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Benign salivary gland tumor

Updated 2026-10-05 Suggest an edit

Overview and definition

Benign salivary gland tumors are a heterogeneous group of neoplasms arising from the epithelial components of major and minor salivary glands.[1][2] They account for approximately 80% of all salivary gland neoplasms.[2][3] Pleomorphic adenoma is by far the most common, representing roughly 60–70% of all salivary gland tumors, followed by Warthin tumor.[1][3][4] The remaining benign subtypes—basal cell adenoma, canalicular adenoma, oncocytoma, myoepithelioma, cystadenoma, and ductal papillomas—are individually uncommon to rare.[1][5] These tumors arise from the intercalated duct reserve cell or myoepithelial cell and typically present as slow-growing, painless, well-circumscribed masses.[1][6] On imaging, the hallmark is a well-defined, often lobulated soft-tissue mass; when arising from minor salivary glands of the palate, smooth pressure remodeling of underlying bone may be seen.[7][8] Complete surgical excision is the standard treatment, with prognosis generally excellent, although pleomorphic adenoma carries a recognized risk of recurrence and malignant transformation.[5][9]

Terminology and classification

The WHO Classification of Head and Neck Tumours (5th edition, 2024) recognizes 11 benign epithelial salivary gland tumor types:[10]

  • Pleomorphic adenoma (PA; synonym: benign mixed tumor)
  • Warthin tumor (synonym: papillary cystadenoma lymphomatosum, adenolymphoma)
  • Myoepithelioma
  • Basal cell adenoma (subtypes: solid, trabecular, tubular, membranous)
  • Oncocytoma (synonym: oxyphilic adenoma)
  • Canalicular adenoma
  • Sebaceous adenoma
  • Lymphadenoma (sebaceous and non-sebaceous)
  • Ductal papillomas (inverted ductal papilloma, intraductal papilloma, sialadenoma papilliferum)
  • Cystadenoma

The term "benign mixed tumor" for pleomorphic adenoma remains widely used but is considered outdated in formal classification. "Adenolymphoma" for Warthin tumor is similarly deprecated.[1] The 2024 WHO update also recognizes emerging entities such as pleomorphic adenoma with canalicular/trabecular phenotype driven by HMGA2 fusions and triphasic basal cell adenoma with CTNNB1 mutations.[10]

Epidemiology

  • Frequency: Salivary gland tumors constitute approximately 6% of head and neck neoplasms. Benign tumors represent ~80% of all salivary gland neoplasms.[2][3][4]
  • Subtype distribution: Pleomorphic adenoma accounts for 60–70% of benign salivary gland tumors; Warthin tumor accounts for 4–26%. All other benign subtypes are individually rare.[1][3][4][5]
  • Age: Peak incidence between the 4th and 6th decades (mean age ~50 years). Warthin tumor tends to present in older patients (6th–7th decades).[1][4][6][11]
  • Sex: Pleomorphic adenoma shows a female predilection (~2:1). Warthin tumor has a strong male predilection, though this gap has narrowed with increased smoking among women.[1][6][11][12]
  • Anatomic distribution:
    • Parotid gland: ~80% of all salivary gland tumors[2][3]
    • Submandibular gland: 10–15%[2]
    • Minor salivary glands: ~10%, with the hard palate being the most common intraoral site, followed by the lip and buccal mucosa[6][7][11]
    • Warthin tumor arises virtually exclusively in the parotid gland[1]
  • Intraosseous occurrence: Primary intraosseous benign salivary gland tumors of the jaws are exceedingly rare; the vast majority of central salivary gland tumors in bone are malignant (mucoepidermoid carcinoma predominating).[13][14]

Clinical presentation

Presentation

  • Painless, slow-growing, firm, mobile mass, typically present for months to years before clinical attention[15][16]
  • Parotid tumors present as preauricular or infraauricular swelling; submandibular tumors as submandibular triangle masses[15]
  • Minor salivary gland tumors of the palate present as smooth, dome-shaped, submucosal swellings, usually on the posterolateral hard palate, with intact overlying mucosa[7][12][17]
  • Lip and buccal lesions present as firm, well-circumscribed submucosal nodules[6]

Specific Subtypes

  • Warthin tumor: May be bilateral (5–10%) or multifocal; occasionally fluctuant due to cystic components; strong association with smoking[1][18]
  • Canalicular adenoma: Characteristically arises in the upper lip of older adults[5]
  • Oncocytoma: Rare; typically parotid; may be bilateral[5]

