Central Retinal Artery Occlusion as an Iatrogenic Complication of Treatment of Central Giant Cell Granuloma of the Mandible Gauri Bhushan, MS,* Swati Gupta, MD,y Urvashi Bhushan, BDS,z and Usha Kaul Raina, MDx Although intralesional steroid injection as a management option for central giant cell granuloma (CGCG) of the mandible is considered safe, central retinal artery occlusion (CRAO) is a dreaded and previously unreported complication of this treatment modality. The present report discusses an iatrogenic case of CRAO that occurred during treatment of CGCG of the mandible. This complication occurred because of high injection pressure, which led to the opening of an anastomosis between the external and internal carotid arteries, leading to retrograde migration of steroid particles. This report also highlights the importance of being aware of such communications. Ó 2015 American Association of Oral and Maxillofacial Surgeons J Oral Maxillofac Surg 73:933.e1-933.e6, 2015
Central giant cell granuloma (CGCG) is a rare benign tumor of the jaw and constitutes fewer than 7% of jaw lesions. Most cases occur in women younger than 30 years. CGCG is more common in the mandible and shows local aggressiveness. Conventional management includes surgical resection, but risk of recurrence and cosmetic deformity has led to the advent of alternative modalities, such as intralesional steroid injection. Central retinal artery occlusion (CRAO) as a complication of an intralesional corticosteroid injection for head and neck tumors, such as eyelid capillary hemangioma, is well reported in the available literature.1 Retrograde embolization of steroid particles has been attributed to high injecting pressure and communication between the hemangioma feeder vessel and the ophthalmic artery.2 However, reported cases of embolization of particles during intralesional steroid injection used for treatment are lacking. The authors encountered 1 such case and have highlighted the importance of being aware of the existence of such an anastomosis between the extra- and intracra-
nial vasculatures resulting in this catastrophic complication.
Report of Case A 13-year-old female patient with CGCG of the right mandible (Figs 1, 2) was given an intralesional injection of triamcinolone acetonide 10 mg mixed with a local anesthetic (2% lignocaine) and 1:100,000 epinephrine. The drug was administered at high injection pressure for better penetration. During the procedure, the patient developed tachycardia and hypertension. After the patient was stabilized hemodynamically, she reported acute loss of vision in the right eye. An ophthalmology consultation was immediately sought. The ocular examination showed that there was no perception of light in the right eye, whereas the left eye had 20/20 vision. The right eye also showed a relative afferent papillary defect. Fundus examination showed whitening of the retina with a cherry-red spot, deposits of triamcinolone
*Senior Resident, Department of Ophthalmology, Guru Nanak Eye Centre, Delhi, India.
Address correspondence and reprint requests to Dr. Gauri Bhushan: B-3/75-B, Lawrence Road, Delhi 110035, India; e-mail:
ySenior Resident, Department of Radiodiagnosis, Maulana Azad Medical College, Delhi, India.
[email protected] Received October 12 2014
zJunior Resident, Department of Pediatric Dentistry, Maulana
Accepted January 20 2015
Azad Institute of Dental Sciences, Delhi, India.
Ó 2015 American Association of Oral and Maxillofacial Surgeons
xDirector Professor, Department of Ophthalmology, Guru Nanak Eye Centre, Delhi, India.
