Vol. 112 No. 3 September 2011

ORAL AND MAXILLOFACIAL SURGERY Editor: David S. Precious

Clinical management of masses arising from the accessoryparotid glandXiao Yang, MD, PhD, Tong Ji, MD, PhD, Li-Zhen Wang, MD, Wen-jun Yang, MD, PhD,Yong-jie Hu, MD, Lai-ping Zhong, MD, PhD, Chen-ping Zhang, MD, PhD, andZhi-yuan Zhang, MD, PhD, Shanghai, ChinaDEPARTMENT OF ORAL AND MAXILLOFACIAL SURGERY, NINTH PEOPLE’S HOSPITAL, SCHOOL OFSTOMATOLOGY, SHANGHAI JIAO TONG UNIVERSITY SCHOOL OF MEDICINE, SHANGHAI KEYLABORATORY OF STOMATOLOGY

Objective. Accessory parotid lesions are clinically rare and its management remains poorly understood. The aim ofthis study was to analyze the clinical management of accessory parotid lesions.Study design. From April 1999 to November 2008, a retrospective analysis of 32 patients with accessory parotidlesions was performed. The preoperative examinations, surgical treatment, and prognosis were recorded and analyzed.Results. Among the 32 patients, there were 8 men and 24 women with an overall average age of 45 years. These patientsalways presented without obvious symptoms, and the masses were moderate to hard in hardness without tenderness,mobile, and with clear boundary. The pathologic diagnoses were 24 benign and 8 malignant lesions. Surgery and surgeryplus radiotherapy were performed in the patients with benign and malignant lesions, respectively, with good prognosis.Conclusions. Accessory parotid lesions are rare, and the clinical manifestation is always the same for benign tumors.Surgical resection and surgical resection plus radiotherapy are the primary choices of treatment for benign andmalignant lesions, respectively. The prognosis is always good. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod

2011;112:290-297)

The accessory parotid gland is a salivary gland sepa-rated from the main parotid gland, and it occurs in�21%-56% of individuals.1,2 It locates �0.6 cm ante-rior to the main parotid gland with its own duct emp-tying into the Stensen duct, superior to the Stensen ductand the masseter muscl, and beneath the buccal andzygomatic branches of the facial nerve.2 The lesionsarising from the accessory parotid gland are clinicallyrare: Among all parotid tumors, the incidence rate ofaccessory parotid tumors is 1%-8%, and among all acces-

The first 2 authors contributed equally to this work.Supported in part by the Program for Innovative Research Team ofthe Shanghai Municipal Education Commission and by research grantno. 2007BAI18B03 from the National Key Technology R&D Pro-gram of China.Received for publication Sep 5, 2010; accepted for publication Oct12, 2010.1079-2104/$ - see front matter© 2011 Mosby, Inc. All rights reserved.

doi:10.1016/j.tripleo.2010.10.023

290

sory parotid tumors the incidence rate of malignant acces-sory parotid tumors is 26%-50%.3,4 So far, 118 lesionsarising from the accessory parotid gland have been re-ported in the English-language literature, including 45malignant tumors, 54 benign tumors, and 19 nontumorlesions.3-28 To better understand the accessory parotidlesions and share our experience on the diagnosis, treat-ment, and prognosis of accessory parotid lesions, we pres-ent herein 32 consecutive patients with lesions arisingfrom the accessory parotid gland, including 8 malignantand 24 benign lesions. We discuss the diagnosis, treat-ment, and prognosis of accessory parotid lesions.

PATIENTS AND METHODSPatients

From April 1999 to November 2008, 32 consecutivepatients with masses arising from the accessory parotidgland at the Department of Oral and MaxillofacialSurgery, Ninth People’s Hospital, Shanghai Jiao TongUniversity School of Medicine, were retrospectively

reviewed with their clinical data (Table I).

suprao

OOOOEVolume 112, Number 3 Yang et al. 291

ManagementAfter signing the informed consent forms, all of the

patients received surgical operation. The final diagnosiswas based on the postoperative pathologic examination.For the patients with malignant tumors, postoperativeradiotherapy was suggested.

