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11 Sonography ofMajor Salivary Glands
239
parotid gland are pathognomonic B-mode criteria for
Sjögren’s syndrome, but they occur in only 40% of cases
[17]. Hypoechoic lesions can be scored by lesional diameter
(0= normal, homogeneous gland; 1=mild inhomogeneity,
hypoechoic areas of 2 mm; 2 = evident inhomogeneity,
hypoechoic areas of 2–6 mm; 3 = gross inhomogeneity,
hypoechoic areas of 6 mm; 4 = adipose degeneration of
gland, with adipose tissue echogenicity and parenchymal
atrophy (Fig.11.11) [21–23]. Grade 1 (mild affection) and
grade 4 (burned-out gland) can hardly be distinguished from
healthy glands (grade 0) by untrained physicians. The maximum diameter of the submandibular gland is often less than
e
Fig. 11.11 B-mode scoring in Sjögren’s syndrome ranging from normal parotid gland (PG) tissue (grade 0, a) through increasing inhomogeneity
(grades 1–3, b–d) to a hyperechoic, burned-out parotid gland (grade 4, e)
240
A. Knopf
3 centimeters (Fig.11.12). In addition, marked hypoechogenic
lesions (grade 3) cannot be distinguished from sarcoidosis,
MALT lymphoma, or HIV-induced lymphoepithelial lesions,
so open parotid gland biopsy is required in these cases [11,
16–18]. Strain elastography visualizes progressive hardened
glands, sometimes including soft cystic areas (Fig. 11.13)
[24]. Highly inammatory salivary glands show hypervascularity in CDS. Although literature reports sensitivity and
specicity higher than 90%, glandular assessment via
B-mode sonography, CDS, or strain elastography requires
great personal expertise [17, 24, 25]. Therefore, shear-wave
elastography was established as a diagnostic tool that reliably identies different disease stages in a quantitative man-
ner (Fig. 11.14), though it is not widely available and is
restricted to specialized centers. Shear-wave velocities
greater than 2.4m/s indicate Sjögren’s syndrome [17, 26].
Sarcoidosis
Sarcoidosis is a granulomatous disease that is based on a
dysfunction in T-cell regulation. The incidence in Caucasians
is estimated to be about 20–40 cases per 100,000 inhabitants.
Sarcoidosis affects patients in the second to fourth decade of
life and shows a balanced gender distribution. Lungs and
mediastinal lymph nodes are predominantly affected.
Cervical lymph nodes represent an extrathoracic hot spot
region [11, 18]. There are notable differences in the clinical
Fig. 11.12 B-mode sonography demonstrates downscaled subman-
dibular gland in grade 3–4 submandibular gland Sjögren’s syndrome
Fig. 11.13 Strain elastography in grade 3 Sjögren’s syndrome, visualizing hardened (red) submandibular gland tissue
Fig. 11.14 Shear-wave elastography in grade 3 parotid gland Sjögren’s
syndrome shows velocities higher than 2.4m/s
ab
11 Sonography ofMajor Salivary Glands
241
course of patients with pulmonary sarcoidosis compared
with their extrathoracic counterparts. Pulmonary sarcoidosis
is often incidentally diagnosed via chest x-ray and has a
chronic clinical course. Heerfordt’s syndrome represents
acute sarcoidosis. Although Heerfordt’s syndrome (syn.
Febris uveoparotid), which includes fever, parotitis, uveitis,
and facultative facial nerve palsy, is traditionally attributed to
the head and neck region, cervical and intra-parotideal lymph
node manifestations are the most frequent head and neck
symptoms in both acute and chronic sarcoidosis [11, 18].
Subsequently, B-mode ultrasound frequently diagnoses
enlarged cervical and intra-parotideal lymph nodes with
hilus hypervascularity in CDS (Fig. 11.15). In addition,
intraparenchymatous manifestations of the parotid in a submandibular gland occur in a minor proportion of patients.
B-mode criteria and CDS cannot distinguish these cases
from Sjögren’s syndrome or MALT lymphoma (Fig.11.15)
[11, 16–18]. In all cases, histological proof of granulomatous
inammation and subsequent clinical differential diagnosis
(e.g., tuberculosis) is mandatory.
