Related Experiment Video
Updated: Jul 5, 2026
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
Published on: June 8, 2014
Medication-related osteonecrosis of the jaw (MRONJ) systemic review: mevalonate pathway mechanisms explored
Jungsuk Cho1, George Feldman2, Ryan Tomlinson2
1Department of Oral and Maxillofacial Surgery, Thomas Jefferson University Hospital, Philadelphia, PA, USA.
Abstract:
Medication-related osteonecrosis of the jaw (MRONJ) is a rare, but devastating condition caused by bisphosphonates, receptor activator of nuclear factor kappa-B ligand inhibitors, anti-angiogenic medications, and disease-modifying antirheumatic drugs. While the clinical spectrum of MRONJ has a wide range, there is a subgroup of patients that do not improve with antibiotics and conservative surgical debridement resulting in pathologic fractures, draining fistulas, and/or osteomyelitis. For the severely affected individuals, the only cure is surgical resection with micro-vascular free flap reconstruction. The etiology of MRONJ is unknown because of the lack of understanding of the biological underpinnings of the disorder connected to the mechanisms of action of the various medications. This limited knowledge has resulted in the classification of patients by clinical presentation rather than underlying pathology. Therefore, the aim of this article is to present a mechanistic framework of MRONJ through the mevalonate pathway in the context of the medications that are known to induce it and explore potential novel therapeutics.
Insights
Medication-related osteonecrosis of the jaw (MRONJ) is a severe condition linked to certain medications. This study proposes a new framework exploring the mevalonate pathway to understand MRONJ
Area of Science:
- Oral and Maxillofacial Surgery
- Pharmacology
- Biochemistry
Background:
- Medication-related osteonecrosis of the jaw (MRONJ) is a serious condition with unknown etiology.
- Current classification relies on clinical presentation, not underlying pathology.
- Severe MRONJ cases require extensive surgical intervention.
Purpose of the Study:
- To present a mechanistic framework for MRONJ pathogenesis.
- To link MRONJ to the mevalonate pathway and causative medications.
- To explore potential novel therapeutic targets for MRONJ.
Main Methods:
- Review of existing literature on MRONJ and related medications.
- Analysis of the mevalonate pathway's role in cellular processes.
- Integration of pharmacological mechanisms with MRONJ clinical manifestations.
Main Results:
- The mevalonate pathway is implicated in the biological underpinnings of MRONJ.
- Specific medications interfere with the mevalonate pathway, contributing to MRONJ.
- A mechanistic framework provides a new perspective on MRONJ etiology.
Conclusions:
- Understanding the mevalonate pathway offers insights into MRONJ development.
- This framework can guide the development of targeted MRONJ therapies.
- Further research into the mevalonate pathway is crucial for MRONJ management.
More Related Videos
06:00Development of a Human Preclinical Model of Osteoclastogenesis from Peripheral Blood Monocytes Co-cultured with Breast Cancer Cell Lines
Published on: September 13, 2017
09:09Treatment with Vancomycin Loaded Calcium Sulphate and Autogenous Bone in an Improved Rabbit Model of Bone Infection
Published on: March 14, 2019
Related Concept Videos
01:31Osteoclasts in Bone Remodeling
01:25Role of Vitamins in Maintaining Bone Health
Vitamin A
Vitamin A is involved in the process of bone remodeling. Retinoic acid, the active metabolite of Vitamin A, has nuclear receptors in osteoblasts and osteoclasts, which are involved in bone remodeling.
Vitamin B12
Vitamin B12 acts as a cofactor during the formation of osteoblast-related proteins, such as osteocalcin. Vitamin B12 plays a role...
01:24Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
01:28Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
01:21Rheumatic Heart Disease III: Medical Management
01:24Peptic Ulcer Disease II: Pathophysiology