Related Experiment Video
Updated: Apr 26, 2026
05:55
Author Spotlight: Developing a Rat Model for Weight-Bearing Intervention to Investigate Osteonecrosis of the Femoral Head
Published on: September 27, 2024
1.1K
Glucocorticoid-induced osteoporosis: 2013 update
1Rheumatology Unit, Department of Clinical and Experimental Medicine, University of Pisa. mmazzant@int.med.unipi.it.
Reumatismo
|July 30, 2014
Summary
Glucocorticoid-induced osteoporosis (GIO) significantly increases fracture risk, with standard bone density scans often insufficient for risk assessment. Early intervention and risk stratification using tools like FRAX are crucial for effective GIO management.
Area of Science:
- Endocrinology
- Orthopedics
- Pharmacology
Background:
- Glucocorticoids are a leading cause of secondary osteoporosis, termed glucocorticoid-induced osteoporosis (GIO).
- Treatment with prednisone (≥10 mg/d for >3 months) dramatically elevates hip and vertebral fracture risks.
- GIO impairs bone quality and mechanical competence, rendering bone mineral density insufficient for accurate fracture risk assessment.
Purpose of the Study:
- To review the pathophysiology and management strategies for glucocorticoid-induced osteoporosis.
- To highlight the limitations of current diagnostic methods and the importance of early intervention.
- To discuss updated guidelines and therapeutic options for GIO.
Main Methods:
- Literature review of glucocorticoid effects on bone.
- Analysis of fracture risk assessment tools, including FRAX.
- Summary of current treatment guidelines and pharmacological interventions for GIO.
Main Results:
- Glucocorticoid use causes significant skeletal fragility and increased fracture incidence.
- Bone mineral density measurements are inadequate for precise GIO fracture risk evaluation.
- Established fracture risk algorithms (FRAX) and updated guidelines aid in GIO management.
Conclusions:
- Early intervention and individualized fracture risk assessment are paramount in managing GIO.
- Bisphosphonates, teriparatide, and denosumab represent key therapeutic options for GIO.
- Surgical interventions like vertebroplasty may offer limited benefit in GIO compared to primary osteoporosis.
Related Concept Videos
01:21Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
689
Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
689
01:24Glucagon-like Receptor Agonists
1.3K
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
1.3K
01:29Bone Disorders
7.9K
Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
7.9K
01:31Osteoclasts in Bone Remodeling
3.8K
Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
3.8K
01:06Oral Hypoglycemic Agents: Glinides
1.0K
Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
1.0K
01:15Hypoglycemia and Glucagon
1.3K
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
1.3K