J Oral MaxillofacSurg 50:59-61.1992
Painful Mass of the Palate DEAN M. DELUKE, DDS,* JAMES J. SCIUBBA, DDS, PHD,t GREGORY LIVANOS, DDS,* AND FRED G. EMMINGS, DDS, PHD§
Case Presentation
inate from either glandular or nerve tissues. Tumors of nerve tissue are regularly found in the palate. The benign varieties, neurofibroma or neurolemmoma, are usually not painful, nor do they cause resorption of bone unless located centrally in the jaws. Central neurofibromas are, however, usually found in the mandible. The pain and bone resorption suggest a malignant schwannoma or neurogenic sarcoma. The diagnostic category with the greatest probability is a malignant tumor of a minor salivary gland. Pain and bone resorption are not usually associated with benign salivary gland tumors, especially tumors of this size. The differential diagnosis would include acinic cell carcinoma, malignant pleomorphic adenoma, adenoid cystic carcinoma, and mucoepidermoid carcinoma. The latter two choices are most likely by virtue of their higher rate of occurrence. Mucoepidermoid carcinomas were once divided into benign and malignant categories, but are now considered by most authorities to be either low- or high-grade malignancies. The former grow slowly and are usually painless, whereas the latter often produce pain as an early symptom. They usually occur in the third to fifth decade of life, infiltrate adjacent tissues, and readily metastasize to regional and distant sites. The adenoid cystic carcinoma, although a more common malignant tumor of minor salivary glands with similar clinical presentation, occurs most often in older patients. Therefore mucoepidermoid carcinoma is the best working diagnosis for this patient. Interestingly, the incisional biopsy site healed much better than expected. Most palatal salivary gland tumors are left ulcerated and occasionally have tumor prolapsing from the site.
A 26-year-old black male presented with a chief complaint of pain in the left maxilla. The past medical history was unremarkable. Clinical examination revealed grossly carious maxillary left first and second molar teeth. In addition, there was a submucosal mass of the left palate, 2 cm in diameter, extending from the canine to the molar region and medially to the midline of the palate. The lesion was firm and nonfluctuant. Occlusal and panoramic radiographs were negative for any intraosseous pathology. Under local anesthesia, the carious first and second molars were removed and an incisional biopsy taken from the center of the palatal mass. Healing of the extraction sites 2 weeks postoperatively was normal, and the palatal mass remained unchanged (Fig 1). Prior to the definitive surgical excision, a computed tomography (CT) scan was obtained that showed a reasonably well-defined mass of the left hemipalate that had resorbed the underlying bone (Fig 2).
Differential
Diagnosis
Fred G. Emmings, DOS, PhD The following discussion assumes normal findings from the extraoral physical examination and normal laboratory examination data other than the CT scan. It also assumes that other levels of the scan effectively ruled out origination of the lesion within the maxillary sinus.
Two major disease categories should be considered: 1) infectious and 2) neoplastic. The first category largely can be eliminated by the clinical characteristics of the swelling and by its persistence following incisional biopsy and removal of the infected teeth. Neoplastic lesions in this location, in a patient this age and with these clinical properties, most likely orig-
SUBSEQUENT CLINICAL COURSE
+ Chief, Department of Dentistry and Oral Surgery, St Glare’s Hospital, Schenectady, NY. t &tending Oral P&ologist and Chairman, Department of Dental Medicine. Lone Island Jewish Medical Center. New Hvde Park. NY. $ StafF’bex&t, St Glare’s Hospital, Schenectady, N?. ’ QProfessor (part-time), University of Rochester School of Medicine
The initial biopsy report was inconclusive, revealing only “benign salivary glands and proliferating nerve trunks, possibly representing traumatic neuroma.” The presurgical working diagnosis had included neoplasia of neural or salivary gland origin. A wide excisional biopsy was performed, including the overlying mucosa with l-cm margins down to bone. The bone underlying the soft-tissue mass exhibited a craterlike area of pressure resorption, with no evidence of infiltration. The wound was packed with iodoform gauze and an acrylic palatal obturator appliance was maintained over the defect for several weeks postoperatively. and removed at regular
and Dentistry, Rochester, NY. Address correspondence and reprint requests to Dr DeLuke: De-
partment of Dentistry and Oral Surgery, St Glare’s Hospital, 600 McClellan St, Schenectady, NY 12304. 0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/5001-0012$3.00/0
59
60
PAINFUL MASS OF THE PALATE
intervals for irrigation and dressing change. The palate healed uneventfully with restoration of normal palatal architecture. The patient has been free of recurrence 24 months postoperatively. Following wide excisional biopsy, a frozen section revealed “marked hyperplasia of salivary gland tissue” and the final biopsy report confirmed a diagnosis of adenomatoid hyperplasia of the palate (Fig 3).
