1230
ARTERIOVENOUS
Even with extremely aggressive treatment, the prognosis of synovial sarcoma is poor; Syear survival rates range from 36% to 5 l%, and lo-year survival rates range from 11.2% to 30%. There does not appear to be any relationship between microscopic type and survival rate. Metastatic lesions occur in almost half of the cases: the lung is the most prevalent site (94%) followed by regional lymph nodes and bone.
761 6. Shmookler
7.
9.
I. Smith LW: Synoviomata. Am J Pathol 3:355, I927 2. Knox LC: Synovial sarcoma: Report ofthree cases. Am J Cancer 28:461, 1936
OF MANDIBLE
3. Stuer J: Eine Ungenwoehnliche Geschwulst der Ellhogengelenksgegend. Inaug Diss Wuerzburg I893 4. Enzinger FM, Weiss SW: Soft Tissue Tumors, Synovial Sarcoma. St Louis, MO, Mosby, 1988, pp 659-688 5. Attie JN, Steckler RM, Platt N: Cervical synovial sarcoma, in Cancer, vol 25. Philadelphia, PA. Lippincott, 1970, pp 758-
8.
References
MALFORMATION
IO.
BM, Enzinger FM, Brannon RB: Oral facial synovial sarcoma. Cancer 50:269-276, 1982 Moore DM. Berke GS: Synovial sarcoma of the head and neck. Arch Otolaryngol Head Neck Surg 113:31 I-313, 1987 Mitcherling JJ, Collins EM, Tomich CE, et al: Synovial sarcoma of the neck: Report of case. Oral Surg 34:64-69. I976 Dieckmann J: Malignant synovioma of the temporomandibular joint. Deutsche Zahnaerztl Zeit 27:853-857. 1972 DelBalso AM, Pyatt RS, Busch RF. et al: Synovial cell sarcoma of the temporomandibular joint. Arch Otolaryngol 108:520522. 1982
J OralMaxillofacSurg 50:1230-1233.
1992
Recurrent Arteriovenous Malformation of the Mandible: A Case Report MUSTAFA AND J.M. SYMINGTON,
6. ABOUZGIA, BDS,* BDS, MSc, PHD, FDSRCS
Congenital arteriovenous malformations (AVMs) are vascular maldevelopments characterized by the presence of abnormal channels joining the arterial to the venous circulation without the interposition of a normal capillary bed; they usually have a high flow. Acquired arteriovenous fistulas are caused by injury. They commonly are single and involve a previously normal circulatory system. These anomalies enlarge by hemodynamic mechanisms rather than by cellular hyperplasia. Intrabony AVMs of the mandible are considered very rare. In their review of the literature, Gallagher et
Received from the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Toronto, and The Toronto Hospital, Toronto, Ontario, Canada. * Senior Resident. t Professor and Department Head. Address correspondence and reprint requests to Dr Symington: Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University ofToronto, 124 Edward St, Toronto, Ontario, M5G lG6 Canada. 0 1992 American 0278-2391/92/501
Association l-001
of Oral and Maxillofacial
7$3.00/O
Surgeons
(ENG)t
al’ found 124 published cases. Various treatment methods were described; of these, the most favorable technique was embolization, followed by resection. Radical surgical excision is reported to have good results, especially with smaller lesions. However, longterm follow-up usually is not reported. Rappaport and Rappaport2 believe that many communicating microfistulae coexist with a major fistula. They also believe that no treatment will effect a cure. While this is somewhat overstated, the principle is important in assessing treatment outcome. In the majority of AVMs, the communications between arteries and veins can be microscopic in size, leading to uncertainty about the anatomical extent of the lesion and resulting in inadequate surgical resections.2-6 Nonfunctioning microfistulae, with no blood flow, probably exist in the tissues surrounding an AVM.2-5 These microfistulae are not demonstrable by angiography.‘,* Coleman and Hoopesg believe that many of the shunts do not show on angiography, but changes in the peripheral resistance allow the shunts to open. Figure 1 represents a summary of the speculated events related to the mechanism of recurrence in congenital arteriovenous malformation.
1231
ABOUZGIA AND SYMINGTON
ARTERIOVENOUS MALFORMATION MACROFISTULAE (microfistulae)
Embolization
Surgery
Fibrosis /‘ Venous thrombosis
I
Collateral Circulation FIGURE 2. Panoramic radiograph (1987) of right side of mandible showing a honeycombed, radiolucent lesion extending from the distal aspect of the first molar to the right angle region.
