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J Am Dent Assoc, Vol 132, No 5, 629-638.
© 2001 American Dental Association
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DENTISTRY & MEDICINE

JADA Continuing Education

Major depressive disorder

Psychopathology, medical management and dental implications



ARTHUR H. FRIEDLANDER, D.D.S. and MICHAEL E. MAHLER, M.D.


   ABSTRACT
TOP
 ABSTRACT
EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 
Background. Major depressive disorder, or MDD, is a psychiatric illness in which mood, thoughts and behavioral patterns are impaired for long periods. The illness distresses the person and impairs his or her social functioning and quality of life. MDD is characterized by marked sadness 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 disability 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 lifetime 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 frequently is associated with a disinterest in performing appropriate oral hygiene techniques, a cariogenic diet, diminished salivary 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 prescribing or administering analgesics and local anesthetics.

Clinical Implications. Dentists cognizant of these signs and symptoms have an opportunity to recognize patients with occult MDD. After confirmation of the diagnosis 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 contribute to the psychotherapeutic aspect of management.

Major depressive disorder (previously known as major depression or unipolar depression), 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 interest or pleasure in previously enjoyed activities such as hobbies and social or sexual interactions) or both.1 A sense of worthlessness or guilt, accompanied by preoccupation over past minor failings and thoughts of suicide, is common.

Dentists have an opportunity to recognize patients with occult major depressive disorder.

In addition to mood change and anhedonia, the patient or a family member may note alterations in appetite that result in weight loss or gain of more than 5 percent; insomnia characterized 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, concentrate 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 interferes with social and occupational functioning.

The onset of the disorder varies, with symptoms developing over days to weeks. Untreated episodes typically last six months or longer. Eventually, the episode 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 withdrawal and household strain.3–6 The risk of recurrence of MDD for people with or without residual symptoms is 50 percent after one episode, 70 percent 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
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 
MDD is common in the United States and is currently 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 percent 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 definitive explanation exists for the sex differences in prevalence rates. The median age at onset of illness is 26 years.10

People at highest risk of experiencing a first episode of depression are those with a family history 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 frequency of depression.16,17 These medically compromised and older people are at almost twice the risk of dying from all causes compared with similarly aged medically compromised people without the mental disorder.18 MDD also is associated with substance abuse. Approximately one-third of people with MDD develop a substance abuse disorder (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
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 
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 structures, 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 circulatory cortisol levels.24 Neuroimaging studies support 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 emotions) in correlation with the severity of depression and increased cortisol levels.25 These abnormalities in blood flow and glucose metabolism recede in most patients after they respond to antidepressant medication.26


   MEDICAL MANAGEMENT
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 
In the United States, treatment for mild or moderately 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, but it is not used often in primary care settings because of unfamiliarity with the techniques, as well as financial and time constraints.27,28 Similar constraints often relegate patients with severe episodes of the disorder to receive pharmacological treatment only, even though a combination of medication and psychotherapy results in greater improvement.29 Electroconvulsive therapy, or ECT, is indicated for patients who cannot tolerate medication and for those at risk of dying imminently because of a refusal to eat or severe suicidal impulses.

Clinicians choose a medication based on the patient’s symptoms and the side-effects profile of a specific drug. If the patient is lethargic, an activating medication will be prescribed; if the patient is anxious, a drug with more sedating qualities will be chosen. Medications with excessive anticholinergic activity (many of the tricyclic antidepressants, or 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 successfully.30 Because of the high rate of relapse, continued use of the medication is recommended for six months to one year beyond the initial recovery.31

The boxGo ("Classification of Commonly Prescribed Antidepressants") shows the major categories of antidepressants, which are based on their mechanisms of action.


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  		CLASSIFICATION OF COMMONLY PRESCRIBED ANTIDEPRESSANTS.

