Osteoporosis in Pediatric Patients Suffering From Chronic Inflammatory Bowel Disease With and Without Steroid Treatment

Walther, Frank; Fusch, Christoph; Radkë, Michaël; Beckert, Sybille; Findeisen, Annette

doi:10.1097/01.mpg.0000228105.91240.80

Cited by 81 publications

(52 citation statements)

References 41 publications

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“…This is supported by the negative correlation between ESR/faecal calprotectin and serum PINP levels in our study and the fact that steroid-naive IBD patients may present with osteoporosis (23,24). Additionally, in active disease other factors such as nutrition or physical inactivity leading to reduced loading of the bones may also contribute to the low PINP levels (25).…”

Section: Discussionsupporting

confidence: 66%

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Vihinen

Kolho²,

Ashorn³

et al. 2008

European Journal of Endocrinology

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Objective: We investigated circulating markers of bone turnover before and during systemic glucocorticoid treatment in paediatric patients with inflammatory bowel disease (IBD). Methods: Twenty-two children (mean age, 12.3 years) with IBD necessitating peroral steroid therapy were studied, with special reference to bone formation and resorption markers amino-terminal type I collagen propeptide (PINP) and carboxyterminal telopeptide of type I collagen (ICTP) respectively. In addition, GH-related IGF-I and sex hormone-binding protein (SHBG) were measured. Bone markers were analyzed at the initiation of the glucocorticoid treatment, at 2 and 5 weeks thereafter and at 1 month following the withdrawal of the steroid. Control group comprised 22 IBD patients in remission.Results: PINP and IGF-I were already lower before glucocorticoid treatment serum in children with active IBD as compared with control children with IBD in remission (median PINP 271 vs 535 mg/l, P!0.05; IGF-I 23 vs 29 nmol/l, P!0.05). After 2 weeks of glucocorticoid treatment serum PINP levels had declined further, from 271 to 163 mg/l (P!0.001), serum ICTP from 14.2 to 9.6 mg/l (P!0.001), and SHBG from 54 to 35 nmol/l (P!0.001) respectively. By contrast, serum IGF-I increased from 23 to 37 nmol/l (P!0.001). One month after the withdrawal of the glucocorticoid, all bone markers restored to levels similar to the controls. Conclusions: Bone formation in children with active IBD appears compromised and systemic glucocorticoid treatment further suppresses bone turnover. After the cessation of the glucocorticoid the bone markers show immediate improvement.European Journal of Endocrinology 159 693-698

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Section: Discussionsupporting

confidence: 66%

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Vihinen

Kolho²,

Ashorn³

et al. 2008

European Journal of Endocrinology

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“…4A) produce pro-osteoclastogenic cytokines such as TNF (50,51), IL-6 (52, 53), and IL-1 (50,54) and could potentially promote osteoclast differentiation and/or function. As such, OsteoMacs may provide a candidate cellular mechanism to explain why chronic inflammation (55) and systemic infection (56) often result in osteopenia/osteoporosis. Based upon their apposition to bone surfaces and their well-known ability to detect dying cells (57), OsteoMacs are also the most obvious candidates to detect and respond to bone damage (e.g., apoptotic death of osteoblasts and osteocytes), a critical event in initiation of bone remodeling and osteoclast recruitment (58).…”

Section: Discussionmentioning

confidence: 99%

Osteal Tissue Macrophages Are Intercalated throughout Human and Mouse Bone Lining Tissues and Regulate Osteoblast Function In Vitro and In Vivo

