing tennis, and dancing are all good weight-bearing exercises. In addition, strength and balance exercises may help you avoid falls, decreasing your chance of breaking a bone Eat foods high in calcium. Getting enough calcium throughout your life helps to build and keep strong bones. People over 50 should get 1, to 1, mg of calcium each day.

Excellent sources of calcium are milk and dairy products low-fat versions are recommended ; a variety of seafood, such as canned fish with bones like salmon and sardines; dark green leafy vegetables, such as kale, collards and broccoli; calcium-fortified orange juice; and breads made with calcium-fortified flour Supplements. If you think you need to take a supplement to get enough calcium, check with your doctor first.

Calcium carbonate and calcium citrate are good forms of calcium supplements. Be careful not to get more than 2, mg of calcium a day very often. That amount can increase your chance of developing kidney problems Vitamin D. Your body uses vitamin D to absorb calcium. You can also get vitamin D from eggs, fatty fish like salmon, cereal and milk fortified with vitamin D, as well as from supplements.

Most people over age 50 can usually safely takeIU of vitamin D a day. However, some patients do not need any vitamin D supplementation. More than 10, IU of vitamin D each day is not recommended unless your caregiver suggests it because it may harm your liver and even lower bone mass. You should talk to your doctor about your individual vitamin D needs Estrogen.

Estrogen, a hormone produced by the ovaries, helps protect against bone loss. Replacing estrogen that is lost after menopause when the ovaries stop most of their estrogen production slows bone loss and improves the body's absorption and retention of calcium.

But because estrogen therapy carries risks, it is only recommended for women at high risk for osteoporosis who have other reasons for using it, such as menopausal symptoms. To learn more, talk to your doctor about the pros and cons of estrogen therapy Avoid certain medications.

Some medications--including steroids, certain drugs used to treat seizures anticonvulsantsblood thinners anticoagulantsand thyroid medications--increase the rate of bone loss if not used as directed. If you are taking any of these medications, speak with your doctor about how to reduce your risk of bone loss through diet and lifestyle changes Other preventive steps.

Limit the amount of alcohol you drink, and do not smoke. Smoking causes your body to make less estrogen, which protects the bones. Too much alcohol can damage your bones and increase your risk of falling and breaking a bone How can I get the calcium my body needs if I'm lactose-intolerant? If you are lactose-intolerant, or have difficulty digesting milk, you may not be getting enough calcium in your diet. Although you may not be able to eat or drink most dairy products, you do have some choices: You might be able to digest some yogurt and hard cheeses.

You can also eat food that contains lactose by first treating it with commercial preparations of lactase which can be added as drops or taken as pills. You can buy lactose-free dairy products. You can also eat lactose-free foods that are high in calcium, such as leafy green vegetables, salmon, and broccoli. What are weight-bearing exercises and how do they help strengthen bone? Weight-bearing exercises are activities that make your muscles work against gravity. Walking, hiking, stair climbing, and jogging are all weight-bearing exercises that help build strong bones.

Thirty minutes of regular exercise at least 4 days a week, or every other day along with a healthy diet may increase peak bone mass in younger people.

Determination of aBMD is particularly convenient in terms of availability of equipment, low exposure to irradiation, reproducibility of the measurement at several sites of the skeleton and, last but not least, its relationship with adult osteoporosis fracture risk as adequately documented in large cohorts of women and men. Because of this last characteristic, aBMD was recognized by several national and international institutions including the World Health Organization WHO ,1 as the variable to be measured for establishing the diagnosis of adult osteoporosis.

These positive aspects do not mean that aBMD measurement integrates all determinants of bone strength. Structural and functional components contribute to the degree of bone fragility and therefore to the risk of experiencing osteoporotic fractures during adult life. The recent use of high-resolution peripheral quantitative computed tomography pQCT can provide additional information on more subtle bone structural mechanical resistance components.

