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14 • Salivary Gland Disease
BA
223
C D
Fig. 14.4 Pleomorphic adenoma of the parotid gland. (A) Axial ultrasound image of a pleomorphic adenoma in the tail of parotid. The lesion is hypoechoic with posterior acoustic enhancement. Skin surface is at the top. (B) is the corresponding magnetic resonance image. (C) is the macroscopic
appearance of a pleomorphic adenoma removed by superficial parotidectomy. Note that in life the adenoma is soft and fluid but after fixation it has a
glistening cream white surface). (D) is the corresponding digital microscopy image.
pleomorphic adenoma and so the only acceptable biopsy is
a superficial parotidectomy (Fig 14.4). This will ensure removal of the tumour together with a surrounding margin
of normal tissue. Fine-needle aspiration or needle core biopsy is acceptable and is without the risk of implantation of
malignant cells in the needle tract. Frozen section may be
useful at surgery for tumours in the parotid gland that are
thought likely to be malignant, to establish whether the facial nerve may be preserved.
OBSTRUCTIVE SALIVARY DISORDERS
Obstructive salivary disease can be acute or chronic. The
clinical features are characteristically pain and swelling of
the affected gland just before meals. Astringent stimuli produce severe symptoms. Sometimes the swelling slowly subsides as saliva leaks past the obstruction, and a bad taste is
suggestive of associated sialadenitis (Fig. 14.5).
Extra-ductal Obstruction
Extra-ductal obstruction is caused by disease outside the
14.3 Salivary Gland Disorders
duct wall. The most important cause is neoplasia, particularly squamous carcinoma in the floor of the mouth or salivary neoplasms. Trauma may also lead to displacement of
LEARNING OBJECTIVE
You should:
• know the features, investigations and management of
salivary gland disorders.
soft or hard tissue, resulting in duct obstruction.
Duct Wall Thickening
Duct wall obstruction may be related to fibrosis, leading to
stricture. The orifices can become stenosed through trauma
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A
Fig. 14.5 An obstructive and infected swelling of the left parotid gland. (A) Extra-oral view showing redness and swelling; (B) intra-oral view showing
mucopurulent saliva.
B
(gonadal swelling) occurs in around 20% of affected adult
males. Diagnosis is made on clinical grounds and bed rest is
advised. As the disease occurs in minor epidemics, infected
persons should avoid contact with those at risk. Virus is
present in the saliva when symptoms commence and
remains for approximately 6 weeks. One episode usually
confers lifelong immunity.
Bacterial Sialadenitis
Acute bacterial sialadenitis principally involves the parotid
glands and is caused by bacteria entering the ductal system
against the salivary flow. Reduced flow is a common predisposing factor and is a feature of many conditions, including
chronic sialadenitis, Sjögren’s syndrome and unwanted effects of drugs. Streptococcus pyogenes, Staphylococcus aureus,
Fig. 14.6 A submandibular calculus in the oral cavity.
Haemophilus species, black-pigmented bacteroides and other
oral bacteria may be detected in mucopurulent discharge
from the duct opening, which is an important clinical sign.
It is accompanied by swelling, pain, fever and erythema of
from dentures or teeth. Rarely, intra-ductal papillomas arise
from the duct wall and obstruct the lumen.
Intra-ductal Obstruction
Salivary calculus is the most common type of obstructive
the overlying skin. Treatment is by antibiotic therapy and
gentle massage to encourage flow. Warm, salty mouthrinses
may be helpful, and patients should be advised against placing a hot-water bottle over the gland as this may lead to a
pointing abscess.
disorder (Fig. 14.6). The submandibular gland is most frequently involved (around 80% of cases), followed by parotid
and, rarely, minor glands. The calculi (sialoliths) tend to be
hard, yellowish and often have a lamellated, concentricring structure. They are composed of calcium phosphates,
thought to be nucleated on microcalculi, which are
commonly found in the major and minor glands. Salivary
calculi may form in ducts within the gland substance.
