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Vol. 94 No. 4 October 2002
ORAL SURGERY
ORAL MEDICINE
ORAL PATHOLOGY
MEDICAL MANAGEMENT UPDATE
Editor: Donald Falace
Late-life depression: Psychopathology, medical interventions,
and dental implications
Arthur H. Friedlander, DDS,a and Dean C. Norman, MD,b Los Angeles, Calif
VETERANS AFFAIRS GREATER LOS ANGELES HEALTHCARE SYSTEM,
UNIVERSITY OF CALIFORNIA–LOS ANGELES
Background. Late-life depression (LLD) initially occurs after age 65 years and is a major public health concern because
the elderly who are at high risk constitute an ever-expanding segment of the population. LLD is a mental illness in
which mood, thought content, and behavioral patterns are impaired, causing the individual distress, compromising
social function, and impairing self-maintenance skills (eg, bathing, dressing, hygiene). LLD characterized by marked
sadness or a loss of interest or pleasure in daily activities and may be accompanied by weight change, sleep
disturbance, fatigue, difficulty in concentration, and a high suicide rate. Diagnosis of LLD is sometimes complicated by
a denial of mood change and an inability to distinguish symptoms of a concurrent physical illness from those of a
depressive etiology. The disorder is most frequently treated with antidepressant medications, and although older
individuals have a recovery rate that is comparable with younger adults, they often take longer to recover, have more
frequent relapses, and are more sensitive to the side effects of the drugs.
Clinical implications. Individuals undergoing treatment for LLD and those whose illness has not been diagnosed or
treated often are seen with significant oral disease by the dentist. Dentists need to be cognizant of how to safely and
compassionately provide care to those already receiving mental health services. They must also be familiar with the
psychiatric symptoms of the disorder to effectuate a timely referral to a physician of those with occult or relapsing
disease. LLD is frequently associated with a disinterest in oral hygiene, a cariogenic diet, diminished salivary flow,
rampant dental decay, 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
necessitates a vigorous preventive dental education program, the use of artificial salivary products, antiseptic
mouthwash, daily fluoride mouth rinse, and special precautions in administration of local anesthetics with
vasoconstrictors and prescription of analgesics.
Conclusion. Dentists who invoke appropriate precautions can usually provide a full range of services to individuals
with LLD, thereby enhancing patient self-esteem and contributing to the psychotherapeutic aspect of management.
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94:404-12)
Late-life depression (LLD) initially begins after age 65
and classically presents as dysphoria (feeling sad, mis-
a
Associate Chief of Staff and Director of Graduate Medical Education, VA Greater Los Angeles Healthcare System, Professor of Oral
and Maxillofacial Surgery and Director of Quality Assurance, Hospital Dental Service, UCLA Medical Center, Los Angeles.
b
Chief of Staff, VA Greater Los Angeles Healthcare System, and
Professor of Internal Medicine, Geriatric Medicine and Infectious
Diseases, UCLA School of Medicine. Los Angeles.
Received for publication Nov 21, 2001; accepted for publication Dec
18, 2001.
© 2002, Mosby, Inc.
