Remodeling is regulated by local cytokines as well as by circulating hormones, including parathyroid hormone PTH , 1,dihydroxyvitamin D 1,OH 2 -D , insulin-like growth factor 1 IGF-1 , and calcitonin. Net bone mass depends on the balance between bone resorption and bone formation. If formation exceeds resorption, as it should during childhood and adolescence, net bone mass increases.

If resorption exceeds formation, net bone mass is reduced. Factors affecting bone health are shown in Table 1. Male subjects have higher bone mass than female subjects, and black women have higher bone mass than white non-Hispanic women or Asian women. Mexican-American women have bone densities between those of white non-Hispanic and black women.

Modifiable determinants of bone mass include nutritional intake of calcium, vitamin D, protein, sodium, and carbonated beverages ie, soda ; exercise and lifestyle; maintenance of a healthy body weight; and hormonal status.

Nutrition and physical activity are each necessary and function synergistically to improve bone acquisition and maintenance.

Calcium is necessary for bone accretion, and dietary calcium intake during infancy, childhood, and adolescence affects bone mass acquisition.

Milk intake during childhood and adolescence is associated with higher BMC and reduced fracture risk in adulthood. Adequate intake is a single value likely to meet the needs of most children and is used for infants younger than 12 months, for whom RDAs have not been established.

The upper limit represents the highest average total daily intake likely to pose no risk of adverse health effects for most people in that age group. Upper limit UL indicates level above which there is risk of adverse events.

The UL is not intended as a target intake no consistent evidence of greater benefit at intake levels above the RDA. Reflects adequate intake reference value rather than RDA.

RDAs have not been established for infants. The primary source of nutrition for healthy term infants in the first year of life is human milk or, alternatively, infant formula if human milk is not available.

Although the BMC may be higher in formula-fed infants than in breastfed infants in the first year of life, the breastfed infant does not demonstrate any evidence of clinical mineral deficiency, and there is no evidence that the breastfed infant should not be the standard for bone mineral accretion.

No data support high mineral intake or supplementation with calcium for healthy breastfed infants. Each 8-oz mL serving of milk provides approximately mg of calcium, and the calcium content of low-fat or flavored milk is similar to that of whole milk Table 3.

One cup of yogurt or 1. Other dietary sources of calcium include green leafy vegetables, legumes, nuts, and calcium-fortified breakfast cereals and fruit juices. Although vegetables are a good source of bioavailable calcium, the quantity of vegetables required to meet daily requirements is substantial, making it difficult to attain dietary calcium requirements with vegetables alone.

Certain cereals eg, whole bran cereals contain phytates, which also reduce bioavailability. Data source: Dietary Guidelines for Americans, Available at: www. For example, one 8-oz serving of skim milk contains no fat and only approximately 80 kcal, approximately the same caloric content as an apple.

In contrast, a can of soda contains kcal. Furthermore, milk provides protein and a number of important nutrients other than calcium, including vitamin D, phosphorus, and magnesium, which are important in bone health.

Milk alternatives, such as soy- or almond-based beverages, may have a reduced amount of bioavailable calcium per glass, even when fortified with calcium. Lactose intolerance occurs in children and adolescents and is more common in black, Hispanic, and Asian subjects. Some of these children and adolescents will be able to tolerate small amounts of dairy products other than milk.

Although a number of studies have demonstrated a positive effect of calcium supplementation on BMC in healthy children and adolescents, 27 , 28 a recent meta-analysis of randomized controlled trials examining the effectiveness of calcium supplementation in increasing BMD in healthy children found that there was no effect of calcium supplementation on BMD of the lumbar spine or femoral neck; a small effect was noted on upper-limb BMD and total body BMC equivalent to approximately a 1.

For most children and adolescents, the emphasis should be on establishing healthy dietary behaviors with a well-balanced diet that includes calcium intake at or near the recommended levels throughout childhood and adolescence. Dietary sources of calcium should be recommended in preference to calcium supplements, not only because of the improved bioavailability of dietary sources of calcium, but also primarily to encourage lifelong healthy dietary habits.

Vitamin D calciferol is a fat-soluble hormone necessary for calcium absorption and utilization. Although there is increasing evidence that vitamin D may also have potential benefits on cardiometabolic risk factors, immunity, and cancer prevention, the focus of the present report is on bone health.

