ma Literature review an

dition of a case

David k. Baker, DDS,” Doiphine Seattle, Wash. CHILDREN’S

HOSPITAL

AND

MEDICAL

Oda, BDS, MSc,’

CENTER,

AND

and Robert

UNIVERSITY

W. T. Myall,

HIS,

:lID,a

OF WASHINGTON

A rapidly growing neoplasm in the buccal mucosa of a &month-old baby was excised. By light and electron microscopy the neoplasm had features that were similar to those described in infantile hemangiopericytoma, a rare neoplasm of vascular origin. By light microscopy the neoplasm was multilobular with highly proliferating round to spindle-shaped cells interspersed with numerous vascular spaces. Ultrastructurally, round to elongated cells with short processes, pinocytotic vesicles, reduplicated basal lamina, and basal lamina-like material were identified. lmmunohistochemically the cells were weakly positive with antibodies to vimentin, focally positive with HHF-35, a smooth-muscle cell antibody, negative with antibodies to S-100 protein, T-200, neuron-specific enolase, neurofilaments, desmin, and cytokeratins 35BHl I and 34BE12. Blood vessels were positive with Ulexeuropaeuslectin, but tumor cells were negative. Reticulin stain decorated a delicate network of fibrils surrounding tumor cells and vascular spaces. Clinically the neoplasm did not recur and the baby has been disease free for more than 26 months. The difficulty of the histologic diagnosis of this neoplasm is discussed and the literature is reviewed, with special emphasis on lesions occurring in the oral cavity. (ORAL SURG ORAL MED ORAL PATHOL

1992;73:596-602)

emangiopericytoma (HPC) is an uncommon vascular neoplasmfirst described by Stout and Murray’ in 1942. It hasbeen suggestedthat this neoplasm originates from pericytes, which are the contractile cells that surround capillaries and regulate blood flow. Becauseof the wide range of maturation of these cells, they can be difficult to distinguish from endothelial cells, fibroblasts, or histiocytes, and this has often lead to erroneous diagnoses.2W4 Histologically HPC has been confused with a wide variety of neoplasms including hemangioendotheliomas, glomus tumors, angiosarcomas, and fibrous histiocytomas.4-6In recent years the pericytes in HPC have been identified ultrastructurally, and this has aided diagnosis.7-9 Immunohistochemistry has recently proven to be beneficial becausethese neoplasmshave been found to be uniformly but weakly positive with antibodies to vimentin. Some have been shown to be focally positive with antibodies to muscle actin.

aDivision of Oral and Maxillofacial Surgery, Children’s Hospital and Medical Center, and University of Washington. bDepartment of Oral Biology, School of Dentistry, University of Washington. 7114129891

596

Although HPCs are found in all age groups, a distinction between adult and infantile forms has been made. Adult HPC is deeply seated, located in muscte tissue, and has been reported asbenign, borderiine, or malignant2 According to Enzinger and Smith,2 malignant HPC has a lo-year survival rate of 70%. Histologically, malignant HPC demonstrates prominent mitotic activity, necrosis,hemorrhage, and increased cellularity. This article defines infantile HPC as a neoplasm present at birth or within the first year of life. It differs from the adult form in its superficial subcutaneous location and presentation as a solitary tumor. Microscopically the tumor has increased mitotic activity and focal necrosis, which are ominous features in the adult form. However, in infants, despite these features, the vast majority of tumors behave in a benign manner.2, lo Enzinger and Smith2 suggestedthat infantile HPC should be regarded asa separatetumor from the adult form because of this peculiarity. Although the literature is replete with casesof HPC in adults” and children,‘* compartively few cases have been reported in infantsi Since 1942 a total of 50 infantile HPCs (in 46 patients) have been reported, including 39 casesreviewed by Baarlen et aLi Our

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Number5 Table I. Infantile HPC: Review of literature since 1942 No. of cases Site

(%I

References

Extremities Trunk Head and neck Total

19 (38)

12,15,20-22,24,25,27-29 1,10,12,20,22,30 1,12-21,23,26,31-33

8 (16) 23 -- (46) 50 (100)

Table II. Head and neck infantile HPC by site Site

Fig. 1. Clinical appea.rance of infantile HPC asprotruding nodulewith ulceratedcenter.

