Odontology (2009) 97:76–83
DOI 10.1007/s10266-008-0099-7
REVIEW ARTICLE
Joel J. Napeñas · Michael T. Brennan · Philip C. Fox
Diagnosis and treatment of xerostomia (dry mouth)
Received: November 14, 2008 / Accepted: December 18, 2008
Abstract Xerostomia (dry mouth) is a common complaint
with widespread implications such as impaired quality of
life, oral pain, and numerous oral complications. There are
a variety of salivary and nonsalivary causes of xerostomia,
the most frequent being medication side effects and sys-
temic disorders. A systematic approach should be employed
to determine the etiology of this condition, with distinctions
made between patients with subjective complaints of xero-
stomia alone and those with measurable salivary gland dys-
function. Management is multidisciplinary and multimodal.
This review summarizes the current literature on the etiol-
ogy, diagnosis, and complications of xerostomia, and on the
management of patients with xerostomia.
Key words Saliva · Xerostomia · Dry mouth
Introduction
Saliva is essential to the function and protection of the oral
cavity and contiguous gastrointestinal epithelium. Common
functions of the fluid component of the salivary secretions
include cleansing and lubricating of oral soft and hard
tissues, solubilization and bolus formation of food, facilita-
tion of taste perception, mastication and speech, and reten-
tion of removable prostheses. Bicarbonate and other buffers
in saliva help maintain saliva’s physiologic pH at 6.5–7.4 and
protect against acidic challenges from bacterial cariogenic
pathogens.1 Glycoproteins such as mucins, histatins, and
numerous other salivary components also have protective
antimicrobial effects against harmful microorganisms. Amy-
J.J. Napeñas · M.T. Brennan · P.C. Fox
Department of Oral Medicine, Carolinas Medical Center, Charlotte,
NC, USA
P.C. Fox (*)
PC Fox Consulting, Via Monterione 29, 06038 Spello (PG), Italy
Tel. +1-301-979-9540 (U.S.); +39-340-948-4780 (Italy)
e-mail: pcfox@comcast.net
© The Society of The Nippon Dental University 2009
lases in saliva aid in digestive function by breakdown of
starch.2
The major salivary glands – the parotid, submandibular
and sublingual glands – account for over 90% of saliva
production. The remainder is produced by the minor sali-
vary glands, located in the submucosa throughout the oro-
pharynx. The primary secretory cells, the acini, produce an
isotonic primary saliva, which is modified by salt reabsorp-
tion within the ductal system, resulting in a final secreted
saliva that is hypotonic with respect to plasma.3 There are
two types of acinar cells: serous-type acinar cells produce a
watery fluid, and mucous-type cells produce a more viscous
fluid. Salivary flow is regulated by the autonomic nervous
system, with the parasympathetic response primarily respon-
sible for stimulating flow and the sympathetic system
involved in salivary protein production.4 Flow rate and sali-
vary composition are dependent upon the type and length
of stimulus, and the gland from which the saliva is
secreted.
Xerostomia is the subjective feeling of dry mouth, a
symptom that may or may not be accompanied by hyposali-
vation, an objective decrease in salivary flow. Though the
most common symptom of hyposalivation is xerostomia,
studies have shown that the former does not necessarily
guarantee the latter.5,6 However, patients that have a greater
than 50% reduction in salivary flow usually experience
xerostomia.7
The prevalence of xerostomia and salivary gland hypo-
function is very difficult to determine with certainty owing
to the limited number of epidemiological studies and differ-
ences in how the two conditions have been defined. More-
over, estimates are hard to obtain because the population
experiencing these conditions is heterogeneous and the
conditions have various causes. A systematic review pub-
lished in 2006 found that the prevalence of self-reported
xerostomia in population-based samples ranged from 0.9%
to 64.8%.8 Another study estimated that 30% of the popula-
tion aged 65 years or older suffered from these disorders.9
Among patients with Sjögren’s syndrome and those having
received head and neck radiation for the treatment of
cancer, the prevalence of xerostomia is nearly 100%.10,11

Causes of xerostomia
There are many causes of xerostomia, both salivary and
nonsalivary (Table 1). Nonsalivary causes include dehydra-
tion, cognitive and neurologic alterations, oral sensory dys-
function, psychological disorders, and idiopathic causes.12
Causes of xerostomia due to salivary gland dysfunction
can be categorized into autoimmune exocrinopathies (most
notably Sjögren’s syndrome), medication side effects, radia-
tion-induced salivary gland dysfunction, and salivary gland
trauma. Other, less common causes that have been reported
include salivary gland tumors, infectious processes, endo-
crine and renal disorders, dementia, cystic fibrosis, and
amyloidosis.13
A distinction must be made between those medications
that cause xerostomia and those that cause hyposalivation.
