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Role of teriparatide in treatment of glucocorticoid-induced osteoporosis.

Lau AN, Adachi JD - Ther Clin Risk Manag (2010)

Bottom Line: GIOP has a significant impact on the morbidity and health-related quality of life of the patients it affects.Some evidence also suggests teriparatide may reduce rates of vertebral fractures in GIOP patients.Overall, this review of the current clinical evidence suggests teriparatide may be an efficacious and promising agent in the treatment of GIOP.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology and Department of Medicine, St Joseph's Healthcare and McMaster University, Hamilton, Ontario, Canada.

ABSTRACT
Glucocorticoids are commonly used in various fields within medicine. One of their most common and clinically significant side effects is glucocorticoid-induced osteoporosis (GIOP). GIOP is a disease leading to progressive decreases in bone mineral density, decreased bone strength, and increased risk of skeletal fractures. GIOP has a significant impact on the morbidity and health-related quality of life of the patients it affects. Glucocorticoids have deleterious effects on bone through promoting osteoblast apoptosis and inhibiting osteoblastogenesis. Teriparatide exerts anabolic effects on bone, so it is understandable why teriparatide is thought to be a rational treatment option. Clinical studies have indicated teriparatide is efficacious in the treatment of GIOP to improve bone mineral density values at the lumbar spine and femoral neck. Some evidence also suggests teriparatide may reduce rates of vertebral fractures in GIOP patients. Overall, this review of the current clinical evidence suggests teriparatide may be an efficacious and promising agent in the treatment of GIOP.

No MeSH data available.


Related in: MedlinePlus

Downstream effect of glucocorticoids on bone metabolism.Abbreviations: PPAR-γ2, peroxisome proliferator-activated receptor-γ2; RANK-L, receptor activation of nuclear factor κB ligand; M-CSF, macrophage colony-stimulating factor; OPG, osteoprotegerin.
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f1-tcrm-6-497: Downstream effect of glucocorticoids on bone metabolism.Abbreviations: PPAR-γ2, peroxisome proliferator-activated receptor-γ2; RANK-L, receptor activation of nuclear factor κB ligand; M-CSF, macrophage colony-stimulating factor; OPG, osteoprotegerin.

Mentions: The mechanisms by which glucocorticoids promote bone resorption are not fully understood. Receptor activation of nuclear factor-κB ligand (RANK-L) likely plays a key role, and the expression of RANK-L is significantly increased in osteoblasts and stromal cells when stimulated by glucocorticoids.11 Macrophage colony-stimulating factor levels are also increased with exposure to glucocorticoids through increased nuclear transcription of the macrophage colony-stimulating factor gene.11 RANK-L and macrophage colony-stimulating factor both play pivotal roles in inducing osteoclastogenesis and decreasing osteoclast apoptosis, thereby leading to increased bone resorption (Figure 1). In addition, osteoprotegerin expression is also decreased in osteoblasts and stromal cells in the presence of glucocorticoids.12 Osteoprotegerin plays a counterregulatory role in the effects of RANK-L, and down-regulation of osteoprotegerin also enhances osteoclastogenesis and decreases rates of osteoclast apoptosis.12


Role of teriparatide in treatment of glucocorticoid-induced osteoporosis.

Lau AN, Adachi JD - Ther Clin Risk Manag (2010)

Downstream effect of glucocorticoids on bone metabolism.Abbreviations: PPAR-γ2, peroxisome proliferator-activated receptor-γ2; RANK-L, receptor activation of nuclear factor κB ligand; M-CSF, macrophage colony-stimulating factor; OPG, osteoprotegerin.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2963159&req=5

f1-tcrm-6-497: Downstream effect of glucocorticoids on bone metabolism.Abbreviations: PPAR-γ2, peroxisome proliferator-activated receptor-γ2; RANK-L, receptor activation of nuclear factor κB ligand; M-CSF, macrophage colony-stimulating factor; OPG, osteoprotegerin.
Mentions: The mechanisms by which glucocorticoids promote bone resorption are not fully understood. Receptor activation of nuclear factor-κB ligand (RANK-L) likely plays a key role, and the expression of RANK-L is significantly increased in osteoblasts and stromal cells when stimulated by glucocorticoids.11 Macrophage colony-stimulating factor levels are also increased with exposure to glucocorticoids through increased nuclear transcription of the macrophage colony-stimulating factor gene.11 RANK-L and macrophage colony-stimulating factor both play pivotal roles in inducing osteoclastogenesis and decreasing osteoclast apoptosis, thereby leading to increased bone resorption (Figure 1). In addition, osteoprotegerin expression is also decreased in osteoblasts and stromal cells in the presence of glucocorticoids.12 Osteoprotegerin plays a counterregulatory role in the effects of RANK-L, and down-regulation of osteoprotegerin also enhances osteoclastogenesis and decreases rates of osteoclast apoptosis.12

Bottom Line: GIOP has a significant impact on the morbidity and health-related quality of life of the patients it affects.Some evidence also suggests teriparatide may reduce rates of vertebral fractures in GIOP patients.Overall, this review of the current clinical evidence suggests teriparatide may be an efficacious and promising agent in the treatment of GIOP.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology and Department of Medicine, St Joseph's Healthcare and McMaster University, Hamilton, Ontario, Canada.

ABSTRACT
Glucocorticoids are commonly used in various fields within medicine. One of their most common and clinically significant side effects is glucocorticoid-induced osteoporosis (GIOP). GIOP is a disease leading to progressive decreases in bone mineral density, decreased bone strength, and increased risk of skeletal fractures. GIOP has a significant impact on the morbidity and health-related quality of life of the patients it affects. Glucocorticoids have deleterious effects on bone through promoting osteoblast apoptosis and inhibiting osteoblastogenesis. Teriparatide exerts anabolic effects on bone, so it is understandable why teriparatide is thought to be a rational treatment option. Clinical studies have indicated teriparatide is efficacious in the treatment of GIOP to improve bone mineral density values at the lumbar spine and femoral neck. Some evidence also suggests teriparatide may reduce rates of vertebral fractures in GIOP patients. Overall, this review of the current clinical evidence suggests teriparatide may be an efficacious and promising agent in the treatment of GIOP.

No MeSH data available.


Related in: MedlinePlus