Radioactive jaw necrosis is a serious complication of head and neck radiotherapy. This complication 's main characteristics are chronic necrosis and infection, and its clinical manifestations are local pain, mouth opening restriction, speech disorder, dysphagia, exposure of dead bone, prolonged healing of facial and neck soft tissue fistula, and even pathological fracture, which brings great pain to the patient's body and mind. Radioactive jaw necrosis has become a clinical problem in the field of medicine, specifically for maxillofacial surgery of the external head and neck. The pathogenesis of radiation-induced jaw necrosis is still unclear, but high radiotherapy dose, extraction of teeth after radiotherapy and surgical trauma are recognized as high-risk factors. The diagnosis of radiation-induced jaw necrosis needs to be combined with the patient's radiotherapy history, clinical symptoms and imaging examination. Conservative or surgical treatment should be selected according to its clinical classification and stages, and the prevention of radiation-induced jaw necrosis should be emphasized. The key points are to remove dental caries, residual roots and crowns before radiotherapy; improve radiotherapy technology; and take preventive measures against high-risk factors. In recent years, the diagnosis and treatment of radiation-induced jaw necrosis has gradually become standardized and individualized. This article reviews the progress of treatment and research on radiation-induced jaw necrosis at home and abroad in terms of its definition, etiology, risk factors, diagnosis, treatment and prevention to provide reference for clinical treatment.

Oral squamous cell carcinoma in the background of/with oral submucous fibrosis (OSCC-OSF) has a unique etiology and is clinically distinct from other OSCCs. We previously identified ADAMTS9-AS2 as a functional tumor suppressor in OSCC-OSF through the regulation of PI3K-AKT signaling. However, its role in metabolic modulation and the underlying mechanisms remain unclear. In this study, we reported for the first time that ADAMTS9-AS2 suppressed aerobic glycolysis by cooperating with let-7a-5p in OSCC cells. Mechanistically, let-7a-5p inhibited HK2 expression by targeting its 3′-UTR, further deregulating glycolytic function, while enhancing HK2 expression rescued the inhibitory effects of the ADAMTS9-AS2/let-7a-5p axis on aerobic glycolysis and OSCC cell growth. Exosomal ADAMTS9-AS2 regulated metabolic reprogramming during OSCC tumorigenesis. ABC transporters in lipid and pyrimidine metabolism were significantly enriched pathways. Changes in several key metabolites were identified after ADAMTS9-AS2 exosome treatment, including increased levels of DL-glutamic acid and D-mannose, along with decreased levels of cytidine and D-maltose. Thus, our findings demonstrate that ADAMTS9-AS2 drives let-7a-5p binding to HK2 to suppress cell growth in OSCC by abolishing aerobic glycolysis. Our data on metabolic reprogramming have greatly expanded the role of the ADAMTS9-AS2/let-7a-5p axis as a key regulator of metabolism during OSCC tumorigenesis.