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Getting to the Bottom of Dry Mouth

Normal salivary physiology, complications, and physical assessment are all part of diagnosing and treating xerostomia.

Xerostomiais a symptom that acts like a disease.1 By definition, xerostomia is the “subjective feeling of oral dryness” and the result of salivary gland hypofunction.2 However, the subjective complaint of dry mouth is not enough for the diagnosis of salivary gland dysfunction, as this can be attributed to both salivary and nonsalivary causes.3 Salivary output must decrease by more than 50% before the perception of dry mouth occurs,4 meaning that a significant reduction in saliva may take place before a patient ever develops an awareness of the problem. Conversely, the perception of dry mouth is not always indicative of an actual reduction or loss of saliva, but rather, the result of psychological influences, such as depression or anxiety.5

Determining the cause of a patient’s xerostomia complaint is important, as a true loss of saliva results in damage to the oral hard and soft tissues. Further, true salivary hypofunction often leads to a major decrease in the quality of life, as patients experience difficulty eating, speaking, swallowing, and wearing dentures or appliances. Taste may be adversely affected as well. These limitations often affect a patient’s nutritional status, leading to poor food choices and/or food avoidance. Some patients lose their desire to interact socially with others when food is part of the event, as mealtimes become fraught with difficulties.

Xerostomia is most frequently reported among the elderly but is not caused by aging. While salivary flow rate does decline somewhat with age, xerostomia is not likely to occur unless the patient’s health is compromised by diseases or drugs used to treat those diseases.1 Older patients are more likely to suffer from chronic conditions, such as heart disease and depression, and take more medications, many of which cause xerostomia as a side effect.


The average adult secretes about 500 ml of saliva in a 24-hour period, but flow rates vary depending on the degree of stimulation, demand, and patient status.6 Salivary flow is controlled by reflex in response to stimulation by taste and chewing.7

Secretion of saliva from the glands is regulated by the two divisions of the autonomic nervous system. The cell-surface receptors on salivary glands receive stimuli from neurotransmitters and transmit signals to structures and enzymes within the cells that comprise the gland. Excitation of either the parasympathetic or sympathetic nerves stimulates salivary secretion, but the effects of the parasympathetic nerves are stronger and last for a longer period of time.6 Rate of salivary flow and the composition of saliva varies, depending on the type and duration of stimulation.7

Parasympathetic stimulation produces the fluid component of the saliva that is high in volume and ions, but low in protein (serous saliva). Sympathetic stimulation produces saliva that is high in protein, but low in volume (mucous saliva). Think of the “fight or flight” sympathetic response, such as that produced by extreme anxiety or fear—often the mouth feels dry.6 Diseases or drugs that alter the number of receptors, receptor function, or signal transduction affect salivary function.8

Unstimulated resting whole saliva is secreted primarily by the submandibular glands, which are mixed salivary glands that produce both serous and mucinous saliva.  The parotid glands, which are serous glands, produce the majority of the watery volume of stimulated whole saliva, such as that secreted while eating. The sublingual glands, while also mixed glands, are primarily mucous type glands and contribute little to the overall total volume of whole saliva. The minor salivary glands found in the oral mucosa contribute about 10% to the total volume of saliva, but continuously secrete a mucinous saliva that is critical for oral mucosal integrity and lubrication.7


Saliva is one of the most complex and vital body fluids and serves many physiological purposes.  Saliva is the first digestive enzyme in the gastrointestinal tract and is necessary for chewing, forming the food bolus, and swallowing.  Salivary amylases are salivary proteins that aid in the breakdown of starches and overall digestive function. The fluid components of saliva cleanse the oral cavity and facilitate the perception of taste sensation.7

Salivary mucins, which are glycoproteins, lubricate oral mucous membranes and protect the tissue from trauma and ulceration.  Lubrication may also prevent the penetration of some carcinogens, toxins, and irritants, and encourages soft tissue repair.9  Saliva maintains the balance of the oral ecosystem with immunologic, nonimmunologic, and antibacterial processes to prevent microbial colonization and reduce bacterial adherence to the teeth and oral tissues.10,11

Bicarbonate and phosphate are electrolytes that serve as salivary buffers for regulating oral and plaque pH. Bicarbonate is the primary buffer at high flow rates and calcium and phosphate keep the saliva saturated with hydroxyapatite.7 Structural integrity of the teeth is maintained by salivary pellicle formation by mucins, the regulation of electrolytes, and remineralization of early enamel lesions by calcium and phosphate.7,10,11


