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Background/Aim: Treatment failure in oral cancer is mainly caused by uncontrolled cervical lymph node (LN) metastasis. We previously reported that CD11b+ cells are recruited into tumor hypoxic areas following radiation, leading to re-vascularization and relapse. Since lymphatic vessel formation has similarities with vascular formation, we examined whether surgery induces hypoxia and stimulates lymphangiogenesis. Materials and Methods: The recruitment of CD11b+ cells and the formation of lymphatic vessels were examined using orthotopic tongue cancer mouse models with glossectomy. Results: Surgery on OSC-19 tumor induced LN metastases and hypoxia, followed by CD11b+ cell influx. These phenomena were not observed in the no tumor or SAT tumor models. Stimulation of lymphangiogenesis was observed in the CD11b+ cell influx area, as the tumor grew. The localization of CD11b+ cells was changed from the lymph nodules to the medullary sinuses. Conclusion: Surgery-induced hypoxia in oral tumors leads to CD11b+ cell infiltration, lymphangiogenesis, and LN metastasis.

The prevalence of medication-related osteonecrosis of the jaw (MRONJ) associated with molecular-targeted therapies such as bevacizumab and sunitinib has been constantly increasing in recent years. MRONJ frequently occurs after invasive dental procedures such as tooth extraction in patients currently or with a previous history of receiving antiresorptive agents including bisphosphonates and/or denosumab. Here, we report a rare case of spontaneously occurring MRONJ of the mandible in a 52-year-old Japanese woman with chronic myelogenous leukemia (CML) who was administered imatinib for 9 years. She had never been treated with antiresorptive agents, and her MRONJ developed spontaneously. Although there have been few reports of MRONJ related to imatinib, our case reported here indicates that imatinib may be capable of causing spontaneous MRONJ.

Various treatments for oral vascular malformation (VM) have been reported. Polidocanol and absolute ethanol have also been reported for sclerotherapy. However, there are still few reports on the therapeutic effect and dosage of polidocanol sclerotherapy. Therefore, we examined its therapeutic effects on oral VM. There were 17 sites of VMs, with nine patients diagnosed with oral VM at the Department of Dental and Oral Surgery, Tsukuba University Hospital. The medical records were retrospectively investigated to determine the site, hemangioma volume, polidocanol injection volume, and therapeutic effect. The volume of hemangiomas was calculated using magnetic resonance images. Based on the site, oral VMs were observed in the tongue, buccal mucosa, lips, and oral floor in eight, three, five, and one patients, respectively. The average size of the site was 3071 mm3. The average injection dose of polidocanol at one site was 2.86 mL, the average number of administrations was 1.6, and the response rate was 88.2%. No adverse events were observed. The median numerical rating scale scores were 2/10 (0–6/10) and 0/10 (0–1/10) the day after surgery and 1 week after surgery, respectively. Univariate regression analysis of the total dose in successful cases provided the following formula: 1.3 + 0.00025 × volume (mm3) (mg). Polidocanol sclerotherapy is an effective treatment method for oral VM.