In , the IOM revised the RDAs for vitamin D intake to be higher than previous recommendations Table 2 , and the AAP endorsed these recommendations. Deficiency is particularly common in those living in northern climates, those with dark skin, and those with inadequate exposure to sunlight, but deficiency also occurs in sunny climates.

Certain medications, such as anticonvulsant, glucocorticoid, antifungal, and antiretroviral medications, increase requirements and predispose subjects to deficiency. Severe vitamin D deficiency is associated with reduced bone mass in adolescents.

Vitamin D 3 is synthesized in the skin from 7-dehydrocholesterol on exposure to sunlight, binds to vitamin D—binding protein, and is transported to the liver where it undergoes hydroxylation to form hydroxyvitamin D OH-D.

The half-life of OH-D is 2 to 3 weeks, and serum OH-D is a good indicator of vitamin D stores. Circulating OH-D undergoes a second round of hydroxylation in the kidney to form 1,OH 2 -D, the active form of the hormone. In contrast to OH-D, 1,OH 2 -D has a half-life of 4 hours. Exposure to UV B radiation in the range of to nm from sunlight is the major source of vitamin D.

Synthesis of vitamin D depends on latitude, skin pigmentation, sunscreen use, and time of day of exposure. Synthesis of vitamin D is minimal during winter months north of 33° latitude in the northern hemisphere and south of 33° latitude in the southern hemisphere.

Exposure of arms and legs to 0. Sunscreen with a sun protection factor 8 or higher effectively prevents transmission of UV B radiation through the skin and blocks the synthesis of vitamin D 3. Maximal synthesis occurs between the hours of am and pm in the spring, summer, and fall.

With decreased synthesis of vitamin D from reduced sun exposure, dietary sources of vitamin D become more important. Natural dietary sources of vitamin D are limited but include cod liver oil, fatty fish eg, salmon, sardines, tuna , and fortified foods.

Farm-raised salmon has lower concentrations of vitamin D than does fresh, wild-caught salmon. In the United States and Canada, all infant formula is fortified with vitamin D. Cow milk, infant formula, and fortified fruit juices each contain approximately IU of vitamin D per 8 oz Table 4.

The RDA is IU for children 1 year and older. Daily supplementation of breastfed infants with IU of vitamin D during the first months of life increases OH-D amounts to normal concentrations.

For those who are unable to achieve adequate amounts of vitamin D in their diet or who have vitamin D deficiency, vitamin D supplements are available in 2 forms: vitamin D 2 ergocalciferol , derived from plants, and vitamin D 3 cholecalciferol , synthesized by mammals.

Some calcium preparations also contain vitamin D. In adolescent girls, supplementation of to IU of vitamin D 3 was effective in increasing BMD in a dose-response manner. Measurement of serum OH-D concentration reflects both endogenous synthesis and dietary intake of vitamin D and is the optimal method of assessment of vitamin D status.

This value was derived on the basis of an assumption of minimal exposure to sunlight and minimal solar vitamin D conversion. In a population of healthy white Danish and Finnish girls, a daily intake of approximately IU of vitamin D was necessary to enable Evidence is insufficient to recommend universal screening for vitamin D deficiency.

The IOM and existing AAP reports do not make recommendations specific to screening. More evidence is needed before recommendations can be made regarding screening of healthy black and Hispanic children or children with obesity.

The recommended screening is measuring serum OH-D concentration, and it is important to be sure this test is chosen instead of measurement of the 1,OH 2 -D concentration, which has little, if any, predictive value related to bone health.

Both vitamin D 2 and vitamin D 3 increase serum OH-D concentrations. In adults, some 52 , 53 but not all 54 studies have suggested that vitamin D 3 is more effective in increasing serum OH-D concentrations than is vitamin D 2.

It is not unusual for a second course of treatment to be necessary to achieve adequate concentrations of serum OH-D.

In , The replacement of milk in the diet by soda can prevent adolescents from achieving adequate calcium and vitamin D intake, and because soda consumption has no health benefit, it should be avoided.

Diets low in protein or high in sodium will predispose subjects to reduced calcium retention. Mechanical forces applied to the skeleton mechanical loading increase bone formation, and weight-bearing exercise improves bone mineral accrual in children and adolescents.

A population-based prospective controlled trial in Sweden demonstrated that a school-based, moderately active, 4-year exercise program increased bone mass and size in children aged 7 through 9 years without increasing fracture risk.