Discussion
FIGURE 1. Mass of the left hemipalate extending from the canine to molar region and expanding to the midline.
FIGURE 2. left maxilla.
Axial CT section showing a well-defined mass of the
Adenomatoid hyperplasia of minor salivary glands was first reported by Giansanti et al in 197 1.’ A review of the literature reveals a total of 17 reported case~.‘-~ The lesion occurs most commonly on the palate and is clinically similar in presentation to palatal tumors of the minor salivary glands. Two cases have been reported in the retromolar region.3*5 Adenomatoid hyperplasia is essentially a benign hyperplasia or hypertrophy of minor accessory salivary glands.’ It consists of a clustering of normal appearing salivary acini with focal areas of mucin spillage.’ Inflammation is generally patchy or absent. Ductal structures appear without any apparent aberration in morphology. The acini are typically crowded, hyperplastic, and hypertrophic, and the overlying epithelium is generally intact, sometimes exhibiting pseudoepitheliomatous hyperplasia or acanthosis.4 The etiology of this condition is uncertain. Salivary gland enlargement (of major salivary glands) has been reported to occur with a variety of systemic conditions’ including endocrine disorders, gout, diabetes mellitus, menopause, hepatic disease, starvation, alcoholism, inflammation, Sjogren’s syndrome, Waldenstrom’s macroglobulinemia, uveoparotid fever, Felty’s syndrome; with certain drugs; and with aging. There is no reported evidence of these conditions occurring in cases of adenomatoid hyperplasia of the minor salivary glands, and none was identifiable in this case.
FIGURE 3. A, Photomicrograph showing hyperplasia of normal-appearing salivary acini. Ductal structures are likewise normal in morphology (hematoxylin-eosin stain, original magnification x 100). B, Higher-power view of the same area showing benign hyperplasia of salivary acini (hematoxylin-eosin stain, original magnification x200).
61
DELUKE ET AL
Some authors would accept the inclusion of this condition under the category of “simple adenoma.“’ Others postulate that the lesion represents a reactive hyperplasia or a hamartomatous proliferation which should be distinguished from true neoplasm.3 Aufdemorte4 does not consider either of the preceding categorizations acceptable and reviews the microscopic criteria for true adenoma. Most authors request further studies to better elucidate the nature of this condition. At present, treatment should include wide excisional biopsy, since the lesion is clinically indistinguishable from salivary gland tumors, and enlargement over time does occur. Recurrence following excision has not been reported.
