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Denosumab, an alternative to bisphosphonates but also associated with osteonecrosis of the jaw – what is the risk? Harlene Kaur Sidhu Dental Update 2024 42:5, 707-709.
Authors
Harlene KaurSidhu
BDS(Birm), MJDF(RCS, Eng), MSc Oral Surg(UCLAN)
The University of Central Lancashire, Lancashire, UK
Most dental professionals will have, or will soon, encounter patients prescribed this novel alternative antiresorptive drug to bisphosphonates, denosumab (Prolia®, Xgeva®). Denosumab is licensed in the UK for the prevention of osteoporotic fractures in postmenopausal women and the prevention of skeletal-related events (SRE) in adults with bone metastases. The presence of osteonecrosis of the jaw in patients receiving non-bisphosphonate antiresorptives has led to the introduction of the term antiresorptive-related osteonecrosis of the jaw or ARONJ. This paper discusses the basic physiology of bone remodelling, the pharmacology of bisphosphonates and denosumab, and the risk of ARONJ.
CPD/Clinical Relevance: What is the potential risk of ARONJ arising from dental treatment that we should be advising for our patients?
Article
Most dental professionals will have, or will soon, encounter patients prescribed this novel alternative antiresorptive drug to bisphosphonates, denosumab (Prolia®, Xgeva® by Amgen) that is administered through subcutanous injection. Denosumab is a monoclonal human antibody that inhibits osteoclast formation, function and survival, thereby decreasing bone resorption.1
Denosumab is licensed in the UK for:
Remodelling of bone is essential for reshaping of the growing skeleton and healing of bone during injury, for example tooth extraction. Bone remodelling is controlled by systemic and local factors:
Remodelling of bone is a balance between bone deposition and resorption. The three central cells to bone remodelling are:
Osteoblasts differentiate from osteocytes and are the key bone-forming cells. Osteocytes maintain ion control and stress communication within bone. Osteoclasts are responsible for bone resorption and originate from the monocyte-macrophage lineage under the influence of cytokine growth factors, especially macrophage colony-stimulating factor (M-CSF), receptor activator of nuclear factor κ-B ligand (RANKL) and vascular endothelial growth factor (VEGF).4
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