Parotitis

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Background

The parotid glands are small exocrine glands that rarely call attention to themselves. Perfect function throughout life is normal.

Dry mouth, drooling, swelling, and pain are essentially the only symptoms caused by dysfunction of the salivary glands.

The major salivary glands and their ducts are strategically situated on either side of the dental occlusal planes to irrigate and saturate a food bolus with saliva during chewing. The parotid gland contacts the mandibular ramus and muscles of mastication, which massage the gland during chewing. The mechanical squeezing and the parasympathetic nervous system, which analyzes a number of sensory inputs, cause the glands to inject an appropriate quantity and quality of saliva into the oral cavity. Minor salivary glands are scattered throughout the oral cavity and pharynx to assist the major glands in moistening, lubricating, and protecting the teeth and mucosa. The normal flow of saliva though the duct prevents oral bacteria from ascending the duct to cause infection.

Inflammatory swelling of the glands may present a serious diagnostic challenge. Parotitis presents in many forms and the symptoms vary from modest to prostrating. Reading the numerous journal on parotitis articles reveals frequent contradictions in the classification, etiology, and treatment of the disorders. A pure viral or bacterial infection, an autoimmune inflammation, or a combination of these can be the etiology. In this article, evolution of the knowledge of parotitis, as well as the diagnosis and treatment, is discussed.

Infectious parotitis

This group of diseases is caused by known infectious agents.

Acute bacterial parotitis

Acute bacterial parotitis is now infrequent, but its historical importance and occasional occurrence today necessitate in-depth knowledge of this entity by the otolaryngologist. Mumps and bacterial parotitis were differentiated by 1800, but neither was effectively treated. The mortality rate for bacterial parotitis was 80%. Before antibiotics and intravenous administration of fluids were available, bacterial parotitis occurred in postoperative patients or other severely ill patients who became dehydrated and contributed to their demise as an incurable sepsis.

Early in the 20th century, surgeons were hesitant to incise and drain parotid abscesses and frequently used ineffective conservative measures until the process was irreversible. They feared the consequences of the unsightly scar and facial paralysis. Parotid abscess is depicted in the image below.


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Elderly man with parotid abscess.

In 1917, Lilienthal described a surgical treatment that was very similar to what is used today.[1] He called parotid abscesses celiac parotitis because they were believed to be metastatic from abdominal infections. Other authors used names such as acute surgical parotitis, acute necrotic parotitis, acute gangrenous parotitis, and other historical designations according to Hemenway and English in 1971.[2]

Lilienthal designed a vertical incision just anterior to the auricle that coursed posteriorly and inferiorly below the ear to join and follow an upper cervical skin crease that paralleled the lower mandibular border as seen in the image below.[1] He elevated the outlined skin flap forward to expose the parotid gland and made multiple incisions into the gland parallel to the facial nerve branches. He then opened the fascia behind the angle of the mandible to drain deeper spaces. The wound was packed and healed by secondary intention, resulting in a surprisingly good cosmetic result. The number of patients treated by this drainage is not known, but this treatment was probably almost anecdotal to Lilienthal’s contemporaries.


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Incision outlined for incision and drainage of parotid abscess.

In 1919, Zachary Cope, a British Army surgeon, described 7 patients with parotitis that he had treated in Baghdad during the exceptionally hot summer of 1917.[3] He recorded that these soldiers had heatstroke or were severely affected by the extreme heat. The patients developed parotid swelling accompanied by fever and general malaise. Cope made wide T-shaped incisions in the gland to allow drainage. Four of the 7 survived after sloughing gangrenous parotid tissue. Cope stated that although the disease was a bacterial infection, the excessive heat and debilitating illness predisposed to its development.

In 1923, Blair and Padgett of St. Louis published an article stating that early surgical drainage of the infected gland was safe and frequently was life saving.[4] They stated that acute suppurative parotitis was an ascending duct infection related to decreased salivary flow, fever, and general debilitation. They cultured the pus and found that Staphylococcus aureus was the most common organism. The treatment proposed by Blair and Padgett did not become the standard practice for several more years. However, the high mortality rate decreased early in the 20th century and was 30-50% by 1930, probably because of more prompt and effective drainage of the abscesses.

