Salivary gland disorders and tumours

• title: "Distribution and Frequency of Salivary Gland Tumours: An International Multicenter Study" authors: Alsanie I, et al. source: "Head Neck Pathol. 2022;16(4):1043-1054" url: https://pmc.ncbi.nlm.nih.gov/articles/PMC9729635/ accessed: 2026-10-31
• title: "Epidemiological Profile of Salivary Gland Tumors in Southern Iranian Population: A Retrospective Study of 405 Cases" authors: Ghaderi H, et al. source: "J Cancer Epidemiol. 2023;2023:8844535" url: https://pmc.ncbi.nlm.nih.gov/articles/PMC10681769/ accessed: 2026-10-31
• title: "Salivary Gland Disorders: Rapid Evidence Review" authors: Kim MJ, Milliren A, Gerold DJ Jr. source: "Am Fam Physician. 2024;109(6):550-559" url: https://www.aafp.org/afp/2024/0600/salivary-gland-disorders accessed: 2026-10-31

• Salivary gland swelling has three large groups: stones and infection (sialolithiasis and sialadenitis), benign tumours, and malignant tumours.
• Sialolithiasis is the most common benign cause of salivary swelling. It most often affects the submandibular gland, men in the 30 to 60 year age group, and usually presents with meal-time swelling and pain. ^[1]
• Pleomorphic adenoma is the commonest benign salivary tumour and Warthin tumour the second; both are usually painless, slow-growing parotid masses.
• Mucoepidermoid carcinoma is the commonest malignant salivary tumour and adenoid cystic carcinoma the classic perineural, late-recurring one.
• Imaging starts with ultrasound for superficial lesions; magnetic resonance imaging is preferred when malignancy is suspected.
• An experienced pathologist can separate malignant from benign on fine needle aspiration in about 90% of cases. Incisional or open biopsies of the major salivary glands are avoided.
• The facial nerve can be involved by tumour or injured at surgery: temporary facial weakness after parotidectomy is reported in 10 to 65% of cases, and permanent weakness in under 5%. ^[3]
• Complete surgical excision is the mainstay for both benign and malignant salivary tumours.

By the end of this page you should be able to:

1. Classify salivary gland swelling and name the common causes in each group.
2. Explain how a stone forms and causes meal-time swelling, and outline conservative and interventional management.
3. Describe pleomorphic adenoma and Warthin tumour and choose appropriate surgery for each.
4. Recognise mucoepidermoid carcinoma and adenoid cystic carcinoma and their differing behaviour.
5. Plan the investigation of a parotid mass, including the roles of ultrasound, contrast-enhanced computed tomography, magnetic resonance imaging and fine needle aspiration.
6. Explain when and how to preserve or sacrifice the facial nerve, and the main complications of parotidectomy.
7. Recognise Sjogren-related salivary swelling and distinguish it from neoplasm and infection.
8. Manage malignant salivary tumour neck disease and follow-up according to grade and stage.

The glands themselves are paired major glands (parotid, submandibular and sublingual) plus hundreds of minor glands in the lips, palate, buccal mucosa and upper aerodigestive tract. Disease in any site can present as a swelling, so location is part of the diagnosis: parotid and submandibular masses are usually palpable on the face or neck, while minor gland lesions present as lumps in the mouth or sinuses.

Clinically the mass is first classified as inflammatory, neoplastic or autoimmune. A neoplasm is then classified by behaviour (benign or malignant), site and histological type, most importantly because histological type predicts recurrence, nodal spread and survival.

The facial nerve (cranial nerve VII) leaves the skull base and passes through the parotid gland, dividing it into superficial and deep lobes. Its five terminal branches control facial movement. Because the nerve lies inside the gland, any parotid operation, benign or malignant, is an operation on the nerve as well as on the tumour. This is the source of the facial nerve risk discussed later.

The submandibular gland drains through Wharton duct, which runs forward and upward to open near the lingual frenulum. Because the duct runs against gravity, stones lodge there easily. The parotid drains through Stensen duct across the masseter. Minor glands have no long ducts, so obstruction there is rare and infection less common.