High vascular. resistance
/ Enlargement of (microfistulae) (Recurrence)
\
I
Hemodynamic factors
FIGURE I. Speculated events related to the mechanism of recurfence of congenital arteriovenous malformations.
Report
the symphysis (Fig 4). Drainage was by large channels that joined the jugular vein at the bulb. On March 30, 1987, embolization with polyvinyl alcohol particles was performed through the right facial artery. It was not possible to selectively catheterize the branch of the internal maxillary artery; therefore, embolization of this vessel was not accomplished. The following day, the patient underwent surgical resection and an immediate reconstruction with an autogenous iliac crest bone graft. The inferior alveolar nerve was preserved.
of Case
A 2 l-year-old white man was referred in March 1987 to the Toronto General Hospital, Department of Oral and Maxillofacial Surgery, with the complaint of a numb right lower lip, mobility of the first and second molars, and pulsatile noises in his right ear of 3 months’ duration. His medical history was noncontributory and no history of previous trauma was disclosed. Physical examination showed a healthy male in no distress. There was a pronounced bruit over the right body of the mandible. Intraoral examination revealed mobility of the lower right first and second molar. The lower right second molar was pulsatile in its socket. There was no palpable lingual or buccal expansion. A panoramic radiograph showed a honeycombed, radiolucent lesion in the right mandible extending from the distal aspect of the first molar to the angle region, with resorption of the roots of the lower second molar (Fig 2). Aspiration under local anesthesia produced a large volume of bright-red blood. A computed tomography (CT) scan with contrast further elucidated the anatomic extent of the lesion and showed disruption of the medial cortex of the mandible (Fig 3). There was no soft-tissue involvement. Angiography confirmed the diagnosis of high-flow intramandibular arteriovenous malformation supplied by the right facial artery, right internal maxillary artery, and left facial artery across
FIGURE 3. CT scan (coronal section, 1987) showing disruption of the medial mandibular cortex.
1232
FIGURE 4. Angiogram (1987) showing AVM of right mandible supplied by the right facial artery and the right internal maxillary artery
The patient did very well until approximately 3 years postoperative, when he began to experience periods of pain and swelling on the right side ofhis face and in the retromandibular and preauricular regions. This occurred at least once a month and lasted for approximately 1 week. In February 199 I. the patient was admitted for investigation. On physical examination, there were no extraoral abnormalities found. Intraoral examination revealed a poorly defined, soft-tissue swelling of approximately 2 cm in diameter with normal overlying mucosa, located at the posteriomedial border of the right mandibular ramus. A panoramic radiograph showed no abnormalities (Fig 5). CT scan with contrast revealed a soft-tissue mass medial to the right mandibular ramus (Fig 6). Angiography showed two small branches from the right internal maxillary artery ending in a very small vascular blush along the posteriomedial aspect of the right mandibular ramus (Fig 7). Magnetic resonance imaging (MRI) with contrast to enhance the blood vessels showed a soft-tissue mass medial to the ascending ramus, adjacent to the deep lobe of the parotid gland (Fig 8). No vascular flow was noted in the soft-tissue mass. The differential diagnosis included a soft-tissue tumor or a recurrent arteriovenous malformation.
FIGURE 5. Panoramic radiography (1991) showing the reconstrutted segment with two integrated implants.
ARTERIOVENOUS
MALFORMATION
OF MANDIBLE
FIGURE 6. CT scan with contrast (coronal section, soft-tissue window, 1991) showing the soft-tissue mass medial to the right mandibular ramus (arrow).
On March 18, 1991, the patient underwent surgery with general anesthesia. Through an external approach with a mandibulotomy, the right parapharyngeal region medial to the ascending ramus was explored. A soft-tissue mass filled with a large blood clot was found, excised, and submitted for histologic examination. The microscopic examination showed multiple dilated blood vessels in a fibrous tissue stroma. Some of the blood vessels contained thrombi undergoing organization.
FIGURE 7. Angiogram (1991) showing two small branches from the right internal maxillary artery ending in a very small vascular blush along the posteriomedial aspect ofthe right mandibular ramus.
1233
ABOUZGIA AND SYMINGTON
that later can respond to changes in hemodynamics, leading to enlargement of the microfistulae and recurrence of the lesion.4 It seems very likely that this was the mechanism of recurrence in this case. Also, tissue adjacent to the AVM is always ischemic4 and, because of the additional ischemia caused by arterial ligation, embolization, and surgical intervention, existing microfistulae can open up, leading to recurrence of the AVM. However, Des Prez et alI4 found no histologic evidence of microfistulae after resection of an AVM. They believe that these lesions represent a diffuse area of ischemia and that &hernia is the stimulus that brings about hypertrophy and hyperplasia of the newly established collateral vessels. References
FIGURE 8. MRI (199 1) showing a soft-tissue mass medial to the ascending ramus, adjacent to the deep lobe of the parotid gland, with no vascular flow (arrow).
