Major Depressive Disorder is a mental illness of at least two weeks duration during which time there is dysphoria (intense sadness) and/or anhedonia, (a loss of interest or pleasure in previously enjoyed activities such as music or sports, social interactions and sexual interaction). A sense of worthlessness, loss of self-esteem, guilt with preoccupation over past minor failings and thoughts of suicide are common. In addition, the patient or a family member may note alterations in appetite that result in weight loss, insomnia characterized by early awakening, self-neglect of personal hygiene, an inability to sit still (agitation), sad-fixed facial expression, slowed speech and body movements (psychomotor retardation), a lack of energy, and an impaired ability to concentrate. This cluster of symptoms is emotionally painful and may cause the individual to withdraw from social and employment activities.1,2 Depression in the elderly is at times more difficult to discern. Elderly individuals often express depression with somatic complaints (bodily aches and pains) and memory impairment but lack a dysphoric mood.3
Prevalence rates for depression determined by a recent sample of respondents selected by Statistics Canada from enumeration areas for the Ontario Health Study reveal 1-year and lifetime prevalence rates of 10.4% and 24.4% respectively.4 These rates are confirmed by yet another recent study conducted in Calgary which determined that the 1 year prevalence rate of major depression was approximately 11%.5 The Ontario Health Study and a study conducted in the 1980s in Edmonton noted that the twelve month and lifetime prevalence rates of depression are twice as high for women as they are for men.6 The reasons for this remain unclear but are probably related to a combination of social and biological influences.7
Only 50% of patients recover fully from depression, 35%-40% recover partially and continue to have residual symptoms; and 10% to 15% do not improve at all despite appropriate treatment.8 Incomplete recovery (that is, persistent symptoms) is associated with impaired function, frequent need for public assistance, absenteeism at work, and social withdrawal. The risk of recurrence for individuals with or without persistent symptoms is 50% after one episode, 70% after a second episode and 90% after a third.
Individuals at highest risk for a first episode of depression are those with a family history of the disease and those who are unemployed, separated, or divorced.9 In addition, there is an increasing prevalence of the disease among the elderly, (> 65 years) especially widows, and men and women with physical illness, physical disablement and high levels of socio-economic deprivation.10 Individuals with depression are very high consumers of general health care, and approximately one-third develop a substance (alcohol, illicit drugs) abuse disorder within their lifetime, and a significant number attempt or complete suicide.11-16
The etiology of depression remains ill defined, however data from longitudinal family studies does demonstrate that emotional stressors such as adversities in early life and/or those of a contemporary nature (death of a child or spouse), reduce blood flow and metabolism in the brain’s limbic system (most notably the amygdala, cingulate cortex and hippocampus) which regulates emotion, sleep, appetite and libido.17,18 This results in a deficiency of the neurotransmitters noradrenaline and serotonin at the synapses between presynaptic neurones (axon) and postsynaptic neurones (dendrite), thus hindering the transmission of impulses along the system’s neural pathways. Emotional stress also causes the hypothalamus to hypersecrete corticotrophin-releasing factor (CRF). This in turn adversely affects the endocrine system because of the rich neuronal connections between the hypothalamus and the pituitary gland. This hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis alters levels of numerous endocrine gland hormones, most notably a rise in circulatory cortisol levels.19
Family practitioners (FPs) usually prescribe antidepressants to manage patients with mild or moderate depressive disorder. Brief psychotherapy while shown to be equally effective for these patients is not often employed because FPs frequently lack the time or skills to counsel patients.20-22 However, individuals with severe episodes of the disorder are often treated by a psychiatrist with both medication and psychotherapy.23 Electroconvulsive therapy is prescribed for those resistant or intolerant of medication and those at risk of imminent death because of a refusal to eat or severe suicidal impulses.24
The Canadian Network for Mood and Anxiety Treatments recommends the use of almost two dozen antidepressants.25 Pharmacologists have divided them into four groups: [tricyclic and related antidepressants (TCAs), selective serotonin re-uptake inhibitors (SSRIs), “other” antidepressant drugs and monoamine oxidase inhibitors (MAOIs)], based on their mechanisms of action (Table 1).26 Physicians choose a medication based on the patient’s symptoms, side effects profile, presence of concurrent medical illness, and cost effectiveness.27 The medications are effective approximately 75% of the time but they take 2-4 weeks to work successfully. The medication regime usually remains in force for months or more after recovery because too rapid a withdrawal is associated with relapse.28
The tricyclic antidepressants (e.g. amitriptyline and desipramine) exert their effect by preventing presynaptic neurones from reabsorbing (blocking re-uptake) noradrenaline and serotonin from the synaptic cleft for recycling. Thus the concentration of these two neurotransmitters is elevated and neuronal activity increased. In the early 1990s the TCAs accounted for approximately 50% of all new prescriptions written for depression however, 40% of patients become non-compliant with the medication because of their significant antimuscarinic side effects.29 These include xerostomia (in 50% of patients), urinary retention, constipation, increased intra-ocular pressure, cardiac arrhythmias, and postural hypotension.
