PATHOLOGY
However, studies by McDowell et al. (1979) suggested that metaplasia may arise
from fully mature cells, such as mucus-secreting cells, which are still capable of
cell division. But more recent findings have indicated that an indirect mechanism
of metaplasia may play a role in this process (Leube and Rustad, 1991).
In the respiratory epithelium, the stem cell normally gives rise to
pseudostratified columnar epithelium, but in the presence of certain stimuli it may
differentiate into squamous epithelium. The lack of vitamin A may be associated
with such squamous metaplasia, since animals deficient in this vitamin show
extensive squamous metaplasia of mucous columnar epithelium; treatment with
vitamin A may reverse the squamous metaplasia.
The mechanism of this metaplasia also appears to result from
redifferentiation of certain stem cells (shown as small black nuclei along the
basement membrane) of each of the epithelia. Because these epithelial cells are
constantly being replaced by progeny of the stem cells, in the absence of vitamin
A or in the presence of some chronic stimulus as yet undefined, the differentiation
of the stem cell may be redirected to the more primitive squamous epithelium.
b. Dysplasia
Squamous cell carcinomas of the larynx follow the growth pattern of all
squamous cell carcinomas. They begin as in situ lesions that later appear as pearly
gray, wrinkled plaques on the mucosal surface, ultimately ulcerating and
fungating (Fig. 17-9). The degree of anaplasia of the laryngeal tumors is highly
variable. Sometimes massive tumor giant cells and multiple bizarre mitotic
figures are seen.
The attachment of the vocal ligaments also limits the spread of carcinoma
from one lateral side to the other. The vocal folds have a relative paucity of
lymphatics, as compared with the supraglottis and the pre-epiglottic space. This
paucity of lymphatic vessels is most marked in the anterior vocal folds and
accounts for the rarity of cervical metastases of T1 glottic carcinomas. The
lymphatic channels of the vocal fold become denser posteriorly in the region of
the arytenoids. Glottic carcinomas may spread by undermining the tissue around
the ventricles (paraglottic region), escaping the endolarynx and spreading
laterally by invading the cricothyroid ligament and the inferior aspect of the
thyroid lamina. Ossified thyroid lamina is more prone to tumor invasion as
compared with the relatively avascular nonossified cartilage. Carcinoma may also
spread superiorly into the vestibular fold by undermining paraglottic ventricular
tissue.
The epiglottis is composed of fenestrated cartilage, which allows for early
tumor spread from the laryngeal surface to the lingual surface and into the preepiglottic space. The latter contains abundant lymphatics; tumor spread into this
space increases the risk for cervical metastasis and worsens prognosis. The preepiglottic space is bound anteriorly by the thyrohyoid membrane. Tumor that
breaches this space invades into the base of tongue. The superior boundary of the
pre-epiglottic space is the hyoepiglottic ligament, which connects the hyoid bone
to the epiglottis. Epiglottic carcinomas, which are inferior to the hyoepiglottic
ligament (infrahyoid tumors), are more commonly encountered than those
superior to the hyoepiglottic ligament (suprahyoid tumors). The hyoepiglottic
ligament provides a barrier blocking the inferior passage of the infrequent
suprahyoid carcinomas into the pre-epiglottic space.
Histologically, SCCs may be recognized by their ability to produce keratin
(Fig. 48-8). Intercellular bridges may be seen as fine hairlike structures between
cells. Well- and moderately differentiated SCCs are usually associated with a
surface mucosal component (in situ carcinoma), which clinically appears as an
erythroleukoplakic irregularities.
Neuroendocrine Tumors
Neuroendocrine tumors of the larynx are divided into two broad
Histologically,
glandular
component
is
common.
Cellular
REFERENCES
Cotran, R.S., Kumar, V.K., Collins, T. 1999 . Head And Neck. In : Robbins :
Pathologic Basis of Diseases. 6th edition. Philadelphia : W.B. Saunders Company.
P. 765 766.
Van De Water, Staecker, H. 2006. Laryngeal Pathology. In : Otolaryngology :
Basic Science and Clinical Review. 1st edition. New York : Thieme Medical
Publisher Inc. p. 579 586.