Follow-upAll of the patients were followed up by return visits.

During their return visits, routine physical examina-tions were performed. If there was any suspicious massin the accessory parotid and neck region, image exam-ination was suggested, and if necessary, fine needleaspiration cytology (FNAC) was suggested.

RESULTSGeneral condition

Among the 32 patients, there were 8 men and 24

Table I. Summary of the 32 patients with different leCase no. Gender Age (y) Diagnosis Surge

1 F 19 PA ERM�PFN�2 F 47 PA ERM�PFN�3 F 39 PA ERM�PFN�4 F 32 PA ERM�PFN�5 F 45 PA ERM�PFN�6 F 30 PA ERM�PFN�7 F 53 PA ERM�PFN�8 F 54 PA ERM�PFN�9 M 36 PA ERM�PFN�

10 F 59 PA ERM�PFN�11 F 40 PA ERM�PFN�12 M 38 PA ERM�PFN�13 F 56 PA ERM�PFN�14 M 29 PA ERM�PFN�15 F 46 PA ERM�PFN�16 F 47 PA ERM�PFN�17 M 27 PA ERM�PFN�18 F 21 PA ERM�PFN�19 F 33 PA ERM�PFN�20 F 68 BCA ERM�PFN�21 M 41 BLEL ERM�PFN�22 F 29 BLEL ERM�PFN�23 M 60 BLEL ERM�PFN�24 M 69 LA ERM�PFN�25 F 59 ACC-w ERM�PSP�26 F 56 ACC-m ERM�PSP�27 F 52 PCC-w ERM�PSP�28 F 64 BCAC-w SP�PFN�LS29 F 44 MyEC-w ERM�PFN�30 F 56 LEC-w ERM�PSP�31 F 59 LEC-p ERM�PFN�32 M 42 MEC-m SP�PFN�LS

F, Female; M, male; PA, pleomorphic adenoma; BCA, basal cell adenocell carcinoma; PCC, papillary cystadenocarcinoma; BCAC, basal cecarcinoma; MEC, mucoepidermoid carcinoma; -w, well differentiatedSP, superficial parotidectomy; PSP, partial superficial parotidectomyligation of Stensen duct; PSD, preservation of Stensen duct; SOND,

women. Their ages ranged from 19 to 69 with a mean

of 45 years, and 72% of the patients were between 30and 60 years old.

LocationThe masses were located in the left side of the

accessory parotid gland in 15 patients and in the rightside in 17 patients.

CourseThe median course of disease was 28 (range 1-248)

months. The median course of the benign lesions was36 (range 1-248) months, and the median course of themalignant lesions was 12 (1 to 84) months.

SymptomsAll the patients had regional gradually growing and

painless masses without obvious symptoms except 1

arising from the accessory parotid glandRadiotherapy Status Follow-up (mo)

No Alive 108No Dead (lung cancer) 84— Lost —No Alive 72No Alive 69No Alive 54No Alive 44No Alive 39No Alive 38No Alive 33— Lost —No Alive 26No Alive 23No Alive 21No Alive 16No Alive 13No Alive 13No Alive 12No Alive 12No Alive 21No Alive 128No Alive 36No Alive 25No Alive 47

SD 60 Gy Alive 47SD 60 Gy Alive 14SD — Lost —

No Alive 86No Alive 80

SD 60 Gy Alive 5060 Gy Alive 25

ND 60 Gy Alive 15

EL, benign lymphoepithelial lesion; LA, lymphadenosis; ACC, aciniccarcinoma; MyEC, myoepithelial carcinoma; LEC, lymphoepithelial-m, moderately differentiated grade; -p, poorly differentiated grade;reservation of facial nerve; ERM, extended resection of mass; LSD,

mohyoid neck dissection.

sionsry

PSDPSDLSDPSDPSDPSDPSDPSDLSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPSDPFN�PPFN�PPFN�PDPSDPFN�LLSDD�SO

ma; BLll adeno

grade;; PFN, p

patient, who felt soft pain of the mass recently in the

ent wit

OOOOE292 Yang et al. September 2011

right accessory parotid region and was postoperativelydiagnosed with adenoid cell carcinoma.