CHRONIC SIALADENITIS
Bacterial Sialadenitis
Chronic bacterial sialadenitis is related to low-grade bacterial invasion through the duct system and often follows
chronic obstructive disease. The submandibular salivary
gland is most commonly affected. Typically, there is recurrent, painful swelling associated with eating or drinking.
ACUTE SIALADENITIS
Viral Sialadenitis
Viral sialadenitis (mumps) is an acute contagious infection
caused by a paramyxovirus. Spread is caused by direct contact with infected saliva and by droplets. There is a 2–3 week
incubation period, and fever and malaise are followed by
sudden, painful swelling of one or both parotid glands. In
adults, viraemia results in involvement of internal organs
such as the central nervous system and gonads. Orchitis
The duct orifice appears inflamed and a mucopurulent discharge may be seen on examination. Patients may complain of a salty or foul taste in the mouth. The gland may
become firm and fibrotic at the end stage. Pathologically
there may be duct ectasia, mucous metaplasia of duct epithelium, periductal fibrosis and elastosis, acinar atrophy
and a chronic inflammatory infiltration (Fig. 14.7). Interlobular fibrosis results in fusion of the lobules. Surgical removal is indicated in intractable disease. On sialograms,
there are combinations of sialectasis (ductal dilatation),
14 • Salivary Gland Disease
225
Fig. 14.7 Chronic sialadenitis of the parotid gland. There is acinar atro-
phy, fibrosis within the between the lobules and chronic inflammatory
infiltration.
Fig. 14.8 Chronic sialadenitis. The main duct has a reasonably normal
diameter and course, but beyond the point of junction with an accessory gland (seen passing vertically upwards from the main duct), the
gland is abnormal. The ducts are dilated and there is some atrophy of
the peripheral ducts. A filling defect is visible centrally, indicating the
presence of a substantial mucus plug or calculus.
strictures, filling defects with calculi or stagnant secretions
and atrophy of minor salivary ducts (Fig. 14.8). In
advanced disease, large abscess cavities may form.
Relapsing Parotitis
Relapsing (recurrent) parotitis is an uncommon disorder
affecting children and sometimes adults. Typically, sialography shows normal main ducts but punctate sialectasis
peripherally. Some cases are bilateral, suggesting a congenital duct abnormality or tendency to reduced flow.
Radiation Sialadenitis
Radiation sialadenitis occurs mostly after radiotherapy,
particularly when given for head and neck cancers. There is
acinar damage and progressive fibrous replacement. Depending on dose, some recovery may be seen. The glands
are shielded where possible to avoid this unwanted effect
and techniques such as intensity modulated radiotherapy
Fig. 14.9 A patient with radiation-related dry mouth, showing cervical
carious lesions, demineralization of enamel and thick mucinous saliva.
Fig. 14.10 Immunohistochemical preparation of IgG4 sialadenitis.
Concentric fibrosis is present and IgG4 positive plasma cells are stained
dark brown.
(IMRT) can be used to direct radiation and spare salivary
glands. Saliva is often thick and frothy on examination and
there is a risk of periodontal disease, enamel demineralisation and dental caries, particularly cervical caries, developing if preventive advice is not given (Fig 14.9). See Sjögren’s
syndrome for treatment of dry mouth.
Chronic Sclerosing Sialadenitis
This disorder presents as a firm tumour-like mass affecting
the submandibular gland. There are increased numbers of
IgG4-secreting plasma cells in the gland parenchyma.
Dense swirling fibrosis and scattered eosinophils are typically also present. The disorder may be bilateral and is often
part of a generalised disorder called IgG4 disease that can
affect the pancreas and other organs (Fig 14.10).
Sarcoidosis
Bilateral parotid swelling may be caused by chronic granulomatous inflammation, as part of the multisystem disorder
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sarcoidosis. Confluent sheets of non-caseating granulomas
(aggregates of macrophages) are found in the gland parenchyma. The lacrimal glands may be involved, resulting in
dry eyes and mouth. Diagnosis may be made by needle core
biopsy and estimating serum angiotensin converting
enzyme levels. Referral to a physician is necessary as pulmonary lesions may be present and systemic immunosuppressive therapy may then be indicated.
