Abstract
Arteriovenous malformations (AVMs) are high-flow lesions of intercommunicating veins and arteries formed by abnormal vessel morphogenesis [1]. Most of the AVMs discussed in previous review articles are congenital lesions that became clinically apparent later in life, whereas acquired AVMs are rare and usually form posttraumatically [2]. Both types of AVMs may produce symptoms of pain, swelling, or discoloration, whereas some AVMs present solely as a mass lesion [3]. The 2 types differ in that congenital AVMs often have multiple communications between arteries and veins, whereas acquired lesions may be solitary arteriovenous communications [1]. Most AVMs are found in the extremities, lungs, and head and neck region, with head and neck lesions approaching 51% of all AVMs [4]. Head and neck lesions are usually intracranial and occur in 0.1% of the population [5]. In contrast, extracranial lesions are considered much more rare, and when they do occur, they are typically located at the carotid or vertebral arteries and can sometimes involve the mandibular bone [2]. Most cases of extracranial AVMs in the literature are cited in female patients with very few cases presenting in males. Furthermore, only 8 cases of submandibular AVMs have been cited in the literature, with all cases presenting in females. Treatment options for AVMs include transvenous or transarterial embolization, radiotherapy, or surgery. Although literature discussing the complications of these treatments is limited, complications that have been described include reperfusion bleeding, ischemic ulceration and necrosis, infection, numbness of the inferior alveolar
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