|Year : 2014 | Volume
| Issue : 4 | Page : 473-476
White lesion: A dormant malignancy?
Vela D Desai1, Priyanka Narang1, Sunil Kumar2, Shruti Maheshwari1
1 Department of Oral Medicine and Radiology, Jaipur Dental College, Jaipur, Rajasthan, India
2 Department of Prosthodontics, Jaipur Dental College, Jaipur, Rajasthan, India
|Date of Submission||11-Jul-2014|
|Date of Acceptance||26-Feb-2015|
|Date of Web Publication||22-Apr-2015|
Vela D Desai
B 406, Trimurty Apartments, Opposite BSNL Telecom Colony, Model Town, Malviya Nagar, Jaipur - 302 017, Rajasthan
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Oral lichen planus (OLP) is a chronic inflammatory mucocutaneous disease that frequently involves the oral mucosa. The authors report a long-term follow-up of a case which presented clinically as lichen planus with apparently benign features but histologically exhibited features of early invasive squamous cell carcinoma. Although a common lesion, the matter concerning malignant potential of OLP and its differentiation from lichenoid reaction still remains unresolved. There is no universally accepted, documented, and approved modality of treatment to prevent the occurrence of cancer development and also literature search reveals no standard methods which can predict cancer development of potentially malignant disorders. Hence every reported case should be well documented. This case report emphasizes the need for histological confirmation, with continuous monitoring 3-6 times annually of clinical lesions that have lichenoid features.
Keywords: Lichenoid reaction, malignant transformation, oral lichen planus, premalignant
|How to cite this article:|
Desai VD, Narang P, Kumar S, Maheshwari S. White lesion: A dormant malignancy?. J Indian Acad Oral Med Radiol 2014;26:473-6
| Introduction|| |
Oral lichen planus (OLP) is a relatively common chronic, cell-mediated autoimmune disease process targeted against basal keratinocytes of the oral mucosa in susceptible individuals. Clinically, it results in reticular white lesions that are usually bilaterally distributed on the oral mucosa. These lesions may be associated with areas of mucosal erosion and ulceration. 
According to literature, about 0.5-1.9% of the population is affected. , Oral lichen planus lesions persist for many years with periods of exacerbations and remissions; complete permanent resolution is rare. ,, Although the World Health Organization (WHO) currently considers OLP to be a disease that may evolve to cancer but its actual potential to evolve malignantly is not proven. The progression rates for oral epithelial dysplasia are varied.  Various studies have shown greater inter and intra-observer variability in the assessment of different grades of dysplasias.  Moderate or severe dysplasias (carcinoma-in-situ) show a greater disposition for malignant transformation compared to mild or non-dysplastic cases;  carcinomatous transformation may also take place in non-dysplastic ones.  Also dysplastic changes have been reported in very small lesions. , Adding up to the present controversy the authors report a case of long-term follow-up of OLP which was apparently asymptomatic but on histopathological evaluation was found to be malignant.
| Case Report|| |
A 22-year-old medically fit male patient reported to the OPD of Oral Medicine and Radiology Department, with the chief complaint of burning sensation on eating spicy food since 6 months. He had the habit of chewing gutkha (Dilbaag) 2-3 pouches/day since 4-5 years which was kept habitually in the right buccal vestibule and occasionally in the left buccal vestibule. His medical history was non-contributory and there was no family history of carcinoma. There was no clinical evidence of lymphadenopathy. Intraoral examination exhibited reticular and finely radiating keratotic striae interspersed with reddish irregular erosions in the right buccal mucosa of approximately 4 × 2 cm in size [Figure 1]. Left buccal mucosa showed interlacing network of white lines of approximately 0.5 × 1 cm in size. On the basis of the clinical features, positive history of consuming pan masala and as the patient kept the quid in the same area of the lesion the provisional diagnosis was given as lichenoid reaction.