Sialosis
Also known as sialadenosis, this condition is characterised by
recurrent bilateral swelling of the salivary glands, most often
the parotids. Sialosis is a non-inflammatory and non-neoplastic
disorder, probably due to abnormality of neurosecretory control. A number of underlying disorders may be present including liver cirrhosis, alcoholism, eating disorders, malnutrition,
drug therapy and hormonal abnormalities. Microscopically,
the acinar cells show hypertrophy and the cytoplasm is packed
with prominent zymogen granules.
SJÖGREN’S SYNDROME
Sjögren’s syndrome is an autoimmune chronic inflammatory
disease involving the salivary and lacrimal glands. It is characterised by polyclonal B-cell proliferation, probably as a
result of loss of T-cell regulation. There is lymphocytic infiltration and destruction of glandular parenchyma (Fig. 14.11).
Sjögren’s syndrome can have widespread manifestations and
is classified into:
n
primary Sjögren’s syndrome: association of dry mouth
and dry eyes
n
secondary Sjögren’s syndrome: association of either dry
mouth and/ or dry eyes and a systemic disorder.
There is some overlap between the two forms, though in
general oral and ocular dryness is more severe in primary
Sjögren’s syndrome. Widespread symptoms may be experienced in both types, including nasal and vaginal dryness,
dysphagia and dry skin. Fatigue syndrome is commonly
present. Autoimmune connective tissue diseases that may
Box 14.1 Autoimmune Diseases in
Secondary Sjögren’s Syndrome
n
Rheumatoid arthritis
n
Systemic lupus erythematosus
n
Progressive systemic sclerosis
n
Primary biliary cirrhosis
n
Mixed connective tissue disorder
be associated with secondary Sjögren’s syndrome are given
in Box 14.1. Rheumatoid disease (arthritis) is the most
commonly associated disorder.
Clinically, middle-aged females are most commonly affected, though Sjögren’s syndrome may occur in childhood.
Sjögren-like features can be seen in other T-cell dysfunctions including HIV infection, therapeutic immunosuppression and graft-versus-host disease. Patients often complain
of difficulty in eating dry foods and the tongue adhering to
the palate. Symptoms are usually worst during the night
and sleep may be disturbed. Difficulty in swallowing, speaking and wearing dentures may be experienced. The oral
mucosa appears glazed and the tongue may become lobulated and beefy-red. Oral candidiasis is common and there
may be patches of erythema or even ulceration. The major
salivary glands may be enlarged. Sudden expansion may be
a result of obstruction, acute infection or transformation to
malignant lymphoma.
Diagnosis
Sjögren’s syndrome is a clinical diagnosis and a number of
investigations may aid in diagnosis. The sensitivity, specificity, clinical utility and costs of laboratory and clinical tests
should be considered, particularly if results do not affect
management.
Estimation of salivary flow (sialometry test) and lacrimal
flow (Schirmer test; Fig. 14.12) are inexpensive simple tests.
Autoantibodies against extractable nuclear antigens (ENA) are
most commonly present and of these, Ro (SS-A) is the most
specific in terms of diagnosis of Primary Sjögren’s syndrome.
Fig. 14.11 Histopathological section of a labial gland biopsy in a patient
with Sjögren’s syndrome showing focal lymphocytic sialadenitis.
Fig. 14.12 Schirmer’s test.
Box 14.2 Diagnosis of Primary Sjögren’s
Syndrome (American College of
Rheumatology [ACR] and European League
Against Rheumatism [EULAR] Classification
Criteria 2016)
Inclusion Criteria
A positive patient response to at least one of five questions:
1. Have you had daily, persistent, troublesome dry eyes for more
than 3 months?
