1. The Salivary Glands diseases

2. Mumps
Etiology
Mumps, the most common salivary gland disease, is a paramyxovirus infection usually of both parotid glands and to some extent the submandibular and sublingual glands.
The usual case involves a child who is not immunized, while a more severe involvement with more complications occurs in adults.
Transmission occurs via infected saliva droplets, which require a 14‐ to 21‐day incubation period before the onset of symptoms.

3. Clinical Presentation
The child usually will develop low‐grade fever and malaise. High‐grade fevers are suggestive of metastatic orchitis (in males) or meningitis.
Both parotid glands become enlarged in 75% of cases, but not always at the same time; therefore, unilateral parotid gland enlargement is frequently observed.
The enlarged parotid glands are tender to the touch and will be uncomfortable during jaw movements. Submandibular glands are frequently tender and enlarged as well.

4. Most cases run a course of slightly less than 2 weeks
Most cases run a course of slightly less than 2 weeks. When the infection resolves, a permanent immunity is incurred. However, in rare cases in children and more commonly in adults, involvement of other organs complicates the usual benign, self‐limiting course.
Orchitis occurs in 25% of adult men and is heralded by testicular swelling and pain. Less frequently, mumps pancreatitis develops, which will produce upper abdominal pain, nausea, and vomiting.
In females, oophoritis parotidea uncommonly develops and is heralded by lower abdominal pain and cramping.
The most severe complication is meningitis, which may eventuate in encephalitis and death in rare cases. Early signs of meningitis are headaches and neck stiffness.

6. Diagnosis
The diagnosis of mumps is confirmed by isolating paramyxovirus from saliva or by paired serum studies that show a fourfold rise in mumps antibody titers.

7. Differential Diagnosis
Bacterial parotitis
Other viral parotitis (coxsackie A virus, cytomegalovirus, echovirus, and parainfluenza viruses)
Obstructive parotitis
Sialosis
Sarcoidosis
Sjögren's syndrome

8. TREATMENT
Mumps, including complications involving other organs, is self‐limiting.
No specific therapy is given other than supportive care, which usually consists of bed rest, antipyretics, analgesics, and hydration.
Orchitis, if it develops, is treated with testicular elevation and ice.
Meningitis, if it develops, may require corticosteroids, elevation of the head, and induced hyperventilation to combat cerebral edema.

9. PROGNOSIS Mumps is self‐limiting and mostly resolves without residua.
Rare deaths occur from meningitis progressing to encephalitis.

10. Bacterial Parotitis Etiology
Bacterial parotitis occurs both in a childhood form (recurrent) and in an adult form.
The recurrent childhood form seems to be unrelated to any predisposing factors or underlying pathology.
The adult form occurs more commonly with advancing age and is often related to dehydration secondary to debilitation, decreased parotid flow secondary to parasympatholytic drug, inspissated mucous plugs producing static salivary flow, or decreased salivary flow related to Sjogren syndrome.

11. Clinical Presentation
In either form, the gland becomes swollen and painful.
In the infection's early stages, the gland will become more swollen and painful with eating, and salivary production further distends the parotid capsule.
The patient is often febrile, but mild cases may not be accompanied by fever.
The opening of Stensen duct is often erythematous, and a suppurative exudate or saliva‐diluted suppurative exudate, which will appear as a milky exudate, may be expressed.
The most common causative organism is Staphylococcus aureus, which is usually the methicillin‐resistant strain (MRSA).
However, the infection usually is not caused by MRSA alone, but is accompanied by several species of streptococci.

12. Severe infections will extend beyond the parotid capsule and may result in a salivary‐cutaneous fistula, a pharyngeal space infection, or an external or middle ear infection.
Bacterial parotitis is much less common than bacterial submandibular gland sialadenitis, probably because of the downward tract of the parotid duct, which makes stasis less likely, and the more proteinaceous parotid secretion.
Unlike the mucoprotein secretions of the submandibular gland, parotid secretions are less viscous and do not support bacterial growth as well.

14. Diagnosis
Culture and sensitivity testing of the exudate. It is important to establish the presence of S aureus and to determine whether it is true MRSA or only penicillin‐resistant via the elaboration of β‐lactamase.
Sialography has been superceded by computed tomography (CT) and magnetic resonance imaging (MRI) because of the more detailed information they offer.
A blood count will usually show a slight leukocytosis with a shift to the left indicative of immature neutrophils.

