Papillomaviruses (HPVs) are double-stranded DNA viruses in the papoviridae family. More than 100 HPV types have been identified, each with a predilection for certain body sites. HPVs are obligatory intranuclear organisms, which exhibit an affinity for keratinocytes, and they must reach mitotically active cells for the establishment of an infection.¹² The viruses presumably reach the basal cells through breaks in the surface epithelium. The mechanism of infection is not clear, but the viral DNA may be maintained as intranuclear, extrachromosomal, circular DNA episomes, which replicate synchronously with the host cell, establishing a latent infection.¹² Under certain circumstances that are still unclear, a latent infection can convert into a productive infection with the assembly of complete infective virions, which then extend to more superficial epithelial layers.¹³ Transmission of infection from one body part to another or from one individual to another appears to be via contact with the superficial epithelial layers where the infective agents are present. These virions induce host cellular mitotic activity resulting in thickening of the epithelium. Increased viral replication also causes cytologic atypia.¹²

An alternative pathway for papillomavirus infection may be the integration of viral DNA into the epithelial cell genome.¹² This appears to be more common with the more high-risk HPV infections that are associated with malignant tumor transformation.¹⁴,¹⁵ Although human papillomavirus often causes clinically apparent warts, it can also exist in a subclinical or latent form. This may account for the frequently observed recurrences rather than from reinfection.⁸

Verruca vulgaris has been reported to arise within tattoos.¹⁶,¹⁷,¹⁸ Various modes of contamination have been proposed such as direct inoculation of virally contaminated tattoo dyes and/or needles, latent verruca in the area of tattoo placement, contamination from the tattoo artist’s saliva,¹⁶,¹⁷ or as a result of HPV infection contracted incidentally with preferential growth within the tattoo environment, because of locally suppressed carbon pigment local immune dysregulation.¹⁹

Periocular verruca vulgaris lesions typically occur near the eyelid margin but can occur anywhere on the periocular skin or conjunctiva. They typically appear as a nonpigmented small papule with a digitated surface or as a filiform lesion with a papillomatous growth pattern (Figure 122.1A). They are flesh-colored growths that may have small finger-like projections (Figure 122.2). The lesions may be pedunculated or broad-based and are often multilobulated (Figure 122.1B). They may be associated with conjunctivitis and keratitis with peripheral corneal vascularization and scarring.²⁰

Clinically, conjunctival warts have a rugose, hyperkeratotic, or scaly crusting appearance (Figure 122.3). When hyperkeratosis is scant or absent, mucosal papillomas may be translucent enough to allow visualization of their frond-like vascular cores.²¹ Pain, telangiectatic vessels, and secondary infection can be seen. When they become large, conjunctival verrucae are often associated with chronic papillary conjunctivitis or punctate epithelial keratitis. Very large lesions can also interfere with eyelid function.

The differential diagnosis of verruca vulgaris includes other benign lesions such as chalazion and hordeolum, epidermal inclusion cyst, molluscum contagiosum, xanthelasma, nevus, and actinic keratosis. It can also be confused with some malignant lesions such as squamous cell carcinoma, basal cell carcinoma, and sebaceous carcinoma.