Osteopenia Pathologic Fractures


Children with special health care needs may have osteopenia for several reasons. These include decreased mobility, decreased calcium and/or vitamin D intake, delayed puberty, and medications, especially some of the antiepileptic medications [Pack: 2003] [Valsamis: 2006] [Sheth: 2004] [Farhat: 2002] that cause osteoporosis. Children with these risk factors may be at increased risk for pathological fractures, fractures that occur with low force. Pathologic fractures can occur with daily care (e.g., during dressing), during positioning for x-rays, during physical therapy or from a seizure. Sometimes a fracture is recognized without any recollection of a traumatic event. Children with CP have a higher fracture rate than the general population [Stevenson: 2006] and this fracture rate may be even higher in children with CP on antiepileptic medications. [Leet: 2006]

Fractures are increased two to six times in patients with epilepsy compared to the general population. [Mattson: 2004] [Vestergaard: 1999] Hepatic enzyme induction by certain anticonvulsant medications appears to contribute to increased metabolism of 25-hydroxyvitamin D to inactive metabolites, which results in metabolic bone disease. There is increasing evidence that anticonvulsant use is associated with a higher risk of osteoporosis and clinical fractures, especially among older agents such as phenobarbital, carbamazepine, phenytoin, and valproate. Valproic acid is thought to directly act on the bone, increasing activity of the osteoclasts, the cells responsible for bone breakdown in the dynamic process of remodeling. [Valsamis: 2006] Not as much information is available regarding the newer antiepileptic drugs, but preliminary reports are favorable. [Farhat: 2002]


All children should receive the recommended daily allowance of vitamin D and calcium in their diet. See Calcium and Vitamin D. If a child’s diet is at risk, supplements may be necessary to achieve recommended daily allowance although it's preferable for the micronutrients to come from the diet when possible. Patients on anticonvulsants might benefit from a higher daily intake of vitamin D than standard recommended daily allowance (in combination with monitoring levels). If a child is high risk for fractures due to immobility, high risk of vitamin D deficiency due to dietary or lifestyle (e.g., low sun exposure) or on anticonvulsants, checking vitamin D levels on a regular basis should be considered with the goal to maintain the level of 25 hydroxy vitamin D in the mid to upper range of normal. Children who have limitation in ambulation should be mobilized as much as possible with walkers and other mobility devices. Children who are not able to stand independently should spend an hour, or more if possible, in a stander daily. Exercise should be encouraged for all children and, for children with limited mobility, identifying adapted forms of exercise which optimize participation is important.

Since bone density drops during casting, minimize the duration of casting when possible. Special care must be taken in handling right after coming out of a a cast to avoid trauma or undue forces to prevent a recurrent fracture in the same area. Hydrotherapy during this time might provide the safest environment to remobilize and strengthen the affected extremity. Protective splinting should be individualized to the particular clinical scenario.


From a practical standpoint, the role of monitoring bone density by by DEXA (Dual-energy X-ray Absorptiometry, a radiological based test that measures bone density) is limited. It is critical to be instituting the strategies above to optimize bone health for all children (not just those with low bone density) and, it is a given that most children with neurodevelopmental disability with limited weight bearing will have a low bone density. The degree of low bone density has not been shown to correlate with the degree of fracture risk. Finally, therapeutic decisions regarding bisphosphonates are rarely made based upon the bone density but rather upon the clinical picture in terms of fracture history. However, on occasion, a clinician might choose to alter a medication regime (e.g., use of a high risk anticonvulsant or use of depoprovera to suppress menses) if they note a very low or declining bone density and in these scenarios measuring bone density might prove useful clinically. Monitoring vitamin D levels is important in selected patients as discussed above. Monitoring “serum calcium” does not provide any guarantee that dietary calcium is adequate, thus monitoring dietary history for calcium intake adequacy is critical.


If pathologic fractures have already occurred, the first step is to review the child’s prevention program to insure adequate vitamin D and calcium intake, assesses vitamin D adequacy (e.g., vitamin D levels), and if possible, reduce exposure to medications that increase the child’s risk (e.g., change to a different anticonvulsant). The clinician should carefully consider any additional factors that might be contributing such as renal or liver conditions, celiac disease or other conditions causing malabsorption of nutrients and hormone imbalances (e.g., delayed puberty, low estrogen or testosterone, hyperthyroidism, hyperparathyroidism) that might be complicating the clinical picture although in most cases these will not be present. Typically a panel of labs is checked to exclude these conditions although, in the child with significant neurodevelopment risk factors, the yield is low.

