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Review Article

An update on oral human papillomavirus infection


Ankit H. Bharti, Kiran Chotaliya, Y. S. Marfatia
Department of Skin and VD, Baroda Medical College, Raopura, Vadodara, Gujarat, India

Address for correspondence:


Dr.Ankit H. Bharti, Baroda Medical College, Raopura, Vadodara390001, Gujarat, India. Email:ankithbharti@gmail.com
Dr.Y. S. Marfatia, Department of Skin and VD, Baroda Medical College, Raopura, Vadodara390001, Gujarat, India. Email: ym11256@gmail.com

Abstract
Human papillomavirus(HPV) constitutes the majority of newly acquired sexually transmitted infections(STIs)
in United States as per the centers for disease control factsheet 2013. Genital HPV is the most common STI
with incidence of about 5.5 million worldwide, nearly 75% of sexually active men and women have been
exposed to HPV at some point in their lives. Oral Sexual behavior is an important contributor to infection of
HPV in the oral mucosa especially in cases known to practice high risk behavior and initiating the same at
an early age. HPV infection of the oral mucosa currents is believed to affect 150% of the general population,
depending on the method used for diagnosis. The immune system clears most HPV naturally within 2years
(about 90%), but the ones that persist can cause serious diseases. HPV is an essential carcinogen being
implicated increasingly in association with cancers occurring at numerous sites in the body. Though there
does not occur any specific treatment for the HPV infection, the diseases it causes are treatable such as
genital warts, cervical and other cancers.

Key words: Human papillomavirus, oral human papillomavirus, oral infection

INTRODUCTION vast majority of them will clear the virus naturally


and never know that they were exposed or had it.
Human papillomavirus(HPV) constitutes the
Sexual partners who have been together for a while
majority of newly acquired sexually transmitted
tend to share HPV. This means that the partner
infections (STIs) in United States as per the
of someone who tests positive for HPV likely has
centers for disease control factsheet 2013. There
HPV already, even though they may have no signs
are nearly 20 million new STI every year, of this
HPV is the most common sexually transmitted or symptoms. Like most Americans, their immune
virus and infection in the United State. [1] There system will clear it in under 2years. India has one
are nearly 200 different strains of HPV, most of of the worlds highest incidence of oral cancer. The
which are harmless and more than 40 HPV types major limitation of the current review was a dearth
that can infect genital and oral mucosa in both of adequate HPV related data in Indian population,
males and females, out of all these, 9 are known to which can establish precise facts and help to
cause cancers. Every day in the US, about 12,000 plot a strategy for its management and verify the
people ages 1524 are infected with HPV. [2] The role of HPV in the head and neck squamous cell
carcinoma(HNSCC).

Access this article online VIROLOGY


Quick Response Code:
Website: HPV is a 55nm deoxyribonucleic acid(DNA) virus,
www.ijstd.org which belongs to papillomaviridae family.[36] The
virion consist of a nonenveloped, singular double
DOI: stranded DNA with nearly 5500 nucleotide base
10.4103/0253-7184.120533 paires.[7] More than 120 genotypically different forms,
with each type having nearly 90% of them sharing

How to cite this article:


Bharti AH, Marfatia YS. An update on oral human papillomavirus infection. Indian J Sex Transm Dis 2013;34:77-82.

Indian Journal of Sexually Transmitted Diseases and AIDS 2013; Vol. 34, No. 2 77
Bharti and Marfatia: An update on oral Human papillomavirus

