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Plantar warts are caused by the human papillomavirus (HPV). Plantar warts were discussed as far back as the ancient Greeks and Romans. They were subsequently identified as being caused by infectious agents in the late 1800s. HPV, a member of the Papovaviridae family, was identified in 1949 and is composed of double-stranded DNA. The peak incidence of plantar warts occurs in the teenage years.1 They are estimated to occur in 10 percent of children and young adults.1 Little is known about how the HPV enters the host cell. It is found in the upper epidermis and results in squamous epithelial cell hyperplasia. Numerous types of HPV exist. Simple plantar warts are mainly due to HPV types 1, 2, or 4.

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Two-thirds of untreated common warts in children regress spontaneously within 2 years.1 Patients seek treatment despite these high remission rates, partly because of their location. Large warts on weight-bearing areas can be painful and disabling. If left untreated, they can be transmitted to adjacent or distant body areas. Patients often present with the plantar wart and request its removal. This chapter summarizes the pathogenesis of plantar warts and two techniques for their removal.

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One must recall the layers of the skin in order to understand the pathogenesis of the HPV (Figure 165-1). The skin is composed of the epidermis, the dermis, and the subcutaneous tissue or hypodermis. The epidermis on the sole of the foot consists mainly of stratified squamous epithelium. The thickness of the epidermis ranges from 0.05 mm on the dorsal surface of the foot to 1.5 mm on the plantar surface.2 HPV replication occurs in the most superficial epidermal layer. The dermis is composed of connective tissue and serves as a scaffold for the skin. The blood vessels, nerves, glands, and hair follicles are located in the dermis.

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HPV is a DNA virus. It gains access to host cells and uses the host’s replicating cell proteins to manufacture viral proteins and DNA. This replication process induces epithelial cell hyperplasia, resulting in the mound of thickened skin observed in a plantar wart. The HPV remains in the epidermis but spreads laterally from the mound of verrucous tissue into what appears to be normal-looking epidermis. Intracellular HPV can remain in the dormant state so long as the host’s cell mediated immunity holds it in check. Untreated, solitary, and small to mid-sized warts have a remission rate of approximately 70 percent in 2 years, with only 20 percent of the initial lesions persisting in immunocompetent individuals.3

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The task force of the American Academy of Dermatology’s Committee on Guidelines of Care has evaluated the indications for treatment of any wart.3 They include patient request for therapy, symptomatic warts (pain, bleeding, itching, or burning), lesions that ...

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