Discussion Initially, this patient was treated successfully by embolization and surgical resection; however, symptoms recurred 3 years later. There was no apparent soft-tissue extension of the AVM in this patient on his initial presentation in 1987. Clinical examination, CT scan with contrast, angiography, and MRI failed to reveal the vascular nature of the recurrent AVM in this patient. A diagnosis of pleomorphic adenoma was considered based on the results of the imaging techniques. However, knowledge of the nature of these vascular lesions favored a diagnosis of recurrent arteriovenous malformation. We believe that the low flow and the thrombi were the responsible factors in causing the diagnostic dilemma. This lesion produces a field change that is in reality much larger than can be detected by current imaging techniques2,’ Occlusion of the proximal artery forces collateral blood flow in the direction of least resistance, which is represented by the fistulas. To treat the malformation definitively and reduce the possibility of recurrence, the abnormal vascular tissue should be removed in its entirety,7.8~10-‘3’18 whenever possible. A widely accepted mechanism of recurrence, in AVMs is based on the belief that microfistulae always exist in the tissue adjacent to the AVM. Therefore, an incomplete resection leaves undetectable microfistulae
1. Gallagher DMK, Hilley D, Epker BN: Surgical treatment of an arteriovenous malformation of the mandible in a child. A case report. J Maxillofac Surg 11:279, 1983 2. Rappaport I, Rappaport J: Congenital arteriovenous listula of the maxillofacial region. Am J Surg 134:39, 1977 3. Morgan RF, Horowitz JH, Wanebo HJ, et al: Surgical management of vascular malformations of the head and neck. Am J Surg 152:424, 1986 4. Leipzig 8, Yau Pak C: Arteriovenous malformation of the pterygomaxillary space. Otolaryngol Head Neck Surg 90:48. 1982 5. Selfe RW. Sherman M. Miller TF: Arteriovenous malformation of the mandible. Otblaryngol Head Neck Surg 86:659, 1978 6. Rappaport I, Yim D: Congenital arteriovenous fistulas of the head and neck. Arch Otolaryngol97:350, 1973 7. Spatz S, Kaltman S, Farber S: Vascular malformation: Report of a case with eight-year follow-up. J Oral Maxillofac Surg 43:281, 1985 8. Vandenakker HP, Kuiper L, Peeters FLM: Embolization of an arteriovenous malformation of the mandible. J Oral Maxillofac Surg 45~255, 1987 9. Coleman C, Hoopes JE: Congenital arteriovenous anomalies of the head and neck. Plast Reconstr Surg 47:354. 1971 10. Anderson JH, Grisus RJ, McKean TW: Arteriovenous malformation of the mandible. Oral Surg 52: 118, 198 1 11. Hurwitz DJ, Kerber CW: Hemodynamic considerations in the treatment of arteriovenous malformations of the face and scalp. Plast Reconstr Surg 67:42 1, 198 1 12. Kelly DE, Terry BC, SmallEW: Arteriovenous malformation of the mandible: Reoort of case. J Oral Sure 35:387, 1977 13. Kaban LB, Mulliken JB: Vascular anomalies oflthe maxillofacial region. J Oral Maxillofac Surg 44:203, 1986 14. Des Prez JD, Kiehn CL, Vlastou C, et al: Malformation of the head and neck. Am J Surg 136424, 1978 15. Mulliken JB: Vascular malformations of the head and neck, in Mulliken JB, Yong AE (eds): Vascular Malformations: Hemangiomas and Malformations. Philadelphia, PA, Saunders, 1988, pp 301-342 16. Frame JW, Wake MJC: Therapeutic arterial embolisation of vascular lesions in maxillofacial region. Br J Oral Maxillofac Surg 25181, 1987 17. Zhao-ju Z, Yun-tang W, Guang-xi S, et al: Clinical application of angiography of oral and maxillofacial hemangiomas. Oral Surg 55:437, 1983 18. Biller HF, Krepsi YP, Som PM: Combined therapy for vascular lesions of the head and neck with intra-arterial embolization and surgical excision. Otolaryngol Head Neck Surg 90:37, 1982
ARTERIOVENOUS
Even with extremely aggressive treatment, the prognosis of synovial sarcoma is poor; Syear survival rates range from 36% to 5 l%, and lo-year survival rates range from 11.2% to 30%. There does not appear to be any relationship between microscopic type and survival rate. Metastatic lesions occur in almost half of the cases: the lung is the most prevalent site (94%) followed by regional lymph nodes and bone.
