Case Description. A 60-year-old woman with a 30-year history of recurrent swellings of her left parotid gland was diagnosed with CP. The diagnosis was based on history, clinical examination, salivary volume and chemistry, computerized tomographic scan and sialography. Treatment was palliative in nature.

Clinical Implication. As a member of the health care team, the dentist must be familiar with the various causes of recurrent parotid infections. Early clinical recognition of CP leads to appropriate and successful care.

The etiology of CP is related to a decreased salivary production or an unknown impedance of its delivery.^1,2 The resulting failure of sufficient ductal lavage by saliva facilitates an ascending duct infection from the oral cavity.

	SIGNS AND SYMPTOMS

TOP ABSTRACT SIGNS AND SYMPTOMS HISTOLOGY CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
Symptoms of CP vary from a mild to a severe intractable form. Each unilateral parotid gland swelling may or may not develop in association with the increased salivary demand made during meals.¹ Usually, middle-aged patients are seen with swollen and mildly tender parotid glands. When the patients are questioned, they often reveal that swellings have developed intermittently over many years and frequently have receded without treatment. Each remission may last from several weeks to several years. A tendency for each exacerbation to progress in intensity with the passage of time is evident.

During an acute episode, a clinical examination will reveal a facial asymmetry caused by unilateral parotid gland swelling. Palpation reveals that the swelling is tender and indurated and follows the anatomical contour of the parotid gland. Cervical lymphadenopathy usually is not present, but fever and malaise may be present. Intraorally, a flow of saliva mixed with pus will be seen exiting from the involved parotid duct orifice when the gland is forcefully massaged. Salivary volume from the acutely inflamed gland will be decreased. With remission, however, normal salivary volume measurements can be obtained.

Imaging has proven to be indispensable to the diagnostic approach. Sialography will depict the duct system clearly. A "sausage-like" sialographic pattern reflects areas of duct wall dilatation and stricturing that result from the effects of the ascending bacterial infection. Stensen’s duct is involved primarily, but the secondary ducts also demonstrate changes in direct proportion to CP’s duration and severity.^1,3,4

Infection leads to stricture formation that, in turn, causes a partial obstruction. The damming effect of the stricture causes a reservoir effect with salivary retention and duct dilatation. The resulting salivary stasis facilitates further infection with more strictures and the consequent duct dilatations. A computerized tomographic, or CT, scan can provide positive data concerning the parenchyma.⁵ The parotid gland normally has a significant complement of fat that is imaged on the scan as irregular areas of lucency admixed with normal areas of parenchymal density. Because of the marked inflammatory infiltrate and fibrosis associated with CP, fat is replaced and an increased parotid gland density is visible on a CT scan.

	HISTOLOGY

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Microscopic evidence testifies to the presence of a nonspecific sialadenitis characterized by a marked infiltrate of chronic inflammatory cells, particularly lymphocytes. Acinar loss, extensive fibrosis and periductal lymphocytosis reflect the chronicity of the condition.^{1,3 5–7} During an acute exacerbation, acute inflammatory cells are superimposed on the features of chronicity.

	CASE REPORT

TOP ABSTRACT SIGNS AND SYMPTOMS HISTOLOGY CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
A 60-year-old woman who had no systemic medical problems was seen in the Salivary Gland Center, or SGC, of Columbia University School of Dental and Oral Surgery in New York City because she had a history of repeated left parotid gland swellings. During the past 30 years, she had had five previous episodes of a moderately painful left parotid gland swelling initiated by eating. Each episode was transient, disappearing after one day without any treatment. The sixth episode of left parotid gland swelling developed one month before her visit to SGC. Because the episode lasted one week and was quite painful, the patient decided to seek care.

We performed the clinical examination three weeks after the latest swelling had receded. The extraoral examination revealed no visible facial swelling. Palpation indicated that the left parotid gland was moderately tender, but its tone was considered to be normal. No cervical lymphadenopathy was present.

The intraoral examination revealed the mucosa to be normally moist. We measured stimulated right, and then left, parotid glands’ salivary volumes using a modified Carlson-Crittenden collector. The right parotid gland’s stimulated salivary volume was 1.0 milliliters per minute (normal is 0.5–1.0 mL/minute), while the left parotid gland produced .6 mL/minute. We observed that the left parotid saliva was cloudy, while the right salivary return was clear.