 
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 presynaptic neurons from reabsorbing (reuptake) serotonin from the synaptic cleft (the space between two neurons) for recycling. Thus, the concentration 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 medications are not lethal, and patients are less likely to discontinue treatment because of adverse drug reactions.32 Although free of annoying anticholinergic and cardiovascular side effects, they do, however, frequently cause diarrhea, nausea, dizziness, insomnia, anxiety or agitation, tremor, headache, sexual dysfunction (that is, decreased libido, ejaculatory and erectile dysfunction, anorgasmia) and, on occasion, an increase in bleeding time.33,34 SSRIs also are effective for symptoms of rumination and obsessive-compulsive types of behavior.

Atypical antidepressants. The atypical antidepressants, or AAs (for example, bupropion [Wellbutrin, GlaxoSmithKline], venlafaxine [Effexor, Wyeth-Ayerst Pharmaceuticals]), exert their effects through varied mechanisms, including selective norepinephrine reuptake inhibition, dopamine reuptake inhibition and antagonist, and reversible inhibition of monoamine oxidase A. These medications are as effective as the SSRIs and, like the SSRIs, are first-line treatments for patients with mild-to-moderate depression, are not lethal in overdoses and have a similar side-effect profile.35 Of specific concern to dentists, maprotiline occasionally is associated with orthostatic hypotension, electrocardiographic changes, tachycardia and agranulocytosis, and mirtazepine has been associated with infrequent reports of agranulocytosis and neutropenia.36

Atypical antidepressants are as effective as the selective serotonin reuptake inhibitors and are first-line treatments for patients with mild-to-moderate depression.

TCAs. The TCAs (for example, amitriptyline [Elavil, AstraZeneca], imipramine [Tofranil, Novartis Pharmaceuticals]) exert their effect by preventing presynaptic neurons from reabsorbing norepinephrine and serotonin from the synaptic cleft for recycling. Thus, the concentration of these two neurotransmitters is elevated and neuronal activity is increased. These agents are used to treat patients with severe disease, as manifested by a depression that is worse in the morning, anhedonia, significant weight loss and psychomotor retardation, as well as for patients whose depression has been refractory to SSRIs. Some TCAs are lethal in overdoses and approximately 40 percent of patients become noncompliant because of unpleasant side effects.

TCAs cause peripheral anticholinergic side effects such as xerostomia, urinary retention, constipation and blurred vision, as well as central anticholinergic side effects such as impaired concentration and confusion. These medications also slow intraventricular conduction, prolonging the QRS, PR and QT intervals on an electrocardiogram. This can cause complete heart block or ventricular dysrhythmias. Many older patients with preexisting medical problems cannot tolerate the adverse side effects associated with TCAs.37

Monoamine oxidase inhibitors. The monoamine oxidase inhibitors, or MAOIs (for example, phenelzine [Nardil, Parke-Davis], tranylcypromine [Parnate, SmithKline Beecham]) exert their antidepressant effect by nonselective inhibition of MAO A and MAO B so that they cannot metabolize norepinephrine and serotonin in the synaptic cleft. Thus, the concentrations of norepinephrine and serotonin are elevated and neuronal activity is enhanced. The MAOIs are used initially to treat patients with moderate-to-severe depression, as well as patients whose depression has been refractory to a course of an SSRI, AA or TCA.

Major side effects associated with the use of MAOIs are dizziness, orthostatic hypotension, insomnia, central nervous system stimulation, weight gain and edema. MAOIs prevent the liver from inactivating tyramine found in aged meats, red wine, beer and some cheeses, causing norepinephrine blood levels to rise and, on occasion, bringing about a fatal hypertensive crisis (consequently, patients receiving treatment with an MAOI should avoid these foods). Severe hypertension also may ensue when a patient concurrently takes an MAOI and a sympathomimetic medication such as ephedrine, which is found in some decongestants, allergy medications and appetite suppressants.38

