D E N T I S T R Y & MEDICINE
Background. Major A D A
Major depressive
disorder
Psychopathology, medical
management and dental
implications
ARTHUR H. FRIEDLANDER, D.D.S.; MICHAEL E.
MAHLER, M.D.
ajor depressive disorder (previously known
M as major depression or unipolar depres-
sion), or MDD, is a psychiatric illness of at
least two weeks’ duration during which
the patient experiences dysphoria (feeling
down or blue, sad, helpless, hopeless, irritable or angry,
agitated or anxious, or any combination
of the preceding), anhedonia (a loss of
Dentists have
interest or pleasure in previously
an opportunity enjoyed activities such as hobbies and
to recognize social or sexual interactions) or both.1 A
patients with sense of worthlessness or guilt, accom-
occult major panied by preoccupation over past minor
depressive failings and thoughts of suicide, is
common.
disorder.
In addition to mood change and anhe-
donia, the patient or a family member
may note alterations in appetite that result in weight
loss or gain of more than 5 percent; insomnia character-
ized by difficulty falling or staying asleep or by early
awakening; an inability to sit still (agitation); slowed
speech and body movements (psychomotor retardation);
extreme fatigue; and an impaired ability to think, con-
centrate or make decisions. Somatic complaints (bodily
aches and pains) without a physiological basis, social
withdrawal and denial of dysphoria also are common
symptoms, especially among older patients.2 The cluster
of depressive symptoms is emotionally painful and inter-
feres with social and occupational functioning.
The onset of the disorder varies, with symptoms
developing over days to weeks. Untreated episodes typi-
cally last six months or longer. Eventually, the episode
Copyright ©1998-2001 American Dental Association. All rights reserved.
ABSTRACT
depressive disorder, or J
✷ ✷
MDD, is a psychiatric ill- 
N
CON
ness in which mood,
IO
thoughts and behavioral
T
T
A
N
I
patterns are impaired for A U I N G E D U C
long periods. The illness R 3
distresses the person and impairs
TICLE
his or her social functioning and quality of
life. MDD is characterized by marked sad-
ness or a loss of interest or pleasure in daily
activities, and is accompanied by weight
change, sleep disturbance, fatigue, difficulty
concentrating, physical impairment and a
high suicide rate. In 2000, the World
Health Organization, or WHO, identified
MDD as the fourth ranked cause of dis-
ability and premature death in the world.
WHO projected that by 2020, MDD would
rise in disease burden to be second only to
ischemic heart disease. The disorder is
common in the United States, with a life-
time prevalence rate of 17 percent and a
recurrence rate of more than 50 percent.
Conclusions. MDD may be associated
with extensive dental disease, and people
may seek dental treatment before becoming
aware of their psychiatric illness. MDD fre-
quently is associated with a disinterest in
performing appropriate oral hygiene tech-
niques, a cariogenic diet, diminished sali-
vary flow, rampant dental caries, advanced
periodontal disease and oral dysesthesias.
Many medications used to treat the disease
magnify the xerostomia and increase the
incidence of dental disease. Appropriate
dental management requires a vigorous
dental education program, the use of saliva
substitutes and anticaries agents containing
fluoride, and special precautions when pre-
scribing or administering analgesics and
local anesthetics.
Clinical Implications. Dentists cog-
nizant of these signs and symptoms have
an opportunity to recognize patients with
occult MDD. After confirmation of the diag-
nosis and institution of treatment by a
mental health practitioner, dentists usually
can provide a full range of services that
may enhance patients’ self-esteem and con-
tribute to the psychotherapeutic aspect of
management.
JADA, Vol. 132, May 2001 629
D E N T I S T R Y & MEDICINE
ends with a complete remission of symptoms in
about 70 percent of patients. The remaining
patients, however, have persistent symptoms and
impairment in function with high use of health
care resources, need for public assistance (such as
subsidized housing), limited ability to perform job
responsibilities, absenteeism at work, social with-
drawal and household strain.3-6 The risk of recur-