When female athletes become amenorrheic, the protective effect of exercise on BMD is lost. Increases in BMD are site specific, depending on the loading patterns of the specific sport.

For example, BMD is greater in gymnasts at the hip and spine, in runners at the femoral neck, and in rowers at the lumbar spine; tennis players have higher radial BMD in the dominant arm than in the nondominant arm. High-impact sports eg, gymnastics, volleyball, karate or odd-impact sports eg, soccer, basketball, racquet sports are associated with higher BMD and enhanced bone geometry.

For most children and adolescents, walking, jogging, jumping, and dancing activities are better for bone health than are swimming or bicycle riding. Excessive high-impact exercise can, however, increase fracture risk.

A prospective longitudinal study of high school girls found that those who participated in more than 8 hours per week of running, basketball, cheerleading, or gymnastics were twice as likely to sustain a fracture compared with less active girls.

The authors suggested that girls who participate in these sports should also include cross-training in lower impact activities. Lifestyle choices may also confer additional risk for BMD deficits.

In adults, smoking, caffeine, and alcohol intake are all associated with reduced BMD, 68 , — 70 and these behaviors should be avoided in children and adolescents. Body weight and composition are important modifiable determinants of bone mass. Mechanical loading during weight-bearing activities stimulates bone formation, and multiple studies in healthy adolescents 8 , 71 , — 73 and in those with anorexia nervosa 74 , — 77 have demonstrated that BMD is directly correlated with BMI.

Lean body mass is most strongly associated with BMD, 78 but increased adiposity can also be associated with increased fracture risk. Several hormones affect bone mass. Estrogen plays an important part in maintaining BMD in women, and estrogen deficiency is associated with increased bone resorption and increased fracture risk.

Testosterone, growth hormone, and IGF-1 all promote bone formation, whereas glucocorticoid excess both increases bone resorption and impairs bone formation. Conditions associated with reduced bone mass and increased fracture risk in children and adolescents are listed in Table 6.

Osteogenesis imperfecta, idiopathic juvenile osteoporosis, and Turner syndrome are rare conditions with increased bone fragility, best managed by pediatric endocrinologists, geneticists, and specialists in pediatric bone health.

Children with chronic illnesses are, however, frequently managed by general pediatricians. Cystic fibrosis, systemic lupus erythematosus, juvenile idiopathic arthritis, inflammatory bowel disease, celiac disease, chronic renal failure, childhood cancers, and cerebral palsy can all be associated with reduced bone mass.

Children with cerebral palsy are at particular risk. Eating disorders are prevalent in adolescents. The degree of reduction of BMD is directly related to the degree of malnutrition, and in girls, is related to the duration of amenorrhea. Low BMD is also found in boys with anorexia nervosa and is associated with low testosterone concentrations.

The energy deficit may be unintentional secondary to a lack of knowledge regarding the increased energy requirements of athletes or it may be intentional and associated with an underlying eating disorder. There is suppression of the hypothalamic-pituitary-ovarian axis, resulting in amenorrhea, a low estrogen state, reduced bone mass, and increased fracture risk.

Endocrine conditions associated with glucocorticoid or PTH excess, hypogonadism, hyperthyroidism, or deficiency of growth hormone or IGF-1 are all associated with low bone mass Table 6. Certain medications, including anticonvulsants and chemotherapeutic agents, prolonged use of proton pump inhibitors, and selective serotonin reuptake inhibitors, can also have a negative effect on bone mass.

Depot medroxyprogesterone acetate DMPA is a very effective long-acting contraceptive that has been credited, to some degree, for the reduction in adolescent pregnancy rates in the United States over the past decade. Prolonged use of DMPA in adolescent girls is associated with hypothalamic suppression and reduced bone mass, however.

Discontinuation of DMPA is associated with rapid improvements in bone mass, although it is not known how much of potential maximum peak bone mass is recovered. The Society for Adolescent Health and Medicine recommends continuing to prescribe DMPA to adolescent girls needing contraception but recommends explanation of the risks and benefits.

The ideal method of assessment of clinically relevant bone health is determination of fracture risk on the basis of longitudinal data. However, there is a paucity of longitudinal studies examining factors affecting bone health in children on the basis of incidence of fractures. Fracture risk depends not only on skeletal fragility but also on age, body weight, history of fractures, and the force of an injury.