From the 1930s to the 1960s, irradiation treatment of numerous diseases became popular, and several authors advocated 4-6 Gy delivered over 4-5 days for bacterial parotitis. Most patients with severe infections required surgical drainage despite radiation treatment. By 1960, most published papers stressed large doses of antibiotics, improved oral hygiene, and increased fluid intake as treatment, with incision and drainage for failures. They found that the parotid capsule and septations required wide exposure and extensive deep incisions parallel to the facial nerve branches to exteriorize the diseased gland. Physicians recognized the importance of hydration and oral hygiene for debilitated patients, and the incidence of bacterial parotitis plummeted.

Parotitis is now more common in elderly patients because many take medications with an atropine effect that retards salivary flow and predisposes to ascending infection. Many psychotropic drugs are relatives of antihistamines.

Acute parotitis in neonates

This rare form of parotitis is lethal without treatment. In January 2004, Spiegel et al reviewed the literature and stated that only 32 cases had been reported in journals during the previous 3 decades.[5] The characteristic clinical picture was of a sick premature infant with unilateral parotid swelling and inflammation. Seventy-five percent of the cases were in male infants. Pus expressed from the duct cultured S aureus in more than half of the cases. Most all of the cultured bacteria were from organisms present in the oral cavity, which suggests an ascending infection from the mouth.

Treatment is prompt administration of gentamicin and antistaphylococcal antibiotics plus adequate hydration, with a cure in approximately 80% of cases. Failure to improve after 24-48 hours of treatment necessitates surgical drainage. Recurrence is uncommon. Acute bacterial parotitis in children between one year of age and adolescence is extremely rare and only a few have been reported. The etiology and treatment is the same as for adults.

Chronic bacterial parotitis

Chronic bacterial parotitis may exist in the presence of calculi or stenosis of the ducts secondary to injury. A number of articles and book chapters describe that chronic infection is a sequela of acute bacterial infection, but the evidence is scant. Most authors have suggested that decreased salivary flow was the common denominator, but reduced flow may be due to the inflammation. In most instances, the chronic disease is either autoimmune or of unknown etiology with superimposed bacterial infections and should not be designated as a chronic bacterial infection.

Acute viral parotitis (mumps)

Mumps, one of the classic childhood infections, is spread by droplets or by direct spread from oropharyngeal secretions that contain the paramyxovirus. Universal immunization, which began in 1977, has made the clinical disease unusual in developed countries. The child should receive the first measles, mumps and rubella (MMR) vaccine at age one year and a second at age 4-6 years.[6, 7]

Occasional outbreaks of mumps are seen, mostly in teenagers or patients in their early twenties who did not receive the second shot. Before the vaccines were available, exposure was almost universal, and clinical disease resulted in 60-70% of those who were exposed. The disease was characterized by grossly enlarged and modestly tender parotid glands. Parotid stimulation caused pain in the gland and ear. Mumps was a benign disease in the vast majority of cases but was occasionally complicated by meningoencephalitis, pancreatitis, orchitis, or deafness especially in young adults. Treatment was and is symptomatic and supportive.

HIV parotitis

Generalized lymphadenopathy has long been associated with HIV, but the localized enlargement of the parotid gland is less well known. The course of the disease is different enough between children and adults to warrant a separate description.

HIV parotitis in children

Salivary gland involvement in children with HIV is well recognized and is much more common than involvement in adults. Characteristically, the gland is firm, nontender, and chronically enlarged (unilateral or bilateral) and usually causes few symptoms. Lymphoepithelial cysts are less common than in adults. Xerostomia with decreased salivary flow rates occurs in adults but is infrequent in children. Infiltration of CD8-positive lymphocytes, possibly as a result of HIV, Epstein-Barr virus (EBV), or an interaction between the 2, enlarges the gland. The diagnosis of HIV parotitis is usually clinical with the typical findings. Other forms of chronic parotitis are rare in children.[8]

The picture is not typical for acute bacterial infection. No specific treatment exists for this parotitis, and none is usually required. Some evidence indicates that parotid involvement is a good prognostic sign.