761 6. Shmookler
7.
9.
I. Smith LW: Synoviomata. Am J Pathol 3:355, I927 2. Knox LC: Synovial sarcoma: Report ofthree cases. Am J Cancer 28:461, 1936
OF MANDIBLE
3. Stuer J: Eine Ungenwoehnliche Geschwulst der Ellhogengelenksgegend. Inaug Diss Wuerzburg I893 4. Enzinger FM, Weiss SW: Soft Tissue Tumors, Synovial Sarcoma. St Louis, MO, Mosby, 1988, pp 659-688 5. Attie JN, Steckler RM, Platt N: Cervical synovial sarcoma, in Cancer, vol 25. Philadelphia, PA. Lippincott, 1970, pp 758-
8.
References
MALFORMATION
IO.
BM, Enzinger FM, Brannon RB: Oral facial synovial sarcoma. Cancer 50:269-276, 1982 Moore DM. Berke GS: Synovial sarcoma of the head and neck. Arch Otolaryngol Head Neck Surg 113:31 I-313, 1987 Mitcherling JJ, Collins EM, Tomich CE, et al: Synovial sarcoma of the neck: Report of case. Oral Surg 34:64-69. I976 Dieckmann J: Malignant synovioma of the temporomandibular joint. Deutsche Zahnaerztl Zeit 27:853-857. 1972 DelBalso AM, Pyatt RS, Busch RF. et al: Synovial cell sarcoma of the temporomandibular joint. Arch Otolaryngol 108:520522. 1982
J OralMaxillofacSurg 50:1230-1233.
1992
Recurrent Arteriovenous Malformation of the Mandible: A Case Report MUSTAFA AND J.M. SYMINGTON,
6. ABOUZGIA, BDS,* BDS, MSc, PHD, FDSRCS
Congenital arteriovenous malformations (AVMs) are vascular maldevelopments characterized by the presence of abnormal channels joining the arterial to the venous circulation without the interposition of a normal capillary bed; they usually have a high flow. Acquired arteriovenous fistulas are caused by injury. They commonly are single and involve a previously normal circulatory system. These anomalies enlarge by hemodynamic mechanisms rather than by cellular hyperplasia. Intrabony AVMs of the mandible are considered very rare. In their review of the literature, Gallagher et
Received from the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Toronto, and The Toronto Hospital, Toronto, Ontario, Canada. * Senior Resident. t Professor and Department Head. Address correspondence and reprint requests to Dr Symington: Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University ofToronto, 124 Edward St, Toronto, Ontario, M5G lG6 Canada. 0 1992 American 0278-2391/92/501
Association l-001
of Oral and Maxillofacial
7$3.00/O
Surgeons
(ENG)t
al’ found 124 published cases. Various treatment methods were described; of these, the most favorable technique was embolization, followed by resection. Radical surgical excision is reported to have good results, especially with smaller lesions. However, longterm follow-up usually is not reported. Rappaport and Rappaport2 believe that many communicating microfistulae coexist with a major fistula. They also believe that no treatment will effect a cure. While this is somewhat overstated, the principle is important in assessing treatment outcome. In the majority of AVMs, the communications between arteries and veins can be microscopic in size, leading to uncertainty about the anatomical extent of the lesion and resulting in inadequate surgical resections.2-6 Nonfunctioning microfistulae, with no blood flow, probably exist in the tissues surrounding an AVM.2-5 These microfistulae are not demonstrable by angiography.‘,* Coleman and Hoopesg believe that many of the shunts do not show on angiography, but changes in the peripheral resistance allow the shunts to open. Figure 1 represents a summary of the speculated events related to the mechanism of recurrence in congenital arteriovenous malformation.
1231
ABOUZGIA AND SYMINGTON
ARTERIOVENOUS MALFORMATION MACROFISTULAE (microfistulae)
Embolization
Surgery
Fibrosis /‘ Venous thrombosis
I
Collateral Circulation FIGURE 2. Panoramic radiograph (1987) of right side of mandible showing a honeycombed, radiolucent lesion extending from the distal aspect of the first molar to the right angle region.
