The mucous membrane of the alimentary tract is composed of numerous small, tubular alveolar glands. Six larger, paired compound glandular structures lying outside the alimentary tract empty their secretions into the tract through collecting ducts. These paired glands are the parotid, submaxillary, and sublingual glands.

The predominant function of the salivary glands is the production of saliva, a watery, viscous fluid containing salts and organic material. The latter is mainly made up of mucin, amylase, and maltase. The functions of saliva include mediation of local immunity, protection of mucous membrane surfaces from drying and microbial invasion, and delivery of taste molecules to receptor sites. Saliva moistens food, transforming it into a semisolid mass that can be swallowed easily. The initial breakdown of food, begun by the salivary enzymes, is unimportant in the overall process of digestion. The salivary glands also assist in the excretion of heavy metals and inorganic and organic materials, and in the maintenance of water balance.

A knowledge of developmental biology is important when congenital defects of salivary gland origin are being assessed. The embryonic primordia of the salivary glands consist of endoderm within the stomaderm, which advances into the adjacent mesenchyme. The parotid bud becomes visible during the fourth week of gestation; the primordia of the sublingual and submandibular glands become visible shortly afterwards. Endoderm of salivary gland origin lies in close proximity to the first and second brachial arches.

The parotid is the largest of the paired salivary glands. Histologically, it is entirely serous, and the entire lobular system is lined by columnar epithelium. The main excretory duct (Stensen's duct) enters the oral cavity adjacent to the second upper molar tooth. The parotid gland occupies the space between the ascending ramus of the mandible, the sternocleidomastoid muscle, and the external auditory meatus. Laterally, the main portion of the gland extends to the anterior border of the masseter muscle in the cheek. The medial extension of the gland, called the deep lobe, lies between the stylomandibular ligament and the angle of the mandible and extends to the medial surface of the ramus and the medial pterygoid muscle. A small portion of the facial process of the parotid gland that accompanies the course of the parotid duct towards its intraoral opening sometimes becomes detached from the main gland. This extension is called the accessory parotid lobe.

Lateral to the gland lies the skin, branches of the greater auricular nerve, superficial blood vessels, and lymph nodes. The buccinator and masseter muscles, the angle and ascending ramus of the mandible, and the temporomandibular joint lie superior and medial to the gland. The external auditory meatus, mastoid tip, sternocleidomastoid muscle, the transverse process of the first cervical vertebra, the posterior belly of the digastric muscle, the styloid process, the carotid and jugular vessels, the stylomastoid foramen, and the VIIth cranial nerve lie posteriorly.

The facial nerve is bounded by the mastoid tip and the sternocleidomastoid muscle posteriorly, by the posterior belly of the digastric muscle and the styloid process medially, and by the base of the tragal cartilage (‘tragal pointer’) laterally and superiorly. Within the gland, the facial nerve divides: the upper division bifurcates to form the frontal and zygomatic orbital branches, while the lower branch divides into the buccal, ramus, and cervical branches. The blood supply of the parotid is derived from the external carotid system through the superficial temporal artery. Venous drainage is by a diffuse collection system into the internal jugular venous system. Parasympathetic innervation of the parotid is by way of preganglionic fibres of the IXth cranial nerve to the otic ganglion. Postganglionic fibres pass through the auriculotemporal branch of the Vth cranial nerve from the otic ganglion to the paratid gland. Preganglionic parasympathetic fibres originate in the inferior salivatory nucleus and accompany the glossopharyngeal nerve to the jugular foramen, where the lesser superficial petrosal nerve is joined by parasympathetic fibres to the ganglion. Postganglionic fibres travel in the walls of the carotid artery and send branches to the parotid, sublingual, and submaxillary glands.

The submaxillary gland is a paired gland of mixed histology, containing mostly serous cells and some mucous cells. The ductal system is lined with columnar epithelium. The submaxillary gland occupies the submandibular triangle, bounded anteriorly by the mylohyoid muscle, inferiorly by the anterior belly of the gastric muscle, and superiorly by the lower border of the body of the mandible. Superficially, the gland relates to the overlying skin and ramus mandibularis nerve, as well as to the platysma muscle. The deep and superior portion of the gland lies on the hypoglossal nerve inferiorly, and on the lingual nerve superiorly. Posteriorly it is pierced by the external facial artery. The external facial vein lies close to the posterior aspect of the gland, providing venous drainage to the superficial and deep systems of the neck. Adjacent lymph nodes relate to the anterior and posterior aspects of the submandibular gland proper. The submandibular duct and the anterior part of the submaxillary gland pass forward on the hyoglossus muscle deep to the mylohyoid muscle. The submandibular duct is crossed twice by the lingual nerve, and runs posterior to the sublingual gland. Wharton's duct opens intraorally in the floor of the mouth through a small papilla at the frenulum of the tongue.