2. Do you have a recurrent sensation of sand or gravel in the
eyes?
3. Do you use tear substitutes more than three times a day?
4. Have you had a daily feeling of dry mouth for more than
3 months?
5. Do you frequently drink liquids to aid swallowing dry food?
Classification Criteria
Total score must be greater or equal to 4
A focus score greater or equal to 1 in a minor salivary gland
biopsy. A focus is defined as an agglomerate of at least
50 mononuclear cells; the focus score is defined by the
number of foci in a 4mm
Antibodies to Ro (SSA). Score 53
Ocular staining score greater or equal to 5 (or van Bijsterfeld
score greater or equal to 4) in at least one eye. Score 51
Schirmer test less than or equal to 5 mm/5 min on at least one
eye. Score 51
Unstimulated whole saliva flow rate less than or equal to 0.1 mm/
min. Score 51
Exclusion Criteria
Past head and neck radiation treatment, acquired immune
deficiency syndrome, sarcoidosis, amyloidosis, graft-versus-
host disease, active hepatitis C, use of anticholinergic drugs
2
area of glandular tissue. Score 53
14 • Salivary Gland Disease
Fig. 14.13 Digital subtraction sialogram in Sjögren’s syndrome. This
patient has fairly classic radiological appearances in the parotid gland.
The main ducts are fairly normal (although the main duct anteriorly is
slightly dilated), but a striking feature is the presence of numerous
small collections of contrast medium (‘snowstorm’) overlying the
gland.
227
Other autoantibodies may be detected by arranging a panel of
tests, as determined by evidence-based laboratory medicine.
Tests that may be utilised for the diagnosis of Sjögren’s syndrome are shown in Box 14.2. Sialographically, the classic
features are varying degrees of punctate and globular sialectasis with fairly normal main ducts. However, secondary
obstruction and infection means that changes often become
similar to chronic sialadenitis (Fig. 14.13). Ultrasound exami-
nation of the salivary glands is increasingly used for the diagnosis of Sjögren’s syndrome (Fig 14.14).
In those cases where other investigations yield insufficient
evidence to confirm the diagnosis, labial gland biopsy is used
to provide a histopathological diagnosis of Sjögren’s syndrome. Infiltration of lymphocytes around intralobular
ducts may be present resulting in focal lymphocytic sialadenitis. In major glands, progressive lymphocytic infiltration
is accompanied by acinar destruction and proliferation of
residual ducts resulting in epimyoepithelial islands. Extensive change of this type results in a salivary lymphoepithelial lesion (SLEL) which in some cases progress to lymphoma.
Management
Sjögren’s syndrome is generally managed by a multidisciplinary team. Dry mouth can be treated by:
n
salivary stimulants if there is residual salivary function,
such as chewing sugar-free gum, sucking specially
Fig. 14.14 Ultrasound image of typical Sjögren’s syndrome showing
heterogeneous hypoechoic foci.
formulated sugar-free pastilles (e.g., Salivix) or tablets
(e.g., saliva-stimulating tablets); sweets must be avoided
because of the high caries risk
n
saliva substitutes: these fall into three main groups:
n
carboxymethylcellulose based (e.g., Saliveze)
n
mucin based (e.g., Saliva Orthana)
n
gels containing enzymes normally present in saliva
(e.g., BioXtra or Biotene oral balance)
n
preventive advice relating to the high risk of caries and
periodontal disease; in dentate individuals, the use of
toothpaste containing 5000 ppm fluoride or a fluoride
mouthwash may be recommended
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n
where xerostomia is severe but residual salivary gland
function is present on stimulation, pilocarpine may be of
benefit in radiation-induced xerostomia and Sjögren’s
syndrome.
Many patients find that dry mouth symptoms are worst
at bedtime and on waking because the oral tissues tend
to stick together and the mouth feels unpleasant. Longeracting gels such as Oral Balance gel are often useful for
patients with these symptoms.