Scalp Face Intraoral Central nervous system Ear Pharynx Trachea Total *One

Fig. 2. Infantile HPC lesionsin their entirety. Note clear multilobular arrangementof this tumor. Also note extensionof tumor to lateral anddeepsurgicalmargins.(Hematoxylin-eosin stain; original magnification,~25.) search of the literature uncovered eight additional cases.i4-18Of all patients described in the literature since 1942, three had recurrences1x-20and three died,21-23one of surgical complications,21 the second of unresectable neck and mediastinal involvement,22 and the third of metastasis or possibly multiple primary tumors. 23The vast majority of patients were treated by surgical excision, and jfew received radiation or chemotherapy.l4,15,18, 1%21,*4,25 The anatomic distribution of infantile HPC is as wide as the distribution of capillaries. The location of all reported infantile HPCs can be found in Table I. Forty-six percent were located in the head and neck, 38% in the extremities, and 16% in the trunk. Details of the head and neck locations of infantile HPC are shownin Table II. The majority of head and neck sites were found on the scalp, face, and the oral cavity. HPC of the oral cavity has been reported to involve

No. of cases (%I

8* 4 4* 3 1 2 -- 1 23

(35) (17) (17) (13) (4) (9) (4) (100)

References

1,12,15,16,18,26,32 15,17,23,31 12,13,19 12,20,33 12 14,26 21

patient had intraoral and scalp lesions.

the lips and the tongue (Table III). Other sites involved were the central nervous system and the pharyngeal-hypopharynx area.14,26 Three of these casesdemonstrated recurrences; one was located on the lower lip, and the other two on the pharyngeal area. This may be due in part to the surgical inaccessibility of the latter area. One case,after a partial resection, spontaneously involuted.13 We report a case in a 4-month-old infant of intraoral HPC occurring on the buccal mucosa.Light microscopy, electron microscopy, and immunohistochemical staining were usedto arrive at the diagnosis. CASEREPORT A 4-month-old,full-term, healthy baby boy wasseenat the Children’sHospital and Medical Center in Seattle for evaluationof an apparentlynonpainfulgrowth on the buccal mucosa.The motherhadnoticedthe lesionabout 1week earlier and reported that the child waschewingonthe area. Despite difficulty in examining the infant, a 1.0 X 0.5 cm soft tissuenoduleon the buccalmucosawasnoted(Fig. 1). It was near Stenson’s duct. The tissue was normal in color except for an erythematous area at the tip. An excisional biopsy with the child under general anesthesia was scheduled. One week later, before the scheduled surgery, the child was seen again at the clinic because of a significant increase in the size of the lesion. Examination demonstrated the lesion to be protruding from the mouth. It was approximately 2 cm in length with an ulcer at the tip. The lesion apparently remained painless. It was rubbery in consistency. The color

598

Baker,

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Table III. Intraoral infantile HPC -Site

/

Lip Posterior region of tongue Lower lip Buccal mucosa

Age at onset

Sex

Unknown Birth

M F

Unknown 4

Birth 4 mo

F M

8 2

1

Size (cm)

Treatment

Recurrence

Excision Excised, reexcised at 3 mo Partial resection Excised at age 4 mo

1

At age 5 yr At age 3 mo No No

Reference

12 19 13 Present case

Table IV. Source and dilution of antibodies used for immunohistochemical staining Antibody

35BHll

Commercial

source

HHF-35

Enzo Biochem, New York, N.Y. Enzo Biochem Dako Corp., Santa Barbara, Calif. Enzo Biochem

S-100 protein Desmin

Dako Dako

T-200 Antineurofilament

Dako Biogenex Laboratories, San Ramon, Calif. Biogenex Vector Laboratories, Burlingame, Calif.

34BEi2 Vimentin

Neuron-specific enolase Ulexeuropaeuslectin

remained

similar to the surrounding

!

Dilution

Cell speciJcity

I:250 after pronase digestion

Simple epithelium

I:500 after trypsin digestion 1:20

Stratified squamous epithelium All mesenchymal cells

1:4000 with 50 mmol/L EDTA 1:lOOO 1:500

Smooth, skeletal, and cardiac muscle Mainly cells of neural crest origin Smooth, skeletal, and cardiac muscle All lymphoid cells Neurons, neural dendrites, peripheral nerve Neurons, APUD Endothelial cells