HIV parotitis in adults

The name lymphoepithelial lesion is frequently applied to HIV parotitis and adds confusion to the many names of parotid inflammatory diseases. A group at the State University of New York (SUNY) presented a series of 50 patients with HIV and masses in the tail of the parotid. Most of the patients were prison inmates and intravenous (IV) drug users. Parotidectomy was performed in 35 patients, with patients earlier in the series undergoing lateral lobectomy and later patients undergoing local excision of involved tissue.

Microscopic examination of the excised specimen revealed 3 types of involvement: (1) follicular hyperplasia of the parotid lymph nodes; (2) diffuse infiltration of the gland by lymphocytes (CD8 T cells) with appearance much like Sjögren disease; and (3) benign lymphoepithelial cysts that are the type of involvement most frequently described in the literature. The cyst walls are lined by stratified epithelium that may be squamous, columnar, cuboidal, or pseudostratified. Aggregates of lymphoid tissue are present within the cyst walls. The salivary parenchyma has a normal appearance. MRI shows the multiple cysts within the enlarged glands and is almost diagnostic. If the enlarged gland causes cosmetic deformity or pain, antiviral therapy, low-dose radiation therapy, or surgical excision may decrease the size of the gland.[9] Most authors suggest enucleation of large cysts. In some individuals, the parotid gland symptoms are very similar to and may be confused with Sjögren syndrome.

Parotitis in tuberculosis

The incidence of pulmonary tuberculosis steadily decreased in the United States until 1985, but the trend reversed and has been slowly increasing since that time with a concurrent rise in extrapulmonary tuberculosis.[10] Tuberculosis is an uncommon cause of parotitis and is not particularly important, except that approximately 25% of patients have pulmonary tuberculosis and may infect their associates. Approximately 3% of patients with AIDS have tuberculosis, and almost 70% of these patients have pulmonary tuberculosis.

In the past, extrapulmonary tuberculosis was apt to be due to atypical tuberculosis, such as the bovine variety, but today, most cases are due to Mycobacterium tuberculosis. Patients have enlarged, nontender, but moderately painful glands. Involvement is most frequently confined to the parotid lymph nodes, but the gland may become diffusely involved with the disease.

The diagnosis is made by typical chest radiograph findings, cultures, or histologic diagnosis after the gland has been removed. The long delay for cultures prolongs the public’s exposure to the disease. A positive skin test is not particularly helpful because of the high incidence of positive skin tests in the general population. Fine-needle aspiration biopsy occasionally yields Langerhans giant cells, which suggest tuberculosis. When diagnosed and treated with antitubercular medications, the gland may return to normal in 1-3 months. Untreated cases progress to draining fistulas and fibrosis.

Chronic punctate parotitis (chronic autoimmune parotitis)

Although acute bacterial parotitis is fairly well understood, chronic enlargement of the salivary glands with recurring infection has caused confusion for more than a century. Numerous terms found in the literature, such as Mikulicz disease, Sjögren syndrome, benign lymphoepithelial lesion of Godwin, chronic punctate sialectasis, and recurrent parotitis of childhood (as seen in the image below), are confusing to the physician. Sialography was commonly used in the workup of parotid disease in the past, and this group demonstrates punctate sialectasis, which implies point like dilatations within the gland.


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Six-year-old girl with recurrent parotitis of childhood.

Mikulicz disease

Johann Mikulicz-Radecki (1850-1905), a professor of surgery in Breslau, Poland, trained under Theodore Billroth of Vienna. In 1888, he encountered a 42-year-old farmer who had experienced lachrymal gland swellings followed by enlargement of the submaxillary and parotid glands. The enlarged lacrimal glands interfered with his vision and were excised by Mikulicz. The submaxillary glands were also excised, but the parotid glands were not removed. Mikulicz recorded in his publication that this was a benign disease and was not related to tuberculosis, leukemia, or malignant lymphoma. He believed the causative factor to be infection. No other patient with an identical disease has been described.

