8
Benign Proliferative Reactions, Intraepithelial Neoplasia, and Invasive cancer of the Uterine cervix
Fig. 8.19 Hyperkeratosis.
Multiple layers of keratin composing the surface
of the squamous epithelium. A granular cell layer has been formed beneath
the keratin layers (H&E x MP).
Fig. 8.20 Anucleated squames
desquamated from the superficial layers of
keratinized— hyperkeratotic— squamous epithelium (Papanicolaou x HP).
Nuclei
are small and often hyperchromatic owing to
pyknosis. Although hyperkeratosis and parakeratosis are usu-
ally associated with a relatively mature squamous epithelium,
a counterpart may overlay an abnormal change such as dys-
plasia or squamous cell carcinoma. Patients with cellular
evidence of hyperkeratosis or parakeratosis should be reexam-
ined to preclude a more serious lesion camouflaged by the
overlying hyperkeratotic or parakeratotic epithelial layer. Phy-
sicians should be advised to take two smears in succession.
The first scrape is intended to remove the superficial, abnor-
mally keratinized layers. In the material obtained with the
second scrape, the true nature of the underlying epithelium
becomes apparent.
Key features of parakeratosis and hyperkeratosis
• Isolated cells or large sheet-like aggregates with anucle-
ate squames;
• Eosinophilic cytoplasm;
Fig. 8.21 Parakeratosis.
Small superficial squamous cells with
sharply outlined cytoplasmic borders and small, often pyknotic nuclei
(Papanicolaou x MP).
• Small round-to-oval nuclei, frequently pyknotic;
• Slight to moderate hyperchromasia; and
• Nucleoli not present.
Squamous Metaplasia
The most common protective mechanism of the endocervical
epithelium of the uterine cervix is squamous metaplasia. The
term metaplasia implies the transformation of one cell type
into another type of cell, the latter being of a lower organiza-
tional order. As applied to the uterine cervix, the term refers to
the process of replacement of simple columnar epithelium lin-
ing the endocervical canal and glands by a stratified squamous
epithelium.
Squamous metaplasia may be arbitrarily subdivided into the
following:
• Reserve cell hyperplasia;
• Immature squamous metaplasia; and
• Mature squamous metaplasia.
Reserve cell hyperplasia is transformed in immature squa-
mous metaplasia, which with increasing differentiation gradu-
ally evolves into mature squamous metaplasia. The maturation
of immature squamous metaplasia tends to be more pronounced
in the distal part of the endocervical canal.
Factors in the initiation and promotion of squamous
metaplasia are chronic irritation of a physical nature, such
as that caused by an intrauterine contraceptive device (IUD),
chemical irritants, inflammation with cell destruction, and
endocrine changes at the beginning of, during, and after
reproductive age. Some of the chemical stimuli that induce
squamous metaplasia in subcolumnar reserve cells are also
capable of inducing cancer in the uterine cervix of experimen-
tal animals.
Squamous metaplasia as such should not be regarded as a
change that necessarily and inevitably precedes the develop-
ment of cancer, but the concept of squamous metaplasia is of
great importance in the understanding of carcinogenesis in the
uterine cervix.
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