rence of MDD for people with or without residual
symptoms is 50 percent after one episode, 70 per-
cent after a second episode and 90 percent after a
third. Risk factors for recurrent episodes include
female sex, never marrying, an initial onset of
depression after age 60 years, long duration of
individual episodes, substance abuse and family
discord.7
EPIDEMIOLOGY OF MAJOR DEPRESSIVE
DISORDER
MDD is common in the United States and is cur-
rently ranked by the World Health Organization
as the fourth most common cause of disability and
premature death in the world.8 The lifetime risk
of developing MDD in the United States ranges
from 10 to 25 percent for women and 5 to 12 per-
cent for men. At any one time, the prevalence rate
is 5 to 9 percent for women and 2 to 3 percent for
men.9 Despite numerous investigations, no defini-
tive explanation exists for the sex differences in
prevalence rates. The median age at onset of ill-
ness is 26 years.10
People at highest risk of experiencing a first
episode of depression are those with a family his-
tory of the disease. Studies of monozygotic and
dizygotic twins have demonstrated that the
propensity to develop MDD is 40 percent genetic
and 60 percent environmental.11,12
People with chronic diseases are at high risk of
developing MDD, with some investigators noting
that the prevalence may be as high as 40 percent
for patients with coronary artery disease and 25
percent for patients with cancer.13,14 Likewise, an
increasing prevalence of the disease exists among
the elderly, such that MDD is the most common
emotional disorder in patients older than 65
years.15 Neurological disorders such as multiple
sclerosis, Parkinson’s disease, stroke and head
trauma also are associated with a higher fre-
quency of depression.16,17 These medically compro-
mised and older people are at almost twice the
risk of dying from all causes compared with simi-
larly aged medically compromised people without
the mental disorder.18 MDD also is associated
630 JADA, Vol. 132, May 2001
Copyright ©1998-2001 American Dental Association. All rights reserved.
with substance abuse. Approximately one-third of
people with MDD develop a substance abuse dis-
order (that is, alcohol, illicit drugs) within their
lifetime.19
Suicide is the most serious outcome of MDD,
with 7 percent of men and 1 percent of women
committing suicide.10,20 In 1990 in the United
States, the estimated cost of treating depression
and the associated cost of premature death from
all causes and impaired workplace productivity
was $53 billion.21
PATHOPHYSIOLOGY
The etiology of MDD remains ill-defined. Some
believe that an emotional stressor identified by
the patient (for example, death of a loved one)
or, occasionally, a stressor not identifiable by
the patient or clinician adversely affects the
brain’s limbic system (which regulates mood
and emotions) and the hypothalamus (which
regulates sleep, appetite and libido).22,23 This
results in a paucity of the neurotransmitters
norepinephrine and serotonin at the synapses
between presynaptic neurons (axon) and post-
synaptic neurons (dendrite), thus hindering the
transmission of impulses in these specific
neural pathways.
Emotional stress also adversely affects the
endocrine system because the hypothalamus
interacts with the pituitary gland via the rich
neuronal connections between these two struc-
tures, which leads to the secretion of hormone-
releasing factors. This hyperactivity of the
hypothalamic-pituitary-adrenocortical, or HPA,
axis alters levels of numerous endocrine gland
hormones, most notably causing a rise in circula-
tory cortisol levels.24 Neuroimaging studies sup-
port this model by demonstrating abnormalities
in blood flow and glucose metabolism in limbic
system structures and the amygdala (areas of the
brain known to be involved with processing emo-
tions) in correlation with the severity of depres-
sion and increased cortisol levels.25 These abnor-
malities in blood flow and glucose metabolism
recede in most patients after they respond to
antidepressant medication.26
MEDICAL MANAGEMENT
In the United States, treatment for mild or mod-
erately severe episodes of MDD usually consists
of administering antidepressant medications.
Brief psychotherapy (15 to 20 sessions) has been
shown to be equally effective for these patients,
 D E N T I S T R Y & MEDICINE