The sublingual gland is the smallest of the paired salivary glands and is located submucosally in the floor of the mouth. Laterally, the gland lies adjacent to the inner surface of the mandible. Medially, the gland rests on the genioglossal muscle. As previously noted, the gland is in contact with the lingual nerve, and submandibular duct, and the mylohyoid muscle. The sublingual gland drains through multiple ducts, each of which enters the floor of the mouth along the plica sublingualis. The arterial supply is through the sublingual and submandibular arteries. Sympathetic innervation of the sublingual and submandibular glands is from the carotid plexus. Preganglionic parasympathetic innervation is by way of fibres that arise from the superior salivatory nucleus and course through the chorda tympani nerve to the submaxillary ganglion. Postganglionic secretomotor fibres are distributed to the glands.

Clinical expression of salivary gland disease relates to the gland involved and the nature of the underlying disease process. Common regional symptoms include pain, subjective swelling, facial paraesthesia, hypersecretion, hyposecretion, aberrations of taste, trismus, dysphasia, difficulty with articulation, weakness of facial movement, and upper airway disturbances. Physical findings may include glandular enlargement, a mass, cloudy or bloody salivary secretion, absence of salivary secretion, diminished taste, weakness of the hypoglossal nerve, varying degrees of facial paralysis, soft palate or lateral pharyngeal wall swelling, diminution of sensation over the face, limitation of jaw movement, and abnormal temporomandibular joint motion.

Both sides of the face should be palpated externally and bimanually. A deep lobe tumour of the parotid may present as a swelling of the lateral pharyngeal wall of the soft palate with no externally visible mass. Saliva should be expressed from Stensen's and Wharton's ducts on both sides when assessing the nature of the salivary excretion. The direction of tongue protrusion or atrophy indicates short-term or long-standing paralysis of the hypoglossal nerve. Diminution of taste suggests disease affecting the lingual and chorda tympani nerve. Facial weakness may be complete or incomplete: parotid disease may occasionally cause facial spasm on the affected side.

Salivary secretion may be collected directly and analysed for composition, microbial contamination, and cellular composition. Cannulation of Wharton's or Stenson's ducts provides evidence of a hypo- or hypersecretory state. Immunological studies and analysis of blood chemistry are particularly valuable in the evaluation of patients whose salivary problems are related to underlying conditions such as Sjögren's syndrome, lymphoma, arthritis, or other collagen or autoimmune diseases. Obstructive salivary gland disease such as ductal stenosis, sialolithiasis, or sialoectasia is best assessed by sialography and polytomography. Potential neoplastic disease of the parotid is best assessed with MRI or CT scanning using dye enhancement. Ultrasonography and arteriography will supplement the results of routine scanning in patients with cystic or vascular disease respectively. Although specialized techniques such as gallium scanning in lymphoma and technetium scanning in Wharton's tumour may assist the clinician in making the diagnosis, the use of these tests is the exception rather than the rule.

Fine needle biopsy should be used routinely in the assessment of suspected neoplastic disease of salivary or parasalivary origin. Open incisional or excisional biopsies may be required if lymphoma, cat scratch disease, atypical mycobacterial lymphadenopathy, or Sjögren's syndrome is suspected. Such biopsies should only be undertaken after careful consideration, however, since they carry the risk of dissemination of benign mixed tumours or malignancy.

Parotitis caused by paramyxoviruses continues to occur in epidemics in non-immunized populations. Although adults may be susceptible, mumps primarily affects children between the ages of 4 and 12 years. A prodrome of malaise develops after an incubation period of 21 days. This precedes the contagious active disease state, when viruses are present in the saliva for 10 days.

Common manifestations of active disease include bilateral, and occasionally unilateral parotid swelling, fever, chills, joint pain, and myalgia. Uncommon manifestations include epididymitis, orchitis, meningoencephalitis, pancreatitis, thyroiditis, and unilateral sensorineural hearing loss.

Treatment relies on isolation of the patient, adequate hydration and nutrition, and control of symptoms.

Dehydration, poor dental hygiene, dental or periodontal disease, or reduced salivary excretion of any cause may result in bacterial infection of the parotid or, less commonly, the submaxillary gland. Neonates, the elderly, and postsurgical patients have an increased risk of developing this condition.