Salivary gland tumours are rare. Malignant salivary gland tumours account for 0.5 to 1.2% of all cancers and about 5% of head and neck cancers ^[4]. Most salivary gland neoplasms are benign. A typical ear, nose and throat surgeon sees many salivary stones and infections but relatively few cancers in a career. ^{[5] [3]}

Parotid gland tumours account for 60 to 75% of all salivary gland tumours, while the submandibular gland accounts for 10 to 15%, with an equal distribution of benign and malignant lesions there ^[4]. Minor salivary gland tumours account for the remainder.

The cancer incidence differs by country. The ESMO-EURACAN Clinical Practice Guideline reports a worldwide crude incidence of salivary gland cancer of 0.69 and an age-adjusted incidence of 0.57 cases per 100,000 people per year, with 53,583 new patients in 2020, and European crude and age-adjusted rates of 1.3 and 0.67 cases per 100,000 people per year, with 9,917 new patients in 2020 ^[5].

Sex distribution and age vary by source and histology, and the usual age at presentation is the sixth or seventh decade, although age at diagnosis varies by histology ^[4][5]. The 5-year relative survival for major salivary gland cancer in Europe is 63%, decreasing with age from about 90% in patients under 25 years to about 70% in patients aged 25 to 64 years ^[5].

Sialolithiasis. The cause is not fully understood. Two dominant theories are proposed: many tiny internal microcalculi are secreted into the ducts and act as a nidus, or there is calcification around a foreign body or debris ^[1]. Anatomical factors that hinder flow (duct stenosis, inflammation), dehydration and reduced salivary flow predispose to stone formation. Only around 80% of stones are radio-opaque ^[1].

Sialadenitis. Reduced salivary secretion and duct obstruction are the major risk factors. Dehydration, immunosuppression, malnutrition, postoperative states, intubation, anticholinergic drugs, antihistamines, diuretics and beta-blockers all reduce salivary flow ^[2]. Retrograde contamination by oral bacteria is common, and staphylococci often lead the polymicrobial cultures of acute suppurative submandibular sialadenitis ^[2].

Tumours. The cause of salivary neoplasms is largely unknown. Reported associations include prior radiation exposure, smoking, viruses (Epstein-Barr virus, human immunodeficiency virus), immunosuppression, occupational exposures, basal cell carcinoma and genetic factors ^[4]. About 50% of radiation-induced salivary tumours are pleomorphic adenomas ^[3]. The histological type is more important than the cause: it determines behaviour.

Obstruction. A stone sits in the duct. When the gland is stimulated to secrete (eating, smelling food), saliva dams up behind the stone, producing swelling and pain. The swelling often subsides between meals, which is why patients describe "meal-time swelling". If the stone remains, pressure, stasis and secondary infection produce acute or chronic sialadenitis.

Infection. Once flow stops, bacteria or viruses invade the acini. Acute infection gives rapid painful swelling, fever and purulent discharge from the duct orifice. Chronic infection gives recurring painful swellings, fibrosis, and eventually a firm gland.

Autoimmunity. In Sjogren disease, lymphocytic infiltration damages the duct epithelium and acini. The result is dry mouth and eyes, bilateral parotid swelling and, in the long term, a raised risk of lymphoma in the gland.

Neoplasm. A benign tumour grows slowly, pushes surrounding tissue aside and becomes encapsulated or pseudo-encapsulated. A malignant tumour invades locally, may follow nerves (adenoid cystic carcinoma), may seed lymph nodes, and may spread to lungs, bone and liver. Grade and stage, not size alone, determine how dangerous it is.

Ask about:

• Swelling: which gland, one side or both, speed of onset, and how long it lasts.
• Meal-time swelling and pain: strongly suggests a stone.
• Fever and foul taste: suggests infection.
• Dry mouth and dry eyes: suggests Sjogren disease.
• Pain at rest or facial weakness: suggests malignancy, especially adenoid cystic carcinoma or salivary duct carcinoma.
• Growth rate: slow and painless favours benign disease; rapid, painful or fixed suggests malignancy.
• Smoking: smoking is a recognised risk factor for salivary tumours, including Warthin tumour, and should be recorded in every parotid mass ^[3].
• Previous radiation to the head and neck: raises the risk of salivary neoplasia.