Unfortunately, the name Mikulicz has been associated with numerous conditions that involve enlarged parotid glands. Early in the 20th century, numerous reports described conditions associated with enlargement or inflammation of the salivary glands. In 1927, Schaffer and Jacobson presented a simplified grouping with only 2 major divisions:[11] (1) cases in which tuberculosis, leukemia, or some other disease had enlarged the gland and (2) Mikulicz disease, in which these other diseases were ruled out. The term "Mikulicz disease" probably should be discarded because of ambiguous definition. However, the term is so popular that it will not soon go away.

Sjögren syndrome

The next major milestone in the understanding of chronic parotitis was the publication of a paper in 1933 by Henrik Sjögren, a Swedish ophthalmologist.[12] In 1930, Sjögren observed his first cases of keratitis sicca and began a systematic study of the disease that lasted more than 20 years. In his landmark publication, he named the disorder keratoconjunctivitis sicca. Sjögren published so extensively that by 1936, the entity was referred to as Sjögren syndrome, a name that today is widely employed throughout the world.

Sjögren reviewed the available literature on the subject and published histopathologic studies of the cornea, conjunctiva, and lachrymal glands. He reported that this disease affected menopausal women in whom the keratoconjunctivitis sicca was a local phenomenon. He stressed that arthritis was a significant feature of the disease and occurred in most patients. Patients had an elevated erythrocyte sedimentation rate. Hypochromic anemia and fever were occasionally present. Sjögren revived the Schirmer test for measuring tear secretion and popularized the use of the Rose Bengal staining technique for the diagnosis.

Sjögren syndrome, similar to other connective tissue diseases, is a multisystem disorder with diverse features. The entity is classified by some as a primary condition (primary Sjögren syndrome) or is associated with autoimmune diseases such as lupus erythematosus or rheumatoid arthritis (secondary Sjögren syndrome). In the fully developed syndrome, most organs seem to be involved.

Most authors classify the disease as definite Sjögren syndrome, which includes (1) objective evidence of keratoconjunctivitis sicca or (2) characteristic pathologic features of the salivary glands. The probable Sjögren syndrome requires 2 out of 3 of the following: (1) recurrent chronic idiopathic salivary gland swelling, (2) unexplained xerostomia, and (3) connective tissue disease.

The disease most commonly appears in people aged 40-60 years, but it may affect small children. In Sjögren syndrome, the prevalence of parotitis in women versus men is approximately 9:1. The involved parotid gland is enlarged and tender at times. Massage of the gland produces clear saliva with flocculated clumps of coagulated proteins.

The next major development in the evolution of knowledge of chronic parotitis was a collective pathologic study of "Mikulicz Disease" by Morgan and Castleman in 1953. They reported 18 cases and stated that the pathologic involvement was uniform in all of these cases. The basic features are massive lymphoid infiltration with atrophy of the acini, proliferation of the cells of the small ducts that leads to narrowing of the lumen, and, finally, obliteration.

The functioning parts of the gland (acini) are destroyed, leaving the appearance of large lymph follicles. However, among this distorted architecture, islands of ductal epithelial cells and myoepithelial cells that appear fairly healthy can be observed. These groupings are called epimyoepithelial islands. The large ducts appear to be normal. In the Morgan and Castleman series, some of the surgical procedures were radical parotidectomies, including severing the facial nerve, because the surgeon believed that the condition was a malignancy.

For further reading on Sjögren syndrome, please see the Medscape Reference articles on the subject in our Pediatrics, Ophthalmology, Emergency Medicine, Rheumatology, and Dermatology sections.

Lymphoepithelial lesion of Godwin

John T. Godwin, a New York pathologist, published a series of 11 parotidectomy cases in 1952 that he diagnosed as benign lymphoepithelial lesion of the parotid gland. Two of the patients had undergone radical parotidectomy followed by irradiation because of the mistaken belief that the lesions were malignant. Three other patients were treated with irradiation. Some had bilateral enlargement of the parotid glands and dry eyes. As a pathologist, he had not interviewed the patients, and the recorded information was incomplete.