Physical examinationThe median size of the masses were 2.0 � 1.5 cm

(range 1.0 � 0.5 cm to 4.0 � 3.0 cm), 84% of thepatients had masses �3.0 � 2.0 cm, and 59% of the

Fig. 1. A, Preoperative front view of a patient with a mass in hC, The buccal branches of facial nerve and the Stensen ductfat pad was used to fill the defect. D, Front view of the pati

patients had masses �2.0 � 2.0 cm. The palpable

masses without tenderness were moderate to hard inhardness, mobile with clear boundary (Fig. 1, A). Themass size did not change with postural variation, andthere was no facial palsy, no obvious obstruction of theStensen duct, and no abnormal secretion from the de-bouch of the Stensen duct. Among the 8 patients withmalignant lesions, 6 patients were at T1 stage and 2

accessory parotid region. B, Standard parotidectomy incision.reserved with complete resection of the mass, and the buccalhout facial palsy (whistling) 1 year after surgery.

er leftwere p

patients were at T2 stage; no clinical positive cervical

OOOOEVolume 112, Number 3 Yang et al. 293

lymph nodes or distant metastasis was detected in thesepatients.

Laboratory examinationIn all of the patients, routine laboratory tests, includ-

ing complete blood count, urine routine test, stool rou-tine test, blood biochemistry test, bleeding time test,and serum protein electrophoresis, were performed, andthe results were almost within the reference ranges.

Image examinationIn this study, 23 patients received ultrasonography, 9

patients received computerized tomography (CT), and3 patients received magnetic resonance imaging (MRI).The majority of the lesions appeared benign on imaging(Fig. 2); when definite infiltration was detected, thelesion was considered to be malignant (Fig. 3).

Preoperative FNACFive patients received this examination: 2 patients

with pleomorphic adenomas, 1 patient with lymphade-nosis, 1 patient with acinic cell carcinoma, and 1 patientwith mucoepidermoid carcinoma. The postoperative di-agnosis of these 5 patients was the same as the preop-erative FNAC.

SurgeryAll of the patients underwent surgical resection of

the masses completely with the standard (Fig. 1, B) ormodified parotidectomy incision or face-lift-type inci-sion. During the surgical process, frozen pathologicexamination was performed: for benign lesions, thebuccal branches of the facial nerve were identified andpreserved carefully (Fig. 1, C); when the Stensen ductcould be separated from the mass, the Stensen duct wasalso preserved; when the Stensen duct had to be dis-connected, anastomosis was performed if possible; li-gation of the Stensen duct was performed in 2 patientswhere the duct length was too short for anastomosis.For the malignant lesions, extended resection of themasses and partial parotidectomy were performed withpreservation of the facial nerve and Stensen duct except

Fig. 2. A, Ultrasonography of pleomorphic adenoma, show-ing a mass with oval shape, clear boundary with intact enve-lope, and low-level echo with nonuniform density. B, Com-puterized tomography of benign lymphoepithelial lesion,showing a mass with clear boundary from its neighboringstructures and uniform density. C, Magnetic resonance imag-ing of pleomorphic adenoma, showing a mass with uniformsignal at T1WI and T2WI stage; the signal was obviously

strengthened when infused with Gd-DTPA through vein.