• Inspect and palpate the gland. A benign neoplasm is typically well circumscribed, mobile and painless. A malignant one is hard, fixed, irregular, and may be associated with enlarged neck lymph nodes.
• Massage the gland and look for saliva at the duct orifice. Purulent discharge confirms infective sialadenitis.
• Test facial movement in every parotid mass: asymmetry of the nasolabial fold, incomplete eye closure, inability to whistle. Facial weakness implies malignant invasion in the absence of previous surgery.
• Examine the neck for cervical lymphadenopathy.
• Inspect the mouth, throat and skin of the head and neck for a primary source if metastasis is possible.
• Bilateral parotid swelling with sicca symptoms raises Sjogren disease, while bilateral Warthin tumour should also be remembered.

Sialolithiasis is the formation of calculi in the ducts of the major salivary glands. It is the most frequent cause of salivary gland swelling. Incidence is estimated at 1 in 10,000 to 1 in 30,000 people ^[1], it commonly affects people aged 30 to 60 years and is more common in men ^[1]. About 85% of sialoliths occur in the submandibular gland, which makes it the most common site ^[1].

Presentation is classic: sudden swelling of the gland before or during meals, with colicky pain, followed by gradual resolution over an hour or two. A stone in the distal Wharton duct may be felt bimanually along the floor of the mouth. If the stone is large and distal, diagnosis is often possible on physical examination alone ^[1].

Diagnosis and imaging are described in the investigations section. Small stones and those in the distal submandibular duct can be missed without careful examination and appropriate imaging.

Acute sialadenitis is bacterial or viral inflammation of the gland. Submandibular sialadenitis is less common than parotid involvement and accounts for about 10% of all cases of sialadenitis ^[2]. Patients are often older or dehydrated.

Management is conservative in the first instance: hydration, warm compresses, gland massage, analgesia such as non-steroidal anti-inflammatory drugs, sialogogues (for example lemon drops or other saliva stimulants), and good oral hygiene. Empiric antibiotics are started when infection is suspected, with amoxicillin-clavulanate or clindamycin, and the choice is refined by culture and sensitivity results ^[2]. Intravenous therapy is used when the patient is systemically unwell. An abscess needs surgical drainage.

Chronic sialadenitis follows recurrent obstruction, often by stones, or persistent infection. It presents with repeated episodes of painful swelling, usually improving between attacks. Histology shows dilated ducts, calculi, chronic inflammation and fibrosis ^[2]. Management is medical in the first instance; if infection supervenes, broad-spectrum antibiotics are added. Where a stone is present, the stone is removed by interventional sialendoscopy or direct surgical removal, and intraglandular stones may be treated with extracorporeal shock-wave lithotripsy under ultrasound guidance ^[2].

Sialadenosis is non-inflammatory, non-neoplastic enlargement of the salivary glands, usually both parotids or both submandibular glands. It is the most common cause of salivary gland swelling overall in some series ^[2] and is strongly associated with chronic alcohol use, diabetes mellitus, hypothyroidism, malnutrition and eating disorders. Histology shows acinar hypertrophy without inflammation ^[2]. Management is expectant: treat the underlying cause. Biopsy is avoided unless the diagnosis is uncertain.

Sjogren disease presents as bilateral, often parotid, swelling with dry mouth and dry eyes, recurrent parotid enlargement, and sometimes a febrile illness. The differential of submandibular swelling includes autoimmune disease, specifically Sjogren disease and systemic lupus erythematosus ^[2]. Key clues are sicca symptoms, abnormal antibodies and characteristic salivary gland biopsy. Any firm, asymmetric or solitary swelling should not be dismissed as Sjogren disease without imaging and tissue diagnosis, because lymphoma can complicate the gland.

Most salivary gland neoplasms are benign. Benign tumours are more common in women, with a male-to-female ratio of 1 to 1.6, and children account for less than 5% of cases ^[3]. The parotid is the commonest major gland involved. ^[4]

Pleomorphic adenoma, also called a benign mixed tumour, is the most common salivary gland tumour. It accounts for 60 to 70% of all benign salivary gland neoplasms ^[3], has a predilection for women and for patients in the third to fifth decades, and occurs in the parotid in 63 to 80% of cases ^[3].