|Figure 1: Buccal mucosa showing red and white lesion with reticular|
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Differential diagnosis of lichen planus was considered because of the bilateral nature of the lesion. As a known etiological agent (Dilbaag, Gutkha) was evident, the patient was counseled to quit the habit of gutkha chewing and was explained about the complications. Antioxidants were prescribed and he was kept under follow-up twice a month for 6 months. Topical applications of corticosteroids were indicated for symptomatic relief. Oral prophylaxis was carried out with instruction for maintaining proper oral hygiene measures. The lesion reduced in size but still persisted even after 6 months of quitting the habit, hence a clinical differential diagnosis of lichen planus was reconsidered [Figure 2]. Considering the malignant potential of lichen planus, complete blood picture, blood sugar, serum cortisol, cytological smear, and toludine blue were recommended after a written consent from the patient. Blood profile was normal but the smear revealed grade IV atypical cells and vital staining was positive. Incisional biopsy of the lesion was taken from the site of toluidine blue retention. Histopathological section revealed squamous cell carcinoma with early invasion [Figure 3], [Figure 4], [Figure 5] and [Figure 6]. The patient was asked to continue the same treatment along with a course of anti-fungal therapy and another biopsy was performed after a gap of 1 month to rule out any disparity, which revealed the same histological changes. Three pathologists from different institutions were consulted for confirmation of histopathological findings to remove interobserver variability. Patient did not consent for further management by surgical intervention. Patient was educated about the malignant potential of the condition. But he insisted on continuing the use of only antioxidants. At a 1-year follow-up, clinically the lesion was seen to slightly increase in size compared to the second visit. Smear taken after 1 year revealed grade IV atypical cells [Figure 7]. Patient did not consent for a third biopsy or surgical management and so conservative treatment was continued and the patient was asked to report if any change (in signs and symptoms) was noticed. Patient is still under observation.
|Figure 3: Low power photomicrograph demonstrating hyperparakeratosis and dysplastic changes extending upto one-third of the epithelium|
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|Figure 4: Medium power photomicrograph demonstrating hyperparakeratosis, hyperchromatic and slightly pleomorphic nuclei in the basal and parabasal cell layers|
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|Figure 5: Medium power photomicrograph showing dysplastic changes extending throughout the entire thickness of the epithelium and showing islands of malignant squamous epithelium invading into lamina propria|
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|Figure 6: High power view showing dysplastic epithelial cells with keratin pearl formation|
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| Discussion|| |
Lichen planus is a chronic inflammatory disease of variable severity that can wax and wane over a long period of time. Above that, the clinical appearance of OLP changes with time which further complicates the issue of premalignancy.  This may be a cause of major error, since malignant transformation occurs over a long period of time  and these patients may belong to the group with largest malignant potential. 
Despite differences in experimental designs, it is striking that the majority of papers report a malignant transformation rate of OLP to approximately 0.5-2% in a 5-year period. This still represents a 10-50-fold greater risk of oral cancer than in the general population. ,, Although the lesion exhibited atypical cells on smear examination after 1 year, yet clinically, it showed no features of malignancy even when it was diagnosed as squamous cell carcinoma 1 year back. Considering the presentation of the lesion at the first visit, the size of the lesion was reduced certainly, because of which, clinically we could ascertain that there was remission of the lesion; but cytology did not support the same. With the fact that OLP can wax and wane, this was a diagnostic dilemma correlating the clinical and histopathological findings. In view of this controversy and common occurrence of OLP, this case report highlights the need for histologic confirmation and follow-up of lesions with lichenoid features. Seldom are such cases reported in literature and they raise an open debatable question "should biopsy be made mandatory for all potentially malignant white lesions." Proper treatment in turn may reduce the morbidity and mortality associated with cancer.
The authors here are considering certain facts or controversies which the literature revealed: Firstly, the possible premalignant potential of OLP is the subject of contrasting views. Secondly, biopsies are not representative of the whole premalignant lesion and also that the course of the premalignant lesions after surgical removal did not appear to be significantly associated with histopathological features of the total lesion. However, Maedda and Kameyama found an increased incidence of carcinoma after excision of hamster tongue mucosa treated with carcinogen in an experimental study. 
