Related Experiment Video
Updated: Aug 4, 2026

07:01
Direct Mouse Trauma/Burn Model of Heterotopic Ossification
Published on: August 6, 2015
Pharmacological interventions for treating acute heterotopic ossification
1Department of Aged Care and Rehabilitation Medicine, Royal North Shore Hospital, Building 12, Pacific Highway, St Leonards, Sydney, 2065, New South Wales, Australia. mharan@med.usyd.edu.au
The Cochrane Database of Systematic Reviews
|October 21, 2004
Summary
Current evidence is insufficient to recommend disodium etidronate for treating heterotopic ossification (HO). More research is needed to assess pharmacological treatments for acute HO with adequate follow-up.
Area of Science:
- Orthopedics
- Pharmacology
- Regenerative Medicine
Background:
- Heterotopic ossification (HO) involves bone formation in soft tissues, often complicating injuries and surgeries.
- HO can lead to significant joint dysfunction and disability.
Purpose of the Study:
- To evaluate the effectiveness of medications in treating acute heterotopic ossification.
- Assessed outcomes included radiological changes, symptom improvement, and functional impairment.
Main Methods:
- Systematic review of randomized and quasi-randomized controlled trials.
- Searched multiple databases for studies on pharmacological treatments for acute HO.
- Included trials confirmed HO by imaging and used radiography to grade severity.
Main Results:
- Two trials involving disodium etidronate versus placebo were analyzed.
- One study suggested disodium etidronate may prevent HO progression, but results were inconsistent.
- Long-term outcomes and side effects were not available, precluding data pooling.
Conclusions:
- Insufficient evidence exists to recommend disodium etidronate for acute HO treatment.
- Concerns remain regarding the long-term efficacy and potential for delayed mineralization.
- Further high-quality studies with extended follow-up are necessary.
Related Concept Videos
Fractures: Bone Repair
Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
Minor fractures with no bone displacement are treated by immobilizing the fractured bone using a cast or splint. However, in the case of fractures with displaced bones, the broken bones are repositioned before immobilization to ensure successful healing without deformation and loss of function. The realignment of fractured bone ends is performed through a process called reduction. If the procedure...
Minor fractures with no bone displacement are treated by immobilizing the fractured bone using a cast or splint. However, in the case of fractures with displaced bones, the broken bones are repositioned before immobilization to ensure successful healing without deformation and loss of function. The realignment of fractured bone ends is performed through a process called reduction. If the procedure...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