Cognitive-behavioral therapy. Cognitive-behavioral therapy or interpersonal psychotherapy is indicated for patients with mild-to-moderate depression who refuse to take medication or are unable to tolerate the side effects of medication.39 These therapies also are frequently used in combination with medication to maximize the effectiveness of treatment and decrease the likelihood of relapse.40 Cognitive-behavioral therapy helps patients recognize and challenge the recurrent negative thoughts and dysfunctional attitudes that may lead to depression or that maintain an episode of depression if dwelled on. Interpersonal psychotherapy focuses on interpersonal role disputes (often marital disputes) 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 psychopharmacological 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. Researchers have postulated that after a number of treatments, neuronal membranes become more responsive to serotonin, thereby enhancing neuronal 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 relaxants to control convulsions have rendered medical 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 permanently 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
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 
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 percent of patients), dysgeusia (altered taste sensations), 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 1Go and 2Go). The use of TCAs is associated with xerostomia (affecting almost 50 percent of patients) and occasionally with sialadenitis, dysgeusia, stomatitis and edema of the tongue (Table 3Go). The MAOIs also occasionally cause xerostomia, but less often than do the TCAs (Table 4Go).


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  		TABLE 1 ADVERSE OROFACIAL REACTIONS TO SELECTIVE SEROTONIN REUPTAKE INHIBITORS.

 

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  		TABLE 2 ADVERSE OROFACIAL REACTIONS TO ATYPICAL ANTIDEPRESSANTS.

 

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  		TABLE 3 ADVERSE OROFACIAL REACTIONS TO TRICYCLIC ANTIDEPRESSANTS.

 

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  		TABLE 4 ADVERSE OROFACIAL REACTIONS TO MONOAMINE OXIDASE INHIBITORS.

 
Patients who report many signs associated with depression are prone to suffer periodontitis.47–50 Researchers have hypothesized that neglect of oral hygiene, increased smoking and altered immune responses facilitate increased colonization 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 developing rampant dental decay because of a disinterest 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 salivary output and a high lactobacillus count.57–60 The SSRIs, AAs and TCAs magnify the problem of xerostomia by blocking parasympathetic stimulation of the salivary glands. Long-term use of TCAs is specifically associated with carbohydrate craving and the potential for increased development of dental caries.61

Chronic facial pain, burning sensation of the oral mucosa (often on the tongue) or a temporomandibular 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 previously implicated as the cause of both depression and inflammatory joint disease.62–69


   DENTAL TREATMENT OF PATIENTS WITH DEPRESSION
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
CONCLUSION
 REFERENCES
 
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 unappreciative 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 regimen. The dentist also must ask the psychiatrist about the patient’s history of alcohol or other substance abuse. Patients with a history of alcohol abuse should undergo liver function tests (that is, blood serum levels of albumin and total proteins), a complete blood cell count and a coagulation profile (that is, prothrombin time and partial thromboplastin time).

Education. Preventive dental education is paramount for these patients and their families. They should receive instruction in proper toothbrushing and flossing methods that maximize removal of dental plaque. Artificial salivary products 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. Profound 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 antidepressants inhibit certain metabolic pathways. Specifically, SSRIs inhibit the cytochrome P-450 isoenzymes needed to adequately metabolize codeine, benzodiazepines, erythromycin and carbamazepine. Therefore, these dental therapeutic agents should be used cautiously and in reduced dosages.71

Adrenergic vasoconstrictors. Dentists must take precautions when administering local anesthetics containing adrenergic vasoconstrictors (such as levonordefrin and epinephrine) to patients receiving TCAs. TCAs block the reuptake of these vasoconstrictors and block muscarinic and {alpha}1-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 interacts with TCAs so that it can be used, but in a dosage not to exceed 0.05 milligrams (the equivalent 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 depressant effects potentiated by tricyclics, and severe respiratory depression may ensue. The administration of medications with anticholinergic properties, 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 prescribing acetaminophen because of its ability to increase TCA levels.73

Patients being treated with MAOIs can receive local anesthetic solutions containing levonordefrin 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 hydrochloride 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 perform a clinical examination and oral prophylaxis at three-month follow-up visits and apply a fluoride gel at a fluorine concentration of at least 10,000 parts per million. Dentists also should correct any defects in the natural dentition or in prostheses during these recall visits. Patients may experience enhanced self-esteem as a result of dental treatment, which may contribute to the psychotherapeutic aspect of management.


