This course was published in the November 2010 issue and expires November 2013. The authors have no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated.
After reading this course, the participant should be able to:
- Describe how Sjögren’s syndrome, diabetes, and radiation therapy reduce salivary flow, causing xerostomia.
- Discuss primary and secondary Sjögren’s syndrome.
- Understand the two types of diabetes.
- Describe the effects of polypharmacy, illegal drug use, and alcoholism on xerostomia.
A variety of factors can contribute to the development of xerostomia—from systemic conditions to lifestyle factors. Dental hygienists are on the front lines of xerostomia diagnosis because they are often the first health care professionals to examine a patient’s oral cavity. The effects of untreated xerostomia can be traumatic, which emphasizes the need to determine the underlying causes of dry mouth so that that the most effective treatment plan can be implemented.
Sjogren’s syndrome is a systemic autoimmune disorder that causes the body’s immune cells to destroy the lacrimal glands (glands that produce tears) and salivary exocrine glands (glands that produce saliva) by targeting ductal epithelial cells. Consequently, salivary composition and flow rate are disturbed, which leads to hyposalivation and dry mouth.1 Approximately 1 million to 4 million people in the United States have Sjogren’s syndrome.2 Most patients are 40 years or older at the time of diagnosis, and women are nine times more likely to develop Sjogren’s than men.3
Patients with primary Sjogren’s syndrome do not have any other autoimmune diseases, while patients with secondary Sjogren’s syndrome have a second autoimmune disorder, such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, mixed connective tissue disease, relapsing polychronditis, or polymyositis. Both primary and secondary forms are responsible for mouth dryness and eye dryness.3 A blood test can identify specific hemotologic markers for the syndrome. High levels of antibodies, such as anti-nuclear antibody (ANA) and rheumatoid factor (RF) are indicative of the syndrome. Positive ANA tests are found in 70% to 90% of patients, while 60% to 90% of patients display positive RF tests.4 Ocular symptoms, of which at least one of the following must be present, include: dry eyes for longer than a 3-month period, recurrent feeling of sand or gravel in eyes, or the use of a tear substitute more than three times a day. Oral symptoms, of which at least one must be present, include: sensation of dry mouth for more than 3 months, swollen glands, or the need to use liquids to help swallow food. At least one of the results from either a Schirmer I test, Rose-Bengal evaluation, or a lacrimal gland biopsy must be abnormal (see Table 1).5,6 At least one of the results from either a salivary gland scintigraphy, parotid sialography, or unstimulated whole saliva sialometry (< 1.5 ml per 15 minutes) must be abnormal. To diagnose secondary Sjogren’s syndrome, proper diagnosis of an established connective tissue disease as well as the presence of either dry mouth or dry eye symptoms and abnormal results from two tests for dry mouth and eyes must occur.4
Radiological evaluation of the parotid gland via magnetic resonance imaging (MRI) or ultrasound can detect glandular insufficiency. Puddling of a radiological contrast across the entire gland after its injection into the parotid/ Stenson’s duct is indicative of Sjogren’s syndrome. Deficiencies in saliva production can be detected by performing stimulated or nonstimulated sialometry.7
Systemic symptoms associated with Sjogren’s syndrome commonly involve inflammatory conditions, such as lung inflammation, nervous system inflammation, kidney disease, muscle inflammation, cutaneous vasculitis, frank arthritis, and aggressive or erosive osteoarthritis. Gynecological concerns include vaginal dryness, urine leakage, and a decreased urine volume. An association between Sjogren’s Syndrome and head and neck lymphomas is also documented.3 Table 2 provides a list of additional symptoms.