It is slow growing, painless, well circumscribed and rubbery. Histologically it contains both epithelial elements (ducts) and mesenchymal elements (cartilage, bone, myxoid tissue), and the mesenchymal component develops through metaplasia of the epithelial cells ^[3]. It is not invasive, but it is not harmless: microscopic pseudopodia extend into surrounding tissue, so enucleation (shelling out) leads to recurrence.

Clinically, recurrence after incomplete excision presents years later, sometimes as multiple nodules. Malignant transformation occurs in up to 25% of untreated pleomorphic adenomas, and the risk of transformation over 15 years is estimated at 5 to 10% ^[4]. A recurrent or long-standing pleomorphic adenoma therefore needs wide excision and long follow-up.

Warthin tumour is the second most common benign salivary tumour, accounting for 15 to 36% of benign salivary gland tumours, with 94.7% of cases in the parotid, especially the tail ^[3]. It favours men and patients in the fourth to seventh decades. It forms a painless, cystic, compressible, encapsulated mass, often at the angle of the jaw, and bilateral lesions are common enough that a bilateral examination is warranted ^[3].

Microscopically it shows a bi-layered oncocytic epithelium with papillary projections over a lymphoid stroma with germinal centres. Its poor blood supply and cystic change explain its compressibility. Recurrence after complete excision is uncommon.

• Myoepithelioma: encapsulated mass of myoepithelial cells, often in the parotid, with little duct formation.
• Basal cell adenoma and canalicular adenoma: well-circumscribed epithelial tumours.
• Oncocytoma: uncommon, elderly patients, mitochondrial-rich cells.
• Sialadenoma papilliferum and ductal papillomas: papillary lesions, often on the palate.

All are managed by complete surgical excision with negative margins. Radiation plays little role, except occasionally for recurrent disease or unresectable tumour ^[3].

Malignant salivary tumours are rare. They comprise 0.5 to 1.2% of all cancers and 5% of head and neck cancers ^[4]. Sex distribution varies by source and histology (see Epidemiology above), and the usual age at presentation is the sixth or seventh decade ^[4][5]. ^[3]

The parotid harbours 60 to 75% of all salivary gland tumours and the submandibular gland 10 to 15%, with an equal mix of benign and malignant lesions in the latter ^[4]. The most common malignant types are mucoepidermoid carcinoma, adenoid cystic carcinoma, carcinoma ex pleomorphic adenoma, adenocarcinoma and squamous cell carcinoma ^[4].

Mucoepidermoid carcinoma is the most common salivary gland malignancy in adults and children. About 89% of cases occur in the parotid, 8.4% in the submandibular gland and 0.4% in the sublingual gland, with equal sex distribution and a peak in the fourth to fifth decades ^[4]. Many cases carry the chromosomal translocation t(11;19)(q21;p13), fusing MECT1 and MAML2 and disrupting NOTCH signalling; this is more often found in low-grade tumours and is associated with a better outlook ^[4].

Histologically it contains mucous, epidermoid and intermediate cells, with cystic spaces and variable solid components. It is graded low, intermediate or high. Low-grade tumours grow slowly and are rarely nodal, whereas high-grade tumours behave aggressively and metastasise. Clinically it often presents as an asymptomatic, firm parotid mass, sometimes with pain or facial weakness ^[4]. First-bite syndrome has been associated with it.

Treatment is wide surgical excision with negative margins, with adjuvant radiotherapy for high grade, advanced stage, positive or close margins, perineural or lymphovascular invasion, nodal disease or extra-glandular extension ^[4].

Adenoid cystic carcinoma accounts for about 10% of all salivary gland neoplasms and 30% of minor salivary gland tumours ^[4], with a peak in the fifth to sixth decades and no clear sex difference, although it is more common in the submandibular gland in women ^[4].

It is slow growing but relentlessly invasive, with a particular tendency for perineural spread and late distant metastasis, especially to lung and bone. Histology shows tubular, cribriform (the classic "Swiss cheese" pattern) and solid patterns; the solid pattern carries the worst prognosis. It presents as a slow-growing solid mass, often with pain from nerve or extra-parenchymal invasion, and cervical nodal metastasis is present in about 20% at presentation, more often with submandibular tumours ^[4]. First-bite syndrome has also been described.