!:20 Prediluted Prediluted 1:500 conjugated to biotin

mucosa except for a

focal areaof ulceration.At biopsythe submucosal extension wasclinically distinct from the underlying buccinatormuscle and no evidenceof invasionof this tissuewasapparent. There wasno unusualamount of bleedingfrom the area. The specimenwas submittedin formalin for microscopic evaluation. So far the infant has beenfollowed for more than 26 monthswith no signsof recurrences. PATHOLOGIC FINDINGS Gross pathology The specimen was submitted as a mucosally covered, solitary, brown nodule measuring 2.0 x 0.6 x 0.7 cm in its greatest dimensions.

cular spaces lined with flat endothelial cells. The classic “staghorn” vascular spaceswere not identified. Numerous mitotic figures were identified (57 per 10 high-power fields), and were present mainly within the areas of the ovoid cells. These particular cells also showed some evidence of pleomorphism (Fig. 3, B). Bizarre tumor cells were not identified in either ovoid or spindle-shaped cells. The latter appeared benign with no evidence of pleomorphism or prominent mitosis. Focal areas of necrosis and hemorrhage were present. The tumor lobules involved both lateral and deep surgical margins (Fig. 2). Reticulin stain demonstrated a meshwork of delicate fibrils surrounding the tumor cells and the vascular spaces(Fig. 4).

Light microscopy Sections from formalin-fixed tissues stained with hematoxylin and eosin exhibited an ulcerated surface epithelium with underlying fibrous connective tissue. The latter was occupied by a lesion arranged in a multilobular fashion (Fig. 2). Lobules were well circumscribed with a smooth periphery surrounded by fibrous connective tissue. They were made up of tightly packed, small, ovoid to spindle-shaped cells with ill-defined borders and round to oval nuclei (Fig. 3). These cells were interspersed by thin-walled vas-

lmmunohistochemistry Immunohistochemical staining on formalin-fixed tissue was performed. Five-micrometer sectionswere deparaffinized and dehydrated, then incubated with primary antibodies. The specificity, commercial source, and dilution of the antibodies are listed in Table IV. Standard avidin-biotin-immunoperoxidase techniques were used. Appropriate negative and positive controls were performed. This tumor expressedthe intermediate filament vi-

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Fig. 3. Higher-power view of section in Fig. 2 shovvs uniform arrangement of spindle-shaped cells around small vascular spaces (A) and pleomorphic round to oval cells with high mitotic rate (B) (Hematoxylin-eosin stain; original magnifications, X400.)

Fig. 4. A, Low-power view showing extensive network of positively stained fibrillar material. B, High-power view showing reticulin fibers surrounding vessels and tumor cells. (Reticulin stain; original magnifications: A, X100; B,

mentin. The Stalin was mild to focally moderate throughout the tumor (Fig. 5, A). Focal positivity with antibodies to muscle-specific actin was also detected (Fig. 5, B). The tumor was nonreactive with antibodies against low- and high-molecular-weight cytokeratins (35BHll and 34BE12), desmin, S-100 protein, T-200, neurofilament, and neuron-specific enolase. Ulex europaeus lectin stained the endothelial cells lining the blood vessels; however, the tumor cells were uniformly negative with this stain (not shown).

tumor cells were found to be completely surrounded by reduplicated basal lamina (Fig. 6). However, the majority of the cells were focally surrounded by basal lamina-likematerial. Poorly developed junctions were identified. Pinocytotic vesicles were present; some were aligned in a linear fashion adjacent to the plasma membrane (Fig. 7). Most tumor cells were of simple appearance with sparse organelles. Fibrillar structures, perhaps representing intermediate filaments, were also noted.

Electron

DISCUSSION

microscopy

Tissue from a fresh1specimen was fixed in 3% glutaraldehyde and processed by standard procedures for ultrastructural examination, which revealed closely associated round and elongated tumor cells with processesof different lengths. These cells were arranged around endothelial-lined vascular spaces similar to those seen at the light microscopic level. Occasional

x400.)

HPC in general, including the infantile variant, has been difficult to diagnose because of the wide spectrum of histologic presentation and resemblance to other neoplasms such as the mesenchymal chondrosarcoma, synovial sarcoma, fibrous histiocytoma, myxomatous liposarcoma, hemangioendothelioma, glomus tumor, and vascular leiomyoma, among oth-

00

Baker, Oda, and Myall

ORAL

SURG ORAL

tvft~

ORAL Pmick May 1992

Fig. 6. Electron microscopy shows occasional tumor c&s with reduplicated basal lamina. (Original magnification, x5000.)

