Dexamethasone Enhances Osteoclast Formation Synergistically with Transforming Growth Factor-β by Stimulating the Priming of Osteoclast Progenitors for Differentiation into Osteoclasts

Takuma, Atsushi; Kaneda, Toshio; Sato, Takuya; Ninomiya, S.; Kumegawa, Masayoshi; Hakeda, Yoshiyuki

doi:10.1074/jbc.m300213200

Cited by 92 publications

(50 citation statements)

References 65 publications

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“…GCs influence the production and action of hormones that regulate bone and calcium metabolism and also have direct effects of GCs on bone. GCs increase the expression of receptor activator of nuclear factor κB ligand (RANK-L) and decrease the expression of its soluble decoy receptor osteoprotegerin (OPG) in stromal and osteoblastic cells [78] and also enhance the expression of macrophage colony-stimulating factor (M-CSF), which in the presence of RANK-L induces osteoclastogene sis [78][79][80] . GCs have direct effects on osteoclasts also by suppressing the expression of an autocrine cytokine, such as interferonⅠ, that normally exerts inhibitory effects on osteoclastogenesis [80] .…”

Section: Corticosteroidsmentioning

confidence: 99%

“…GCs increase the expression of receptor activator of nuclear factor κB ligand (RANK-L) and decrease the expression of its soluble decoy receptor osteoprotegerin (OPG) in stromal and osteoblastic cells [78] and also enhance the expression of macrophage colony-stimulating factor (M-CSF), which in the presence of RANK-L induces osteoclastogene sis [78][79][80] . GCs have direct effects on osteoclasts also by suppressing the expression of an autocrine cytokine, such as interferonⅠ, that normally exerts inhibitory effects on osteoclastogenesis [80] . Also they inhibit the function of mature osteoblasts and suppress the synthesis of insulin-like growth factor-Ⅰ, an agent that enhances bone formation [78,79] .…”

Section: Corticosteroidsmentioning

confidence: 99%

See 1 more Smart Citation

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Rodríguez-Bores

Barahona-Garrido²,

Yamamoto‐Furusho³

2007

WJG

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Lor e n a R o d r í g u e z -B o r e s , J o s u é B a r a h o n a G ar r ido, Jesús K Yamamoto-Furusho, IBD Clinic, Department of Gastroenterology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. AbstractLow bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease (IBD) has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors (VDRs) and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B (RANK), RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography (QCT), radiographic absorptiometry, and ultrasound.DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, while new emergent therapies such as calcitonin and teriparatide among others remain to be assessed.

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Section: Corticosteroidsmentioning

confidence: 99%

Section: Corticosteroidsmentioning

confidence: 99%

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Rodríguez-Bores

Barahona-Garrido²,

Yamamoto‐Furusho³

2007

WJG

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“…Glucocorticoids also act on osteoclastogenesis through osteoblastic signals on the receptor activator of the nuclear factor kB ligand (RANK-L) -osteoprotegerin (OPG) axis. Glucocorticoids enhance RANK-L, which binds and activates RANK on the surface of osteoclasts precursor, and also inhibit OPG production, with a consequent induction of osteoclastogenesis (8) and an early increase in bone resorption in GIO. This increased bone resorption can explain the response to antiresorbing drugs in the management of GIO.…”

Section: Mechanisms Of Glucocorticoid Action On Bonementioning

confidence: 99%

“…Glucocorticoid therapy can enhance bone resorption, but the most important effect of glucocorticoid is suppression of bone formation through several mechanisms (6)(7)(8). Glucocorticoids decrease gastrointestinal calcium absorption and increase renal calcium excretion, which may result in modest elevations in serum levels of Parathyroid Hormone (PTH) that cannot explain all skeletal changes observed in glucocorticoid-induced osteoporosis (GIO).…”

mentioning

confidence: 99%

Glucocorticoid-induced osteoporosis

Gregório¹,

Lacativa²,

Melazzi³

et al. 2006

Arq Bras Endocrinol Metab

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Glucocorticoid-induced osteoporosis is the most frequent cause of secondary osteoporosis. Glucocorticoids cause a rapid bone loss in the first few months of use, but the most important effect of the drug is suppression of bone formation. The administration of oral glucocorticoid is associated with an increased risk of fractures at the spine and hip. The risk is related to the dose, but even small doses can increase the risk. Patients on glucocorticoid therapy lose more trabecular than cortical bone and the fractures are more frequent at the spine than at the hip. Calcium, vitamin D and activated forms of vitamin D can prevent bone loss and antiresorptive agents are effective for prevention and treatment of bone loss and to decrease fracture risk. Despite the known effects of glucocorticoids on bone, only a few patients are advised to take preventive measures and treat glucocorticoid-induced osteoporosis. RESUMOOsteoporose Induzida por Glicocorticóide. A osteoporose induzida por glicocorticóides é a causa mais freqüente de osteoporose secundária. Os glicocorticóides causam uma perda óssea rápida nos primeiros meses de uso da medicação; entretanto, o seu efeito mais importante é uma supressão significativa da formação óssea. A administração oral de glicocorticóides está associada a um aumento no risco de fraturas na coluna e no quadril. O risco é dose dependente; entretanto, mesmo doses baixas de glicocorticóides podem aumentar o risco de fraturas. Os pacientes em uso de glicocorticóides perdem mais osso trabecular que osso cortical; em conseqüên-cia, as fraturas são mais freqüentes na coluna que no quadril. O uso concomitante de cálcio e vitamina D ou formas ativas da vitamina D previne a perda óssea, e as drogas anti-reabsortivas são efetivas na prevenção e tratamento da perda óssea e diminuem o risco de fraturas. Apesar de os efeitos deletérios dos glicocorticóides sobre o osso serem bastante conhecidos, poucos pacientes são orientados ou recebem tratamento preventivo associado à terapia com glicocorticóides.

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“…The main reason for that is the fact that long term glucocorticoid therapy can induce rapid and severe bone loss which eventually heightens the risk of fractures. An analysis of General Practice Research Database (UK) at Veterans Affair Medical Centers shows that 40% of respiratory patients who underwent glucocorticoid therapy with daily dosage addition were facing a relative increased risk of femur and spine fractures (Abu 2000, Adler 2003, Takuma 2003, Jia 2006, Kim 2006, Swanson 2006, Lu 2007.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Long Term Administration of Glucocorticoid to Bone Lining Cells Apoptosis

Sari¹

2017

FMI

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Dexamethasone Enhances Osteoclast Formation Synergistically with Transforming Growth Factor-β by Stimulating the Priming of Osteoclast Progenitors for Differentiation into Osteoclasts

Cited by 92 publications

References 65 publications

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Glucocorticoid-induced osteoporosis

The Effect of Long Term Administration of Glucocorticoid to Bone Lining Cells Apoptosis

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