Godwin discussed the work of Mikulicz but did not mention Sjögren, although the history of the cases reveals that some undoubtedly were Sjögren syndrome. Several of the patients underwent sialography that revealed punctate sialectasis. He suggested that sialography might be helpful in the diagnosis but that a needle-aspiration biopsy was not adequate for diagnosis. He suggested incisional biopsy for diagnosis and determined that extensive surgery was not necessary. Godwin noted that several of the glands were diffusely involved, while some had well-circumscribed areas of tumor.

The Godwin name is most frequently associated with a circumscribed tumor with the histologic features of Sjögren syndrome. Why an autoimmune process directed against the salivary gland tissue would be so localized within the gland is difficult to understand.

Pathogenesis of autoimmune parotitis

The autoimmune diseases listed above appear to be the same disease process with different manifestations. Initial insult to the gland may be a viral infection. Peptides derived from viral antigens and autoantigens become associated with class II histocompatibility molecules in the cytoplasm of the epithelial cell, and the human leukocyte antigen (HLA) complex is subsequently expressed on the cell surface. CD4+ T cells recognize these antigens and release a series of cytokines, which promote further T-cell activation.

B cells enter the gland and produce autoantibodies, including anti–Sjögren syndrome antibodies (ie, anti–SS-A, anti–SS-B) and rheumatoid factor (RF). B cells with cell surface RF can concentrate immune complexes and present antigens to CD4+ T cells. The acini are destroyed by this autoimmune mechanism. Continued cell division of specific B cells leads to oligoclonal expansion and increased chance of karyotypic error associated with neoplastic transformation.

Diseases of uncertain etiology

Pathophysiology

The pathophysiology varies with the type of parotitis and is discussed under Background.

Epidemiology

Mortality/Morbidity

Death from parotitis is extremely unusual. Parotitis most frequently is a complication of an underlying process. Morbidity is generally proportional to the original disease.

Race

Parotitis occurs with equal frequency in people of all races.

Sex

Chronicparotitis occurs with equal frequency in both sexes. The parotitis of Sjögren syndrome has a male-to-female ratio of 1:9. Recurrent parotitis of childhood is more common in males.

Age

Viral parotitis (mumps) occurs most frequently in children. Parotitis that accompanies systemic diseases (eg, rheumatoid arthritis or HIV) mirrors the occurrence of those diseases.

History

Symptoms include the following:

Physical

Causes

Laboratory Studies

Imaging Studies

Procedures

Interventional sialoendoscopy

This technique is growing in popularity and availability and seems to be the best method of treatment.[14] The duct is anesthetized and dilated to insert a telescope for inspection of the large ducts. A working channel in the telescope permits irrigation, suction, and insertion of forceps, wire loop, or even laser energy via a glass fiber to remove the calculi. The clinician has much more information as to the condition of the duct system. This instrument is useful for the assessment and treatment of several inflammatory disorders of the gland.

Advances in the management of chronic sialoadenitis include endoscopic-assisted approaches. Initially, salivary endoscopy is performed to identify any stones. If none is located, ultrasonography or CT imaging is recommended. The endoscopic-assisted management technique is a safe and often effective means of evaluating the anatomy, administering various irrigations (eg, saline, antibiotics, steroids), performing sialodochoplasty, removing stones, and placing stents. In Europe, this technique is mainly performed with the patient under local anesthesia, but in the United States, general anesthesia is preferred since more aggressive procedures can be readily performed at a single setting with the patient under anesthesia if the endoscopic approach is not successful. Studies suggest a high rate of symptom control, and future studies are underway to further address a possibly larger role for this technique.[15, 16, 17, 18]

Incisional biopsy

Under local anesthesia, a biopsy of the tail of the gland may be obtained by an experienced surgeon without injury to the facial nerve. Fine-needle aspiration biopsy frequently is diagnostic for tumors and may be helpful to identify cell types and to obtain material for cultures when the clinical picture suggests infection. Excisional biopsy of a labial minor salivary gland may be diagnostic when the clinical picture suggests Sjögren syndrome.