a similar DNA base pair homology.[8] Nearly 40 HPV TRANSMISSION


types are known to infect the genital tract mucosa
HPV infection of oral and oropharyngeal mucosa
and 14 are detected in the majority of biopsies,
are associated with orogenital sex and high risk
of invasive cervical carcinoma and are therefore
sexual behavior of cohabiting numerous partners,
considered high risk[Table1] or oncogenic.[1]
particularly when initiated at an early age.[1519]
IMUNOPATHOGENESIS HPV infection is more strongly related to couples
The precise mechanism of entrance of HPV into who practiced oral sex as against couples who solely
the cell are not yet validated. It is known that the practiced vaginal sex.[17,20]
HPV capsid proteins play an essential role in host
epithelial cell entry and delivery of the viral DNA Oral and oropharyngeal HPV infections are primarily
to the nucleus.[9] acquired through sexual activities, mouth to mouth
contact between partners or family members,
HPV CLEARANCE autoinoculation and vertical transmission during
birth are also some of the known routes which can
Acquiring new HPV infection is now strongly
establish HPV infection. [17,21,22] Mucosotropic HPV
being associated with sexual behavior with female
strains are capable of causing benign lesions in the
and male sexual partners. So is the probability of
upper aerodigestive tract.[23]
clearing existing HPV infection is also being strongly
associated with sexual behavior. No association
has been found with age and incidence of any, CLINICAL MANIFESTATIONS
oncogenic, or nononcogenic HPV types, although Focal epithelial hyperplasia(heck disease)
the probability of clearing these infections increased Hecks disease or focal epithelial hyperplasia was
with age. The risk of HPV infection decreases with first described in 1965, it is seen most commonly
increasing age in women,[10,11] men on the other hand in Alaska Eskimos and in American native or
seem to have a constant risk for acquiring new HPV Indians, South Africa and occasionally in Israel.
infections throughout their life.[12] A study of men in It affects oral mucosa, lips, tongue, notably lower
the USA, noted that the incidence of HPV infection lip and more rarely the palate, floor of the mouth
was constant over the age range 1844years.[13] and
and oropharynx more commonly in the age group
yet another study, claims that the incidence was
of 318, but can be seen in all age groups.[24] It is
constant in men aged 1870years and residing in
strongly associated with HPV types 13 and 32 which
Brazil, Mexico and USA.[12]
are seen in about 90% of infections. [25,26] Usually
regresses spontaneously but treatment is often
Markowitz etal. reported faster clearance of
taken to mitigate esthetic problems or repeated bite
oncogenic HPV infections in men with increasing
injuries.
age. [12] thus more rapid clearance noted in older
men might be related to a higher prevalence of HPV
antibodies in older men.[14] Oral squamous papilloma
Oral Squamous papilloma is a benign tumor se en
In consensus to what has been reported in women, in all age groups, more commonly in 3050years of
the median time to clearance of HPV 16 is nearly age. The lesions in children are commonly seen in
2times longer(about 12months) than with other the laryngotracheobronchial complex and in the oral
oncogenic HPV types(e.g.63months for HPV mucosa over soft palate, lingual, frenulum, lower lip
18). Clearance of specific HPV types by age group and uvula among adults.[24] It is mainly related to
needs to be further assessed in Indian population HPV 6 and 11. Surgical removal is the first choice of
especially by metaanalysis studies. The median treatment, but electrocauterization, cryosurgery and
time for clearance of any type of HPV infection interferon injections are also used.
was significantly longer in men aged 1830years as
compared to other age groups.[12] Oral condyloma acuminata
Condyloma is derived from the Greek word
Table1: HPV genotypes and oncogenic risk kondilus i.e. round tumors and acuminatum
Risk type HPV type from the Latin word acuminare; i.e.to become
High 16, 18 pointed. The sexual route remains the main route
Intermediate 31, 33, 35, 39, 45, 51, 52, 58, 59, 68 of transmission (20%)[27] and people who have oral
Low 6, 11, 42, 43, 44 sex have a 50% chance to acquire the oral infection.
HPV=Human papillomavirus Incubation period ranges from 2 to 8weeks. It is

78 Indian Journal of Sexually Transmitted Diseases and AIDS 2013; Vol. 34, No. 2
Bharti and Marfatia: An update on oral human papillomavirus