This technical approach is expected to improve the prediction of bone strength as compared to the current use of the variables that can easily be captured by DXA: In addition, at some skeletal sites an estimate of volumetric v BMD, cortical thickness, cross-sectional area and moment of inertia can be computed.

Osteoporosis - Symptoms and causes - Mayo Clinic

Quantitative ultrasonography QUS has been compared to DXA for identifying adults with osteoporosis and fragility fractures. Although QUS parameters determined in some but not all tested devices can predict the osteoporotic fracture risk, their use is still not recommended for the diagnosis or treatment monitoring of adult osteoporosis. Calcaneous QUS measurements can detect low bone mass during childhood and adolescence.

However, as recently argued, this technique remains a research tool in the pediatric population. During growth, aBMD increment is essentially due to an increase in bone size,4 which is closely linked to a virtually commensurate increment in the amount of mineralized tissue contained within the periosteal envelope. Consequently, vBMD increases very little from infancy to the end of the growth period.

In healthy girls, longitudinal examination of the lumbar spine development during pubertal maturation indicates that the standard deviation scores Z-scores of aBMD, BMC, vBMD, as well as vertebral body width and height are highly correlated, with "r" coefficients ranging from 0.

There is no evidence of a gender difference in bone mass at birth; the vBMD appears to be similar in female and male newborns. This absence of substantial sex differences in bone mass is maintained until the onset of pubertal maturation. The gender difference in bone mass is expressed during puberty. This difference appears to be due mainly to a more prolonged bone maturation period in males than in females, with a larger resulting increase in bone size and cortical thickness.

Puberty affects bone size much more than it does vBMD. There is no significant sex difference in volumetric trabecular density at the end of pubertal maturation. The increment in bone mass gain is less marked in long bone diaphyses. It certainly represents an important macro-architectural determinant of the difference in the incidence of vertebral fragility fractures observed between female and male subjects in later life.

Within each gender, this structural property also plays an important role in vertebral fracture risk. In postmenopausal women, a smaller cross-sectional area of vertebral bodies was measured in those with than without vertebral fractures despite the fact that the two groups displayed equally low trabecular vBMD as determined by spinal QCT. There is an asynchrony between the gain in standing height and the growth of bone mineral mass during pubertal maturation. It is possible that some of these fractures may also be determined by tracking, from infancy to the end of skeletal maturation, along a relatively low bone mass percentile Z-score.

In adolescent females, gain in bone mass declines rapidly after menarche; no further statistical gains are observed 2 years later at least in sites such as the lumbar spine or femoral neck. As described above the change in vBMD during growth is very modest as compared to the increment in bone size. Furthermore the increased vBMD as measured by QCT has been detected in vertebral cancellous bone but not in appendicular cortical tissue. This is in keeping with numerous observations indicating that at most skeletal sites, total bone mineral mass does not significantly increase from the third to the fifth decade.

Nevertheless, a few cross-sectional studies suggest that bone mass acquisition may still be substantial during the third and fourth decades. In any case, the balance of published data does not sustain the concept that bone mass at any skeletal site, in either gender and in any ethnic geographic population group, continues to accumulate through the fourth decade.

However, several observations are not consistent with such an increased range in aBMD values in relation to age. In untreated post-menopausal women, the standard deviation SD of bone mineral mass measured at both the proximal and distal radius was not greater in women aged 70 to 75 compared to 55 to 59 years.

Thus, at both the lumbar spine and femoral neck, the range of aBMD values was no wider in women aged 70 to 90 years old than in women aged 20 to 30 years. The notion of 'tracking' has two important implications.

First, the prediction of fracture risk based on one single measurement of femoral neck aBMD remains reliable in the long term. From these two implications, it can be inferred that the bone mass acquired at the end of the growth period appears to be more important than the bone loss occuring during adult life. Load was determined by upper body weight, height and the muscle moment arm, and bone strength estimated from the bone cross-sectional area CSA and vBMD.