Fig. 5. Immunohistochemical staining shows tumor cells positively stained with antibodies to vimentin (A) and to smooth muscle. (B). (Original magnifications, x400.)

ers. The articles by Enzinger and Smith2 and Dardick et a1.7 provide thorough reviews. Infantile lesions differ from the adult form in their histologic features, clinical presentation, and biologic behavior. Histologically they have a tendency toward being multilobular.2, 3 Clinically they are usually subcutaneous2 and have a benign behavior despite the high rate of mitotic activity, necrosis, and hemorrhage.2% 3, I2 These lesions are uncommon in general and are extremely rare in the oral cavity. Including this case, only four have been reported in the oral cavity (Table III). All lesions were surgically removed. Histologically, this case constituted a diagnostic problem. Neoplasms such as embryonal rhabdomyosarcoma, lymphoma, and infantile fi’jrosarcoma were included in the differential diagnosis. Embryonal rhabdomyosarcoma was excluded because of the absence of rhabdomyoblasts, absence of the loose arrangement of cells, the multilobular arrangement of

Fig. 7. Electron microscopy shows elongated cells with pinocytotic vesicles, some aligned at periphery of cell membrane. Also note basal lamina-like material present focally. (Original magnification, X5000.)

the lesion, negative stainings with antibody to desmin, lack of contractile elements ultrastructurally, and lack of clinical aggressive behavior (i.e., recurrence after conservative surgical removal) (Fig. 2) where the neoplastic tissue extended to all surgical margins. Lymphoma was also considered but was excluded on the basis of the presence of two types of oval and spindle-shaped cells, multilobular arrangement, and negative staining with T-200 antibody. Cells were ultrastructurallynot consistent with hematopoieticcells. Infantile fibrosarcoma was one of the most difficult neoplasms to exclude; this is a problem well recognized and reported in the literature.2‘4 Allen34 stated that at times a distinction between these two neoplasms may be impossible. Both neoplasms have

Volume 73 Number 5

Fig. 8. The area healed postoperatively with minimal scarring.Photographwastaken 1 year after surgery.

spindle-shaped to oval cells and both may have marked vascularity. However, HPC usually has more prominent, dilated vascular spaces, some with a staghorn appearance. Our case lacked the prominent vasculature, which made the diagnosismore difficult. However, it should be mentioned that it is not unusual for the infantile type of HPC to lack prominent vasculature.12 The blood vesselsin this casewere abundant but were thin and collapsed, being slit shaped. Reticulin stain (Fig. 4) brought out the vascu1a.rnature of this lesion and demonstrated that tumor cells were located outside the vascular sheath (Fig. 4, B). The prominent histologic feature present that assistedin separating infantile HPC from fibrosarcoma was the multilobular arrangement of this case (Fig. 2). This is an important histologic criterion used to differentiate between the two entities2 Other features in support of HPC were lack of inffiltrative pattern of the tumor and absenceof the storiform pattern seen in fibrosarcomas. In addition, electron microscopy demonstrated markecl perivascular arrangement of tumor cells, cells with reduplicated basal lamina (Fig. 6), the presenceof occasional intercellular junctions, and the lack of cytoplasmic organelles (Fig. 7). These features were more in support of IHPC than of fibrosarcoma. The immunohistochemical pattern of weak but uniform positive staining with antibody to vimentin and focal positive staining with antibody to smooth-muscle actin (Fig. 5) were also more in support of HPC7 than of fibrosarcoma. Last, the clinical behavior of no recurrence or metastasisis consistent with the behavior of a HPC rather than any sarcoma, including low-grade infantile fibrosarcoma. The latter is known to be locally aggressive and to have a tendency for local recurrence.39 This patient healed