Skeletal fragility, in turn, is dependent on a number of factors in addition to bone mass, including bone size, geometry, microarchitecture, and bending strength. For example, bending strength depends on the radius of a bone, and a large bone will be more resistant to fracture than a smaller bone, even when both bones have the same BMC or BMD.

Dual-energy x-ray absorptiometry DXA is the preferred method of assessment of bone mass because of its availability, speed, precision, and low dose of radiation 5—6 mSv for the lumbar spine, hip, and whole body, which is less than the radiation exposure of a transcontinental flight and one-tenth that of a standard chest radiograph.

DXA machines are widely available, and robust pediatric reference databases for children older than 5 years are included with the software of the major DXA manufacturers.

Scanning time of the hip or spine is less than 1 minute; for the whole body, it is approximately 5 minutes. In adults, each SD reduction in BMD below the young adult mean doubles the fracture risk.

Osteoporosis is operationally defined as a BMD 2. However, caution should be used in interpreting DXA results in children.

First, because children have not yet achieved peak bone mass, z scores the number of SDs below the age-matched mean should be used instead of T scores. Second, DXA measures 2-dimensional areal BMD expressed as grams per square centimeter , as opposed to 3-dimensional volumetric BMD expressed in grams per cubic centimeter , and areal BMD underestimates true volumetric BMD in subjects with smaller bones.

Third, many children with chronic illness have growth retardation and delayed puberty. Therefore, a correction should be made for height or height age, and a number of mathematical corrections have been proposed. In contrast to adults, in pediatrics, there is no specific BMD z score below which fractures are more likely to occur, but there is a growing body of literature demonstrating an association between low bone mass measured by using DXA and fracture risk in children.

Limited evidence is available to guide pediatricians regarding when to order a DXA. In general, a DXA should be performed to identify children and adolescents at risk for skeletal fragility fractures and to guide treatment decisions.

DXA scans are usually repeated after 1 year and should not be repeated at an interval of less than 6 months. Quantitative computed tomography measures true volumetric BMD, but the radiation exposure dose is high 30— mSv.

Newer modalities, such as peripheral quantitative computed tomography, can measure volumetric BMD of the appendicular skeleton with much lower radiation doses but are not widely available for clinical use. Quantitative ultrasonography is a noninvasive method of assessing bone health by measuring speed of an ultrasound wave as it is propagated along the surface of bone.

This method is difficult to interpret because of a lack of pediatric reference data, however, and poor precision in the pediatric population. In most chronic diseases associated with low BMD, treatment of the underlying condition helps improve bone mass, and specific interventions will depend on the underlying condition.

Depending on the medical condition, for those children and adolescents who are unable to consume enough calcium from dietary sources, including fortified foods, calcium supplementation can be prescribed.

Calcium carbonate should be taken with meals to promote absorption, but calcium citrate does not require gastric acid for absorption and can be taken on an empty stomach. Screening for vitamin D deficiency by obtaining a serum OH-D concentration is recommended in patients at increased risk of bone fragility and in those with recurrent low-impact fractures.

Bisphosphonates inhibit osteoclast-mediated bone resorption and have been used to increase BMD and reduce fracture risk in children with osteogenesis imperfecta, , — cerebral palsy, and connective tissue disorders , and children treated with corticosteroids.

Bisphosphonates are incorporated into bone and may be slowly released from the bone even after the medication has been discontinued. Because of the paucity of studies on efficacy and long-term safety, at this time these agents should not be used to treat asymptomatic reduction in bone mass in children, and their use should be restricted to osteogenesis imperfecta and other select conditions with recurrent fractures, severe pain, or vertebral collapse.

Adolescent girls with anorexia nervosa or the female athlete triad are frequently prescribed oral contraceptives to improve bone mass, even with no evidence of their efficacy. In girls with anorexia nervosa, oral contraceptives will induce monthly menstruation, which may be incorrectly interpreted as an indication of adequate weight restoration.

Suggested ages to ask these questions are 3 years, 9 years, and during the annual adolescent health maintenance visits. Encourage increased dietary intake of calcium- and vitamin D—containing foods and beverages.

Dairy products constitute the major source of dietary calcium, but calcium-fortified drinks and cereals are available. Low-fat dairy products, including nonfat milk and low-fat yogurts, are good sources of calcium.