  • People don’t notice they have dry mouth until salivary output has been reduced by about 50%.4
  • The feeling of dry mouth can be caused by anxiety and depression.
  • The average adult secretes approximatley 500 ml of saliva—approximately 2 cups—in a 24-hour period.
  • Saliva has an antiviral effect so patients with xerostomia are at a higher risk of viral infections.
  • The four complaints that are most relative to a reduced salivary flow are oral dryness when eating, the need to sip liquids to swallow dry foods, difficulty swallowing, and the perception of too little saliva in the mouth.3


The antibacterial and buffering capacities, coupled with the natural mechanical cleansing of saliva, protect the oral cavity from caries and periodontal diseases.11 As salivary flow decreases, salivary buffers become even more important. As oral pH becomes more acidic, oral sugar clearance is prolonged and plaque bacteria adhere more readily to the teeth.7,10,11 Thus, in a xerostomic patient, saliva is less able to protect the teeth from the acid attack of cariogenic bacteria, such as lactobacillus and Streptococcus mutans, and significant caries activity often develops, predominately on exposed root surfaces.7,10,11

Decreased salivary production also places the patient at risk for opportunistic infections, especially fungal infections caused by Candida organisms. Parotid saliva contains peptides that have antifungal properties against Candida albicans.12 Fungal infections are a common complication in patients with immunosuppression, diabetes, or HIV infection, and in those taking antibiotics, hormones, or chemotherapy.11 Fungal infections can be a recurrent problem for patients with chronic xerostomia.

Saliva also demonstrates an antiviral effect. Salivary and mucosal antibodies protect the oral cavity against multiple viruses.  Salivary mucins protect the oral tissues from herpes simplex virus and HIV virus.10,11,13,14  Therefore, viral infections must be considered a risk in xerostomic patients.11

Dental professionals must thoroughly assess for and educate their patients about the multiple oral complications associated with xerostomia. These complications include dental caries; periodontal diseases and tooth loss; oral trauma, ulcerations, and pain; fungal and viral infections; and alterations in the oral functions of mastication, speech, and swallowing. Interventions used to manage these effects include fluoride therapy; salivary stimulation and replacement therapy; antimicrobial, antifungal, and antiviral therapies; pain control; tobacco cessation; and mechanical plaque removal.11


When a patient reports dry mouth symptoms, conducting a proper evaluation to determine whether salivary flow is actually diminished and to determine the underlying etiology of the condition is integral to proper treatment. Several objective measurements exist that measure salivary function and can be used to diagnose salivary hypofunction. However, their availability function is best achieved with repeated or serial measurements, given the wide variation in the normal range of function.3,15

The first aspect of patient evaluation is a thorough medical history review. It is important to obtain a history of medication use, presence or history of disease, or medical treatment that may affect salivary gland function. These conditions may include a history of radiation therapy to the head and neck region; neurological impairments, such as stroke or nerve damage; salivary tumors; or a systemic disease, such as Sjögren’s syndrome.3

Evaluating patient symptoms can help determine whether the perceived dryness is actually due to salivary hypofunction. Fox describes the four complaints most likely to correlate to actual decreased glandular function including: oral dryness when eating, the need to sip liquids to swallow dry foods, difficulty swallowing, and the perception of too little saliva in the mouth.3

Physical inspection of the oral cavity reveals many changes to the hard and soft tissues in a patient with true xerostomia.  Palpation of the major salivary glands may reveal chronic enlargement and possible tenderness.  The oral mucosa will appear friable, and the mouth mirror or the clinician’s fingers may stick to the oral mucosa. The tongue may appear fissured with atrophy of the papilla.  Pressure on the salivary ducts with the blunt end of a mouth mirror or cotton swab reveals little or no secretion. Opportunistic fungal infections may be present on the tongue, mucosa, and as angular cheilitis.  Aphthous and viral lesions may also be visible. Gingival disease may appear, or if already present, may increase in extent and severity.  Finally, carious lesions, especially on root surfaces and on the cusp tips, are highly characteristic of a chronic dry mouth.3,11