OOOOE294 Yang et al. September 2011

in 3 patients. For those 3 patients, 1 patient was withepitheliomyoepithelial carcinoma, for whom partial pa-rotidectomy was performed; another patient was withbasal cell adenocarcinoma, for whom superficial parot-idectomy was performed; and the third patient was withmucoepidermoid carcinoma, for whom superficial pa-rotidectomy and supraomohyoid neck dissection wereperformed. After removal of the lesions, the wound wasdirectly closed. If the defect was large, the buccal fat

Fig. 3. A, Ultrasonography of mucoepidermoid carcinoma,showing a mass with oval shape, clear boundary with intactenvelope, and mixed-level echo with fluid content. B, Com-puterized tomography of mucoepidermoid carcinoma, show-ing a mass with unclear boundary, nonuniform density, andinfiltration to the masseter muscle.

pad or local flap was used to fill the defect.

Intraoperative frozen pathologic examinationIntraoperative frozen pathologic examination was

performed in all of the patients, and no misdiagnosisfrom benign to malignant lesions or vice versa oc-curred. The total accuracy rate of frozen pathologicdiagnosis was 94% according to the postoperativepathologic diagnosis. For the 24 patients with benignlesions, the accuracy rate was 96%; only 1 lesion waspostoperatively diagnosed as pleomorphic adenomaswhereas the frozen pathologic diagnosis was myoepthe-lioma. For the 8 patients with malignant lesions, theaccuracy rate was 88%; only 1 lesion was postopera-tively diagnosed as papillary cystadenocarcinoma (welldifferentiated grade) whereas the frozen pathologic di-agnosis was adenoid cystic carcinoma (well differenti-ated grade).

Postoperative pathologic diagnosisPostoperative pathologic examination confirmed 24 be-

nign lesions and 8 malignant lesions. Among the 24benign lesions, there were 19 pleomorphic adenomas, 3benign lymphoepithelial lesions, 1 basal cell adenoma,and 1 lymphadenosis. Among the 8 malignant lesions,there were 2 acinic cell carcinomas, 2 lymphoepithelialcarcinomas, 1 papillary cystadenocarcinoma, 1 basalcell adenocarcinoma, 1 myoepithelial carcinoma, and 1mucoepidermoid carcinoma.

Postoperative radiotherapyFor the 8 patients with malignant tumors (6 patients

at clinical stage T1N0M0 and 2 patients at clinical stageT2N0M0), postoperative radiotherapy was suggested.Specifically, 5 patients received postoperative 60 Gyradiotherapy, 2 patients did not accept postoperativeradiotherapy, and 1 patient was lost after surgery. Noserious complications occurred during radiotherapy.

Wound healing and postoperative facial nervefunction

Primary wound healing without salivary fistula wasachieved in all of the patients. Postoperative parotidgland function and facial nerve function was good andsymmetric in the patients with benign lesions. In thepatients with malignant lesions, xerostomia was obvi-ous after radiotherapy; it was acceptable for these pa-tients with symptomatic treatment. Postoperative facialnerve function was good and symmetric in 5 patients; inthe remaining 3 patients receiving superficial parotid-ectomy or partial parotidectomy with dissection of fa-cial nerve, postoperative temporal facial palsy oc-curred, but the facial nerve function recovered in 6months after surgery by using neurotrophic drugs. Dur-ing the follow-up period, the facial nerve function was

good (Fig. 1, D).

OOOOEVolume 112, Number 3 Yang et al. 295

PrognosisAll of the patients were followed up, except for 3

patients who were lost after surgery. The median fol-low-up period was 36 (12 to 128) months. During thefollow-up period, no recurrence of the lesion was ob-served, the life quality of each patient was good, andtheir lives were not affected by the surgical treatment.Especially for the patients with malignancy, no tumorrecurrence and metastasis occurred during the fol-low-up period. All of the patients were alive, except 1patient with pleomorphic adenoma who died of lungcancer.