Children 4 through 8 years of age require 2 to 3 servings of dairy products or equivalent per day. Adolescents require 4 servings per day Table 3. The RDA of vitamin D for children 1 year and older is IU.

Children who are obese and children on anticonvulsant, glucocorticoid, antifungal, or retroviral medications may require higher doses, but specific end points and targets remain poorly defined. Encourage weight-bearing activities. Walking, jumping, skipping, running, and dancing activities are preferable to swimming or cycling to optimize bone health.

Routine screening of healthy children and adolescents for vitamin D deficiency is not recommended. Those with conditions associated with reduced bone mass Table 6 or recurrent low-impact fractures should have a serum OH-D concentration measured.

Those who have vitamin D deficiency should be treated and have OH-D concentrations measured after completion of treatment. Consider a DXA in medical conditions associated with reduced bone mass and increased bone fragility and in children and adolescents with clinically significant fractures sustained after minimal trauma.

In children, z scores should be used instead of T scores. In those with growth or maturational delay, corrections should be made for height or height age. In adolescent female subjects, discourage preoccupation with extreme thinness. A DXA should be considered in an adolescent athlete who has been amenorrheic for more than 6 months.

Athletes, parents, and coaches should be educated about the female athlete triad. There is no evidence to support prescribing oral contraceptives to increase bone mass in those with anorexia nervosa or the female athlete triad. Until more studies demonstrating safety and efficacy in other populations have been conducted, use of bisphosphonates in children and adolescents should be restricted to osteogenesis imperfecta and conditions associated with recurrent fractures, severe pain, or vertebral collapse.

The authors have indicated they do not have a financial relationship relevant to this article to disclose. This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors.

All authors have filed conflict of interest statements with the American Academy of Pediatrics. Any conflicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication.

The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.

This clinical report has been endorsed by American Bone Health, a national, community-based organization that provides education programs, tools, and resources to help the public understand bone disease and bone health.

All clinical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at or before that time.

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Previous Article Next Article. Bone Acquisition During Childhood and Adolescence. Primary Prevention: Optimizing Bone Health in Healthy Children. Sources of Calcium. Calcium Supplementation. Vitamin D. Sources of Vitamin D. Recommended Daily Intake and Vitamin D Supplementation.

Assessment of Vitamin D Status. Screening for Vitamin D Deficiency. Treatment of Vitamin D Deficiency. Soda Consumption, Protein, and Other Minerals. Exercise and Lifestyle. Body Weight. Hormonal Status. Secondary Prevention: Assessment of Populations at Risk for Increased Bone Fragility.

Conditions Associated With Reduced Bone Mass in Children and Adolescents. Assessment of Bone Health. Tertiary Prevention: Specific Treatments to Increase Bone Mass in Populations at Increased Risk of Fracture.

Oral Contraceptives. The Role of the Pediatrician. Lead Authors. Committee on Nutrition, — Former Committee Member. POTENTIAL CONFLICT OF INTEREST:. Article Navigation. From the American Academy of Pediatrics Clinical Report October 01 Optimizing Bone Health in Children and Adolescents Neville H.

Golden, MD ; Neville H. Golden, MD. This Site. Google Scholar. Steven A. Abrams, MD ; Steven A. Abrams, MD. COMMITTEE ON NUTRITION ; COMMITTEE ON NUTRITION. Stephen R. Daniels, MD ; Stephen R. Information about a therapy, service, product or treatment does not in any way endorse or support such therapy, service, product or treatment and is not intended to replace advice from your doctor or other registered health professional.

The information and materials contained on this website are not intended to constitute a comprehensive guide concerning all aspects of the therapy, product or treatment described on the website.

All users are urged to always seek advice from a registered health care professional for diagnosis and answers to their medical questions and to ascertain whether the particular therapy, service, product or treatment described on the website is suitable in their circumstances.

The State of Victoria and the Department of Health shall not bear any liability for reliance by any user on the materials contained on this website.

Skip to main content. Bones muscles and joints. Home Bones muscles and joints. Osteoporosis in children. Actions for this page Listen Print. Summary Read the full fact sheet. On this page.

Our bones Causes of juvenile osteoporosis Diagnosing juvenile osteoporosis Idiopathic juvenile osteoporosis Long-term risks of osteoporosis in children Treating juvenile osteoporosis Where to get help.