As much as 20% of surgically treated non-homogenous leukoplakias have reported to develop carcinoma compared to previous and present reported frequencies of malignant development of such lesions without surgical interventions.  Genetically altered epithelial cells unrevealed by routine histological examination and even in areas with normal histology may account for the lack of correlations. Field cancerization may result in unrevealed incomplete resection leading to recurrence of lesions or development of frank carcinoma from residual genetically altered cells. ,
| Conclusion|| |
Although OLP, in many cases, may be diagnosed clinically, it requires appropriate histological examination for assessment of oral cancer risk. This further enhances the need for patient education and management, appropriate medical treatment and long-term review. Lichenoid or OLP presenting with features of early invasive carcinoma was a factor of major concern and diagnostic dilemma. Secondly, the lesion clinically presented with benign features with clinical remission, yet histology showed type IV dysplastic cell. Also it is mandatory to carry out more randomized clinical trials with long-term follow-up. It would be unethical to do any therapy without knowing the outcome of the same. In this scenario, any case with different presentations should be mentioned in the literature for better understanding.
| References|| |
Thornhill MH. The current understanding of the aetiology of oral lichen planus. Oral Dis 2010;16:507-8.
Regezi JA, Sciubba JJ, Jordan RC. Oral pathology: Clinical pathologic correlations. 5 th
ed. USA: Saunders; 2008. p. 90-5.
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 3 rd
ed. USA: WB Saunders; 2009. p. 782-7.
Eisenberg E. Lichen planus and oral cancer: Is there a connection between the two? J Am Dent Assoc 1992;123:104-8.
Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoid reactions: Etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci 2007;49:89-106.
Irani S. Squamous cell carcinoma arising in oral lichen planus. Avicenna J Dent Res 2010;1:49-52.
Lumerman H, Freedman P, Kempel S. Oral epithelial dysplasia and the development of invasive squamous cell carcinoma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:321-9.
Fischer DJ, Epstein JB, Morton TH, Schwartz SM. Interobserver reliability in the histopathologic diagnosis of oral pre-malignant and malignant lesions. J Oral Pathol Med 2004;33:65-70.
Bouquot JE, Whitaker SB. Oral leukoplakia - Rationale for diagnosis and prognosis of its clinical subtypes or "phases". Quintessence Int 1994;25:133-40.
Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Long-term treatment outcome of oral premalignant lesions. Oral Oncol 2006;42:461-74.
Waldron CA, Shafer WG. Leukoplakia revisited. A clinicopathologic study 3256 oral leukoplakias. Cancer 1975; 36:1386-92.
Neville BW, Day TA. Oral cancer and precancerous lesions. CA Cancer J Clin 2002;52:195-215.
Mattsson U, Jontell M, Holmstrup P. Oral lichen planus and malignant transformation: Is a recall of patients justified? Crit Rev Oral Biol Med 2002;13:390-6.
Holmstrup P, Thorn JJ, Rindum J, Pindborg JJ. Malignant development of oral lichen planus-affected oral mucosa. J Oral Pathol 1988;17:219-25.
Holmstrup P. The malignant potential of oral lichen planus. Oral Dis 2010;16:509-10.
Macdonald DG, Rennie JS. Oral epithelial atypia in denture induced hyperplasia, lichen planus and squamous cell papilloma. Int J Oral Surg 1975;4:40-5.
Drangsholt M, Truelove E, Morton T, Epstein J. A man with a 30-year history of oral lesions. J Evid Base Dent Pract 2001; 1:123-35.
Maeda H. Kameyama Y. Effect of excisional wounding on DMBA-induced hamster tongue carcinogenesis. J Oral Pathol 1986;15:21-7.
Holmstrup P, Vedtofte P, Reibel J, Stoltze K. Oral premalignant lesions: Is a biopsy reliable? J Oral Pathol Med 2007;36:262-6.
Holmstrup P, Vedtofte P, Reibel J Stoltze K. Long term treatment outcomes of oral premalignant lesions. Oral Oncol 2006;42:461-74.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]