DISCUSSIONIn this study, 75% of the accessory parotid lesions

are benign and the rest are malignant. The pleomorphicadenoma is the most common benign tumor, the benignlymphoepithelial lesion is the most common nontumorlesion, and the acinic cell carcinoma and lymphoepi-thelial carcinoma are the most common malignant le-sions. Combined with the previously reported 118 cases,there are 53 malignant tumors, 74 benign tumors, and 23nontumor lesions in the total 150 cases (Table II).3-28 Themost common malignant tumor is mucoepidermoid car-

Table II. Constituent ratio of the 150 accessory parotidgland lesions

Type of lesios n %

Malignant tumors 53Mucoepidermoid carcinoma 29 55%Acinic cell carcinoma 7 13%Malignant pleomorphic adenoma 3 6%Lymphoma 3 6%Basal cell adenocarcinoma 2 4%Myoepithelial carcinoma 2 4%Lymphoepithelial carcinoma 2 4%Squamous cell carcinoma 2 4%Papillary cystadenocarcinoma 1 2%Adenoid cystic carcinoma 1 2%Undifferentiated carcinoma 1 2%

Benign tumors 74Pleomorphic adenoma 64 87%Myoepithelioma 5 7%Basal cell adenoma 2 3%Monochromic adenomas 2 3%Papillary cystadenoma 1 1%

Nontumor lesions 23Benign lymphoepithelial lesion 7 30%Chronic sclerosing sialadenitis 6 26%Chronic inflammation 4 17%Cyst 3 13%Abscess 1 4%Fibrosis 1 4%Fibromatosis 1 4%

cinoma, the most common benign tumor is pleomor-

phic adenoma, and the most common nontumor lesionis benign lymphoepithelial lesion.

DiagnosisFor the patients with accessory parotid lesions, they

consistently complained of a painless mass in the mid-cheek without obvious symptoms. It is sometimes hardto reach the final diagnosis clinically. The physicalexamination always reveals a solid mass in the mid-cheek, and the mass is always palpable, moderate tohard in hardness, without tenderness, mobile, and withclear boundary. These findings could help us to differ-entiate the mass of the lesions arising from adiposetissue from other types of vascular malformation, ex-cept for the capillary vascular malformation, which isalmost the same as in solid masses and has no changein size with postural variation. Furthermore, some otherdifferential diagnoses should be considered for tumorsarising from nerve, fiber, lymph node, appendages ofthe skin, and so on. In general, from the location of themass, we can always make a simple judgment on theorigin of the mass from the accessory parotid gland.

Further auxiliary examinations could help make thecorrect diagnosis, such as sialography, ultrasonogra-phy, CT, MRI, positron-emission tomography (PET),and FNAC. Currently, FNAC is the most reliable toolof histologic examination before surgery. Although theoccasional misdiagnosis occurs,15 this approach is stillthe primary diagnostic option to diagnose a solid massin the accessory parotid gland, because it is safe, accu-rate, and fast. Besides the histologic examination byFNAC, frozen section is exclusively used during thesurgical operation when FNAC is not available beforesurgery. In the present study, FNAC was used in 5patients, who also received frozen section during thesurgical operation as a routine procedure, and the di-agnosis was same to the postoperative histologic exam-ination. The other 27 patients received the frozen sec-tion during the surgery, and based on the frozen sectionresults we confirmed the surgical plan during the sur-gery. The accurate rate of frozen section was 94% inour patients, and there was no misdiagnosis from be-nign to malignant lesions or vice versa. The frozensection is routinely used in our clinical practice and theFNAC is suggested before surgery for cytologic exam-ination.

Conventional sialography is now not commonly usedin the accessory parotid mass examination, except fordetermining the relationship between the Stensen ductand the mass as well as the accessory parotid gland.Ultrasonography is a relatively inexpensive and conve-nient tool for accessory parotid lesion examination. Theappearance of benign accessory parotid lesions is al-

ways oval in shape, has a clear boundary with intact

OOOOE296 Yang et al. September 2011

envelope, and has a low-level echo.13,15,27 The appear-ance of malignant lesions varies with different patho-logic diagnoses. The mucoepidermoid carcinoma couldshow an oval shape and clear boundary with intactenvelope, but the internal echo is mixed with fluidcontent; this difference may be due to the mixed con-tent of the tumor. Basal cell adenocarcinoma and pap-illary cystadenocarcinoma appear almost the same asbenign tumors, because of the uniform density of tu-mors. CT and MRI are widely used in the accessoryparotid lesion, and they can clearly show the locationand size of the lesions as well as their relationship withthe neighboring anatomic structures, such as theStensen duct, main parotid gland, masseter muscle, andso on. PET is always used to detect recurrent or distantmetastatic malignancies.23,26 Although there are manypreoperative examinations available, we suggest thatthe frozen section be used to confirm the treatment planduring surgery.