From young to older adulthood, this index increased more in women Chinese and Caucasian than men of the same ethnicity. Similar conclusion was reached concerning the construction of the femoral neck. Determinants of peak bone mass and strength Several interconnected factors influence bone mass accumulation during growth.

These physiological determinants classically include heredity, vitamin D and bonetropic nutrients calcium, proteinsendocrine factors sex steroids, IGF-I, 1. Quantitatively, the most prominent determinant appears to be genetically related. Heredity Mass Parent-offspring comparison studies reveal a significant relationship in the risk of osteoporosis within families, with apparent transmission from either mothers or fathers to their children.

This "genetic effect" appears to be greater in skeletal sites such as the lumbar spine compared to the femoral neck. Two main approaches have dominated the search for genetic factors that would influence bone acquisition and thereby modify the susceptibility to osteoporosis in later life. One approach is to search by genome-wide screening for loci flanked by DNA micro-satellite markers that would co-segregate with the phenotype of interest in a population of related individuals.

The pedigrees investigated to date consist mainly of families with a member at either extreme of the skeletal phenotype spectrum, particularly those exhibiting either very high or very low bone mineral mass or areal density. The second most frequently used approach is to search for an association between allelic variants or polymorphisms of genes coding for products that are implicated in bone acquisition or loss.

Numerous polymorphisms of "candidate" genes have been found to be associated with aBMD, so far the most convenient measurable surrogate of bone mass and strength. The genes studied code for molecules implicated in bone function and structure such as circulating endocrine factors, hormone receptors, local regulators of bone modeling and remodeling or matrix molecules.

None of these genes appears to account for more than a few percent of PBM variance. Identifying the implicated genes interacting with bone-specific nutrients and the response to mechanical loading represents a formidable, but hopefully not intractable, challenge. As specified above, the development of bone mineral mass during the entire growth period, including during pubertal maturation, is essentially due to an increase in bone size, with very mild changes in the amount of mineralized tissue within the bone envelope.

In adulthood, patients affected by the androgen insensitivity syndrome, with XY genotype and a marked female phenotype are taller than the average standing height of the corresponding female population. They exert biphasic effects by accelerating bone growth at the beginning of puberty whereas in both genders, estrogens are key determinants for the closing of growth plates.

In female subjects, bone mineral mass increases more by endosteal than periosteal accrual. To a large extent, they explain the greater risk of osteoporotic fractures occurring in adult women than men. The increased bone mineral apposition at the level of the endosteal surface during puberty in female subjects may teleologically represent a biological adaptation allowing the rapid mobilization of bone mineral in response to the increased needs during pregnancy and lactation.

A later age at menarche was found to be associated with lower aBMD in the spine and proximal femur35,36 and higher risk of vertebral37 and hip fracture38 in adulthood. Indirect evidence from a retrospective epidemiological survey suggests that this association is likely to be related to the influence of pubertal timing on PBM attainment.

In premenopausal women, early compared to late menarche, is associated with higher aBMD. Although this intuitive explanation appears to be quite reasonable, there is no unequivocal evidence demonstrating that sex hormone exposure is the essential causal factor accounting for the association between pubertal timing and the risk of osteoporosis. The growth hormone-insulin-like growth factor-1 system From birth to the end of adolescence, the GH-IGF-1 system is essential for harmonious skeleton development.

During puberty, the plasma level of IGF-1 rises transiently according to a pattern that is similar to the curve of the gain in bone mass and size. This factor exerts a direct action on both growth plate chondrocytes and osteogenic cells responsible for building both cortical and trabecular bone tissue constituents.

This activity is also expressed by parallel changes in the circulating biochemical markers of bone formation, osteocalcin and alkaline phosphatase.

In addition, IGF-1 exerts an important impact on renal endocrine and transport functions that are essential for bone mineral economy. IGF-1 receptors are localized in the renal tubular cells. They are connected to both the production machinery of the hormonal form of vitamin D, namely 1,25 OH 2D and to the transport system of inorganic phosphate Pi localized in the luminal membrane of the tubular cells. Coupled to the stimulation of the tubular capacity to reabsorb Pi, the extra cellular Ca-Pi product is increased by IGF-1, which, through this dual renal action, favors the mineralization of the bone matrix.

