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Pediatric Osteoporosis

  • Author: Manasa Mantravadi, MD, MS; Chief Editor: Jatinder Bhatia, MBBS, FAAP  more...
 
Updated: May 25, 2016
 

Background

There are several commonly used definitions for osteoporosis. At the 2000 National Institutes of Health (NIH) Consensus Conference, osteoporosis was defined as a skeletal disorder characterized by compromised bone strength that predisposes to an increased risk of fracture.[1] The World Health Organization (WHO) defines osteoporosis in adults as a bone mineral density (BMD) at least 2.5 standard deviations below peak (defined as the BMD achieved by healthy young adults of the same race and gender aged 18-30 y). For adults BMD is commonly expressed in T-scores, defined by standard deviations (SD) from the mean peak bone mineral density with T-scores at the lumbar spine or hip of <-2.5 defining osteoporosis .

Although this definition is functionally valid for adults, it is not appropriate for children as they have not yet attained peak bone mass. Because the T-score is a measure of bone mineral density compared to early adulthood, its use in children whose BMD and bone mineral content (BMC, in grams) have not yet reached peak will generally yield a low value. Instead, Z scores are used in children as they reflect SD scores from the mean in comparison to BMD and BMC of healthy children of the same age, gender, and body size. Some but not all Z-score measures also incorporate race.

It is also important to note that BMD is derived from an areal measure, defined as the bone mineral content (BMC) in grams per selected bone area measured in centimeters squared (see Pathophysiology below). It therefore is not a true volumetric density.  Unlike adult patients in whom the bone volume does not change over time, a child’s bones grow and model over time, with the growth of individual bones not happening uniformly in three dimensions. Sufficient population-based data correlating BMD measures with fracture rates in healthy children are also not available. For all these reasons, the official WHO definition of osteoporosis cannot pertain to children.

In 2007, at the first Pediatric Consensus Development Conference (sponsored by the International Society for Clinical Densitometry (ISCD)) an official position on the use and interpretation of densitometric studies in children based on expert opinion was released; it was subsequently updated in 2013. The following are the most recent pediatric osteoporosis definitions and fracture risk positions in children[2, 3] :

  • “The diagnosis of osteoporosis in children and adolescents should not be made on the basis of densitometric criteria alone.”
  • “The finding of one or more vertebral compression (crush) fractures is indicative of osteoporosis, in the absence of local disease or high-energy trauma. In such children and adolescents, measuring BMD (bone mineral density) adds to the overall assessment of bone health.”
  • “In the absence of vertebral compression (crush) fractures, the diagnosis of osteoporosis is indicated by the presence of both a clinically significant fracture history and BMD Z-score ≤ -2.0. A clinically significant fracture history is one or more of the following: 1) two or more long bone fractures by age 10 years; 2) three or more long bone fractures at any age up to age 19 years.”
  • “A BMC/BMD Z-score > -2.0 does not preclude the possibility of skeletal fragility and increased fracture risk.”

The ISCD guidelines additionally stipulate that dual-energy x-ray absorptiometry (DXA) is the preferred method for assessing BMC and areal BMD (aBMD) in children and adolescents.Although population-based data on the relationship between BMD and fracture are still limited, population-based reference curves for DXA assessments of BMC and aBMD for total body less head (TBLH), lumbar spine, hip, femoral neck and distal one-third radius for black and nonblack children in the United States are now available from the Bone Mineral Density in Childhood Study (BMDCS).[4]

Unlike in adults, where osteopenia is defined as a T-score between -1 and -2.5, use of the word “osteopenia” is not appropriate when referring to pediatric BMC/BMD values. Instead, low BMCs or areal bone mineral densities (aBMDs) are defined by Z-scores –2.0 or less adjusted for age, sex and body size (height z-score). ‘Low bone mineral mass or bone mineral density’ is the phrase that is recommended for low BMC or aBMD in the absence of a fracture history suggestive of osteoporosis rather than osteopenia or osteoporosis.[3]

Go to Osteoporosis for complete information on non-pediatric osteoporosis.

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Pathophysiology

Low BMD in adults is generally due to net bone loss after peak accrual. In children low BMD can result from loss of bone or, more commonly failure to accrue adequate bone mineral for the bone size. Some causes of low BMD are also due to inherited conditions, particularly ones that affect collagen amount or function (such as osteogenesis imperfecta).

DXA provides aBMD measures, which are 2-dimensional measurements derived by dividing BMC measured in grams in a specified bone region (eg, lumbar spine) by the bone area (BA) in cm2.  Since it does not account for the depth of the bone, it gives “density” as a reading in g/cm2. This method of assessing BMD is limited because changes in bone volume are not accounted for. This can result in inaccurate estimations of the degree of bone loss or the skeletal response to treatment. 