0278-2391/15/00073-7 http://dx.doi.org/10.1016/j.joms.2015.01.018
933.e1
933.e2
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG
FIGURE 1. Radiograph showing a multilocular radiolucent lesion of the right mandible. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
acetonide in multiple small arterioles and venules, and scattered intraretinal hemorrhages (Fig 3). Fluorescein angiography was performed and findings were consistent with CRAO of the right eye (Fig 4). Examination of the left eye did not disclose any abnormalities. Conventional treatment for CRAO, which included an ocular massage and anterior chamber paracentesis,
FIGURE 2. Highly cellular section showing numerous multinucleated giant cells admixed with disorganized fibrovascular connective tissue consistent with central giant cell granuloma (hematoxylin and eosin stain; magnification, 400). Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
was given, but there was no alleviation of symptoms. The possibility of inadvertent injection of triamcinolone acetonide in the arterial system was considered and the patient was advised for angiography of the head and neck region to look for possible communication between the arterial systems of the internal carotid artery (ICA) and the external carotid artery (ECA). Computed tomographic angiography visualized a tuft of vessels in the substance of the right medial and lateral pterygoid muscles (Fig 5) with likely communication between branches of the internal maxillary artery (branch of the ECA) and the cavernous portion of the ICA (Fig 6). These angiographic findings suggested a possible route for retrograde arterial embolization of triamcinolone acetonide crystals in the central retinal artery. Triamcinolone crystals were injected into the inferior alveolar branch of the right maxillary artery. From this site, an embolus probably entered the middle meningeal artery, which is a branch of the internal maxillary artery. An anastomosis is normally present between the middle meningeal artery and the cavernous segment of the ICA, which can open up under a high-pressure injection. The clinical signs and symptoms at presentation occurred owing to the subsequent entry of steroid particles into the central retinal artery. The authors followed up with the patient after 1 week and subsequently after 4 weeks. The follow-up showed that the crystals of triamcinolone acetonide in
BHUSHAN ET AL
FIGURE 3. Fundus photograph of the right eye at presentation shows deposition of triamcinolone crystals in the retinal vessels, particularly around the macula. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
the retinal vessels had disappeared (Figs 7, 8). However, there was no visual improvement. Additional intralesional steroid injections were not given and the patient underwent surgical resection of the tumor.
Discussion CGCG of the jaw is a rare, benign tumor seen more commonly in the mandible than in the maxilla. Conventional treatment is surgical resection and curettage,
FIGURE 4. Fluorescein angiogram depicts nonperfusion of retinal vessels around the macula. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
933.e3 which has a higher success rate than other treatment modalities. Nonetheless, recurrences have been reported in up to 11 to 49% of cases. Cosmetic deformity and mutilating complications are a concern, especially with large tumors.3 During the past few years, other treatment options have been increasingly used. These options include intralesional steroid injections, calcitonin spray, and subcutaneous interferon-a2a. The practice of intralesional steroid injections (triamcinolone) was first introduced by Terry and Jacoway,3 in which a 50:50 mixture of 2% lidocaine with 1:100,000 epinephrine was found to be effective, with minimal complications, although multiple weekly injections were needed. Histologic resemblance of the lesion to sarcoid, for which steroids are the first-line treatment, is the rationale behind the use of the steroid to treat CGCG. Another histologic study of CGCG found that dexamethasone can inhibit multinucleated giant cells of the tumor, which are actually osteoclasts.4 This hypothesis is supported by the inhibition of osteoclast-like cells in a marrow culture by the steroid.5 Because of the frequent multilocular nature of the tumor (as seen at radiography), injecting steroids at a high pressure and at multiple sites (2 mL of solution is injected every 2 cm of visible lesions by radiography) ensures complete penetration of the drug throughout the lesion for acceptable results.6 The injections are conventionally repeated 6 times at weekly intervals. The expansile nature of the lesion makes the overlying cortex thin, which enables easy injection of steroid into the tumor. Numerous case reports also have shown successful treatment of CGCG with calcitonin. Although patients with CGCG do not have classic hyperparathyroidism, the histologic similarity to a brown tumor of hyperparathyroidism can be the reason behind the response of this tumor to calcitonin. It is administered through a subcutaneous route or through intranasal spray. During the course of treatment with calcitonin, a myriad of side effects is encountered, ranging from dizziness, flushing, nausea, diarrhea, and interaction with parathormone leading to possible effects on calcium and bone metabolism.7,8 Although intranasal spray eliminates most of these complications, many patients are unable to tolerate the side-effects. Another treatment modality that has recently been discussed is interferon-a. Interferon has been used in the past few years to treat patients with metastatic or locally advanced, nonresectable giant cell lesions of the long bones. It is administered subcutaneously for the treatment of CGCG of the mandible with the rationale that the antiangiogenic property of interferon will inhibit angiogenesis within the lesion and thus cause its involution.9 However, histologic analysis has shown that markers for vascular endothelium are located only in the periphery, and although scattered cases of
933.e4
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG
FIGURE 5. Computed tomographic angiogram of the head and neck displays an anomalous tuft of vessels in the pterygoid region (arrow). Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
CGCG have shown successful response to interferon treatment, the rationale is not well supported. Treatment of CGCG with steroids is the safest of all treatment modalities with the fewest side-effects. This is perhaps due to the fact that it is administered locally rather than systemically. Even after an extensive review of the literature, the authors did not come across any reported case of CRAO after an intralesional steroid injection. CRAO and systemic symptoms in the present case raised the possibility of inadvertent steroid injection into the vascular network in or around the lesion. An injecting pressure higher than the systemic arterial pressure can cause retrograde migration of the emboli by opening pre-existing anastomotic routes. There are several known potential orbital collateral routes connecting the ECA to the ophthalmic artery,10 and 1 of them has been highlighted in the present case.