Surgical treatmentThe primary treatment of the accessory parotid solid

lesions is surgery, especially for the benign lesions, andradical surgery is the major choice. Several types ofincision have been described: cheek skin incision, per-oral incision, standard parotidectomy incision, modi-fied standard parotidectomy incision, facelift-type inci-sion, and so on. However, considering the lesionexposure, facial nerve protection, and cosmetic defor-mity avoidance, the standard parotidectomy incision isstrongly recommended. The cheek skin and peroralincisions have been seldom used, because of the poten-tial risk of facial nerve deficit and Stensen duct dam-age.5 The indication of the cheek skin and peroralincisions should be strictly controlled, such as a singlelesion with size �3 cm in diameter, pleomorphic ade-noma localizing within the accessory parotid gland,patient’s preference, and so on.18,22 Modified standardparotidectomy incision and facelift-type incision areboth based on the standard parotidectomy incision forcosmetic consideration.7,14,16

During the operation, the Stensen duct should beprotected if possible. For benign lesions, the Stensenduct should be protected when there is no direct rela-tionship between the lesion and the Stensen duct. Whenthe Stensen duct has to be partially resected, it shouldbe anastomosed if its length is adequate. In the presentstudy, all of the Stensen ducts in the patients withbenign lesions were protected or anastomosed except 1duct ligation that was too short for anastomosis. Some-times, to reconstruct the duct or reduce the damage tothe duct, a thin catheter can be used to keep the ductopen followed by suturing the defect; then the catheter

is removed through the mouth 7-10 days after surgery.

For the malignant lesions, the Stensen ducts had to beresected when the duct was invaded or for the safetymargin of resection; other Stensen ducts should beprotected with postoperative radiotherapy. The facialnerve should definitely be protected during the surgery,especially the buccal and zygomatic branches, locatednear the accessory parotid gland and the Stensen duct.When the branches of facial nerve are resected becauseof invasion or safety margin, neural transplantationshould be considered. The great auricular nerve is pri-marily recommended for neural transplantation.

Treatment protocol and prognosisThe treatment protocol of accessory parotid lesions

depends on the pathologic diagnosis. For benign lesions,surgical resection is the first choice of treatment, and theprognosis is always good, without tumor recurrence ormetastasis.8,14,16,17,19,21,27 In the present study, the pa-tients with benign lesions are all alive, except for 1 whodied of lung cancer, and the longest follow-up periodwas 128 months. For malignant lesions, because theirsize is always small at the clinical stage of T1 and T2and lymph node metastasis is uncommon, surgical re-section plus postoperative radiotherapy or chemother-apy is suggested according to the pathologic diagnosis.This treatment is similar to malignant lesions arisingfrom the main parotid gland. A systematic review of4,631 cases by Jeannon et al.29 revealed that postoper-ative radiotherapy can improve the overall survival rateof patients with parotid carcinomas. Another report byZbären et al.30 suggested that postoperative radiother-apy benefits T1 and T2 parotid carcinoma, includingreduction of local recurrence and increase of 5-yearsurvival rate. For the accessory parotid malignancies,surgical resection plus postoperative radiotherapy hasbeen most used and has produced good results formucoepidermoid carcinoma, squamous cell carcinoma,carcinoma ex pleomorphic adenoma, basal cell adeno-carcinoma, and undifferentiated carcinoma,11,12,18,23,27