High vascular. resistance
/ Enlargement of (microfistulae) (Recurrence)
\
I
Hemodynamic factors
FIGURE I. Speculated events related to the mechanism of recurfence of congenital arteriovenous malformations.
Report
the symphysis (Fig 4). Drainage was by large channels that joined the jugular vein at the bulb. On March 30, 1987, embolization with polyvinyl alcohol particles was performed through the right facial artery. It was not possible to selectively catheterize the branch of the internal maxillary artery; therefore, embolization of this vessel was not accomplished. The following day, the patient underwent surgical resection and an immediate reconstruction with an autogenous iliac crest bone graft. The inferior alveolar nerve was preserved.
of Case
A 2 l-year-old white man was referred in March 1987 to the Toronto General Hospital, Department of Oral and Maxillofacial Surgery, with the complaint of a numb right lower lip, mobility of the first and second molars, and pulsatile noises in his right ear of 3 months’ duration. His medical history was noncontributory and no history of previous trauma was disclosed. Physical examination showed a healthy male in no distress. There was a pronounced bruit over the right body of the mandible. Intraoral examination revealed mobility of the lower right first and second molar. The lower right second molar was pulsatile in its socket. There was no palpable lingual or buccal expansion. A panoramic radiograph showed a honeycombed, radiolucent lesion in the right mandible extending from the distal aspect of the first molar to the angle region, with resorption of the roots of the lower second molar (Fig 2). Aspiration under local anesthesia produced a large volume of bright-red blood. A computed tomography (CT) scan with contrast further elucidated the anatomic extent of the lesion and showed disruption of the medial cortex of the mandible (Fig 3). There was no soft-tissue involvement. Angiography confirmed the diagnosis of high-flow intramandibular arteriovenous malformation supplied by the right facial artery, right internal maxillary artery, and left facial artery across
FIGURE 3. CT scan (coronal section, 1987) showing disruption of the medial mandibular cortex.
1232
FIGURE 4. Angiogram (1987) showing AVM of right mandible supplied by the right facial artery and the right internal maxillary artery
The patient did very well until approximately 3 years postoperative, when he began to experience periods of pain and swelling on the right side ofhis face and in the retromandibular and preauricular regions. This occurred at least once a month and lasted for approximately 1 week. In February 199 I. the patient was admitted for investigation. On physical examination, there were no extraoral abnormalities found. Intraoral examination revealed a poorly defined, soft-tissue swelling of approximately 2 cm in diameter with normal overlying mucosa, located at the posteriomedial border of the right mandibular ramus. A panoramic radiograph showed no abnormalities (Fig 5). CT scan with contrast revealed a soft-tissue mass medial to the right mandibular ramus (Fig 6). Angiography showed two small branches from the right internal maxillary artery ending in a very small vascular blush along the posteriomedial aspect of the right mandibular ramus (Fig 7). Magnetic resonance imaging (MRI) with contrast to enhance the blood vessels showed a soft-tissue mass medial to the ascending ramus, adjacent to the deep lobe of the parotid gland (Fig 8). No vascular flow was noted in the soft-tissue mass. The differential diagnosis included a soft-tissue tumor or a recurrent arteriovenous malformation.
FIGURE 5. Panoramic radiography (1991) showing the reconstrutted segment with two integrated implants.
ARTERIOVENOUS
MALFORMATION
OF MANDIBLE
FIGURE 6. CT scan with contrast (coronal section, soft-tissue window, 1991) showing the soft-tissue mass medial to the right mandibular ramus (arrow).
On March 18, 1991, the patient underwent surgery with general anesthesia. Through an external approach with a mandibulotomy, the right parapharyngeal region medial to the ascending ramus was explored. A soft-tissue mass filled with a large blood clot was found, excised, and submitted for histologic examination. The microscopic examination showed multiple dilated blood vessels in a fibrous tissue stroma. Some of the blood vessels contained thrombi undergoing organization.
FIGURE 7. Angiogram (1991) showing two small branches from the right internal maxillary artery ending in a very small vascular blush along the posteriomedial aspect ofthe right mandibular ramus.
1233
ABOUZGIA AND SYMINGTON
that later can respond to changes in hemodynamics, leading to enlargement of the microfistulae and recurrence of the lesion.4 It seems very likely that this was the mechanism of recurrence in this case. Also, tissue adjacent to the AVM is always ischemic4 and, because of the additional ischemia caused by arterial ligation, embolization, and surgical intervention, existing microfistulae can open up, leading to recurrence of the AVM. However, Des Prez et alI4 found no histologic evidence of microfistulae after resection of an AVM. They believe that these lesions represent a diffuse area of ischemia and that &hernia is the stimulus that brings about hypertrophy and hyperplasia of the newly established collateral vessels. References
FIGURE 8. MRI (199 1) showing a soft-tissue mass medial to the ascending ramus, adjacent to the deep lobe of the parotid gland, with no vascular flow (arrow).
