Manejo Dental

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 VOLUME 39 NUMBER 2 FEBRUARY  2008  139 QUINTESSENCE INTERNATIONAL  Thyroid activity is controlled by the hypothal- amic-pituitary-thyroid axis. Thyroid-releasing hormone (TRH), secreted by the hypothala- mus, induces the secretion of thyroid stimu- lating hormone (TSH) by the anterior pitu- itary, which in turn stimulates thyroid hor- mone synthesis and secretion by the thyroid gland. 1–3 The thyroid gland is a bilobular structure that lies on either side of the tra- chea. 1 Its functional unit is the thyroid follicle made up of thyroid follicular cells (TFCs). 4 TFCs selectively remove iodine from the blood and synthesize iodothyronines (thyrox- ine [T 4 ], triiodothyroxine [T 3 ], and reverse  triiodot hyron ine [rT 3 ]). 1 The enzyme respon- sible for the synthesis of iodothyronines is  thyr oid pero xidase (TPO). The appro ximate proportions of T 4 , T 3 , and rT 3 produced are 90%, 10%, and less than 1%, respectively. rT 3 appears to have no biologic function. 5 Once secreted into the bloodstream, approximately 70% of T 4 and T 3 binds to thyroxine-binding globulin (TBG), while the remaining 30% binds to transthyretin, albumin, and lipopro-  teins. 1 A small percentage of T 3 and T 4 (< 0.2%) circulates in an unbound, free state and acts to maintain physiological hormone levels by negative feedback mechanisms involving the hypothalamus, pituitary, and  thyr oid gland s. 6 Risk stratification and dental management of the patient with thyroid dysfunction Michaell A. Huber, DDS 1  /Géz a T. Terézhalmy, DDS, MA 2 The thyroid gland produces hormones critical to the maintenance of the cellular metabolic rate. The actions of these hormones are far-reaching, affecting thermoregulation and calorigenesis; the metabolism of carbohy drates, fats, and proteins; and oxygen utilization. Thyroid hormon es also appear to act synergistically with epinephrine and enhance tissue sensitivity to catecholamines. Signs and symptoms of hypothyr oidism include listlessness, fatigue, cold intolerance, dry skin, hair loss, constipation, weight gain, muscle soreness, and slow heart rate. Signs and symptoms of hyperthyroidism include irritability, heat intol- erance, tremors, increased sweating, frequent bowel movements, and quickened heart rate. The effect of inadequately treated or undiagnosed hyperthyroidism on the heart car- ries perioperative risks. To provide competent dental care to patients with thyroid dysfunc-  tion, clinicians must understand the disease, its treatment, and the impact the disease and its treatment may have on the patient’s ability to undergo and respond to dental care. (Quintessence Int 2008;39:139–150) Key words: dental care, hyperthyroid, hypothyroid, thyroid dysfunction 1 Associate Prof essor and Head, Division of Oral Medicine, Department of Dental Dia gnostic Science, The University of  Texas Health Science Cente r at San Antonio,Dental School, San Antonio,Texas. 2 Endowed Professor in C linical Dentistry, Dental School, and Professor, Department of Pharmacology, Graduate School of Biomedical Sciences, The University of T exas Health Science Center at San Antonio,San Antonio,Texas. Correspondence: Dr Michaell A. Huber , Divisi on of Or al Medicine, Depart ment of Dental Diagnosti c Science, The University of Texas Health Science Center at San Antonio,Dental School , Mail Code 7919 , 7703 F loyd Cur l Drive, San Ant onio,  Texas, 78229-3900. Fax: 210-567-6348. E-mail: huberm@ uthscsa.edu COPYRIGHT © 2008 BY QUINTESSENCE PUBLISHING CO, INC. PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY. NO PART OF THIS ARTICLE MAY BE REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER

description

pacientes con problemas de tiroides

Transcript of Manejo Dental

  • VOLUME 39 NUMBER 2 FEBRUARY 2008 139

    QUINTESSENCE INTERNATIONAL

    Thyroid activity is controlled by the hypothal-

    amic-pituitary-thyroid axis. Thyroid-releasing

    hormone (TRH), secreted by the hypothala-

    mus, induces the secretion of thyroid stimu-

    lating hormone (TSH) by the anterior pitu-

    itary, which in turn stimulates thyroid hor-

    mone synthesis and secretion by the thyroid

    gland.13 The thyroid gland is a bilobular

    structure that lies on either side of the tra-

    chea.1 Its functional unit is the thyroid follicle

    made up of thyroid follicular cells (TFCs).4

    TFCs selectively remove iodine from the

    blood and synthesize iodothyronines (thyrox-

    ine [T4], triiodothyroxine [T3], and reverse

    triiodothyronine [rT3]).1 The enzyme respon-

    sible for the synthesis of iodothyronines is

    thyroid peroxidase (TPO). The approximate

    proportions of T4, T3, and rT3 produced are

    90%, 10%, and less than 1%, respectively. rT3appears to have no biologic function.5 Once

    secreted into the bloodstream, approximately

    70% of T4 and T3 binds to thyroxine-binding

    globulin (TBG), while the remaining 30%

    binds to transthyretin, albumin, and lipopro-

    teins.1 A small percentage of T3 and T4(< 0.2%) circulates in an unbound, free state

    and acts to maintain physiological hormone

    levels by negative feedback mechanisms

    involving the hypothalamus, pituitary, and

    thyroid glands.6

    Risk stratification and dental management of the patient with thyroid dysfunctionMichaell A. Huber, DDS1/Gza T. Terzhalmy, DDS, MA2

    The thyroid gland produces hormones critical to the maintenance of the cellular metabolic

    rate. The actions of these hormones are far-reaching, affecting thermoregulation and

    calorigenesis; the metabolism of carbohydrates, fats, and proteins; and oxygen utilization.

    Thyroid hormones also appear to act synergistically with epinephrine and enhance tissue

    sensitivity to catecholamines. Signs and symptoms of hypothyroidism include listlessness,

    fatigue, cold intolerance, dry skin, hair loss, constipation, weight gain, muscle soreness,

    and slow heart rate. Signs and symptoms of hyperthyroidism include irritability, heat intol-

    erance, tremors, increased sweating, frequent bowel movements, and quickened heart

    rate. The effect of inadequately treated or undiagnosed hyperthyroidism on the heart car-

    ries perioperative risks. To provide competent dental care to patients with thyroid dysfunc-

    tion, clinicians must understand the disease, its treatment, and the impact the disease and

    its treatment may have on the patients ability to undergo and respond to dental care.

    (Quintessence Int 2008;39:139150)

    Key words: dental care, hyperthyroid, hypothyroid, thyroid dysfunction

    1Associate Professor and Head, Division of Oral Medicine,

    Department of Dental Diagnostic Science, The University of

    Texas Health Science Center at San Antonio, Dental School, San

    Antonio, Texas.

    2Endowed Professor in Clinical Dentistry, Dental School, and

    Professor, Department of Pharmacology, Graduate School of

    Biomedical Sciences, The University of Texas Health Science

    Center at San Antonio, San Antonio, Texas.

    Correspondence: Dr Michaell A. Huber, Division of Oral

    Medicine, Department of Dental Diagnostic Science, The

    University of Texas Health Science Center at San Antonio, Dental

    School, Mail Code 7919, 7703 Floyd Curl Drive, San Antonio,

    Texas, 78229-3900. Fax: 210-567-6348. E-mail: huberm@

    uthscsa.edu

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  • 140 VOLUME 39 NUMBER 2 FEBRUARY 2008

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    ETIOLOGY AND EPIDEMIOLOGY

    T4 serves as a prohormone for the extrathy-

    roidal production of T3, which, in its free form,

    accounts for most of the biological activity of

    thyroid hormones.6 T3 stimulates RNA poly-

    merase and phosphoprotein kinases and the

    synthesis of nuclear proteins, which are

    involved in the regulation of growth and

    development; thermoregulation and calorige-

    nesis; the metabolism of carbohydrates, pro-

    teins, and lipids; and oxygen consumption.1

    Thyroid hormones also appear to act syner-

    gistically with epinephrine to enhance

    glycogenolysis and hyperglycemia and

    enhance tissue sensitivity to catecholamines.