Excision with wide margins is required, and adjuvant radiotherapy is commonly used. Because recurrence can appear many years later, long follow-up is essential.

• Acinic cell carcinoma (ACC): usually parotid (over 80%), with submandibular (4%) and minor gland (17%) cases. Bilateral parotid involvement occurs in 3 to 5%. It favours women in the fifth decade and presents as a slow-growing solitary mass ^[4]. High-grade transformation, though rare, can occur.
• Carcinoma ex pleomorphic adenoma: 5 to 15% of salivary malignancies, arising in a pre-existing or recurrent pleomorphic adenoma; malignant transformation risk 5 to 10% over 15 years and up to 25% in untreated tumours. It may present as a longstanding benign mass that suddenly accelerates ^[4].
• Salivary duct carcinoma: high grade, often with facial weakness and aggressive behaviour.
• Polymorphous low-grade adenocarcinoma: occurs almost exclusively in minor salivary glands, often on the palate, and may resemble adenoid cystic carcinoma.
• Lymphoma and melanoma: less common; lymphoma is the commonest malignancy whose treatment is primarily medical.

Parotid malignancies that present as large, fixed preauricular masses are often associated with cervical nodal metastasis. Facial nerve paralysis occurs in up to 12 to 15% of cases and is often associated with adenoid cystic carcinoma, mucoepidermoid carcinoma and salivary duct carcinoma ^[4]. Preoperative facial weakness changes the surgical plan and justifies sacrificing the involved nerve segment.

• Ultrasound is the first non-invasive investigation for major superficial salivary gland lesions. It localises the tumour, distinguishes solid from cystic, guides fine needle aspiration and shows heterogenous echogenicity, poorly defined margins, local invasion and lymphadenopathy, which suggest malignancy ^[3][4].
• Contrast-enhanced computed tomography (CT) evaluates tumour extent, bony infiltration and cervical lymphadenopathy. Dental artefact and poorer soft tissue resolution limit it, particularly for mucoepidermoid and adenoid cystic carcinoma, and it may underestimate the lesion ^[4]. It is preferred for suspected bony invasion.
• Magnetic resonance imaging (MRI) is recommended to assess tumour extent, soft tissue and nerve invasion for lesions in the deep parotid lobe, sublingual glands and minor salivary glands, and to detect the facial nerve branches and their relationship to the tumour for surgical planning ^[4]. MRI has higher sensitivity and specificity than CT for salivary gland lesions ^[3][4].
• Positron emission tomography (PET) is used to detect locoregional and distant metastasis, particularly in high-grade salivary gland cancer; it cannot reliably distinguish benign from malignant tumours because pleomorphic adenoma and Warthin tumour also take up tracer ^[4].
• MR sialography and ultrasound are useful for stones. Conventional radiographs detect large radiopaque stones but miss smaller and intraglandular ones, and only around 80% of stones are radio-opaque ^[1]. Non-contrast CT is a valid tool for diagnosing sialolithiasis when the stone is large enough or when slices are obtained every millimetre. MR sialography avoids radiation and gives excellent duct visualisation, while ultrasonography shows a hyperechoic focus with posterior shadowing ^[1].

MRI is the preferred modality whenever malignancy is suspected ^[5]. Contrast-enhanced CT is mostly reserved for patients in whom MRI is contraindicated ^[5]. Imaging should include the neck lymph nodes ^[5].

Ultrasound-guided salivary gland fine needle aspiration (FNA) cytology has become the accepted minimally invasive method for evaluating parotid and submandibular gland tumours before operation. In experienced hands it can distinguish malignant from benign disease in about 90% of cases ^[5], and the result should be reported according to the Milan System, with a defined risk of malignancy and suggested management ^[5].

If FNA is non-diagnostic, or histotype detail is needed, ultrasound-guided core needle biopsy can be used: it obtains more tissue and has a higher diagnostic yield than FNA, with a lower rate of inadequate sampling, but carries a slightly higher risk of pain, facial nerve injury and bleeding ^[5].

Fine needle aspiration has a sensitivity of about 73% and a specificity of about 91% for distinguishing benign from malignant salivary tumours in systematic reviews ^[3].

