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Erschienen in:
01.07.2010 | Invited Commentary
Osteonecrosis of the jaw and bevacizumab therapy
Erschienen in: Breast Cancer Research and Treatment | Ausgabe 1/2010
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Osteonecrosis of the jaw (ONJ) initially came to attention through case reporting. It appears to occur in 1–18% of patients with metastatic bone disease treated with bisphosphonate therapy [1, 2] and is seen less frequently in patients treated with bisphosphonates for osteoporosis or Paget’s Disease of Bone [3]. ONJ is seen uncommonly in patients with early stage breast cancer treated with bisphosphonates as was demonstrated in the recent meta-analysis of breast cancer adjuvant bisphosphonate studies where the incidence of ONJ was 0.24% [4]. ONJ may be uncommon, but it is clinically significant to the patient, medical, and dental communities [5]. Risk factors for developing ONJ appear to be bisphosphonate exposure, cancer and its therapies (possibly including antiangiogenesis therapies), bone invasive dental procedures, lifestyle, and behaviors [6, 7]. There are many potential mechanisms of ONJ (Table 1). The etiology of ONJ is presently unknown.
Table 1
Potential mechanisms of ONJ [19]
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Inhibition of bone remodeling
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Compromised bone microenvironment functioning affecting bone remodeling and repair
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Vascular
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Antiangiogenic affects delaying wound healing and/or affecting micro-infarction in bone and/or soft tissues
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Infection and inflammation
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Microorganisms of the oral cavity promoting cell death in the bone and/or oral soft tissues
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Genetic predisposition
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Genetic polymorphisms affecting drug metabolism, excretion, or drug targets within pathways of bone metabolism and/or wound healing
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Drug interactions
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Drug interactions between chemotherapy and bisphosphonate selectively promoting cell death
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