Acute bacterial sialoadenitis usually presents as a swollen, painful, and enlarging parotid or submaxillary gland. Fever, chills, trismus, dysphagia, and painful swallowing are often present; examination reveals progressive swelling with erythema of the overlying skin. Unchecked diffuse cellulitis of the glandular parenchyma results in formation of a microabscess, which progresses to a macroabscess. The common causes are Staphylococcus aureus, Streptococcus viridans, Escherichia coli, and anaerobic bacteria. Broad-spectrum antibiotics and hydration are required; late disease may need surgical drainage.

Sialoadenitis may occasionally be chronic and recurrent, with periods of quiescence between active infections. The results of sialography are normal, and fibrosis eventually results in resolution of the condition. Surgical removal of the affected gland is rarely required.

Mycobacterium tuberculosis causes a granulomatous inflammatory disease that may involve the parenchyma of the submaxillary or parotid glands. Retrograde or haematogenous spread is the usual route of infection. Perilymphatic enlargement and active disease may occur primarily or secondary to primary glandular disease. Diagnostic tests should include standard radiographic evaluation (including CT and MRI scans) and skin testing. Fine needle or open biopsy will establish the presence of a caseating granulomatous process. The gland is excised rarely.

Treatment of infection due to an atypical mycobacterium, such as M. avis, requires surgical excision of all diseased parenchymal and nodal tissue since antibiotic therapy is ineffective. The diagnosis of AIDS should also be excluded.

The actinomycetes are filamentous or rod-shaped, fastidious anaerobes. Salivary gland infection is usually associated with spread of the organism from dental or periodontal disease or from the intestine. Parenchymal disease is characterized by granulomatous inflammation with abscess and fistula formation. ‘Sulphur granules’ may be found associated with cyst and abscess formation. Long-term penicillin therapy is the treatment of choice.

This diagnosis is suggested by a history of cat scratch followed by fever, malaise, and enlargement of the salivary glands and lymph nodes. Identification of the causative bacterium by histology or culture is difficult and impractical. A variant of this syndrome is oculoglandular fever, characterized by nodal hypertrophy and conjunctivitis.

Treatment consists of hydration, drainage of the abscess, and antibiotic treatment of secondary bacterial infection. Gradual resolution over weeks to months is the rule.

With the exception of atypical mycobacterial disease, surgical excision of the parotid and submaxillary glands is not usually necessary. A history of rapid glandular enlargement, pain, and fever, and clinical findings of rash and lymph node enlargement suggest infection. Appropriate clinical studies, which should only be performed after an exhaustive history and physical examination, include a complete blood count, sedimentation rate, sinus and chest radiographs, CT scan of the neck, and culture and Gram staining of material obtained from oral and sinonasal sampling. Fine needle biopsy may be required: if this does not yield samples which allow a diagnosis to be made, cone needle or open biopsy can be undertaken. Material drained from abscesses or suppurative areas should be subjected to full microbiological assessment.

Salivary flow may be obstructed at the parenchyma, the peripheral ductule, or at Wharton's or Stensen's ducts or their orifices.

Wharton's or Stensen's duct may become narrowed as a result of repeated infection, iatrogenic injury, congenital abnormality, trauma, or through compression by a tumour.

Narrowing of the duct orifices is the simplest diagnosis to establish. There is a history of poor dental hygiene, dental infection, caries, or ill-fitting dentures, coupled with difficulty or inability to cannulate the duct. Duct stricture may not be so readily apparent. The single best study for identifying the site of obstruction is polytomographic sialography.

Orifice stenosis or distal duct stricture is treated conservatively by repeated dilations. Formal stenotomy and cannulation or marsupialization of the duct orifice is required in patients who fail to respond. Duct reimplantation or ligation, or excision of the gland, is only occasionally required.

Proximal perihilar duct stricture, recurrence of stricture at any site, or post-traumatic anastomotic stricture after stenting predicts repeated episodes of progressive obstruction and the eventual need for formal gland excision. In older patients and those who refuse surgery duct ligation, or rarely radiotherapy (100 cGy), are alternative methods of treatment.

Mucinous plugs may occur at any level of the ductile system in debilitated, irradiated, or immunocompromised patients, resulting in intermittent gland swelling and repeated infections due to stasis. Treatment is usually conservative, involving rehydration, massage, elimination of any medication which may be contributing to the problem, and, occasionally, administration of antibiotics. Surgical intervention is rarely needed.

