Xerostomia -- Clinical Evaluation and Treatment in General Practice

Xerostomia is a common symptom with various causes that, if ignored, can lead to serious oral consequences. Clinical evaluation of patients complaining of dry mouth must include some additional history and specific examination of the salivary glands, oral mucosa, and teeth. Additional evaluation may include consultation with the patient’s physician, request for microbial culture, or labial salivary gland biopsy. No one form of treatment for patients with chronic xerostomia is sufficient, but comprehensive treatment is effective in improving patient oral comfort and function, and preventing unnecessary loss of teeth. This treatment must include ongoing dental caries prevention and treatment, salivary flow stimulation, recognition and treatment of oral candidiasis, selective use of saliva substitutes, and possible changes in the patients’ prescription and nonprescription drug use.

Xerostomia (dry mouth) is a subjective symptom that is usually, but not always, associated with salivary hypofunction, in which there are both decreased saliva production and qualitative changes in saliva. This symptom is encountered with greater frequency in dental practice as a result of increasing use of systemic prescription drugs, which can singly or in combination affect salivary function, and because of increasing public awareness of this symptom and its significance.¹

Causes of Xerostomia

As noted in Table 1, salivary hypofunction can be divided into temporary and chronic forms, depending on the cause. The chronic forms are of greatest concern because of their long-term potential to cause dental and oral mucosal disease as well as to adversely affect oral function. Another difference between the temporary and chronic forms of salivary hypofunction is that most short-term salivary hypofunction affects only resting (basal) secretion, and patients retain their ability to respond normally to gustatory, masticatory, or olfactory stimuli. However, most of the chronic causes of salivary hypofunction decrease both resting and stimulated secretion rates, creating both greater symptoms and potentially less response to treatment.

Prescription drug use is the most common cause of chronic salivary hypofunction. Categories of drugs most frequently causing clinically significant salivary function are listed in Table 1. There are, however, literally hundreds of drugs that can produce symptoms of dry mouth, but most do so with lesser severity and affect a smaller proportion of patients. It is interesting to note that patients’ salivary flow rates may decrease simply in proportion to the number of prescription drugs they are taking.² Thus, there may be an unknown additive or synergistic effect on salivary function when multiple prescription drugs are taken.

Clinical Effects of Chronic Xerostomia

The results of a chronic lack of saliva follow from the well-known functions of normal saliva,³ which include:

* Maintaining a neutral oral pH through various buffer systems;

* Supporting ongoing remineralization of teeth by providing a reservoir of calcium and phosphate ions;

* Coating the oral mucosa and teeth to protect them against harmful substances;

* Lubricating the mouth to facilitate chewing, swallowing, and speech;

* Providing local antimicrobial activity through enzymes, immunoglobulin A, and histatins; and

* Serving as a solvent for the taste mechanism.

Therefore, the loss of saliva is thought to be associated with a loss of "protection." Some of the oral consequences of chronic salivary hypofunction occur in approximate proportion to the severity of the hypofunction. These include progressive dental caries -- primarily in cervical, incisal, or marginal locations -- and various kinds of oral dysfunction (i.e., difficulty with chewing, dysphagia, dysphonia, or dysgeusia), and dysfunction of lower complete dentures. Signs of chronic erythematous candidiasis are seen in about one-third of patients with chronic salivary hypofunction⁴ and caused by Candida albicans or other Candida species.^5,6 Interestingly, the white plaques of pseudomembranous candidiasis (thrush) are rarely seen in these patients. Patients with chronic salivary hypofunction may also develop alterations in their sense of taste, with or without candidiasis.

Diagnosis of Xerostomia in General Practice

History

As generated from the routine medical history, patients’ descriptions of prescription and nonprescription drug use may reveal the cause of their symptoms of dry mouth. Given the rapid proliferation of new drug names, this analysis may require a standard reference such as the Handbook of Clinical Drug Data, the Physicians Desk Reference, or other source. As noted above, medications are the most common cause of xerostomia and salivary hypofunction. If the drug history does not reveal a probable cause, additional information must be obtained from those patients complaining of xerostomia.

