Superficial arteriovenous hemangioma of the oral cavity

Objective, Superficial arteriovenous hemangioma (AH) is a benign vascular l esion that often affects the head and neck, but only 3 histologically prove n intraoral lesions have been previously reported. The aim of this study wa s to analyze the clinical and histologic features of 36 oral AHs from 35 pa tients. Study design, All vascular lesions, other than pyogenic granulomas, accessi oned between 1952 and 2000 were retrieved, and clinical details were gleane d from the request forms or, when available, from the case notes. Histologi c sections stained with hematoxylin-eosin were reviewed, and all selected c ases were stained for smooth muscle actin and elastin. Results, The age range was 12 to 90 (mean, 53 years; median, 59). Of ail pa tients, 54% were female. All the lesions were solitary. The labial mucosa o r vermilion was affected in ii (49%) patients, the tongue in 5, the hard pa late and cheek mucosa in 4 each, the gingiva or alveolar mucosa in 3, and t he floor of the mouth in 1. Clinical presentation was most often a raised l esion smaller than 20 mm. Duration ranged from months to many years. Four l esions recurred. The consistent histopathologic feature was an unencapsulat ed mass of blood vessels located in the lamina propria, the submucosa, or b oth, but 3 patterns could be discerned. The most common (in 44% of cases) c omprised a diffuse mixture of thick-walled and thin-walled vessels in varia ble proportions. The second pattern (42%) showed a lobular arrangement of s maller vessels of uniform wall thickness, sometimes associated with an arte riole. The remaining 14% showed a tortuous pattern of angular, branching, t hick-walled vessels lacking inner elastic laminae one lesion showed both th is pattern and the first pattern, one showed both the lobular morphology an d the third pattern. Of the patients with the lobular arrangement, 64% were female. Smooth muscle actin was a major component of the lesional vessel w alls regardless of thickness, but although most contained some fibrillary e lastin, none had inner elastic laminae as prominent as those seen in adjace nt true arteries. All AHs contained plump endothelial cells, and mast cell numbers were increased. Conclusions, The etiology of AH is uncertain; endocrine and inflammatory st imuli may activate an underlying vascular malformation. Some lesions, espec ially those in younger patients, may be true hamartomas.