Open or incisional biopsy of major salivary gland lesions should be avoided, because of the risk of facial nerve injury, spillage and seeding and of complicating definitive surgery ^[3][5]. Incisional biopsy is appropriate for submucosal minor salivary gland lesions, taken by an experienced surgeon with the surrounding stroma ^[5].

Malignant salivary gland tumours are staged clinically before treatment and pathologically after resection, using the UICC TNM eighth edition classification; minor salivary gland tumours are staged according to the site from which they arise ^[5]. Intraoperative frozen sections may be used to assess margins, perineural invasion or nodes if the result will change management at the time of surgery ^[5].

Sialolithiasis. Management begins conservatively: massage of the gland, non-steroidal anti-inflammatory drugs and sialogogues. Signs of infection (cervical adenopathy, purulent discharge or erythema over the duct) indicate antibiotic therapy ^[1].

Further treatment depends on stone size and site:

• Intraparenchymal stones of 5 to 7 mm that can be visualised may be extracted endoscopically. ^[1]
• Larger stones require transoral slitting.
• External shock-wave lithotripsy is used for smaller stones that are not palpable and not visible endoscopically, and is generally unsuccessful for larger stones.
• External shock-wave lithotripsy is also an option for non-palpable stones or for stones visualised endoscopically ^[1].
• Refractory intraglandular stones can be treated with extracorporeal shock-wave lithotripsy under ultrasound guidance ^[2].

Acute sialadenitis. Most cases resolve with conservative medical management: hydration, warm compresses, gland massage, analgesia, sialogogues and good oral hygiene ^[2]. Empiric therapy starts with amoxicillin-clavulanate or clindamycin, with antibiotic selection refined by culture and sensitivity reports. Intravenous antibiotics are used when the patient is systemically unwell, and abscess requires drainage ^[2].

Chronic sialadenitis. Medical management (hydration, oral hygiene, analgesia, sialogogues) comes first; broad-spectrum antibiotics are added for infection. When sialolithiasis is present, stone removal is by interventional sialendoscopy or direct surgical removal, with extracorporeal shock-wave lithotripsy for intraglandular stones ^[2].

Sialadenosis. Expectant management with treatment of the underlying cause (alcohol cessation, glycaemic control, nutritional rehabilitation) ^[2].

Complete surgical excision with negative margins is the mainstay ^[3]. Radiation has only a limited role, for recurrent disease, for unresectable tumour, or when there is extensive facial nerve involvement ^[3].

• Pleomorphic adenoma: enucleation is inappropriate because of capsule irregularity and recurrence. A superficial or partial parotidectomy with facial nerve preservation, removing the tumour with a cuff of normal parotid, is standard ^[3]. If the tumour is in the deep lobe, a total parotidectomy may be needed.
• Warthin tumour: complete excision with a margin. Because Warthin tumour often occurs in older smokers and may be bilateral, a conservative gland-preserving approach is favoured where possible, and a second Warthin should be looked for.
• Extracapsular dissection removes the tumour with its immediate capsule without identifying or dissecting the facial nerve branches. It has lower reported rates of facial nerve weakness, salivary fistula and Frey syndrome in selected benign lesions, and good local control (over 95%) is achieved with negative margins ^[3].
• Total or superficial parotidectomy with facial nerve preservation is used for large or deep benign parotid tumours ^[3].

After complete excision, recurrence of benign disease is low. Follow-up is long because pleomorphic adenoma can recur decades later and because malignant transformation, although uncommon, is serious.

Treatment is multimodal and should be planned by a multidisciplinary team in a specialised head and neck unit ^[5].

