Squamous papilloma is the most common benign epithelial tumor of the oral mucosa [1]. The World Health Organization defines papilloma as “a range of localized hyperplastic exophytic and polypoid lesions of hyperplastic epithelium with a verrucous or cauliflower-like morphology” [2]. It represents for approximately 2.5% of papillary lesions in the oral cavity and can also be found in other locations such as the larynx, bronchial tree, esophagus, bladder, anus, and genital tract  [1][3].

The etiology of oral squamous papilloma remains unknown, although associations with human papillomavirus (HPV) and local trauma have been reported [2][4].

HPV has been found to have the ability to invade the nuclei of cells in the spinous layer resulting in proliferative tissue growth. A recent report in the scientific literature, however, suggests that presence of HPV may be merely an incidental finding unrelated to the development of a squamous papilloma [4].

Its clinical appearance may sometimes mimic exophytic carcinoma, verrucous carcinoma, or condyloma acuminatum. This underscores the necessity of a thorough clinical examination, complemented by histopathological analysis, to establish an accurate diagnosis [2][4].

Based on two clinical cases, we highlight the oral locations of papillomas, their pathogenesis, clinical features, and therapeutic approaches.

Oral squamous papilloma is a generic term that is used to include papillary and verrucous growths composed of benign epithelium and minor amounts of supporting connective tissue [3]. It is a benign tumor that develops from the stratified squamous epithelium, usually as a result of localized epithelial hyperplasia. It is most often associated with infection by human papillomavirus (HPV), particularly types 6 and 11, which are considered low-risk oncogenic strains [2][4].

HPV is transmitted through sexual, perinatal, horizontal, or autoinoculation. In adults, contamination is most commonly linked to sexual activity, particularly through orogenital or orobuccal contact. In children, transmission is generally non-sexual, occurring either perinatally during passage through the birth canal, by autoinoculation from cutaneous warts, or, more rarely, via indirect contact with contaminated objects. Horizontal transmission between individuals (saliva or hands) is also possible [2]-[5].

Once inoculated, usually through mucosal erosions or microabrasions, HPV reaches the basal layers of the stratified epithelium, which represent the only permissive site for viral replication. The virus then expresses early proteins, such as E6 and E7, which interfere with cell cycle regulators, thereby inducing the proliferation of infected keratinocytes. These infected cells subsequently migrate toward the superficial epithelial layers while continuing to express the viral genome. This process results in epithelial hyperplasia, which is histologically characterized by acanthosis, papillomatosis, and hyperkeratosis—features that explain the typical clinical appearance of oral papillomatous lesions. Among the most frequently HPV-associated lesions in the oral cavity are squamous papilloma, verruca vulgaris, condyloma acuminatum, and focal epithelial hyperplasia [1][5][6].

However, not all oral papillomas are necessarily of viral origin. Non-viral etiologies have also been described, involving chronic irritative or inflammatory factors. These include tobacco use, alcoholism, repeated mechanical trauma (such as ill-fitting prostheses or uncorrected edentulous areas), as well as poor oral hygiene [7].

Although oral papilloma is usually diagnosed between the ages of 20 and 50, it can occur at any age, as illustrated by our two cases, affecting both a child and an elderly adult [1][2].

Clinically, oral papilloma presents as an exophytic proliferation with a papillary or verrucous surface, often pedunculated but sometimes sessile, and generally asymptomatic. Its size is usually less than 1 cm. The color, ranging from white to pink, depends on the degree of keratinization, which is itself influenced by the duration of the lesion’s development [3][4][8][9].

In our cases, keratinization was more pronounced in the child, whose long-standing lesion appeared whitish, whereas in the adult, the more recent lesion was pinkish with less keratinization.

The most common locations are the hard palate and tongue, but other sites such as the labial mucosa and edentulous ridges may also be involved, as observed in our cases [3][4][8][9].

The diagnosis is clinical and histopathological [2][8]. Histopathological examination reveals characteristic features such as hyperpapillomatosis, hyperkeratosis, and acanthosis [3]-[5]. The presence of koilocytes, vacuolated keratinocytes with enlarged nuclei indicative of viral involvement, was not observed in the cases presented, was not observed in the cases presented. The virus itself can be detected using techniques such as in situ hybridization and polymerase chain reaction (PCR) [5].

The standard treatment for oral papilloma remains complete surgical excision, which serves both to confirm the histopathological diagnosis and to ensure curative management. Various techniques can be employed, including cold blade excision, electrocautery, laser ablation, cryosurgery, and, in some cases, intralesional interferon injections [4][5]. The choice of method depends on several factors, such as the lesion’s location, size, the patient’s age, and the available technical resources.

Two approaches were successfully employed in our patients: cold blade excision and diode laser removal.

The choice of laser was guided by its numerous clinical advantages. This technique provides excellent hemostasis, allows for high precision in tissue ablation, minimizes local trauma, and eliminates the need for sutures. Moreover, it is associated with significantly reduced postoperative pain and edema, ensuring greater patient comfort and faster healing. Furthermore, the use of high-power laser surgery is believed to vaporize virus-infected cells, with the thermal effect extending beyond the visible lesion margins. This mechanism contributes to reducing the residual viral load and, consequently, lowers the risk of recurrence [10]-[12].

For both patients, the postoperative evolution was favorable, with no short-term recurrence observed.

Oral papilloma is a benign lesion commonly associated with HPV. Diagnosis relies on clinical examination and histopathological analysis. Complete excision, by various methods including laser, remains the treatment of choice. Laser offers advantages such as better hemostasis and reduced postoperative pain. In our cases, the postoperative course was favorable with no short-term recurrence.