Effect of systemic glucocorticoid therapy on bone metabolism and the osteoprotegerin system in patients with active Crohn's disease

Tirpitz, Christian von; Epp, Sonja; Klaus, Jochen; Mason, Richard; Hawa, Gerhard; Brinskelle-Schmal, Natascha; Hofbauer, Lorenz C.; Adler, Guido; Kratzer, Wolfgang; Reinshagen, Max

doi:10.1097/00042737-200311000-00003

Cited by 49 publications

(23 citation statements)

References 34 publications

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“…Furthermore, we also noted a trend towards lower bone mass in children with CD compared to UC. The differences in bone mass between CD and UC patients have been described previously [27,28]. Malnutrition was significant in the IBD group, especially in CD patients.…”

Section: Discussionsupporting

confidence: 63%

Osteoprotegerin and soluble receptor activator of nuclear factor κB ligand in children with inflammatory bowel disease

Jankowska

Gutowska-Owsiak

Kamińska³

et al. 2013

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Section: Discussionsupporting

confidence: 63%

Osteoprotegerin and soluble receptor activator of nuclear factor κB ligand in children with inflammatory bowel disease

Jankowska

Gutowska-Owsiak

Kamińska³

et al. 2013

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“…In patients with renal disease, a decrease in both OPG and OC serum circulating levels was shown, with a parallel increase in bone resorption markers during the first two weeks of GCs treatment (13). In addition, during a 3-month period of high-dose GC treatment (60 mg prednisolone per day), it was observed that OPG decreased after 2 weeks and returned to baseline after 3 months, while soluble RANKL serum levels increased (30). In contrast, considering CS, in three studies, OPG serum levels were found to be higher in patients compared to healthy controls (14,31,32).…”

Section: Discussionmentioning

confidence: 96%

Persistent increase of osteoprotegerin levels after cortisol normalization in patients with Cushing's syndrome

Camozzi¹,

Sanguin²,

Albigier³

et al. 2010

European Journal of Endocrinology

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Objective: Osteoprotegerin (OPG) has been identified as a decoy receptor that inhibits osteoclast differentiation and, more recently, as a paracrine regulator of vascular calcification. OPG is suppressed by glucocorticoids (GC); however, results from experimental and clinical studies are not univocal. The aim of this study was to evaluate OPG and bone metabolism in patients with Cushing's syndrome (CS) before and after cure. Design and methods: Twenty-six patients with CS (all women, mean age: 39.1G11.9 years) and 24 ageand gonadal status-matched healthy women were studied for bone mineral density, bone metabolism, OPG, and receptor activator of nuclear factor-kB ligand at baseline. Twelve patients were also studied 6-18 months after surgery, with persistent normalization of cortisol levels. Results: OPG was significantly higher and osteocalcin (OC) was significantly lower in CS patients than in controls (OPG: 4.17G1.23 vs 2.95G0.79 pmol/l, PZ0.00001; OC: 15.0G6.1 vs 18.8 G6.8 ng/ml, PZ0.04 in CS and controls respectively). After cure, we found no difference in OPG levels, despite a significant increase in OC levels (from 16.4G11 to 37.2G15 ng/ml, PZ0.03). Conclusion: Patients with CS showed increased OPG serum levels that remained unchanged after recovery, despite a restoration of bone formation. We speculate that high levels of OPG could reflect the persistent damage of the GCs on cardiovascular system. European Journal of Endocrinology 162 85-90

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“…This enhanced bone resorption activity is not anymore balanced by the osteoblast bone formation activity, causing a loss in bone mass and a progressive destruction of bone microarchitecture. Induced androgen and estrogen deficiency, systemic glucocorticoid exposure (22), T cell activation as in rheumatoid arthritis and skeletal malignancies (23,24) also enhance the release of RANKL, ending up in promoting osteoclastogenesis and inducing unbalanced bone loss. Denosumab is a fully human monoclonal antibody that binds with high affinity and high specificity to RANKL, thereby preventing RANKL from binding to RANK (25).…”

Section: Pharmacological Approach To Osteoporosismentioning

confidence: 99%

The contribution of cortical and trabecular tissues to bone strength: insights from denosumab studies

Iolascon¹,

Napolano²,

Gioia³

et al. 2013

CCMBM

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SummaryAll materials undergo an aging process which is characterized essentially by changes of the rigidity (stiffness), of the ability to absorb the stresses (toughness) and then ultimately in the mechanical resistance (strength). Both cortical and trabecular bone undergo a continuous process of structural remodeling with the main aim to preserve their biomechanical properties. An imbalance in this process, which promotes bone resorption, results in a quantitative loss of bone tissue and in a qualitative alteration of the skeletal microarchitecture, as you can see in osteoporosis, rheumatoid arthritis or bone metastases. Cortical component has a prominent role on strength therefore loss of cortical bone that is prevalent in elderly may explain the higher frequency of fractures of bones composed mainly of cortical bone such as the proximal femur. Remodeling inhibition with denosumab improved structural strength without altering material properties, that can be primarily explained by the combined effects of increased trabecular and cortical bone mass, and reductions in trabecular eroded surfaces and particularly cortical porosity. Denosumab for its mechanism of action and pharmacokinetics results in a significant, early and continued increase in BMD with enhanced bone strength improving both cortical and trabecular bone.

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Effect of systemic glucocorticoid therapy on bone metabolism and the osteoprotegerin system in patients with active Crohn's disease

Cited by 49 publications

References 34 publications

Osteoprotegerin and soluble receptor activator of nuclear factor κB ligand in children with inflammatory bowel disease

Osteoprotegerin and soluble receptor activator of nuclear factor κB ligand in children with inflammatory bowel disease

Persistent increase of osteoprotegerin levels after cortisol normalization in patients with Cushing's syndrome

The contribution of cortical and trabecular tissues to bone strength: insights from denosumab studies

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