References I. Giansanti JS, Baker JO, Waldron CA: Intraoral mutinous minor salivary gland lesions presenting clinically as tumors. Oral Surg 32:918, 1971 2. Devildos LR, Langlois CC: Minor salivary gland lesions presenting clinically as tumor. Oral Surg 41:657, 1976 3. Arafat A, Brannon RB, Ellis GL: Adenomatoid hyperplasia of mucous salivary glands. Oral Surg 52:5 1, 198 I 4. Aufdemorte TB. Ramzv MD. Holt GR. et al: Focal adenomatoid hyperplasia of salivary glands. Acta-Cytol 29:23, 1985 5. Brannon RB, Houston GD, Meader CL: Adenomatoid hyperplasia of mucous salivary glands: A case involving the retromolar area. Oral Surg 60: 188, 1985 6. Brown FI-I, Houston GD, Lubow RM. et al: Adenomatoid hyperplasia of mucous salivary glands. J Periodontol 58: 125. 1987 7. Shafer WG, Hine MR, Levy BM: A Textbook of Oral Pathology (ed 4). Philadelphia, PA. Saunders, 1983
Painful Mass of the Palate DEAN M. DELUKE, DDS,* JAMES J. SCIUBBA, DDS, PHD,t GREGORY LIVANOS, DDS,* AND FRED G. EMMINGS, DDS, PHD§
Case Presentation
inate from either glandular or nerve tissues. Tumors of nerve tissue are regularly found in the palate. The benign varieties, neurofibroma or neurolemmoma, are usually not painful, nor do they cause resorption of bone unless located centrally in the jaws. Central neurofibromas are, however, usually found in the mandible. The pain and bone resorption suggest a malignant schwannoma or neurogenic sarcoma. The diagnostic category with the greatest probability is a malignant tumor of a minor salivary gland. Pain and bone resorption are not usually associated with benign salivary gland tumors, especially tumors of this size. The differential diagnosis would include acinic cell carcinoma, malignant pleomorphic adenoma, adenoid cystic carcinoma, and mucoepidermoid carcinoma. The latter two choices are most likely by virtue of their higher rate of occurrence. Mucoepidermoid carcinomas were once divided into benign and malignant categories, but are now considered by most authorities to be either low- or high-grade malignancies. The former grow slowly and are usually painless, whereas the latter often produce pain as an early symptom. They usually occur in the third to fifth decade of life, infiltrate adjacent tissues, and readily metastasize to regional and distant sites. The adenoid cystic carcinoma, although a more common malignant tumor of minor salivary glands with similar clinical presentation, occurs most often in older patients. Therefore mucoepidermoid carcinoma is the best working diagnosis for this patient. Interestingly, the incisional biopsy site healed much better than expected. Most palatal salivary gland tumors are left ulcerated and occasionally have tumor prolapsing from the site.
A 26-year-old black male presented with a chief complaint of pain in the left maxilla. The past medical history was unremarkable. Clinical examination revealed grossly carious maxillary left first and second molar teeth. In addition, there was a submucosal mass of the left palate, 2 cm in diameter, extending from the canine to the molar region and medially to the midline of the palate. The lesion was firm and nonfluctuant. Occlusal and panoramic radiographs were negative for any intraosseous pathology. Under local anesthesia, the carious first and second molars were removed and an incisional biopsy taken from the center of the palatal mass. Healing of the extraction sites 2 weeks postoperatively was normal, and the palatal mass remained unchanged (Fig 1). Prior to the definitive surgical excision, a computed tomography (CT) scan was obtained that showed a reasonably well-defined mass of the left hemipalate that had resorbed the underlying bone (Fig 2).
Differential
Diagnosis
Fred G. Emmings, DOS, PhD The following discussion assumes normal findings from the extraoral physical examination and normal laboratory examination data other than the CT scan. It also assumes that other levels of the scan effectively ruled out origination of the lesion within the maxillary sinus.
Two major disease categories should be considered: 1) infectious and 2) neoplastic. The first category largely can be eliminated by the clinical characteristics of the swelling and by its persistence following incisional biopsy and removal of the infected teeth. Neoplastic lesions in this location, in a patient this age and with these clinical properties, most likely orig-
SUBSEQUENT CLINICAL COURSE
+ Chief, Department of Dentistry and Oral Surgery, St Glare’s Hospital, Schenectady, NY. t &tending Oral P&ologist and Chairman, Department of Dental Medicine. Lone Island Jewish Medical Center. New Hvde Park. NY. $ StafF’bex&t, St Glare’s Hospital, Schenectady, N?. ’ QProfessor (part-time), University of Rochester School of Medicine
The initial biopsy report was inconclusive, revealing only “benign salivary glands and proliferating nerve trunks, possibly representing traumatic neuroma.” The presurgical working diagnosis had included neoplasia of neural or salivary gland origin. A wide excisional biopsy was performed, including the overlying mucosa with l-cm margins down to bone. The bone underlying the soft-tissue mass exhibited a craterlike area of pressure resorption, with no evidence of infiltration. The wound was packed with iodoform gauze and an acrylic palatal obturator appliance was maintained over the defect for several weeks postoperatively. and removed at regular
and Dentistry, Rochester, NY. Address correspondence and reprint requests to Dr DeLuke: De-
partment of Dentistry and Oral Surgery, St Glare’s Hospital, 600 McClellan St, Schenectady, NY 12304. 0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/5001-0012$3.00/0
59
60
PAINFUL MASS OF THE PALATE
intervals for irrigation and dressing change. The palate healed uneventfully with restoration of normal palatal architecture. The patient has been free of recurrence 24 months postoperatively. Following wide excisional biopsy, a frozen section revealed “marked hyperplasia of salivary gland tissue” and the final biopsy report confirmed a diagnosis of adenomatoid hyperplasia of the palate (Fig 3).