Low BMD in children results when there is an imbalance between the rates of bone formation and resorption. Low-turnover conditions, characterized by low bone formation, include chronic liver disease, burn injuries, and conditions that affect the bone marrow (eg, leukemias) or their treatments. High-turnover states, such as hyperparathyroidism or hyperthyroidism, can result in an increase in bone resorption.

Bone will not accrue normally when there are deficits of calcium, phosphate, and/or vitamin D or when bone is not exposed to normal physical/mechanical stresses and strains. One population particularly at risk for failure to accrue bone are infants born prematurely.  Because most calcium is transmitted from mother to fetus during the third trimester, premature infants do not receive in utero all the calcium their bodies need to normally mineralize. With rapid postnatal increases in bone turnover, fewer opportunities are available for the bones to mineralize.[5] Furthermore, most of these children receive parenteral nutrition (first as IV fluids and then later as total parenteral nutrition (TPN)) for the first several weeks of life. Calcium and phosphorus requirements are generally not able to be met by TPN in any age group, and infants, especially the very premature infant, can present with poor bone mass and metabolic bone disease.

Other populations of children experience secondary bone loss from adaptations to trauma and infection or threat of infection. These include bone loss due to immobilization as well as loss due to the stress response, in which endogenous glucocorticoids act in the same manner as exogenously administered steroids. These compounds cause an initial increase in osteoblast production of the receptor activator of nuclear transcription factor kappa B ligand (RANKL), which stimulates marrow to produce osteoclastic cells, increasing bone resorption. However, steroids also promote osteoblast apoptosis and reduce marrow cell osteoblast differentiation, eventually leading to a low-turnover bone loss or adynamic bone.

Another mechanism linked to bone loss is the inflammatory response. This involves the production of the cytokines interleukin (IL)–1 beta and IL-6, as well as tumor necrosis factor (TNF) alpha. These can increase bone resorption via stimulation of osteoblast production of RANKL.

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Etiology

Bone mass and, for children, the ultimate achievement of young adult peak bone mass, is predominately determined by genetics. Adequate dietary intake and absorption of calcium, phosphorus, and vitamin D are also critical for normal bone accrual.  Phosphorus is relatively plentiful in most Western diets, and therefore dietary phosphorus deficiency that is significant enough to cause bone disease is very rare.  Calcium intake is much more likely to be deficient in children, particularly young adolescent girls. The NIH Consensus Conference on Osteoporosis recommended that preadolescent and young adolescent girls have a calcium intake that is 50% more than the intake recommended for younger children and older adults.[6] Dietary calcium supplementation in the preadolescent years may be a key factor in optimizing peak bone mass. However, when dietary calcium supplementation is stopped, data suggest that the increase in bone mass is not maintained.

A third factor critical for optimal bone accrual is exercise. In 2014, literature from The Bone Mineral Density in Childhood study showed that self-reported weight-bearing physical activity contributed to significantly greater BMC accrual after adjustment for age, height velocity, Tanner stage, prior visit BMC, and calcium intake in both sexes and both racial subgroups (defined as blacks and non-blacks in this study).[7]

Multiple conditions that can adversely affect bone mineralization and bone strength, and result in pediatric osteoporosis. Primary osteoporosis occurs due to an intrinsic skeletal defect of genetic or idiopathic origin. Osteogenesis imperfecta (OI) is the most common of the genetic conditions. Secondary osteoporosis stems from chronic systemic illnesses in children due to either the effects of the disease process on the skeleton or their treatment. Causes for secondary osteoporosis include immobility, leukemia, inflammatory conditions, glucocorticoid therapy, hypogonadism and poor nutrition.[8]

The following table lists some of the most frequent conditions that result in reduced bone mass in children.[9]

Table 1: Conditions Associated with Reduced Bone Mass in Children and Adolescents (Open Table in a new window)

Genetic conditions
   Osteogenesis imperfecta
   Idiopathic juvenile osteoporosis
   Turner syndrome
Chronic illness
   Cystic fibrosis
   Connective tissue disorders (lupus, juvenile idiopathic arthritis, juvenile dermatomyositis)
   Inflammatory bowel disease, celiac disease
   Chronic renal failure
   Childhood cancer
   Cerebral palsy
   Chronic immobilization
Eating disorders, including anorexia nervosa, bulimia nervosa, eating disorders not otherwise specified, and the female athlete triad
Endocrine disorders
   Cushing syndrome
   Hypogonadism
   Hyperthyroidism
   Hyperparathyroidism
   Growth hormone deficiency
   Diabetes mellitus
Medications
   Glucocorticoids
   Anticonvulsants
   Chemotherapy
   Leuprolide acetate
   Proton pump inhibitors
   Selective serotonin reuptake inhibitors
   DMPA

Table from: Golden NH, Abrams SA, Committee on Nutrition. Optimizing bone health in children and adolescents. Pediatrics. 2014 Oct. 134 (4):e1229-43.