Our bones Our bones are living tissue that is constantly growing, rebuilding, replacing and repairing. Causes of juvenile osteoporosis In most cases, juvenile osteoporosis is caused by an underlying medical condition, certain medications used to treat a medical condition or a lifestyle factor.

Inadequate dietary intake, smoking and alcohol may also lead to juvenile osteoporosis. Diagnosing juvenile osteoporosis Juvenile osteoporosis is usually diagnosed after a child has broken a bone.

Diagnosis may include: medical history physical examination medical histories of family members to find out if a genetic disorder is the cause a bone scan — dual energy x-ray absorptiometry DEXA to test bone density blood tests.

Idiopathic juvenile osteoporosis Sometimes no underlying cause can be found. Treating juvenile osteoporosis In most cases, juvenile osteoporosis can be treated.

Discuss medication options with your doctor. Where to get help Your GP doctor Paediatrician Physiotherapist Exercise physiologist Dietitian Healthy Bones External Link. Tel: Musculoskeletal Australia External Link. Tel: What is juvenile osteoporosis? What are the types? External Link , WebMD.

Juvenile osteoporosis External Link , NIH Osteoporosis and Related Bone Diseases National Resource Center, USA. Pediatric osteoporosis External Link , , Medscape. Give feedback about this page. Was this page helpful? Yes No.

If your child has a condition related to bone minerals, low bone density, rickets, or any related condition, our team can create an individualized treatment plan that meets their wide-ranging needs.

We strive to provide empathetic and compassionate care that involves the input of your family. During an appointment for bone health evaluation, your child can anticipate a comprehensive assessment of their skeletal well-being. It is recommended that patients come prepared with a list of any previous fractures, including details on the age of the fracture and the mechanism of the injury.

Families are also encouraged to bring along nutritional information about their child, with details on their calcium and vitamin D intake. Depending on the physician's recommendations, your child might be advised to have x-rays , bone density testing, and laboratory work, either before or during their visit.

The appointment aims to evaluate bone health status, identify potential risk factors, and develop personalized strategies for optimal bone health maintenance. Breadcrumb Home Programs Bone Health Program. However, in some children disability may extend into adulthood.

The reason for this is unknown. The more bone mass we have, the stronger our bones, and the lower the risk of osteoporosis later in life. In most cases, juvenile osteoporosis can be treated.

Treatment depends on the cause but may include:. This page has been produced in consultation with and approved by:. Content on this website is provided for information purposes only. Information about a therapy, service, product or treatment does not in any way endorse or support such therapy, service, product or treatment and is not intended to replace advice from your doctor or other registered health professional.

The information and materials contained on this website are not intended to constitute a comprehensive guide concerning all aspects of the therapy, product or treatment described on the website. All users are urged to always seek advice from a registered health care professional for diagnosis and answers to their medical questions and to ascertain whether the particular therapy, service, product or treatment described on the website is suitable in their circumstances.

The State of Victoria and the Department of Health shall not bear any liability for reliance by any user on the materials contained on this website. Skip to main content. Bones muscles and joints. Home Bones muscles and joints. Osteoporosis in children. Actions for this page Listen Print.

Summary Read the full fact sheet. On this page. Our bones Causes of juvenile osteoporosis Diagnosing juvenile osteoporosis Idiopathic juvenile osteoporosis Long-term risks of osteoporosis in children Treating juvenile osteoporosis Where to get help.

Our bones Our bones are living tissue that is constantly growing, rebuilding, replacing and repairing. Causes of juvenile osteoporosis In most cases, juvenile osteoporosis is caused by an underlying medical condition, certain medications used to treat a medical condition or a lifestyle factor.

Inadequate dietary intake, smoking and alcohol may also lead to juvenile osteoporosis. Diagnosing juvenile osteoporosis Juvenile osteoporosis is usually diagnosed after a child has broken a bone.

Diagnosis may include: medical history physical examination medical histories of family members to find out if a genetic disorder is the cause a bone scan — dual energy x-ray absorptiometry DEXA to test bone density blood tests. Idiopathic juvenile osteoporosis Sometimes no underlying cause can be found.

Treating juvenile osteoporosis In most cases, juvenile osteoporosis can be treated. Discuss medication options with your doctor. Where to get help Your GP doctor Paediatrician Physiotherapist Exercise physiologist Dietitian Healthy Bones External Link.

Tel: Musculoskeletal Australia External Link. Tel: What is juvenile osteoporosis?