GLUCOCORTICOID-INDUCED BONE DISEASE: MECHANISMS AND IMPORTANCE IN PEDIATRIC PRACTICE

Abstract

Objective: To describe mechanisms by which glucocorticoids cause osteoporosis, with fracture risk, combining this learning with a possible professional behavior change.

Data sources: A systematic search on SciELO, PubMed, Scopus, and Medline databases was carried out for consensus, review articles, including systematic reviews and meta-analysis, which were published in English, between 2000 and 2016. Keywords used on the search were the following: glucocorticoids, fractures, osteoporosis, bone health, vitamin D, children, and adolescents.

Data synthesis: The review was divided into four topics: 1) introduction, with a brief focus on pediatric fractures; 2) osteoporosis in children and adolescents, highlighting it as a silent cause of fractures; 3) glucocorticoids and secondary bone disease, describing deleterious mechanisms of this steroids group on bone structure; 4) molecular effects of glucocorticoids excess on bone, with details about the harmful mechanisms on bone molecular level.

Conclusions: Glucocorticoids excess determines early bone disease, favoring the occurrence of fractures. Thus, a child or an adolescent who uses glucocorticoids, especially systemically and chronically, but also repeats cycles at high cumulative doses of the medication, needs care and guidance related to bone health at the onset of treatment. On the other hand, the presence of fractures, even if related to trauma, can be a sign of underlying and unknown bone fragility, which may be secondary to the use of glucocorticoids and/or vitamin D deficiency.

Figure 1:. Pathogenesis of fractures related to glucocorticoids (GC) excess.

Figure 2:. Genomic mechanism of action of GC and the hydroxysteroid dehydrogenase (HSD) enzymatic system.

Figure 3:. Synthesis of the main deleterious actions of glucocorticoids excess in the bone.