The selective serotonin re-uptake inhibitors (e.g. fluoxetine) exert their antidepressant effect by preventing presynaptic neurones from reabsorbing (“re-uptake”) serotonin (5-hydroxytrytamine; 5-HT) from the synaptic cleft for recycling.30 Thus, the concentration of serotonin in the cleft is heightened and neuronal activity is enhanced. Unlike the majority of TCAs, these medications are not lethal in overdose and are less sedating and have fewer antimuscarinic (causing xerostomia in only 18% of patients) and cardiotoxic effects.31 These medications do however frequently cause gastrointestinal distress, insomnia, agitation, sexual dysfunction, and on occasion an increase in bleeding time.32,33 By the late 1990s the SSRIs were increasingly being used as the first-line agents in the treatment of depression.34
A third group, known as the “other” antidepressants consists of a heterogeneous collection of medications which exert their effects through varied mechanisms. Bupropion’s exact antidepressant mechanism remains illusive, however it does weakly block the reuptake of serotonin, norepinephrine and dopamine. Nefazodone inhibits re-uptake of serotonin and also selectively blocks serotonin receptors. Venlafaxine acts as a serotonin and noradrenaline re-uptake inhibitor (SNRI).
The monoamine oxidase inhibitors (e.g. phenelzine) exert their antidepressant effect by preventing monoamine oxidase (MAO) A and B from breaking down (metabolizing) noradrenaline and serotonin in the synaptic cleft. Thus the concentrations of these two neurotransmitters are elevated and neuronal activity is enhanced. The MAOIs are reserved for those whose depression has been refractory to a course of TCAs, SSRIs or the “other” antidepressants. The rationale for the limited use of these medications (less than 10% of antidepressant prescriptions) arises because of dangerous dietary and drug-drug interactions which may cause severe hypertension. MAOIs prevent the gut wall and liver from inactivating exogenous amines (e.g. tyramine found in aged cheeses, meats, and red wine). The amines reach the systemic circulation and thence noradrenergic nerve endings where they release noradrenaline resulting in vasoconstriction; hypertension and possibly death from an intracranial hemorrhage. Severe hypertension may also occur when a patient concurrently takes an MAOI and an indirect-acting sympathomimetic medication such as ephedrine which is found in decongestant preparations.35 Other major side effects associated with the use of MAOIs are dizziness, orthostatic hypotension, restlessness, insomnia, dry mouth and weight gain.
Moclobemide, a reversible inhibitor of monoamine oxidase type A (RIMA) differs from the traditional (irreversible) MAOIs in that it produces significantly less potentiation of oral tyramine, however patients are advised to avoid consuming large amounts of tyramine-rich foods. Similarly, the risk of adverse drug interactions with sympathomimetics such as ephedrine, pseudophedrine and phenylpropanolamine is claimed to be less but patients still need to avoid these medications. Adverse drug interactions, specifically with opiods occur frequently and must be avoided. The drug is well tolerated by the elderly for it does not affect blood pressure, psychomotor performance, nor cause insomnia, dry mouth and weight gain.
