Page 31 - GP fall 2023

If a patient presents with bilateral parotid pression, and family history. This chronic
swelling, HIV will need to be ruled out, and disease leads to the consumption of great
the patient should be sent for further testing. quantities of alcohol that may eventually
There is a chance that the patient is unaware cause alcoholic hepatic cirrhosis (AHC) in
of the possible HIV infection since approx- some patients. The destruction of the hepat-
imately 20% of patients who are HIV posi- ic parenchyma and functions of bodily or-
tive do not know their status. gans are also compromised by AHC. A pa-
tient who suffers from alcoholism or AHC,
Sjögren’s syndrome can present with asymptomatic bilateral
Sjögren’s syndrome (SS) is a systemic auto- parotid swelling that is commonly accom-
immune disease of unknown etiology and is panied by xerostomia. Rhinophyma, facial
characterized by chronic inflammation and edema, jaundiced mucosa or skin, dilated
tissue damage of salivary glands and lacri- Figure 5. Sjögrens Syndrome. blood vessels and a red or flushed facial
mal glands, leading to sicca symptoms, such appearance are other clinical findings that a
as dry mouth and dry eye, associated with or cytomegalovirus (both human herpes dental professional should be aware of and
decreased secretion of saliva and tears. An viruses). It is thought that viruses may trig- observe.
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estimated 3 million people in the U.S. have ger an autoimmune response in susceptible
Sjögren’s syndrome and it occurs more of- individuals. Because of the combination of
ten in women (86%) than in men, with peak parotid swelling and associated xerostomia,
incidence occurring around age 50 years. oral healthcare providers are often the first
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to see patients with Sjögren’s syndrome.
Although parotid swelling is seen in most
patients with Sjögren’s syndrome, other
oral conditions, including xerostomia, can-
didiasis, root/cervical, and incisal/occlu-
sal caries, are often seen in these patients.
Accurate diagnosis of Sjögren’s syndrome
is essential as these patients need to be Figure 6. Alcoholism.
monitored. A small percentage of patients
with Sjögren’s syndrome will develop a Sialadenosis is non-neoplastic, non-in-
B-cell lymphoma. Typically, this only de- flammatory swelling of the salivary gland
velops after the patient has been living with in association with acinar hypertrophy and
Figure 3. Sjögren’s Syndrome. Sjögren’s for some time. It is a result of ductal atrophy. Sialadenosis presents as
Sjögren’s syndrome with gland inflamma- the B-cell infiltrate that surround the ducts non-tender swelling that is often bilateral
tion (resulting in dry eyes and mouth, etc.) making them both less capable of producing and symmetric. Sialadenosis is often asso-
that is not associated with another connec- saliva as well as creating a monoclonal pro- ciated with systemic metabolic conditions.
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tive tissue disease is referred to as primary liferation of the B-cells themselves. Blood A factor that may have contributed to the
Sjögren’s syndrome. Sjögren’s syndrome, tests for Sjögren’s should include antinu- more frequent observations of sialadenosis
which is also associated with a connective clear antibodies (ANA) which are present in conjunction with alcohol use may be re-
tissue disease, such as rheumatoid arthritis, in most patients. Other antibodies found in flective of the high prevalence of alcoholic
systemic lupus erythematosus, and sclero- most patients with Sjögren’s syndrome are liver disease among patients with cirrhosis.
derma, is referred to as secondary Sjögren’s SS-A and SS-B, also known as anti-Ro and
syndrome. Primary SS (pSS) is a chronic, anti-La, rheumatoid factor as well as thyroid
systemic autoimmune disease characterized antibodies. Other conditions such as anemia
by oral and ocular sicca complaints. Inflam- and abnormal sedimentation rates and levels
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mation of the salivary and lacrimal glands is of C-reactive protein may also be present.
a hallmark of the disease and plays a central Treatment is predominantly palliative. Top-
role in the current classification criteria. 9 ical fluoride is indicated for all patients as
well as non-fluoride remineralizing systems
which repair caries by enhancing fluoride
efficiency. Salagen or pilocarpine can be
used systemically to increase salivary out- Figure 7. Alcoholism.
put and tear production, although they both
have side effects since they can make the This has been estimated to be between 60
patient sweaty and uncomfortable. OTC and 70% in Western Europe and the United
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products can be effective, including sugar- States. Alcoholism and alcoholic cirrhosis
less gum and candy as well as sipping water became the most frequently cited predispos-
and using artificial saliva. ing factors for sialadenosis with incidence
Figure 4. Sjögrens Syndrome. estimates of 30–86%. Since alcohol is hep-
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Alcoholism atotoxic, this can cause malnutrition. The
With respect to potential etiologies, the Throughout the years, there has been an metabolism of alcohol leads to the forma-
consensus is that Sjögren’s is influenced by upward trend in alcoholism rates. Possible tion of acetaldehyde and other products that
both genetic and environmental factors, in- causes and contributing factors that can lead can cause fatty liver, cirrhosis with fibrosis,
cluding a history of a family member with to alcoholism are drinking at an early age, or acute inflammation (alcoholic hepatitis).
Sjögren’s or another connective tissue dis- stress, mental health problems, such as de- Thus, the impact of alcoholic cirrhosis on
ease or infection with Epstein Barr virus the development and progression of nutri-
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