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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 (COX-2),...
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Related Experiment Video

Updated: Jun 22, 2026

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats
05:55

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Published on: September 27, 2024

[Glucocorticoid-induced osteoporosis treatment algorithm].

J Payer1, Z Killinger, K Brázdilová

  • 1V. interná klinika Lekárskej fakulty UKa FNsP Bratislava, Slovenská republika. payer@ruzinov.fnspba.sk

Vnitrni Lekarstvi
|June 12, 2009
PubMed
Summary
This summary is machine-generated.

Excess glucocorticoids cause secondary osteoporosis, leading to bone density loss and fractures. This review covers prevention and treatment strategies for glucocorticoid-induced osteoporosis (GIO).

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Last Updated: Jun 22, 2026

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats
05:55

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Published on: September 27, 2024

Area of Science:

  • Endocrinology
  • Bone Metabolism
  • Pharmacology

Context:

  • Glucocorticoids are a leading cause of secondary osteoporosis.
  • Both exogenous and endogenous hypercorticism increase fracture risk.
  • Long-term glucocorticoid use necessitates proactive bone health management.

Purpose:

  • To review current prevention and treatment methods for glucocorticoid-induced osteoporosis (GIO).
  • To propose a comprehensive approach for managing GIO in at-risk patients.

Summary:

  • Excessive glucocorticoid exposure significantly elevates the risk of secondary osteoporosis.
  • Patients with hypercorticism, including those on glucocorticoid therapy, experience bone density loss and pathological fractures.
  • This review consolidates existing GIO prevention and treatment strategies and offers a proposed management plan.

Impact:

  • Provides clinicians with evidence-based strategies for GIO prevention and treatment.
  • Aims to reduce the incidence of fractures in patients exposed to glucocorticoids.
  • Offers a framework for managing bone health in long-term glucocorticoid users.