Learning the patient’s occurrence pattern of dry mouth symptoms can be helpful. For example, the continuous presence of dry mouth symptoms throughout the day is usually associated with significant salivary hypofunction and loss of the protective effects of saliva. Alternatively, the gradual daily onset of such symptoms may be associated with less severe hypofunction, mouth breathing, or an excessive awareness by the patient of the amount of saliva in their mouth. Symptoms of dry mouth occurring only at night, on awakening from sleep, usually are not associated with abnormal salivary function because salivary flow normally approaches zero during sleep. There are also some additional questions to ask patients who complain of dry mouth, which, if positive, are moderately predictive of salivary hypofunction: Do you sip liquids to aid swallowing dry foods? Does your mouth feel dry when eating? Do you have difficulty swallowing any foods?⁷ If patients complain of regional or generalized mucosal pain, often described as "burning," or they describe intolerance to spicy or acidic foods, which may have forced them to significantly alter their diet, the labial angles and oral mucosa should be carefully examined for signs of erythematous candidiasis, as described below (Table 2).

Patients with depression may or may not include that diagnosis on a history form. Two recent studies illustrate its relationship to the symptom of xerostomia. One study of apparently healthy individuals with normal unstimulated and stimulated whole salivary flow rates, found symptoms of depression in 21 percent of those who also had symptoms of dry mouth, but in only 3 percent of those who did not have symptoms of dry mouth.⁸ Another study sampled all the 55-year-old men and women in a European city and found that 26 percent of the men and 33 percent of the women complained of the subjective sensation of dry mouth. After dealing statistically with the confounding variables of smoking and prescription drugs and diseases that could cause xerostomia, the authors found that depressive symptoms were significantly associated with the symptom or oral dryness.⁹ In diagnosing such patients, it is important to remember that depression can mask a chronic disease associated with salivary hypofunction, and patients with xerostomia and self-identified depression or currently using antidepressant drugs must be fully evaluated.

Physical Examination -- Extraoral

For patients who complain of xerostomia, it may be most convenient to begin with the extraoral examination. As noted in Table 1, some of the conditions causing salivary hypofunction may also cause enlargement of the parotid and/or submandibular glands. For example, between one-third and one-half of patients with Sjögren’s syndrome develop enlargement of major salivary glands. In cases of Sjögren’s syndrome, sarcoidosis, or HIV infection, this enlargement is usually firm and nontender to palpation, affects all or most of the gland, and is usually bilateral, although one side may be larger than the other. It should be noted, however, that while these patients can have clinically similar swelling of major salivary glands, the histological features are different. At the beginning of this examination, it is useful to visually examine the duct openings in the mucosa for each parotid and submandibular gland, while applying gentle extraoral pressure to the corresponding gland (Figure 1). This permits observation of the saliva being expressed; is it clear, water-like and flowing freely (the normal condition), or cloudy, viscous and hanging from the duct orifice, or does nothing come out when pressing on the gland?

Parotid glands are easy to palpate because of their superficial location over the mandibular ramus, but they must be distinguished from the masseter muscle, which they overlie. Submandibular glands are best palpated between an index finger placed in the distal mouth floor and another placed extraorally on the skin medial to the mandibular angle. The normal parotid or submandibular glands are not usually palpable because they are softer than their surrounding tissues. Therefore, if the parotid or submandibular glands can be anatomically defined by palpation, then some degree of induration is probable.

Physical Examination -- Intraoral

The intraoral examination of patients complaining of xerostomia should focus on the appearance and lubricity of the mucosa and the location and distribution of dental caries. Does a gloved finger slide easily over the mucosa during examination; is there resistance to sliding; or is there a sticky quality to the mucosa? During the oral examination, has saliva pooled in the mouth floor? (Figure 2)

Erythematous candidiasis involves thinning of the mucosa, which causes the red color and symptoms described above. Clinically, it is characterized by erythema and atrophy of the filiform papilla on the dorsal tongue, leaving a smooth, cobble-stone, or fissured surface on the dorsal tongue (Figure 3A). Other signs include patchy oral mucosal erythema, particularly on the palate or buccal mucosa, or under dentures, and angular cheilitis. The latter rarely occurs without the presence of intraoral candidiasis¹⁰ (Table 2). In patients with these signs, the diagnosis can be confirmed by fungal culture of a swab specimen from the dorsal tongue, or other erythematous lesion, from which a substantial number of colony forming units (double digits or more) can be identified through culture. A colony forming unit assessment can be performed by the clinical laboratory and is necessary because small quantities of Candida may be present in the normal oral flora.¹¹ Adequate treatment of oral candidiasis (described below) will usually eliminate the patient’s symptoms of mucosal burning and intolerance to acidic or spicy foods, in spite of continuing salivary hypofunction, and it will lead to restoration of the mucosa⁴ (Figure 3B).