Red Flags Suggesting Malignancy

  • Rapid growth, pain, fixation to skin or deep structures[15][19]
  • Facial nerve (CN VII) dysfunction: paresis or paralysis[19]
  • Cervical lymphadenopathy[19]
  • Mucosal ulceration overlying a minor salivary gland mass (uncommon in benign tumors but reported rarely in pleomorphic adenoma)[17]

Radiographic findings

Benign salivary gland tumors are predominantly soft-tissue masses of the major or minor salivary glands and are not primarily intraosseous lesions. Conventional dental radiographs (periapical, panoramic) are therefore most relevant when minor salivary gland tumors of the palate, retromolar region, or floor of mouth produce secondary effects on adjacent bone, or when an intraosseous salivary gland neoplasm is encountered.

Location and Distribution

  • Minor salivary gland tumors of the palate are centered in the posterolateral hard palate or junction of hard and soft palate, virtually never arising in the midline, reflecting the anatomic distribution of palatal salivary glands.[7]
  • Retromolar and floor-of-mouth minor salivary gland tumors may abut the mandible.[13]
  • Primary intraosseous benign salivary gland tumors are exceedingly rare; the mandible is more commonly affected than the maxilla when central salivary gland neoplasms occur, but the overwhelming majority of intraosseous salivary gland tumors are malignant.[13][14][20]

Periphery and Shape

  • When a palatal minor salivary gland tumor produces changes visible on occlusal or periapical radiographs, the underlying bone typically shows smooth, well-corticated pressure remodeling (saucerization) rather than destructive invasion, reflecting the slow, expansile growth of benign tumors.[7][8]
  • On panoramic radiographs, a retromolar or posterior mandibular benign salivary gland tumor may appear as a well-defined, corticated, extrinsic soft-tissue mass with smooth scalloping of the adjacent cortex.[21][22]
  • The rare primary intraosseous benign salivary gland tumor (e.g., intraosseous myoepithelioma) presents as a well-circumscribed, unilocular radiolucency with a corticated border.[14]

Internal Architecture

  • Benign salivary gland tumors are predominantly soft-tissue density and appear radiolucent when superimposed on bone on conventional radiographs.
  • Calcification within benign salivary gland tumors is uncommon but may occasionally be seen in long-standing pleomorphic adenomas as punctate or amorphous radiopacities.[23][24]
  • Phleboliths are not a feature; their presence should raise consideration of a vascular lesion.

Effects on Teeth and Adjacent Structures

  • Palatal tumors may displace teeth or cause divergence of roots when large.[7]
  • Root resorption is uncommon in benign salivary gland tumors and, when present, should raise concern for a more aggressive or malignant process.[21]
  • Tooth vitality is typically preserved.
  • Large palatal tumors may thin or remodel the nasal floor or maxillary sinus floor, visible on panoramic or occlusal radiographs.[7]

Growth Pattern and Cortical Involvement

  • Benign tumors produce smooth, expansile remodeling of adjacent bone without cortical destruction.[8]
  • Aggressive-appearing bone destruction is atypical for benign salivary gland tumors and has been described only rarely in pleomorphic adenoma; its presence warrants consideration of malignancy.[8]
  • CBCT can more accurately assess the extent of cortical thinning, expansion, and the integrity of cortical boundaries compared with panoramic radiography, which is particularly useful for palatal tumors where the relationship to the nasal cavity and maxillary sinus must be defined.[25]

Extent

  • CBCT provides superior three-dimensional delineation of the interface between a palatal soft-tissue mass and the underlying palatal bone, identifying cortical continuity or perforation that may not be apparent on two-dimensional radiographs.[25]
  • For retromolar or posterior mandibular lesions, CBCT clarifies the relationship to the inferior alveolar canal and lingual cortex.[25]

Variants

  • Warthin tumor: Exclusively parotid; no direct jaw involvement expected on dental radiographs. Bilateral or multifocal parotid masses may be incidentally noted on panoramic radiographs as soft-tissue opacities overlying the ramus.[1]
  • Canalicular adenoma: Upper lip location; no bone involvement expected.
  • Intraosseous myoepithelioma: Reported as a well-circumscribed unilocular radiolucency in the mandibular premolar-molar region, mimicking an odontogenic cyst or ameloblastoma.[14]

Other imaging findings

MRI

MRI is the preferred advanced imaging modality for characterizing salivary gland tumors and is superior to CT for soft-tissue delineation, capsule detection, and assessment of perineural spread.[24][26][27]