Osteogenesis imperfecta (OI), a rare genetic disorder of type 1 collagen, is perhaps the most studied form of primary osteoporosis. Individuals with OI present with varying degrees of fracture, blue sclerae, dentinogenesis imperfecta, ligament laxity, and hearing impairment.[10] Bone biopsy shows decreased cortical and cancellous bone mass.[11] Dominant mutations in COL1A1 and COL1A2 account for 95% of OI cases.[12]

For more on OI, visit http://emedicine.medscape.com/article/1256726-overview

Idiopathic juvenile osteoporosis (IJO) is another rare form of primary osteoporosis and is a diagnosis of exclusion. IJO typically presents before puberty and spontaneously remits after puberty. Its characteristic features are bone pain, walking difficulties, and metaphyseal and vertebral fractures.[13]

Secondary forms of pediatric osteoporosis can be the result both of the primary disease but also from the treatments for that disease or concomitant features. Sarcopenia, malnutrition, malabsorption, proinflammatory cytokines, sunlight avoidance, immobilization, endocrine dysfunction, and chronic glucocorticoid exposure are among the list of factors that contribute to the deleterious effects on bone.  

Medications, such as tenofovir, corticosteroids, cyclosporine, and other cytotoxic agents, may contribute to bone loss. Chronic long-term glucocorticoid use decreases bone formation and increases resorption. A 2008 study indicated that the risk of bone loss secondary to oral steroid use is higher in boys than in girls, whereas cumulative inhaled corticosteroids did not increase the risk of bone loss in either boys or girls.[14] However, more recent studies show that children with asthma receiving budesonide and beclomethasone dipropionate have decreased linear growth, and that children who receive long-term inhaled corticosteroid therapy for asthma have height deficits 1–2 years after treatment initiation that persist into adulthood.[15]  Thus, long-term therapy with inhaled corticosteroid therapy is safer than frequent bursts of oral corticosteroids on bone mineral accretion.[15] However, an attempt to minimize any adverse effects with use of lowest effective dose is recommended.

 

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Epidemiology

Highly powered studies do not exist currently for pediatric osteoporosis so the data on the prevalence of pediatric osteoporosis are inadequate.  For example, through 1991, the rare condition of idiopathic juvenile osteoporosis had been reported in only 60 cases. However, numerous observational studies have shown that survivors of pediatric and adolescent cancers are at risk for low bone mass after completion of therapy. Other studies have shown secondary bone fragility occurs early in the disease process, with 16% of children with acute lymphoblastic leukemia and 7% of children with a rheumatologic condition having evidence of vertebral compression fractures within 30 days of diagnosis.[16, 17]

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Prognosis

Prognosis depends on the underlying cause and the severity of the bone disease. While osteoporosis in children is not linked to increased mortality as in adults, it may have serious effects on a child’s quality of life including pain, poor school performance, loss of function, and other long-term consequences. In extreme cases, including idiopathic juvenile osteoporosis and low BMD for age in immobile children with severe developmental delay, crippling bony deformities may lead to cardiopulmonary compromise.

Genetic condition leading to increased bone resorption may have a satisfactory prognosis if the antiresorptive agents can eliminate further bone loss. (See Treatment and Management.)

In the case of trauma-induced or burn-induced low BMD for age in which bone formation is primarily affected, prognosis depends on the patient’s genetically determined peak bone mass and efficacy of clinically experimental therapies, such as anabolic steroids and pamidronate along with correction of progressive vitamin D deficiency that is a consequence of the skin’s failure to make adequate vitamin D with ultraviolet light exposure, similar to what is seen elderly persons. (See Treatment and Management.)

Although theories suggest that early-onset bone loss may be overcome as new healthy bone replaces compromised bone, a long-term outcome study in 144 young adults who were born with very low birth weight and were studied around the time of peak bone mass have significantly lower BMD at the lumbar spine and femoral neck compared to term-born peers.[18] Some studies have evaluated the impact of bone-involving diseases during childhood (anorexia nervosa, malignancy, and juvenile rheumatoid arthritis) on BMD and fracture risk in adult age.[19, 20, 21] These have demonstrated that even after resolution of some childhood diseases, permanent bone damage (in terms of reduced BMD and increased fracture risk) can be seen in adulthood.