The role of bispohosphonate treatment in children with neurodevelopmental disability and pathologic fractures is evolving. Bisphosphonates do increase bone density but the evidence that they reduce fracture rate over the long term is preliminary (based on case series data). Additionally, little is defined in terms of length of treatment and long term side effects. Obtaining a bone density to make a decision about whether to proceed with bisphosphonate treatment is of little utility as, in the presence of multiple pathologic fractures, bone density will certainly be low and the actual extent of low bone density has not been shown to correlate with future fracture risk. Rather, based upon the clinical picture, a careful discussion with the family regarding the balance of continued risk of pathologic fractures versus our current research data for use of bisphosphonates should occur and an individual decision made whether to proceed with their use. Generally intravenous bisphosphonates are used given the risk of esophagitis in many children with neurodevelopmental disability but this should be tailored to the particular clinical situation. Protocols for treatment with biphosphonates (dose, interval, choice of medication duration of therapy) vary among treatment centers somewhat and, if exploring such treatment, it might be best done with referral to a clinician with expertise in the area.

Bisphosphonate treatment may either be parenteral (most commonly pamidronate or zolendronate given every q 2-4 months) or oral (most of the experience with children is with alendronate, 35 mg for children under 40 kg, 70 mg for those over 40 kg, q week, however the data for impact of oral bisphosphonates (which are less active and also have low bioavailability) is even more limited than the data for effectiveness of IV formulations and concerns for esophagitis limite their use in many children. Alendronate is taken weekly, must be taken on an empty stomache, must be followed by adequate fluid intake to insure passage through the esophagus, and must be followed by at least 30 minutes of upright positioning ). In the event bisphosphontes will be used, a base line bone density by DEXA should be obtained. It is important to note that the vertebral bone density is of limited value as the lower extremity bone density is more impacted by non-weight bearing and thus more clinically relevant. Measuring and interpreting bone density is challenging and is best done at a pediatric center with extensive experience in measuring bone density in children. For children with neurodevelopmental disability with positioning challenges or internal metal hardware, special views may be needed (e.g., lateral femur). For children with atypical body composition (e.g., very small stature for age, very low muscle mass for age or size) clinical interpretation can be particularly challenging. Generally, before starting therpay with biphosponates a variety of baseline labs are obtained to insure adequate vitamin D level, exclude other contributing causes to low bone density (see above), to insure no contraindication (e.g.., low serum calcium) and to confirm normal liver/renal function and blood counts since use of these medications can rarely impact these through time. These labs are typically monitored yearly and bone density is remeasured in approximatley 12 months after initiation of therapy. Duration of therapy is unclear but often is 1-2 years. This may evolve as more is understood about the impacts of treatment and persistence of treatment effect. Bisphosphonates have been associated with a number of rare bur serious side effects. One of these is the potential for osteonecrosis of the jaw. Children who are taking bisphosphonates should be seen regularly by a pediatric dentist with caries and other oral problems treated as this might minimize this possibility.



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Authors: Lisa Samson-Fang, MD - 1/2014
Lynne M. Kerr, MD, PhD - 1/2014
Content Last Updated: 1/2014

Page Bibliography

Farhat G, Yamout B, Mikati MA, Demirjian S, Sawaya R, El-Hajj Fuleihan G.
Effect of antiepileptic drugs on bone density in ambulatory patients.
Neurology. 2002;58(9):1348-53. PubMed abstract

Leet AI, Mesfin A, Pichard C, Launay F, Brintzenhofeszoc K, Levey EB, D Sponseller P.
Fractures in children with cerebral palsy.
J Pediatr Orthop. 2006;26(5):624-7. PubMed abstract

Mattson RH, Gidal BE.
Fractures, epilepsy, and antiepileptic drugs.
Epilepsy Behav. 2004;5 Suppl 2:S36-40. PubMed abstract

Pack, Alison.
The Association between Antiepileptic Drugs and Bone Disease.
Epilepsy Curr. 2003;3(3):91-95. PubMed abstract

Sheth RD.
Bone health in pediatric epilepsy.
Epilepsy Behav. 2004;5 Suppl 2:S30-5. PubMed abstract

Stevenson RD, Conaway M, Barrington JW, Cuthill SL, Worley G, Henderson RC.
Fracture rate in children with cerebral palsy.
Pediatr Rehabil. 2006;9(4):396-403. PubMed abstract

Valsamis HA, Arora SK, Labban B, McFarlane SI.
Antiepileptic drugs and bone metabolism.
Nutr Metab (Lond). 2006;3:36. PubMed abstract / Full Text

Vestergaard P, Tigaran S, Rejnmark L, Tigaran C, Dam M, Mosekilde L.
Fracture risk is increased in epilepsy.
Acta Neurol Scand. 1999;99(5):269-75. PubMed abstract