Despite early institution of the treatment for CRAO, there was no apparent clinical improvement, possibly because of multiple emboli in the small vessels of the retina that failed to dislodge. In light of this catastrophic complication in this case, the authors recommend injecting intralesional steroids at low pressure after taking care not to inadvertently inject it into a vessel to avoid retrograde embolization of drug. However, multiple injections sites can be used in the same sitting to ensure adequate drug delivery. Although the complication encountered is a rare one, patients should be cautioned about possible vision loss or stroke during preoperative risk counseling. The authors also highlight the need for simultaneous indirect ophthalmoscopy for pediatric patients undergoing intralesional corticosteroid injection for mandibular tumors and other tumors of the head and neck who might not be able to report symptomatic
933.e5
BHUSHAN ET AL
FIGURE 6. Connection between a branch of the internal maxillary artery and the cavernous portion of the internal carotid artery (arrow) is visualized on computed tomographic angiogram. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
FIGURE 7. Fundus photograph after 6 weeks shows absorption of triamcinolone particles.
FIGURE 8. Fluorescein angiogram 6 weeks later visualizes limited retinal vessel filling at the macula.
Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
933.e6 vision loss. The authors further recommend that the interventionist should have sound knowledge and must keep in mind the existence of these dormant anastomotic communications between the ECA and ICA that can open up under high-pressure injection in the head and neck region. Acknowledgments We thank Dr. Neeraj Nischal (MD) and Ms. Poorva Singal for their help in editing the manuscript.
References 1. Egbert JE, Schwartz GS, Walsh AW: Diagnosis and treatment of an ophthalmic artery occlusion during an intralesional injection of corticosteroid into an eyelid capillary hemangioma. Am J Ophthalmol 121:638, 1996 2. Egbert JE, Paul S, Engel WK, et al: High injection pressure during intralesional injection of corticosteroids into capillary hemangiomas. Arch Ophthalmol 119:677, 2001
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG 3. Terry BC, Jacoway JR: Management of central giant cell granuloma: An alternative to surgical therapy. Oral Maxillofac Surg Clin North Am 6:579, 1994 4. Flanagan AM, Nuo B, Tinkler SM, et al: The multinucleate cells in giant cell granulomas of jaws are osteoclasts. Cancer 62:1139, 1988 5. Pharoah MJ, Heersche JNM: Dexamethasone inhibits formation of osteoclast like cells in bone marrow cultures. J Dent Res 65: 1006, 1986 6. Kermer C, Millesi W, Watzke IM: Local injection of corticosteroids for central giant cell granuloma. Int J Oral Maxillofac Surg 23:366, 1994 7. Pogrel MA, Harris ST, Regezi J, et al: Calcitonin treatment for central giant cell granulomas. J Oral Maxillofac Surg 55(suppl):38, 1997 8. de Lange J, Rosenberg AJWP, van den Akker HP, et al: Treatment of central giant cell granuloma of the jaw with calcitonin. Int J Oral Maxillofac Surg 28:372, 1999 9. Kaban LB, Troulis MJ, Ebb D, et al: Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaw. J Oral Maxillofac Surg 60:1103, 2002 10. Geibprasert S, Pongpech S, Armstrong D, et al: Dangerous extracranial-Intracranial anastomoses and supply to the cranial nerves: Vessels the neurointerventionalist needs to know. AJNR Am J Neuroradiol 30:1459, 2009
Central giant cell granuloma (CGCG) is a rare benign tumor of the jaw and constitutes fewer than 7% of jaw lesions. Most cases occur in women younger than 30 years. CGCG is more common in the mandible and shows local aggressiveness. Conventional management includes surgical resection, but risk of recurrence and cosmetic deformity has led to the advent of alternative modalities, such as intralesional steroid injection. Central retinal artery occlusion (CRAO) as a complication of an intralesional corticosteroid injection for head and neck tumors, such as eyelid capillary hemangioma, is well reported in the available literature.1 Retrograde embolization of steroid particles has been attributed to high injecting pressure and communication between the hemangioma feeder vessel and the ophthalmic artery.2 However, reported cases of embolization of particles during intralesional steroid injection used for treatment are lacking. The authors encountered 1 such case and have highlighted the importance of being aware of the existence of such an anastomosis between the extra- and intracra-