   CONCLUSION
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
REFERENCES
 
We must emphasize that dentistry, in concert with medicine, has much to offer patients with MDD. Our goal is to encourage dentists to recognize patients with occult MDD, make knowledgeable referrals to mental health practitioners for confirmation of the diagnosis and treatment, and to offer these patients the full range of dental treatment options.



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  		Dr. Friedlander is associate chief of staff for graduate medical education, Veterans Affairs Greater Los Angeles Healthcare System (14), 11301 Wilshire Blvd., Los Angeles, Calif. 90073, e-mail "arthur.friedlander{at}med.va.gov". He also is the director of quality assurance, Hospital Dental Service, University of California Los Angeles Medical Center, and a professor of oral and maxillo-facial surgery, University of California Los Angeles School of Dentistry. Address reprint requests to Dr. Friedlander.

 


   FOOTNOTES
 

Dr. Mahler is the vice president for specialty and hospital-based services, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, an attending neurologist, Neurobehavior Clinic at the Veterans Affairs Greater Los Angeles Healthcare System, and a clinical professor of neurology, University of California Los Angeles School of Medicine.


   REFERENCES
TOP
 ABSTRACT
 EPIDEMIOLOGY OF MAJOR DEPRESSIVE...
 PATHOPHYSIOLOGY
 MEDICAL MANAGEMENT
 DENTAL FINDINGS
 DENTAL TREATMENT OF PATIENTS...
 CONCLUSION
 REFERENCES
 

  1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (DSM-IV). 4th ed. Washington: American Psychiatric Association; 1994:317–89.

  2. Mulsant BH, Ganguli M. Epidemiology and diagnosis of depression in late life. J Clin Psychiatry 1999;60(suppl 20):9–15.[Medline]

  3. Judd LL. Pleomorphic expressions of unipolar depressive disease: summary of the 1996 CINP President’s Workshop. J Affect Disord 1997;45(1–2):109–16.[Medline]

  4. Judd LL, Akiskal HS, Zeller PJ, et al. Psychosocial disability during long-term course of unipolar depressive disorder. Arch Gen Psychiatry 2000;57(4):375–80.[Abstract/Free Full Text]

  5. Druss BG, Rosenheck RA. Patterns of health care costs associated with depression and substance abuse in a national sample. Psychiatr Serv 1999;50(2):214–8.[Abstract/Free Full Text]

  6. Pearson SD, Katzelnick DJ, Simon GE, Manning WG, Helstad CP, Henk HJ. Depression among high utilizers of medical care. J Gen Intern Med 1999;14(8):461–8.[Medline]

  7. Mueller TI, Leon AC, Keller MB, et al. Recurrence after recovery from major depressive disorder during 15 years of observational follow-up. Am J Psychiatry 1999;156(7):1000–6.[Abstract/Free Full Text]

  8. Murray CJ, Lopez AD, eds. The global burden of disease. Cambridge, Mass.: Harvard University Press; 1996:21.

  9. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence for DSM-III-R psychiatric disorders in the United States: results from the National Comorbidity Survey. Arch Gen Psychiatry 1994;51(1):8–19.[Abstract/Free Full Text]

  10. Weissman MM, Bland RC, Canino GJ, et al. Cross-national epidemiology of major depression and bipolar disorder. JAMA 1996; 276(4):293–9.[Abstract/Free Full Text]

  11. Andrew M, McGuffin P, Katz R. Genetic and non-genetic subtypes of major depressive disorder. Br J Psychiatry 1998;173:523–6.[Abstract/Free Full Text]

  12. Kendler KS, Prescott CA. A population-based twin study of lifetime major depression in men and women. Arch Gen Psychiatry 1999;56(1):39–44.[Abstract/Free Full Text]

  13. Patten SB. Long-term medical conditions and major depression in the Canadian population. Can J Psychiatry 1999;44(2):151–7.[Medline]

  14. Musselman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment. Arch Gen Psychiatry 1998;55(7):580–92.[Abstract/Free Full Text]