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remarkably well and has not shown any evidence of recurrence during a 26-month period (Fig. 8). HPC in general, including the infantile type, may be extremely difficult to diagnose, and at times the diagnosisis made by exclusion. However, certain light microscopic features such as the multilobularity and lack of infiltrative pattern in the infantile type have been of assistance.Electron microscopic features of this neoplasmhave also been of assistancein the differentiation from other neoplasms.7,9 A spectrum of ultrastructural features are identified, depending on the stage of differentiation of the tumorous pericyte. Certain HPCs, especially those of the central nervous system,tend to produce more classicfeatures of tumor cells with basal lamina, pinocytotic vesicles, long cytoplasmic extensions, and intermediate-sized cytoplasmic processesas compared with those of soft tissue (peripheral). The latter may show these features but less prominently. Our case had ultrastructural features that are more related to those seenin the soft tissue, with discrete to focal basal lamina predominating. Occasionally, reduplicated basal lamina was noted (Fig. 6). Primitive cell junctions (not shown) and pinocytotic vesicles were present (Fig. 7). Cytoplasmic organelles were not prominent. Immunohistochemical staining of HPC is a more recent development and hasbeen usedto study the cell of origin of this neoplasm.This procedure has been of significance in differentiating HPC from other neoplasms.Recent reports demonstrate the uniform mild to moderate staining of the tumor cells with antibodies to vimentin (Fig. 5, A).7~ l3 A few caseshave been shown to be focally positive for muscle protein antibodies such as HHF-35.7 Our case was also focally positive with this antibody (Fig. 5, B). This reaction suggeststhe possiblesmooth muscleorigin of HPC. However, ultrastructurally no evidence of well-developed myofibrils or densebodies were identified in our caseor in the literature. The positivity of the tumor cells with antibodies to muscle protein may reflect the ability of pericytes to differentiate into smooth muscle cells.7 Considerable variability exists in the clinical course of the infantile form of HPC, from spontaneousinvo1ution”3,25to possible metastasis and death.19 With such small numbers of infantile HPC reported, it is difficult to predict clinical behavior on the basis of histology and therefore long-term follow-up is mandatory. Most casesin the literature were treated by surgical excision. The therapeutic modality did not influence the prognosis, which was generally favorable. Both radiation and chemotherapy have been attempted with variable success.3’ 4 The three recur-

02

Baker,

Oda, and Myall

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MED

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PATE~L

May

rences can most likely be attributed to incomplete excision. One case recurred 5 years after removal,t2 which seems to emphasize further the need for longterm follow-up. SUMMARY

HPCs have been reported in the oral cavity in the past.35M3XIt is a rare neoplasm in infants, with only four reported cases (present case included). The tumor generally behaves in a clinically benign manner despite its seemingly malignant histologic features. We report a case of intraoral infantile hemangiopericytoma of the buccal mucosa diagnosed with light microscopy, electron microscopy, and immunohistochemical staining. The neoplasm was conservatively excised surgically, and the healing was unremarkable, with no evidence of recurrence during 26 months of follow-up. However, children with this tumor need to be reexamined at regular intervals for many years. We thank Ms. Audrey Was for the electron microscopy and photography printing.

16.

17. 18.

19.

20. 21. 22,

23.

24. 25. 26.

21. REFERENCES

1. 2. 3. 4. 5. 6. I.

8. 9.

10. 11.

12. 13. 14.

15.

Stout AP, Murray MR. Hemangiopericytcma, vascuiar tumor featuring Zimmermann’s pericytes. Ann Surg 1942;116:26-33. Enzinger FM, Smith BH. Hemangiopericytoma, an analysis of 106 cases. Hum Path01 1976;7:61-82. Enzinger FM, Weiss SW. Soft tissue tumors. St Louis: CV Mosby, 1983:463-81. Jaffe BF. Unusual laryngeal problems in children. Ann Otol 1973;82:637-42. Stout AP. Tumors featuring pericytes, glomus tumor and hemangiopericytoma. Lab Invest 1956;5:217-23. Pitluk HC, Corm J Jr. Hemangiopericytoma, literature review and clinical presentations. Am J Surg 1979;137:413-6. Dardick I, Hammer SP, Scheithouer BW. Ultrastructural spectrum of hemangiopericytoma: a comparative study of fetal, adult, and neoplastic pericytes. Ultrastruct Path01 1989;13:111-54. Elmoto T. Ultrastructure of an infantile hemangiopericytoma. Cancer 1977;40:2161-70. Nunnery EW, Kahn LB, Reddick RL, et al. Hemangiopericytoma: a light microscopic and ultrastructural study. Cancer 1981;47:906-14. Tulenko JF. Congenital hemangiopericytoma: case report. Plast Reconstr Surg 1986;41:276-7. McMaster MJ, Soule EH, Ivins JC. Hemangiopericytoma, a clinicopathologic study and long-term follow up of 60 patients. Cancer 1975;36:2232-44. Kauffman SL, Stout AP. Hemangiopericytoma in children. Cancer 1960;13:695-710. Baarlen JV, Drogtrop AP, Bax NMA. Congenital hemangiopericytoma: report of a case. Pediatr Path01 1988;8:109-15. Baden M, Papageorgiou A, Joshi VV, Stern L. Upper airway obstruction in a newborn secondary to HPC. Can Med Assoc J 1972;107:1202-4. Chana RS, Narasimharoo KL, Bannerjee CK, Mitra SK,

