718
Multiple Focal Pigmented Lesions in the Maxillary Tuberosity and Hard Palate: A Unique Display of Intraoral Junctional Nevi Aaron R. Biesbrock* and Alfredo Aguirre*
The pigmented conditions located in the oral cavity have a diverse genesis ranging from vascular lesions to exogenous and endogenous pigmentations. In this report we have documented the unusual occurrence of multiple intraoral junctional nevi in a patient. A review of the patient's past dental records revealed that 2 of these lesions were first noticed 8 years earlier; however, no efforts were made to identity the nature of the pigmentations. Removal of 4 lesions and subsequent histopathological analysis revealed the presence of junctional nevi. This case illustrates the importance of a thorough clinical and histological work-up when dealing with pigmented lesions in the oral cavity. The excision of all suspected oral nevi is warranted because they cannot be clinically differentiated from other pigmented lesions, including oral melanoma. In addition, the potential of junctional nevi to undergo malignant transformation in the oral cavity is undetermined. / Periodontol 1992; 63:718-721.
Key Words: Nevus, intraoral; pigmentation, oral.
Pigmented nevi are benign tumors of the skin and mucosa characterized by the presence of melanin-producing, neuroectodermal derived cells.1 While commonly found on the skin, pigmented nevi are relatively uncommon in the oral cavity.1'2 Nevi are classified based upon histologie differences and tissue location as junctional, compound, intradermal, intramucosal, or blue. The junctional nevus, which is comprised of nests of nevus cells located at the dermoepidermal junction, is rarely found in the mouth and comprises only 5% of all oral pigmented nevi.3 To the best of our knowledge, this is the first documented clinical and histopathologic report of multiple intraoral junctional nevi occurring in a single individual. CASE REPORT A 73 year-old Caucasian female presented to the postgraduate periodontics clinic, School of Dental Medicine, State University of New York at Buffalo, for a periodontal evaluation of her dentition. A review of her past medical history revealed rheumatoid arthritis and aortic valve stenosis. Therefore, for her dental appointments, the patient was pre-
*Department of Oral Biology and
Dental Research Institute, and Departof Periodontics, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY. department of Oral Biology and Dental Research Institute, and Department of Stomatology and Interdisciplinary Sciences, School of Dental Medicine. ment
medicated with amoxicillin per American Heart Association
guidelines.4'5 The patient was taking no medications other than antibiotic premedication. Her vital signs were well
within normal limits, with a blood pressure of 134/68 and a pulse of 72 beats/minute. The patient had a light complexion with numerous skin pigmented macules (freckles). No swelling could be detected upon palpation of lymph nodes. Upon oral examination a subepithelial, flat, smooth, firm, black-brown pigmented lesion 4 mm in diameter in the region of the left maxillary tuberosity was noted. The lesion exhibited a somewhat diffuse margin (Fig. 1). Three more lesions of similar appearance, 2 to 4 mm in diameter, were noted in the midline of the hard palate (Fig. 2). Further questioning of the patient and a thorough review of her past dental records revealed that 2 of these lesions were first documented 8 years previously. The lesions were diagnosed on the basis of clinical presentation as normal pigmentation or "freckles." The size of the lesions was not documented and no biopsy was performed. Additional inquiries failed to reveal the presence of systemic conditions related to oral
pigmentation (including endocrinic, metabolic, genetic, chemical, and pharmacologie). Tobacco usage and familial history of cancer were negative. Thus, an excisional biopsy was indicated based on a clinical differential diagnosis that included: pigmented nevus, melanotic macule, amalgam tattoo, and malignant melanoma. Four lesions were removed by 3 separate excisional biopsies and a full coverage
Volume 63 Number 8
BIESBROCK, AGUIRRE
719
ceived. The specimen obtained from the maxillary tuberosity measured 5x5x3 mm at its largest dimensions, while the 2 specimens from the hard palate measured 8 x 5x2 and 5x3x2 mm. The specimens were bisected for embedding.
