Superficial arteriovenous hemangioma of the oral cavity.

OBJECTIVE: Superficial arteriovenous hemangioma (AH) is a benign vascular lesion that often affects the head and neck, but only 3 histologically proven intraoral lesions have been previously reported. The aim of this study was to analyze the clinical and histologic features of 36 oral AHs from 35 patients.

STUDY DESIGN: All vascular lesions, other than pyogenic granulomas, accessioned between 1952 and 2000 were retrieved, and clinical details were gleaned from the request forms or, when available, from the case notes. Histologic sections stained with hematoxylin-eosin were reviewed, and all selected cases were stained for smooth muscle actin and elastin.

RESULTS: The age range was 12 to 90 (mean, 53 years; median, 59). Of all patients, 54% were female. All the lesions were solitary. The labial mucosa or vermilion was affected in 17 (49%) patients, the tongue in 5, the hard palate and cheek mucosa in 4 each, the gingiva or alveolar mucosa in 3, and the floor of the mouth in 1. Clinical presentation was most often a raised lesion smaller than 20 mm. Duration ranged from months to many years. Four lesions recurred. The consistent histopathologic feature was an unencapsulated mass of blood vessels located in the lamina propria, the submucosa, or both, but 3 patterns could be discerned. The most common (in 44% of cases) comprised a diffuse mixture of thick-walled and thin-walled vessels in variable proportions. The second pattern (42%) showed a lobular arrangement of smaller vessels of uniform wall thickness, sometimes associated with an arteriole. The remaining 14% showed a tortuous pattern of angular, branching, thick-walled vessels lacking inner elastic laminae; one lesion showed both this pattern and the first pattern, one showed both the lobular morphology and the third pattern. Of the patients with the lobular arrangement, 64% were female. Smooth muscle actin was a major component of the lesional vessel walls regardless of thickness, but although most contained some fibrillary elastin, none had inner elastic laminae as prominent as those seen in adjacent true arteries. All AHs contained plump endothelial cells, and mast cell numbers were increased.

CONCLUSIONS: The etiology of AH is uncertain; endocrine and inflammatory stimuli may activate an underlying vascular malformation. Some lesions, especially those in younger patients, may be true hamartomas.