1079-2104/2002/$35.00 ⫹ 0 7/13/122434
doi:10.1067/moe.2002.122434
404
erable, helpless, and hopeless) and anhedonia (an inability to enjoy oneself). Among community-dwelling
individuals, this may appear as a loss of interest or
pleasure in activities that were formerly sources of
enjoyment, such as watching television or playing with
grandchildren. For nursing home residents, this may
take the form of no longer eating dinner in the group
dining room or going to concerts, movies, or discussion
groups. A loss of self-esteem, or a preoccupation over
past minor failings, and thoughts of suicide may accompany the dysphoria and anhedonia. In addition,
alterations may be seen in appetite that result in weight
loss or gain, insomnia, neglect of personal hygiene, an
inability to sit still (agitation), sad fixed facial expres-
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
Volume 94, Number 4
sion, slowed speech and body movements (psychomotor retardation), lack of energy, and cognitive impairment (ie, difficulty in thinking, concentrating, and
making decisions). This cluster of symptoms is emotionally painful for the individual and impairs their
social interactions and activities of daily living (eg,
ability to groom, bathe, and perform oral hygiene).1-3
LLD is at times difficult to diagnose (masked depression) because many symptoms of the disorder, such as
sleep disturbance, fatigue, and impaired concentration,
overlap with symptoms of other medical problems,
such as heart disease, lung disease, and cancer, that are
prevalent in older persons.4,5 Similarly, appetite disturbance may be caused by factors such as age-related
diminished smell and taste, medication-derived xerostomia, and an absence of teeth.6 LLD may also be
difficult to diagnose because some elderly individuals
express depression with complaints about numerous
bodily aches and pains that lack objective signs or with
denial of a depressive mood and symptoms of guilt and
self-reproach. This often results in the patient being
provided medication for the somatic complaints but
with the depression going undiagnosed and untreated.7-9
EPIDEMIOLOGY
The overall prevalence rate for LLD is 3.3% for
women and 1.4% for men; however, when broken
down by setting, there is marked variation.10 The illness
is relatively uncommon (1%) among the physically
healthy elderly living independently in the community,
but the prevalence increases (12%) among those hospitalized for medical illnesses (eg, diabetes, angina,
myocardial infarction), neurologic disease (eg, stroke),
and surgical conditions and rises even further (20% to
25%) among chronically ill but cognitively intact patients in nursing homes.11,12
This epidemiologic pattern of LLD occurring in relation to age-related physical illness, chronic disabilities, and social isolation is a major public health concern because it is estimated that between 2002 and 2040
the segment of the population over age 65 years will
grow by 160% and that over age 75 years will grow by
270%.13-15 The reasons for the greater prevalence of the
disorder among women remain unclear but is probably
related to social influences.16 Women on average live 7
years longer than men and outnumber men 3 to 2 in the
population at the age of 65 years and 5 to 2 in the
population aged 85 years and older. Thus, they are at
greater risk than men of having multiple vulnerabilities
that lead to increased risk of institutionalization and
concomitant depression.
The relapse rate of LLD is approximately 60%, with
those at highest risk having a concurrent severe medical
Friedlander and Norman 405
illness, an absence of a social support network, or a
history of relapse.17-21 Individuals with LLD are high
consumers of general healthcare, may abuse alcohol
and sedative-hypnotic agents, and have an increased
overall mortality rate compared with that of nondepressed peers.22
Risk of suicide is a major concern for those with
LLD. From 1980 to 1992, the suicide rate for men and
women aged 65 years and older increased 9%, and for
those aged 80 to 84 years, it increased 35%.23 At
highest risk of suicide are elderly white males without
friends or social support with an initial onset of mild to
moderately severe depression uncomplicated by substance abuse.24,25 However, even with these profiles, it
is still uniquely difficult to predict which individuals
will commit suicide. Seventy-five percent of depressed
individuals who commit suicide have visited a primary
care physician within the prior month and 39% within
the prior week, but their mental illness was neither
recognized nor treated.26,27
PATHOPHYSIOLOGY
The etiology of late-onset depression remains ill
defined; however, it appears to be an acquired condition
that arises from a combination of the physiologic effects of aging, medical illnesses, physical disabilities,
medications, and psychosocial stress (eg, death of a
spouse, enforced change of residence, increased dependency).28,29 Data from computerized tomographic scans
often reveal regional cerebral atrophy, such as smaller
prefrontal lobe volume. Magnetic resonance imaging
studies show enlarged cerebral ventricles and whitematter hyperintensities, which are construed to be areas
of compromised brain tissue resulting from hypertension-induced, small blood vessel ischemic occlusive
disease (silent infarctions/silent strokes).30 Similarly,
functional neuroimaging with positron emission tomographic scanning shows decreased regional cerebral
blood flow and decreased cerebral glucose metabolism.31 Aging also is associated with a decline in the
levels of the neurotransmitter hormones norepinephrine
and serotonin (because of neuronal loss, decreased synthesis, or increased degradation) and in the number of
␤-adrenergic and serotonin postsynaptic binding sites.