Are there carious lesions or signs of decalcification in cervical or incisal areas of the teeth? Are recurrent caries present in subgingival crown margins or around existing class five restorations? (Figures 2 and 4) In patients with chronic salivary hypofunction, the extent of their dental caries may be greater than would be suggested by the adequacy of their plaque and calculus control.

Clinically Assessing Salivary Hypofunction

Salivary flow rates can be measured for whole, parotid or submandibular secretions under resting or stimulated conditions. However, the range of flow rates for each of these is very wide among healthy individuals who have no known diseases and who are not taking any medications.¹² Therefore, a clear distinction between "normal" and "abnormal" flow rates may not be possible.¹³ In addition, measuring salivary flow rates is not a usual part of most dental practices, can be quite time-consuming, and may be difficult to standardize when done only occasionally.

Various investigators have tried to identify an unstimulated whole salivary flow rate that distinguishes normal from abnormal function. In reviewing previous studies and conducting their own, Navazesh and colleagues found that rates of 0.12 to 0.16 mL/min seem to define the range below which there is a higher rate of oral soft and hard tissue abnormalities.¹⁴ Using that as a baseline, they identified a set of four clinical measures that, when used together in a formula, reasonably predicted the presence or absence of salivary hypofunction. The clinical measures were dryness of the buccal mucosa; absence of saliva expressible from the ducts; the total number of decayed, missing and filled teeth; and dryness of the lips. In summary, salivary hypofunction can be assessed by the clinical methods described in this section for clinical decision-making, without measuring salivary flow rates (Table 2).

Various tests have been proposed to determine a patient’s risk of developing caries. These tests include salivary flow rates, salivary buffer capacity, and quantifying mutans streptococci and lactobacilli from the saliva. However, a review of these caries risk assessment notes that these tests are better at selecting people who will not develop caries than they are at selecting people who will, and that no single test has yet proven to be successful in predicting caries development for the majority of populations studied.¹⁵

Chronic Diseases Causing Xerostomia

Sjögren’s syndrome is the second most common connective tissue disease, after rheumatoid arthritis. Patients with primary Sjögren’s syndrome have the salivary and ocular components of Sjögren’s syndrome and may develop other organ system manifestations. Patients with secondary Sjögren’s syndrome first have another connective tissue disease (e.g. rheumatoid arthritis, systemic lupus erythematosus, or mixed connective tissue disease) and later develop the salivary and/or ocular components (Figure 4). Patients in a dental practice may be suspected of having Sjögren’s syndrome, because they already have the diagnosis of a connective tissue disease or, because they have clinical evidence of significant salivary hypofunction that is not otherwise explained from information in their history and, on questioning, they may complain of ocular symptoms (e.g. an inability to tear, ocular pain or burning, or having a foreign-body sensation in their eyes). It is helpful to contact the patient’s physician concerning the patient’s diagnoses and blood test results. Several serological markers that are highly associated with the connective tissue diseases are commonly seen in patients with Sjögren’s syndrome and may raise the suspicion of it, but none of them are sufficiently specific to permit it to be diagnosed by blood tests. Those that are commonly associated with Sjögren’s syndrome include the following "autoantibodies": antinuclear antibody, rheumatoid factor, anti-Ro (SS-A), and anti-La (SS-B).

In patients who have clinical evidence of significant salivary hypofunction but do not have another connective tissue disease, the dentist should refer the patient to an ophthalmologist to assess whether they have the ocular component of Sjögren’s syndrome, called keratoconjunctivitis sicca.¹⁶ If they do have keratoconjunctivitis sicca, they should then be referred to someone experienced in performing a labial salivary gland biopsy¹⁷ to assess whether they have focal lymphocytic sialadenitis in that specimen, which represents the salivary component of Sjögren’s syndrome.¹⁸ A patient having keratoconjunctivitis sicca and focal lymphocytic sialadenitis in a salivary biopsy has primary Sjögren’s syndrome, a diagnosis that should be reported to the patient’s physician. A labial salivary gland biopsy may also reveal another systemic disease, such as sarcoidosis (Figure 1), which can clinically mimic Sjögren’s syndrome,¹⁹ and should be reported to the patient’s physician.

