Epithelioid hemangioma is an unusual, which was at first described as angiolymphoid hyperplasia with eosinophilia (ALHE) in 1969 and misinterpreted as the same disease with Kimura’s disease. But now it represents a distinctive vascular tumor, a different entity with those inflammatory conditions. Here, we present a case of epithelioid hemangioma appearing as a diffuse gingival nodular mass in 33‐year‐old male who had suffered from the idiopathic sharp pain of left mandible area previously and later extended to left maxillary region, therefore the gingival lesion was clinically estimated as malignancy associated with neural invasion. CT images revealed the soft tissue mass restricted to left maxillary gingiva without infiltration to underlying maxillary alveolar bone. Histologically, the circumscribed soft tissue mass consist of solid sheets of epithelioid to spindled cells, expressing reactivity for neither cytokeratin AE1/3 nor HMB‐45, but for CD31, endothelial cell marker. Therefore, the lesion was pathologically diagnosed as epithelioid hemangioma. Diagnostic evaluation for the neurologic symptoms of the patient revealed the trigeminal neuralgia, accompanying with the present epithelioid hemangioma incidentally. Awareness of epithelioid hemangioma should be emphasized not to be misdiagnosed as malignant disease like an invasive squamous cell carcinoma, malignant melanoma, or angiosarcoma. Proper evaluation and interpretation for neural symptom may lead to the correct differential diagnosis and therapeutic intervention

We recently described a novel animal model of trigeminal neuropathic pain following compression of the trigeminal ganglion (Ahn et al., 2009). In our present study, we adapted this model using male Sprague-Dawley rats weighing between 250-260 g and then analyzed the behavioral responses of these animals following modified chronic compression of the trigeminal ganglion. Under anesthesia, the rats were mounted onto a stereotaxic frame and a 4% agar solution (10μL) was injected in each case on the dorsal surface of the trigeminal ganglion to achieve compression without causing injury. In the control group, the rats received a sham operation without agar injection. Air-puff, acetone, and heat tests were performed at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, 40, 55, and 70 days after surgery. Compression of the trigeminal ganglion produced nociceptive behavior in the trigeminal territory. Mechanical allodynia was established within 3 days and recovered to preoperative levels at approximately 60 days following compression. Mechanical hyperalgesia was also observed at 7 days after compression and persisted until the postoperative day 40. Cold hypersensitivity was established within 3 days after compression and lasted beyond postoperative day 55. In contrast, compression of the trigeminal ganglion did not produce any significant thermal hypersensitivity when compared with the sham operated group. These findings suggest that compression of the trigeminal ganglion without any injury produces prolonged nociceptive behavior and that our rat model is a useful system for further analysis of trigeminal neuralgia.