A red lesion on the palate
Brad W. Neville, DDS,
Angela C. Chi, DMD and
Molly Jeter
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THE CHALLENGE
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An 82-year-old man visited the dental clinic for fabrication of a new maxillary denture. During his comprehensive head-and-neck examination, the clinician discovered an asymptomatic 1.5 x 1.5-centimeter red, macular lesion on the left posterior lateral hard palate and tuberosity region (Figure 1
). The patient was not wearing a denture, and no other obvious source of irritation could be identified. He reported having smoked cigarettes when he was much younger, but he indicated that he had quit smoking more than 50 years ago. He stated that he did not drink alcohol.
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Figure 1. A flat, red, triangular patch of mucosa located on the left posterior hard palate and tuberosity.
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On the basis of the differential diagnosis, the clinician decided to observe the lesion for a brief period but noted no changes at the patient’s follow-up visit two weeks later. Therefore, the clinician performed an incisional biopsy of the lesion. At low and medium power, the epithelium demonstrated a slightly papillary surface with hyperplasia of the rete ridges (Figure 2). At higher magnification, the cells exhibited a disorderly maturation pattern with hyperchromatism, pleomorphism and increased nuclear size (Figure 3). These changes focally involved the entire thickness of the epithelium.
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Figure 2. A medium-power photomicrograph showing epithelial hyperplasia with a rough, pebbly surface. The epithelial cells appear crowded and disorganized (hematoxylin-eosin stain, original magnification x200).
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Figure 3. A high-power photomicrograph showing hyperchromatic and pleomorphic cells that extend to the epithelial surface (hematoxylin-eosin stain, original magnification x400).
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Can you make the diagnosis?
- candidiasis
- erythroplakia
- pizza burn
- trauma from an ill-fitting denture
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THE DIAGNOSIS
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B. erythroplakia
"Erythroplakia," the red counterpart of leukoplakia, is a clinical term referring to a red patch of the oral mucosa that cannot be defined clinically or pathologically as resulting from any other condition.1,2 Although erythroplakia is not encountered nearly as often as is leukoplakia, it is a more worrisome lesion with regard to dysplastic or malignant changes. Virtually all true erythroplakias exhibit significant epithelial dysplasia. Shafer and Waldron3 conducted a study and found that 51 percent of erythroplakias exhibited invasive carcinoma, 40 percent exhibited severe dysplasia or carcinoma in situ (CIS) and the remaining 9 percent exhibited mild-to-moderate dysplasia. In contrast, the same authors4 reported that leukoplakias exhibited dysplastic or malignant changes in approximately 20 percent of all cases.
In this case, the biopsy specimen revealed CIS. CIS represents a transitional stage between pre-malignant epithelial dysplasia and invasive squamous cell carcinoma. By definition, CIS is characterized by dysplastic changes that involve the entire thickness of the surface epithelium, but without invasion of tumor cells through the basement membrane into the underlying connective tissue.5 Although CIS is considered to be a cancer, theoretically it cannot metastasize at this stage, because the tumor cells have not yet gained access to the lymphovascular structures in the lamina propria. However, it is important to evaluate the entire lesion microscopically to ensure that early invasion has not occurred elsewhere in the specimen.
Clinical erythroplakia often is associated with a history of tobacco or alcohol use, although some cases develop with no identifiable causative factors. Treatment usually involves total surgical removal of the lesion with clear margins. Also, because many patients with oral carcinoma or epithelial dysplasia exhibit multifocal involvement (so-called "field cancerization"), the clinician should perform a detailed oral and oropharyngeal examination to identify any other possible lesions.6 In addition, periodic follow-up of the area is advisable for the rest of the patient’s life.5
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CONCLUSION
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Oral premalignant lesions that exhibit significant dysplasia microscopically are at great risk of progressing to invasive carcinoma.7 Many researchers are working to identify genetic markers that can be used as more objective measures of the risk of malignant transformation than is the histopathologic grade of dysplasia. For example, various investigators have demonstrated that loss of heterozygosity at certain loci (for example, 3p, 9p, 4q, 8p, 11q, 17p) is more common in dysplastic lesions that progress to malignancy than in those that do not progress.8–11 Other investigations regarding markers of cell proliferation, differentiation, apoptosis, angiogenesis and tumor invasion have yielded variable results. In the future, analysis of molecular markers may be used more widely to supplement conventional microscopic examination for prognostic evaluation.
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FOOTNOTES
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Dr. Neville is a distinguished university professor, Division of Oral Pathology, Department of Stomatology, College of Dental Medicine, Medical University of South Carolina, 173 Ashley Ave., Charleston, S.C. 29425, e-mail "nevilleb{at}musc.edu". Address reprint requests to Dr. Neville.
Dr. Chi is an assistant professor, Division of Oral Pathology, Department of Stomatology, College of Dental Medicine, Medical University of South Carolina, Charleston.
Ms. Jeter is a fourth-year dental student, College of Dental Medicine, Medical University of South Carolina, Charleston.
Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine.
The authors thank Dr. Mary Richardson for providing slides of the biopsy specimens.
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REFERENCES
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- Kramer IR, Lucas RB, Pindborg JJ, Sobin LH. Definition of oral leukoplakia and related lesions: an aid to studies on oral precancer. Oral Surg Oral Med Oral Pathol 1978;46(4):518–39.[Medline]
- Neville BW, Day TA. Oral cancer and precancerous lesions. CA Cancer J Clin 2002;52(4):195–215.[Abstract/Free Full Text]
- Shafer WG, Waldron CA. Erythroplakia of the oral cavity. Cancer 1975;36(3):1021–8.[Medline]
- Waldron CA, Shafer WG. Leukoplakia revisited: a clinicopathological study of 3,256 oral leukoplakias. Cancer 1975;36(4):1386–92.[Medline]
- Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. Philadelphia: Saunders; 2002:344–6.
- Lippman SM, Hong WK. Second malignant tumors in head and neck squamous cell carcinoma: the overshadowing threat for patients with early-stage disease. Int J Radiat Oncol Biol Phys 1989;17(3):691–4.[Medline]
- Silverman S Jr, Gorsky M, Lozada F. Oral leukoplakia and malignant transformation: a follow-up study of 257 patients. Cancer 1984;53(3):563–8.[Medline]
- Rosin MP, Cheng X, Poh C, et al. Use of allelic loss to predict malignant risk for low-grade oral epithelial dysplasia. Clin Cancer Res 2000;6(2):357–62.[Abstract/Free Full Text]
- Califano J, van der Riet P, Westra W, et al. Genetic progression model for head and neck cancer: implications for field cancerization. Cancer Res 1996;56(11):2488–92.[Abstract/Free Full Text]
- Mao L, Lee JS, Fan YH, et al. Frequent microsatellite alterations at chromosomes 9p21 and 3p14 in oral premalignant lesions and their value in cancer risk assessment. Nat Med 1996;2(6):682–5.[Medline]
- Partridge M, Pateromichelakis S, Phillips E, Emilion GG, A’Hern RP, Langdon JD. A case-control study confirms that microsatellite assay can identify patients at risk of developing oral squamous cell carcinoma within a field of cancerization. Cancer Res 2000;60(14):3893–8.[Abstract/Free Full Text]
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THE CHALLENGE
THE DIAGNOSIS