but it is not used often in

primary care settings CLASSIFICATION OF COMMONLY PRESCRIBED
because of unfamiliarity ANTIDEPRESSANTS.
with the techniques, as
SELECTIVE SEROTONIN REUPTAKE INHIBITORS
well as financial and time
constraints. 27,28
Similar dCitalopram (Celexa, Forest Pharmaceuticals)

constraints often relegate dFluoxetine (Prozac, Eli Lilly)

patients with severe dFluvoxamine (Luvox, Solvay Pharmaceuticals)
episodes of the disorder to
receive pharmacological dParoxetine (Paxil, SmithKline Beecham)

treatment only, even dSertraline (Zoloft, Pfizer)

though a combination of
medication and psycho-
therapy results in greater
29
improvement. Electrocon-
vulsive therapy, or ECT, is
indicated for patients who
cannot tolerate medication
ATYPICAL ANTIDEPRESSANTS
dBupropion (Wellbutrin, GlaxoSmithKline)
dMaprotiline (Ludiomil, Ciba Pharmaceuticals)
dMirtazepine (Remeron, Organon)
dNefazodone (Serzone, Bristol-Meyers Squibb)

and for those at risk of dTrazodone (Desyrel, Apothecon, a Bristol-Myers Squibb company)
dying imminently because dVenlafaxine (Effexor, Wyeth-Ayerst Pharmaceuticals)
of a refusal to eat or severe
suicidal impulses. TRICYCLIC ANTIDEPRESSANTS

Clinicians choose a med- dAmitriptyline (Elavil, AstraZeneca)

ication based on the pa- dClomipramine (Anafranil, Geneva Pharmaceuticals)
tient’s symptoms and the
side-effects profile of a spe- dDesipramine (Norpramin, Aventis Pharmaceuticals)

cific drug. If the patient is dDoxepin (Sinequan, Pfizer/Adapin, Lotus Pharmaceuticals)

lethargic, an activating dImipramine (Tofranil, Novartis Pharmaceuticals)
medication will be pre-
scribed; if the patient is dNortriptyline (Pamelor, Novartis Pharmaceuticals)

anxious, a drug with more dProtriptyline (Vivactil, Merck)

sedating qualities will be dTrimipramine (Surmontil, Wyeth-Ayerst Pharmaceuticals)
chosen. Medications with
excessive anticholinergic MONOAMINE OXIDASE INHIBITORS

activity (many of the tri- dPhenelzine (Nardil, Parke-Davis)

cyclic antidepressants, or dTranylcypromine (Parnate, SmithKline Beecham)
TCAs) are contraindicated
in elderly patients because
they produce confusion, exacerbate glaucoma and
cause urinary retention. Many antidepressant
medications cause sexual dysfunction, and people
who are sexually active usually prefer to avoid
these drugs. Antidepressant medications are
effective for approximately 75 percent of patients,
but they take two to four weeks to work success-
fully.30 Because of the high rate of relapse, con-
tinued use of the medication is recommended for
six months to one year beyond the initial
recovery.31
The box (“Classification of Commonly Pre-
scribed Antidepressants”) shows the major cate-
gories of antidepressants, which are based on
their mechanisms of action.
Selective serotonin reuptake inhibitors.
The selective serotonin reuptake inhibitors, or
SSRIs (for example, fluoxetine [Prozac, Eli Lilly],
paroxetine [Paxil, SmithKline Beecham]) exert
their antidepressant effect by preventing presyn-
aptic neurons from reabsorbing (reuptake) sero-
tonin from the synaptic cleft (the space between
two neurons) for recycling. Thus, the concentra-
tion of serotonin in the cleft is heightened and
neuronal activity is enhanced. SSRIs are the
first-line treatment for patients with mild-to-
moderate depression. Overdoses of these medica-
tions are not lethal, and patients are less likely
to discontinue treatment because of adverse drug
reactions.32 Although free of annoying anticholin-

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Copyright ©1998-2001 American Dental Association. All rights reserved.
D E N T I S T R Y & MEDICINE