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Pathak IC. Hemangiopericytoma in infants and children. Indian J Pediatr 1984;51:95-8. Chabalko JJ, Fraumeni JF Jr. Blood-vessel neoplasms in children: epidemiologic aspects. Med Pediatr Oncol 1975; I:i 35 41. Boyle J, Kennedy C, Berry J, Mott MG. Congenital haemanuiouericvtoma. J R Sot Med 1985:78(suoo1):20-3. Mathur’SN, Kriplani A, Arora N,’ Jain S: Vanjani RN. Recurrent congenital haemangiopericytoma at an unusual site. J Indian Med Assoc 1988;86:69-70. Alpers CE, Rosenau W, Finkbeiner WE, deLorimier AA, Kronish D. Congenital (infantile) hemangiopericytoma of the tongue and sublingual region. Am J Clin Path01 1984;81:37782. Kauffman SL, Stout AP. Congenital mesenchymal tumors. Cancer 1965;18:460-76. Isaacs H. Perinatal (congenital and neonatal) neoplasms: a report of 110 cases. Pediatr Path01 1985;3:165-216. Atkinson JB, Mahour GH, Isaacs H Jr, Ortega JA. Hemangiopericytoma in infants and children: a report of six patients. Am J Surg 1984;148:372-4. Morgan A, Evbuomwan I. Congenital haemangiopericytoma of the face with earlv distant metastasis. J R Co11 Sure Edinb 1983;28:123-5. ' Maillet P, Lamesch A, Dawagne MP. L’hemangiopericytome congenital. Chir Pediatr 1985;26:22-5. Jenkins JJ III. Congenital malignant hemangiopericytoma. Pediatr Path01 1987;7:119-22. Seibert JJ, Seibert RW, Weisenburger DFS, Allsbrook W. Multiple congenital HPC of the head and neck. Laryngoscope 1978;88:1006-12. Cole HN Jr, Reagan JW, Lund HZ. Hemangiopericytoma. AMA Arch Dermatol 1955;72:328-34. Stout AP. Hemangiopericytoma: a study of 25 new cases. Cancer 1949;2:1027-35. Chen KTK, Kessel SE, Medrano VA. Congenital hemangiopericytoma. J Surg Oncol 1986;31:127-9. Hammoudi SM, Corkery JJ. Congenital hemangiopericytoma of duodenum. J Pediatr Surg 1985;20:559-60. Dingman RO. Hemangiopericytoma: report of two cases-one of congenital origin. Plast Reconstr Surg 1985;21:393-8. Stout AP, Lattes R. Tumors of the soft tissues. In: Atlas of tumor pathology; fascicle 1,2nd series. Washington, DC: Armed Forces Institute of Pathology, 1967. Wyler AR, Hered J, Smith JR, Loeser JD. Subarachnoid hemorrhage in infancy due to brain tumor. Arch Nemo1 1973;29:4i7-78. Allen PW. The fibromatoses: a clinicoparhologic classification based on 140 cases: Dart 2. Am J Sure Path01 1977:1:305-21. Brockbank J. Hemangiopericytoma o? the oral cavity: report of a case and review of the literature. J Oral Surg 1979;37:659710. Genet PE, Bernstein ML, Alpert B, Small I. Vascular lesions of the mandible. J Oral Maxillofac Surg 1984;42:537-42. Aduana V, Mohammad H, Vaiana J, Ghosh L. Hemangiopericytoma arising in a solitary plexiform neurofibroma: report of a case and review of the literature. J Oral Maxillofac Surg 1988;46:1106-9. Goldwasser MS, Daw JL. Hemangiopericytoma of the palate: case report. J Oral Maxillofacial Surg 1990;48:211-5. Gonzalez-Crussi F. Ultrastructure of congenital fibrosarcoma. Cancer 1970;26:1289-99.

Reprint requests: Dolphine Oda, BDS, MSc Division of Oral Pathology, University of Washington Seattle, WA 98195

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Intraoral infantile hemangiopericytoma: literature review and addition of a case.

A rapidly growing neoplasm in the buccal mucosa of a 4-month-old baby was excised. By light and electron microscopy the neoplasm had features that wer...
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