Vertebral Histomorphometry in a Child with Glucocorticoid-Induced Osteoporosis

Abstract

Vertebral fractures are an under-recognized problem in children with glucocorticoid-induced osteoporosis (GIO). They cause severe back pain and spinal column deformity with a decrease of quality of life. For evaluating the bone mass, bone mineral density measurements have been widely carried out using dual energy X-ray absorptiometry. However, bone histomorphometric analyses of GIO in children are scarce. Bone histomorphometric analyses of vertebral bodies have not been reported. Our aim is to report the first bone histomorphometric data for vertebrae from an autopsied child with GIO. A 15-year-old girl with systemic lupus erythematosus was started on a daily oral dose of 10 mg of prednisolone at 6 years of age. She presented with back pain from 12 years of age. Magnetic resonance imaging at 14 years of age showed a compression fracture of the first lumbar (L1) vertebral body. At 15 years of age, she died of heart failure owing to pulmonary hypertension. Collapsed (L1) and non-collapsed (seventh thoracic vertebrae; T7) vertebral bodies were autopsied for bone histomorphometry and compared. T7 showed severe osteoporosis (bone volume, 4.99%; trabecular thickness, 59 μ m; trabecular separation, 1,134 μ m). Compared with T7, L1 showed increased bone volume (33.9%) and trabecular thickness (77 μm), and decreased trabecular separation (156 μ m) owing to the impact of the vertebral fracture. The bone formation and bone resorption parameters were comparable between the two vertebrae. These histological findings suggest that severe osteoporosis developed after long-term glucocorticoid administration, and that the remodeling activities were similar in the fractured and non-fractured vertebrae.Keywords: bisphosphonate; bone histomorphometry; glucocorticoid-induced osteoporosis; growth; osteoblast Tohoku J. Exp. Med., 2012, 227 (4), 263-267. © 2012 Tohoku University Medical Press Glucocorticoid-induced osteoporosis (GIO) is the most common cause of secondary osteoporosis in adults, and is the result of profound effects of glucocorticoids on bone cells (Canalis et al. 2004). Glucocorticoids inhibit osteoblastogenesis and promote osteoblast apoptosis, thereby leading to significant reductions in bone formation (Weinstein et al. 1998). The growing skeleton may be especially vulnerable to the adverse effects of glucocorticoids on bone formation, which could possibly compromise trabecular and cortical bone accretion.Compression fractures of the vertebral body are an under-recognized problem in children with GIO (Varonos et al. 1987;Valta et al. 2007; Huber et al. 2010). They cause severe back pain and spinal column deformity with a decrease of quality of life. For evaluating the bone mass, bone mineral density measurements have been widely carried out using dual energy X-ray absorptiometry. However, bone histomorphometric analyses of GIO in children are scarce. A histomorphometric evaluation of GIO in children with chronic illnesses has been reported for specimens obtained by iliac bone biopsy (Ward et al. 2004). To the best of...

Effects of Glucocorticoids on Bone: What we can Learn from Pediatric Endogenous Cushing’s Syndrome

“…On bone biopsies and imaging studies, the above mechanisms result in unequal effects on the microarchitecture of the different types of bone [42][43][44]. It seems that the trabecular bone is principally affected, with decrease of its thickness and the development of trabecular perforations, while the cortical bone seems to be relatively spared [43][44][45]. At the same time, there is increased fat infiltration of the bone marrow which is also attributed to the excess GCS [45].…”

“…It seems that the trabecular bone is principally affected, with decrease of its thickness and the development of trabecular perforations, while the cortical bone seems to be relatively spared [43][44][45]. At the same time, there is increased fat infiltration of the bone marrow which is also attributed to the excess GCS [45]. Given the fact that the trabecular bone plays a significant role in the maintenance mechanical strength of the bone, the above alterations decrease bone quality and result in the increased risk for fractures [46].…”

Severe Kyphosis Secondary to Glucocorticoid-Induced Osteoporosis in Adolescent Twins with Congenital Adrenal Hyperplasia - A Case Report and Literature Review

“…Vertebral compression fractures, that frequently appear in osteoporosis, could be a cause for the spinal deformity [15]. The hyperkyphosis in these cases are similar to the Scheuermann kyphosis with a fixed angular kyphosis presenting an anterior wedging of the vertebra.…”

“…Vertebral fractures are an important issue in children with GC induced osteoporosis, but the BMD values may not be able to adequately reflect the increased risk of fractures. The alteration in bone microstructure must be considered when assessing the risk of fracture and can be measured with TBS, that can be extracted from DXA images of the lumbar spine [14,15]. A low bone density or deterioration to the bone microstructure of the vertebrae and possible vertebral fracture can lead to deformities of the spine.…”

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