IgG4-Associated Sialadenitis
Mikulicz-Radecki rst described systemic disease including
the lacrimal and submandibular glands in 1892. Later, a
hardened, indolent, and tumor-like submandibular gland was
described as Küttner’s tumor [27]. In 2001, Hamano et al.
demonstrated for the rst time increased serum IgG4 levels
in sclerosing pancreatitis [28]. Today, IgG4-associated diseases involve 14 organ systems, including lacrimal and salivary glands (Mikulicz syndrome, Küttner’s tumor) [29].
Interestingly, salivary gland manifestation has shown a
strong predilection for the submandibular gland; involvement of the parotid, sublingual, and minor salivary glands
are rare events [2, 3, 11, 17]. B-mode ultrasound usually
visualizes a downscaled submandibular gland with maxi-
mum diameter often less than 3cm. An intraglandular, irregular border and hypoechogenicity represent the B-mode
sonographic correlate of chronic inammation (Fig.11.16).
CDS shows irregular intralesional vascularity of the
hypoechoic region (Fig. 11.17). B-mode sonography and
CDS show signicant overlap with submandibular gland carcinoma, so diagnostic submandibulectomy represents the
surgical approach of choice [3].
11.2.3 Radiation-Induced Sialadenitis
Radiation-induced sialadenitis occurs in both transcutaneous
radiotherapy of head and neck cancer and radioiodine (
therapy of well-differentiated thyroid cancer [30, 31].
Fig. 11.16 B-mode sonography of IgG4-associated disease shows
irregular-bordered, hypoechoic lesions in the anterior part of the right
submandibular gland. mhm m. mylohyoideus, smg submandibular
gland
131
I)
Fig. 11.15 B-mode sonography of parotid gland sarcoidosis visualizes a large intra-parotideal lymph node with marked hilus structure (a) or a
parenchymatous manifestation with multiple echo-free areas (b). JA jaw angle, PG parotid gland
242
A. Knopf
Fig. 11.17 Corresponding color-coded duplex sonography of IgG4-
associated disease shows irregular intralesional vascularity
Fig. 11.18 B-mode sonography in acute radiation-induced sialadenitis
of the right parotid gland demonstrates diffuse glandular enlargement
and hypoechoic lesions. JA jaw angle
Fig. 11.19 B-mode sonography in chronic radiation-induced sialade-
nitis visualizes a downscaled and inhomogeneous right submandibular
gland
Fig. 11.20 Shear-wave elastography in chronic radiation-induced sial-
adenitis shows shear-wave velocities of the right parotid gland higher
than 2m/s
Transcutaneous radiotherapy with cumulative doses greater
than 30 gray causes permanent salivary gland dysfunction
from damage to epithelial and connective tissue elements
such as blood vessels, from direct damage of salivary acini
and ducts, or both [31, 32]. The
131
I accumulates in the salivary glands, giving rise to transient or permanent salivary
gland damage [30, 33]. Serous salivary tissue of the parotid
gland demonstrates particularly high sensitivity to transcuta-
131
neous
I radiation therapy. In acute sialadenitis, B-mode
ultrasound demonstrates enlarged salivary glands with diffuse hypoechoic inhomogeneity (Fig. 11.18). CDS shows
hypervascularized glandular tissue. However, chronic tissue
destruction occurs more often and can be seen as hyperechoic,
sclerosing, and down-scaled salivary glands (Fig. 11.19).
Strain elastogram shows salivary glands that are harder than
circumjacent tissue. More recently, acoustic structure quantication and shear-wave elastography were established to
reliably identify radiation-induced salivary damage. Shearwave velocities >2 m/s indicate chronic glandular tissue
destruction (Fig.11.20) [34–36].
11.2.4 Chronic Recurrent Parotitis
Chronic recurrent parotitis represents a nonobstructive parotitis that can be divided into juvenile and adult forms. The
etiopathogenesis is still unknown; dysontogenetic duct ectasia and autoimmune conditions are discussed. In nearly all
11 Sonography ofMajor Salivary Glands
243
patients, the condition becomes clinically apparent with a
painful, unilateral, or bilateral swelling of the parotid gland
after bacteria superinfection. B-mode ultrasound visualizes
hypoechoic and echo-free lesions, referring to intraparotideal lymph nodes and ductal ectasia (Fig. 11.21).
Peripheral hypervascularity occurs in acute bacterial superinfection (Fig.11.22). Strain elastography attributes the soft
tissue pattern to echo-free areas (Fig.11.23). More recently,
shear-wave elastography was suggested as reliable diagnostic tool for the assessment of disease severity and progression [37]. However, there is no ultrasonographic proof of
chronic recurrent parotitis, so a detailed history of the clinical course may be required for the diagnostic workup, and
differential diagnosis of lymphoepithelial lesions is necessary in the adult form.