Microscopic Findings The specimens were overlaid by a hyperplastic keratinized stratified squamous epithelium presenting well-circumscribed nests of cuboidally and spindle-shaped nevus cells in the basal cell layer. Some of these nevus nests contained melanin, and were bulged downward into the papillary connective tissue creating the appearance of "dropping off." The underlying fibrous connective tissue contained occasional melanophages and abundant endothelial lined spaces (Figs. 3 and 4). The microscopic diagnosis was junctional nevi.
Figure 1. Initial presentation of intraoral functional nevus of the maxillary tuberosity.
2. Initial presentation of intraoral functional nevi of the hard Three discrete pigmented flat lesions (arrows) were observed in the root of the palate. Adjacent teeth are out offocus.
Figure palate.
acrylic surgical Stent was inserted for the patient's comfort. Healing of the biopsy sites was uneventful. All the speci-
fixed in 10% buffered formalin. The gross and microscopic findings were virtually identical for all the mens were
specimens.
Macroscopic Description Three
of soft tissue containing 4 brown-black flat discolorations on the mucosal surface were re-
wedges
pigmented
DISCUSSION This case is unique in that it is the only documented occurrence of multiple intraoral junctional nevi in a patient. A review of the dental and medical literature revealed that only 11 intraoral junctional nevi have been reported (Table 1). Based on clinical examination alone junctional nevi cannot be differentiated from other pigmented lesions, including oral melanoma.12 Dark brown, black, or bluish discolorations of the oral mucosa can be separated into 3 categories: vascular lesions and exogenous or endogenous pigmentations.13 The vascular lesions originate from traumatic purpuric submucosal hemorrhages characterized by the retention of blood, intracellular fluid, and/or hemosiderin pigment in the tissues. These lesions do not blanch with diascopy (firmly pressing a microscope slide or a piece of clear plastic over a lesion). However, they tend to resolve and disappear with time. Hemangiomas can also present with similar clinical features, although they can be differentiated by their blanching characteristics when diascopy is applied. Exogenous pigmentations include metallic tattoos (caused by the introduction of heavy metals, primarily amalgam, directly into soft tissues), foreign bodies (lead pencil, ink, carbon, etc.), occupational exposure (to lead, zinc, cadmium, copper, tin, manganese), and locally acting biological agents (chromogenic bacteria producing black hairy tongue).13 All these etiological agents were ruled out by direct careful anamnesis as the genesis of this patient's focal pigmentations. Endogenous pigmentations result from increased melanin concentrations at localized mucosal tissue sites. Melanotic lesions of the oral cavity include pigmented nevi, melanocytic macules, smoker's melanosis, and lesions associated with drug therapy (antimalarials, minocycline hydrochloride, phenopthalein, and chlorpromazine) or systemic diseases (Addison's, Peutz-Jegher's, Albright's, and von Recklinghausen's syndromes). The color of pigmented lesions is a function of both the amount of chromatic material, as well as the tissue depth at which it is deposited.
720
J Periodontol August 1992
INTRAORAL JUNCTIONAL NEVI
Table 1. Documented Cases of Intraoral Junctional Nevi*
Author
(Reference)
Age/Sex/Race Size*
Couch, (6) Trodahl, Sprague (7) Kaufman
Lourides
50/F/W 3/M/W
20/M/W 54/M/W 27/F/W 21/M/W 65/F/W 22/F/B 4/M/W 22/F/H 10/F/H 73/F/W
(8)
Gossman, Miller (1) Silverman
(9)
Buchner, Hansen (10) Hansen, Buchner (11) Buchner, Hansen (3) Biesbrock, Aguirre
(present report)
*
*
Figure 3. Junctional nevus, low power view. The surgical specimens showed a hyperkeratinized hyperplastic stratified squamous epithelium with nests of nevus cells showing junctional activity (arrow) and melanophages in the underlying fibrous connective tissue papillae (arrowheads) (hematoxylin-eosin stain; original magnification x 100).