Though many medications have xerostomia as a side effect,
very few have been tested for objective changes in salivary
flow. Medications with anticholinergic activity presumably
inhibit salivary secretion, and in most cases the effect is
reversed upon discontinuance of the drugs.14,15 Tricyclic
antidepressants are potent inhibitors of salivation that act
by binding to muscarinic–cholinergic receptors. Antihyper-
tensive medications are commonly cited for side effects of
xerostomia or hyposalivation. Whereas α-adrenergic agonist
antagonists (e.g., clonidine, guanfacine, and methyldopa)
consistently cause hyposalivation,16 β-blockers and angio-
tensin-converting enzyme inhibitors have been shown to
77
17–19
cause neither hyposalivation nor xerostomia. Diuretics
have been implicated in xerostomia but not hyposaliva-
tion.20,21 Other classes of medications responsible for
hyposalivation due to anticholinergic effects are antispas-
modic drugs, which contain anticholinergic alkaloids, and
some barbiturates.13
Sjögren’s syndrome (SS) is a chronic, autoimmune,
inflammatory disorder characterized by lymphocytic infil-
tration of the exocrine glands in multiple sites, most com-
monly the lacrimal and salivary glands. It can occur alone
(primary SS), or in conjunction with another autoimmune
rheumatic disease (secondary SS). The estimated preva-
lence in the population is 0.6%, with the highest prevalence
in the fourth or fifth decade of life.22 Ninety percent of
patients are women. The focal lymphocytic infiltration of
the exocrine glands may lead to germinal center formation,
production of antibodies, and focal sialadenitis.23 The patho-
genesis is not known, but is thought to be multifactorial in
nature. It is believed to involve an interplay of autoantibod-
ies [e.g., SS-A (or anti-Ro) and SS-B (or anti-La)] and
cytokines (e.g., B-cell activating factor, tumor necrosis
factor) with multiple potential triggers.22
Clinically, patients with SS most often present with a
complaint of dry eyes (keratoconjunctivitis sicca) and dry
mouth; however, extraglandular manifestations may also
occur. Transient or chronic bilateral enlargement of the
parotid or submandibular glands is seen in 20%–30% of
patients in combination with hyposalivation and symptoms
of fatigue and arthralgias.24 Other extraglandular manifesta-

Table 1. Causes of complaints of xerostomia

Nonsalivary
Dehydration
Cognitive alteration
Neurological dysfunction
Oral sensory dysfunction
Psychological
Mouth breathing

Salivary (hyposalivation and/or altered salivary composition)

Disease
Sjögren’s syndrome
Autoimmune disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis, scleroderma, primary biliary cirrhosis)
Diabetes mellitus
Human immunodeficiency virus
Sarcoidosis
Herpes virus family (e.g., cytomegalovirus, Epstein-Barr virus)
Hepatitis C
End-stage renal disease
Treatment side effects
Medications
Tricyclic antidepressants
Antihypertensive medications (e.g., diuretics, α-adrenergic agonist antagonists)
Antispasmodic drugs
Other
Radiation therapy
External beam radiation therapy (head and neck, mantle, whole body)
Radioiodine therapy (131I)
Salivary gland trauma
Salivary gland tumor
Nutritional deficiencies, and/or eating disorders (anorexia/bulimia)
78
tions include vasculitis, thyroid insufficiency, interstitial
pneumonia, and renal tubular acidosis.13 Diagnosis and
careful continuing follow-up of SS are essential, in particu-
lar because the risk of developing non-Hodgkin lymphoma
in primary SS patients is over 18 times that in the general
population.25,26
Secondary SS is seen in 25%–35% of rheumatoid arth-
ritis patients.27,28 Systemic lupus erythematosus has been
associated with a decreased unstimulated whole saliva flow
rate, a 75% incidence of oral complaints (e.g., xerostomia,
pain), and secondary SS in one-third of patients.29–31 Primary
biliary cirrhosis is associated with xerostomia, as 70% of
patients have a coexisting autoimmune disease such as SS
and 90% exhibit focal sialadenitis.22,32 Fifteen percent of
patients with scleroderma show lymphocytic infiltrates, but
there is no evidence of increased xerostomia or hyposaliva-
tion.33 Sarcoidosis patients can present with signs and symp-
toms highly suggestive of primary SS; therefore, they should
be differentiated by a salivary gland biopsy, which will show
granulomatous inflammation rather than the lymphocytic
infiltration found in SS. Although it has been reported that
hepatitis C virus (HCV)-infected individuals have mild sial-
adenitis, clinical evidence of hyposalivation, xerostomia, or
dry eyes is often absent.34 There is conflicting evidence
about links between HCV and SS, and even though pres-
ence of HCV is an exclusion criterion in the American–