HIV or hepatitis C infections can cause salivary hypofunction and salivary gland enlargement, or salivary hypofunction only, respectively. They are both definitively diagnosed by serological tests. Diagnoses of amyloidosis, diabetes, or a central nervous system disease should be apparent from the patient’s medical history, as would therapeutic radiation to the head and neck or bone marrow transplantation. As noted above, there is an association between the symptom of xerostomia and depression.

Treatment of Patients With Xerostomia

There is no one form of treatment that is effective for patients with chronic salivary hypofunction, but there is clear evidence that comprehensive treatment is effective. Such treatment needs to consider five categories:

* Ongoing dental caries prevention and treatment;

* Salivary flow stimulation;

* Oral candidiasis recognition and treatment;

* Selective use of saliva substitutes; and

* Review of the patient’s current prescription drug regimen and elimination, where possible, of concurrent use of drugs having anticholinergic effects.²⁰

Caries Prevention and Treatment

Patients who develop severe salivary hypofunction -- for example, from radiation therapy to the head and neck -- and do not receive nor follow necessary instructions and support to prevent dental caries, can lose their entire dentition to caries in a few years. An example of such a patient is seen in Figure 5; similar results can occur in patients with Sjögren’s syndrome or on multiple drug therapy, but more slowly.

In a landmark study of caries prevention in patients who had undergone radiation therapy to the head and neck, there were three treatment groups: 1) those receiving oral hygiene instructions only, 2) those receiving oral hygiene instructions and daily 1 percent tray-applied sodium fluoride gel, and 3) those receiving both of the above and placed on a sucrose restricted diet.²¹ Group 1 had an average monthly increase in the number of decayed, missing or filled dental surfaces of 2.51, which was 12 times greater than the DMFS increase seen in group 2. Furthermore, group 2 had a DMFS increase five times greater than that seen in group 3. While each of the three prevention strategies studied on these patients with severe salivary hypofunction had some effect, the combination of oral hygiene instructions, daily topical fluoride application, and dietary sucrose restriction was 63 times more effective in preventing caries than oral hygiene instructions alone. This is a good place to apply the old saying, the whole is worth more than the sum of its parts.

Patients with moderate to severe salivary hypofunction must become part of their treatment by being taught the role of dietary sugars in the development of dental caries, the need to limit sugar intake to meals and eliminate it between meals, and how to remove dental plaque effectively. Strategies with topical fluoride need to be based on the severity of the patient’s salivary hypofunction and their caries experience. These can include professionally applied high concentration fluoride solutions in a tray (e.g. 1.23 percent fluoride in acidulated phosphate fluoride gel for four minutes), or a 2.26 percent fluoride varnish applied directly to the teeth, four times per year.^{22, 23} Patient-applied sodium fluoride gel (0.5 percent fluoride) in a custom-fitted tray for five minutes daily can be used to supplement professionally applied fluoride. For lower risk patients, a daily rinse with a 0.05 percent sodium fluoride can be a useful addition to professionally applied fluorides. Neutral sodium fluoride preparations are generally preferred to stannous fluoride preparations because they are better-tolerated by patients.

For patients at highest risk of caries, or those without evidence of lesion arrest or remineralization, additional strategies can include the periodic use of chlorhexidine to control the quantity of mutans streptococci in the flora. This can be in the form of a patient-applied 0.12 percent chlorhexidine gluconate rinse, one minute daily for two weeks²² (Table 3).

The caries associated with chronic salivary hypofunction often attacks the margins of existing restorations in both supragingival and subgingival locations (Figures 2 and 4). For the initial treatment of such patients, dental restorations with subgingival margins should be avoided wherever possible (Figure 6). Subgingival margins are difficult to clean and are less accessible to topical fluoride application. Recurrent caries at this location is common in these patients and difficult to detect and treat. Full veneer crowns, if ultimately necessary, should not be placed until caries are under complete control (i.e., the patient has been free of new lesions for at least one year).