ergic and cardiovascular side effects, they do, medications also slow intraventricular conduc-
however, frequently cause diarrhea, nausea, tion, prolonging the QRS, PR and QT intervals
dizziness, insomnia, anxiety or agitation, tremor, on an electrocardiogram. This can cause com-
headache, sexual dysfunction (that is, decreased plete heart block or ventricular dysrhythmias.
libido, ejaculatory and erectile dysfunction, anor- Many older patients with preexisting medical
gasmia) and, on occasion, an increase in bleeding problems cannot tolerate the adverse side
time.33,34 SSRIs also are effective for symptoms of effects associated with TCAs.37
rumination and obsessive-compulsive types of Monoamine oxidase inhibitors. The
behavior. monoamine oxidase inhibitors, or MAOIs (for
Atypical antidepressants. The atypical example, phenelzine [Nardil, Parke-Davis],
antidepressants, or AAs (for example, bupropion tranylcypromine [Parnate, SmithKline Beecham])
[Wellbutrin, GlaxoSmithKline], venlafaxine exert their antidepressant effect by nonselective
[Effexor, Wyeth-Ayerst Pharmaceuticals]), exert inhibition of MAO A and MAO B so that they
their effects through varied mechanisms, cannot metabolize norepinephrine and serotonin
including selective norepinephrine in the synaptic cleft. Thus, the con-
reuptake inhibition, dopamine centrations of norepinephrine and
reuptake inhibition and antagonist, Atypical serotonin are elevated and neuronal
and reversible inhibition of antidepressants are activity is enhanced. The MAOIs are
monoamine oxidase A. These medi- as effective as the used initially to treat patients with
cations are as effective as the selective serotonin moderate-to-severe depression, as
SSRIs and, like the SSRIs, are well as patients whose depression
reuptake inhibitors
first-line treatments for patients has been refractory to a course of an
with mild-to-moderate depression, and are first-line SSRI, AA or TCA.
are not lethal in overdoses and treatments for Major side effects associated
have a similar side-effect profile.35 patients with mild-to- with the use of MAOIs are dizzi-
Of specific concern to dentists, moderate depression. ness, orthostatic hypotension,
maprotiline occasionally is associ- insomnia, central nervous system
ated with orthostatic hypotension, stimulation, weight gain and
electrocardiographic changes, tachycardia and edema. MAOIs prevent the liver from inacti-
agranulocytosis, and mirtazepine has been asso- vating tyramine found in aged meats, red wine,
ciated with infrequent reports of agranulocy- beer and some cheeses, causing norepinephrine
tosis and neutropenia.36 blood levels to rise and, on occasion, bringing
TCAs. The TCAs (for example, amitriptyline about a fatal hypertensive crisis (consequently,
[Elavil, AstraZeneca], imipramine [Tofranil, patients receiving treatment with an MAOI
Novartis Pharmaceuticals]) exert their effect by should avoid these foods). Severe hypertension
preventing presynaptic neurons from reabsorbing also may ensue when a patient concurrently
norepinephrine and serotonin from the synaptic takes an MAOI and a sympathomimetic medica-
cleft for recycling. Thus, the concentration of tion such as ephedrine, which is found in some
these two neurotransmitters is elevated and neu- decongestants, allergy medications and appetite
ronal activity is increased. These agents are used suppressants.38
to treat patients with severe disease, as mani- Cognitive-behavioral therapy. Cognitive-
fested by a depression that is worse in the behavioral therapy or interpersonal psycho-
morning, anhedonia, significant weight loss and therapy is indicated for patients with mild-to-
psychomotor retardation, as well as for patients moderate depression who refuse to take
whose depression has been refractory to SSRIs. medication or are unable to tolerate the side
Some TCAs are lethal in overdoses and approxi- effects of medication.39 These therapies also are
mately 40 percent of patients become noncom- frequently used in combination with medication
pliant because of unpleasant side effects. to maximize the effectiveness of treatment and
TCAs cause peripheral anticholinergic side decrease the likelihood of relapse.40 Cognitive-
effects such as xerostomia, urinary retention, behavioral therapy helps patients recognize and
constipation and blurred vision, as well as cen- challenge the recurrent negative thoughts and
tral anticholinergic side effects such as dysfunctional attitudes that may lead to depres-
impaired concentration and confusion. These sion or that maintain an episode of depression if

632 JADA, Vol. 132, May 2001

Copyright ©1998-2001 American Dental Association. All rights reserved.
 D E N T I S T R Y & MEDICINE

TABLE 1

ADVERSE OROFACIAL REACTIONS TO SELECTIVE SEROTONIN

REUPTAKE INHIBITORS.
MEDICATION ADVERSE OROFACIAL REACTIONS*

Xero- Sialadenitis Dysgeusia Sto- Gingi- Glossitis Tongue Discolored Brux- Miscellaneous
stomia matitis vitis Edema Tongue ism

Citalopram + 0 + + + + 0 0 + 0
(Celexa,
Forest
Pharmaceuti-
cals)

Fluoxetine + + + + + + 0 + + Jaw pain,

(Prozac, Eli buccal
Lilly) glossal
syndrome

Fluvoxamine + 0 + + + + 0 0 0 Toothache
(Luvox,
Solvay
Pharmaceuti-
cals)

Paroxetine + + + + + + + + + Caries,
(Paxil, dysphagia
SmithKline
Beecham)

Sertraline + 0 + + 0 + + 0 + Dysphagia,
(Zoloft, gingival
Pfizer) hyperplasia

* Plus sign indicates “yes”; zero, “no.”