Stone formation in the parotid or submaxillary ductile system may be primary or secondary. Primary lithiasis is most common in the submaxillary glandular duct. Stasis, or slow clearance of salivary gland secretions, is usually combined with one or more predisposing factors, including anatomical alterations in the duct, damage to the duct epithelium from infection or trauma, stricture, changes in physicochemical characteristics of salivary secretions, and systemic metabolic disease (particularly hyperparathyroidism, hyperuricaemia, and hypercalcaemia).

A history of recurrent progressive glandular swelling, initially associated with meals, is common. Palpation may disclose a stone along the course of Wharton's or Stensen's duct. Salivary secretion from the affected duct is cloudy, and a calcium phosphate precipitate is visible on microscopy.

Calculi are composed predominantly of calcium phosphate; the majority are, therefore, radio-opaque. A sialogram is the most useful test for identifying and locating calculi.

Treatment is determined by the location and size of the stone, and the frequency of the disease. Large stones can be excised, the duct opening being stented or marsupialized. Proximal hilar stones are best removed by excision of the duct and gland. Mid-ductal calculi or multiple small stones in the duct occasionally respond to evacuation, irrigation, stenting, and ductoplasty.

In primary Sjögren's syndrome, a complicated array of autoimmune events ultimately leads to atrophy of the salivary and lacrimal glands. So-called secondary disease is associated with systemic (connective tissue) disease such as rheumatoid arthritis, systemic lupus erythematosus, polymyositis, polyarteritis, and Waldenstrom's macroglobulinaemia (Table 1) 606.

The diagnosis of Sjögren's syndrome requires a high index of suspicion; a complete history and physical examination, together with extensive haematological and immunochemical studies should be undertaken. The single most specific test is biopsy from the salivary glands of the inner lip, which shows lymphocytic infiltration. As the disease progresses, repeated episodes of sialectasia cause segmental duct strictures, local or widespread globular dilatation, and cyst formation. Sialography reveals areas of dye extravasation.

Treatment is based on relief of symptoms and management of any underlying systemic disease. Affected patients need to be monitored for the development of serious concomitant conditions, including lymphoma and carcinoma of the oesophagus.

Benign or malignant tumours of the salivary glands account for less than 4 per cent of all tumours of the head and neck. Salivary gland tumours are most common in the parotid (85 per cent): 60 per cent of these are benign, the most common type being benign mixed tumour. The likelihood of a tumour being malignant is 40 per cent in the parotid gland, 60 per cent in the submaxillary gland, and 90 per cent in the sublingual gland.

Histologically, mucoepidermoid carcinoma accounts for the majority of parotid malignancies. Adenocarcinoma and adenocystic carcinoma are the most frequent malignant tumours in the submaxillary and sublingual glands. The incidence of occult and nodal disease and of recurrent disease exceeds 40 per cent in patients with high-grade mucoepidermoid and squamous cell carcinoma. Adenocystic carcinoma, and undifferentiated and high-grade mucoepidermoid carcinoma are prone to metastasize to distant sites, including the brain, lung, and bone.

A history suggestive of a tumour is an indication for extensive tests and repeated examination. If bulging or asymmetry of the cheek, or a mass of the upper neck, the submaxillary or submental triangle, the floor of the mouth, or the soft palate is detected, fine needle biopsy and radiography should be undertaken.

In the absence of an obvious mass, a tumour is suggested by local or referred facial pain, spasm of the masseter or temporalis muscle, trismus or unexplained temporomandibular joint dysfunction, bloody or discoloured saliva, and cranial nerve deficits.

Examination of the head and neck should include bimanual examination of the soft tissue and bones of the face and mandible, analysis of cranial nerve function, auscultation over the orbits, cheeks, and neck, and assessment of the patency of Wharton's and Stensen's ducts.

Radiographs will document the presence, size and extent of any tumour, along with associated pathology, such as bony destruction. CT scanning with contrast is excellent for the assessment of soft tissue and bone; MRI with gadolinium enhancement provides good soft tissue imaging, and is more sensitive to salivary gland neoplasia than is CT. MRI will also detect vascular lesions such as haemangioma or lymphangioma; these can be confirmed by arteriography. Cystic lesions, including vascular lakes, can be identified on ultrasonography. Technetium-99m sulphur-colloid scanning is positive in most patients with Wharton's tumours and oncocytomas. A positive gallium scan is suggestive of a lymphomatous or inflammatory condition. Chest radiography should be performed routinely when a parotid neoplasia is identified.