Salivary Flow Stimulation

Patients’ residual salivary function can be stimulated by physiological or pharmacological means to reduce symptoms of xerostomia. Physiological stimulation can be provided by masticatory or gustatory stimuli, through sugar-free chewing gum (e.g., xylitol gum) or sugar-free hard candies, used as needed during the day to relieve oral symptoms. To avoid enhancing dental caries development in high caries-risk patients, either of these physiological stimulatory methods must use sugar-free, not "sugarless" products. Both methods can increase salivary flow, but only while the stimulus is present in the mouth.

Pharmacological stimulation can be provided through prescription of various systemically administered cholinergic drugs, which may give the patient up to several hours of increased salivary flow and reduced oral symptoms. Pilocarpine has long been know to increase salivary secretion^24,25 and is initially prescribed at 5 mg, three to four times daily. It should not be prescribed for patients with uncontrolled asthma or narrow-angle glaucoma and should be used with caution in patients with significant cardiovascular or pulmonary disease. There is no evidence yet that either physiological or pharmacological salivary stimulation will prevent dental caries or oral candidiasis.

Oral Candidiasis

When erythematous oral candidiasis occurs in patients with only mild to moderate salivary hypofunction, fluconazole or other systemic antifungal drugs can be used for a few weeks, with usually satisfactory results (as assessed by the treatment end-points described below). More commonly, erythematous oral candidiasis occurs in patients with severe chronic hyposalivation,²⁶ whose treatment is best accomplished with topical forms of polyene or imidazole anti-fungal drugs²⁷ for periods of weeks or months. Because these patients are at very high risk for progressive dental caries, they must utilize forms of these topical drugs that are the least cariogenic, i.e. those that do not contain sucrose or glucose. Topical forms are necessary because in patients having severe salivary hypofunction, systemically administered antifungal drugs do not reach the mouth of such patients in therapeutically adequate amounts.

All currently available "oral" topical antifungal drugs contain substantial amounts of sucrose or glucose (i.e. brands of clotrimazole oral troches, nystatin oral pastilles, and nystatin oral suspension), which creates significant risk for supporting dental caries development when used as directed. Therefore, the best topical antifungal drug to use with patients at high risk for dental caries is nystatin vaginal tablets. These do contain lactose, which is a potentially cariogenic carbohydrate, but much less so than either sucrose or glucose. They must be dissolved slowly in the mouth for 15-20 minutes, two or three times per day. Such patients usually must take frequent sips of water to allow the tablet to dissolve in that time. The treatment end-point for erythematous candidiasis should be resolution of all the mucosal erythema, return of filiform papillae to the dorsal tongue, and resolution of associated oral symptoms.⁴

For patients wearing partial or complete dentures, additional instructions and treatment are needed:

* Dentures must be removed from the mouth before using any topical antifungal drug.

* Dentures must be disinfected by soaking overnight in a fungicidal substance compatible with the denture materials and rinsed before reinserting in the mouth.

* Nystatin topical powder may be applied on the fitting surface of a clean denture (while wet) just before reinserting it in the mouth. Since this powder contains talc, care must be taken to insure that patients do not inhale the dry powder.²⁰

The presence of angular cheilitis almost always indicates concurrent intraoral candidiasis.¹⁰ Angular cheilitis can be treated by nystatin or clotrimazole creme, but in most cases this only should be done with concurrent treatment of the intraoral infection. After treatment is completed, recurrence of erythematous candidiasis is common and the patient the needs to be re-treated as described above. If recurrence is frequent, re-treatment should be followed by maintenance therapy (e.g. continued use of half of a nystatin vaginal tablet slowly dissolved in the mouth each day).⁴

Saliva Substitutes

These over-the-counter products can be helpful for patients with fairly severe chronic hyposalivation, particularly those wearing a complete denture, but are less helpful for patients with more saliva. These products are usually most effective for patients at their bedside when awakening during the night, while talking, or while traveling. None replace all the functions of natural saliva, and none have long duration because they are swallowed. There are several types available. Most are carboxymethylcellulose-based, while others are mucin-based or glycerate polymer gel-based. In comparative studies, carboxymethylcellulose-based preparations usually have the lowest objective and subjective ratings; mucin-based products are usually rated higher by patients, but are not available in the United States. The glycerate polymer gel-based product appears to provide better reduction in oral dry mouth symptoms than carboxymethylcellulose-based substitutes²⁸ particularly in patients with severe xerostomia.²⁹ None of these products has been shown to prevent dental caries or oral candidiasis.