nial vasculatures resulting in this catastrophic complication.
Report of Case A 13-year-old female patient with CGCG of the right mandible (Figs 1, 2) was given an intralesional injection of triamcinolone acetonide 10 mg mixed with a local anesthetic (2% lignocaine) and 1:100,000 epinephrine. The drug was administered at high injection pressure for better penetration. During the procedure, the patient developed tachycardia and hypertension. After the patient was stabilized hemodynamically, she reported acute loss of vision in the right eye. An ophthalmology consultation was immediately sought. The ocular examination showed that there was no perception of light in the right eye, whereas the left eye had 20/20 vision. The right eye also showed a relative afferent papillary defect. Fundus examination showed whitening of the retina with a cherry-red spot, deposits of triamcinolone
*Senior Resident, Department of Ophthalmology, Guru Nanak Eye Centre, Delhi, India.
Address correspondence and reprint requests to Dr. Gauri Bhushan: B-3/75-B, Lawrence Road, Delhi 110035, India; e-mail:
ySenior Resident, Department of Radiodiagnosis, Maulana Azad Medical College, Delhi, India.
[email protected] Received October 12 2014
zJunior Resident, Department of Pediatric Dentistry, Maulana
Accepted January 20 2015
Azad Institute of Dental Sciences, Delhi, India.
Ó 2015 American Association of Oral and Maxillofacial Surgeons
xDirector Professor, Department of Ophthalmology, Guru Nanak Eye Centre, Delhi, India.
0278-2391/15/00073-7 http://dx.doi.org/10.1016/j.joms.2015.01.018
933.e1
933.e2
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG
FIGURE 1. Radiograph showing a multilocular radiolucent lesion of the right mandible. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
acetonide in multiple small arterioles and venules, and scattered intraretinal hemorrhages (Fig 3). Fluorescein angiography was performed and findings were consistent with CRAO of the right eye (Fig 4). Examination of the left eye did not disclose any abnormalities. Conventional treatment for CRAO, which included an ocular massage and anterior chamber paracentesis,
FIGURE 2. Highly cellular section showing numerous multinucleated giant cells admixed with disorganized fibrovascular connective tissue consistent with central giant cell granuloma (hematoxylin and eosin stain; magnification, 400). Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
was given, but there was no alleviation of symptoms. The possibility of inadvertent injection of triamcinolone acetonide in the arterial system was considered and the patient was advised for angiography of the head and neck region to look for possible communication between the arterial systems of the internal carotid artery (ICA) and the external carotid artery (ECA). Computed tomographic angiography visualized a tuft of vessels in the substance of the right medial and lateral pterygoid muscles (Fig 5) with likely communication between branches of the internal maxillary artery (branch of the ECA) and the cavernous portion of the ICA (Fig 6). These angiographic findings suggested a possible route for retrograde arterial embolization of triamcinolone acetonide crystals in the central retinal artery. Triamcinolone crystals were injected into the inferior alveolar branch of the right maxillary artery. From this site, an embolus probably entered the middle meningeal artery, which is a branch of the internal maxillary artery. An anastomosis is normally present between the middle meningeal artery and the cavernous segment of the ICA, which can open up under a high-pressure injection. The clinical signs and symptoms at presentation occurred owing to the subsequent entry of steroid particles into the central retinal artery. The authors followed up with the patient after 1 week and subsequently after 4 weeks. The follow-up showed that the crystals of triamcinolone acetonide in
BHUSHAN ET AL
FIGURE 3. Fundus photograph of the right eye at presentation shows deposition of triamcinolone crystals in the retinal vessels, particularly around the macula. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
the retinal vessels had disappeared (Figs 7, 8). However, there was no visual improvement. Additional intralesional steroid injections were not given and the patient underwent surgical resection of the tumor.