These deficits also are believed responsible for LLD in
some individuals because they hinder the transmission
of neural impulses in the limbic system (amygdala and
hippocampus), areas of the brain responsible for the
regulation of mood, sleep, appetite, libido, and memory.32
LLD differs from early-onset disease with less prominence of depressed mood, delayed diagnosis because
of greater difficulty in distinguishing the disease from
the overlapping symptoms of physical illness, a lower
406 Friedlander and Norman
Table I. Antidepressant medications
Heterocyclic antidepressant drugs
Secondary amines
Desipramine hydrochloride
Nortriptyline hydrochloride
Tertiary amines
Amitriptyline hydrochloride
Clomipramine hydrochloride
Doxepin hydrochloride
Imipramine
Trimipramine
SSRIs
Citalopram hydrobromide
Fluoxetine
Fluvoxamine
Paroxetine hydrochloride
Sertraline hydrochloride
Atypical antidepressant drugs
Bupropion hydrochloride
Maprotiline
Mirtazapine
Nefazodone hydrochloride
Trazodone hydrochloride
Venlafaxine hydrochloride
MAOIs
Phenelzine sulfate
Tranylcypromine sulfate
frequency of family history of the disease but a higher
frequency of cognitive impairment, anatomic and physiologic changes in the brain, increased time lag in
therapeutic response, treatment resistance, and increased mortality from medical illness and suicide.
MEDICAL MANAGEMENT
Pharmacotherapy, psychotherapy, or a combination
of both is used with great efficacy to treat the disorder.33 Electroconvulsive therapy is reserved for those
who cannot tolerate medication or are at risk of imminent death because of a refusal to eat or suicidal tendency.
More than 2 dozen antidepressant medications are
currently available and are divided into 4 groups: heterocyclic antidepressants, selective serotonin reuptake
inhibitors (SSRIs), “atypical” antidepressants, and
monoamine oxidase inhibitors (MAOIs; Table I). Medications are chosen on the basis of the patient’s symptoms, drug side effect profile, and the presence of
concurrent medical illness. If the patient is agitated (ie,
restlessness and insomnia), an antidepressant with sedative qualities will be chosen; however, if the patient is
lethargic, a less sedating drug will be prescribed.34
Older patients are more likely to have side effects
because of age-related pharmacokinetic alterations in
drug absorption, binding, distribution, metabolism, and
excretion. Medications with excessive anticholinergic
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
October 2002
activity are avoided in individuals whose medical conditions (eg, glaucoma) could be worsened by these side
effects, and antidepressants that cause sexual dysfunction are avoided in those who remain sexually active.
These medications are effective approximately 75% of
the time, with patients usually responding in 6 to 12
weeks. The medication regime commonly remains in
force for at least 1 year after recovery because of the
propensity for relapse.
The heterocyclic antidepressants (also known as the
tricyclic antidepressants) exert their effect by preventing presynaptic neurones from reabsorbing (blocking
reuptake) noradrenaline and serotonin from the synaptic cleft for recycling. Thus, the concentration of these
2 neurotransmitters is elevated and neuronal activity is
increased. The heterocyclic antidepressants are divided
into 2 subgroups. The secondary amines (eg, desipramine hydrochloride, nortriptyline hydrochloride) have
relatively mild, peripheral, and central anticholinergic
profiles and have been used for many years to treat
elderly patients. The tertiary amines (eg, amitriptyline
hydrochloride, doxepin hydrochloride) have more pronounced anticholinergic effects (eg, fecal impaction,
urinary retention, falls and hip fractures, xerostomia,
and altered cardiac rate and rhythm) and are less commonly used.35
The SSRIs (eg, fluoxetine) exert their antidepressant
effect by preventing presynaptic neurones from reabsorbing (reuptake) serotonin from the synaptic cleft for
recycling.36 Thus, the concentration of serotonin in the
cleft is elevated and neuronal activity is enhanced. The
SSRIs are becoming the drugs of choice in the physically ill depressed patient because of their reduced
anticholinergic side effects, reduced cardiotoxicity, and
much diminished likelihood of inducing confusion.37
The use of these medications, however, may be of
concern to dentists because of the potentially increased
bleeding time secondary to a disruption in platelet
function.38,39
A third group, known as the atypical antidepressants,
consists of a heterogeneous collection of medications
that exert their effects through varied mechanisms. Mirtazapine enhances presynaptic norepinephrine release
and secondarily enhances serotonin neurotransmission.