European classification of SS, it is not thought to be a cause
of SS. Xerostomia has been reported in people with diabe-
tes mellitus, although no definitive association between this
condition and hyposalivation has been established.35
Radiation therapy (RT) combined with surgery is the
main therapy for head and neck cancers. Depending on
the site and extension of primary tumors and the path of
lymphatic spread, all or part of the major and minor sali-
vary glands are included within the radiation fields. Stan-
dard radiotherapy for advanced head and neck carcinomas
consists of fractionated doses of approximately 10 Gy per
week over 5–7 weeks. Salivary gland exposure to radiation
results in severe hypofunction and changes in saliva com-
position. Glandular damage includes inflammatory cell and
lymphocytic infiltration, degeneration, necrosis, atrophy,
fibrosis and duct dilatation, with damage primarily to
serous acinar cells.1 The severity of salivary gland damage
is dependent on the volume of glandular tissue in the radia-
tion field and the radiation dose. Profound salivary hypo-
function is believed to occur when greater than 50% of
the parotid gland volume is irradiated.36 Reversible
decreases in the salivary flow rate have been seen with
doses as low as 2.25 Gy and as high as 20 Gy.37,38 A thresh-
old effect between reversible and irreversible salivary gland
damage has been suggested at a dose of 26 Gy.39 Parotid
glands receiving doses in excess of 60 Gy sustain perma-
nent damage.40 An 80% reduction in both parotid and
submandibular/sublingual flow rates occurs after the first
2 weeks of RT, and deterioration toward undetectable
levels is seen at 6–8 weeks.41 Improvements in xerostomic
symptoms can occur a few months after therapy, despite
a continuing decline in salivation, suggesting adaptation.42
However, xerostomia and salivary gland hypofunction
persist for the remainder of the patient’s lifetime. Xero-
stomia and hyposalivation may also occur after lower dose
partial and whole-body irradiation for hematologic
malignancies.43
Older individuals experience xerostomia for a number of
reasons, including the ones stated above. Salivary glands
are known to undergo significant histological changes with
age, with secretory (acinar) components being replaced by
fibrous and adipose tissue.44 This phenomenon is most
evident in the submandibular glands, and less so in the
minor and parotid glands, resulting in an overall decreased
weight of the glands. However, it has been shown that clini-
cally significant decreases in major salivary gland flow do
not occur in healthy older people,45 although age-related
changes in salivary electrolytes have been found, including
decreased Na+ and increased K+ concentrations.46 Further,
studies have shown increases with age in IgA, proline-rich
proteins (which are involved in tooth remineralization), and
the antimicrobial proteins lactoferrin and lysozyme.47,48 It
has been shown that, in the absence of major medical prob-
lems and medication use, such constituents remain stable in
the aged.49 Therefore, one cannot simply attribute changes
in salivary quantity and quality to aging; rather, it is more
likely that such changes are due to the additive effects of
medications and systemic disorders.
Diagnosis
A systematic approach should be used to distinguish patients
with symptoms of xerostomia versus those with measurable
salivary gland hypofunction (Table 2). The chief complaint
should be noted and explored in detail. Certain complaints
are highly predictive of impaired salivary flow rates, whereas
others do not correlate with hyposalivation. Specifically,
positive responses to any of the following complaints are
associated significantly with hyposalivation: oral dryness
when eating; need to sip liquids to swallow dry foods; diffi-
culty swallowing (deglutition); and the perception of too
little saliva.5 Complaints that may or may not accompany
decreased salivary flow include a feeling of dryness upon
awakening and at night; use of chewing gum, candies, or
mints to stimulate salivary flow; and keeping a glass of water
at the bedside. All these are common complaints but do not
reliably predict salivary gland hypofunction.5 Other symp-
toms are speech and eating difficulties, which may compro-
mise nutritional status and cause problems in the patient’s
social life. Patients may have taste disturbances due to the
need for saliva to stimulate gustatory receptors and deliver
tastants to the buds.50 Other complaints include halitosis,
stomatodynia (burning mouth and tongue), and intolerance
of acidic or spicy foods.51 Denture wearers may have more
sore spots, and difficulty in retention of prostheses.