  15. Snow V, Lascher S, Mottur-Pilson C. Pharmacologic treatment of acute major depression and dysthymia. American College of Physicians–American Society of Internal Medicine. Ann Intern Med 2000;132(9):738–42.[Free Full Text]

  16. Patten SB, Metz LM, Reimer MA. Biopsychosocial correlates of lifetime major depression in a multiple sclerosis population. Mult Scler 2000;6(2):115–20.[Abstract/Free Full Text]

  17. Poewe W, Luginger E. Depression in Parkinson’s disease: impediments to recognition and treatment options. Neurology 1999;52(7 suppl 3):S2–6.[Medline]

  18. Penninx BW, Geerlings SW, Deeg DJ, van Eijk JT, van Tilburg W, Beekman AT. Minor and major depression and the risk of death in older persons. Arch Gen Psychiatry 1999;56(10):889–95.[Abstract/Free Full Text]

  19. Abraham HD, Fava M. Order of onset of substance abuse and depression in a sample of depressed outpatients. Compr Psychiatry 1999;40(1):44–50.[Medline]

  20. Blair-West GW, Cantor CH, Mellsop GW, Eyeson-Annan ML. Lifetime suicide risk in major depression: sex and age determinants. J Affect Disord 1999;55(2–3):171–8.[Medline]

  21. Meagher D, Murray D. Depression. Lancet 1997;349(suppl 1): 117–20.

  22. Kendler KS, Karkowski LM, Prescott CA. Causal relationship between stressful life events and the onset of major depression. Am J Psychiatry 1999;156(6):837–41.[Abstract/Free Full Text]

  23. De Marco RR. The epidemiology of major depression: implications of occurrence, recurrence, and stress in a Canadian community sample. Can J Psychiatry 2000;45(1):67–74.[Medline]

  24. Musselman DL, DiBattistia C, Nathan KI, Kilts CD, Schatzberg AF, Nemeroff CB. Biology of mood disorders. In: American Psychiatric Press textbook of psychopharmacology. 2nd ed. Washington: American Psychiatric Press; 1998:550–8.

  25. Drevets WC. Prefrontal cortical-amygdalar metabolism in major depression. Ann N Y Acad Sci 1999;877:614–37.[Medline]

  26. Brody AL, Saxena S, Silverman DH, et al. Brain metabolic changes in major depressive disorder from pre- to post-treatment with paroxetine. Psychiatry Res 1999;91(3):127–39.[Medline]

  27. Scott J. Treatment of chronic depression. N Engl J Med 2000;342(20):1518–20.[Free Full Text]

  28. Goldman LS, Nielsen NH, Champion HC. Awareness, diagnosis, and treatment of depression. J Gen Intern Med 1999;14(9):569–80.[Medline]

  29. Scott J. Where there’s a will: cognitive therapy for people with chronic depressive disorders. In: Tarrier N, Wells A, Haddock G, eds. Treating complex cases: The cognitive behavioural therapy approach. Chichester, England: Wiley; 1998:81–104.

  30. Clinical practice guideline number 5: depression in primary care, 2—treatment of major depression. Rockville, Md.: U.S. Department of Health and Human Services, Agency for Health Care Policy and Research; 1993. AHCPR publication 93–0551.

  31. Williams JW, Mulrow CD, Chiquette E, Noel PH, Aguilar C, Cornell J. A systematic review of newer pharmacotherapies for depression in adults: evidence report summary. Ann Intern Med 2000;132(9): 743–56.[Abstract/Free Full Text]

  32. Montgomery SA, Henry J, McDonald G, et al. Selective serotonin reuptake inhibitors: a meta-analysis of discontinuation rates. Int Clin Psychopharmacol 1994;9(1):47–53.[Medline]

  33. Edwards JG, Anderson I. Systematic review and guide to selection of selective serotonin reuptake inhibitors. Drugs 1999;57(4): 507–33.[Medline]

  34. Spigset O. Adverse reactions to selective serotonin reuptake inhibitors: reports from a spontaneous reporting system. Drug Saf 1999;20(3):277–87.[Medline]