Fine needle biopsy often allows a specific histological diagnosis to be made with minimal risk of complications or tumour dissemination. Open biopsy is justified in patients with clinically obvious malignancy and in those for whom surgery is not an option.

This tumour accounts for 70 per cent of all benign salivary gland tumours. The lateral lobe of the parotid gland is most commonly affected, and women in the fifth decade of life are predominantly affected.

The history is usually that of a slowly growing mass in the parotid, with no pain and no other symptoms of head and neck disease. Examination discloses an asymmetrical parotid gland with a well-circumscribed mass in the body or tail of the lateral lobe. Lymphadenopathy is not usually present; sensation and motion in the face are normal. Surgical excision, with preservation of the facial nerve, is the treatment of choice: the pseudoencapsulated tumour can usually be dissected away from the facial nerve and its branches. Histological examination reveals pleomorphism of the microscopic myoepithelial cells.

Recurrent disease is not uncommon, particularly in younger patients. This may follow incomplete removal of the tumour or following rupture of the pseudocapsule during surgery. Recurrence can be a major problem when it is associated with miliary spread and encapsulation of the facial nerve. Treatment must be tailored to the individual patient: aggressive surgical treatment requires removal of all or part of the facial nerve and its surrounding tissue, followed by major reconstruction. Postoperative radiotherapy is advisable after major ablation, or after nerve-sparing surgery.

Papillary cystadenoma lymphomatosum, the second most common benign tumour, is found exclusively in the parotid gland, and affects predominantly men, the peak age incidence being 55 years. There is a high incidence of bilateral disease.

The tumour is typically slow growing, asymptomatic, soft, and lobulated. Needle aspiration yields a brownish fluid. Histological examination reveals two layers of epithelial cells surrounding a lymphoid stroma with a cystic centre. T and B lymphocytes show a normal distribution and ratio. Malignant degeneration is rare, and the most likely diagnostic confusion would be with lymphoma or a lymphoproliferative disorder. The treatment of choice is long-term observation, or surgical extirpation.

These diverse, rare, benign tumours are characterized by proliferation of epithelial elements in the absence of cells of mesenchymal origin. The evaluation and treatment of these tumours, which include sebaceous lymphadenoma, basal cell adenoma, and myoepithelioma, is similar to that of Warthin's tumour.

This benign tumour affects the elderly, and may originate in any of the salivary glands. It presents as a slow-growing, painless mass which is well circumscribed and soft. Confusion with lipoma is not unusual. Histologically, this tumour is characterized by polyhedral cells with eosinophilic cytoplasm. Electron microscopy shows these to be laden with mitochondria. Treatment is by surgical extirpation with preservation of surrounding structures.

Mucoepidermoid carcinoma of the salivary glands is the most common malignancy of the parotid gland. The peak incidence is in the fifth decade, and women are affected more frequently than men. Histological features reveal the derivation of the tumour from the mucous and basal cells of the salivary gland ducts: mucous cells, cystic spaces with stromal penetration, inflammation, and squamous differentiation may all be seen. Classification of tumours as high or low grade relates to pathological staging and also predicts clinical behaviour. High-grade tumours show more aggressive growth and have a poorer prognosis, with a 5-year survival rate of 40 per cent compared to 90 per cent for patients with low-grade tumours. The incidence of lymph node metastasis is approximately 40 per cent; the recurrence rate is 30 per cent. Common sites of metastasis include regional lymph nodes, brain, skin, bone, and lung.

This aggressive tumour originates from the reserve cells of the intercalated ducts and canaliculi. Histological examination shows a basic pattern of basaloid cells in a cribriform, tubular, and solid field. The growth rate of the tumour is variable, and the minor salivary glands and the submaxillary gland are usually affected. The incidence peaks at the fifth decade; both sexes are affected equally. Sixty per cent of patients have early perineural invasion, and the incidence of local and distant recurrences exceeds 50 per cent. The 5- and 2-year survival rates are 60 per cent and 20 per cent, respectively. Common sites of distant metastasis are the brain and lung.

This tumour is principally found in the parotid, where it often shows a transition from slow to rapid growth. Histological features are those of a mixed tumour showing features of both anaplasia and invasion. The peak incidence is in the sixth to seventh decade of life; both sexes are affected equally. There is a 20 per cent incidence of regional lymph node metastasis and an overall recurrence rate of 50 per cent. Principal sites of metastasis are regional lymph nodes and the lungs. The 5-year survival rate is 50 per cent.