Electroconvulsive therapy (ECT) is reserved for patients with severe depression unresponsive to medication, refusal to eat, or multiple attempts at suicide.36 It is administered with a general anesthetic, and muscle relaxant (which attenuates the skeletal muscle contractions of the seizure) two times a week for several weeks until the patient improves. The electrical stimulus administered to the brain via electrodes placed on the temples stimulates the centrencephalic structures to produce a bilateral gran mal seizure. The resultant depolarization of neurones alters cerebral blood flow and metabolism, stimulates the hypothalamus to discharge its hormones restoring the normal interactions among HPA hormones and renders the neuronal membranes more responsive to neurotransmitters, thereby enhancing neuronal activity.37 As noted in the University of British Columbia study, this results in approximately 75% of patients having remission of their depression.38 Medical complications are rare, however, the procedure is associated with a brief headache, and possibly, temporary amnesia.39
Irrespective of these issues, two thirds of patients who have had ECT report that the experience was no more upsetting than a visit to the dentist.40
The British Royal Colleges of Psychiatrists and Anesthesiologists recommend that an anesthetist assess the patient prior to ECT in order to determine the health of the dentition and temporomandibular joint (TMJ). The Colleges warn that broken or loose teeth may be aspirated during treatment, and that upper airway obstruction due to arthritis of the TMJ, dental abscesses and facial deformity may preclude treatment.41 During the procedure, an anesthetist applies a bite-block between the maxillary and mandibular teeth to protect them and the tongue from clenching which results from the stimulation of the masseter muscles.42
Individuals with untreated depression often exhibit psychomotor retardation with reduced facial muscle activity as measured by electromyography. This may explain the often encountered fixed facial expression and deep furrows in the forehead and beside the mouth.43 Individuals with untreated depression are also at high risk of developing rampant dental decay because of a disinterest in performing oral hygiene, a preference for carbohydrates because of reduced serotonin centrally, a craving for intense sweets (because of impaired taste perception), and a high lactobacillus count.44-47 Patients being treated for depression are also at high risk of developing rampant dental decay because most of the antidepressants cause xerostomia by blocking parasympathetic stimulation of the salivary glands. Long-term use of TCA’s is also associated with an increase in dental decay because these medications induce a craving for carbohydrates.48
Individuals who report a great number of signs associated with depression are also prone to suffer periodontitis.49-52 It is hypothesized that neglect of oral hygiene, xerostomia, increase in smoking and altered immune response facilitate increased colonization by pathogenic bacteria. This leads to a breakdown of the periodontal attachment.53,54 Individuals receiving SSRIs or the “other antidepressants” may on occasion develop a movement disorder which includes clenching and/or grinding of the teeth (bruxism) further worsening the periodontal condition.55-57 This may occur because these medications increase extrapyramidal levels of serotonin thereby inhibiting dopaminergic pathways which control movements.58
A typical facial pain (“neuralgia”), burning sensation of the oral mucosa (often on the tongue), or some temporomandibular joint disorder are frequently the somatic complaints that bring the depressed patient to the dentist.59,60 It is 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.61-67
The results of the initial drug approval trials for some of the most frequently prescribed medications from each of the four groups of antidepressants confirm a significant number of adverse orofacial reactions.68 These complications, include: xerostomia, sialadenitis, gingivitis, stomatitis dysgeusia and edema and discoloration of the tongue are delineated on Tables 2-5.
Some patients receiving psychiatric treatment for depression may be reluctant to admit it because of local or historic stigma associated with mental illness. In order to overcome such barriers and obtain necessary information, the dentist should display a supportive, non-judgmental attitude and advise their patients that such information will be held confidential and is indispensable to the provision of safe dental care.
Depressed patients may on occasion be uncooperative and irritable during dental treatment and may appear unappreciative because of numerous complaints that are inconsistent with objective findings.69 Before a patient begins dental treatment, their FP should be consulted. Information requested should include the patient’s current psychological status and current psychotropic medication regimen. The physician must also be questioned as to the patient’s history of alcohol or other substance abuse. Patients with a history of alcohol abuse should have liver function tests (blood serum levels of albumin and total proteins), a complete blood cell count, and a coagulation profile (prothrombin time and partial thromboplastin time).