Next, a thorough and complete medical history to iden-
tify conditions, treatments, and medications that may cause
xerostomia or hyposalivation should be obtained. This
should be followed by a physical examination of oral hard
and soft tissues to identify signs of hyposalivation, which
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Table 2. Evaluation of salivary function

History
Focus on:
Systemic or local diseases
Trauma
Medication list
Symptom questions
Predictive of hyposalivation (Fox et al., 1987)5
“Do you sip liquids to aid in swallowing dry foods?”
“Does your mouth feel dry when eating a meal?”
“Do you have difficulties swallowing any foods?”
“Does the amount of saliva in your mouth seem to be too little, too much, or you don’t
notice it?”
Physical examination
Extraoral examination
Major salivary glands
Lymph nodes
Intraoral examination
Soft tissues
Periodontium
Dentition
Measurement of salivary output
Unstimulated whole saliva flow
Stimulated whole saliva flow
Ductal flow of major salivary glands (e.g., parotid, submandibular/sublingual)
Sialochemical analyses
Serum laboratory studies
Complete blood count with differential
Autoimmune markers (e.g., antinuclear antibody, anti-SS-A, anti-SS-B, rheumatoid factor)
Serum immunoglobulins
Erythrocyte sedimentation rate
Salivary imaging
Sialography
Scintigraphy (99mTc)
Ultrasonography
Magnetic resonance imaging
Plain film
Computed tomography
Salivary biopsy
Labial minor salivary gland
Fine-needle aspiration
Major salivary gland

may include dried and chapped lips, glossy or desiccated
oral mucosa; fissured, red, or depapillated tongue; and lack
of salivary pooling in the floor of mouth. The quantity and
quality of saliva should be examined, with a more viscous
consistency indicative of salivary gland hypofunction. The
examiner should try to express saliva from the four major
salivary gland ducts: the two parotid (Stensen’s) ducts in the
buccal mucosa adjacent to the upper first molars, and the
two submandibular (Wharton’s) ducts on the floor of mouth.
The presence of a cloudy or purulent discharge from the
ducts may indicate an infection within the major salivary
glands.
Oral candidiasis of all varieties (e.g., pseudomembrane-
ous, erythematous, median rhomboid glossitis, and angular
cheilitis) may be seen in patients with hyposalivation. It is
usually diagnosed on the basis of clinical findings; however,
it can be confirmed microbiologically with a direct smear.
Dental caries are also frequently found in these patients,
especially in older adults, those with more dental restora-
tions, and those with gingival recession that exposes more
caries-prone root surfaces.
Enlarged salivary glands, unilateral or bilateral, may be
seen in patients with hyposalivation. Lack of salivary flow
may lead to bacterial or viral infection, although individuals
with SS may experience swelling and sialadeniti without
infection.
Measurement of salivary output is imperative to differ-
entiate between salivary and nonsalivary causes of xerosto-
mia. A number of methods for measurement of unstimulated
whole saliva (UWS) and stimulated whole saliva (SWS)
flow rates have been described that require no specialized
equipment, are controlled and reproducible, and can be
performed in any office setting.52 Individualized collectors
can be used to get specialized measurements of salivary flow
from the major salivary glands. Salivary flow rates are useful
for diagnosing autoimmune exocrinopathies; specifically,
they are an objective criterion in the American–European
Classification Criteria for diagnosis of SS.53 A UWS below
80
0.12–0.16 ml/min and a SWS flow rate below 0.5 ml/min,
obtained using a standardized technique, are considered
indicative of hyposalivation.52,54 Salivary function can also
be measured by scintigraphy. 99mTechnetium pertechnetate
(Tc) is a gamma ray-emitting radionuclide that is taken up
by salivary glands after intravenous injection and then
secreted. Measurement of uptake and secretion into the
oral cavity can determine the presence and extent of func-
tional acinar tissue. Major gland function can be graded by
applying a scoring system to the scans.55
A number of other imaging techniques can aid in iden-
tifying salivary gland abnormalities. Magnetic resonance
imaging, with its ability to visualize water-containing struc-
tures, can identify solid and cystic masses in the glands and
lymph nodes. Plain films may also be useful in identifying
salivary tumors. Sialography is a useful technique to visual-
ize the anatomy of ducts, acinar integrity, calcifications, and
some tumors.56 The gland anatomy is well delineated by
retrograde instillation of a radio-opaque fluid through a
major salivary gland duct orifice. Ultrasonography is an
effective and noninvasive means of identifying changes
within the gland parenchyma and periglandular and intra-
and extraductal structures, particularly cysts.57
Salivary gland biopsy provides a definitive diagnosis of
glandular pathology. A labial minor salivary gland biopsy
is more readily and commonly performed than a biopsy of
the major salivary glands. In cases of suspected SS, the pres-
ence of focal, periductal lymphocytic infiltration beyond a
graded threshold is the best criterion for definitive diagnosis
of the salivary component.58 Fine-needle aspiration of
enlarged major salivary glands followed by immunocyto-
chemical analyses is useful for differentiating between a
benign polyclonal lymphocytic infiltration and a malignant
monoclonal infiltration as found in lymphoma.