characterized by little pinkish or whitish nodules, clinically or histologically as any other disease. It is
which proliferate over tongue, lips, palate and floor considered to be premalignant lesion of oral cavity
of mouth which can be sessile or pedunculated. and has a potential of 1662% of getting converted
The surface contour is usually cauliflower like. HPV into oral SCC.[36] Oral leukoplakia is commonly caused
types 6 and 11 have commonly been detected with by HPV types 6, 11 and 16.[37] No consensus as to the
immunohistochemistry and by hybridization with best treatment course and prevention remains the best
7585% positivity.[28,29] approach. Nonsurgical treatment based on topical
bleomycin and systemic retinoids. Invasive treatment
Common warts(Verruca vulgaris) includes cryosurgery, CO2 laser and surgical resection.
Verruca vulgaris is one of the most common They are effective in the short run, nut lesions may
manifestation seen mainly in children can infect oral relapse in the long run.
mucosa.[24] It is usually seen on lips, hard palate,
gingival and dorsal surface of tongue. The most Oral squamous cell carcinoma
common HPV types affecting the musocostrofics(6, In 1976, the first description of relation between
11 and 16) and the cutaneoustrofic(1, 2, 4 and 7) OSCC and HPV was described by Zur Hausen, since
and HPV2 and HPV4 are detected in more than then it has been as an exclusive cause for Cervical
55% of oral lesions.[30] Usually warts are selflimited Carcinoma.[31] HPV was seen in association to 20%
and resolve within 2years. Treatment is sought of OSCC cases as reported in 1983 by Syrjanen.[38]
usually because of esthetic discomfort or to avoid
bite injuries. HNSCC are a major cause of morbidity and mortality
worldwide especially in the Indian subcontinent
with>90% of which are SCC and rank sixth among
Oral lichen planus
all malignancies worldwide.[39]
OLP chronic immunomediated disease with
unknown etiology, which is seen commonly in
More than 90% HNSCC and anogenital cancers are
relation with skin and mucosal lesions associated
caused by HPV16 type. It represents 3% of malignant
with HPV. [31,32] It is commonly seen in age group
transformation, i.e.more than 5,000 diagnosed cases a
of 3060years predominantly in females, though
day and more than 90% of oral cancers. HPV infection
it can also be seen in children and adolescents.
influences the prognosis of the SCC[Table2]. The
The lesions of OLP are generally bilateral and
similarities between the oral and genital injuries along
symmetrical, affects the oral mucosa, gingival, the
with the following factors point toward a role of HPV
dorsum of tongue and lip mucosa. HPV types 11 and infection in oral mucosa, i.e.Affinity to epithelial
16 are commonly found in about 87% of patients. cells, type of genital and oropharyngeal epithelia and
Treatment with corticosteroids reduces the symptoms oncogenic potential of HPV.[40]
but does not cure the condition, treatment with
calcineurin inhibitors, topical retinoids are also used
as additive therapy.[33,34]
Recurrent respiratory papillomatosis
It is characterized by the proliferation of benign
squamous papillomas within the aerodigestive
Oral verrucous carcinoma tract.[4143] In 75% of children with RRP, the diagnosis
A variant of squamous cell carcinoma (SCC), which was made before the childs 50 th birthday and in
is benign with welldistinguished morphology adults in fourth decade. [44] It is mainly caused
and clinical presentation. It is a rare tumor by HPV6 and HPV11, found usually over oral
described by Ackerman in 1948 as a cancer that mucosa, trachea and bronchi and esophagus. In
commonly involves lips, oropharynx and laryngeal 1998, Wanget al. reported this disease presenting
mucosa. It is also known as Achermans tumor, in age<5years it is referred as Juvenile Onset
florid papilomatosis, epithelioma cuniculatum and RRP is thought to be vertically transmitted during
carcinoma cuniculatum[35] and Buschke Loewestein. the childbirth, although transplacental transmission
Commonly caused by HPV types 6, 11, 16 and has also been reported. [45] Treatment modalities
18.[24] The treatment of choice is surgical resection, include cold steel excision, CO2 laser and adjuvant
Radiotherapy with resection, cytostatic drugs like modalities such as interferon, ribavarin, cidofovir,
interferon. Recurrence rate is high when isolated photodynamic therapy, HPV vaccine etc.
surgical resection or radiotherapy is performed.[35]
WHIM syndrome
Oral leukoplakia It is a rare Autosomal Dominant syndrome
MartorellCalatayud A. described oral leukoplakia as characterized by warts, hypogammaglobulinemia,
a white patch or plaque that cannot be characterized infections and retention of mature neutrophils in