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Patient Education

Use education as a means of prevention and treatment. As early as possible, inform patients of any age with low BMD for age or osteoporosis why bone loss has occurred and how to keep bone loss under control. Also inform patients with low BMD for age or osteoporosis of the consequences of bone loss. Instruct children, adolescents, and their families that the roots of adult-onset osteoporosis may begin in childhood.

The American Academy of Pediatrics (AAP) recommends that pediatricians assess children’s calcium and vitamin D consumption at ages 3, 9 and yearly in the pre-teen and teen years. Most children can get the recommended amount of calcium by eating three servings a day of low-fat dairy products – four servings for adolescents. Infants less than one year old should receive 400IU of vitamin D daily. Children greater than 1 and adolescents receive 600 IU of vitamin D daily through diet or supplements. The AAP also encourages physical activity, primarily weight-bearing exercise, as an important part of keeping bones healthy.[9]

For patient education resources, see the Bone Health Center, as well as Osteoporosis and Understanding Osteoporosis Medications.

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Contributor Information and Disclosures
Author

Manasa Mantravadi, MD, MS Assistant Research Professor in Endocrinology/Diabetology, Department of Pediatrics, Indiana University School of Medicine

Manasa Mantravadi, MD, MS is a member of the following medical societies: American Academy of Pediatrics, American Telugu Association

Disclosure: Nothing to disclose.

Coauthor(s)

Linda A DiMeglio, MD, MPH Associate Professor of Pediatrics, Section of Pediatric Endocrinology and Diabetology, Department of Pediatrics, Indiana University School of Medicine; Director, Type 1 Diabetes Research Team, Riley Hospital for Children at Indiana University Health

Linda A DiMeglio, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Society for Bone and Mineral Research, Endocrine Society, Midwest Pediatric Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Janssen<br/>Received research grant from: Alexion.

Stephanie E Woerner, RN, MSN, FNP-C, CDE Family Nurse Practitioner, Pediatric Endocrinology and Diabetology, Riley Hospital for Children at Indiana University Health, Indiana University School of Medicine; Family Nurse Practitioner, MinuteClinic, Inc

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Jatinder Bhatia, MBBS, FAAP Professor of Pediatrics, Medical College of Georgia, Georgia Regents University; Chief, Division of Neonatology, Director, Fellowship Program in Neonatal-Perinatal Medicine, Director, Transport/ECMO/Nutrition, Vice Chair, Clinical Research, Department of Pediatrics, Children's Hospital of Georgia

Jatinder Bhatia, MBBS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Society for Nutrition, American Society for Parenteral and Enteral Nutrition, Academy of Nutrition and Dietetics, Society for Pediatric Research, Southern Society for Pediatric Research

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Gerber.

Additional Contributors

Steven M Schwarz, MD, FAAP, FACN, AGAF Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center

Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American Association for Physician Leadership, New York Academy of Medicine, Gastroenterology Research Group, American Gastroenterological Association, American Pediatric Society, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

Gordon L Klein, MD, MPH Clinical Professor of Orthopedic Surgery and Rehabilitation, University of Texas Medical Branch School of Medicine

Gordon L Klein, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American Gastroenterological Association, American Pediatric Society, American Society for Bone and Mineral Research, American Society for Nutritional Sciences, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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Prediction of bone loss with biochemical bone markers. Adapted from Ross PD, Knowlton W. Rapid bone loss is associated with increased levels of biochemical markers. (DPD stands for deoxypyridinoline.) J Bone Miner Res 1998 Feb; 13(2): 297-302.
Table 1: Conditions Associated with Reduced Bone Mass in Children and Adolescents
Genetic conditions
   Osteogenesis imperfecta
   Idiopathic juvenile osteoporosis
   Turner syndrome
Chronic illness
   Cystic fibrosis
   Connective tissue disorders (lupus, juvenile idiopathic arthritis, juvenile dermatomyositis)
   Inflammatory bowel disease, celiac disease
   Chronic renal failure
   Childhood cancer
   Cerebral palsy
   Chronic immobilization
Eating disorders, including anorexia nervosa, bulimia nervosa, eating disorders not otherwise specified, and the female athlete triad
Endocrine disorders
   Cushing syndrome
   Hypogonadism
   Hyperthyroidism
   Hyperparathyroidism
   Growth hormone deficiency
   Diabetes mellitus
Medications
   Glucocorticoids
   Anticonvulsants
   Chemotherapy
   Leuprolide acetate
   Proton pump inhibitors
   Selective serotonin reuptake inhibitors
   DMPA
Table 2: Calcium and Vitamin D Dietary Reference Intakes [9]