  • Pleomorphic adenoma: Characteristically T2-hyperintense (reflecting myxoid/chondroid stroma), well-circumscribed, with homogeneous gadolinium enhancement; the capsule is often visible as a low-signal rim on T2-weighted images. Lobulated borders and inhomogeneous internal signal are common in larger tumors. Mean ADC values are relatively high (~1.9 × 10⁻³ mm²/s), helping distinguish pleomorphic adenoma from malignant tumors.[1][24][26][28]
  • Warthin tumor: Complex T1 and T2 signal due to mixed solid and cystic components; characteristically lacks gadolinium enhancement; lower ADC values (~1.0 × 10⁻³ mm²/s) than pleomorphic adenoma, which can cause diagnostic confusion with malignancy. Warthin tumors concentrate ⁹⁹ᵐTc-pertechnetate on scintigraphy, a distinguishing feature.[1][28]
  • Malignant features on MRI: T2 hypointensity, irregular margins, invasion of adjacent structures, and restricted diffusion suggest malignancy.[29]

CT

  • Contrast-enhanced CT delineates the relationship of salivary gland tumors to adjacent bone (mandible, skull base) and is useful when osseous invasion is suspected.[27]
  • Two-phase helical CT can help differentiate tumor subtypes: pleomorphic adenomas show progressive enhancement (increasing attenuation at delayed phase), whereas Warthin tumors show early enhancement with washout (decreasing attenuation at delayed phase).[30]
  • CT is superior to MRI for detecting cortical erosion and sialolithiasis.[27]

Ultrasound

  • First-line imaging for superficial parotid and submandibular masses.[15][31]
  • Pleomorphic adenomas appear as hypoechoic, well-defined, lobulated lesions with posterior acoustic enhancement; may contain calcifications.[23]
  • Warthin tumors are oval, hypoechoic, well-defined, often with anechoic cystic areas and increased vascularity.[23][32]
  • Ultrasound-guided FNA improves diagnostic yield.[31]

Differential diagnosis

When a well-defined soft-tissue mass is identified in the region of a major or minor salivary gland, the primary differential centers on distinguishing among benign salivary gland tumor subtypes and excluding low-grade malignancy. For intraoral minor salivary gland tumors of the palate, the differential also includes non-salivary soft-tissue and bony lesions. Imaging alone cannot reliably distinguish benign from malignant salivary gland tumors in all cases.[27][33]

EntityWhy it is consideredBest discriminator
Mucoepidermoid carcinomaMost common malignant salivary gland tumor; may arise in the palate or rarely as a primary intraosseous jaw lesionIll-defined margins, cortical destruction, and internal amorphous sclerotic bone favor mucoepidermoid carcinoma over a benign tumor[7][34][35]
Adenoid cystic carcinomaSecond most common malignant minor salivary gland tumor of the palate; perineural spreadPerineural invasion on MRI, irregular margins, and T2 hypointensity distinguish from benign tumors[7][29]
Polymorphous adenocarcinomaLow-grade malignancy with predilection for minor salivary glands of the palate; may mimic pleomorphic adenoma clinicallyInfiltrative growth pattern on histopathology; imaging overlap with pleomorphic adenoma necessitates biopsy[7][36]
Palatal abscess or minor salivary gland mucoceleInflammatory or obstructive palatal swelling mimicking a neoplasmClinical fluctuance, tenderness, and rapid onset distinguish from the slow, painless growth of benign tumors[16]

The highest-risk diagnostic pitfall is misidentifying a low-grade malignancy (particularly polymorphous adenocarcinoma or low-grade mucoepidermoid carcinoma) as a benign pleomorphic adenoma on incisional biopsy, given overlapping histomorphology at the palatal site.[36] FNA or incisional biopsy with adequate tissue sampling is essential; excisional biopsy with complete histopathological examination may be required for definitive diagnosis.[36]

Histopathology

Pleomorphic Adenoma

The hallmark is morphological diversity, with a biphasic population of epithelial and myoepithelial cells set in a variable mesenchymal-like stroma:[36][37][38]

