Squamous Papilloma of the Tongue: A case report

INTRODUCTION

Squamous cell papilloma or Oral Squamous Papilloma (OSP) is a benign, hyperplastic wart-like localized proliferation, representing an exaggerated growth of normal squamous epithelium.¹ Abbey et al. have studied series of 464 oral squamous cell papillomas, their data reported a slightly higher occurrence rate in males than in females and in white population as opposed to black patients. Papillomas were most abundant on the palatal complex, dorsum and lateral tongue borders, and lower lips, respectively.² Given the myriad subtypes of HPV, clinicians have sounded a note of due caution against high-risk human papilloma virus in oral pathoses. The lesion is preferably excised surgically. Recurrence is usually uncommon.^3,4

CASE REPORT

A 17-year-old female presented to our clinic with a chief complaint of a cauliflower-shaped pedunculated pinkish white lesion on the lateral border of the tongue which began to be a source of concern (Figure 1). The patient reported an insidious onset of such asymptomatic solitary lesion. The patient was assured and educated about the benignancy of the condition before scheduling her for surgery. Upon getting the guardian’s consent, the lesion was excised and sent out for the microscopic examination.

The histological examination revealed a heavy keratinization over the hyperplastic and acanthotic squamous epithelium. The submucosal fibrovascular connective tissues displayed a stroma of numerous anastomosing projections and scattered chronic inflammatory cells in small numbers. Neither malignancy nor dysplasia was evident. The diagnosis was established as an oral squamous papilloma (Figures 2 & 3).

DISCUSSION

Oral Squamous Papilloma (OSP) is a benign, hyperplastic wart-like localized proliferation, representing an exaggerated growth of normal squamous epithelium. OSP may be found on the vermilion portion of the lips and on any intra-oral mucosal site, with predilection for the hard and soft palate and the uvula. Lesions range from flat-topped plaques to verruciform or cauliflower-shaped.¹ The presence of HPV virion components ultrastructurally and immunocytochemically indicates active viral replication in the lesion. This viral infection appears to be transmitted horizontally, venereally, perinatally, vertically or even autoinoculatively.² HPV, the putative etiologic agent of papillomas of the upper aerodigestive tract, is a member of the papova-virus group. It is a DNA virus containing a single molecule of double-stranded DNA comprising approximately 8000 nucleotide base pairs. A wide variety of HPV subtypes, including 16 and 18, can be demonstrated in these lesions.^5,6 HPV has also shown to immortalize epithelial cells and has a synergistic effect with chemicals, like tobacco. This combined mutagenic effect plays a key role in HPV-induced carcinogenesis.³ Although many oral squamous papillomas appear to be virally induced, the infectivity of the HPV is low. The route of transmission of the virus is unknown for oral lesions, although direct contact in an area of local trauma would be favored.²

Histologically, the covering squamous epithelium shows a normal maturation pattern. Occasional papillomas demonstrate pronounced basilar hyperplasia and mild mitotic activity. Scattered chronic inflammatory cells in small numbers are common in the stroma, presumably from chronic low-grade trauma to the lesion. Submucosal fibrovascular connective tissues are contiguous with the stroma of the stalk, the body of the mass and the surface projections. The surface keratin is often quite thickened, usually with parakeratin.⁷

The differential diagnosis of oral squamous papilloma, includes verruciform xanthoma, papillary hyperplasia, and condyloma acuminatum, evus unius lateris (ichthyosis hystrix), acanthosis nigricans, tuberous sclerosis and focal dermal hypoplasia (Goltz-Gorlin) syndrome. Verruciform Xanthoma (VX) may resemble squamous papilloma. VX has, however, a distinct predilection for the gingiva and the alveolar ridge and contains foamy cells in the connective tissue papillae.^1,2,7 Moreover, an innocuous oral squamous papilloma may herald the serious precancer proliferative verruciform leukoplakia.⁸

Removal by surgical excision is the treatment of choice. Laser ablation is also effective but does not offer the opportunity for microscopic examination of the lesion to confirm the diagnosis. Recurrence is uncommon, except for lesions in patients infected with HIV.⁷

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

REFERENCES

1. 1. Eversole L. Papillary lesions of the oral cavity: relationship to human papillomaviruses. J Calif Dent Assoc. 2000;28(12):922-7.
2. 2. Abbey L, Page D, Sawyer D. The clinical and histopathologic features of a series of 464 oral squamous cell papillomas. Oral Surg Oral Med Oral Pathol. 1980;49:419-24.
3. 3. Dhanapal R, Ranganathan K, Kondaiah P, Devi R, Joshua E, Saraswathi T. High-risk human papilloma virus in archival tissues of oral pathosis and normal oral mucosa. Contemp Clin Dent. 2015;6(2):148-52.
4. 4. Prabhu S, Wilson D. Human papillomavirus and oral disease-emerging evidence: a review. Aust Dent J. 2013;58:2-10.
5. 5. Subramanyam D, Krishna S. c-Myc substitutes for Notch1-CBF1 functions in cooperative transformation with papillomavirus oncogenes. Virology. 2006;347:191-8.
6. 6. Fan X, Liu Y, Chen JJ. Down-regulation of p21 contributes to apoptosis induced by HPV E6 in human mammary epithelial cells. Apoptosis. 2005;10:63-73.
7. 7. Neville BW, Damm DD, Allen CM, Bouquot JE. Squamous papilloma. In: Neville BW, Damm DD, Allen CM, Bouquot JE, eds. Oral and Maxillofacial Pathology. 3rd ed. India: Guanabara Koogan ed, de Janeiro; 2010: 362-364.
8. 8. Scully C, Porter S. Orofacial disease: update for the dental clinical team: 3. White lesions. Dental Update. 1999;26:123-9.