11.3 Sialadenosis
Sialadenosis is dened as noninammatory and nonneoplastic swelling of major salivary glands. Underlying conditions range from dystrophic, endocrine, neurogenic, or
medication- associated conditions to anorexia or bulimia
[38]. There is no typical sonographic appearance. Mostly,
B-mode ultrasound visualizes a hyperechoic, slightly inhomogeneous, bilateral enlargement of the parotid glands
Fig. 11.21 B-mode sonography in chronic recurrent parotitis shows
multiple hypoechoic lesions in an enlarged right parotid gland. JA jaw
angle
Fig. 11.23 Strain elastography in chronic recurrent parotitis validates color-coded duplex sonography and visualizes avascular areas as soft (blue)
and vascularized hypoechoic areas as hard (red)
Fig. 11.22 Color-coded duplex sonography in chronic recurrent par-
otitis attributes hypoechoic areas to intra-parotideal lymph nodes with
hilus vessels and duct ectasia with peripheral vascularity. JA jaw angle
244
A. Knopf
Fig. 11.24 B-mode sonography of parotid gland sialadenosis shows
diffuse enlargement of the pre-auricular parotid gland, with regular
echotexture
(Fig. 11.24) [4]. A detailed history, clinical examination,
and laboratory testing are needed to exclude a broad variety
of chronic parotid gland diseases.
11.4 Duct-Associated Disease
11.4.1 Obstructive Sialadenitis
Stenosis and stricture of salivary ducts, as well as ductal
concrements (sialolithiasis), result in obstructive sialadenitis. Stenosis and stricture may be due to dysontogenetic,
posttraumatic, post-inammatory, and iatrogenic conditions; sialolithiasis represents the most important etiopathogenetic condition (Fig. 11.25) [39]. About 90% of
sialolithiasis affects the submandibular gland; concrements
of the parotid or sublingual glands occur infrequently.
Concrements can be diagnosed in the glandular hilus, in the
central part, and in the peripheral parts of the Wharton’s
and Stenson’s duct. The diagnostic setup in obstructive
sialadenitis comprises sonography, MR sialography, and
sialendoscopy [40]. Concrements larger than 2 mm can
usually be diagnosed via B-mode ultrasound, which has an
estimated diagnostic sensitivity of 94%, with 100% specicity [3, 41]. A history of digestion- associated swelling of
the affected gland with B-mode visualization of cortical
concrement reex, dorsal acoustic shadows, and pre-stenotic ductal dilatation validate the hypothesis of sialolithiasis (Fig. 11.26). Bacterial ascensus with subsequent
sialadenitis is frequently diagnosed (Fig.11.27). Intraductal
application of contrast enhancers and elastographic assessment is currently under consideration but is not part of a
standardized diagnostic approach [42, 43].
Fig. 11.25 Stenosis of Stenson’s duct papilla with proximal duct dila-
tation. JA jaw angle, MM masseter muscle
11.4.2 Duct Cysts
Salivary gland duct cysts are nonneoplastic lesions with an
epithelium lining inside, so they can therefore be differentiated from sialocele after facial injury [44]. True salivary
gland cysts are acquired as a result of ductal obstruction [44].
The vast majority of lesions originate in the main body of the
supercial parotid gland lobe or are associated with Stenson’s
duct (Fig.11.28). A substantial proportion of these parotid
gland cysts are diagnosed due to bacterial superinfection.
Dysontogenetic cysts show predilection for the sublingual
gland (ranula) and can be diagnosed by inspection of the
oor of the mouth (Fig.11.29). Some of these cysts exhibit
transcervical extension, perforating the mylohyoid muscle or
coiling its posterior border (Fig. 11.30). Cysts appear
hypoechoic or echo-free because of differences in liquid viscosity. Intralesional vascularization fails to be diagnosed in
CDS, but hypervascularization of the circumjacent tissue can
occur after inammation (Fig.11.31).