  35. Horst WD, Preskorn SH. Mechanisms of action and clinical characteristics of three atypical antidepressants: venlafaxine, nefazodone, bupropion. J Affect Disord 1998;51(3):237–54.[Medline]

  36. Majeroni BA, Hess A. The pharmacologic treatment of depression. J Am Board Fam Pract 1998;11(2):127–39.[Medline]

  37. Lebowitz BD, Pearson JL, Schneider LS, et al. Diagnosis and treatment of depression in late life: consensus statement update. JAMA 1997;278(14):1186–90.[Abstract/Free Full Text]

  38. Baldessarini RJ. Drugs and the treatment of psychiatric disorders. In: Hardman JG, Limbird LE, Molinoff PB, Ruddon RW, Gilman AG, eds. Goodman & Gilman’s the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill; 1996:431–59.

  39. Frank E, Thase ME. Natural history and preventative treatment of recurrent mood disorders. Ann Rev Med 1999;50:453–68.[Medline]

  40. Keller MB, McCullough JP, Klein DN, et al. A comparison of nefazodone, the cognitive behavioral-analysis system of psychotherapy, and their combination for the treatment of chronic depression. N Engl J Med 2000;342(20):1462–70.[Abstract/Free Full Text]

  41. Tew JD, Mulsant BH, Haskett RF, et al. Acute efficacy of ECT in the treatment of major depression in the old-old. Am J Psychiatry 1999;156(2):1865–70.[Abstract/Free Full Text]

  42. Blier P, de Montigny C. Serotonin and drug-induced therapeutic response in major depression, obsessive-compulsive and panic disorders. Neuropsychopharmacology 1999;21(2 suppl):91S–8S.[Medline]

  43. Sackeim HA, Prudic J, Devanand DP, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328(12):839–46.[Abstract/Free Full Text]

  44. Dubovsky SL. Electroconvulsive therapy. In: Kaplan HI, Sadock BJ, eds. Comprehensive textbook of psychiatry/VI. 6th ed. Baltimore: Williams & Wilkins; 1995:2129–40.

  45. Bailine SH, Rifkin A, Kayne E, et al. Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry 2000;157(1): 121–3.[Abstract/Free Full Text]

  46. Physicians’ desk reference. 54th ed. Montvale, N.J.: Medical Economics; 2000.

  47. Elter JR, Beck JD, Slade GD, Offenbacher S. Etiologic models for incident periodontal attachment loss in older adults. J Clin Periodontol 1999;26(2):113–23.[Medline]

  48. Monteiro da Silva AM, Oakley DA, Newman HN, Nohl FS, Lloyd HM. Psychosocial factors and adult onset rapidly progressive periodontitis. J Clin Periodontol 1996;23(8):789–94.[Medline]

  49. da Silva AM, Newman HN, Oakley DA. Psychosocial factors in inflammatory periodontal diseases: a review. J Clin Periodontol 1995;22:516–26.[Medline]

  50. Kurer JR, Watts TL, Weinman J, Gower DB. Psychological mood of regular dental attenders in relation to oral hygiene behaviour and gingival health. J Clin Periodontol 1995;22(1):52–5.[Medline]

  51. Moss ME, Beck JD, Kaplan BH, et al. Exploratory case-control analysis of psychosocial factors and adult periodontitis. J Periodontol 1996;67(10 suppl):1060–9.[Medline]

  52. Schleifer SJ, Keller SE, Bartlett JA, Eckholdt HM, Delaney BR. Immunity in young adults with major depressive disorder. Am J Psychiatry 1996;153(4):477–82.[Abstract/Free Full Text]

  53. Gerber PE, Lynd LD. Selective serotonin-reuptake inhibitor-induced movement disorders. Ann Pharmacother 1998;32(6):692–8.[Abstract]

  54. Brown ES, Hong SC. Antidepressant-induced bruxism successfully treated with gabapentin. JADA 1999;130(10):1467–9.[Abstract/Free Full Text]