dwelled on. Interpersonal psychotherapy focuses
on interpersonal role disputes (often marital dis-
putes) and social functioning. It can help patients
explore issues in their past (such as bereavement)
that may have made them more vulnerable to
depression.
ECT. This therapy is indicated for patients
with especially severe depression marked by
unresponsiveness to medication or an inability to
tolerate the side effects of routine psychopharma-
cological agents, refusal to eat or multiple
attempts at suicide. For these reasons, physicians
often select ECT as a first-line treatment for
elderly patients with severe MDD.41 The electrical
currents used in ECT create massive neuronal
electrical discharges in the central nervous
system similar to a seizure or convulsion. Re-
searchers have postulated that after a number of
treatments, neuronal membranes become more
responsive to serotonin, thereby enhancing neu-
ronal activity.42 ECT usually is administered two
to three times a week for several weeks until the
patient’s condition improves. Approximately
90 percent of patients enter a remission within
one to two weeks after treatment begins.
Full oxygenation and the use of muscle relax-
ants to control convulsions have rendered medi-
cal complications of ECT rare. However, the
procedure is associated with a brief headache
and possibly retrograde memory loss (that is,
inability to recall events that occurred just
before the treatment). ECT does not perma-
nently impair memory, intelligence, reasoning,
abstract thinking or visuomotor or perceptual
skills.43 Most psychiatrists recommend a dental
examination for their geriatric patients before
ECT to determine if the anesthetist needs to
adjust the procedure because of dentures or
problematic teeth (that is, those that might be
fractured or swallowed during the procedure).44
Positioning the electrodes farther away from the
masseter muscles is associated with decreased
dental injuries.45
DENTAL FINDINGS
The official U.S. Food and Drug Administration
medication package insert accompanying each of
the antidepressant medications is reprinted in
the Physicians’ Desk Reference46 and identifies
adverse orofacial reactions that may occur. The
majority of SSRIs and AAs have been shown to
cause xerostomia (affecting approximately 18

JADA, Vol. 132, May 2001 633

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D E N T I S T R Y & MEDICINE

TABLE 2

ADVERSE OROFACIAL REACTIONS TO ATYPICAL ANTIDEPRESSANTS.

MEDICATION ADVERSE OROFACIAL REACTIONS*

Xero- Sialadenitis Dysgeusia Sto- Gingi- Glossitis Tongue Discolored Brux- Miscellaneous
stomia matitis vitis Edema Tongue ism

Bupropion + 0 + + 0 + 0 0 + Toothache,
(Wellbutrin, oral edema,
GlaxoSmith- dysphagia
Kline)

Maprotiline + + + + 0 0 0 + 0 Dysphagia
(Ludiomil,
Ciba Pharma-
ceuticals)

Mirtazepine + + + + + + + + 0 Facial
(Remeron, edema
Organon)

Nefazodone + 0 + + + + 0 0 0 Monoliasis,
(Serzone, dysphagia,
Bristol- periodontal
Meyers abscesses,
Squibb) oral ulcers

Trazodone + 0 + 0 0 0 0 0 0 Sinusitis
(Desyrel,
Apothecon)

Venlafaxine + 0 + + + + + + + Monoliasis,
(Effexor, dysphagia,
Wyeth-Ayerst halitosis,
Pharma- oral ulcers
ceuticals)

* Plus sign indicates “yes”; zero, “no.”