Chang

Raggatt

Alexander

et al. 2008

The Journal of Immunology

618

646

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Resident macrophages are an integral component of many tissues and are important in homeostasis and repair. This study examines the contribution of resident tissue macrophages to bone physiology. Using immunohistochemistry, we showed that a discrete population of resident macrophages, OsteoMacs, was intercalated throughout murine and human osteal tissues. OsteoMacs were distributed among other bone lining cells within both endosteum and periosteum. Furthermore, OsteoMacs were coisolated with osteoblasts in murine bone explant and calvarial preparations. OsteoMacs made up 15.9% of calvarial preparations and persisted throughout standard osteoblast differentiation cultures. Contrary to previous studies, we showed that it was OsteoMacs and not osteoblasts within these preparations that responded to pathophysiological concentrations of LPS by secreting TNF. Removal of OsteoMacs from calvarial cultures significantly decreased osteocalcin mRNA induction and osteoblast mineralization in vitro. In a Transwell coculture system of enriched osteoblasts and macrophages, we demonstrated that macrophages were required for efficient osteoblast mineralization in response to the physiological remodeling stimulus, elevated extracellular calcium. Notably, OsteoMacs were closely associated with areas of bone modeling in situ, forming a distinctive canopy structure covering >75% of mature osteoblasts on diaphyseal endosteal surfaces in young growing mice. Depletion of OsteoMacs in vivo using the macrophage-Fas-induced apoptosis (MAFIA) mouse caused complete loss of osteoblast bone-forming surface at this modeling site. Overall, we have demonstrated that OsteoMacs are an integral component of bone tissues and play a novel role in bone homeostasis through regulating osteoblast function. These observations implicate OsteoMacs, in addition to osteoclasts and osteoblasts, as principal participants in bone dynamics.

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“…Many previous studies that used DXA have reported reduced BMD measurements for patients with short stature and/or genetic syndromes associated with short stature; this result could be explained by reduced height because BMD is a measurement of area and these patients have reduced height, which negatively affects their BMD values (9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 89%

Bone density and metabolism in subjects with microdeletion of chromosome 22q11 (del22q11)

Stagi¹,

Lapi

Gambineri³

et al. 2010

European Journal of Endocrinology

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Introduction: Although hypoparathyroidism with hypocalcaemia is one of the most frequent clinical features of monoallelic microdeletion of chromosome 22q11 (22q11DS), bone mass and metabolism have not yet been assessed in these patients. Design: This study aimed to evaluate bone mass and metabolism in a cohort of patients, both children and adults, with 22q11DS. Methods: In twenty-eight patients with 22q11DS (median age 12.5, range 6.1-42.8 years), serum levels of ionised and total calcium, phosphate, parathyroid hormone (PTH), 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, osteocalcin and bone-specific alkaline phosphatase (BSAP), and urinary deoxypyridinoline concentrations were evaluated. In these patients, bone mineral density (BMD) was evaluated by dual-energy X-ray absorptiometry (DXA) examination, and volumetric BMD (bone mineral apparent density (BMAD)) was calculated. The data obtained from paediatric and adult patients were compared with two age-, sex-and body sizematched healthy subject control groups. Results: Patients with 22q11DS showed a reduced BMAD Z-score compared with controls (P!0.001). These patients also had significantly lower ionised (P!0.001) and total calcium (P!0.05) levels as well as lower PTH levels (P!0.05), compared with the controls. In particular, children and young patients with 22q11DS had significantly lower serum osteocalcin levels (P!0.001), BSAP levels (P!0.001) and urinary deoxypyridinoline concentrations (P!0.001) than controls. These results were not confirmed in adults. Finally, patients with hypoparathyroidism and/or hypocalcaemia at the time of the study showed significantly lower ionised (P!0.001) and total calcium levels (P!0.001), PTH levels (P!0.05), BSAP levels (P!0.001), osteocalcin levels (P!0.001) and urinary deoxypyridinoline concentrations (P!0.001), compared with patients without hypoparathyroidism and/or hypocalcaemia. Nonetheless, the BMAD Z-score did not show substantial differences between these two groups. Conclusions: Subjects with 22q11DS have a significant reduction in bone mass that appears to be more severe in adults who have already attained peak bone mass than in children who are still growing. Therefore, we suggest a close monitoring of bone mass and metabolism in 22q11DS patients.

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Osteoporosis in Pediatric Patients Suffering From Chronic Inflammatory Bowel Disease With and Without Steroid Treatment

Cited by 81 publications

References 41 publications

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Bone turnover and metabolism in paediatric patients with inflammatory bowel disease treated with systemic glucocorticoids

Osteal Tissue Macrophages Are Intercalated throughout Human and Mouse Bone Lining Tissues and Regulate Osteoblast Function In Vitro and In Vivo

Bone density and metabolism in subjects with microdeletion of chromosome 22q11 (del22q11)

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