There is no cure for Sjogren’s syndrome so addressing the symptoms is the main avenue of treatment. Treatments are generally directed at the associated autoimmune disorders.1 Antirheumatics such as nonsteroidal anti-inflammatory drugs (NSAIDs) suppress inflammation and aid in the relief of musculoskeletal symptoms.1 Methotrexate, a disease-modifying anti-rheumatic drug, may improve mouth and eye dryness. 8 Certain studies show that hydroxychloroquine, a class of drugs used to prevent and treat malaria, decrease immunoglobulin serum concentrations as well as slightly improve oral and ocular symptoms and arthralgia/ myalgia.9,10 Patients with severe complications can also try corticosteroids or immunosuppressive drugs.
Diabetes mellitus is a chronic disorder of carbohydrate, fat, and protein metabolism that causes the levels of glucose to become too high in the blood because of deficits in insulin secretion and/or insulin action. Approximately 23.6 million people in the United States have diabetes. 11 There are two major types: type 1 and 2. Type 1 diabetes makes up approximately 5% to 10% of all diabetes cases.12 Type 1 is further characterized into two subgroups. In the most common form, Type 1A, the body destroys its own pancreatic beta cells responsible for producing insulin.12 In Type 1B, a severe insulin deficiency exists but is not caused by autoimmunity.
Onset of types 1A and 1B can occur at any age, although they most typically present during childhood or adolescence.12 Type 2 diabetes is caused by impaired insulin function.12 The lack of insulin or insulin resistance triggers an inability to respond to an elevated blood glucose level. As a result, insulindependent cells are unable to use the glucose as energy. Stored triglycerides are used as an alternative energy source and are metabolized into fatty acids. Blood glucose levels become elevated. Because the kidneys cannot completely absorb the excess glucose, a component of the glucose continues to reside in the urine.
This keeps the kidneys from reabsorbing water, which leads to the production of large volumes of pale urine accompanied by fluid loss. Water found in body cells replenishes the lost blood volume, which causes dehydration and increased thirst. One effect of this dehydration may be the development of xerostomia. Xerostomia occurs in about 40% to 80% of patients with diabetes.13 Patients with poorly controlled diabetes experience the lowest stimulated parotid flow rates and are also more likely to have asymptomatic bilateral parotid gland enlargement (Figure 1).14 Patients with diabetes are also predisposed to oral candidiasis, median rhomboid glossitis, denture stomatitis, and angular chelitis.15
Burning mouth or tongue is associated with undiagnosed type 2 diabetes.16 Mild impairment of sweet receptors in patients with diabetes is caused by xerostomia.17 Increased salivary glucose levels and xerostomia may also increase the prevalence of caries in these patients.12 The specific treatment for diabetes induced xerostomia is proper glycemic control to reduce the effect of glycosuria and subsequent dehydration.
Hyposalivation is a common side effect of radiation therapy used in the treatment of tumors of the head and neck.18 Radiation therapies for squamous cell cancers of the oral cavity, oropharynx, and sinuses; brain tumors, melanomas; lymphomas; sarcomas; and salivary gland tumors can all cause xerostomia.18 The most radiosensitive salivary gland is the parotidgland, followed by submandibular, sublingual, and minor salivary glands (Figure 1).19 Radiation damage results from fibrosis of salivary glands, loss of acinar cells, reduced blood flow due to possible damage to the vasculature, and interference with nerve transmission.20 A 60% to 90% decline in salivary function typically occurs within 1 week of receiving 10 Gy of radiation. Recovery is possible if the total dosage to salivary tissue is less than 25 Gy.21 Radiation doses higher than 23 Gy and 25 Gy cause irreversible salivary gland destruction. 22 Following a radiation dose higher than 60 Gy, salivary glands begin to atrophy and undergo fibrosis. Patients often develop sticky and viscous saliva, later followed by the lack of saliva production and the development of xerostomia.22 The effects of radiation are dependent on the number of salivary glands exposed, dose, and time frame of the radiation therapy.22,23
To spare salivary function and improve quality of life, salivary gland exposure to radiation can be minimized by using intensity modulated radiation therapy, three-dimensional treatment planning, and dose delivery techniques.23,24 The use of the radioprotective agent amifostine may reduce radiation-induced hyposalivation.25 Surgical replacement of submandibular glands is one way of protecting them from the path of radiation.22 Complications with radiation therapy are not limited to radiation exposure. The radioactive iodine used in thyroid cancer treatment can also disrupt parotid gland function.26