  • Epithelial component: Ductal and tubular structures lined by inner luminal epithelial cells and outer myoepithelial cells; sheets, cords, and islands of cells[36][39]
  • Myoepithelial component: Plasmacytoid, spindle, clear, and stellate cell morphologies; myoepithelial cells undergo progressive modification ("melting") into the surrounding stroma[36][37][40]
  • Stroma: Myxoid, chondroid, hyaline, and fibrous areas in varying proportions; the chondromyxoid stroma is the most characteristic feature[38][39]
  • Capsule: Complete encapsulation in ~25% of cases; incomplete or absent capsule in the majority, particularly in minor salivary gland tumors of the palate (~84% partially or non-encapsulated). Pseudopod extensions through the capsule are common and contribute to recurrence risk.[1][9][11][12]
  • Subtypes: Classic (balanced epithelial and stromal components), cellular (cell-rich), and myxoid (stroma-rich)[11][39]
  • Squamous metaplasia (~25–43%), cystic degeneration (~43%), and keratin pearl formation are recognized features[11]

Molecular Findings

  • PLAG1 rearrangements are the most characteristic molecular alteration in pleomorphic adenoma and are present in neoplastic ductal, myoepithelial, and chondroid cells but not in non-neoplastic stromal elements.[41]
  • HMGA2 fusions are identified in a subset, particularly those with canalicular/trabecular phenotype.[10]
  • PLAG1 immunohistochemistry is useful for confirming the diagnosis and distinguishing pleomorphic adenoma from histologic mimics.[41]

Other Benign Subtypes

  • Warthin tumor: Bilayered oncocytic epithelium with papillary-cystic architecture and dense lymphoid stroma with germinal centers[1]
  • Basal cell adenoma: Basaloid cells in solid, trabecular, tubular, or membranous patterns; the membranous subtype has a higher recurrence risk[5]
  • Myoepithelioma: Composed exclusively of myoepithelial cells without ductal differentiation[1]

Radiologic-Pathologic Correlation

The high T2 signal intensity of pleomorphic adenoma on MRI corresponds to the myxoid/chondroid stromal component, while more cellular tumors show lower T2 signal.[1][26] Warthin tumor's mixed solid-cystic MRI appearance reflects its papillary-cystic architecture with lymphoid stroma.[1]

Management and prognosis

Workup and Referral

  • FNA biopsy is the standard initial tissue-sampling technique for major salivary gland masses, with a positive predictive value exceeding 95% for pleomorphic adenoma.[19][26]
  • Cross-sectional imaging (MRI preferred; CT when bone involvement is suspected) is indicated for deep lobe parotid tumors, tumors suspicious for malignancy, and all non-parotid salivary gland subsites.[19][29][31]
  • Referral to an oral and maxillofacial surgeon or head and neck surgeon is appropriate for all salivary gland masses requiring excision.[19]

Surgical Treatment

  • Parotid tumors: Superficial parotidectomy or partial superficial parotidectomy is the standard for superficial lobe pleomorphic adenomas; total parotidectomy with facial nerve preservation for deep lobe tumors. Extracapsular dissection is increasingly accepted for small, mobile, superficial tumors, with recurrence rates comparable to formal parotidectomy (~3%).[1][42][43][44]
  • Enucleation is no longer recommended due to unacceptably high recurrence rates (up to 45–79%).[45][46]
  • Minor salivary gland tumors: Wide local excision with a margin of normal tissue, including periosteum; bone resection is performed only when imaging demonstrates bone invasion.[1][12][17]
  • Warthin tumor and other benign subtypes: Conservative excision is generally curative.[1][5]

Recurrence

  • Pleomorphic adenoma recurrence rates with modern surgical techniques are 1–5% at 5 years and up to 7% at 10 years.[1][9][44][47]
  • Risk factors for recurrence: young age.[9][44][46]
  • Recurrent pleomorphic adenoma is often multinodular and difficult to eradicate; 48% of recurrent tumors recur again, mostly within 10 years.[9][48]
  • Recurrence is very uncommon in minor salivary gland pleomorphic adenomas after adequate excision.[1][12]
  • Other benign subtypes rarely recur, with the exception of the membranous type of basal cell adenoma and occasionally oncocytoma and canalicular adenoma.[5]

Malignant Transformation

  • Pleomorphic adenoma carries a 5–15% lifetime risk of malignant transformation to carcinoma ex pleomorphic adenoma, with risk increasing with tumor duration. Contemporary data suggest the risk is approximately 1.5% within the first 5 years.[5][43][49][50]
  • Basal cell adenoma and Warthin tumor carry a much lower but recognized risk of malignant transformation.[5]
  • The remaining benign subtypes virtually never undergo malignant change.[5]