Nefazodone hydrochloride inhibits reuptake of serotonin and also selectively blocks serotonin receptors, and
venlafaxine hydrochloride inhibits reuptake of serotonin and noradrenaline.
The MAOIs (eg, phenelzine sulfate, tranylcypromine
sulfate) exert their antidepressant effect by downregulating ␤-noradrenergic and ␣2-noradrenergic receptors
and serotonin1 and serotonin2 receptors. The MAOIs
are used infrequently and are reserved for those whose
depression has been refractory to a course of heterocy-
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
Volume 94, Number 4
clics, SSRIs, or the atypical antidepressants. The rationale for the limited use of these medications (⬍10% of
antidepressant prescriptions) arises because of dangerous dietary and drug interactions (eg, with ephedrine)
that may cause severe, acute hypertension. MAOIs
prevent the gut wall and liver from inactivating exogenous amines (eg, tyramine found in aged cheeses,
meats, and red wine). The amines reach the systemic
circulation and then noradrenergic nerve endings where
they release noradrenaline, resulting in vasoconstriction
and hypertension.40 Older individuals with fragile cerebral vasculature are potentially at high risk of death
from a hypertensive-induced intracranial hemorrhage.
Other major side effects associated with the use of
MAOIs are orthostatic hypotension, xerostomia, and
weight gain.
Psychotherapeutic intervention, without adjunctive
medication, is effective treatment for some patients
with LLD. It is an especially attractive option in the
frail medically ill to avoid drug side effects and drugdrug interactions. Psychotherapy also is frequently used
in combination with drugs in severely ill patients to
increase compliance with medication use and decrease
the likelihood of relapse.41,42 Psychotherapeutic interventions include cognitive-behavior therapy and interpersonal psychotherapy.43,44
Electroconvulsive therapy (ECT) is another form of
treatment for LLD with antidepressant effects that occur much more rapidly (within 7 to 10 days) than those
obtained with antidepressive medication. For this reason, it is considered a first-line treatment for patients
with LLD who refuse to eat or are in danger of a
completed suicide.45 ECT is also indicated for patients
with LLD who are medication resistant or for those
with concomitant medical conditions (eg, cardiovascular disease) that preclude the administration of adequate
dosages of psychopharmacologic agents.46,47 With general anesthesia, a brief electric stimulus is administered
to the brain via electrodes placed on the temples. The
current passes through the central parts of the brain
stimulating the centrencephalic structures to produce a
grand mal seizure. The massive depolarization of neurones alters cerebral blood flow and metabolism and
renders the neuronal membranes more responsive to
noradrenaline, thereby enhancing neuronal activity.48
This results in approximately 75% of patients having
remission of their depression; however, to prevent relapse, an antidepressant may be prescribed for 1 year
after the patient has completed the course of ECT.49
Medical complications of ECT are rare; however, the
procedure is associated with a brief headache and an
increased vulnerability to cognitive side effects.50,51
Anterograde amnesia (newly learned information is
rapidly forgotten) and retrograde amnesia (deficits in
Friedlander and Norman 407
recall or recognition of events that occurred closest in
time to the treatment) commonly occur. After termination of ECT, anterograde amnesia typically resolves
within a few weeks, but retrograde amnesia diminishes
more gradually and may possibly persist.52 Irrespective
of these issues, two thirds of patients who have had
ECT report that the experience was no more challenging than a visit to the dentist.53
An often overlooked aspect of the pre-ECT work-up
is the orofacial examination, which could identify broken or loose teeth that may be aspirated during the
seizure, upper airway obstruction from destructive arthritis of the temporomandibular joint, dental abscesses, or facial deformities that may preclude