All nevi presented with Diameter in cm.
as
Benign melanocytic nevi are very common in the skin, demonstrated by the Trodahl and Sprague7 and Stegmaier
and Becker14 studies, which indicated that the mean number of cutaneous pigmented nevi per person is 40. In contrast, intraoral pigmented nevi are extremely rare in comparison to their cutaneous counterpart, with an estimated 0.1% in-
pigmentation.
cidence.15 Junctional nevi comprise only 2.8% to 5.0% of oral nevi.1-11 Clinically they have the appearance of dark pigmented, smooth, flat mucosal lesions that are most often found on the palate, maxillary alveolar ridge, and buccal mucosa. Histologically, they are characterized by nests or cords of cuboidal to spindle-shaped nevus cells located at the junction between epithelium and connective tissue.1 These nevus cell nests bulge downward creating a "dropping off" appearance. Nevus cells are thought to originate from melanocytes and have hydropic swollen nucleoli that occupy a large portion of the nucleus.1'9 Electron microscopic studies of intraoral junctional nevi have revealed a number of nevus cell abnormalities including hyperplasia, nuclear pleomorphism, prolific melanin synthesis (with diverse patterns of disaggregation), increased number of digestive bodies, and fragmentation of the basal lamina.9 This peculiar junctional cellular activity resembles the early stages of malignant melanoma and may have an underlying potential for malignant transformation.9'11 In addition, chronic trauma has been suggested as a possible initiator of malignant
Figure 4. High power view ofjunctional nevus. Nests of cuboidal hyperchromatic nevus cells at the epithelial-connective tissue interface showing the characteristic artifactual shrinkage that separate them from the surrounding tissues (arrows). Numerous melanophages containing dark-brown pigmented melanin in the cytoplasm (arrowheads) were observed in the fibrous connective tissue papilla (hematoxylin-eosin stain; original magnification X 400).
Site
1.0 Palate N/D Lower lip, vermilion border N/D Lower lip, vermilion border N/D Palate 0.5 Buccal mucosa 0.2 Palate N/D Lower labial mucosa 1.0 Palate 0.2 Palate 0.3 Palate 0.2 Palate 0.3 Maxillary tuberosity 0.4 Palate 0.2 Palate 0.2 Palate
transformation.11
Malignant melanoma is a neoplasm that arises from melanocytes at the epithelial-connective tissue junction.16'17 Malignant melanomas are classified as superficial spreading melanoma (70%), nodular melanoma (15%), acrai lentiginous melanoma (8%), and lentigo maligna melanoma (5%).18 Lentigo maligna melanoma and superficial spreading melanoma are characterized by an early stage of radial enlargement, which precedes a secondary stage of vertical invasion and metastasis. The radial enlargement stage is absent in nodular melanoma,
so
metastasis
occurs
much earlier lead-
ing to a more severe fatality rate. Oral melanomas are rare, comprising 0.2% to 8.0% of all melanomas.16'17'19-20 They have
predilection for the maxillary alveolar ridge and where 80% of the lesions occur, show a slight prefpalate, erence for males (58%), and usually emerge between the fifth and seventh decades of life.16'20 Oral melanomas have a very poor prognosis and have been shown to have a 5a
Volume 63 Number 8
year survival rate of between 5.2% to 20%.16·20 Thirty to 35% of oral melanomas have been associated with preexisting benign melanosis.16,19-22 Although it is recognized that melanomas of the skin can arise in pre-existing lentigo maligna, congenital 26melanocytic nevi, and in dysplastic melanocytic nevi,23 the relationship between oral junctional nevi and melanoma remains unclear.11 However, Taylor and Lewis16 have recently documented the clinical and histological progression of a benign melanosis into mel-
5-year period. A systematic and careful diagnostic approach should be used when confronting pigmented lesions in the oral cavity, where vascular, exogenous, and endogenous sources of pigmentation should be considered when formulating a differential diagnosis. No treatment is usually recommended for vascular and exogenous pigmentations. Similarly, a conservative approach is used for melanocytic macules, smoker's melanosis, pigmentations associated with drug therapy, and systemic diseases. In contrast, surgical removal of suspected pigmented nevi is recommended because the oral mucosa is under continuous frictional, thermal, and biological challenges, and the potential of the junctional variant to undergo malignant transformations remains to be established. Furthermore, intraoral pigmented nevi and early melanoma cannot be differentiated on clinical grounds and microscopic examination becomes essential for the diagnosis. anoma over a
Acknowledgment
This work was supported in part by U.S. Public Health Service Grants DE08240 and DE00158.