SYSTEMIC DISORDERS AND SALIVARY FUNCTION
Numerous medications, including many over-the-counter
drugs, produce dry mouth as an unwanted effect. The more
likely types to cause dry mouth are certain drugs used to
treat depression, high blood pressure and anxiety, as well as
antihistamines, decongestants, muscle relaxants and pain
medications. Increasing dry mouth is also associated with
aging and may be related to a reduced ability to excrete
drugs. Dosage may need to be reviewed or prescription of
an alternative which does not have dry mouth as a side effect discussed with the patient’s physician. Recreational
drug use (e.g., marijuana) is also a cause of dry mouth.
Methamphetamine use can cause severe dry mouth and
damage to teeth.
Dry mouth can be due to poor nutrition, diabetes, stroke,
dementia, nerve damage and can be a feature of cystic
fibrosis. Snoring and mouth breathing also can contribute
to dry mouth. Drinking alcohol and smoking or chewing
tobacco can increase dry mouth symptoms. Anxiety can
also reduce salivary flow.
Hypersalivation and drooling can be distressing conditions. Temporary hypersalivation may be caused by infection, gastroesophageal reflux, pregnancy, medications and
exposure to toxins, such as mercury. Chronic hypersalivation
is most often caused by conditions of disordered muscle control that affect ability to swallow, leading to saliva build-up.
Hypersalivation may be seen in association with macroglossia, cerebral palsy, facial nerve palsy, Parkinson’s disease,
amyotrophic lateral sclerosis and stroke. Drug and surgical
options may be used to treat hypersalivation in some cases.
SALIVARY GLAND TUMOURS
Salivary tumours account for around 3% of human tumours but malignancy is comparatively rare. Most arise in
the parotid gland, where around 90% of tumours are benign adenomas and only 10% are malignant. There is a
higher relative proportion of malignant tumours in the submandibular and minor salivary glands; for example, around
45% of salivary neoplasms arising in the palate (Fig. 14.15)
prove to be malignant.
Many histopathological types have been classified and
their clinical behaviour is variable (Box 14.3). Only the
most common types are described.
Benign Tumours
Pleomorphic Adenoma
Pleomorphic salivary adenoma is the most commonly encountered neoplasm, accounting for around 80%–90% of
Box 14.3 Principal Types of Salivary Tumour
Adenomas
Pleomorphic adenoma
Warthin’s tumour
Canalicular adenoma
Basal cell adenoma
Oncocytoma
Carcinomas
Mucoepidermoid carcinoma
Acinic cell carcinoma
Adenoid cystic carcinoma
Polymorphous adenocarcinoma
Epithelial-myoepithelial carcinoma
Salivary duct carcinoma
Basal cell adenocarcinoma
Carcinoma ex pleomorphic adenoma
Oncocytic carcinoma
Adenocarcinoma NOS
Soft Tissue Tumours
Sialolipoma
Haemangioma
A BB
Fig. 14.15 (A) A mucoepidermoid carcinoma arising in the palate, showing prominent vasculature over the surface of a rubbery swelling. (B) Microscopic
appearance of a low grade muco-epidermoid carcinoma, showing squamous and mucous differentiation.
14 • Salivary Gland Disease
229
all salivary tumours. In the major salivary glands, they
present as slow-growing, painless nodules, often detected
on routine extra-oral examination or palpation. The nodule
can be soft or firm in texture and is freely moveable. In the
minor glands, pleomorphic adenoma typically presents as
a rubbery nodule, principally in the palate and upper lip
submucosa (Fig 14.16). Palatal lesions may be secondarily
ulcerated.