• Surgery is the mainstay. The reference procedure for parotid cancer is total parotidectomy. For low-grade, early stage (cT1-T2N0) tumours in the superficial lobe, superficial parotidectomy can suffice. For advanced-stage, intermediate- or high-grade, or preoperatively known malignant tumours, total parotidectomy is preferable ^[5].
• The facial nerve is preserved if there is no preoperative paralysis and no intraoperative macroscopic invasion. It is sacrificed if there is preoperative paralysis. Where invasion is found intraoperatively, the decision between sacrifice and preservation is taken on oncological and functional grounds ^[5].
• For submandibular gland carcinoma, resection of the gland with surrounding level Ib nodes is required to ensure negative margins; a selective neck dissection of levels I to III is standard for high-grade disease without clinically involved nodes ^[5].
• Adjuvant radiotherapy improves locoregional control and survival in high-grade disease, advanced stage, positive or close margins, perineural invasion, lymphovascular invasion, nodal metastases or extra-glandular extension ^[4].
• Primary radiotherapy is reserved for unresectable disease, poor surgical candidates, unacceptable surgical morbidity, or palliation ^[4].
• Chemotherapy is not routine; it is the mainstay for salivary gland lymphoma.
• Targeted systemic therapy is evolving. Androgen receptor and HER2 status should be confirmed in salivary duct carcinoma and adenocarcinoma not otherwise specified with distant metastases; NTRK fusion testing is mandatory for secretory carcinoma and acinic cell carcinoma ^[5].
• Advanced salivary duct carcinoma may be treated with androgen deprivation therapy or anti-HER2 therapy in selected patients, and TRK inhibitors for NTRK fusion tumours ^[5]. Aggressive or recurrent tumours can also receive platinum-based chemotherapy.

Cervical nodal metastases occur in 10 to 40% of parotid carcinomas, more often in high grade, advanced T stage, facial nerve involvement and extra-glandular extension; the most frequently involved levels are II, III and IV ^[5]. The incidence of nodal metastasis in submandibular carcinoma at presentation is around 8 to 33%, usually levels I to III, with possible skip metastasis to levels IV and V ^[5]. ^[4]

For a clinically node-negative neck, elective neck dissection is strongly recommended when the estimated risk of occult metastasis is 15 to 20% ^[5]. Risk factors include age over 54 years, pain, facial nerve dysfunction and T stage above T2 ^[5]. Some centres prefer elective neck irradiation or level II dissection with frozen section, extending dissection only if nodes are positive ^[5]. For high-risk disease, levels I to V are addressed, with levels I and V added on indication ^[5].

The operation is performed under general anaesthesia with the patient positioned to allow facial nerve monitoring. The skin flap is raised over the parotid capsule, the facial nerve trunk is identified at its exit from the stylomastoid foramen, and dissection proceeds along the nerve branches from proximal to distal. The tumour is removed before any additional procedure. Intraoperative facial nerve monitoring helps, though it does not replace careful dissection. Intraoperative frozen sections assess margins.

Complications include:

• Temporary facial nerve weakness in 10 to 65% of cases and permanent weakness in under 5% ^[3][4].
• Frey syndrome (gustatory sweating) can occur after parotidectomy; reported frequency varies widely with time since surgery and assessment method ^[4].
• Haematoma, infection, sialocele and salivary fistula.
• Xerostomia, altered sensation and cosmetic contour defect.
• First-bite syndrome after deep-lobe or parapharyngeal dissection.

Frey syndrome is treated with topical antiperspirants, botulinum toxin or, rarely, further surgery. Facial nerve reconstruction (nerve grafting or dynamic procedures) should be considered early if the nerve is sacrificed.

Surveillance after salivary cancer aims to detect locoregional recurrence and metastasis. High-grade mucoepidermoid and adenoid cystic carcinomas need long-term imaging and careful examination of the nerve. Late recurrence of adenoid cystic carcinoma is common, so follow-up of 10 to 15 years or longer is prudent.

• Obstruction and infection: acute and chronic sialadenitis, abscess, gland atrophy.
• Facial nerve dysfunction: whether from tumour invasion or surgery.
• Recurrence: especially pleomorphic adenoma after incomplete excision and adenoid cystic carcinoma.
• Malignant transformation: of long-standing pleomorphic adenoma.
• Xerostomia: after radiation or extensive surgery, with dental caries.
• Systemic: Sjogren disease increases lymphoma risk; malignant lymphoma of the gland needs medical therapy.

Benign tumours have an excellent prognosis after complete excision, with over 95% local control ^[3]. Recurrence is the main long-term risk, particularly after enucleation of pleomorphic adenoma.