REFERENCES 1. Gossman JR, Miller GA. Intraoral junctional nevus: Review of the literature and report of case. / Oral Surg 1975; 33:275-281. 2. Brown FH, Houston GD. Smoker's melanosis. A case report. J Periodontol 1991; 62:524-527. 3. Büchner A, Hansen LS. Pigmented nevi of the oral mucosa: A clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part 2: Analysis of 191 cases. Oral Surg Oral Med 4.
5. 6. 7.
8.
Oral Pathol 1987; 63:676-682. Dajani AS, Bisno AL, Chung KY, et al. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. JAMA 1990; 264:2919-2922. Pallasch TJ, Slots J. Antibiotic prophylaxis for medical-risk patients. J Periodontol 1991; 62:227-231. Couch CD, Kaufman M. Junctional nevus of the palate: Report of case. / Oral Surg 1956; 14:334-336. Trodahl JN, Sprague WG. Benign and malignant melanocytic lesions of the oral mucosa: An analysis of 135 cases. Cancer 1970; 25:812823. Lourides 0. Report of an unusual case of chorioepithelial nevus of the oral mucosa. Odontol Proodos 1970; 24:195.
BIESBROCK, AGUIRRE
721
9. Silverman S,
Greenspan JS, Christie TM. Junctional nevus of the oral Light and electron microscopic observations. Oral Surg Oral Med Oral Pathol 1975; 39:259-267. Büchner A, Hansen LS. Pigmented nevi of the oral mucosa: A clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part 1: A clinicopathologic study of 36 new cases. Oral Surg Oral Med Oral Pathol 1987; 63:566-572. Hansen LS, Buchner A. Changing concepts of the junctional nevus mucosa:
10.
11.
and melanoma: Review of the literature and
Surg 1981; 39:961-965.
report of case. J Oral
12. Eisen D, Voorhees JJ. Oral melanoma and other pigmented lesions of the oral cavity. J Am Acad Dermatol 1990; 24:527-537. 13. Archard HO. Biology and pathology of the oral mucosa. In: Fitzpatrick TB, Eisen AZ, Wolff , Freedberg IM, Austen KF, eds. Dermatology in General Medicine, 3rd ed. NY: McGraw-Hill Book Company; 1987:1152-1239. 14. Stegmaier OC, Becker SW Jr. Incidence of melanocytic nevi in young adults. J Invest Dermatol 1960; 34:125-129. 15. King OH, Blankenship JP, King WA, Coleman SA. The frequency of pigmented nevi in the oral cavity: Report of 5 cases. Oral Surg Oral Med Oral Pathol 1967; 23:82-90. 16. Taylor CO, Lewis JS. Histologically documented transformation of benign oral melanosis into malignant melanoma: A case report. J Oral Maxillofac Surg 1990; 48:732-734. 17. Eckardt A. Primary malignant melanoma of the oral mucosa: Report of a case. / Oral Maxillofac Surg 1987; 45:1065-1068. 18. Lever WF, Schaumburg-Lever G. Melanocytic nevi and malignant melanoma. In: Lever WF, and Schaumburg-Lever G, eds. Histopathology of the Skin, 6th ed. Philadelphia: J. B. Lippincott Company; 1983:681-725. 19. Bucci E, Mignogna MD, Lo Muzio L. Primary malignant melanoma of the oral cavity: A case report. / Oral Maxillofac Surg 1989; 47:621622. 20. Rapini RP, Golitz LE, Greer RO, Krekorian EA, Poulson T. Primary malignant melanoma of the oral cavity: A review of 177 cases. Cancer 1985; 55:1543-1551. 21. Chaudhry AP, Hampel A, Gorlin RJ. Primary malignant melanoma of the oral cavity. Cancer 1958; 11:923-928. 22. Peckitt NS, Wood GA. Malignant melanoma of the oral cavity: A case report. Oral Surg Oral Med Oral Pathol 1990; 70:161-164. 23. Sober AJ, Rhodes AR, Mihm MC, Fitzpatrick TB. Neoplasms: Malignant melanoma. In: Fitzpatrick TB, Eisen AZ, Wolff , Freedberg IM, Austen KF, eds. Dermatology in General Medicine, 3rd ed. NY: McGraw-Hill Book Company; 1987:947-966. 24. Sagebiel RW. The dysplastic melanocytic nevus. J Am Acad Dermatol 1989; 20:496-501. 25. Halpern AC, Guerry D, Elder DE, et al. Dysplastic nevi as risk markers of sporadic (nonfamilial) melanoma. Arch Dermatol 1991; 127:995-999. 26. Langer , Rappersberger , Steiner A, Wolff . The ultrastructure of dysplastic nevi: Comparison with superficial spreading melanoma and common naevocellular naevi. Arch Dermatol Res 1990; 282:353362. Send reprint requests to: Dr. Aaron R. Biesbrock, Department of Oral Biology, Foster Hall, School of Dental Medicine, State University of New York, Buffalo, New York 14214. Accepted for publication February 3, 1991.