Suspected pleomorphic adenomas are normally biopsied
prior to excision with a margin of normal tissue. The
adenomas are variable in appearance microscopically but
are distinctive in having characteristic cellular and stromal
Fig. 14.16 A pleomorphic adenoma arising in a minor salivary gland at
the junction of the hard and soft palate.
elements. The cellular component is of ductal epithelial and
myoepithelial cells, and these are arranged in sheets and
strands (Fig 14.17A). Ducts may form and sometimes squamous differentiation is present. The stromal component is
rich in proteoglycans and can be organised as loose (myxoid) tissue or cartilage-like (chondroid) tissue; both types
may be present (Fig 14.17B). An important pathological
feature to be aware of is that a pseudocapsule of compressed fibrous tissue forms around pleomorphic adenoma
(Fig 14.17C). Islands of tumour cells may extend beyond
the capsule and “shelling out” the adenoma in the past led
to multifocal recurrence. Extracapsular dissection with or
without removal of adjacent salivary parenchyma is most
often used to treat pleomorphic adenoma, and multifocal
recurrence is rare, only occurring if the pseudocapsule is
ruptured during surgery.
Warthin’s Tumour
Warthin’s tumour affects predominantly older men and
arises almost exclusively in the parotid. Approximately
10% of cases are bilateral and the tumour presents as a
discrete nodule, rarely exceeding 3 cm in diameter. Macroscopically Warthin’s tumour has a characteristic tan-grey
multicystic appearance on sectioning in the pathology
laboratory (Fig. 14.18A). Microscopically, these tumours
have a papillary cystic structure comprising double layered, eosinophilic ductal cells supported by a lymphoid
stroma (Fig 14.18B). Smoking is known to be an important aetiological factor and may affect mitochondrial
biology resulting in oncocytic hyperplasia of the ductal
epithelium.
AA BB
CC
Fig. 14.17 Microscopic features of pleomorphic adenoma. (A) shows a
cellular area with ductal differentiation, (B) shows myxochondroid
stroma (left) and cellular areas (right), (C) shows the pseudocapsule that
adjoins salivary parenchyma (top).
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Fig. 14.18 Macroscopic and corresponding digital pathology image of
a Warthin’s tumour.
Acinic-Cell Carcinoma
The acinic-cell carcinoma is uncommon. It shows differentiation towards salivary acinar cells; it is generally low
grade but can undergo high-grade transformation.
Secretory Carcinoma
This tumour has similarities to acinic cell carcinoma and
was only included in the WHO classification is recent years.
It is mostly a low-grade cancer that can be successfully
treated by local excision with a margin but high-grade
transformation has been described. The neoplasm has a
characteristic gene fusion, ETV6-NTRK3 or rarely ETV6RET and molecular testing is required for diagnosis.
Polymorphous Adenocarcinoma
Typically, polymorphous adenocarcinoma occurs on the
posterior palate. It is a mostly a low-grade malignant tumour with a good prognosis despite its infiltrative growth
pattern and tendency to swirl around nerves. It can also
occur in the tongue where some cases behave in a more aggressive way and show a cribriform architecture.
Other Adenomas
Other adenomas with varying patterns arise. These include basal cell, canalicular, trabecular and oncocytic
types. Treatment is the same as for pleomorphic adenoma.
Canalicular adenoma is most common in the upper lip and
can be multifocal.
Soft Tissue Salivary Tumours
Benign fatty tumours may arise in the salivary gland and
those that contain salivary parenchyma are known as
sialolipoma, though conventional lipomas, peripheral
nerve tumours and haemangiomas may occur, particularly
in the parotid gland.
Malignant Tumours
Outcome in malignant salivary gland tumours depends
on histological type and grade as well as stage. Advanced
malignant tumours with extensive spread or metastasis
have a far worse prognosis than early-stage tumours.
Adenoid Cystic Carcinoma
Adenoid cystic carcinoma affects middle-aged or elderly
patients and accounts for around 30% of minor gland tumours. It is slow growing but may cause pain, palsy or
paraesthesia because of its particular tendency to invade
and spread along nerve pathways. Histopathologically, it
shows a Swiss-cheese appearance owing to microcysts
filled by basement membrane material. Small, darkly
staining cells with indistinct outlines are typical. It is infiltrative; metastasis develops as a late event and it has a poor
long-term prognosis. It is treated by surgery, often with
adjuvant radiotherapy (Fig 14.19).
