Pediatric Osteoporosis Treatment & Management

Updated: May 19, 2020
  • Author: Manasa Mantravadi, MD, MS; Chief Editor: Jatinder Bhatia, MBBS, FAAP  more...
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Approach Considerations

Management is primarily medical, depending on the underlying condition. If the underlying condition is optimally managed and low bone density for age persists, then management depends on bone dynamics. See Osteoporosis and Nonoperative Treatment of Osteoporotic Compression Fractures for more information on these topics.

The primary goals of the management of osteoporosis are prevention of fractures, including vertebral fractures, and scoliosis and improvement in function, mobility, and pain. [10]


Medical Management of High Bone Resorption

When bone resorption exceeds bone formation, an antiresorptive agent such as a bisphosphonate may be used. A review has been developed for educational purposes by the Drug and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society regarding bisphosphonates in the treatment of pediatric osteoporosis. The following information is from the executive summary. [34]

Bisphosphonates are chemical analogs of pyrophosphate, in which the oxygen atom is replaced by a carbon atom (P-C-P instead of P-O-P). By adhering to the bone surface, bisphosphonates come into close contact with osteoclasts, where they exert their therapeutic actions.

Bisphosphonates have the potential to bring about sizeable changes in bone density and the reshaping of vertebral bodies in children. A greater response to bisphosphonates in bone mineral density (BMD) and content is seen in children compared with adults, since the cortical surfaces of bone thicken as the bisphosphonate interferes with modeling, while skeletal resorption is blunted along endocortical surfaces.

Bisphosphonate administration, particularly intravenous, in children with moderate and severe forms of osteogenesis imperfecta (OI) has been adopted as part of routine clinical care. However, in children with mild forms of OI or osteoporosis caused by chronic illness, the evidence suggests that bisphosphonate therapy should be relegated to well-designed clinical trials or used on compassionate grounds for such children who, in addition, show clinical evidence of bone fragility associated with low bone mass or density. There are insufficient data on the use of bisphosphonates as preventative agents to recommend their administration to children with asymptomatic reductions in bone mass or density alone.

Bisphosphonates have been widely used in children with OI. Reported therapeutic effects include improvement in bone density, grip strength, vertebral height, cortical thickness, trabecular number, quality of life and mobility, decreased bone pain, and bone turnover and fracture rate.

The first step in treating children with osteoporosis caused by systemic illness is to identify and manage modifiable risk factors by quelling the underlying disease, restoring the normal hormonal milieu (eg, growth hormone and sex steroid status), correcting vitamin D deficiency, and rectifying underweight or overweight status and physical deconditioning. However, if these measures are insufficient, consideration of treatment with a bisphosphonate is warranted for those with low BMD or bone mineral content and bone fragility.

In neuromuscular diseases, most of the clinical studies examining the use of bisphosphonates have been carried out in children with bone fragility or low BMD that is secondary to cerebral palsy. Both randomized clinical trials and small, uncontrolled studies have tested the efficacy of intravenous pamidronate in increasing BMD among nonambulatory children with cerebral palsy and have noted skeletal gains at the spine, femoral neck, and/or total body and the absence of serious adverse effects.

There is a lack of consensus regarding the use of bisphosphonates in idiopathic juvenile osteoporosis. Complicating the issue is the fact that many of the reports of bisphosphonate use for idiopathic juvenile osteoporosis include data from heterogeneous case series that include patients with osteoporosis of varying etiologies.

Short-term safety issues with bisphosphonates include transient hypocalcemia; a brief acute-phase reaction, including influenza-like symptoms such as low-grade fever, headache, nausea, vomiting, rash, tachycardia, myalgia, and bone pain; and esophageal irritation. Uncommon short-term safety issues are nephrotoxicity, anterior uveitis and atrial fibrillation.

Potential long-term adverse effects include radiographic metaphyseal bands, iatrogenic osteopetrosis, fractures after bisphosphonate discontinuation in growing children, delayed healing at osteotomy sites, esophageal cancer, and osteonecrosis of the jaw. It is noteworthy that no cases of some of these adverse effects (eg, esophageal cancer and osteonecrosis of the jaw) have been seen in children.

The current generation of oral bisphosphonates includes alendronate and risedronate. The primary parenterally administered bisphosphonate is pamidronate.

To date, there is no consensus on the optimal agent, dosage, or duration of therapy. In the absence of numerous randomized, controlled trials comparing different agents, doses, and durations in various bone disorders, it is impossible to state whether one treatment protocol is more efficacious than another. However, the response to intravenous therapy seems to be more consistently positive than the response to oral agents. [34] A Cochrane Database Systemic Review confirmed that bisphosphonates increase bone density in children and adolescents with OI. [35]

Preliminary data suggest that zoledronic acid (ZA) is as effective as pamidronate in preventing bone loss. [36] Acute adverse events related to ZA infusion in youths are common, occur principally after the first ZA infusion in bisphosphonate-naive patients, and are typically mild and easily managed. Future prospective studies are needed to determine the potential long-term risks as well as benefits of ZA therapy in the pediatric population. [37]