15. DIFFERENTIAL DIAGNOSIS
Most cases of infectious parotitis are evident by the clinical signs and symptoms of an enlarged, painful parotid gland with an altered salivary flow.
However, in adults, an underlying pathosis should be considered. In the absence of debilitation or drug‐induced xerostomia, one must consider a sialolith or early Sjogren syndrome, particularly in women, and a benign lymphoepithelial lesion in either sex.
HIV parotitis also produces a painful parotid enlargement, although it is caused not by bacteria but by multiple lymphoepithelial cysts.
In addition, sarcoidosis and sialosis cause parotid enlargement; however, the pain associated with these conditions is mild and pus is not produced.

16. TREATMENT
Initial treatment includes hydration, which may require intravenous fluids and antibiotics.
If cultures identify S aureus that is not MRSA and the usual streptococci, then antibiotics such as ampicillin with sulbactam, 1.5 g every 6 hours intravenously, is a good choice, as is ciprofloxacin, 400 mg every 12 hours intravenously.
If the cultures identify MRSA, the best therapy is 500 mg vancomycin administered intravenously every 12 hours.
PROGNOSIS
Specific antibiotics and hydration therapy are very effective. Persistent infection should alert the clinician to look for several possibilities: a parotid mucous plug or sialolith; immunosuppression; resistant bacteria; incorrect initial interpretation of cultures; an undiagnosed abscess; or an unrecognized underlying pathology such as Sjogren syndrome.

17. Benign Lymphoepithelial Lesion
Etiology
The etiology of benign lymphoepithelial lesion is unknown. It has been speculated that autoimmune, viral, or genetic factors are the trigger.

18. Clinical Presentation
The benign lymphoepithelial lesion can be conceptualized as a Sjogren‐like infiltration and enlargement of the parotid glands without the mucosal dryness (sicca syndrome) and without the rheumatoid manifestations.
As the disease progresses, both parotid glands become involved in nearly all cases.
The parotid gland enlargements are diffuse and soft at first, becoming more firm throughout the years.
Secondary bacterial parotitis frequently occurs because of stasis of salivary flow and ductal obstruction.
Lymphoepithelial lesions may include a single lymphoepithelial cyst. However, in HIV infection, multiple cysts are the rule.

19. Differential diagnosis
Incisional parotid biopsy.
Differential diagnosis
Parotid neoplasms
Sarcoidosis
nutritional sialosis
HIV parotitis
mumps.

20. Prognosis Treatment Treatment is palliative.
The possibility of neoplastic transformation is a concern. The detection of a monoclonal lymphocytic infiltrate is thought to be suggestive of a low-grade lymphoma.
Treatment is controversial; some clinicians advocate irradiation therapy whereas others recommend monitoring when the disease is limited to the salivary glands.
Prognosis
Most BLELs remain benign. Only 5% to 10% progress to a lymphoma, most of which are B cell lymphomas.

23. Treatment that is available for the dry mouth patient can be divided into four main categories:
(1) preventive therapy,
(2) symptomatic treatment,
(3) local or topical salivary stimulation,
(4) systemic salivary stimulation.
Effective treatment of an underlying systemic disorder associated with salivary gland dysfunction may correct the salivary complaint as well.

26. Pleomorphic Adenoma
The pleomorphic adenoma is the prototypical benign yet true neoplasm; that is, it will continue to grow—or regrow if not completely removed—but it is incapable of metastasis.
It occurs at different statistical incidences in all salivary glands. Eighty percent of tumors that occur in the parotid gland are benign.
Pleomorphic adenomas, and salivary gland tumors in general, are not commonly found in the submandibular and sublingual glands.

27. Clinical Presentation
Eighty percent of all pleomorphic adenomas in the parotid gland develop in the superficial lobe, which constitutes 80% of the parotid gland.
It presents as a freely movable, firm mass. Peculiarly and rarely, these can fluctuate in size or be painful.
Pleomorphic adenomas do not induce facial nerve paresis. Any facial nerve weakness not attributable to previous surgery should be considered a malignancy until proven otherwise.
When a pleomorphic adenoma arises from the deep lobe of the parotid gland, it usually goes unrecognized for a number of years until its size creates symptoms of dysphagia or gagging.

