2019
DOI: 10.1111/1756-185x.13680
|View full text |Cite
|
Sign up to set email alerts
|

Management of glucocorticoid‐induced osteoporosis: What is new?

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
4
0

Year Published

2021
2021
2022
2022

Publication Types

Select...
4

Relationship

0
4

Authors

Journals

citations
Cited by 4 publications
(4 citation statements)
references
References 38 publications
(61 reference statements)
0
4
0
Order By: Relevance
“…Glucocorticoid and diabetes induced osteoporosis share pathophysiological characteristics: a predominant decrease in bone formation rather than an increase in bone resorption and an increase in bone marrow adiposity [60][61][62]. In glucocorticoid-induced osteoporosis, after an early transient increase in bone resorption, there is a long-term suppression of bone formation related to an increased sclerostin secretion and up-regulation of peroxisome proliferator-activated receptor that favor the differentiation of pluripotent precursor cells to adipocytes rather than osteoblasts, contributing to bone marrow adipocyte expansion [63,64]. Fragility fractures are now recognized as an important complication of both diabetes mellitus type 1 and type 2, particularly in those with long-term disease, poor glycaemic control, β cells failure and insulin treatment [65].…”
Section: Oxytocin As a Therapeutic Agent: Perspectivesmentioning
confidence: 99%
“…Glucocorticoid and diabetes induced osteoporosis share pathophysiological characteristics: a predominant decrease in bone formation rather than an increase in bone resorption and an increase in bone marrow adiposity [60][61][62]. In glucocorticoid-induced osteoporosis, after an early transient increase in bone resorption, there is a long-term suppression of bone formation related to an increased sclerostin secretion and up-regulation of peroxisome proliferator-activated receptor that favor the differentiation of pluripotent precursor cells to adipocytes rather than osteoblasts, contributing to bone marrow adipocyte expansion [63,64]. Fragility fractures are now recognized as an important complication of both diabetes mellitus type 1 and type 2, particularly in those with long-term disease, poor glycaemic control, β cells failure and insulin treatment [65].…”
Section: Oxytocin As a Therapeutic Agent: Perspectivesmentioning
confidence: 99%
“…Decreased bone formation is responsible for the pathogenesis of glucocorticoid-induced osteoporosis [ 123 ]. Recent evidence has shown that glucocorticoid administration enhances KLF15 expression, which leads to a reduction in osteoblast function [ 124 ].…”
Section: Roles Of Klfs In Normal Bone Physiology ( Table 1 ...mentioning
confidence: 99%
“…Osteoporosis is a systemic chronic pathology that requires long-term management after disease onset. Most osteoporotic patients are elderly; however, similar pathological conditions can be observed in patients undergoing long-term therapeutic glucocorticoid treatment (glucocorticoid-induced osteoporosis—GIO) [ 123 ]. The skeletons of patients show low bone mass and microstructural bone quality [ 146 ].…”
Section: Role Of Klfs In Osteoarthritis Osteoporosis and Osteosarcomamentioning
confidence: 99%
“…Osteoporosis is a major health problem, leading to fragility fractures which cause significant mortality in affected patients up to 3–4 times higher than the general population within one year after diagnosis 1 3 . With the growing ageing population, this results in substantially increasing costs to global health-care systems 4 . The goals of osteoporosis treatment are to reduce risk of osteoporotic fractures and improve bone mineral density (BMD), a gold standard tool for diagnosing osteoporosis and assessing response to therapy 5 , 6 .…”
Section: Introductionmentioning
confidence: 99%