Contrary to popular belief, salivary gland hypofunction is not a normal sign of aging. There is no significant age-related change to the responsiveness of salivary mucous cells.27,28 However, as people age they take more medications and xerostomia is commonly caused by the side effects of prescribed medications. In fact, medications are the most common cause of dry mouth, due to the secondary decrease in salivary function.22 Close to 80% of the most commonly prescribed medications induce xerostomia.22 More than 75% of people older than age 65 are taking at least one prescription medication.29
Determining relative xerostomia incidence rates for specific drugs is difficult; nonetheless, complaints of xerostomia increase with the number of medications being taken.29 Older adults often have a slower metabolism, which makes them more susceptible to the effects of medications.29 Therapeutic doses of medications do not damage salivary gland anatomy and any damage is reversible with discontinued use of xerogenic drugs.19,23 The classes of drugs associated with the development of dry mouth include anticholinergic and antiparkinsonian agents, antidepressants, systemic antihistamines, antipsychotic and antihypertensive medications, central nervous system stimulants, and sedatives.23
Chemotherapy medications are also associated with reduced salivation, however, these effects tend to be transient.22 The sensation of oral dryness can be caused by analgesics and diuretics due to modified sensory function and/or mucosal or total body dehydration.30 Anti-cholinergic medications are the most commonly prescribed medications that reduce salivary flow.22 The substitution of medications with fewer xerostomic side effects should be considered. For example, selective serotonin reuptake inhibitors cause fewer dry mouth symptoms than tricyclic antidepressants.31 Dividing a large dose of medication into smaller doses can eliminate or mitigate the xerostomic effect of the drug.22
ILLICIT DRUG USE
Illicit drug use is a common cause of dry mouth, particularly the use of methamphetamine (MA). MA is a highly addictive central nervous system stimulant that has a high potential for abuse. MA acts by stimulating the release and then reuptake of dopamine, norepinephrine, and serotonin in the brain.32,33 Intense emotions, euphoria, increased alertness, insomnia, hyperactivity, decreased appetite, increased respiration, and hyperthermia are the common short-term effects. One of many long-term effects includes psychological (but not physical) dependence on MA.34-36 MA use causes hyposalivation via the stimulation of receptors within salivary gland vasculature inducing vasoconstriction, thus reducing salivary flow.37
Reducing salivary flow causes teeth to become more susceptible to demineralization and caries by limiting the protective capacity of saliva.38 MA-induced xerostomia is exacerbated by dehydration caused by the drug user’s elevated metabolism and increased physical activity.39 This dehydration may stimulate the user to ingest large quantities of liquids, especially carbonated sugary soft drinks, fueling caries development. The situation is further compounded by an accompanying lack of concern for personal and oral hygiene.39,40
The drug’s ability to increase motor activity, such as excessive bruxism, along with the acidic nature of the drug itself, contribute to the destruction of dentition associated with MA use.40 MA users are predisposed to extensive caries, a condition termed “meth mouth,” which is characterized by rampant caries, particularly located on the buccal smooth surfaces and interproximal surfaces of anterior teeth.44,46 The teeth appear blackened, stained, and rotted, and are often beyond salvaging and must be extracted.38,41
Alcoholism affects 14 million Americans and is characterized by impaired social functioning and many serious health problems.42 The disease affects genetically vulnerable individuals who are susceptible to cravings for alcohol via the actions of neurotransmitter systems within the brain’s pleasure center. Dental disease is extensive in people with alcoholism. Alcohol use decreases salivary flow and many people with alcoholism become disinterested in personal and oral hygiene.43
Additional diseases may contribute to the presence of xerostomia, either through pathophysiology of the disease process and/or due to the medications used in treating the disease and its symptoms. Table 3 provides a list. Looking beyond the oral cavity is important when addressing xerostomia in patients. Patients’ systemic health and lifestyle choices have a profound effect on their oral health, particularly in the development of xerostomia. Addressing these causes of xerostomia is the first step toward effective treatment of dry mouth.