Management
After establishing a diagnosis, a step-wise management
approach should be implemented. This consists of alleviat-
ing symptoms, instituting preventive measures, treating oral
conditions, improving salivary function (if possible), and
managing any underlying systemic conditions (Table 3). A
multidisciplinary approach among health-care providers is
required.
There are many palliative measures available to alleviate
symptoms. Salivary substitutes and lubricants with moisten-
ing properties are designed to provide prolonged mucosal
wetting.59 Products include “artificial” salivas, rinses, gels,
and sprays, which may contain carboxymethylcellulose
(CMC), a mucopolysaccharide, glycerate polymer gel base,
or natural mucins, singly or in combination. Toothpastes
are available that contain a synthetic detergent (sodium
lauryl sulfate) and an osmoprotectant (glycine betaine
BET). In clinical studies of post-RT patients, these products
have collectively exhibited a mild effect on the subjective
complaint of xerostomia but no effect on objective mea-
surements of hyposalivation. Patients express a mild prefer-
ence for CMC-based products over mucins.11 Attempts
should be made in all patients to stimulate the remaining
salivary function by using topical or systemic approaches.
Sugar-free candies and chewing gums that contain xylitol
are intended to stimulate salivary flow and can provide
transient relief of xerostomia. Such products have been
shown to have more positive effects than lubricants in post-
RT and hemodialysis patients.11,22 There is not sufficient
clinical evidence to support the definitive recommendation
of any single palliative product; therefore, it is best for the
patient to try several agents and select the one that gives
greatest relief. Use of a humidifier, particularly at the
bedside during sleep, can alleviate symptoms of xerostomia
and dry eyes and nasal passages. Patients can also make
adjustments in their diet to avoid dry or acidic foods, to
accompany dry foods with frequent sips of water, and to
avoid caffeine-containing or alcoholic beverages that cause
dehydration and increase oral dryness symptoms.
Preventive care should be addressed next. Extra mea-
sures should be instituted to prevent oral complications
from low salivary output. This starts with frequent dental
and oral evaluations, with examinations every 4–6 months
and radiographs performed annually. To prevent dental
caries, meticulous oral hygiene, a low-sugar diet, and regular
use of topical fluoride are recommended. Daily use of
neutral pH sodium fluoride is the most effective means
of preventing rampant hyposalivation-induced caries.11
Fluorides and remineralizing solutions are available as var-
nishes, dentifrices, gels, and rinses, which can be used with
or without applicator trays. The specific preventive fluoride
regimen should be determined by the dentist and patient by
considering the extent of salivary gland hypofunction and
the caries rate.
Oral candidiasis is a common oral complication in xero-
stomia and salivary gland hypofunction patients. A number
of topical antifungal agents, in the form of rinses, ointments,
pastilles, and troches, are effective therapeutics. Systemic
antifungal therapy should be reserved for cases refractory
to topical therapy, and for immunocompromised patients.
Denture users should prevent fungal colonization through
daily immersion of prostheses in benzoic acid, chlorhexi-
dine 0.12% solution, or 1% sodium hypochlorite. Angular
cheilitis can be treated with topical antifungal and anti-
inflammatory agents.