    Yet, there appears to be a paradoxical

    inverse relationship between circulating nor-

    epinephrine and thyroid hormone levels.710

    While the myocardial effects of excess thy-

    roid hormone mimic a hyperadrenergic state,

    the levels of circulating catecholamines, in

    these scenarios, are actually low or normal. It

    is postulated that the increased sympath-

    omimetic response may be due to thyroid

    hormone-induced increase in myocardial

    sensitivity, increased responsiveness to !-

    adrenergic receptor activation or possibly an

    up-regulation of adrenergic receptors.7 The

    reduced peripheral resistance observed in

    thyroid excess may be associated with a

    reduced contractile response to norepineph-

    rine (possibly through !1-adrenergic and/or

    !2-adrenergic receptor modulation) and

    enhanced acetylcholine-induced vasodilata-

    tion.11 However, others postulate that

    increased endothelial production of nitric

    oxide (NO), observed in thyroid excess,

    underlies the reduced peripheral resistance

    observed.9

    Patients with thyroid dysfunction may be

    characterized as euthyroid, hypothyroid, or

    hyperthyroid to reflect normal, inadequate, or

    excessive hormonal secretion, respectively

    (Table 1).12 Some thyroid disorders manifest

    polar clinical progressions, whereby initial

    glandular hypersecretion evolves into a state of

    hyposecretion. Many of the more common thy-

    roid disorders (Graves disease, Hashimotos

    thyroiditis, postpartum thyroid dysfunction,

    and painless sporadic thyroiditis) represent

    autoimmune phenomenas.13,14 In addition to

    genetic predisposition, numerous environ-

    mental factors, such as low birth weight, iodine

    deficiency or excess, selenium deficiency, the

    use of oral contraceptives and other medica-

    tions, stress, allergy, smoking, ionizing radia-

    tion, and bacterial or viral infection, have been

    postulated to contribute to etiopathogenesis of

    autoimmune thyroid disease.14

    Disorders characterized by euthyroidismEuthyroid goiter (diffuse, nodular, multinodular)Benign tumorsMalignant tumors

    Differentiated (papillary, follicular)Undifferentiated (small cell, giant cell)Medullary

    ThyroiditisAcuteSubacute thyroiditis (de Quervains)Chronic autoimmune (Hashimotos disease)PostpartumReidels thyroiditis

    Disorders characterized by hypothyroidismWith hypothyroidism

    Primary hypothyroidismChronic autoimmune thyroiditis Iatrogenic (surgery, 131I [radioiodine] therapy)Diffuse and nodular goiterSevere iodine deficiency

    Neonatal congenital hypothyroidismSecondary hypothyroidism

    Pituitary hypothyroidismTertiary hypothyroidism

    Hypothalamic hypothyroidismWithout hypothyroidism

    Generalized and peripheral resistance to thyroidhormones

    Transient hypothyroidism (iodinedeficiency/excess, druginduced, postpartum)

    Disorders characterized by hyperthyroidismGlandular hyperfunction

    Diffuse hyperthyroid goiter with thyroid associatedophthalmopathy (Graves disease)

    Multinodular hyperthyroid goiter or Plummersdisease

    Autonomous noduleThyrotoxicosis (without thyroid gland hyperfunction)

    Excessive exogenous thyroid hormonesPost-inflammatory or from glandular destructionAmiodarone induced

    Transient hyperthyroidism

    Table 1 Common thyroid disorders12

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  • VOLUME 39 NUMBER 2 FEBRUARY 2008 141

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    The actual prevalence of thyroid disorders

    is unknown. The Thyroid Foundation of

    America estimates that 10 million Americans

    suffer from a hypothyroid disorder and 4.5

    million Americans suffer from a hyperthyroid

    disorder, of whom 8 million and 600,000,

    respectively, are undiagnosed.15 As is the

    case with most autoimmune diseases, there

    is a clear female preponderance, with a

    female-to-male ratio of about 5 to 10:1.14 An

    estimated 5% of individuals in the United

    States have palpable thyroid nodules, of

    which 95% are benign (roughly 85% hyper-

    plastic nodules, 15% adenomas, and less

    than 1% cysts).16 In 2006, an estimated

    30,180 cases of thyroid carcinoma were diag-

    nosed in the United States (7,590 men and

    22,590 women).17 Thyroid carcinoma is most

    frequently papillary (81%), followed by follicu-

    lar and Hrthle-cell (14%), medullary (3%),

    and anaplastic (2%) forms.16

    CLINICAL MANIFESTATIONS

    It must be emphasized that, in many cases,

    the natural history of a thyroid disorder may

    be marked by subtle periods of remission

    and exacerbations.12 Conversely, either

    extreme hypothyroidism or extreme hyper-

    thyroidism may evolve into a life-threatening

    medical emergency.

