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Jaw Bone Samples From Bisphosphonate-Treated Patients: A Pilot Cohort Study.
Carina Cardemil1,2, Peter Thomsen1,3, Cecilia Larsson Wexell1,4
1Department of Biomaterials, Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden.
Clinical Implant Dentistry and Related Research
|April 29, 2015
Summary
Bisphosphonate treatment can cause osteonecrosis of the jaw (ONJ). This study found increased IL-1β and decreased Casp8 expression in ONJ patients, suggesting a need for further research into molecular mechanisms.
Area of Science:
- Oral and Maxillofacial Surgery
- Oncology
- Pharmacology
Background:
- Osteonecrosis of the jaw (ONJ) is a serious complication associated with bisphosphonate therapy.
- Understanding the cellular and molecular changes in jawbone affected by ONJ is crucial for patient management.
Purpose of the Study:
- To conduct a detailed tissue and cellular-level characterization of jawbone from bisphosphonate-treated patients with and without ONJ.
- To analyze gene expression profiles related to bone metabolism, inflammation, and apoptosis in ONJ.
Main Methods:
- Histological analysis of alveolar bone samples from patients with ONJ, without ONJ, and healthy controls.
- Gene expression analysis of markers for bone formation, resorption, inflammation, angiogenesis, and apoptosis.
Main Results:
- Histological examination revealed low to moderate inflammation with inflammatory infiltrates and the presence of multinuclear giant cells and osteoclasts in both patient groups.
- Significantly upregulated expression of the pro-inflammatory marker interleukin-1 beta (IL-1β) was observed in patients with ONJ compared to controls.
- A downregulated expression of Caspase-8 (Casp8) was noted in bisphosphonate-treated patients.
Conclusions:
- The study highlights distinct molecular alterations in jawbone associated with bisphosphonate-related ONJ, particularly involving IL-1β and Casp8.
- Similar receptor activator of NF-kappaB ligand (RANKL)/osteoprotegerin (OPG) ratios were found across groups.
- Further investigation into the molecular mechanisms underlying ONJ in patients receiving antiresorptive therapy is warranted.
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