For xerostomic patients, or hyposalivation patients with
an appreciable difference between UWS and SWS flow
rates, systemic secretogogues may be of benefit. Even in
patients with minimal salivary function, stimulation of
secretion may be of benefit, both for relieving dryness
symptoms and providing the protective effects of natural
saliva. Parasympathomimetics that are agonists for musca-
rinic receptors can stimulate salivary flow. Two parasympa-
thomimetic drugs, pilocarpine and cevimeline, are approved
by the U.S. Food and Drug Administration for treatment
of xerostomia; pilocarpine is approved for SS- and RT-
induced xerostomia, and cevimeline for SS. Pilocarpine is a
nonselective muscarinic agonist, whereas cevimeline has
specific affinity for receptor subtypes not present in cardiac
and respiratory tissue. There is sufficient evidence from
 81

Table 3. Treatment of xerostomia, hyposalivation, and related oral complications

Management of symptoms
Diet and habit modifications
Frequent and regular sips of water
Avoidance of dry, hard, sticky, acidic foods
Avoidance of excess caffeine and alcohol
Salivary substitutes and lubricants
Artificial saliva
Rinses
Gels
Sprays
Toothpastes
Use of bedside humidifier during sleeping hours
Preventive measures
Increased frequency of oral/dental evaluation
Topical fluoride application
Varnish (0.5% NaF)
Daily use of fluoridated dentifrice
Topical: over-the-counter (0.05% NaF); prescription (1.0% NaF, 0.4% SnF)
Treatment of oral conditions
Dental caries
Restorative therapy, topical fluoride
Oral candidiasis
Chlorhexidine (CHX) 0.12%: rinse, swish, and spit 10 ml twice daily
Nystatin/triamcinolone ointment for angular cheilitis: apply topically 4 times daily
Clotrimazole troches: 10 mg dissolved orally 4–5 times daily for 10 days
Systemic therapy for immunocompromised patients
Denture antifungal treatment: soaking of denture for 30 min daily in CHX or 1% sodium
hypochlorite
Bacterial infections
Systemic antibiotics for 7–10 days
Ill or poor fitting prostheses
Denture adjustment
Hard and soft reline
Use of denture adhesives
Implant-borne prostheses
Increase salivary flow
Sugar-free, xylitol-containing mints, candies, and gum
Sialogogues
Pilocarpine: 5–10 mg orally 3 times daily
Cevimeline: 30 mg orally 3 times daily
Acupuncture
Manage underlying systemic conditions
Multidisciplinary management with other health-care providers

randomized controlled clinical trials that oral forms of pilo-
carpine and cevimeline both increase saliva flow rates and
alleviate symptoms.22 Pilocarpine in the form of a mouth-
wash, used orally for 1 min, was shown in one randomized
controlled trial with healthy patients to increase salivary
flow and affect subjective dryness as well.60 However, other
topical forms of pilocarpine (e.g., spray, pastilles) did not
have the same beneficial outcome in post-RT patients.61,62
Both drugs have side effects, including excessive sweating,
rhinitis, increased pancreatic secretion, and urinary and gas-
trointestinal disturbances. Less common and more serious
adverse side effects of pilocarpine and cevimeline involve
the cardiovascular and respiratory systems. The use of pilo-
carpine and cevimeline is contraindicated in patients with
gastric ulcer, uncontrolled asthma, or hypertension, or in
patients on β-blockers. Acupuncture has been investigated
for treatment of hyposalivation and xerostomia, but the
results are conflicting.22
The xerostomic side effects of medications may be allevi-
ated or reduced by substituting for the problem medications
similar drugs that have lesser side effects. For instance,
selective serotonin reuptake inhibitors cause less xerosto-
mia than do tricyclic antidepressants.63 Moreover, altera-
tions in the timing or dosing schedule of medications, such
as avoidance of medication doses at nighttime when salivary
flow is normally at its lowest, may minimize xerostomic
effects. Multidisciplinary management of underlying sys-
temic conditions is imperative to reduce oral complications.
For instance, primary care providers should help diabetic
patients maintain good glycemic control. A rheumatologist
may treat a patient with SS with other therapeutics involv-
ing cytokines or immunoregulators (e.g., rituximab or
hydroxychloroquine) or with systemic steroids. Prominent
complaints of xerostomia in patients with end-stage renal
disease have been shown to improve following renal
transplantation.64
82
Summary and conclusions
A systematic approach to the management of the xerosto-
mic patient is imperative to recognize and distinguish
patients with subjective complaints from those who have
evidence of salivary gland hypofunction as well. Establish-
ing a definitive diagnosis (or, at a minimum, recognizing the
extent of hyposalivation) is necessary to determine the
appropriate therapeutic measures to moderate symptoms,
improve objective signs, and prevent oral complications.
Management of these conditions requires a multidisci-
plinary approach, with close follow-up by a dental practi-
tioner familiar with the complexities of salivary gland
dysfunction.
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