ECT.54-57 Similarly, it is recommended that loose teeth
than cannot be protected during the procedure be prophylactically extracted before ECT.58,59 This latter admonition is important because of the severe jaw clenching that results from the stimulation of the masseter
muscles.60
OROFACIAL FINDINGS
Persons with undiagnosed, untreated, or treatmentresistant LLD may present with numerous orofacial
complications. These individuals may appear to have a
fixed facial expression and deep furrows in the forehead
and beside the mouth, which can accompany psychomotor retardation.61 Studies with standarized psychologic tests (eg, Beck Depression Inventory, Minnesota Multiphasic Personality Inventory) to evaluate
older individuals seeking treatment for chronic facial
pain or a burning sensation of the oral mucosa and
tongue reveal that approximately 40% would qualify
for a diagnosis of LLD.62-69 Studies that evaluated the
oral health of patients with LLD receiving long-term
treatment with antidepressant medications have noted
that these individuals evidence extensive dental decay.
This is likely the result of many factors, including a
disinterest in oral hygiene, a preference for carbohydrates because of reduced serotonin centrally, a craving
for intense sweets (because of impaired taste perception), a decrement in whole mouth and parotid gland
saliva (because depression itself is related to increased
anticholinergic activity), and a high lactobacillus
count.70-77 Individuals with LLD are also at high risk of
advanced periodontal disease because of neglect of oral
hygiene, xerostomia, an increase in smoking, and an
altered immune response facilitating increased colonization by pathogenic bacteria, thus leading to a breakdown of the periodontal attachment.78,79
Individuals with diagnosed LLD under treatment are
also at risk of development of dental decay because
many antidepressants add to the xerostomia by blocking parasympathetic stimulation of the salivary glands.
408 Friedlander and Norman
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
October 2002
Table II. Adverse orofacial reactions to heterocyclic antidepressant medications
Medication
Xerostomia
Sialadenitis
Dysgeusia
Stomatitis
Gingivitis
Glossitis
Bruxism
Miscellaneous
Amitriptyline hydrochloride
Clomipramine hydrochloride
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
0
⫹
0
⫹
0
0
Desipramine hydrochloride
Doxepin hydrochloride
Imipramine
Nortriptyline hydrochloride
Protriptyline hydrochloride
Trimipramine
⫹
⫹
⫹
⫹
⫹
⫹
⫹
0
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
0
⫹
⫹
⫹
0
⫹
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Caries, cheilitis,
dysphagia, oral ulcers,
halitosis, sinusitis
Facial edema
0
Facial edema
Facial edema
Facial edema
Facial edema
A metaanalysis of the results of double-blind, randomized control trials has shown that the crude rates of
occurrence of xerostomia are 27% for heterocyclics and
22% for the SSRIs.80 However, even though this is a
statistically significant difference, studies reveal that
individuals receiving both classifications of drugs evidence extensive dental decay secondary to the medications’ xerostomic effects.81,82 Long-term use of heterocyclic agents also is associated with an increase in
dental decay because this group of medications enhances the craving for carbohydrates by a still unexplained mechanism.83 Similarly, individuals receiving
SSRIs or the atypical antidepressants may on occasion
have a movement disorder develop that includes
clenching or bruxing of the teeth, further worsening the
periodontal condition.84 This may occur because these
medications increase extrapyramidal levels of serotonin, thereby inhibiting dopaminergic pathways that
control movements.85
The most frequently prescribed antidepressant medications are associated with a significant number of
adverse orofacial reactions.86,87 These complications
(ie, xerostomia, sialadenitis, gingivitis, dysgeusia, and
stomatitis) almost always arise because of medicationinduced salivary gland dysfunction (Tables II to V).