Water Consumption

Some patients with chronic salivary hypofunction consume water excessively. Patients should understand that dry mouth is rarely associated with systemic dehydration and that consuming large quantities of water does not overcome oral dryness. Frequent small sips of water during the day will help reduce oral symptoms. However, excessive consumption of water can remove the mucus coating the oral surfaces and further increase the patients symptoms of dryness. Milk may be a better, but less convenient, liquid to sip.

Nocturia

Patients may have frequent sleep interruption caused by nocturia if they consume water at night. To avoid nocturia, beginning one hour before sleep patients should not drink water and when they awaken during the night they should use a small volume of a saliva substitute, instead of drinking water.

Prescription Drug Review

Patients’ current prescription drug use should regularly be reviewed to identify those drugs whose principal effect, or side effects, contribute to decreased salivary function. If such drugs are being used, the problem should be discussed with the prescriber of the drug; it may be possible to eliminate the drug or to substitute with one that has less effect on salivary function.

Summary

Xerostomia is a common clinical problem. Patients with that symptom must be evaluated by their dentists’ obtaining additional history and performing examinations that are clearly in the scope of general dental practice. The cause of a patient’s xerostomia should be determined, the severity of associated salivary function should be estimated, and appropriate treatment initiated. The goal of that treatment is to improve the patient’s oral symptoms and function and to prevent and restore dental caries. Effective treatment of chronic salivary hypofunction requires patient education and treatment, proportional to its severity and include caries prevention, appropriate dental restoration, saliva stimulation, selective use of saliva substitutes and, where appropriate, changes in the patient’s use of prescription drugs.

Acknowledgment

The authors are grateful to Dr. Hiromi Mochizuki for her valuable criticism of the manuscript.

Authors

Troy E. Daniels, DDS, MS, is a professor of oral medicine and oral pathology at the University of California at San Francisco School of Dentistry.

Ava J. Wu, DDS, is an associate clinical professor of oral medicine at UCSF School of Dentistry.

References

1. Parker-Pope T, A common side effect, dry mouth, can cause serious tooth decay. Wall Street Journal. March 10, 2000.

2. Wu AJ, Ship JA, A characterization of major salivary gland flow rates in the presence of medications and systemic diseases. Oral Surg Oral Med Oral Pathol 76:301-6, 1993.

3. Mandel ID, The role of saliva in maintaining oral homeostasis. J Am Dent Assoc 119:298-304, 1989.

4. Hernandez YL, Daniels TE, Oral candidiasis in Sjögren’s syndrome: Prevalence, clinical correlations and treatment. Oral Surg Oral Med Oral Pathol 68:324-9, 1989.

5. Tapper-Jones L, Aldred M, Walker DM, Prevalence and intraoral distribution of Candida albicans in Sjögren’s syndrome. J Clin Path 33:282-7, 1980.

6. Crockett DN, O’Grady JF, Reade PC, Candida species and Candida albicans morphotypes in erythematous candidiasis. Oral Surg Oral Med Oral Pathol 73:559-63, 1992.

7. Fox PC, Busch KA, Baum BJ, Subjective reports of xerostomia and objective measures of salivary gland performance. J Am Dent Assoc 115:581-4, 1987.

8. Bergdahl M, Bergdahl J, Johansson I, Depressive symptoms in individuals with idiopathic subjective dry mouth. J Oral Pathol Med 26:448-50, 1997.

9. Antilla SS, Knuuttila ML, Sakki TK, Depressive symptoms as an underlying factor of the sensation of dry mouth. Psychosom Med 60:215-8, 1998.

10. Ohman SC, Dahlen G, et al, Angular cheilitis: a clinical and microbial study. J Oral Pathol 15:213-7, 1986.

11. Arendorf TM, Walker DM, The prevalence and intraoral distribution of Candida albicans in man. Arch Oral Biol 25:1-10, 1980.

12. Ship JA, Fox PC, Baum BJ, How much saliva is enough? Normal function defined. J Am Dent Assoc 122:63-9, 1991.

13. Skopouli FN, Siouna-Fatourou HI, et al, Evaluation of unstimulated whole saliva flow rate and stimulated parotid flow as confirmatory tests for xerostomia. Clin Exp Rheumatol 7:127-9, 1989.

