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SALIVARY GLANDS - ALCOHOLIC SIALADENOSIS
Sialadenosis (sialosis, asymptomatic parotid hypertrophy) is defined
as a persistent non-inflammatory bilateral painless soft symmetric
enlargement of the parotid glands with infrequent involvement of
the submandibular salivary glands. Swellings are caused by metabolic
and secretory disorders of the glandular parenchyma. The entity
is seen in a variety of endocrinopathies including diabetes, malnutritional
syndromes and following the use of some medications. Clinically,
sialadenosis is most commonly alcohol related, with approximately
40% of the alcoholics showing signs of parotid enlargement.
Sialadenosis is thought to originate from a dysregulation of the
autonomic nervous system. Such neuropathies are part of a pattern
often seen in alcoholism. Since sympathetic innervation of the parotid
gland
is concerned with protein synthesis and protein secretion, sympathetic
denervation of the acinar cells leads to inhibition of this activity
and intracellular accumulation of zymogen granules. Acinar cells
may increase to as much as three times their normal size causing
parotid enlargement. However, in cases of long standing alcoholism,
the parotid gland swelling may be due to a fatty infiltration resulting
from a disturbance in fat metabolism secondary to liver dysfunction.
Accurate diagnosis requires differentiation from inflammatory or
neoplastic salivary gland disease and mandates a search for liver
pathology. When the classic signs of sialadenosis are coupled with
an alcoholic history, diagnosis is facilitated. Confirmation of
the clinical diagnosis can be clinched with imaging techniques --
sialography and CT scanning.
The Salivary Gland Center (SGC) has found that the overall sialographic
pattern is essentially normal. Nevertheless, because of the increase
in parotid gland size and compression of the duct radicles by acinar
swelling, a relative sparsity and thinness of ducts are visualized
by the dye study. With CT scanning, a significant increase in parotid
density, representing parenchymal hypertrophy, is usually evident.
Conversely, late stage alcoholic patients show a decreased parotid
density due to increased fat content.
Treatment is directed at the more serious complications of alcoholism.
Some diminution in parotid swelling can be anticipated with abstinence
and improvement in liver function. Total resolution is not the rule.
The Salivary Gland Center (SGC) was developed because a void existed
in the diagnostic and comprehensive care of patients with salivary
gland problems and/or secretory dysfunction. Since the diversity
of these salivary conditions presents challenges to the clinician,
the SGC is available for referrals.
Louis Mandel, DDS
Director, Salivary Gland Center
(212) 305-9982
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