We also performed salivary chemistry (sodium; chloride; lactoferrin; immunoglobulin A, or IgA; and albumin). We determined that the right parotid gland’s salivary chemical parameters were within normal limits. However, marked changes in the left parotid gland’s salivary chemistry were present, and all of the tested chemical levels were elevated. Such findings are characteristic of the existence of a chronic inflammatory process.

We requested a CT scan to rule out the presence of a sialolith. No calcifications were revealed, but we noted an asymmetry in the density of the right and left parotid glands with increased density of the left parotid gland (Figure 1).

View larger version (114K): [in this window] [in a new window]   Figure 1. Chronic parotitis in the left parotid gland. The computerized tomographic scan demonstrates increased parenchymal density of the left parotid gland (arrow) compared with the right parotid gland.

View larger version (62K): [in this window] [in a new window]   Figure 2. A. Left parotid sialogram demonstrates the gross "sausagelike" pattern of Stensen’s duct associated with patient’s chronic parotitis. B. Normal parotid sialogram shows normal caliber and contour of Stensen’s duct (arrows).

	DISCUSSION

TOP ABSTRACT SIGNS AND SYMPTOMS HISTOLOGY CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
The initial cause of the ascending infection in CP can be anticholinergic medications (for example, antihistamines, psychotherapeutics), which will decrease salivary production. No such agents, however, were used by the patient. With decreased lavage due to whatever reason, infection gains a foothold in the duct, and damage to the duct wall ensues. The resulting duct inflammation with healing creates wall irregularities and strictures. These duct-surface distortions favor salivary stasis and offer opportunities for bacterial growth. Mucopus is produced and serves to clog the duct lumen leading to conditions that favor further bacterial growth and stasis. Inevitably, a perpetuating cycle of obstruction and infection is established, thus producing the intermittent symptomatology associated with CP.

Chronic parotitis should not be confused with secondary infections that occur in the presence of a sialolith or Sjögren’s syndrome, or SS. Sialoliths cause obstruction, and the salivary stasis that results also can lead to repeated infectious exacerbations that may or may not resolve with stone removal. The sialolith, however, is the known primary factor that acts to cause the parotitis, which is secondary. In CP, no known primary cause can be ascertained except for the hypothesized decreased salivary production or delivery. Similarly in SS, the manifestations of a chronic ascending infection with acute exacerbations may be present. Patients who have SS have a marked decrease in salivary production that facilitates the development of an ascending infectious process, which becomes superimposed on the SS. Again, such a situation differs from CP in that patients who have SS have a known cause for their secondary parotitis. No predisposing factor such as SS exists in patients with true CP.

A true acute parotitis may mimic the acute exacerbation seen in CP. Its differentiation from CP is determined by its presence in a severely dehydrated patient with no history of parotid swelling. The dehydration leads to xerostomia, which then facilitates an ascending duct infection. Transient and chronic parotid gland swellings also occur in patients who have received therapeutic radioactive iodine for thyroid cancer. The radioactive iodine is concentrated actively by the parotid gland, damages the gland and causes inflammatory changes. Parotid gland swellings associated with neoplasms, sialadenosis, human immunodeficiency virus and sarcoid do not manifest clinically as intermittent swellings. They are slow in onset, persistent and usually painless and usually do not disappear spontaneously.

The SGC uses salivary volume and sialochemistry as diagnostic tools. We found stimulated right parotid gland volume to be within normal limits in our patient. The left parotid gland, however, revealed an entirely different story. The patient’s long history of CP terminated in the loss of secreting acini. Saliva could be obtained, but in a decreased amount. Although the salivary volume we collected from the left parotid gland was considered to be within normal limits, it was significantly decreased compared with the return from the asymptomatic, normal right parotid gland.

Volume measurements may vary widely in a gland affected by CP. Flow rates are dependent on whether an acute exacerbation is in existence. Obviously in such states, inflammatory obstruction is present and will result in an enhanced salivary diminution. During the intermittent and often prolonged remission periods, salivary flow recovers and, at times, may even be normal.

Sialochemistry serves to further substantiate the existence of CP. Because of the damaged duct wall, sodium and chloride are not adequately resorbed as the saliva moves toward the duct orifice. Elevated salivary levels of these electrolytes are the end product.⁸ The elevated levels of salivary albumin reflect the failure of the damaged duct wall to filter out surrounding serum albumin and prevent its entry into the lumenal saliva. Lactoferrin and IgA mirror the existence of the infection associated with CP.⁹

Conservative therapy for the acute chronic parotitis attack often is sufficient and usually leads to patient satisfaction if the acute attacks are dispersed widely by prolonged asymptomatic periods.