and the radiation dose ranges from 60 to 68 Gy. Tumorrecurrence was reported in only 1 patient.26 On theother hand, because surgery alone is used in somepatients with malignant tumors without postoperativeradiotherapy or chemotherapy,12,13 tumor recurrence isreported.20 Therefore, for patients with accessory pa-rotid malignancies, especially for the patients with thetumor at stages T1 and T2, surgical resection pluspostoperative radiotherapy can benefit them, and theprognosis is good. Further prospective studies should beperformed to clarify the benefit of postoperative radiother-apy in accessory parotid malignancies. In the presentstudy, among the 7 patients who could be followed up, 5patients received 60 Gy postoperative radiotherapy, and

they were all alive without tumor recurrence or metastasis.

OOOOEVolume 112, Number 3 Yang et al. 297

Interestingly, the other 2 patients who refused to re-ceive postoperative radiotherapy were also alive with-out tumor recurrence or metastasis. Owing to the lowmorbility of accessory parotid malignancy, the differ-ence of survival rate is undetected between the patientswith and without postoperative radiotherapy. Again,further prospective clinical trial on this issue is greatlyneeded.

CONCLUSIONSAccessory parotid lesions are rare in clinics; the

clinical manifestation and imaging characteristics arealways the same for benign lesions. Auxiliary exami-nation techniques of ultrasonography, CT, MRI, PET,and FNAC are useful for clinical diagnosis. FNAC isthe best method for preoperative diagnosis. Surgicalresection is the first choice of treatment for benignaccessory parotid lesions and provides a good progno-sis. Surgical resection plus postoperative radiotherapyis recommended for malignant accessory parotid le-sions, and the prognosis is good.

REFERENCES1. Frommer J. The human accessory parotid gland: its incidence,

nature, and significance. Oral Surg Oral Med Oral Pathol OralRadiol Endod 1977;43:671-6.

2. Toh H, Kodama J, Fukuda J, Rittman B, Mackenzie I. Incidenceand histology of human accessory parotid glands. Anat Rec1993;236:586-90.

3. Perzik SL, White IL. Surgical management of preauricular tumorsof the accessory parotid apparatus. Am J Surg 1966;112:498-503.

4. Ferguson MM, MacDonald DG. Persistent sialadenitis in anaccessory parotid gland. Oral Surg Oral Med Oral Pathol OralRadiol Endod 1978;45:696-700.

5. Johnson FE, Spiro RH. Tumors arising in accessory parotidtissue. Am J Surg 1979;38:576-8.

6. Polayes JM, Rankow RM. Cysts, masses, and tumors of theaccessory parotid gland. Plast Reconstr Surg 1979;64:17-23.

7. Richards AT, Chait LA, Skudowitz RB. Tumours of accessoryparotid glands. S Afr Med J 1984;65:971-2.

8. Afify SE, Maynard JD. Tumours of the accessory lobe of theparotid gland. Postgrad Med J 1992;68:461-2.

9. Slater LJ, Edwards RC, Faircloth WJ Jr, Sorensen DC. Lym-phoepithelial lesion of accessory parotid presenting as a buccalspace mass. J Oral Maxillofac Surg 1992;50:1131-5.

10. Rodino W, Shaha AR. Surgical management of accessory parotidtumors. J Surg Oncol 1993;54:153-6.

11. Sakurai K, Urade M, Kishimoto H, Takahashi Y, Hozumi S,Yanagisawa T. Primary squamous cell carcinoma of accessoryparotid gland duct epithelium: report of a case. Oral Surg OralMed Oral Pathol Oral Radiol Endod 1998;85:447-51.

12. Yoshihara T, Suzuki S, Nagao K. Mucoepidermoid carcinomaarising in the accessory parotid gland. Int J Pediatr Otorhinolar-yngol 1999;48:47-52.

13. Lewkowicz A, Levy Y, Zeltser R, Zagury A, Nahlieli O. Acces-sory parotid gland masses. Oral Surg Oral Med Oral Pathol OralRadiol Endod 2000;89:610-2.