Discussion CGCG of the jaw is a rare, benign tumor seen more commonly in the mandible than in the maxilla. Conventional treatment is surgical resection and curettage,
FIGURE 4. Fluorescein angiogram depicts nonperfusion of retinal vessels around the macula. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
933.e3 which has a higher success rate than other treatment modalities. Nonetheless, recurrences have been reported in up to 11 to 49% of cases. Cosmetic deformity and mutilating complications are a concern, especially with large tumors.3 During the past few years, other treatment options have been increasingly used. These options include intralesional steroid injections, calcitonin spray, and subcutaneous interferon-a2a. The practice of intralesional steroid injections (triamcinolone) was first introduced by Terry and Jacoway,3 in which a 50:50 mixture of 2% lidocaine with 1:100,000 epinephrine was found to be effective, with minimal complications, although multiple weekly injections were needed. Histologic resemblance of the lesion to sarcoid, for which steroids are the first-line treatment, is the rationale behind the use of the steroid to treat CGCG. Another histologic study of CGCG found that dexamethasone can inhibit multinucleated giant cells of the tumor, which are actually osteoclasts.4 This hypothesis is supported by the inhibition of osteoclast-like cells in a marrow culture by the steroid.5 Because of the frequent multilocular nature of the tumor (as seen at radiography), injecting steroids at a high pressure and at multiple sites (2 mL of solution is injected every 2 cm of visible lesions by radiography) ensures complete penetration of the drug throughout the lesion for acceptable results.6 The injections are conventionally repeated 6 times at weekly intervals. The expansile nature of the lesion makes the overlying cortex thin, which enables easy injection of steroid into the tumor. Numerous case reports also have shown successful treatment of CGCG with calcitonin. Although patients with CGCG do not have classic hyperparathyroidism, the histologic similarity to a brown tumor of hyperparathyroidism can be the reason behind the response of this tumor to calcitonin. It is administered through a subcutaneous route or through intranasal spray. During the course of treatment with calcitonin, a myriad of side effects is encountered, ranging from dizziness, flushing, nausea, diarrhea, and interaction with parathormone leading to possible effects on calcium and bone metabolism.7,8 Although intranasal spray eliminates most of these complications, many patients are unable to tolerate the side-effects. Another treatment modality that has recently been discussed is interferon-a. Interferon has been used in the past few years to treat patients with metastatic or locally advanced, nonresectable giant cell lesions of the long bones. It is administered subcutaneously for the treatment of CGCG of the mandible with the rationale that the antiangiogenic property of interferon will inhibit angiogenesis within the lesion and thus cause its involution.9 However, histologic analysis has shown that markers for vascular endothelium are located only in the periphery, and although scattered cases of
933.e4
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG
FIGURE 5. Computed tomographic angiogram of the head and neck displays an anomalous tuft of vessels in the pterygoid region (arrow). Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
CGCG have shown successful response to interferon treatment, the rationale is not well supported. Treatment of CGCG with steroids is the safest of all treatment modalities with the fewest side-effects. This is perhaps due to the fact that it is administered locally rather than systemically. Even after an extensive review of the literature, the authors did not come across any reported case of CRAO after an intralesional steroid injection. CRAO and systemic symptoms in the present case raised the possibility of inadvertent steroid injection into the vascular network in or around the lesion. An injecting pressure higher than the systemic arterial pressure can cause retrograde migration of the emboli by opening pre-existing anastomotic routes. There are several known potential orbital collateral routes connecting the ECA to the ophthalmic artery,10 and 1 of them has been highlighted in the present case.