  55. Study shows link between antidepressants, bruxism. JADA 2000;131(3):297.[Free Full Text]

  56. Bostwick JM, Jaffee MS. Buspirone as an antidote to SSRI-induced bruxism in 4 cases. J Clin Psychiatry 1999;60(12):857–60.[Medline]

  57. Amsterdam JD, Settle RG, Doty RL, Abelman E, Winokur A. Taste and smell perception in depression. Biol Psychiatry 1987;22(2):1481–5.[Medline]

  58. Anttila SS, Knuuttila ML, Sakki TK. Depressive symptoms favor abundant growth of salivary lactobacilli. Psychosom Med 1999;61(4): 508–12.[Abstract/Free Full Text]

  59. Wallin MS, Rissanen AM. Food and mood: relationship between food, serotonin and affective disorders. Acta Psychiatr Scand Suppl 1994;377:36–40.[Medline]

  60. Christensen L, Somers S. Comparison of nutrient intake among depressed and nondepressed individuals. Int J Eat Disord 1996;20(1): 105–9.[Medline]

  61. Potter W, Manji H, Rudorfer M. Tricyclics and tetracyclics. In: Schatzberg A, Nemeroff C, eds. The American Psychiatric Press textbook of psychopharmacology. 2nd ed. Washington: American Psychiatric Press; 1998:199–218.

  62. Gallagher RM, Marbach JJ, Raphael KG, Dohrenwend BP, Cloitre M. Is major depression comorbid with temporomandibular pain and dysfunction syndrome? A pilot study. Clin J Pain 1991;7(3):219–25.[Medline]

  63. Korszun A, Hinderstein B, Wong M. Comorbidity of depression with chronic facial pain and temporomandibular disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;82(5):496–500.[Medline]

  64. Gatchel RJ, Garofalo JP, Ellis E, Holt C. Major psychological disorders in acute and chronic TMD: an initial examination. JADA 1996;127(9):1365–74.[Abstract/Free Full Text]

  65. Sternberg EM, Young WS, Bernardini R, et al. A central nervous system defect in biosynthesis of corticotropin-releasing hormone is associated with susceptibility to streptococcal cell wall-induced arthritis in Lewis rats. Proc Natl Acad Sci USA 1989;86(12):4771–5.[Abstract/Free Full Text]

  66. Marbach JJ. Medically unexplained chronic orofacial pain: temporomandibular pain and dysfunction syndrome, orofacial phantom pain, burning mouth syndrome, and trigeminal neuralgia. Med Clin North Am 1999;83(3):691–710.[Medline]

  67. Bergdahl M, Bergdahl J. Burning mouth syndrome: prevalence and associated factors. J Oral Pathol Med 1999;28(8):350–4.[Medline]

  68. Drage LA, Rogers RS. Clinical assessment and outcome in 70 patients with complaints of burning or sore mouth symptoms. Mayo Clin Proc 1999;74(3):223–8.[Abstract]

  69. Demange C, Husson C, Poi-Vet D, Escande JP. Paresthesies buccales psychogenes et depresion: une approche psychanalytique [Burning mouth syndromes and depression: a psychoanalytic approach]. Rev Stomatol Chir Maxillofac 1996;97(4):244–52.[Medline]

  70. Korszun A, Ship JA. Diagnosing depression in patients with chronic pain. JADA 1997;128:1680–6.[Abstract/Free Full Text]

  71. Callahan AM, Marangell LB, Ketter TA. Evaluating the clinical significance of drug interactions: a systematic approach. Harv Rev Psychiatry 1996;4(3):153–8.[Medline]

  72. Ganzberg S. Psychoactive drugs. In: ADA guide to dental therapeutics. 2nd ed. Chicago: ADA Publishing, a division of ADA Business Enterprises Inc.; 2000:376–405.

  73. Broquet KE. Status of treatment of depression. South Med J 1999;92(9):846–56.[Medline]

  74. Yagiela JA. Adverse drug interactions in dental practice: interactions associated with vasoconstrictors—part V of a series. JADA 1999;130(5):701–9.[Abstract/Free Full Text]




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