Histologic Findings

Excision of parotid tissue is infrequently used for diagnosis. When removed for acute infection, acute necrosis of the glandular elements is observed. Autoimmune parotitis occasionally progresses to lymphoma, and biopsy is performed when suspected. Invasion by lymphocytes and destruction of the glandular elements are observed.

Medical Care

Surgical Care

The treatment of chronic parotitis is based on the symptoms of the patient and decisions are, by definition, subjective.

Consultations

Patients with autoimmune parotitis experience xerostomia and excessive tooth decay. These patients should have dental consultation and frequent dental care.

Diet

The diet does not significantly affect cases of parotitis.

Medication Summary

Parotitis occurs in a variety of situations, and the drugs prescribed are those to treat the underlying disease.

Further Inpatient Care

Hospitalization for parotitis is extremely unusual. Parotitis may arise in hospitalized patients who are severely ill, and it is treated as indicated above (see Treatment).

Inpatient & Outpatient Medications

Treatment of generic parotitis involves no specific medications. Discontinue medicines with atropinelike effects and substitute other medications when feasible.

Deterrence/Prevention

Complications

Prognosis

The prognosis is good for all forms of parotitis. Associated or underlying diseases are the actual determinants of the prognosis.

Author

Jerry W Templer, MD, Professor, Department of Otolaryngology, University of Missouri-Columbia School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Benjamin Daniel Liess, MD, Assistant Professor, Department of Otolaryngology, University of Missouri-Columbia School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Ted L Tewfik, MD, Professor, Department of Otolaryngology-Head and Neck Surgery, Director of Continuing Medical Education of Otolaryngology; and Professor of Pediatric Surgery, McGill Faculty of Medicine, Senior Staff Montreal Children's Hospital, Montreal General Hospital and Royal Victoria Hospital

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Dominique Dorion, MD, MSc, FRCSC, FACS, Deputy Dean and Associate Dean of Resources, Professor of Surgery, Division of Otolaryngology-Head and Neck Surgery, Faculty of Medicine, Université de Sherbrooke, Canada

Disclosure: Nothing to disclose.

Christopher L Slack, MD, Private Practice in Otolaryngology and Facial Plastic Surgery, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Disclosure: Axis Three Corporation Ownership interest Consulting; Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting

References

  1. Lilienthal HA. A method of incising parotid abscess without injury to the facial nerve distribution. Am J Surg. 1917;31(4):101-2.
  2. Hemenway WG, English GM. Surgical treatment of acute bacterial parotitis. Postgrad Med. Oct 1971;50(4):114-9. [View Abstract]
  3. Cope VZ. Acute necrotic parotitis. Br J Surg. 1919;7:130-3.
  4. Blair VP, Padgett EC. Pyogenic infection of the parotid glands and ducts. Arch Surg. 1923;7(1):1-36.
  5. Spiegel R, Miron D, Sakran W, Horovitz Y. Acute neonatal suppurative parotitis: case reports and review. Pediatr Infect Dis J. Jan 2004;23(1):76-8. [View Abstract]
  6. van Boven M, Ruijs WL, Wallinga J, O'Neill PD, Hahné S. Estimation of vaccine efficacy and critical vaccination coverage in partially observed outbreaks. PLoS Comput Biol. May 2013;9(5):e1003061. [View Abstract]
  7. Waaijenborg S, Hahné SJ, Mollema L, Smits GP, Berbers GA, van der Klis FR, et al. Waning of Maternal Antibodies Against Measles, Mumps, Rubella, and Varicella in Communities With Contrasting Vaccination Coverage. J Infect Dis. May 8 2013;[View Abstract]
  8. Baurmash HD. Chronic recurrent parotitis: a closer look at its origin, diagnosis, and management. J Oral Maxillofac Surg. Aug 2004;62(8):1010-8. [View Abstract]
  9. Beitler JJ, Vikram B, Silver CE, et al. Low-dose radiotherapy for multicystic benign lymphoepithelial lesions of the parotid gland in HIV-positive patients: long-term results. Head Neck. Jan-Feb 1995;17(1):31-5. [View Abstract]
  10. Henderson SO, Mallon WK. Tuberculosis as the cause of diffuse parotitis. Ann Emerg Med. Sep 1995;26(3):376-9. [View Abstract]
  11. Shaffer AJ, Jacobsen AW. Mikulicz's syndrome, a report of ten cases. Amer J Dis Child. 1927;34:342-6.
  12. Sjogren H. Keratoconjunctivitis sicca. Acta Ophthalmologica. 1933;Supplement 2:1-145.
  13. Hemenway WG. Chronic punctate parotitis. Laryngoscope. Apr 1971;81(4):485-509. [View Abstract]
  14. Papadaki ME, McCain JP, Kim K, Katz RL, Kaban LB, Troulis MJ. Interventional sialoendoscopy: early clinical results. J Oral Maxillofac Surg. May 2008;66(5):954-62. [View Abstract]
  15. Gillespie MB, Intaphan J, Nguyen SA. Endoscopic-assisted management of chronic sialadenitis. Head Neck. Sep 2011;33(9):1346-51. [View Abstract]
  16. Iro H, Zenk J, Escudier MP, et al. Outcome of minimally invasive management of salivary calculi in 4,691 patients. Laryngoscope. Feb 2009;119(2):263-8. [View Abstract]
  17. Marchal F, Dulguerov P. Sialolithiasis management: the state of the art. Arch Otolaryngol Head Neck Surg. Sep 2003;129(9):951-6. [View Abstract]
  18. Koch M, Iro H, Zenk J. Role of sialoscopy in the treatment of Stensen's duct strictures. Ann Otol Rhinol Laryngol. Apr 2008;117(4):271-8. [View Abstract]
  19. Ericson S, Zetterlund B, Ohman J. Recurrent parotitis and sialectasis in childhood. Clinical, radiologic, immunologic, bacteriologic, and histologic study. Ann Otol Rhinol Laryngol. Jul 1991;100(7):527-35. [View Abstract]
  20. Ferraro FJ Jr, Rush BF Jr, Ruark D, Oleske J. Enucleation of parotid lymphoepithelial cyst in patients who are human immunodeficiency virus positive. Surg Gynecol Obstet. Nov 1993;177(5):524-6. [View Abstract]
  21. Fox RI, Kang HI. Pathogenesis of Sjögren's syndrome. Rheum Dis Clin North Am. Aug 1992;18(3):517-38. [View Abstract]
  22. Godwin JT. Benign lymphoepithelial lesion of the parotid gland adenolymphoma, chronic inflammation, lymphoepithelioma, lymphocytic tumor, Mikulicz disease. Cancer. Nov 1952;5(6):1089-103. [View Abstract]
  23. Mandel L, Witek EL. Chronic parotitis: diagnosis and treatment. J Am Dent Assoc. Dec 2001;132(12):1707-11; quiz 1727. [View Abstract]
  24. Morgan WS, Castleman B. A clinicopathologic study of Mikulicz's disease. Am J Pathol. May-Jun 1953;29(3):471-503. [View Abstract]
  25. Shaha AR, DiMaio T, Webber C, Thelmo W, Jaffe BM. Benign lymphoepithelial lesions of the parotid. Am J Surg. Oct 1993;166(4):403-6. [View Abstract]
  26. Wang S, Li J, Zhu X, et al. Gland atrophy following retrograde injection of methyl violet as a treatment in chronic obstructive parotitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Mar 1998;85(3):276-81. [View Abstract]
  27. Watkin GT, Hobsley M. Natural history of patients with recurrent parotitis and punctate sialectasis. Br J Surg. Sep 1986;73(9):745-8. [View Abstract]

Elderly man with parotid abscess.

Incision outlined for incision and drainage of parotid abscess.

Six-year-old girl with recurrent parotitis of childhood.

Sialogram of patient with sialectasis. Notice the appearance of a tree with leaves.

Elderly man with parotid abscess.

Six-year-old girl with recurrent parotitis of childhood.

Sialogram of patient with sialectasis. Notice the appearance of a tree with leaves.

Incision outlined for incision and drainage of parotid abscess.

Parotid gland anatomy.