    HypothyroidismHypothyroidism is a clinical disease state

    occurring when there is insufficient thyroid

    hormone available to target tissues (Table 1).

    Classification (cretinism versus myxedema)

    by age of onset is important because the

    clinical presentations will vary substantially.

    CretinismCongenital hypothyroidism occurs at an over-

    all incidence of approximately 1:3,000 to

    4,000 births, with a slightly higher prevalence

    in the Hispanic population and a decreased

    prevalence in African-Americans.18 About

    85% of the cases are likely due to sporadic

    thyroid dysgenesis (agenesis), while the

    other 15% are due to an autosomal recessive

    mode of inheritance.19 Congenital hypothy-

    roidism (cretinism) is a recognized cause of

    mental retardation. The clinical manifesta-

    tions of hypothyroidism are difficult to recog-

    nize at birth, and it isnt usually until the third

    month of life that symptoms begin to appear.

    By this time, substantial neurological and

    mental retardation may have occurred.

    MyxedemaMyxedema usually develops gradually over a

    period of months or years (Fig 1). Signs and

    symptoms include coarse facial features

    (such as thick lips, puffy eyelids, and a sad

    expression), dry hair, slow speech, lethargy,

    memory impairment (depression), cardiovas-

    cular abnormalities (including slow pulse

    rate, hypotension, cardiomegaly, low-ampli-

    tude QRS, and inverted T waves), increased

    sensitivity to cold, decreased sweating, dry

    and cold skin, muscle weakness, and

    reduced respiratory rate. A characteristic

    nonpitting tissue edema is frequently ob-

    Fig 1 Myxedema is characterized by coarse facialfeatures,accented by thick lips,macroglossia,puffy eye-lids, dry hair and skin, and a lethargic sad expression.

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  • QUINTESSENCE INTERNATIONALHuber/Terzhalmy

    served.8,20 It is postulated to be a conse-

    quence of the deposition of mucopolysac-

    charides and a viscid proteinaceous fluid

    within tissues.21,22 The tongue and laryngeal

    tissues are often affected, resulting in slurred

    speech, hoarseness, and impaired sleep pat-

    terns.21,23 A rather characteristic loss of the

    outer third of the eyebrow is frequently

    observed.20,21,24 Laboratory abnormalities

    may include evidence of anemia and elevat-

    ed levels of aspartate transaminase, alanine

    transaminase, lactate dehydrogenase, creati-

    nine, and cholesterol.5

    Myxedema coma is an extreme life-threat-

    ening complication of hypothyroidism.

    Typically, the patient is elderly and has a his-

    tory of hypothyroidism.3,25 Most cases are

    preceded by precipitating factors such as

    infection, exposure to cold, sedative drug

    therapy, lung disease, stroke, congestive

    heart failure, gastrointestinal bleeding, acute

    trauma, or noncompliance with thyroid sup-

    plementation.26 The patient manifests wors-

    ening alveolar hypoventilation, hypothermia,

    bradycardia and decreased cardiac contrac-

    tility, hyponatremia and decreased glomeru-

    lar filtration, and rarely coma.27 Management

    requires prompt administration of thyroid

    hormone and supportive measures (ie, venti-

    latory support, fluid restoration, glucose

    administration, and glucocorticoid adminis-

    tration) to stabilize and reverse the down-

    ward spiral. Mortality rates of 20% to 60%

    have been reported. 27

    HyperthyroidismHyperthyroidism is a clinical disease state

    produced by the effects of excessive thyroid

    hormone on peripheral tissues (Table 1). The

    severity of the illness caused by thyrotoxico-

    sis is related to the severity and duration of

    the hormone excess, the age of the patient,

    and the presence or absence of other disease.