Multiple Focal Pigmented Lesions in the Maxillary Tuberosity and Hard Palate: A Unique Display of Intraoral Junctional Nevi Aaron R. Biesbrock* and Alfredo Aguirre*
The pigmented conditions located in the oral cavity have a diverse genesis ranging from vascular lesions to exogenous and endogenous pigmentations. In this report we have documented the unusual occurrence of multiple intraoral junctional nevi in a patient. A review of the patient's past dental records revealed that 2 of these lesions were first noticed 8 years earlier; however, no efforts were made to identity the nature of the pigmentations. Removal of 4 lesions and subsequent histopathological analysis revealed the presence of junctional nevi. This case illustrates the importance of a thorough clinical and histological work-up when dealing with pigmented lesions in the oral cavity. The excision of all suspected oral nevi is warranted because they cannot be clinically differentiated from other pigmented lesions, including oral melanoma. In addition, the potential of junctional nevi to undergo malignant transformation in the oral cavity is undetermined. / Periodontol 1992; 63:718-721.
Key Words: Nevus, intraoral; pigmentation, oral.
Pigmented nevi are benign tumors of the skin and mucosa characterized by the presence of melanin-producing, neuroectodermal derived cells.1 While commonly found on the skin, pigmented nevi are relatively uncommon in the oral cavity.1'2 Nevi are classified based upon histologie differences and tissue location as junctional, compound, intradermal, intramucosal, or blue. The junctional nevus, which is comprised of nests of nevus cells located at the dermoepidermal junction, is rarely found in the mouth and comprises only 5% of all oral pigmented nevi.3 To the best of our knowledge, this is the first documented clinical and histopathologic report of multiple intraoral junctional nevi occurring in a single individual. CASE REPORT A 73 year-old Caucasian female presented to the postgraduate periodontics clinic, School of Dental Medicine, State University of New York at Buffalo, for a periodontal evaluation of her dentition. A review of her past medical history revealed rheumatoid arthritis and aortic valve stenosis. Therefore, for her dental appointments, the patient was pre-
*Department of Oral Biology and
Dental Research Institute, and Departof Periodontics, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY. department of Oral Biology and Dental Research Institute, and Department of Stomatology and Interdisciplinary Sciences, School of Dental Medicine. ment
medicated with amoxicillin per American Heart Association
guidelines.4'5 The patient was taking no medications other than antibiotic premedication. Her vital signs were well
within normal limits, with a blood pressure of 134/68 and a pulse of 72 beats/minute. The patient had a light complexion with numerous skin pigmented macules (freckles). No swelling could be detected upon palpation of lymph nodes. Upon oral examination a subepithelial, flat, smooth, firm, black-brown pigmented lesion 4 mm in diameter in the region of the left maxillary tuberosity was noted. The lesion exhibited a somewhat diffuse margin (Fig. 1). Three more lesions of similar appearance, 2 to 4 mm in diameter, were noted in the midline of the hard palate (Fig. 2). Further questioning of the patient and a thorough review of her past dental records revealed that 2 of these lesions were first documented 8 years previously. The lesions were diagnosed on the basis of clinical presentation as normal pigmentation or "freckles." The size of the lesions was not documented and no biopsy was performed. Additional inquiries failed to reveal the presence of systemic conditions related to oral