- Van der Reijden WA, Vissink A, Veerman EC, Nieuw Amerongen AV. Treatment of oral dryness related complaints (xerostomia) in Sjogren’s syndrome. Ann Rheum Dis. 1999;58:465-473.
- Kassan SS, Moutsopoulos HM. Clinical manifestations and early diagnosis of Sjogren’s syndrome. Arch Intern Med. 2004;64:1275-1284.
- Fox PC. Autoimmune diseases and Sjogren’s syndrome: an autoimmune exocrinopathy. Ann NY Acad Sci. 2007;1098:15-21.
- Fox RI. Sjogren’s syndrome. Lancet. 2005;366:321-331.
- Medline Plus. Sjogren’s syndrome. Available at:www.nlm.nih.gov/medlineplus. Accessed October 11, 2010.
- Krachmer JH, Mannis MJ, Holland EJ. Cornea Volume 1. 2nd ed. Philadelphia: Elsevier Mosby;2005:526.
- Kalk WWI, Vissink A, Spijkervet FKL, Bootsma H, Kalleberg CGM, Roodenburg JLN. Parotid sialography for diagnosing Sjogren’s syndrome. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.2002;94:131-137.
- Skopouli FN, Jagiello P, Tsifetaki N, Moutsopoulos HM. Methotrexate in primary Sjogren’s syndrome.Clin Exp Rheumatol. 1996;14:555-558.
- Yavuz S, Asfurolu E, Bicakcigil M, Toker E. Hydroxychloroquine improves dry eye symptoms of patients with primary Sjogren’s syndrome. Rheumatol Int. 2010 Mar 23. [Epub ahead of print].
- Rihl M, Ulbricht K, Schmidt RE, Witte T. Treatment of sicca symptoms with hydroxychloroquine in patients with Sjogren’s syndrome. Rheumatology. 2009;48:796-799.
- National Diabetes Information Clearinghouse.National Diabetes Statistics, 2007. Available at:http://diabetes.niddk.nih.gov/dm/pubs/statistics.Accessed October 15, 2010.
- Lalla RJ, D’Ambrosio JA. Dental management considerations for the patient with diabetes mellitus. J Am Dent Assoc. 2001;132:1425-1432.
- Sreebny LM, Yu A, Green A, Valdini A. Xerostomia in diabetes mellitus. Diabetes Care.1992;15:900-904.
- Nassour DN, Patel SV, Kosseifi SG, Jordan RM, Peiris AN. Marked bilateral parotid enlargement in metabolic syndrome: a case report and review of the literature. Tenn Med. 2007;100:39-41.
- Quirino MR, Birman EG, Paula CR. Oral manifestations of diabetes mellitus in controlled and uncontrolled patients. Braz Dent J. 1995;6:131-136.
- Gibson J, Lamey PJ, Lewis M, Frier B. Oral manifestations of previously undiagnosed noninsulin dependent diabetes mellitus. Oral Pathol Med. 1990;19:284-287.
- Zhou LH, Liu XM, Feng XH, Han LO, Liu GD. Expression of alpha-gustducin in the circumvallate papillae of taste buds of diabetic rats. Acta Histochem. 2009;111:145-149.
- Guggenheimer J, Moore PA. Xerostomia: etiology, recognition and treatment. J Am Dent Assoc. 2003;134:61-69.
- Sreebny LM. Saliva in health and disease: an appraisal and update. Int Dent J. 2000;50:140-161.
- Hensley ML, Hagerty KL, Kewalramani T, et al. American Society of Clinical Oncology 2008 clinical practice guideline update: use of chemotherapy and radiation therapy protectants. J Clin Oncol. 2009;27:127-145.