Prognosis

  • Overall prognosis for benign salivary gland tumors is excellent after complete excision.[5][47]
  • Long-term surveillance is recommended for pleomorphic adenoma given the prolonged interval to recurrence (median ~7.5 years) and the risk of late malignant transformation. Patient self-monitoring may be as effective as routine imaging surveillance for detecting recurrence.[47][51]

Special considerations

PLAG1 and HMGA2 as Diagnostic Adjuncts

PLAG1 rearrangements are highly specific for pleomorphic adenoma among salivary gland tumors and can be detected by FISH or immunohistochemistry.[41] PLAG1 immunohistochemistry may show false-negative results on cytology cell-block material due to fixation differences.[52] HMGA2 fusions characterize a subset of pleomorphic adenomas with canalicular/trabecular phenotype and have been incorporated into the post-2024 WHO classification framework.[10]

Pediatric Considerations

Salivary gland tumors are uncommon in children. Pleomorphic adenoma is the most common benign salivary gland neoplasm in the pediatric population, but the differential diagnosis is broader, including vascular malformations, infantile hemangiomas, and first branchial cleft cysts.[31][53] Age below 18 years is an independent risk factor for recurrence after parotidectomy for pleomorphic adenoma (HR ~31).[44]

ORAD reference data

Radiographic characteristics

18 characteristics

Banded distributions from the ORAD reference database.

Clinical Features

What is the sex of your patient? Female · commonly
What is the sex of your patient?
FindingFrequency
Male commonly
Female commonly
Unknown rarely
What is the race of your patient? Nonblack · usually
What is the race of your patient?
FindingFrequency
Black occasionally
Nonblack usually
Unknown rarely
What is the age of your patient? 26 - 50 · commonly
What is the age of your patient?
FindingFrequency
0 - 10 rarely
11 - 25 occasionally
26 - 50 commonly
50 + commonly
Unknown rarely
Does your patient have pain or paresthesia? No pain · usually
Does your patient have pain or paresthesia?
FindingFrequency
Pain sometimes
No pain usually
Unknown rarely

Radiographic Features

Which jaw contains the lesion? Maxilla only · commonly
Which jaw contains the lesion?
FindingFrequency
Maxilla only commonly
Mandible only commonly
Both jaws occasionally
The lesion center is in what region ? Molar region · commonly
The lesion center is in what region ?
FindingFrequency
Incisor region sometimes
Canine/Premolar Region sometimes
Molar region commonly
Ramus region rarely
TMJ region rarely
Sinus region rarely
The relationship of the lesion to teeth is: Not tooth associated · usually
The relationship of the lesion to teeth is:
FindingFrequency
Crown associated rarely
Root associated rarely
Apex associated rarely
Missing tooth associated rarely
Not tooth associated usually
Is the tooth associated with the lesion vital? Vital · usually
Is the tooth associated with the lesion vital?
FindingFrequency
Vital usually
Not vital rarely
Unknown rarely
Please estimate the number of lesions: One · usually
Please estimate the number of lesions:
FindingFrequency
One usually
Two not reported
Three or more not reported
Generalized not reported
What is the maximum size of the lesion? Greater than 3 cm · usually
What is the maximum size of the lesion?
FindingFrequency
Less than 2 cm occasionally
2 to 3 cm occasionally
Greater than 3 cm usually
Where is the origin of the lesion? Peripheral · usually
Where is the origin of the lesion?
FindingFrequency
Central sometimes
Peripheral usually
The borders of the lesion are: Corticated · usually
The borders of the lesion are:
FindingFrequency
Corticated usually
Defined but not corticated occasionally
Diffuse occasionally
The loculation of the lesion is: Not loculated · sometimes
The loculation of the lesion is:
FindingFrequency
Unilocular sometimes
Multilocular sometimes
Not loculated sometimes
The contents of the lesions are: Radiolucent · usually
The contents of the lesions are:
FindingFrequency
Radiolucent usually
Radiopaque not reported
Mixed sometimes
Radiolucent with flecks not reported
Does the lesion contain one or more teeth ? No · usually
Does the lesion contain one or more teeth ?
FindingFrequency
Yes occasionally
No usually
Unknown occasionally
Does the lesion expand the bony cortex? Yes · commonly
Does the lesion expand the bony cortex?
FindingFrequency
Yes commonly
No commonly
Does the lesion cause root resorption ? No · usually
Does the lesion cause root resorption ?
FindingFrequency
Yes occasionally
No usually
Does the lesion cause tooth displacement or impaction? Yes · commonly
Does the lesion cause tooth displacement or impaction?
FindingFrequency
Yes commonly
No commonly
Atlas sources

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