In this episode we explore the biology of human papillomavirus (HPV), how plantar warts develop, why certain patients are more susceptible, how to distinguish verrucae from other plantar lesions, and the evolution of treatment from historical remedies to modern immunotherapy and surgical excision. The most important take home message is that removing the visible wart is not necessarily the same as eliminating the viral infection. That distinction explains much of the difficulty surrounding recurrence and treatment-resistant lesions.
Certain HPV variants are associated with plantar warts, these are types 1, 2, 4, 27, and 57. Exposure to these types by susceptible individuals can result in the classic pedunculated, involuted lesions known as 'plantar warts.' Generally, this is because of a breakdown in the epithelial structure allowing the virus to enter skin cells. These can be microscopic scratches in the skin, for example from walking on sand which is extremely abrasive.
The appearance of plantar warts varies, but classically it appears as roughened skin with abnormal edges, interruption of the normal skin lines (dermatoglyphics), and contains small black dots which are essentially coagulated capillaries. Rarely does a plantar wart protrude since they are under constant compression. Often isolated lesions exist, or several isolated lesions, but a mosaic pattern may emerge if the virus spreads to surrounding skin, which appears as multiple round or irregularly shaped 'tiles' of keratosis clustered together.
Common OTC preparations include 17% salicylic acid. This medication comes in single use bandages or as a gel in a small tube like toothpaste, and requires daily applications, sometimes for several weeks. Another common OTC option is freezing spray. My experience with these is that failure is very common especially if the wart is on a weight bearing area of the foot since the skin is too thick for a deep enough frost from freezing or complete keratin disruption to remove all infected cells.
In my clinic if nothing has been tried previously, topical daily acid application after careful deep debridement is often first line treatment. If this fails, Cantharone application is employed. This is a blistering agent that causes local inflammation and eruption of the infected tissue. Sometimes a few applications is required however this has a success rate higher than topical acids.
For stubborn cases, local excision is preferred. Scarring can be avoided if the dermal barrier is not violated. I use special curettes to avoid violating the basement membrane. This alleviates the need for suture material and development of a scar. Concomitant application of phenol 90% strength is used at the time to bathe the wound site after excision in an effort to ensure total destruction of any viral material in the area. This method has an extremely high success rate, although recurrence and reinfection are possible even with this method.
Lasers are also an effective surgical option. I have also used Plasma Jet, which is an argon-gas ablative tool. As you can see, multiple options exist, since there is no universal procedure that works for everyone every time.
When multiple methods have failed, I have used immunotherapy on occasion. Topical imiquimod cream has shown efficacy in mosaic patterns and in recurrence situations.