However, if stomatitis develops in a patient taking
mirtazapine, it may represent the initial signs of medication-induced bone marrow suppression (ie, agranulocytosis, leucopenia, or granulocytosis), a potentially
fatal event.
DENTAL MANAGEMENT
Some patients who undergo psychiatric treatment for
depression may be reluctant to admit it because of local
or historic stigma attached to a psychiatric diagnosis.
To overcome such barriers and obtain necessary information, the dentist should display a supportive, nonjudgmental attitude and advise patients that such information will be held confidential and is indispensable to
the provision of safe dental care.
Before a patient with LLD begins dental treatment,
their physician should be consulted. With consent of
the patient, information requested should include the
patient’s current psychologic status and current psychotropic medication regimen and any history of alcohol
or other substance abuse.
Preventive dental education is paramount for these
patients. Family members, however, must also be involved during the development of the preventative dental regime; if the depression does not adequately respond to therapy, the patient may lack the motivation
and concentration necessary to autonomously comply.
Instructions should be given in proper tooth brushing
and flossing methods that maximize dental plaque removal. Artificial salivary products, antiseptic mouthwash (eg, chlorhexidine), and a 0.05% sodium fluoride
mouth rinse may be prescribed for patients with xerostomia. Dental treatment should consist of subgingival
scaling, root planing and curettage, caries control, application of fluoride gel, and dental restorations. Effective local anesthesia is mandatory in depressed and
often anxious individuals.
Use of local anesthetic solutions containing epinephrine as a vasoconstrictor for patients receiving heterocyclics is controversial because of the fear of precipitating a hypertensive crisis or a cardiac arrhythmia. The
primary mechanism for terminating the pressor action
of adrenergic amines (eg, epinephrine) is their reuptake
by presynaptic sympathetic nerve fibers, which precludes their continued access to receptor sites. Heterocyclics block this reuptake process. The heterocyclics
also block muscarinic and ␣1-adrenergic receptors,
thereby directly depressing the heart. Thus, the combination of a heterocyclic antidepressant and epinephrine
may potentially result in an increase in systolic blood
pressure or a cardiac arrhythmia. Therefore, Howe and
Whitehead88 recommend the use of anesthetic solutions
that do not contain epinephrine (for instance, 3% mepivacaine hydrochloride). However, others do not report
any untoward results with the use of epinephrine in
Friedlander and Norman 409
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY
Volume 94, Number 4
Table III. Adverse orofacial reactions to SSRIs
Medication
Xerostomia
Sialadenitis
Dysgeusia
Stomatitis
Gingivitis
Glossitis
Bruxism
Miscellaneous
Citalopram hydrochloride
Fluoxetine
⫹
⫹
0
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
Fluvoxamine
Paroxetine hydrochloride
Sertraline hydrochloride
⫹
⫹
⫹
0
⫹
0
⫹
⫹
⫹
⫹
⫹
⫹
⫹
⫹
0
⫹
⫹
⫹
0
⫹
⫹
0
Jaw pain, buccal glossal
syndrome
Toothache
Caries, dysphagia
Dysphagia,
gingival hyperplasia
Table IV. Adverse orofacial reactions to atypical antidepressant drugs
Medication
Xerostomia Sialadenitis Dysgeusia
Stomatitis
Gingivitis Glossitis Bruxism
Bupropion hydrochloride
⫹
0
⫹
⫹
0
⫹
⫹
Maprotiline
Mirtazapine
⫹
⫹
⫹
⫹
⫹
⫹
⫹
See Miscellaneous
0
⫹
0
⫹
0
0
Nefazodone hydrochloride
⫹
0
⫹
⫹
⫹
⫹
0
Trazodone hydrochloride
Venlafaxine hydrochloride
⫹
⫹
0
0
⫹
⫹
0
⫹
0
⫹
0
⫹
0
⫹
Miscellaneous
Toothache, oral edema,
dysphagia
Dysphagia
Stomatitis may indicate
agranulocytosis,