Discussion
FIGURE 1. Mass of the left hemipalate extending from the canine to molar region and expanding to the midline.
FIGURE 2. left maxilla.
Axial CT section showing a well-defined mass of the
Adenomatoid hyperplasia of minor salivary glands was first reported by Giansanti et al in 197 1.’ A review of the literature reveals a total of 17 reported case~.‘-~ The lesion occurs most commonly on the palate and is clinically similar in presentation to palatal tumors of the minor salivary glands. Two cases have been reported in the retromolar region.3*5 Adenomatoid hyperplasia is essentially a benign hyperplasia or hypertrophy of minor accessory salivary glands.’ It consists of a clustering of normal appearing salivary acini with focal areas of mucin spillage.’ Inflammation is generally patchy or absent. Ductal structures appear without any apparent aberration in morphology. The acini are typically crowded, hyperplastic, and hypertrophic, and the overlying epithelium is generally intact, sometimes exhibiting pseudoepitheliomatous hyperplasia or acanthosis.4 The etiology of this condition is uncertain. Salivary gland enlargement (of major salivary glands) has been reported to occur with a variety of systemic conditions’ including endocrine disorders, gout, diabetes mellitus, menopause, hepatic disease, starvation, alcoholism, inflammation, Sjogren’s syndrome, Waldenstrom’s macroglobulinemia, uveoparotid fever, Felty’s syndrome; with certain drugs; and with aging. There is no reported evidence of these conditions occurring in cases of adenomatoid hyperplasia of the minor salivary glands, and none was identifiable in this case.
FIGURE 3. A, Photomicrograph showing hyperplasia of normal-appearing salivary acini. Ductal structures are likewise normal in morphology (hematoxylin-eosin stain, original magnification x 100). B, Higher-power view of the same area showing benign hyperplasia of salivary acini (hematoxylin-eosin stain, original magnification x200).
61
DELUKE ET AL
Some authors would accept the inclusion of this condition under the category of “simple adenoma.“’ Others postulate that the lesion represents a reactive hyperplasia or a hamartomatous proliferation which should be distinguished from true neoplasm.3 Aufdemorte4 does not consider either of the preceding categorizations acceptable and reviews the microscopic criteria for true adenoma. Most authors request further studies to better elucidate the nature of this condition. At present, treatment should include wide excisional biopsy, since the lesion is clinically indistinguishable from salivary gland tumors, and enlargement over time does occur. Recurrence following excision has not been reported.
References I. Giansanti JS, Baker JO, Waldron CA: Intraoral mutinous minor salivary gland lesions presenting clinically as tumors. Oral Surg 32:918, 1971 2. Devildos LR, Langlois CC: Minor salivary gland lesions presenting clinically as tumor. Oral Surg 41:657, 1976 3. Arafat A, Brannon RB, Ellis GL: Adenomatoid hyperplasia of mucous salivary glands. Oral Surg 52:5 1, 198 I 4. Aufdemorte TB. Ramzv MD. Holt GR. et al: Focal adenomatoid hyperplasia of salivary glands. Acta-Cytol 29:23, 1985 5. Brannon RB, Houston GD, Meader CL: Adenomatoid hyperplasia of mucous salivary glands: A case involving the retromolar area. Oral Surg 60: 188, 1985 6. Brown FI-I, Houston GD, Lubow RM. et al: Adenomatoid hyperplasia of mucous salivary glands. J Periodontol 58: 125. 1987 7. Shafer WG, Hine MR, Levy BM: A Textbook of Oral Pathology (ed 4). Philadelphia, PA. Saunders, 1983
