North Texas Dentistry Volume 8 Issue 2 2018 ISSUE 2 DE | Page 12

oral cancer
HPV-Related Oral and
Oropharyngeal Carcinoma
T
by David D. Vu MD, DDS, PharmD and David R. Kang MD, DDS, MS, FACS
he human papillomavirus, more commonly known as “HPV”
is ubiquitous. It is a virus that most people will be infected
with at some point in their lives (over 80% of women, and
over 90% of men). It commonly causes warts, which may be sub-
tle, appearing as small bumps, or have a more characteristic cau-
liflower appearance, oftentimes, patients being asymptomatic
altogether. The warts appear on any part of the body, including
the genitals, where they have a similar appearance. Most indi-
viduals clear an HPV infection within one or two years, although
it may persist in others.
There are over 400 types of HPV (types designated by numbers),
and around 40 of these are spread through direct sexual contact.
It is the most commonly sexually transmitted disease in the U.S.
with an incidence of 14 million per year, with about 12,000 peo-
ple between 15 and 24 years infected daily. Transmission occurs
via skin or mucous membrane either by direct genital to genital
contact, or from genital contact to the mouth and throat, such
as in oral sex. It is believed to affect men more commonly due to
an increased viral load encountered in the cervix of women dur-
ing oral sex.
HPV is important not only as a sexually transmitted disease, but
also as a potential cause of cancer. It is a DNA virus that encodes
for two important oncogenes, E6 and E7. After infecting ker-
atinocytes of the skin and mucous membranes, it synthesizes the
12 NORTH TEXAS DENTISTRY | www.northtexasdentistry.com
protein products of E6 and E7, which inactivate two key tumor
suppressor genes, p53 and retinoblastoma (Rb). Inactivation of
the latter is associated with an increase in p16, one of the mark-
ers used in testing for HPV infection. Rb and p53 are important
in regulating cell cycle and directing the normal life cycle of a
cell, including programmed cell death or apoptosis. If inacti-
vated, cell growth goes unchecked, setting the stage for develop-
ment of a cancer. It is a slow process, however, taking 10 to 30
years after the initial infection before a tumor develops.
Low risk HPV 6 and 11 may often cause genital warts or condy-
loma acuminatum, but not cancer. High risk HPV can cause can-
cer and includes types 16, 18, 33, 35, 45, and others, which are
responsible for most HPV-caused cancers, especially HPV 16.
Like other types of HPV, high risk HPV is often asymptomatic
and clears after 1 to 2 years. Risk of cancer increases if the infec-
tion persists beyond the usual time.
Virtually, all cervical cancers are caused by HPV, about 70% of
which are due to HPV 16 and 18. 95% of anal cancers are caused
by HPV, most by HPV 16. Approximately, 70% of oropharyngeal
cancers are caused by HPV, over half of which are attributed to
HPV 16. Other cancers caused by HPV include 65% of vaginal,
50% of vulvar, and 35% of penile cancers. Most of these are due
to HPV 16.