11.5 Neoplasms
The incidence of salivary gland tumors is estimated to be
about 40 cases per million inhabitants, representing 3% of all
head and neck neoplasms [45, 46]. Pleomorphic adenomas
and Warthin’s tumors (syn. cystadenolymphoma) are the
most frequent entities, but a variety of other benign lesions
are also reported [2, 45–48]. The vast majority of salivary
gland lesions originate in the parotid gland, but the relative
number of major salivary gland malignancies increases from
the parotid and submandibular glands to the sublingual gland
[46]. Salivary gland malignancy is estimated to be about nine
ab
11 Sonography ofMajor Salivary Glands
Fig. 11.26 (a) Proximal duct dilatation (arrows) due to distal sialolithiasis of the right submandibular gland. (b) Concrement shows cortical reex
with dorsal acoustic shadow
245
Fig. 11.27 B-mode ultrasound shows bacterial superinfection in sialoli-
thiasis of the left submandibular gland. Seen are diffuse glandular inhomogeneity with hypoechoic lymphatic septa, and a peripheral concrement
(C) with proximal duct dilatation (arrows). MHM—mylohyoid muscle
Fig. 11.29 B-mode ultrasound shows an intraoral echo-free lesion
(ranula). MHM mylohyoid muscle, SLG sublingual gland, SMG submandibular gland, T tongue
Fig. 11.28 B-mode sonography of an intra-parotideal duct cyst visual-
izes an echo-free lesion in the central part of the left parotid gland. JA
jaw angle
Fig. 11.30 B-mode ultrasound of a ranula with cervical extension
bypassing the mylohyoid muscle (MHM). SMG submandibular gland
246
A. Knopf
propriate standard deviation in the measured region of interest, causing value exclusion. Second, shear-wave velocities
are markedly higher than the measurement range of the ultrasound device [53]. In accordance with ndings in CDS,
CEUS demonstrates poorly microvascularized tumors
(Fig.11.32b, c) [52, 54, 56].
Miliary seeding of pleomorphic adenoma after surgical
intervention appears as tumor multilocularity in the submandibular triangle or the parotid region, including subcutaneous tissue and head and neck muscles. Tumors demonstrate
well-dened borders, a round or lobulated shape, and often
marked hypoechogenicity (Fig. 11.33). Tumor seeding is
often much wider than expected from the initial surgical
attempt (Fig.11.34).
Fig. 11.31 Corresponding color-coded duplex sonography validates
the ranula by demonstrating the avascularity of the echo-free lesion
cases per million inhabitants; mucoepidermoid carcinoma is
the most common primary cancer [2, 45, 47]. In contrast to
the submandibular and sublingual glands, the parotid gland
harbors lymph nodes, so it represents an organ of locoregional metastasis [2, 49]. Salivary gland lymphoma or other
malignancies occur infrequently [2].
11.5.1 Benign Tumors
Pleomorphic Adenoma
Pleomorphic adenomas are the most frequent tumor entity of
the major salivary glands. In contrast to Warthin’s tumors,
multilocularity in pleomorphic adenomas exclusively occurs
after prior parotid gland surgery, most likely linked to an iatrogenic rupture of the tumor’s pseudo-capsule [2]. The risk
of intraoperative tumor dissemination and the risk of malignant transformation highlight the necessity of reliable preoperative tumor identication in order to optimize treatment
regimens. B-mode ultrasound characterizes pleomorphic
adenomas as being sharply bordered and lobulated tumors
with moderate to strong acoustic enhancement [3, 45, 50,
51]. Echogenicity varies because of different extents of epi-
thelial and stromal components (Fig.11.32) [3, 45, 52–54].
CDS usually visualizes poor intralesional vascularization
(Fig.11.32b) [3, 45, 50, 52–54]. More recently, strain and
shear-wave elastography, as well as CEUS, have been used
to increase the preoperative identication and differentiation
of pleomorphic adenomas. Strain elastography shows a pleomorphic adenoma that is harder than the circumjacent glandular tissue (“dense core”) (Fig. 11.32a) [53, 55].
Interestingly, analysis of shear-wave velocities demonstrates
heterogeneous results, with a high rate of measurement dropout [53]. There are two explanations for these contradictory
results: rst, lesional tissue heterogeneity results in an inap-
Monomorphic Adenoma
Monomorphic adenomas represent a heterogeneous group of
salivary gland tumors. Warthin’s tumor is the most important
monomorphic adenoma, accounting for approximately the
half of all benign tumors [2, 57]. Today’s balanced distribution of pleomorphic adenoma and Warthin’s tumors refers
most likely to an increased patients’ age, nicotine abuse,
improved diagnostic applications, and a general demographic
change toward an older population [2, 57]. Interestingly,
Warthin’s tumor does not affect the sublingual or submandibular gland, but de novo unilateral or bilateral parotideal
multilocularity occurs in 5–10% of cases [2]. In addition, a
substantial proportion of Warthin’s tumors show an eccentric
growing pattern in level IIa that impedes the differentiation to
cervical lymph nodes or branchial cleft cysts [3, 58]. These
ndings refer to the hypothesis of an inclusion of glandular
cells in parotid gland lymph nodes during embryogenesis
[59–61]. Other histological subtypes of monomorphic adenoma, such as oncocytoma, basal cell adenoma, or myoepithelioma, occur infrequently [2]. However, pretherapeutic
differentiation might be of high clinical impact, because
oncocytoma and basal cell adenoma also demonstrate miliary
seeding after surgical rupture of the tumor capsule [2].