leucopenia, or
granulocytosis; facial
edema
Moniliasis, dysphagia,
periodontal abscesses,
oral ulcers
sinusitis
Moniliasis, dysphagia,
halitosis, oral ulcers
Table V. Adverse orofacial reactions to MAOIs
Medication
Phenelzine sulfate
Tranylcypromine sulfate
Xerostomia
Sialadenitis
Dysgeusia
Stomatitis
Gingivitis
Glossitis
Bruxism
Miscellaneous
⫹
⫹
0
0
0
0
0
0
0
0
0
0
0
0
0
0
patients taking heterocyclic antidepressants and conclude that the amount of epinephrine used in dental
anesthetic preparations is too insignificant to interact
with the heterocyclics.89,90 Regardless, it may be prudent to administer no more than 50 ␮g of epinephrine,
as is found in 2 to 3 cartridges of 2% lidocaine with
1:100,000 epinephrine, with care being taken to avoid
intravenous administration. Similarly, the American
Dental Association Guide to Dental Therapeutics suggests cautious use of epinephrine and in as low a dose
as is feasible but avoidance of the use of levonordefrin
and norepinephrine.91 It is also recommended that gingival retraction cords impregnated with epinephrine be
avoided.92
Other adverse drug interactions between heterocyclics and medications used in dentistry may occur. The
respiratory depressant effects of narcotic analgesics
(eg, codeine) are potentiated by tricyclics. Barbiturates
(eg, phenobarbital) may accelerate the metabolism of
heterocyclics and attenuate their antidepressant effects.
The administration of medications with anticholinergic
properties, such as atropine or scopolamine, can cause
an increase in intraocular pressure and precipitate or
worsen narrow angle glaucoma. Finally, care should be
observed when prescribing acetaminophen because of
its ability to decrease the metabolic rate of heterocyclics.93
Patients taking MAOIs can receive local anesthetic
solutions containing epinephrine because the MAOIs
do not potentiate the pressor or cardiac effects of this
direct-acting sympathomimetic.94 The use of meperidine hydrochloride by a patient taking MAOIs may
result in fatal elevations in body temperature (hyperpyrexia) because of increased serotonin release.
MAOIs also interfere with the detoxification of barbiturates and anticholinergic drugs (eg, atropine, scopolamine) and thus potentiate their effects.95
Adverse interactions between the SSRIs and some
410 Friedlander and Norman
medications used in dentistry may occur because these
antidepressants inhibit certain metabolic pathways.
Specifically, the SSRIs inhibit P-450 isoenzymes
needed to adequately metabolize codeine, benzodiazepines, erythromycin, and carbamazepine. These dental
therapeutic agents therefore should be used cautiously
and in reduced dosages.96
At 3-month follow-up visits, a clinical examination,
oral prophylaxis, and application of a fluoride gel with
a concentration at least 10,000 ppm are performed.
Correction of defects in the natural dentition or prosthetic replacements are also performed during these
recall visits. A consequent enhancement of self-esteem
in these patients is often noticed by family and friends
and may potentially contribute to the psychotherapeutic
aspect of management.
CONCLUSION
The purpose of this paper is to familiarize dentists
with LLD so that patients may safely and compassionately be treated and to help dentists recognize individuals who present with signs and symptoms consistent
with occult depression so that they can knowledgeably
refer them to a physician for evaluation and treatment.
In addition, some within our own profession may suffer
from this disorder, either diagnosed or occult, and this
information may be of benefit to them. It should be
recognized that dentistry, in concert with medicine, has
much to offer patients with depression.
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