pigmentation (including endocrinic, metabolic, genetic, chemical, and pharmacologie). Tobacco usage and familial history of cancer were negative. Thus, an excisional biopsy was indicated based on a clinical differential diagnosis that included: pigmented nevus, melanotic macule, amalgam tattoo, and malignant melanoma. Four lesions were removed by 3 separate excisional biopsies and a full coverage
Volume 63 Number 8
BIESBROCK, AGUIRRE
719
ceived. The specimen obtained from the maxillary tuberosity measured 5x5x3 mm at its largest dimensions, while the 2 specimens from the hard palate measured 8 x 5x2 and 5x3x2 mm. The specimens were bisected for embedding.
Microscopic Findings The specimens were overlaid by a hyperplastic keratinized stratified squamous epithelium presenting well-circumscribed nests of cuboidally and spindle-shaped nevus cells in the basal cell layer. Some of these nevus nests contained melanin, and were bulged downward into the papillary connective tissue creating the appearance of "dropping off." The underlying fibrous connective tissue contained occasional melanophages and abundant endothelial lined spaces (Figs. 3 and 4). The microscopic diagnosis was junctional nevi.
Figure 1. Initial presentation of intraoral functional nevus of the maxillary tuberosity.
2. Initial presentation of intraoral functional nevi of the hard Three discrete pigmented flat lesions (arrows) were observed in the root of the palate. Adjacent teeth are out offocus.
Figure palate.
acrylic surgical Stent was inserted for the patient's comfort. Healing of the biopsy sites was uneventful. All the speci-
fixed in 10% buffered formalin. The gross and microscopic findings were virtually identical for all the mens were
specimens.
Macroscopic Description Three
of soft tissue containing 4 brown-black flat discolorations on the mucosal surface were re-
wedges
pigmented
DISCUSSION This case is unique in that it is the only documented occurrence of multiple intraoral junctional nevi in a patient. A review of the dental and medical literature revealed that only 11 intraoral junctional nevi have been reported (Table 1). Based on clinical examination alone junctional nevi cannot be differentiated from other pigmented lesions, including oral melanoma.12 Dark brown, black, or bluish discolorations of the oral mucosa can be separated into 3 categories: vascular lesions and exogenous or endogenous pigmentations.13 The vascular lesions originate from traumatic purpuric submucosal hemorrhages characterized by the retention of blood, intracellular fluid, and/or hemosiderin pigment in the tissues. These lesions do not blanch with diascopy (firmly pressing a microscope slide or a piece of clear plastic over a lesion). However, they tend to resolve and disappear with time. Hemangiomas can also present with similar clinical features, although they can be differentiated by their blanching characteristics when diascopy is applied. Exogenous pigmentations include metallic tattoos (caused by the introduction of heavy metals, primarily amalgam, directly into soft tissues), foreign bodies (lead pencil, ink, carbon, etc.), occupational exposure (to lead, zinc, cadmium, copper, tin, manganese), and locally acting biological agents (chromogenic bacteria producing black hairy tongue).13 All these etiological agents were ruled out by direct careful anamnesis as the genesis of this patient's focal pigmentations. Endogenous pigmentations result from increased melanin concentrations at localized mucosal tissue sites. Melanotic lesions of the oral cavity include pigmented nevi, melanocytic macules, smoker's melanosis, and lesions associated with drug therapy (antimalarials, minocycline hydrochloride, phenopthalein, and chlorpromazine) or systemic diseases (Addison's, Peutz-Jegher's, Albright's, and von Recklinghausen's syndromes). The color of pigmented lesions is a function of both the amount of chromatic material, as well as the tissue depth at which it is deposited.