B-mode ultrasound visualizes a round, oval, or polycyclic
tumor with well-dened borders (Fig.11.35). Monomorphic
adenoma appears as a hypoechoic tumor with moderate to
strong acoustic enhancement (Fig.11.35a). Echo-free areas
occur in cystic parts of Warthin’s tumor. Complex cysts can
be seen due to septal segmentation [3, 52–54]. Monomorphic
adenoma usually shows peripheral and/or central hypervascularity, which can be validated with a fast and strong perfusion
in CEUS (Fig.11.35b, c) [52–54]. Particularly in Warthin’s
tumor, strain elastography shows soft and hard areas representing solid and cystic parts (“half and half”) (Fig.11.35a)
[53, 55]. Other monomorphic adenomas appear harder as the
circumjacent glandular tissue [53]. Sonographic ndings
after miliary seeding of basal cell adenoma and oncocytoma
are often similar to pleomorphic adenoma.
bc
11 Sonography ofMajor Salivary Glands
a
247
Fig. 11.32 (a) B-mode ultrasound of pleomorphic adenoma demon-
strates a hypoechoic intra-parotideal lesion with regular borders that
appears hard (red) in strain elastography. (b, c) Hypovascularity and
hypoperfusion are visualized in color-coded duplex sonography and
contrast-enhanced ultrasound. The white line outlines the parotid gland;
the red line indicates the tumor
Fig. 11.33 B-mode sonography of miliary seeding of pleomorphic
adenoma. Hypoechoic tumors (arrows) originated in the subcutaneous
tissue after parotidectomy. MM masseter muscle
Fig. 11.34 Coronal magnetic resonance (MR) tomography of miliary
seeding of pleomorphic adenoma
248
bc
A. Knopf
a
Fig. 11.35 (a) B-mode ultrasound of Warthin’s tumor demonstrates a
hypoechoic intra-parotideal lesion with regular borders that appears
with hard (red) and soft (blue) areas in strain elastography. (b, c)
11.5.2 Malignant Tumors
Hypervascularity and hyperperfusion are visualized in color-coded
duplex sonography and contrast-enhanced ultrasound. The white line
outlines the parotid gland; the red line indicates the tumor
metastasis in recent decades is likely the result of the
increased elderly population and failure to recommend elec-
Primary andSecondary Epithelial Malignancy
Carcinomas of major salivary glands occur infrequently,
with an incidence estimated to be about nine cases per million inhabitants [2, 45, 47]. The broad variety of salivary
gland carcinomas comprises 24 histological subtypes listed
by the World Health Organization (WHO). Cancer of the
parotid gland represents almost 15% of all parotid gland
lesions and can be divided into primary carcinoma and secondary carcinoma (intra-parotideal lymph node metastasis)
[2]. Lymph node metastasis most commonly involves cutaneous malignancy, such as squamous cell carcinoma, malignant melanoma, and Merkel cell carcinoma [62, 63]. A
dramatic increase of metachronous intra-parotideal
tive parotidectomy and neck dissection in cases of cutaneous
squamous cell carcinoma [2, 64]. The proportions of primary
carcinomas increase from about 20% for the parotid gland to
about 50% for the submandibular gland and about 95% for
sublingual glands [65]. Mucoepidermoid, adenoid cystic,
acinic cell, and adenocarcinoma, as well as carcinoma ex
pleomorphic adenoma are the most common histological
subtypes [2, 65]. The clinical appearance differs dramatically between different histological subtypes. Whereas a
minor proportion of low-grade mucoepidermoid, myoepithelial, or adenoid cystic carcinomas exhibit lymph node metastases, lymph node positivity is frequently diagnosed in
high-grade mucoepidermoid carcinoma and carcinoma ex