Mucoepidermoid Carcinoma
Mucoepidermoid carcinoma affects younger and middleaged patients and it accounts for around 5% of minor gland
tumours. Histopathologically, it shows mucous, squamous
and intermediate differentiation (Fig. 14.15). Clinically, it
shows a range of clinical behaviour, from low-grade to
highly malignant types.
Carcinoma Arising in Pleomorphic Adenoma
Carcinomas can arise in longstanding pleomorphic adenomas.
The carcinoma can be intracapsular or minimally invasive, in
which case the tumour is managed clinically as a conventional
pleomorphic adenoma. However, when the carcinoma component invades the salivary parenchyma, the tumour is regarded
as frankly malignant. High grade carcinoma of salivary duct or
undifferentiated type is most common in invasive carcinoma
arising in pleomorphic adenoma and then the prognosis is the
worst of all salivary tumours. Treatment may involve resection,
neck dissection and chemoradiotherapy. Any of the malignant
salivary tumour types may arise in pleomorphic adenoma and
mixed patterns are also encountered.
Other Carcinomas
Salivary duct carcinoma, basal cell adenocarcinoma, sebaceous carcinoma, myoepithelial carcinoma, epimyoepithelial carcinoma and other rare types of carcinoma occur.
Prognosis depends on the type, grade and stage.
Other Malignant Tumours
Salivary glands can also develop malignant melanoma,
lymphoma (sometimes arising in Sjögren’s syndrome), metastases, myoepithelial tumours and rare types.
Molecular Pathology of Salivary Glands
In recent years, it has been discovered that many salivary tumours have characteristic gene fusions or alterations and
these are now used in routine diagnosis (Table 14.1). Accurate
diagnosis of salivary tumours is based on morphology, but
histochemistry, immunohistochemistry and molecular techniques are also useful for rare or problematic cases. Genomic
sequencing can be used in advanced and metastatic salivary
cancer to identify targets for chemotherapy.
Salivary Gland Cysts
The most common salivary cysts occur in the minor salivary glands as a result of trauma. They present as blue,
fluctuant swellings, which typically have a relapsing history. There are two types.
14 • Salivary Gland Disease
231
A
C
C D
Fig. 14.19 (A) Ultrasound Doppler image of adenoid cystic carcinoma of midline of palate. Colour corresponds to blood flow in the position of the
greater palatine foramen. (B) Corresponding axial magnetic resonance image to Fig. 14.19A showing an adenoid cystic carcinoma in the midline palate.
(C) Adenoid cystic carcinoma showing the “Swiss cheese” appearance. The cells have angular hyperchromatic nuclei and enclose microcysts filled by
basement membrane material. (D) A section of the facial nerve invaded by adenoid cystic carcinoma. From Anita Sengupta, Jackie Brown, Meena
Rudralingam: The use of intraoral ultrasound in the characterization of minor salivary gland malignancy: report of two cases, Vol 45(4), https://doi.org/10.1259/
dmfr.20150354
D
B
Mucous Extravasation Mucocoele
Table 14.1 Molecular Pathology of Salivary
Gland Disease
Salivary Tumour Molecular Pathology
Acinic cell carcinoma NR4A3 upregulation
Adenoid cystic carcinoma MYB-NFIB, MYB1-NFIB fusion
Hyalinising clear cell
carcinoma
Mucoepidermoid carcinoma CRTC1-MAML2, CRTC3-
Polymorphous adenocarcinoma PRKD1 fusions and
Salivary duct carcinoma HER2 amplification, NCOA4-
Secretory carcinoma ETV6-NTRK3, ETV6-RET
EWSR1-ATF1 fusion
MAML2, EWSR1-POU5F1
mutations, PRKD2 and
3 changes
RET, TRIM27-RET fusion
This is the most frequent type, and it occurs in the lower
labial mucosa (Fig. 14.20), buccal mucosa and rarely at
other sites. Trauma results in tearing of the duct, with leakage of saliva into the connective tissue. A granulation
tissue capsule forms and mucin-filled, foamy macrophages
are typically seen in the cyst fluid. Chronic inflammatory
infiltration is usually seen also.