720
J Periodontol August 1992
INTRAORAL JUNCTIONAL NEVI
Table 1. Documented Cases of Intraoral Junctional Nevi*
Author
(Reference)
Age/Sex/Race Size*
Couch, (6) Trodahl, Sprague (7) Kaufman
Lourides
50/F/W 3/M/W
20/M/W 54/M/W 27/F/W 21/M/W 65/F/W 22/F/B 4/M/W 22/F/H 10/F/H 73/F/W
(8)
Gossman, Miller (1) Silverman
(9)
Buchner, Hansen (10) Hansen, Buchner (11) Buchner, Hansen (3) Biesbrock, Aguirre
(present report)
*
*
Figure 3. Junctional nevus, low power view. The surgical specimens showed a hyperkeratinized hyperplastic stratified squamous epithelium with nests of nevus cells showing junctional activity (arrow) and melanophages in the underlying fibrous connective tissue papillae (arrowheads) (hematoxylin-eosin stain; original magnification x 100).
All nevi presented with Diameter in cm.
as
Benign melanocytic nevi are very common in the skin, demonstrated by the Trodahl and Sprague7 and Stegmaier
and Becker14 studies, which indicated that the mean number of cutaneous pigmented nevi per person is 40. In contrast, intraoral pigmented nevi are extremely rare in comparison to their cutaneous counterpart, with an estimated 0.1% in-
pigmentation.
cidence.15 Junctional nevi comprise only 2.8% to 5.0% of oral nevi.1-11 Clinically they have the appearance of dark pigmented, smooth, flat mucosal lesions that are most often found on the palate, maxillary alveolar ridge, and buccal mucosa. Histologically, they are characterized by nests or cords of cuboidal to spindle-shaped nevus cells located at the junction between epithelium and connective tissue.1 These nevus cell nests bulge downward creating a "dropping off" appearance. Nevus cells are thought to originate from melanocytes and have hydropic swollen nucleoli that occupy a large portion of the nucleus.1'9 Electron microscopic studies of intraoral junctional nevi have revealed a number of nevus cell abnormalities including hyperplasia, nuclear pleomorphism, prolific melanin synthesis (with diverse patterns of disaggregation), increased number of digestive bodies, and fragmentation of the basal lamina.9 This peculiar junctional cellular activity resembles the early stages of malignant melanoma and may have an underlying potential for malignant transformation.9'11 In addition, chronic trauma has been suggested as a possible initiator of malignant
Figure 4. High power view ofjunctional nevus. Nests of cuboidal hyperchromatic nevus cells at the epithelial-connective tissue interface showing the characteristic artifactual shrinkage that separate them from the surrounding tissues (arrows). Numerous melanophages containing dark-brown pigmented melanin in the cytoplasm (arrowheads) were observed in the fibrous connective tissue papilla (hematoxylin-eosin stain; original magnification X 400).
