PART TWO
Diagnostic Cytology
as they may mask a more serious underlying disease process.
These changes—hyperkeratosis, parakeratosis, basal cell hyper-
plasia,
pseudoparakeratosis,
and
dyskeratosis—have
been
discussed elsewhere in this book. They reflect abnormalities of
maturation with normal keratin formation in cells that normally
do not reveal these changes.
Squamous epithelial cell changes
• Hyperkeratosis;
• Parakeratosis;
• Basal cell hyperplasia;
• Pseudoparakeratosis; and
• Dyskeratosis.
Dyskeratosis is mentioned here because of its relationship
with viral infections and developing cancer. This represents an
abnormality of the squamous cells in which the cytoplasmic
maturation is altered. The affected cells reveal premature, hyper-
mature, or atypical keratinization. It is a common occurrence
in the presence of chronic infections, such as those caused by
human papillomavirus (HPV). The cytomorphologic features
are further detailed in the appropriate sections.
Endocervical Columnar Epithelium
In addition to the squamous metaplasia discussed earlier,
endocervical cells may undergo other morphologic changes
including columnar cell hyperplasia and hyperplastic polyp
formation.
Columnar Cell Hyperplasia
Endocervical cells frequently enlarge and produce excessive
mucus. Such changes occur with chronic irritation of the endo-
cervical canal, such as among women using IUDs8 or hormonal
contraceptives, and who are exposed to certain infections; these
are discussed separately.
Hyperplastic Polyp
Hyperplastic endocervical columnar cells may proliferate to
produce finger-like epithelial processes—polyps. As described
by Ramzy9 and Frost,10 these polyps are three-dimensional struc-
tures with three distinct planes—a floor or base composed of a
sheet of polygonal cells, a middle plane that makes up the sides
of the polyp, and a top or surface layer that, like the base, is also
a sheet of polygonal cells. In the center of the polyp, a connec-
tive tissue core that contains fibroblasts, collagen, and capillary
vessels, may be recognizable.
Tubal Metaplasia
Generally, endocervical epithelium may contain ciliated colum-
nar cells only in small numbers (5-10%). Under conditions
of chronic irritation, sheets of ciliated cells representing tubal
metaplasia may occur in the specimens collected from the trans-
formation zone and the adjacent endocervix. These cells may
show pseudostratification and atypia and can be a common
source of misinterpretation as neoplastic cells.11
Tubal metaplas-
tic cells may stain positively with p16INK
4A
antibodies,12 which
may lead to confusion with neoplastic processes.
Columnar epithelial cell changes
• Hyperplasia
• Polyp formation
• Squamous metaplasia
• Tubal metaplasia
Endometrium
Heavy acute inflammation, with pronounced reactive, degen-
erative, and metaplastic changes may be observed in these
cells during the later half of menstrual bleeding, following
instrumentation, in the postpartum period, and in association
with the usage of an IUD. Retained gestational products and
foreign bodies may result in extensive squamous metaplasia,
multinucleated giant cell reaction, and calcification. Some of
these changes are discussed later in this chapter.
Infections of the Female Genital Tract
Bacterial infections
Bacteria most commonly infect the female genital tract. Bibbo
and Wied13 reported nonspecific organisms including mixed
bacteria and coccobacilli in nearly 20% of patients. Among chil-
dren these infections occur commonly and may be hormonally
dependent. Vaginal or vaginopancervical smears often reveal a
number of bacilli and coccid organisms (mixed infections) as
detailed by Wied and Bibbo.14 These organisms, although dif-
fusely scattered, may occur in clumps and as microcolonies.
Appropriate microbiologic isolation techniques are necessary
for specific species identification but is generally not considered
necessary for clinical management of the disease.
Bacterial vaginitis (nonspecific vaginitis) was first described
by Gardner and Dukes.15 They stated, "Any woman whose ovar-
ian activity is normal and who has a gray, homogenous, mal-
odorous vaginal discharge with a pH of 5.0 to 5.5 that yields no
Trichomonads is likely to have
Haemophilus vaginalis
vaginitis."
It is also known as nonspecific vaginosis/vaginitis so named by
Blackwell and Barlow,16 or bacterial vaginosis (BV), a term used
by the International Agency for Research on Cancer.17 This is the
most common cause for the clinical entity of bacterial vaginosis.
Instead of making a specific diagnosis of
G. vaginalis
infection,
reporting of a "shift in the bacterial flora" is the current term
used to describe the organism variously named as
Haemophilus
vaginalis
and
Corynebacterium vaginalis.
Gardner and Dukes18
first described these organisms. Regarding the etiology of BV, the
statement by Fredricks and Marrazzo that "BV probably results
from infection with complex communities of bacteria that
consist of metabolically interdependent (syntrophic) species"
appears true.19
Morphologically, the organisms are Gram-negative or Gram-
variable, are 0.1-0.8 nm in diameter, and appear bacillary or coc-
cobacillary. The microbe, although it shares many characteristics
with
Corynebacterium
, is catalase-negative and is now classified
separately. Petersdorf and colleagues20 and Ledger and associ-
ates21 found that as many as 40-50% of women may have vaginal
infection with
G. vaginalis
and be asymptomatic. Among symp-
tomatic women, leucorrhoea and pruritus with inflamed vaginal
mucosa and occasional punctate hemorrhages are commonly
observed. Increased growth and concentration of these organ-
isms may not denote pathogenicity.17 It is believed that patients
with pure
G. vaginalis
infection are asymptomatic when the
vaginal pH is less than 4.5. Secondary organisms interplay with
G. vaginalis
and alter this synergistic relationship. A raised pH
over 4.5 (5.0 to 6.5) and an interaction with various bacteroides
and peptococci may produce clinical disease. Recently, consider-
able interest has been exhibited in the study of BV. Molecular
identification of the associated bacteria has revealed the presence
96
previous page 98 ComprehensiveCytopathology 1104p 2008 read online next page 100 ComprehensiveCytopathology 1104p 2008 read online Home Toggle text on/off