14. Klotz DA, Coniglio JR. Prudent management of the midcheek mass:

revisiting the accessory parotid gland tumor. Laryngoscope 2000;110:1627-32.

15. Kawashima Y, Kobayashi D, Ishikawa N, Kishimoto S. A caseof myoepithelioma arising in an accessory parotid gland. JLaryngol Otol 2002;116:474-6.

16. Lin DT, Coppit GL, Burkey BB, Netterville JL. Tumors of theaccessory lobe of the parotid gland: a 10-year experience. La-ryngoscope 2004;114:1652-5.

17. Isogai R, Kawada A, Ueno K, Aragane Y, Tezuka T. Myoepi-thelioma possibly originating from the accessory parotid gland.Dermatology 2004;208:74-8.

18. Hamano T, Okami K, Sekine M, Odagiri K, Onuki J, Iida M, etal. A case of accessory parotid gland tumor. Tokai J Exp ClinMed 2004;29:131-3.

19. Osborne RF, Purohit MR, Hamilton JS. Pleomorphic adenoma ofthe accessory parotid gland. Ear Nose Throat J 2005;84:274-5.

20. Currarino G, Votteler TP. Lesions of the accessory parotid glandin children. Pediatr Radiol 2006;36:1-7.

21. Ferri E, Pavon I, Armato E, Cavaleri S, Capuzzo P, Ianniello F.Myoepithelioma of a minor salivary gland of the cheek: casereport. Acta Otorhinolaryngol Ital 2006;26:43-6.

22. Schmutzhard J, Schwentner IM, Andrle J, Gunkel AR, Sprinzl GM.Resection of accessory parotid gland tumors through a peroral approachwith facial nerve monitoring. J Craniofac Surg 2007;18:1419-21.

23. Osborne RF. Squamous cell carcinoma of the accessory parotidgland. Ear Nose Throat J 2007;86:602-4.

24. Breeze J, Ramesar K, Williams MD, Howlett DC. Pleomorphicadenoma arising from accessory parotid tissue presenting asdysphonia. J R Army Med Corps 2008;154:57-9.

25. Stenner M, Preuss SF, Hüttenbrink KB, Klussmann JP. Acces-sory parotid gland lesions: case report and review of literature.Eur Arch Otorhinolaryngol 2008;265:1135-8.

26. Gomes M, Pepe G, Bomanji J, Al-Salihi O, Du Y, Gacinovic S,et al. High-grade mucoepidermoid carcinoma of the accessoryparotid gland with distant metastases identified by 18F-FDGPET-CT. Pediatr Blood Cancer 2008;50:395-7.

27. Sun G, Hu Q, Tang E, Yang X, Huang X. Diagnosis andtreatment of accessory parotid-gland tumors. J Oral MaxillofacSurg 2009;67:1520-3.

28. Tamiolakis D, Chimona TS, Georgiou G, Proimos E, NikolaidouS, Perogamvrakis G, et al. Accessory parotid gland carcinoma expleomorphic adenoma. Case study diagnosed by fine needleaspiration. Stomatologija 2009;11:37-40.

29. Jeannon JP, Calman F, Gleeson M, McGurk M, Morgan P,O’Connell M, et al. Management of advanced parotid cancer. Asystematic review. Eur J Surg Oncol 2009;35:908-15.

30. Zbären P, Nuyens M, Caversaccio M, Greiner R, Stauffer E. Post-operative radiation therapy for T1 and T2 primary parotid carci-noma: is it useful? Otolaryngol Head Neck Surg 2006;135:140-3.

Reprint requests:

Lai-ping Zhong, MD, PhDDepartment of Oral and Maxillofacial SurgeryNinth People’s HospitalSchool of StomatologyShanghai Jiao Tong University School of MedicineShanghai Key Laboratory of Stomatology639 Zhizaoju RdShanghai 200011China

zhonglp@hotmail.com