Site
1.0 Palate N/D Lower lip, vermilion border N/D Lower lip, vermilion border N/D Palate 0.5 Buccal mucosa 0.2 Palate N/D Lower labial mucosa 1.0 Palate 0.2 Palate 0.3 Palate 0.2 Palate 0.3 Maxillary tuberosity 0.4 Palate 0.2 Palate 0.2 Palate
transformation.11
Malignant melanoma is a neoplasm that arises from melanocytes at the epithelial-connective tissue junction.16'17 Malignant melanomas are classified as superficial spreading melanoma (70%), nodular melanoma (15%), acrai lentiginous melanoma (8%), and lentigo maligna melanoma (5%).18 Lentigo maligna melanoma and superficial spreading melanoma are characterized by an early stage of radial enlargement, which precedes a secondary stage of vertical invasion and metastasis. The radial enlargement stage is absent in nodular melanoma,
so
metastasis
occurs
much earlier lead-
ing to a more severe fatality rate. Oral melanomas are rare, comprising 0.2% to 8.0% of all melanomas.16'17'19-20 They have
predilection for the maxillary alveolar ridge and where 80% of the lesions occur, show a slight prefpalate, erence for males (58%), and usually emerge between the fifth and seventh decades of life.16'20 Oral melanomas have a very poor prognosis and have been shown to have a 5a
Volume 63 Number 8
year survival rate of between 5.2% to 20%.16·20 Thirty to 35% of oral melanomas have been associated with preexisting benign melanosis.16,19-22 Although it is recognized that melanomas of the skin can arise in pre-existing lentigo maligna, congenital 26melanocytic nevi, and in dysplastic melanocytic nevi,23 the relationship between oral junctional nevi and melanoma remains unclear.11 However, Taylor and Lewis16 have recently documented the clinical and histological progression of a benign melanosis into mel-
5-year period. A systematic and careful diagnostic approach should be used when confronting pigmented lesions in the oral cavity, where vascular, exogenous, and endogenous sources of pigmentation should be considered when formulating a differential diagnosis. No treatment is usually recommended for vascular and exogenous pigmentations. Similarly, a conservative approach is used for melanocytic macules, smoker's melanosis, pigmentations associated with drug therapy, and systemic diseases. In contrast, surgical removal of suspected pigmented nevi is recommended because the oral mucosa is under continuous frictional, thermal, and biological challenges, and the potential of the junctional variant to undergo malignant transformations remains to be established. Furthermore, intraoral pigmented nevi and early melanoma cannot be differentiated on clinical grounds and microscopic examination becomes essential for the diagnosis. anoma over a
Acknowledgment
This work was supported in part by U.S. Public Health Service Grants DE08240 and DE00158.
REFERENCES 1. Gossman JR, Miller GA. Intraoral junctional nevus: Review of the literature and report of case. / Oral Surg 1975; 33:275-281. 2. Brown FH, Houston GD. Smoker's melanosis. A case report. J Periodontol 1991; 62:524-527. 3. Büchner A, Hansen LS. Pigmented nevi of the oral mucosa: A clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part 2: Analysis of 191 cases. Oral Surg Oral Med 4.
5. 6. 7.
8.
Oral Pathol 1987; 63:676-682. Dajani AS, Bisno AL, Chung KY, et al. Prevention of bacterial endocarditis: Recommendations by the American Heart Association. JAMA 1990; 264:2919-2922. Pallasch TJ, Slots J. Antibiotic prophylaxis for medical-risk patients. J Periodontol 1991; 62:227-231. Couch CD, Kaufman M. Junctional nevus of the palate: Report of case. / Oral Surg 1956; 14:334-336. Trodahl JN, Sprague WG. Benign and malignant melanocytic lesions of the oral mucosa: An analysis of 135 cases. Cancer 1970; 25:812823. Lourides 0. Report of an unusual case of chorioepithelial nevus of the oral mucosa. Odontol Proodos 1970; 24:195.
BIESBROCK, AGUIRRE
721
9. Silverman S,
Greenspan JS, Christie TM. Junctional nevus of the oral Light and electron microscopic observations. Oral Surg Oral Med Oral Pathol 1975; 39:259-267. Büchner A, Hansen LS. Pigmented nevi of the oral mucosa: A clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part 1: A clinicopathologic study of 36 new cases. Oral Surg Oral Med Oral Pathol 1987; 63:566-572. Hansen LS, Buchner A. Changing concepts of the junctional nevus mucosa:
10.
11.
and melanoma: Review of the literature and
Surg 1981; 39:961-965.
report of case. J Oral
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