Benign and Malignant Lesions of

the Cervix
Andy Teodoro K. Paningbatan, MD, FPOGS
• Cervix
– Ectocervix
• non-keratinizing,
stratified squamous
epithelium
– Endocervix
• simple columnar
epithelium
Squamocolumnar junction (SCJ)
– junction between the squamous epithelium and the
columnar epithelium. Its location on the cervix is variable.
BENIGN LESIONS OF THE CERVIX
 Nabothian Cyst
• Develops when squamous
epithelium covers a nests of
glandular cells, predisposing
them to accumulation of
secretions.
• As this benign process
continues, smooth, clear or
yellow glandular elevations
are visible during routine
examination.
• Nabothian cysts warrant no
further therapy.
 Endocervical Polyps
• hyperplastic
projection of the
endocervical folds
• associated with
leukorrhea or
postcoital spotting
 Micropapillomatosis labialis
• a benign anatomic variant of the vulva
characterized by minute epithelial projections
on the inner labia minora and lower vagina
• projections are uniform in size and shape and
arise singly from their base attachments
• often shows spontaneous regression and
treatment is not indicated
PREMALIGNANT & MALIGNANT
NEOPLASMS OF THE CERVIX
Cervical Intra-epithelial Neoplasia
• histological abnormality of the cervix in which
abnormal epithelial cells, that are potential
precursors to invasive cancer, are present in
the squamous epithelium.
 Abnormal
cells
extending
Abnormal cells up to the
extending to the upper
middle third third
Abnormal cells confined to
the lower third
Cervical Intra-epithelial Neoplasia
• Epidemiology and Etiology
– Human Papillomavirus (97.8%)
– HPV types 16 and 18 are associated with the
development of CIN
– the majority of women will clear the virus; a
minority retain oncogenic HPV that can lead to the
development of CIN.
 Cervical Intra-epithelial Neoplasia
• Other associated factors include:
– smoking;
– immunocompromise, e.g. human
immunodeficiency virus;
– genital warts;
– high-risk male partner.
 Cervical Intra-epithelial Neoplasia
• Pathophysiology
– During puberty, estrogens and a lower vaginal pH
cause the columnar epithelium lining the
endocervix to undergo metaplasia to
squamous epithelium.
– The area where metaplasia occurs is called the
‘transformation zone’.
– Cells in the transformation zone are subsequently
more prone to CIN.
 Cervical Intra-epithelial Neoplasia
• Clinical features
– usually asymptomatic; identified by cervical
screening;
– not visible on the cervix.
 Cervical Intra-epithelial Neoplasia
• Investigations
 Cervical screening (Pap smear)
o Cervical smears are performed on women 21
years every 3 years until the age of 50.
o Between the ages of 50 and 64, smears are 5
yearly provided that results are normal.
 Cervical Intra-epithelial Neoplasia
• Investigations
 HPV testing
o improves the sensitivity of cervical screening.
o Its value lies in its extremely high
negative predictive power, which means that if a
woman tests high-risk HPV negative, her risk of
developing cervical cancer over the next 5–10
years is exceptionally low.
 Cervical Intra-epithelial Neoplasia
• Investigations
 HPV testing
o Never offered as a screening test for HPV infection
outside of current guidelines.
o Appropriate clinical uses for HR HPV testing include:
a) cotesting with cervical cytology screening in
women aged 30 years or older,
b) triage or surveillance of certain abnormal cytology
results and untreated CIN, and
c) posttreatment surveillance
 Cervical Intra-epithelial Neoplasia
• Investigations
 Colposcopy
o Performed if a cervical smear is severely or
persistently abnormal.
o Enables visualization of the cervix with bright light
and magnification.
o Acetic acid or Lugol’s iodine
Cervical Intra-epithelial Neoplasia
 Cervical Intra-epithelial Neoplasia
• Treatment:
= The aim is to treat pre-cancer before it
progresses to invasion.
• CIN I can be treated or observed:
– smear is repeated in 6 months time.
• CIN II and III are treated by large loop excision
of the transformation zone.
• Cervical Cancer
– 3rd most common cancer in women, worldwide
– 2nd leading cause of female cancer in the
Philippines
– 6,670 new cervical cancer cases annually (2012)
– 2nd leading cause of female cancer deaths in the
Philippines
– 2,832 cervical cancer deaths annually (2012)
• High-risk HPVs are by far the most important
factor in the development of cervical cancer.
• Human Papilloma Virus
– DNA viruses
– 15 high risk HPVs that
are currently identified
• HPV-16
• HPV-18
• HPV-45
– High risk HPVs are also implicated in
squamous cell carcinomas arising at many other sites,
including the vagina, vulva, penis, anus, tonsil, and
other oropharyngeal locations.
– Low oncogenic risk HPVs are the cause of the sexually
transmitted vulvar, perineal, and perianal warts
(condyloma acuminatum).
• HPVs infect immature basal cells of the
squamous epithelium in areas of epithelial
breaks, or immature metaplastic squamous
cells present at the squamocolumnar
junction.
• Once infected, these basal cells may become a
viral reservoir.
• Genital HPV infections
– Latent infection refers to – Productive infections are
that in which cells are characterized by viral
infected, but life-cycle completion and
HPV remains quiescent plentiful production of
infectious viral particles
– Express as genital warts
or subclinical infections
• Genital HPV infections
– Extremely common
– Asymptomatic
– Transient: eliminated by the immune response in
the course of months.
On average, 50% of HPV infections are cleared
within 8 months, and 90% of infections are cleared
within 2 years.
Infections with high-risk HPVs last longer than
infections with low oncogenic risk HPVs.
• Even though HPV has been firmly established
as a common cause of cervical cancer, it is not
sufficient to cause cancer.
• Risk Factors
– HPV Infection
– Increased number of sexual partners
– Early age of first intercourse
– High parity
– Cigarette smoking
– Low socioeconomic status

• The most important risk actors or the acquisition

of genital HPV infection are the number of
lifetime and recent sexual partners and early age
at first sexual intercourse.
• Clinical features:
= post-coital bleeding;
= inter-menstrual bleeding;
= post-menopausal bleeding;
= bloodstained, offensive
smelling vaginal discharge;
= on examination the cervix
may appear normal in early
disease; later it
may be ulcerated or
replaced by an irregular
mass.
• Advanced cervical carcinoma spreads by direct
extension to contiguous tissues.
• Lymphatic spread via the paracervical and
parametrial lymph nodes
Cervical Cancer
• Treatment
– Stage 1: Radical Hysterectomy
– Stage 2 and above: Chemo-radiation
• Papanicolaou Smear
– Cytologic examination which detect abnormal
cells shed premalignant lesions
– first smear should be at age 21 years or within 3
years of onset of sexual activity then yearly
thereafter
– If result of a Pap test is abnormal, a colposcopic
examination of the cervix and vagina is performed
to identify the lesion.
• A new aspect of cervical cancer prevention is
vaccination against high-risk oncogenic HPVs
• The bivalent vaccine
prevents
persistent infection
with HPV types 16
and 18, which
together are
responsible for more
than 70% of cases
of cervical cancer.
• The quadrivalent
vaccine,
additionally
protects against
HPV types 6 and
11, the main
perpetrators of
genital warts.
• The nanovalent
vaccine, protects
against HPV
types 6, 11, 16,
18, 31, 33, 45,
52, & 58
END