14. Navazesh M, Christensen C, Brightman V. Clinical criteria for the diagnosis of salivary gland hypofunction. J Dent Res 71:1363-9, 1992.

15. Powell LV, Caries risk assessment: relevance to the practitioner. J Am Dent Assoc 129:349-53, 1998.

16. Bloch KJ, Buchanan WW, et al, Sjögren’s syndrome: a clinical, pathological and serological study of sixty-two cases. Medicine 44:187-231, 1965.

17. Daniels TE, Benign lymphoepithelial lesion and Sjögren’s syndrome. In, Ellis G, Auclair P, Gnepp D, eds, Surgical Pathology of Salivary Glands. WB Saunders, Philadelphia, 1991, 83-106.

18. Daniels TE, Whitcher JP, Association of patterns of labial salivary gland inflammation with keratoconjunctivitis sicca: analysis of 618 patients with suspected Sjögren’s syndrome. Arthritis Rheum 37:869-77, 1994.

19. Sack KE, Whitcher JP, et al, Sarcoidosis Mimicking Sjögren’s syndrome: Histopathological Observations. J Clin Rheumatol 4:13-6, 1998.

20. Daniels TE, Newbrun E, Oral Treatment and Prevention of Dental Decay. In, Carsons S, Harris E, eds. The New Sjögren’s Syndrome Handbook. Oxford Press, 1998, pp156-62.

21. Dreizen S, Brown LR, et al, Prevention of xerostomia-related dental caries in irradiated cancer patients. J Dent Res 56:99-104, 1977.

22. Newbrun E, Current treatment modalities of oral problems of patients with Sjögren’s syndrome: Caries prevention. Adv Dent Res 10:29-34, 1996.

23. Beltrán-Aguilar ED, Goldstein JW, Lockwood SA, Fluoride varnishes. A review of their clinical use, cariostatic mechanism, efficacy and safety. J Am Dent Assoc 131:589-96, 2000

24. Greenspan D, Daniels TE, Effectiveness of pilocarpine in postradiation xerostomia. Cancer 59:1123-5, 1987.

25. Fox PC, Atkinson JC, et al, Pilocarpine treatment of salivary gland hypofunction and dry mouth (xerostomia). Arch Intern Med 151:1149-52, 1991.

26. Abraham CM, Al-Hashimi I, Haghighat N, Evaluation of the levels of oral Candida in patients with Sjögren’s syndrome. Oral Surg Oral Med Oral Pathol 86:65-8, 1998.

27. Ellepola ANB, Samaranayake LP, The in vitro post-antifungal effect of nystatin on Candida species of oral origin. J Oral Pathol Med 28:112-6, 1999.

28. Furumoto EK, Barker GJ, et al, Subjective and clinical evaluation of oral lubricants in xerostomic patients. Spec Care Dentistry 18:113-8, 1998.

29. Regelink G, Vissink A, et al, Efficacy of a synthetic polymer saliva substitute in reducing oral complaints of patients suffering from irradiation-induced xerostomia. Quintessence Int 29:383-8, 1998.

To request a printed copy of this article, please contact: Troy E. Daniels, DDS, MS, School of Dentistry, S-630, University of California, San Francisco, CA 94143-0430 or at danielst@dentistry.ucsf.edu

Legends

Figure 1. This man complained of xerostomia, had slight, diffuse, bilateral parotid enlargement and intraoral signs of salivary hypofunction. This thickened, cloudy secretion was expressible from the left parotid duct during examination, but the major salivary glands were not painful or tender to palpation. A labial salivary gland biopsy revealed noncaseating granulomas, confirming the diagnosis of sarcoidosis.

Figure 2. This patient with primary Sjögren’s syndrome has severe salivary hypofunction. Note parchment-like mucosa on the mouth floor and caries in incisal, cervical, and marginal locations. Caries are also detectable at the subgingival crown margins.

Figure 3A. This 26-year-old woman complains of dry and burning mouth and intolerance to spicy foods. She has signs of erythematous candidiasis including angular cheilitis, erythema of the dorsal tongue, and atrophy of the filiform papillae.