Discussion Initially, this patient was treated successfully by embolization and surgical resection; however, symptoms recurred 3 years later. There was no apparent soft-tissue extension of the AVM in this patient on his initial presentation in 1987. Clinical examination, CT scan with contrast, angiography, and MRI failed to reveal the vascular nature of the recurrent AVM in this patient. A diagnosis of pleomorphic adenoma was considered based on the results of the imaging techniques. However, knowledge of the nature of these vascular lesions favored a diagnosis of recurrent arteriovenous malformation. We believe that the low flow and the thrombi were the responsible factors in causing the diagnostic dilemma. This lesion produces a field change that is in reality much larger than can be detected by current imaging techniques2,’ Occlusion of the proximal artery forces collateral blood flow in the direction of least resistance, which is represented by the fistulas. To treat the malformation definitively and reduce the possibility of recurrence, the abnormal vascular tissue should be removed in its entirety,7.8~10-‘3’18 whenever possible. A widely accepted mechanism of recurrence, in AVMs is based on the belief that microfistulae always exist in the tissue adjacent to the AVM. Therefore, an incomplete resection leaves undetectable microfistulae
1. Gallagher DMK, Hilley D, Epker BN: Surgical treatment of an arteriovenous malformation of the mandible in a child. A case report. J Maxillofac Surg 11:279, 1983 2. Rappaport I, Rappaport J: Congenital arteriovenous listula of the maxillofacial region. Am J Surg 134:39, 1977 3. Morgan RF, Horowitz JH, Wanebo HJ, et al: Surgical management of vascular malformations of the head and neck. Am J Surg 152:424, 1986 4. Leipzig 8, Yau Pak C: Arteriovenous malformation of the pterygomaxillary space. Otolaryngol Head Neck Surg 90:48. 1982 5. Selfe RW. Sherman M. Miller TF: Arteriovenous malformation of the mandible. Otblaryngol Head Neck Surg 86:659, 1978 6. Rappaport I, Yim D: Congenital arteriovenous fistulas of the head and neck. Arch Otolaryngol97:350, 1973 7. Spatz S, Kaltman S, Farber S: Vascular malformation: Report of a case with eight-year follow-up. J Oral Maxillofac Surg 43:281, 1985 8. Vandenakker HP, Kuiper L, Peeters FLM: Embolization of an arteriovenous malformation of the mandible. J Oral Maxillofac Surg 45~255, 1987 9. Coleman C, Hoopes JE: Congenital arteriovenous anomalies of the head and neck. Plast Reconstr Surg 47:354. 1971 10. Anderson JH, Grisus RJ, McKean TW: Arteriovenous malformation of the mandible. Oral Surg 52: 118, 198 1 11. Hurwitz DJ, Kerber CW: Hemodynamic considerations in the treatment of arteriovenous malformations of the face and scalp. Plast Reconstr Surg 67:42 1, 198 1 12. Kelly DE, Terry BC, SmallEW: Arteriovenous malformation of the mandible: Reoort of case. J Oral Sure 35:387, 1977 13. Kaban LB, Mulliken JB: Vascular anomalies oflthe maxillofacial region. J Oral Maxillofac Surg 44:203, 1986 14. Des Prez JD, Kiehn CL, Vlastou C, et al: Malformation of the head and neck. Am J Surg 136424, 1978 15. Mulliken JB: Vascular malformations of the head and neck, in Mulliken JB, Yong AE (eds): Vascular Malformations: Hemangiomas and Malformations. Philadelphia, PA, Saunders, 1988, pp 301-342 16. Frame JW, Wake MJC: Therapeutic arterial embolisation of vascular lesions in maxillofacial region. Br J Oral Maxillofac Surg 25181, 1987 17. Zhao-ju Z, Yun-tang W, Guang-xi S, et al: Clinical application of angiography of oral and maxillofacial hemangiomas. Oral Surg 55:437, 1983 18. Biller HF, Krepsi YP, Som PM: Combined therapy for vascular lesions of the head and neck with intra-arterial embolization and surgical excision. Otolaryngol Head Neck Surg 90:37, 1982