This tumour usually appears as a solitary, encapsulated, low-grade, slowly growing nodule in the parotid gland. It is frequently bilateral and mainly affects women in the sixth decade of life. Histologically, it is a serous cell tumour originating from reserve cells of the terminal ducts. The incidence of regional lymph node metastasis is 10 per cent; distant metastases predominantly occur by haematogenous spread to the bone and lung. The overall recurrence rate is 50 per cent, and the 5-year survival rate exceeds 50 per cent.

There are many types of adenocarcinoma, including mucinous cell, ductal cell, and clear cell adenocarcinoma of intercalated duct cell origin. All share the basic characteristics of a firm, solitary, nodular mass in a salivary gland containing papillary or non-papillary cells, which may or may not secrete mucus, growing in sheets, cords, or cylinders. The incidence of local lymph node metastasis approaches 25 per cent; the overall recurrence rate is 40 per cent. Common sites of metastasis include regional lymph nodes, lung, and bone. The 5-year survival rate is 65 per cent.

Squamous cell carcinoma in a salivary gland should be considered to be metastatic until proved otherwise. The tumour arises from ductile epithelial cells, and histological examination reveals characteristic pearl formation, keratin production, and intracellular bridges. It is most common in the submaxillary gland of individuals in the fifth decade of life. The firm, well-defined mass has a variable growth rate, and frequently shows fixation to surrounding structures and nodularity. Lymphadenopathy is common. The overall recurrence rate is 50 per cent, with a 5-year survival rate of 50 per cent.

This tumour characteristically presents as a solitary, firm, rapidly growing mass, usually of the parotid gland, in the seventh or eighth decade of life. Histological examination reveals anaplastic invasion of spherical or spindle cells growing in sheets. The overall recurrence rate is 40 per cent, with a 25 per cent incidence of regional lymph node metastasis. The 5-year survival rate is 35 per cent.

Surgical treatment carries the best results. Subtotal or total parotidectomy is required, with preservation of the facial nerve when possible. The facial nerve should be resected if its preservation is likely to be associated with incomplete resection of the tumour. Primary nerve graft, reconstruction, or reanimation procedures will then be required.

Regional lymph node dissection should be considered in patients with mucoepidermoid or squamous cell carcinoma of the parotid or submaxillary gland, which is associated with a greater than 40 per cent incidence of metastasis to regional nodes. Neck dissection should be undertaken in all patients with palpable nodes.

Surgery may be contraindicated if disease is extensive, or in severely debilitated patients: chemotherapy or radiotherapy are alternative options. Postoperative radiotherapy is indicated if surgical margins are close or positive for tumour cells, and in patients with suspected subclinical lymph node disease, extranodal disease, or tumours such as adenocystic carcinoma, and high grade mucoepidermoid carcinoma that show a propensity for early metastasis.

The use of chemotherapy is controversial. At best it provides palliation or adjuvant therapy in patients who fail to respond to standard treatment or who exhibit diffuse distant metastasis.

Blunt and penetrating injury and exposure to radiation account for the majority of injuries to the salivary gland. Trauma may also arise through poor dental hygiene, and chemical and iatrogenic injury. Assessment of injury to the salivary glands must also take into account the surrounding structures. The head and neck should be thoroughly examined. Retrograde injection of methylene blue into Stensen's or Wharton's ducts will reveal any interruption of salivary flow. Patients who have suffered animal or human bites or other penetrating injury should receive tetanus toxoid; potentially rabid animals should be isolated and tested. Most patients should receive broad-spectrum antibiotics. Blunt trauma may result in haematoma or a loculated infection, which necessitates drainage.

Surgical treatment of trauma to the salivary glands follows the basic principles of trauma surgery. Major mucosal or skin flap repairs are best reserved for secondary repair, unless no other means of covering a defect is available: skin grafting is always an option. Repair of all nerves, especially the lingual, hypoglossal, and facial nerve, is crucial. The best possible repair is a direct end-to-end anastomosis; sural nerve cable grafting is the next best procedure.

Salivary ducts should be repaired using an operating microscope. Large distal ducts and orifices can be repaired by marsupialization and duct reimplantation; repair of central and more distal ducts is more difficult, and late stenosis is common. All repairs should be made over an internal silastic stent.

The salivary glands are frequently damaged during radiotherapy to the head and neck. A dose above 1000 cGy causes significant atrophy and a change in the volume and characteristics of the salivary secretion. Patients experience progressive dental caries, periodontal disease and poor taste and appetite.

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