- Blanco AI, Chao KS, El Naqa I, et al. Dosevolume modeling of salivary function in patients with head-and-neck cancer receiving radiotherapy. Int J Radiat Oncol Biol Phys. 2005;62:1055-1069.
- Gupta A, Epstein JB, Sroussi H. Hyposalivation in elderly patients. J Can Dent Assoc. 2006;72:841– 846.
- Diaz-Arnold AM, Marek CA. The impact of saliva on patient care: a literature review. J Prosthet Dent.2002;88:337-343.
- Chambers MS, Garden AS, Kies MS, Martin JW. Radiation-induced xerostomia in patients with head and neck cancer: pathogenesis, impact on quality of life, and management. Head Neck. 2004;26:9.
- Jensen SB, Pedersen AM, Vissink A, et al. A systematic review of salivary gland hypofunction and xerostomia induced by cancer therapies: management strategies and economic impact. Support Care Cancer. 2010;18:1061-1079.
- Caglar M, Tuncel M, Alpar R. Scintigraphic evaluation of salivary gland dysfunction in patients with thyroid cancer after radioiodine treatment. Clin Nucl Med. 2002;27:767-771.
- Allweiss P, Braunstein GD, Karz A, Waxman A. Sialadenitis following I-131 therapy for thyroid carcinoma: concise communication. J Nucl Med.1984;25:755-758.
- Aguirre A, Testa-Weintraub LA, Banderas JA, Haraszthy GG, Reddy MS, Levine MJ. Sialochemistry: a diagnostic toll? Crit Rev Oral Biol Med. 1993;4:343-350.
- Ship JA, Pillemer SR, Baum BJ. Xerostomia and the geriatric patient. J Am Geriatr Soc. 2002;50:535-543.
- Napeñas JJ, Brennan MT, Fox PC. Diagnosis and treatment of xerostomia (dry mouth). Odontology. 2009;97:76-83.
- Hunter KD, Wilson WS. The effects of antidepressant drugs on salivary flow and content of sodium and potassium ions in human parotid saliva. Arch Oral Biol. 1995;40:983-989.
- Rothman RB, Baumann MH, Dersch CM, et al. Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin. Synapse. 2001;39:32-41.
- Sulzer D, Sonders MS, Poulsen NW, Galli A. Mechanisms of neurotransmitter release by amphetamines:a review. Prog Neurobiol. 2005;75:406-433.
- Beebe DK, Walley E. Smokable methamphetamine (‘ice’): an old drug in a different form. Am Fam Physician. 1995;51:449-453.
- Yu Q, Larson DF, Watson RR. Heart disease, methamphetamine and AIDS. Life Sci.2003;73:129-140.
- Gotway MB, Marder SR, Hanks DK, et al.Thoracic complications of illicit drug use: an organ system approach. Radiographics. 2002;22(Spec No):S119–S125.
- Meth Mouth. Available at: www.ada.org/3056.aspx. Accessed October 13, 2010.
- Klasser GD, Epstein J. Methamphetamine and its impact on dental care. Can Dent Assoc. 2005;71:759-762.
- Shaner JW. Caries associated with methamphetamine abuse. J Mich Dent Assoc. 2002;84:42-47.
- McGrath C, Chan B. Oral health sensations associated with illicit drug abuse. Br Dent J.2005;198:159-162.
- Canadian Dental Association. “Meth mouth” in the news. J Can Dent Assoc. 2005;71:454.
- Grant BF, Dawson DA, Stinson FS, Chou SP, Dufour MC, Pickering RP. The 12-month prevalence and trends in DSM-IV alcohol abuse and dependence: United States, 1991-1992 and 2001-2002. Drug Alcohol Depend. 2004;74:223-234.
- Friedlander AH, Marder SR, Pisegna JR. Alcohol abuse and dependence: psycopathology, medical management and dental implications. J Am Dent Assoc. 2003;134:1306.
From Dimensions of Dental Hygiene. November 2010; 8(11): 50-53.