Denosumab, the monoclonal antibody to receptor activator of nuclear transcription factor kappa B ligand (RANKL), can successfully prevent bone loss in adults with osteoporosis; however, data on its safety and efficacy in children are limited. [38]


Medical Management of Low Bone Formation

Anabolic steroids (eg, testosterone, oxandrolone) may be helpful in forming new bone; however, consider the risks of premature closure of the epiphyses, short stature, and hirsutism. Also consider the potentially increased risk of tumor development. However, when oxandrolone was given for 1 year to a group of children following burn injury, no epiphyseal closure was demonstrated, and only 2 cases of clitoral hypertrophy were observed (both were reversed after cessation of the drug). [39]

Recombinant human growth hormone is a useful anabolic agent for children with growth hormone deficiency; its benefits for others with low bone density for age have not been extensively studied. It does improve bone mineral content (BMC) in children with burn injury if given for a year, but the need for repeated injections and the cost limit its use. [40]

The absence of a safe and effective anabolic agent makes bone loss secondary to low bone formation more difficult to manage than bone loss secondary to high bone resorption. Parathyroid hormone (PTH), which is potentially very promising when given intermittently to osteoporotic adults, is not approved for use in children because of the detection of osteogenic sarcoma in mice that were given very high test doses. [41]


Surgical Care

Unless a resectable tumor can be identified as the cause of low bone density for age or osteoporosis, surgery is unlikely to play a role in treatment. In most cases, the cause is systemic and results in widespread disease. Surgeries may be necessary for rod placement or for stabilization of fracture.


Dietary Measures

Calcium and vitamin D are the most important dietary nutrients to help prevent adult osteoporosis, although a study suggests that calcium supplementation does not promote a significant accumulation in the appendicular skeleton in children. [42] A diet rich in dairy products is recommended to help provide the calcium and vitamin D required. [43]

The American Academy of Pediatrics (AAP) endorses recommended dietary allowances for calcium and vitamin D as shown in the following table. The AAP also supports testing for vitamin D deficiency in children and adolescents with conditions associated with increased bone fragility. [44] The Global Consensus Recommendations on Prevention and Management of Nutritional Rickets released similar information including universal supplementation of all infants with vitamin D from birth to 12 months of age, independent of their mode of feeding. [45]


Table 2. Calcium and Vitamin D Dietary Reference Intakes [11] (Open Table in a new window)








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  

   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

a 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 recommended dietary allowance [RDA]).

b Reflects adequate intake reference value rather than RDA. RDAs have not been established for infants.

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


The following tables show dietary sources of both calcium and vitamin D. [11]


Table 3. Dietary Sources of Calcium (Open Table in a new window)



Serving Size 


Calories per Portion  


Calcium Content (mg)


Dairy foods      
       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
       Plain yogurt, low-fat    8 oz      143     415
       Fruit yogurt, low-fat    8 oz      232     345
       Plain yogurt, nonfat    8 oz      127     452
       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

a Not all soy beverages are fortified to this level.

Table from: Dietary Guidelines for Americans, 2010. Available at:


Table 4. Sources of Vitamin D (Open Table in a new window)

Food     Serving Size             Vitamin D Contenta (IU)         
Natural sources                
        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
    Shiitake 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, 10,000, 50,000 

a The activity of 40 IU of vitamin D is equivalent to 1 µg.

b Not all brands of orange juice, yogurt, and cheese are fortified with vitamin D.



Activity plays a role in the prevention of osteoporotic fractures. Several studies in the United States and in Europe have established that regular weight-bearing exercise, such as jumping, in school-aged children improves bone mass. [46, 9] Encouraging such exercises as walking, running, tennis, volleyball, hiking, hockey, dancing, skiing, basketball, gymnastics, soccer, aerobics, jumping rope, and lifting weights can help with contribution to BMC in children and adolescents.

Lack of locomotion, due to either recurrent fractures in children with OI or chronic illnesses, reduces mobility, muscle force, and subsequently bone strength. Based on studies in adults, high frequency, low amplitude whole body vibration (WBV) is being developed as a non-drug therapy to increase muscle force and mobility in children. [10]



Experts in pediatric osteoporosis may come from several subspecialties. Traditionally, osteoporosis is often the province of the pediatric endocrinologist, but experts may be found in pediatric nephrology, gastroenterology, genetics, or orthopedic surgery as well.


Long-term Monitoring

Generally, children with osteoporosis do not require hospitalization unless they have a complication such as a hip fracture. This is a very uncommon occurrence in children; however, following a fracture, anticipatory intervention is needed to minimize future hospital stays and to identify individuals at risk for repeated fracture.

The aim of outpatient care is to closely monitor bone mineral density to determine if ongoing bone loss occurs or if the process has reached a plateau. The AAP recommendation for repeating bone densitometry testing is that, although 6 months should normally elapse between measurements, it might be appropriate in some cases to wait at least 1 year. [47]  In situations of ongoing bone loss, measurements of biochemical markers of calcium metabolism, vitamin D status, and bone formation and resorption can help guide management.

Transferring a patient is not necessary unless pediatric subspecialty care is unavailable at the institution.