Furthermore, at the bone level, IGF-1 still directly enhances the osteoblastic formation of the extra cellular matrix. In growth plate chondrocytes as well as in their plasma membrane derived extra cellular matrix vesicles are equipped by a phosphate transport system that plays a key role in the process of primary calcification and thereby in bone development. This Pi transport system is also present in other osteogenic cells43 and interestingly, is regulated by IGF The hepatic production of IGF-1, which is the main source of its circulating level, is influenced not only by GH, but also by other factors, particularly by amino acids from dietary proteins figure 2.

The modalities of this interaction have still to be delineated in humans. From animal studies, relatively low concentrations of estrogens would appear to stimulate the hepatic production of IGF-1, whereas large concentrations apparently exert an inhibitory effect.

Mechanical forces impinge on the skeleton by enhancing osteoblastic bone formation, while inhibiting osteoclastic bone resorption. Some appear to be produced by the osteocytes. The density, distribution and extensive communication network of osteocytes make them particularly well structured to function as detectors of mechanical strain by sensing fluid movement within the bone canaliculi. They can direct the formation of new bone by activating lining cells to differentiate in preosteoblasts.

Sclerostin can bind and antagonize LRP5, a Wnt co-receptor that is required for bone formation in response to mechanical load. Mechanical loading can induce a marked reduction of sclerostin in both osteocytes and in the canaliculi network. The mechanosensation and transduction in osteocytes still involve other factors including nitric oxide NOprostaglandins and ATP.

Age and optimal response to loading. Growing bones are usually more responsive to mechanical loading than adult bones.

Peak bone mass and osteoporosis prevention.

Physical activity increases bone mineral mass accumulation in both children and adolescents. However, the impact appears to be stronger before than during or after the period of pubertal maturation.

The greater gain in aBMD or BMC in young athletes compared with less active controls is preferentially localized in weight bearing bones, such as the proximal femur. Studies in adult elite athletes strongly indicate that increased bone mass gains resulting from intense physical activity during childhood and adolescence are maintained after training attenuates or even completely ceases.

Exercise during growth and fracture prevention in adulthood. The question whether the increased PBM induced by physical exercise will be maintained into old age and confer a reduction in fracture rate remains uncertain. A cross-sectional study of retired Australian elite soccer players suggested that this might not be the case.

In the perspective of public health programs aimed at increasing bone mineral mass gain in children and adolescents, it is obvious that only physical exercise of moderate intensity, duration and frequency, but which would still be effective, can be taken into consideration. In children, prepubertal individuals or those at an early stage of sexual maturation, several interventions implemented within the school curriculum indicate that moderate exercise can impact positively on bone development.

Nevertheless, it remains uncertain to what extent the greater aBMD gain in response to moderate and readily accessible weight-bearing exercise is associated with a commensurate increase in bone strength.

The magnitude of benefit in terms of bone strength will depend upon the nature of the structural change. An effect consisting primarily of an increased periosteal apposition and consecutive diameter will confer greater mechanical resistance than a response limited to the endosteal apposition rate leading essentially to a reduction in the endocortical diameter.

Here are five things to know about osteoporosis and what can be done to prevent it. Osteoporosis affects bone mass Osteoporosis is a disease affecting the bones. Over time, a person with osteoporosis will lose bone density. The bones become more fragile and porous, which increases the risk of a fracture. Bones naturally have holes and spaces in them, but with osteoporosis, the holes and spaces grow much larger.

Talk with your healthcare provider if you experience prolonged back pain, loss of height, and a change in posture. Those are sometimes indicators of bone loss. White and Asian women also have a higher risk, as do people who have a family member with osteoporosis. People with smaller body frames also have a higher chance of getting the disease.