Laboratory tests can evaluate those with a suspected history of Sjögren’s syndrome, as these patients possess specific autoantibodies that are immune markers that aid in the diagnosis of this disease.6 Labial minor salivary gland biopsy is the best criterion for the diagnosis of the salivary component of Sjögren’s syndrome.16

Diagnostic imaging is also helpful in visualizing solid tumors, salivary stones, ductal abnormalities, and pathology of the glandular tissues.3 Magnetic resonance imaging (MRI) is helpful to assess chronic lymphadenopathy and solid masses. Sialography uses a radiopaque fluid injected into the gland through the main duct to visualize the anatomy of the gland.3,17,18 Scintiscanning, also known as a Tc scan, is a measure of secretory function that uses an intravenously injected gamma-emitting radionuclide drug (Tc = technetium pertechnetate) that is taken up by the salivary glands and secreted into the mouth. The presence of Tc in the salivary glands indicates a functional glandular tissue.19 This technique is used to determine whether a patient with functional glands will benefit from salivary stimulating medications.3  Hematologic and immunologic testing also may be useful in formulating a differential diagnosis of long-term xerostomia.6


  1. Ettinger RL. Review: xerostomia: a symptom which acts like a disease. Age Ageing. 1996;25:409-412.
  2. Sreebny LM. Dry mouth and salivary gland hypofunction. Part I: Diagnosis. Compendium. 1988;9:569-578.
  3. Fox PC. Differentiation of dry mouth etiology. Adv Dent Res. 1996;10:13-16.
  4. Dawes C. Physiologic factors affecting salivary flow rate, oral sugar clearance, and the sensation of dry mouth in man. J Dent Res. 1987;66(special issue):648-653.
  5. Bergdahl M, Bergdahl J. Low unstimulated salivary flow and subjective oral dryness: association with medication, anxiety, depression, and stress. J Dent Res. 2000;79:1652-1658.
  6. Porter SR, Scully C, Hegarty AM. An update of the etiology and management of xerostomia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;97:28-46.
  7. Jensen SB, Pedersen AM, Reibel J, Nauntofte B. Xerostomia and hypofunction of the salivary glands in cancer therapy. Support Care Cancer. 2003;11:207-225.
  8. Enwonwu CO. Ascorbate status and xerostomia. Med Hypotheses. 1992;39:53-57.
  9. Tabak LA, Levine MJ, Mandel ID, Ellison SA. Role of salivary mucins in the protection of the oral cavity. J Oral Pathol. 1982;11:1-17.
  10. Mandel ID. The role of saliva in maintaining oral homeostasis. J Am Dent Assoc. 1989;119:298-304.
  11. Spolarich AE. Managing the side effects of medications. J Dent Hyg. 2000;74:57-69.
  12. Pollock JJ, Denepitiya L, MacKay BJ, Iacono VJ. Fungistatic and fungicidal activity of the human parotid salivary histidine-rich polypeptides on Candida albicans. Infect Immun. 1984;44:702-707.
  13. Heineman HS, Greenberg MS. Cell protective effect of human saliva specific for herpes simplex virus. Arch Oral Biol. 1980;25:257-261.
  14. Fox PC, Wolff A, Yeh CK, Atkinson JC, Baum BJ. Saliva inhibits HIV-1 infectivity. J Am Dent Assoc. 1988;116:635-637.
  15. Ship JA, Fox PC, Baum BJ. How much saliva is enough? ‘Normal’ function defined. J Am Dent Assoc. 1991;122:63-69.
  16. Daniels TE. Labial salivary gland biopsy in Sjögren’s syndrome: assessment as a diagnostic criterion in 362 suspected cases. Arthritis Rheum. 1984;27:147-156.
  17. Luyk NH, Doyle T, Ferguson MM. Recent trends in imaging the salivary glands. Dentomaxillofac Radiol. 1991;20:3-10.
  18. Daniels, TE, Benn DK. Is sialography effective in diagnosing the salivary component of Sjögren’s syndrome? Adv Dent Res. 1996;10:25-28.
  19. Kohn WG, Ship JA, Atkinson JC, Patton LL, Fox PC.Salivary gland 99mTc-scintigraphy: a grading scale and correlation with major salivary gland flow rates. J Oral Pathol Med. 1992;21:70-74.

From Dimensions of Dental Hygiene. April 2005;3(4):22-24.

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