29. When a pleomorphic adenoma presents in the mucosa of the hard palate‐soft palate junction, it will be a firm, painless mass with intact overlying mucosa.
If the mucosa is ulcerated and the ulceration is not attributable to trauma or a biopsy, the mass should be considered a malignancy.
In the palatal mucosa, the mass will seem to be fixed to the palate.
Since the pleomorphic adenoma cannot invade bone, this is not caused by bony invasion but rather by the inelasticity of the palatal mucosa, which becomes distended by the tumor mass and may eventuate in a cupped‐out resorption of bone.
In other oral mucosal sites, the pleomorphic adenoma presents as a freely movable, circumscribed mass.
Pleomorphic adenomas can arise at any age but are somewhat more common between the ages of 30 and 50 years and are slightly more common in women.

31. Diagnosis
For a mass in the parotid gland, a computed tomography (CT) scan or magnetic resonance imaging (MRI) scan is valuable to confirm its location in the parotid, specifically in the superficial lobe.
For a mass in the palatal mucosa, a CT scan, particularly coronal views, also is recommended to determine its extent and the degree of any resorption of the palate. A deep incisional biopsy of the mass is recommended in its center to establish a firm permanent‐section diagnosis prior to planning definitive surgery.

32. Differential Diagnosis
The differential diagnosis of a firm mass in the parotid gland must include a
Warthin tumor
Basal cell adenoma
Mucoepidermoid,Adenoid cystic, Acinic cell carcinomas.
Nonsalivary gland neoplasms that are known to occur in the parotid gland—ie, hemangiomas, lymphangiomas, lipomas, and lymphomas within parotid lymph nodes—may also present in a similar fashion.

33. The differential diagnosis of a firm mass in the palatal mucosa with intact overlying epithelium is primarily a subset of other salivary gland neoplasms. In order of statistical likelihood, they are adenoid cystic, mucoepidermoid, and polymorphous low‐grade adenocarcinomas.
Another benign tumor that requires some consideration is the canalicular adenoma.
In addition, several nonsalivary gland tumors may present with a similar appearance, such as non‐Hodgkin lymphoma and neurofibroma.

34. Treatment The treatment of choice is surgical excision.
Enucleation of parotid mixed tumors is not advisable because of the risk of recurrence due to extension of tumor through capsular defects.
Removal of mixed tumors arising within the parotid gland is complicated by the presence of the facial nerve.
Resection of the submandibular gland is the preferred treatment for mixed tumors in this location.
Lesions of the palate or gingiva often involve or abut, periosteum or bone, making complete removal difficult unless some bone is removed.

35. Prognosis
Inadequate initial removal of mixed tumors in major glands may result in recurrence, often with multiple, discrete tumor foci.
With each recurrence there is an increased possibility of malignant transformation (carcinoma ex-mixed tumor).

36. Warthin Tumor
Papillary cystadenoma lymphomatosum is a benign hamartomatous or reactive proliferation of ductal salivary gland cells and lymphoid elements that is commonly referred to as a Warthin tumor.

37. Clinical Presentation
The tumor will present almost exclusively in the superficial lobe of the parotid gland as a firm to doughy painless mass of several months' duration.
It is said to occur most frequently in the "tail" of the parotid gland, which is the most inferior and posterior portion of the gland below the ear and the angle of the mandible.
Men are affected more frequently than women by a 3:1 ratio, and it affects those between 30 and 70 years of age.
Warthin tumors are known to occur bilaterally (synchronous tumors) in about 4% to 6% of cases, or two or more tumors are known to occur simultaneously in the same gland (also synchronous tumors).

38. Diagnosis
A CT scan may be performed to document the tumor's location in the parotid gland, but an experienced clinician can determine the same by examination.
A fine‐needle aspirate is quick and straightforward and may be the most yielding study.
It will identify the lesion as a Warthin tumor or at least rule out a malignancy, which would require a more aggressive surgery.

39. Differential Diagnosis
Pleomorphic adenoma.
Basal cell adenoma.
Malignant parotid tumors.

40. TREATMENT
A Warthin tumor is excised with a superficial parotidectomy, representing both a diagnostic biopsy and the definitive treatment for this tumor. The cut gross specimen will often reveal the characteristic finding of a soft, sponge‐like multicystic lesion containing a thin brown fluid.

41. Prognosis
A superficial parotidectomy is curative for a Warthin tumor. In rare instances, an apparent recurrence is noted, but such phenomena probably represent new tumors arising from residual gland elements.

42. Mucoepidermoid Carcinoma