Pediatric low bone density: when to refer

Abstract

Osteoporosis is a highly prevalent disease-causing high morbidity and health-care expenditures. As bone mass structure rarely varies from that of young adulthood, it is important for early recognition of low bone density disorders during childhood. This article will differentiate the common conditions causing low bone density and help Pediatricians promptly identify the patients in need of a Pediatric Endocrinologist referral by explaining the pathophysiology, evaluation, and management of these conditions.

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Abbreviations: DEXA, dual-energy X-ray absorptiometry;
BMD, bone mineral density; BMC, bone mineral content; aBMD,
areal bone mineral density; BMAD, bone mineral apparent density;
TBLH, total body less head; VFA, vertebral fracture assessment; CP,
cerebral palsy; OI, osteogenesis imperfecta
Introduction
There are multiple medical conditions that predispose to low
bone density and fragility fractures. As a primary care provider, it is
important to recognize indications for referral to a Pediatric Endocrine
bone clinic.
Children are at a greater risk for fractures than adults. Around
42% to 64% of boys and 27% to 40% of girls can potentially develop
a fracture between birth and 16 years of age. The upper extremity
fractures, especially the forearm, are more common, as more than
65% of all long bone fractures take place in this area.1
Osteoporosis is a skeletal condition in which bone density is
low and there is increased risk for fractures. A denite indication
of osteoporosis is the presence of a vertebral compression fracture
without any underlying lesion or impactful trauma. A patient can also
be diagnosed with osteoporosis if he/she has a clinically signicant
fracture history and a bone mineral density (BMD) Z-score less than/
equal to -2.0. This can be a result of two or more long bone fractures
before 10 years of age or three or more long bone fractures before
19 years of age. Factors such as the location of the injury, imaging
features, and the clinical context should all be reviewed when
considering a complete pathology evaluation and/or diagnosis of the
disease. If choosing to proceed, the primary step is to rule out any
evidence of mineral disorders followed by evaluation for any acute or
chronic systemic illnesses. If all these tests results are reassuring, then
proceed with X-ray spine (with/without skeletal survey) and a dual-
energy X-ray absorptiometry (DEXA) scan.2
Bone mineral density is a strong indicator of a patient’s overall
bone health. The dual-energy X-ray absorptiometry (DEXA) scan
can report bone mineral content (BMC), areal bone mineral density
(aBMD in gm/cm²), bone mineral apparent density (BMAD). Bone
mineral density is reported as Z-scores in pediatric subjects, in which
these scores are corrected to the height of the subject. If the Z-score
is less than or equal to -2.0 standard deviations, then it is indicative of
“low bone mineral mass or bone mineral density”. The most frequent
areas measured for assessing BMD in children are the posterior-
anterior spine and the total body score without including the head.
Distal forearm, proximal femur, lateral distal femur, and vertebral
fracture assessment can also serve as alternate sites in the case of non-
removable artifacts and/or skeletal deformities causing diculties
with positioning. Factors outside of the DEXA score are also equally
important criteria in the diagnosis of osteoporosis.2,3
As a primary care provider, it is especially important to identify
key conditions that can potentially increase the risk for low bone
mineral mass. Predisposing conditions such as cerebral palsy, long-
term use of steroids, hypogonadism, and certain genetic conditions
like osteogenesis imperfecta can negatively aect the subject’s overall
bone health and deter long-term growth.
The most common condition predisposing to low bone density
is cerebral palsy (CP). Calcium intake, medications, and weight-
bearing status are the three primary determining factors of bone
mass in these patients. Although calcium intake is typically low in
these patients, these numbers are not reected in lab results due to
compensatory mechanisms. Medications (such as anticonvulsants,
depot medroxyprogesterone acetate, etc.) can deter absorption and/
or metabolism of vital nutrients, which has a negative eect on
bone health. Bone structures are regulated by simultaneous action of
osteoblasts and osteoclast cells; the activities of these cells are highly
dependent on the weight-bearing status of the subject. It is shown that
children who are non-weight bearing have thinner, more fragile bones
than those who can walk.4 Therefore, these children are inherently at
a higher risk for developing fractures (around 4% per year) than those
who are weight-bearing. This fracture rate can increase to 7% per year
once the child develops a single fracture. Coincidingly as the child’s
bone health deteriorates, the morbidity rate increases, demonstrating
the need for early-recognition of this complication.
Long-term use of steroids can also negatively aect bone health.
Eects of long-term use of corticosteroids on skeleton include
apoptosis of all bone cells including osteoblasts, osteocytes, and
osteoclasts. Osteoblastogenesis is reduced whereas osteoclastogenesis
is increased. There is reduction in the synthesis of insulin like growth
factor-1 (IGF-1) and collagen. Bone loss can occur in two phases.
The initial 10-15% of loss happens in the rst few months of steroid
use and is followed by phases of 2-5% of bone loss yearly. A daily
prednisone dose of ≥7.5 mg for 3 months or more cause signicant
bone loss and double the risk for fractures. Inhaled steroids on a
long term can also potentially aect bone density. Patients who are
susceptible for bone loss include those who have elevated parathyroid
hormone (PTH), impaired calcium absorption, increased urinary
calcium excretion, vitamin D deciency, and acidosis.5,6
Endocrinol Metab Int J. 2022;10(1):1‒2. 1
©2022 Sukumaran. This is an open access article distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and build upon your work non-commercially.
Pediatric low bone density: when to refer
Volume 10 Issue 1 - 2022
Anju Sukumaran
Associate Professor at University of Mississippi, USA
Correspondence: Anju Sukumaran MD, Associate Professor
at University of Mississippi, 2500 N state Street, University of
Mississippi Medical Center, Jackson, MS, US 39216,
Tel 6019845246, Email
Received: January 25, 2022 | Published: February 08, 2022
Abstract
Osteoporosis is a highly prevalent disease-causing high morbidity and health-care
expenditures. As bone mass structure rarely varies from that of young adulthood, it is
important for early recognition of low bone density disorders during childhood. This article
will dierentiate the common conditions causing low bone density and help Pediatricians
promptly identify the patients in need of a Pediatric Endocrinologist referral by explaining
the pathophysiology, evaluation, and management of these conditions.
Keywords: bone fragility, low bone density
Endocrinology & Metabolism International Journal
Short Communication Open Access