Malignant salivary cancer prognosis depends on histological type, grade, stage, facial nerve involvement, nodal status and margin status. The ESMO guideline reports a 5-year relative survival for major salivary gland cancer in Europe of 63%, ranging down to 70% in patients aged 25 to 64 years and about 90% in patients under 25 years ^[5]. Advanced stage, high grade, perineural invasion and nodal metastases worsen the outlook. Adenoid cystic carcinoma has a reasonable 5-year but poor 10- to 20-year survival because of late metastasis. Mucoepidermoid carcinoma ranges from indolent (low grade) to highly aggressive (high grade). ^[4]

Children. Salivary gland tumours are rare in children, accounting for less than 5% of cases, and most are benign or vascular. Mucoepidermoid carcinoma is the most common malignant salivary tumour in children. A paediatric parotid mass always needs specialist assessment and imaging before any operation.

Older adults. Acute sialadenitis is more common in older and dehydrated patients. Secretory drugs and dehydration should be reviewed before antibiotics. Malignancy must be excluded in any new salivary mass in an older smoker.

Pregnancy. Sialolithiasis can flare because of relative dehydration. Ultrasound is the imaging of choice. Surgical excision of a tumour is usually deferred unless there is strong suspicion of malignancy, with multidisciplinary planning.

Immunocompromised patients. HIV and other immunosuppression predispose to lymphoepithelial and cystic salivary disease and to lymphoma. Management targets the underlying condition as well as the gland.

• Most salivary swellings can be diagnosed clinically. Meal-time swelling points strongly to a stone, and a firm fixed parotid mass with facial weakness suggests malignancy.
• Ultrasound, widely available and inexpensive, is the best first imaging test. CT and MRI may not be accessible; their absence should not delay referral of a suspected cancer.
• Conservative measures for stones and sialadenitis (hydration, massage, sialogogues, simple analgesics) are effective and low cost.
• Fine needle aspiration by an experienced pathologist (or even a trained clinician) is feasible where core biopsy is not.
• Surgery for benign salivary tumours needs facial nerve preservation; where specialist surgery is unavailable, patients should be referred before biopsy or excision that could damage the nerve.
• Radiotherapy for malignant disease may not be available locally; referral pathways should be established early.
• Histopathology of every excised salivary mass should be obtained, even if processing is delayed or sent to a regional centre.

• Salivary gland swelling is grouped as obstruction and infection, benign tumour, malignant tumour and autoimmune disease.
• Sialolithiasis is the commonest benign cause of salivary swelling; it usually affects the submandibular gland, men aged 30 to 60, and presents with meal-time swelling and pain.
• About 85% of sialoliths are submandibular and only around 80% are radio-opaque.
• Acute sialadenitis is managed conservatively with hydration, analgesia and sialogogues, with amoxicillin-clavulanate or clindamycin when infection is present.
• Sialadenosis is non-inflammatory enlargement treated by treating the cause.
• Pleomorphic adenoma is the commonest benign salivary tumour (60 to 70% of benign tumours) and Warthin tumour the second (15 to 36%).
• Enucleation of pleomorphic adenoma invites recurrence; excision with a cuff of normal gland is required.
• Malignant salivary tumours are 0.5 to 1.2% of all cancers; mucoepidermoid carcinoma is the commonest malignant type and adenoid cystic carcinoma the classic perineural, late-metastasising type.
• Facial nerve paralysis in a parotid mass suggests malignancy and occurs in up to 12 to 15% of cases.
• Ultrasound is first-line imaging; MRI is preferred when malignancy is suspected.
• Fine needle aspiration distinguishes benign from malignant in about 90% of cases in experienced hands.
• Open or incisional biopsy of a major salivary gland should be avoided.
• Complete surgical excision is the mainstay for benign and malignant salivary tumours.
• Total parotidectomy is the reference operation for parotid cancer, with superficial parotidectomy acceptable for low-grade T1-T2N0 superficial lesions.
• Parotidectomy carries a 10 to 65% rate of temporary and under 5% rate of permanent facial weakness, and Frey syndrome can occur afterward. ^[4]
• Adenoid cystic carcinoma and other salivary cancers need long follow-up because of late recurrence.

• "Head and neck cancer" and "lymphoma" (see your local index) for related neck disease.
• "Swelling of the neck and parotid region" for the broader differential.
• "Sjogren syndrome" for autoimmune salivary disease.
• "Facial nerve palsy" and "parotidectomy" for nerve complications.
• "Xerostomia" for reduced salivation and its consequences.