percent of patients), dysgeusia (altered taste sen-
sations), stomatitis and glossitis. A few drugs in
these two categories of medications also have
been identified as causing sialadenitis, gingivitis,
and edema and discoloration of the tongue
(Tables 1 and 2). The use of TCAs is associated
with xerostomia (affecting almost 50 percent of
patients) and occasionally with sialadenitis, dys-
geusia, stomatitis and edema of the tongue
(Table 3). The MAOIs also occasionally cause
xerostomia, but less often than do the TCAs
(Table 4).
Patients who report many signs associated
with depression are prone to suffer periodon-
titis.47-50 Researchers have hypothesized that
neglect of oral hygiene, increased smoking and
altered immune responses facilitate increased col-
onization by pathogenic bacteria. This leads to a
breakdown of the periodontal attachment.51,52
Patients receiving SSRIs or AAs may develop a
movement disorder that includes clenching,
grinding of the teeth (bruxism) or both, further
worsening the periodontal condition.53-55 This may
occur because these medications increase
extrapyramidal levels of serotonin, thereby
inhibiting dopaminergic pathways that control
movements.56
Patients with MDD are at high risk of devel-
oping rampant dental decay because of a disin-
terest in performing oral hygiene practices, a
preference for carbohydrates resulting from
reduced serotonin levels, a craving for intense
sweets because of impaired taste perception, a
decrement in whole-mouth and parotid gland sali-
vary output and a high lactobacillus count.57-60 The
SSRIs, AAs and TCAs magnify the problem of
xerostomia by blocking parasympathetic stimula-
tion of the salivary glands. Long-term use of
TCAs is specifically associated with carbohydrate
craving and the potential for increased develop-
ment of dental caries.61
Chronic facial pain, burning sensation of the
oral mucosa (often on the tongue) or a temporo-
mandibular joint disorder is frequently the
somatic complaint that brings the depressed
patient to the dentist. Some researchers have
hypothesized that the pain may arise from stress-
induced disruption of the HPA axis, a mechanism

634 JADA, Vol. 132, May 2001

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 D E N T I S T R Y & MEDICINE

TABLE 3

ADVERSE OROFACIAL REACTIONS TO TRICYCLIC ANTIDEPRESSANTS.

MEDICATION ADVERSE OROFACIAL REACTIONS*

Xero- Sialadenitis Dysgeusia Sto- Gingi- Glossitis Tongue Discolored Brux- Miscellaneous
stomia matitis vitis Edema Tongue ism

Amitriptyline + + + + 0 0 + + 0 0
(Elavil,
AstraZeneca)

Clomipramine + + + + + + 0 0 0 Caries,
(Anafranil, cheilitis,
Geneva Phar- dysphagia,
maceuticals) oral ulcers,
halitosis,
sinusitis

Desipramine + + + 0 0 0 + + 0 Facial
(Norpramin, edema
Aventis Phar-
maceuticals)

Doxepine + 0 + + 0 0 0 0 0 0
(Sinequan,
Pfizer/Adapin,
Lotus Phar-
maceuticals)

Imipramine + + + + 0 0 + + 0 Facial
(Tofranil, edema
Novartis
Pharma-
ceuticals)

Nortriptyline + + + + 0 0 + + 0 Facial
(Pamelor, edema
Novartis
Pharma-
ceuticals)

Protriptyline + + + 0 0 0 + + 0 Facial
(Vivactil, edema
Merck)

Trimipramine + + + + 0 0 + + 0 Facial
(Surmontil, edema
Wyeth-Ayerst
Pharma-
ceuticals)

* Plus sign indicates “yes”; zero, “no.”

previously implicated as the cause of both depres-
sion and inflammatory joint disease.62-69
DENTAL TREATMENT OF PATIENTS WITH
DEPRESSION
Some patients who receive psychiatric treatment
for depression may be reluctant to admit it
because of the perceived stigma associated with
mental illness. To overcome such barriers and
obtain necessary information, the dentist should
exhibit a supportive, nonjudgmental attitude and
advise patients that such information will be held
confidential and is indispensable to the provision
of safe dental care.
Depressed patients may be uncooperative and
irritable during dental treatment, appear unap-
preciative and have numerous complaints that
are inconsistent with objective findings.70 Before a
patient begins dental treatment, the dentist
should consult with his or her psychiatrist (after
informing the patient). Information requested
should include the patient’s current psychological
status and current psychotropic medication regi-
men. The dentist also must ask the psychiatrist
about the patient’s history of alcohol or other sub-
stance abuse. Patients with a history of alcohol
abuse should undergo liver function tests (that is,
blood serum levels of albumin and total proteins),