Preventive dental education is paramount for these patients and their families. They should receive instruction in proper tooth brushing and flossing methods that maximize dental plaque removal. Artificial salivary products, antiseptic mouthwash, and a 0.05% sodium fluoride mouthrinse are prescribed for many patients with signs of xerostomia. Dental treatment should consist of subgingival scaling, root planing and curettage, caries control, application of fluoride gel, and dental restorations. Profound local anesthesia is mandatory to adequately perform these procedures in depressed and often anxious individuals.
Use of local anesthetic solutions containing adrenaline as a vasoconstrictor for patients receiving TCAs is controversial because of fear of precipitating a hypertensive crisis, and/or a cardiac arrhythmia. The primary mechanism for terminating the pressor action of adrenergic amines (e.g. epinephrine) is their re-uptake by sympathetic nerve fibers which precludes their continued access to receptor sites, however TCAs block this re-uptake process. The TCAs also block muscarinic and (1-adrenergic receptors thereby directly depressing the heart. Thus, it is feared by some that the combination of a TCA and adrenaline may result in an increase in systolic blood pressure and/or a cardiac arrhythmia. Therefore, Howe and Whitehead recommend standard doses of anesthetic solutions that do not contain epinephrine, for instance, 3% mepivacaine.70 However, the editors of the British Dental Practitioners’ Formulary (DPF) and Meechan, Robb and Seymour have not seen any untoward results and they conclude that the amount of adrenaline used in dental anesthetic preparations is too insignificant to interact with the TCAs.71,72 Prudence, however, dictates the latter group of authors to recommend administering no more than two carpules of 2% lidocaine with 1/100,000 epinephrine and that great care be taken to avoid intravenous administration.
Other adverse drug interactions between TCAs and medications used in dentistry may occur. The respiratory depressant effects of narcotic analgesics are potentiated by tricyclics and the barbiturates may accelerate the metabolism of TCAs thereby attenuating their antidepressant effects. 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. Lastly, care should be observed when prescribing acetaminophen because of its ability to decrease the metabolic rate of TCAs.73
Adverse interactions between the SSRI’s and some medications used in dentistry may occur because these antidepressants inhibit certain metabolic pathways. Specifically the SSRI’s inhibit the cytochrome 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.74
Patients taking MAOIs (including Moclobemide) can receive local anesthetic solutions containing adrenaline because the MAOIs do not potentiate the pressor or cardiac effects of this direct-acting sympathomimetic.75 However, the prescribing of meperidine hydrochloride or dihydrocodeine for these patients should be avoided or the dosages markedly reduced because of a potentially toxic interaction in which there is either severe CNS excitation (i.e., restlessness, muscular rigidity, hyperpyrexia and hyperreflexia) or severe CNS depression (i.e., respiratory depression, hypotension, and coma).76
At 3-month follow-up visits a clinical examination, oral prophylactics, and application of a fluoride gel at a fluorine 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 and may contribute to the psychotherapeutic aspect of management.
We wrote this paper to familiarize dentists with major depressive disorder so that they could safely and compassionately treat those with previously diagnosed disease. We also wrote this paper to help dentists recognize individuals who present to them with oral manifestations and an affect that is consistent with occult depression so that they could knowledgeably refer them to a physician for evaluation and treatment. This latter scenario is quite plausible because the majority of cases of depression in the community are neither recognized, diagnosed nor treated. In addition, it would be imprudent not to acknowledge that some within our own profession suffer from this disorder, either diagnosed or occult and hopefully this material will also benefit them. It must be emphasized that dentistry in concert with medicine has much to offer patients with depression.OH
Dr. Friedlander is Associate Chief of Staff for Graduate Medical Education, VA Greater Los Angeles Healthcare System, Director of Quality Assurance, Hospital Dental Service, UCLA Medical Center, and Professor of Oral and Maxillofacial Surgery, UCLA School of Dentistry, Los Angeles, CA.
Mrs. Friedlander is a Public Health Nurse at the Mid-Valley Health Center/Los Angeles County Department of Health in Van Nuys, California and a Research Associate at the VA Sepulveda Dental Service, Sepulveda, CA.
Oral Health welcomes this original article.
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