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.
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.
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.
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
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