Despite early institution of the treatment for CRAO, there was no apparent clinical improvement, possibly because of multiple emboli in the small vessels of the retina that failed to dislodge. In light of this catastrophic complication in this case, the authors recommend injecting intralesional steroids at low pressure after taking care not to inadvertently inject it into a vessel to avoid retrograde embolization of drug. However, multiple injections sites can be used in the same sitting to ensure adequate drug delivery. Although the complication encountered is a rare one, patients should be cautioned about possible vision loss or stroke during preoperative risk counseling. The authors also highlight the need for simultaneous indirect ophthalmoscopy for pediatric patients undergoing intralesional corticosteroid injection for mandibular tumors and other tumors of the head and neck who might not be able to report symptomatic
933.e5
BHUSHAN ET AL
FIGURE 6. Connection between a branch of the internal maxillary artery and the cavernous portion of the internal carotid artery (arrow) is visualized on computed tomographic angiogram. Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
FIGURE 7. Fundus photograph after 6 weeks shows absorption of triamcinolone particles.
FIGURE 8. Fluorescein angiogram 6 weeks later visualizes limited retinal vessel filling at the macula.
Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
Bhushan et al. Central Retinal Artery Occlusion in CGCG. J Oral Maxillofac Surg 2015.
933.e6 vision loss. The authors further recommend that the interventionist should have sound knowledge and must keep in mind the existence of these dormant anastomotic communications between the ECA and ICA that can open up under high-pressure injection in the head and neck region. Acknowledgments We thank Dr. Neeraj Nischal (MD) and Ms. Poorva Singal for their help in editing the manuscript.
References 1. Egbert JE, Schwartz GS, Walsh AW: Diagnosis and treatment of an ophthalmic artery occlusion during an intralesional injection of corticosteroid into an eyelid capillary hemangioma. Am J Ophthalmol 121:638, 1996 2. Egbert JE, Paul S, Engel WK, et al: High injection pressure during intralesional injection of corticosteroids into capillary hemangiomas. Arch Ophthalmol 119:677, 2001
CENTRAL RETINAL ARTERY OCCLUSION IN CGCG 3. Terry BC, Jacoway JR: Management of central giant cell granuloma: An alternative to surgical therapy. Oral Maxillofac Surg Clin North Am 6:579, 1994 4. Flanagan AM, Nuo B, Tinkler SM, et al: The multinucleate cells in giant cell granulomas of jaws are osteoclasts. Cancer 62:1139, 1988 5. Pharoah MJ, Heersche JNM: Dexamethasone inhibits formation of osteoclast like cells in bone marrow cultures. J Dent Res 65: 1006, 1986 6. Kermer C, Millesi W, Watzke IM: Local injection of corticosteroids for central giant cell granuloma. Int J Oral Maxillofac Surg 23:366, 1994 7. Pogrel MA, Harris ST, Regezi J, et al: Calcitonin treatment for central giant cell granulomas. J Oral Maxillofac Surg 55(suppl):38, 1997 8. de Lange J, Rosenberg AJWP, van den Akker HP, et al: Treatment of central giant cell granuloma of the jaw with calcitonin. Int J Oral Maxillofac Surg 28:372, 1999 9. Kaban LB, Troulis MJ, Ebb D, et al: Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaw. J Oral Maxillofac Surg 60:1103, 2002 10. Geibprasert S, Pongpech S, Armstrong D, et al: Dangerous extracranial-Intracranial anastomoses and supply to the cranial nerves: Vessels the neurointerventionalist needs to know. AJNR Am J Neuroradiol 30:1459, 2009