In CP cases, the CT scan has two functions. It can be used to uncover the existence of a parotid stone, and it depicts the extent of parenchymal involvement. Parotid stones are difficult to detect with standard radiography because of the superimposition of bony structures; the surrounding calcified bone serves to blot out the opacity of a small, calcified parotid stone. Furthermore, the parotid stone may be only minimally calcified, and radiography will fail to show its presence. Because the CT scan is exquisitely sensitive to insignificant amounts of calcification, it will reveal these radiolucent stones clearly.¹⁰

While the CT scan demonstrates parenchymal changes, sialography serves to illustrate duct contour and distribution. In the case we report, a startling gross "sausaging" of Stensen’s duct confirmed the existence of advanced degenerative changes in the left parotid gland. The duct "sausaging" represents areas of stricture with duct dilatation from the resulting salivary obstruction and retention. The virulence of the involved organisms and the duration of the CP would seem to directly affect the degree of duct damage.

Patients who have CP are treated on the basis of their symptomatology. Treatment for an acute attack can be conservative because the pain and swelling are self-limiting and transient. Antibiotics are helpful in an acute attack. Effective therapy requires identification of the involved organisms followed by the administration of the appropriate antibiotic protocol. To increase duct lavage, sialogogues may be used. However, autonomic agents that have side effects, such as pilocarpine, need not be used. Sufficient glandular secreting cells are present and will respond to stimulation caused by sugarless chewing gum or sour candy. Increased fluid intake, parotid gland massage, duct probing to break up mucopus blockages, good oral hygiene and analgesics all are very helpful adjuncts. Sialographic dye introduction lavages the duct system with an antiseptic iodine solution, giving the procedure a dual function: diagnosis and therapy.

Conservative therapy for the acute attack often is sufficient and usually leads to patient satisfaction if the acute attacks are dispersed widely by prolonged asymptomatic periods. With frequent repeated severe attacks, a more aggressive stance is mandated. Duct ligation performed to encourage gland atrophy has not met with great success, and neither has tympanectomy, which is used to interrupt parasympathetic parotid stimulation from the tympanic plexus.⁷ Retrograde duct injection of methyl violet performed to cause inflammation with panductal fibrosis and resulting gland atrophy recently has been advocated.¹¹

Provided that the symptomatology of CP is sufficiently severe, superficial parotid lobectomy has become the most accepted surgical approach.^1,2,12,13 Complications can occur and include a facial nerve palsy, which usually is transient; sialocele; salivary fistulae; and Frey’s syndrome,¹ which develops when parasympathetic fibers that previously innervated the parotid gland synapse with fibers to the facial sweat glands. In patients who have undergone surgery, gustatory sweating replaces salivary production when the patient eats.

The most conservative approach is to treat the condition palliatively. This decision is based on the objective symptoms, patient discomfort and cosmetic concern. In this case report, we did not offer aggressive therapy to the patient, who had six transient episodes of left parotid gland swelling over 30 years. We decided that the symptomatology was not compelling enough to opt for anything more than conservative treatment of the acute phases of CP. Similarly, during the quiescent remission stage, no known treatment is available nor need be offered. Regardless, periodic checkups are indicated.

	CONCLUSION

TOP ABSTRACT SIGNS AND SYMPTOMS HISTOLOGY CASE REPORT DISCUSSION CONCLUSION REFERENCES

 
Dentists are in the unique position to diagnose a patient with CP. The ability to perform a thorough clinical examination, salivary examination and imaging procedure facilitates the differentiation of CP from infection seen in entities such as sialolithiasis and SS. The patient benefits from an accurate diagnosis, which in turn leads to an appropriate therapeutic approach.

View larger version (96K): [in this window] [in a new window]   Dr. Mandel is the director, Salivary Gland Center; a clinical professor, Division of Oral and Maxillofacial Surgery; and an assistant dean, Columbia University School of Dental and Oral Surgery, 630 W. 168th St., New York, N.Y. 10032. Address reprint requests to Dr. Mandel.

View larger version (144K): [in this window] [in a new window]   Ms. Witek is a research assistant, Salivary Gland Center; and a fourth-year dental student, Columbia University School of Dental and Oral Surgery, New York.