Figure 3B. After about three months of treatment with topical antifungal drugs, her oral symptoms have resolved and filiform papillae have returned to the dorsal tongue, but her chronic salivary hypofunction and primary Sjögren’s syndrome continue.

igure 4. This 41-year-old patient with rheumatoid arthritis, mild secondary Sjögren’s syndrome, depression, and multiple drug treatment has rapidly progressing dental caries. Note the pattern of new and recurrent caries.

Figure 5. This patient underwent radiation therapy for a carcinoma of the oropharynx 21 months prior to this photograph. At the onset of radiation treatment she had a bicuspid dentition, a few small restorations, and no active caries. After completion of treatment, she was non-compliant with home dental care procedures and failed her dental recall appointments.

Figure 6. Several years prior to this photograph, this middle-aged patient complained of xerostomia and had many areas of cervical caries at the time these crowns and bridges were placed. Within a few years, recurrent caries had affected the margins of most of the abutments, necessitating the supplemental class V amalgam restorations. The patient has primary Sjögren’s syndrome and ongoing salivary hypofunction.

Table 1. Differential Diagnosis of Salivary Hypofunction

Temporary hypofunction (usually, only resting secretion is decreased):

* Effects of short-term drug use (e.g. antihistamines)

* Virus infections** (e.g. mumps)

* Dehydration (e.g. thermal or trauma)

* Psychogenic conditions (e.g. anxiety)

Chronic hypofunction (usually, both resting and stimulated secretion rates are decreased):

* Effects of chronically administered drugs

-- Antidepressants (e.g. amitriptyline)

-- Neuroleptics (e.g. phenothiazines, lithium)

-- Parasympatholytics (e.g. anti-Parkinsonian drugs)

-- Some antihypertensive drugs (e.g. clonidine) and many combinations (e.g. beta-blocker and diuretic)

* Chronic diseases

-- Sjögren’s syndrome**

-- Sarcoidosis**

-- HIV** or Hepatitis C infection

-- Depression

-- Diabetes mellitus, uncontrolled

-- Amyloidosis (primary or secondary)

-- Central nervous system diseases

-- Rarely, absent or malformed glands

* Other effects of treatment

-- Therapeutic radiation to the head and neck

-- Graft vs. host disease (following bone marrow transplantation)

**may also cause major salivary gland enlargement

Table 2. Symptoms and Signs Suggesting Chronic Salivary Hypofunction

Symptoms

* Positive responses to specific questions:⁷

-- Do you sip liquids to aid swallowing dry foods?

-- Does your mouth feel dry when eating?

-- Do you have difficulty swallowing any foods?

* Complaints of burning mucosa and/or intolerance to spicy foods (usually associated with erythematous candidiasis)

Signs

* Little or no pooled saliva in the mouth floor during examination

* Dry or sticky mucosal surfaces

* Multiple caries in cervical, incisal, or marginal locations

* Thick or cloudy saliva expressible from parotid or submandibular gland ducts

* Bilateral salivary gland enlargement

* Signs of erythematous candidiasis:

-- Dorsal tongue with erythema, loss of filiform papillae, and fissured or cobblestone appearance

-- Angular cheilitis

-- Patchy erythema on other mucosal surfaces

Table 3. Products Selectively Useful for Treating Patients With Chronic Salivary Hypofunction

Anti-caries agents

* Professionally applied

-- 1.23% fluoride in acidulated phosphate fluoride gel

-- 2.26% fluoride varnish²³

* Patient-applied

-- 0.5% fluoride in neutral sodium fluoride gel

-- 0.05% sodium fluoride mouth rinse

-- 0.12% chlorhexidine gluconate mouth rinse

Saliva stimulants

* Sugar-free chewing gum or hard candies

* Pilocarpine hydrochloride tablets, 5 mg, initially prescribed at one tablet three times daily

Antifungal drugs

* Fluconazole, 100 mg tablets, 200 mg on first day then 100 mg per day for 14 days

* Nystatin Vaginal Tablets, 100,000 units per tablet, dissolve slowly in mouth (15-20 minutes), using sips of water as necessary to aid dissolution, 2 to 4 tablets per day, for 3 to 12 weeks, depending on the severity and clinical response (see text)

* Nystatin or 1% Clotrimazole cream, 15 gm tube (see text)

* Nystatin Topical Powder, 15 gm (see text)

Note: This table is meant as a supplement to the text. It is not a comprehensive outline for treatment.