 Age          

 

 

 

      

Calcium     

                                           

Vitamin D              

                

RDA (mg/d) (Intake That Meets Needs of ≥97.5% of Population)

                                  

UL (mg/d)a

RDA (IU/d) (Intake That Meets Needs of ≥97.5% of Population)

                                             

UL (IU/d)a  

Infants        
   0–6 mo                         200b            1000                      400b                 1000
   6–12 mo                         260b            1500                      400b                 1500
   1–3 y                         700            2500                      600                 2500
   4–8 y                         1000            2500                      600                 3000
   9–13 y                         1300            3000                      600                 4000
   14–18 y                         1300            3000                      600                 4000
Table 3: Dietary Sources of Calcium

                 Food                

 

Serving Size 

 

Calories per Portion  

 

Calcium Content (mg)

  

Dairy foods      
   Milk      
       Whole milk    8 oz      149     276
       Reduced fat milk (2%)    8 oz      122     293
       Low-fat milk (1%)    8 oz      102     305
       Skim milk (nonfat)    8 oz       83     299
       Reduced-fat chocolate milk (2%)    8 oz      190     275
       Low-fat chocolate milk (1%)    8 oz      158     290
   Yogurt      
       Plain yogurt, low-fat    8 oz      143     415
       Fruit yogurt, low-fat    8 oz      232     345
       Plain yogurt, nonfat    8 oz      127     452
   Cheese      
       Romano cheese    1.5 oz      165     452
       Swiss cheese    1.5 oz      162     336
       Pasteurized processed American cheese      2 oz      187     323
       Mozzarella cheese, part skim    1.5 oz      128     311
       Cheddar cheese    1.5 oz      171     307
       Muenster cheese    1.5 oz      156     305
   Nondairy foods      
       Salmon      3 oz       76      32
       Sardines, canned      3 oz      177     325
       White beans, cooked    1 cup      307     191
       Broccoli, cooked    1 cup       44      72
       Broccoli, raw    1 cup       25      42
       Collards, cooked    1 cup       49     226
       Spinach, cooked    1 cup       41     249
       Spinach, raw    1 cup        7      30
       Baked beans, canned    1 cup      680     120
       Tomatoes, canned    1 cup       71      84
   Calcium-fortified food      
       Orange juice     8 oz      117     500
       Breakfast cereals    1 cup   100-210  250-1000
       Tofu, made with calcium    0.5 cup       94     434
       Soy milk, calcium fortifieda     8 oz      104     299
Table 4: Sources of Vitamin D
Food     Serving Size             Vitamin D Contenta (IU)         
Natural sources                
    Salmon    
        Fresh wild    3.5 oz               600-1000
        Fresh farmed    3.5 oz               100-250
    Sardines, canned    3.5 oz                  300
    Mackerel, canned    3.5 oz                  250
    Tuna, canned    3.5 oz                  236
    Shitake mushroom    
        Fresh    3.5 oz                  100
        Canned    3.5 oz                1600
    Egg, hard-boiled    3.5 oz                   20
Vitamin D-fortified foods    
    Infant formula   1 cup (8 oz)                  100
    Milk   1 cup (8 oz)                  100
    Orange juiceb   1 cup (8 oz)                  100
 Yogurtsb   1 cup (8 oz)                  100
    Cheesesb    3 oz                  100
    Breakfast cerealsb   1 serving               40-100
Pharmaceutical sources in the United States          
    Vitamin D2 (ergocalciferol)   1 capsule                50000
    Drisdol (vitamin D2) liquid    1 cc                8000
    Supplemental sources    
    Multivitamin            400, 500, 1000
    Vitamin D3    400, 800, 1000, 2000, 5000, 10000, 50000 
Table 5: Treatment of Vitamin D Deficiency
Age Preparation and Dosea                                                                                
Infants, 0–12 mo Vitamin D2 or D3 50 000 IU weekly for 6 wk  



 



or



Vitamin D2 or D3 2000 IU daily for 6 wk
Followed by a maintenance dose of 400–1000 IU daily                                                  Followed by a maintenance dose of 400–1000 IU daily                             
Children and adolescents, 1–18y                                                         Vitamin D2 or D3 50 000 IU weekly for 6-8 wk  



 



or



 



 



 



Vitamin D2 or D3 2000 IU daily for 6–8 wk
Followed by a maintenance dose of 600–1000 IU daily Followed by a maintenance dose of 600–1000 IU daily
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