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D E N T I S T R Y & MEDICINE
TABLE 4
ADVERSE OROFACIAL REACTIONS TO MONOAMINE OXIDASE INHIBITORS.
MEDICATION ADVERSE OROFACIAL REACTIONS
Xero- Sialadenitis Dysgeusia Sto-
stomia matitis
Phenelzine + 0 0 0
(Nardil,
Parke-Davis)
Tranyl- + 0 0 0
cypromine
(Parnate,
SmithKline
Beecham)
* Plus sign indicates “yes”; zero, “no.”
a complete blood cell count and a coagulation pro-
file (that is, prothrombin time and partial throm-
boplastin time).
Education. Preventive dental education is
paramount for these patients and their families.
They should receive instruction in proper tooth-
brushing and flossing methods that maximize
removal of dental plaque. Artificial salivary prod-
ucts are prescribed for many patients with signs
of xerostomia. Dental treatment should consist of
subgingival scaling, root planing and curettage,
caries control and restorative treatment. Pro-
found local anesthesia is mandatory to perform
these procedures adequately in depressed and
often anxious patients.
Adverse interactions. Adverse interactions
between SSRIs and some medications used in
dentistry may occur because these antidepres-
sants inhibit certain metabolic pathways. Specifi-
cally, SSRIs inhibit the cytochrome P-450 isoen-
zymes needed to adequately metabolize codeine,
benzodiazepines, erythromycin and carba-
mazepine. Therefore, these dental therapeutic
agents should be used cautiously and in reduced
dosages.71
Adrenergic vasoconstrictors. Dentists must
take precautions when administering local anes-
thetics containing adrenergic vasoconstrictors
(such as levonordefrin and epinephrine) to
patients receiving TCAs. TCAs block the reuptake
of these vasoconstrictors and block muscarinic
and α1-adrenergic receptors, thereby directly
depressing the heart. Levonordefrin adversely
interacts with TCAs, resulting in dramatic
increases in systolic blood pressure and cardiac
dysrhythmias.72 Epinephrine more modestly inter-
acts with TCAs so that it can be used, but in a
636 JADA, Vol. 132, May 2001
Copyright ©1998-2001 American Dental Association. All rights reserved.
Gingi- Glossitis Tongue Discolored Brux- Miscellaneous
vitis Edema Tongue ism
0 0 0 0 0 0
0 0 0 0 0 0
dosage not to exceed 0.05 milligrams (the equiva-
lent of three cartridges of 1:100,000 epinephrine)
per half-hour and with careful aspiration to avoid
intravascular administration.
Other adverse drug interactions between TCAs
and medications used in dentistry may produce
significant morbid reactions. Sedative-hypnotics,
barbiturates and narcotics may have their depres-
sant effects potentiated by tricyclics, and severe
respiratory depression may ensue. The adminis-
tration of medications with anticholinergic prop-
erties, such as atropine or scopolamine, can cause
an increase in intraocular pressure and worsen
occult or known narrow-angle glaucoma. Last,
dental professionals should take care when pre-
scribing acetaminophen because of its ability to
increase TCA levels.73
Patients being treated with MAOIs can receive
local anesthetic solutions containing levonorde-
frin or epinephrine, because the MAOIs do not
potentiate the pressor or cardiac effects of these
direct-acting catecholamines.74 However, dentists
should avoid prescribing meperidine hydrochlo-
ride for these patients because of a potentially
toxic interaction in which severe hyperthermia,
hypertension and tachycardia may develop.
Animal studies have shown that MAOIs also
increase the potency of other narcotic analgesics.
Therefore, it is prudent to prescribe only one-half
the usual dosage of narcotic and to titrate slowly
any additional medication until a symptomatic
response is achieved.
We recommend that dental professionals per-
form a clinical examination and oral prophylaxis
at three-month follow-up visits and apply a fluo-
ride gel at a fluorine concentration of at least
10,000 parts per million. Dentists also should cor-
 D E N T I S T R Y & MEDICINE

rect any defects in the natural depression to cardiovascular disease: epidemiology, biology, and treat-
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Dr. Friedlander is asso-
of dental treatment, which may 2000;6(2):115-20.
ciate chief of staff for contribute to the psychothera- 17. Poewe W, Luginger E. Depression in Parkinson’s disease: impedi-
graduate medical edu-
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Greater Los Angeles
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Healthcare System (14), CONCLUSION W, Beekman AT. Minor and major depression and the risk of death in
11301 Wilshire Blvd.,
older persons. Arch Gen Psychiatry 1999;56(10):889-95.
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90073, e-mail
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“arthur.friedlander@
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med.va.gov”. He also is has much to offer patients with 20. Blair-West GW, Cantor CH, Mellsop GW, Eyeson-Annan ML.
the director of quality
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assurance, Hospital
MDD. Our goal is to encourage J Affect Disord 1999;55(2-3):171-8.
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sity of California Los
117-20.
Angeles Medical
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Angeles School of
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Dr. Friedlander.
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