Indian Journal of Sexually Transmitted Diseases and AIDS 2013; Vol. 34, No. 2 79
Bharti and Marfatia: An update on oral Human papillomavirus

Table2: Difference between oropharyngeal variety of stem cells and progenitor cells, but its role
cancer HPV+ and HPV is not wellcharacterized.[46]
HPV positives HPV negatives
Age Younger Older RELATION TO HUMAN
individuals (3050) individuals (5070) IMMUNODEFICIENCY VIRUS
Risk factors Oral sex, french kiss, H/O tobacco
high number of sexual and/or alcohol Sikora et al. proved that seropositive individuals
partners consumption show a higher prevalence of oral infection with high
Incidence Increasing Decreasing oncogenic risk HPV, which increase with age, male
Location Base of tongue, Oral mucosa gender and infection by Virion Host Shutoff2
amygdalae
protein.[29]
Field No Yes
cancerization
Histology Poorly Clearly
Seropositive individuals also have a higher risk of
differentiated basaloid differentiated getting oral HPV infection from more than one HPV
Stage of T34, N23 Variable types, further increasing the oncogenic potential
diagnosis of the infection. [21] The risk of infection by high
Biomarkers Overexpressed P16, Loss of P16; P53 oncogenic types of HPV is 13times greater in HIV
inactivation of P16 and and pRb mutation; positive individuals who practiced oral sex with
pRb cyclin D1, EGFR
more than one person during the previous year.[29,47]
and survivine
overexpression
Chromosomal Less frequent Frequent RELATION TO PREGNANCY
mutations
Prognosis Very good, increased Poor
Genital warts in pregnancy flourish well with
sensitivity to increase in size and number, which is believed to
radiotherapy and be due to hormonal influence, increased vascularity
chemotherapy and relative immunedeficiency. Elective caesarean
Distant Rare Frequent is advised in case of genital warts as vertical
metastasis
transmission of HPV DNA from an HPV infected
Second Rare Frequent
primaries
mother to a neonate is increased if the infant is
Five years 6090 2070
delivered through an infected cervix. However the
survival rate % absence of persistent infections infection infants
HPV=Human papillomavirus; EGFR=Epidermal growth factor receptor at 6months after delivery may suggest temporary
inoculation rather than true vertical infection.[48]
Table3: Laboratory investigations
Despite the overwhelming evidence for a sexual
Laboratory investigations for detection of human papilloma
virus transmission of highrisk HPVs, other routes of
Direct method transmission have been proposed. Several studies
Light microscopy: Microscopic cellular features. Low sensibility have explored whether HPVs can be vertically
and does not indicate HPV types transmitted from mother to child by direct contact
Electron microscopy: HPV particles can be identified during labor, or horizontally through manipulation
Drawbacks of the child with infected hands, bathing, towels
HPV types cannot be detected and fomites. 19.7% of the 66 infants born to HPV
Molecular methods positive mothers and 16.9% of the 77 infants
Nonamplified technique born to HPVnegative mothers tested HPVDNA
In situ hybridization positive at some point during followup thus
Southern blot and dot blot Children of mothers who were HPVpositive at the
Amplified technique postpartum visit are nearly 5times more likely to
Target amplification test HPVpositive than children of corresponding
Hybrid captured technology
HPVnegative mothers.[49] The oncogenic HPV types
HPV=Human papillomavirus
16, 18, 31, 33 and 35 are common, whereas HPV
types 6 and 11 are rarely seen. The interaction
the bone marrow(myelokathexis) also associated between oral HPV and Pregnancy is yet to be studied.
with increased susceptibility to HPV infections is
also reported. The occurrence of HPV related SCC
in two sibling with WHIM syndrome was reported
CONCLUSION
by Cipriani etal. Amutation in chemokine receptor Oropharyngeal HPV infection is primarily associated
CXCR4, a 7transmembrane protein expressed in a with sexual activities especially orogenital sex

80 Indian Journal of Sexually Transmitted Diseases and AIDS 2013; Vol. 34, No. 2
Bharti and Marfatia: An update on oral human papillomavirus

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