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Osteonecrosis of the jaw is a major public health concern throughout the world. Use of radiotherapy for head and neck cancer and bone antiresorptives and antiangiogenic agents have increased its incidence. Medication-related osteonecrosis of the jaw is more common relative to other types of osteonecrosis. Osteoradionecrosis occurs despite better treatment planning and shielding to minimize collateral damage to bone. Other related necrotic lesions are secondary to usage of recreational drugs and steroids. This article provides comprehensive information about these different types of bone necrosis; provides the readers with radiographic diagnostic criteria and updates on current theories on pathophysiology of osteonecrosis., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objectives: Osteoradionecrosis (ORN) is common in the jaws after radiotherapy. We hypothesized that the mandible is more susceptible to ORN than the tibia, based on site disparity in hypoxic, hypocellular, and hypovascular tissue breakdown., Study Design: Twelve rats received 50 Gy irradiation to mandible or tibia; 4 of the rats further received minor surgical trauma to the irradiated sites. Structural and cellular skeletal changes were assessed with computerized tomography, histology, and immunostaining., Results: Mandible developed ORN with 70% mean bone loss 10 weeks after irradiation (P < .05), whereas tibia was structurally and radiologically intact 20 weeks after irradiation. Hypocellularity, hypoxia, and oxidative stress were higher in irradiated mandible (P < .001) than tibia (P < .01) but vascular damage was similar at both skeletal sites. Combined effects of radiation and minor trauma promoted mandibular alveolar bone loss and tibial fracture., Conclusions: ORN has a more rapid onset in mandible than in tibia in the rat., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Jaw osteoradionecrosis (ORN) is a major complication of head and neck cancer radiotherapy. Treatment complications account for most of the poor outcomes for head and neck cancers and the associated racial health disparities in cancer survivorship. The global incidence of jaw ORN is improving due to pre-radiotherapy patient preparations and improved head and neck cancer radiotherapy protocols. The diagnosis and management of jaw ORN are based on the patient's history and clinical presentation combined with radiological and histopathological tests. Evidence-based jaw ORN therapies focus on preventive, palliative, and surgical principles. However, new and innovative therapeutic approaches based on the cellular and molecular pathophysiological processes of jaw ORN and the jawbone's susceptibility to radiation bone damage are limited. The rationale for this narrative review is to highlight the current diagnostic approaches to jaw ORN and the pathophysiological basis for new therapeutic options for ORN. [ABSTRACT FROM AUTHOR]

Objectives: Oropharyngeal cancer (OPC) is the sixth most common cancer worldwide. Focus on risk factors, improved diagnostic methods and effective management strategies have made it possible to successfully treat OPC. However, the 5-year survival rate has not improved for several years due to multiple treatment complications, tissue morbidity, loss of function, and diminished quality of life. Survivors are faced with complications like oral mucositis, hyposalivation, osteoradionecrosis, tissue fibrosis, morbidity from jaw resection, disfigurement, and loss of function that further diminish quality of life. The aim of this review is to highlight major complications associated with treatment of OPC via a literature search and review of available options for identification and management of these complications. Data sources: Relevant publications on oral complications of OPC therapy were thoroughly reviewed from the literature published between the years 1988 and 2012. We evaluated reported incidence, prevalence, and risk factors for oral complications of chemotherapy and radiotherapy for OPC. The authors conducted an electronic search using English language databases, namely PubMed Plus, Medline (Pre-Medline and Medline), Cochrane Database of Systematic Reviews (evidence-based medicine), Dentistry & Oral Sciences Source, A ccessScience, Embase, Evidence-Based Medicine Reviews Multifile, Google Scholar, ISI Journal Citation Reports, and Ovid Multi-Database. Conclusion: We identified the most common complications associated with the treatment of oral cancers. Based on the information gathered, there is evidence that survival of OPC extends beyond eradication of the diseased tissue. Understanding the potential treatment complications and utilizing available resources to prevent and minimize them are important. Caring for OPC survivors should be a multidisciplinary team approach involving the dentist, oncologist, internist, and social worker to improve the currently stagnant 5-year survival rate of OPC. More emphasis on improved quality of life after elimination of the cancer will ultimately improve OPC survivorship. [ABSTRACT FROM AUTHOR]

Cancer radiotherapy is often complicated by a spectrum of changes in the neighboring bone from mild osteopenia to osteoradionecrosis. We previously reported that parathyroid hormone (PTH, 1-34), an anabolic agent for osteoporosis, reversed bone structural deterioration caused by multiple microcomputed tomography (microCT) scans in adolescent rats. To simulate clinical radiotherapy for cancer patients and to search for remedies, we focally irradiated the tibial metaphyseal region of adult rats with a newly available small animal radiation research platform (SARRP) and treated these rats with intermittent injections of PTH1-34. Using a unique 3D image registration method that we recently developed, we traced the local changes of the same trabecular bone before and after treatments, and observed that, while radiation caused a loss of small trabecular elements leading to significant decreases in bone mass and strength, PTH1-34 preserved all trabecular elements in irradiated bone with remarkable increases in bone mass and strength. Histomorphometry demonstrated that SARRP radiation severely reduced osteoblast number and activity, which were impressively reversed by PTH treatment. In contrast, suppressing bone resorption by alendronate failed to rescue radiation-induced bone loss and to block the rescue effect of PTH1-34. Furthermore, histological analyses revealed that PTH1-34 protected osteoblasts and osteocytes from radiation-induced apoptosis and attenuated radiation-induced bone marrow adiposity. Taken together, our data strongly support a robust radioprotective effect of PTH on trabecular bone integrity through preserving bone formation and shed light on further investigations of an anabolic therapy for radiation-induced bone damage. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Orofacial bone is commonly affected by osteoradionecrosis (ORN) during head and neck cancer radiotherapy possibly due to interactions of several factors including radiation damage to resident bone marrow stromal cells (BMSCs). Irradiation causes DNA damage, triggers p53-dependent signalling resulting in either cell-cycle arrest or apoptosis. In same individuals, disproportionately higher rapid growth of orofacial BMSCs relative to those of axial/appendicular bones suggests their response to radiation is skeletally site-specific. We hypothesised that survival and osteogenic recovery capacity of irradiated human BMSCs is site-dependent based on anatomic skeletal site of origin. Methods: Early passage BMSCs from maxilla, mandible and iliac crest of four normal volunteers were exposed to 2.5 to 10Gy gamma radiation to evaluate clonogenic survival, effects on cell cycle, DNA damage, p53-related response and in vivo osteogenic regenerative capacity. Results: Orofacial bone marrow stromal cells (OF-MSCs) survived higher radiation doses and recovered quicker than iliac crest (IC-MSCs) based on clonogenic survival, proliferation and accumulation in G0G1 phase. Post-irradiation p53 level was relatively unchanged but expression of p21, a downstream effector was moderately increased in OF-MSCs. Re-establishment of in vivo bone regeneration was delayed more in irradiated IC-MSCs relative to OF-MSCs. Conclusions: Effect of irradiation on human BMSCs was skeletal site-specific with OF-MSCs displaying higher radio-resistance and quicker recovery than IC-MSCs. [Copyright &y& Elsevier]