Pediatric low bone density: when to refer 2
Copyright:
©2022 Sukumaran
Citation: Sukumaran A. Pediatric low bone density: when to refer. Endocrinol Metab Int J. 2022;10(1):1‒2. DOI: 10.15406/emij.2022.10.00311
Hypogonadism is another condition that can predispose to low bone
density. Although estrogen and androgen can both prolong osteoblast
and osteocyte survival, they shorten the lifespan of osteoclasts.
Evaluation for hypogonadism starts with checking levels of luteinizing
hormone, follicle stimulating hormone, testosterone, estradiol. This
can be managed by treating the cause and/or replacement therapy with
sex steroids, which has shown to improve bone density.7
There are certain genetic conditions that can cause low BMD such
as osteogenesis imperfecta (OI), WNT1 mutations, etc. The altered
collagen formation and deposition in these conditions cause recurrent
fractures. Biochemical tests are usually unremarkable. Bone turnover
markers are helpful only as a response to treatment and not for
diagnosis. Bisphosphonate infusions are usually used as supportive
therapy during bone growth. In the case of continued bone pain after
reaching maximum bone growth, then bisphosphonates can continue
to be used.
Management of low BMD includes ensuring adequate intake of
minerals such as calcium, phosphorus, zinc, magnesium, and vitamin
D. In those who are non-ambulatory, it is recommended that their serum
25-hydroxy vitamin D level is at least 30 to 40ng/mL. Weight-bearing
exercises, especially by physical therapy, are extremely important.
Aquatic therapies can also be very benecial. Pharmacologic
management using bisphosphonates are also considered for those
with increased bone fragility. Bisphosphonates serve to increase bone
mineral density by inactivating osteoclasts, which are responsible for
the breakdown of existing bone cells. Bone mineral density typically
increases during the period of treatment and then decreases back to
baseline within 2 years of discontinuation. Despite this return, a high
proportion of children remain fracture free for 5 years or more.
Conclusion
Evaluation of bone health should identify children who may
benet from interventions to decrease their elevated risk of a clinically
signicant fracture. Indications for referral include a history of
multiple fractures and non-weight bearing situations such as cerebral
palsy, chronic use of steroids, hypogonadism, and genetic conditions
like osteogenesis imperfecta. Early identication and management of
these conditions are equally important to reduce both the morbidity of
the subject as well as health-care costs.
Acknowledgments
None.
Funding
None.
Conicts of interest
The authors declare no conict of interest.
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