Mucous Retention Mucocoele
This type occurs less frequently and tends to be found in the
upper labial mucosa. Trauma results in duct stricture and
then expansion, forming a cyst lined by ductal epithelium.
The cyst contains clear saliva, with minimal inflammatory
or macrophage reaction.
Bilateral and multiple lymphoepithelial parotid cysts can
be a feature of HIV infection. The cysts occur early in
HIV disease and are not typically seen in advanced AIDS.
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Fig. 14.20 A mucous extravasation mucocoele arising from minor
glands in the lower labial mucosa.
Surgical removal of minor salivary glands is the treatment
of choice for mucous extravasation and retention cysts and
tumours. Surgery of the major salivary glands is carried
out when there is neoplastic disease, obstruction and sometimes in inflammatory disease.
MINOR SALIVARY GLANDS
Excision of a cyst with associated glands and duct may be
undertaken under local anaesthesia. Swellings thought to
be tumours because of their history, site and appearance
require wider excision. Ranulae (mucocoeles arising from
the sublingual gland) should be excised together with the
associated lingual gland. If large in size, then this may be
more readily performed under general anaesthesia.
Cryosurgery, in which sub-zero cooling is used to destroy
tissues, may be used to remove small cysts. The probe of a
liquid nitrogen apparatus is placed on the cyst for two to five
cycles of about 30 seconds at 2100° C. The extreme cold
results in an acute inflammatory response and tissue damage. The technique, which is very simple to use, results in
significant postoperative swelling but excellent healing
without a surgical scar. The disadvantage is that there is no
histopathological examination. Cryosurgery may also be
used for small vascular lesions such as haemangiomas.
Fig. 14.21 Ranula arising in the right floor of the mouth from the sublingual gland.
Diagnosis is based on fine-needle aspiration and imaging.
No intervention is normally required but if lymphomatous
infiltration is suspected, surgical excision may be performed.
Ranula
Mucous cysts arising from the sublingual gland can form in
the floor of the mouth where they are known as a ranula
(Fig 14.21). Rarely the cyst may track down through mylohyoid to produce a swelling in the submandibular area,
known as a plunging ranula (see Chapter 13).
14.4 Surgery
SUBMANDIBULAR SALIVARY GLAND
Surgical removal of a calculus from the anterior part of the
duct of the submandibular salivary gland may be undertaken under local anaesthesia. A suture is placed about the
duct behind the calculus to prevent it moving back into the
gland and then the duct is dissected and opened via an intra oral approach. The calculus is removed and the duct sutured
open to prevent stricture. Should the calculus be sited more
proximally, then removal of the gland may be necessary. In
the case of surgical removal of the submandibular gland for
this or another reason, the patient is advised of the following
risks of the operation:
n
Possible facial nerve damage resulting in weakness of
the lower lip.
n
Possible lingual nerve damage resulting in lingual
paraesthesia.
Surgical removal of the submandibular gland is undertaken under general anaesthesia with the patient supine and
the head turned to the opposite side and extended. The skin
is prepared and the submandibular incision made 2.5 cm
below the mandible to avoid the facial nerve (Fig. 14.22).
During dissection, vessels are identified and ligated before the
gland is removed. A vacuum drain is placed to minimise haematoma formation and the wound is closed with sutures.
An alternative to surgery for calculus removal is radiologically guided retrieval of the calculus through the duct
orifice using a basket retrieval catheter. This works best
with small, freely moving calculi.
LEARNING OBJECTIVE
You should:
• know the principles of surgery to remove salivary
glands.
PAROTID SALIVARY GLAND
A calculus in the anterior part of the parotid salivary duct
may be removed by an intraoral approach under local anaesthesia, again with a suture placed behind to prevent the