    Hyperthyroidism occurs most frequently in

    women of childbearing age and may mani-

    fest as a goiter, tremor, excitability, emotional

    instability, rapid pulse rate (tachycardia, atrial

    fibrillation), heart murmur, hypertension,

    rapid respiration, facial flushing, warm and

    moist skin, increased appetite with weight

    loss, muscle wasting, enlarged palpable

    lymph nodes, and exophthalmos often asso-

    ciated with symptoms of a gritty sensation,

    light sensitivity, increased tearing, double

    vision, and a feeling of retroocular pressure

    (Figs 2 and 3).28 Laboratory abnormalities

    may include hypercalcemia and elevated lev-

    els of alkaline phosphatase, aspartate

    transaminase, and alanine transaminase.5

    Osteoporosis typically affects cortical (hip

    and forearm) rather than trabecular bone

    (spine). 29

    142 VOLUME 39 NUMBER 2 FEBRUARY 2008

    Figs 2 and 3 Common signs and symptoms ofhyperthyroidism include a goiter and exophthalmosoften associated with symptoms of a gritty sensa-tion, light sensitivity, increased tearing, doublevision, and a feeling of retroocular pressure.

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  • VOLUME 39 NUMBER 2 FEBRUARY 2008 143

    QUINTESSENCE INTERNATIONALHuber/Terzhalmy

    Thyroid storm is the extreme manifesta-

    tion of hyperthyroidism. Its uncommon and

    occurs most frequently in patients with

    Graves disease, toxic adenomas, toxic

    multinodular goiters, and hypersecretory thy-

    roid carcinoma.26 Predisposing factors

    include infection, nonthyroid trauma, psy-

    chosis, parturition, myocardial infarction,

    intake of radioiodine and high doses of

    iodine-containing compounds, thyroid trau-

    ma, the discontinuation of antithyroid drug

    therapy, and the recent institution of amio-

    darone therapy.25 Cardinal clinical findings

    include fever (greater than 101.3F), tachy-

    cardia, CNS dysfunction (including agitation,

    confusion, and delirium), and gastrointestinal

    dysfunction (such as nausea, vomiting, and

    diarrhea).25,26 Other potential findings include

    diaphoresis, atrial fibrillation, and congestive

    heart failure.3,26 Management in an intensive

    care unit includes the administration of !-

    adrenergic blocking agents, propylthiouracil,

    and supportive measures (such as external

    cooling and careful fluid resuscitation). 25

    DIAGNOSIS

    Patients with a suspected thyroid disorder

    should undergo a thorough physical evalua-

    tion, including an exhaustive medical history,

    physical examination, and appropriate labo-

    ratory testing. A thyroid disorder may develop

    insidiously over time, and the suspect signs

    and symptoms are easy to overlook. This

    fact, combined with the dynamic nature of

    some thyroid disorders and the limited sensi-

    tivity/specificity of available tests, can chal-

    lenge the diagnostic acumen of even the

    most experienced clinician.

    CretinismMandatory screening of TSH levels in new-

    borns allows for the early identification of con-

    genital hypothyroidism and the prompt institu-

    tion of management strategies aimed at reduc-

    ing neurological impairment (cretinism).30,31

    Adult Hypo- or HyperthyroidismSerum TSH concentrations represent the

    most reliable indicator of thyroid status.26 The

    American Thyroid Association recommends

    that all patients obtain a serum TSH determi-

    nation at age 35 and every 5 years there-

    after.32 In general, results demonstrating a

    high TSH and low free T4 (FT4) are indicative

    of hypothyroidism, while results demonstrat-

    ing a low TSH and a high FT4 are indicative

    of hyperthyroidism.6 Following initial TSH

    measurements, specialized testing may be

    performed.33 For nodular disease, this may

    include a needle-aspiration biopsy to rule out

    malignancy.34,35 For cases of suspected

    autoimmune thyroid disease, antithyroid anti-

    body testing (antithyroglobulin antibody

    [TgAb], anti-TPO antibody [TPOAb], antithy-

    roid receptor antibody [TRAb], and thyroid

    stimulating antibody) may prove valuable.6

    Scintigraphy may be useful in determining

    nodular functional status in hyperthyroidism

    (Graves disease or multinodular goiter), fol-

    licular neoplasm, and multinodular goiter.36,37

    PRINCIPLES OF MEDICALMANAGEMENT

    HypothyroidismWith early detection and medical manage-

    ment, permanent mental retardation may be

    avoided in the young. Purified or synthetic

    thyroid preparations are available for replace-

    ment therapy. Thyroxine, in the form of

    levothyroxine, is the most widely prescribed

    treatment for hypothyroidism in the United

    States (Table 2).38 The amount of thyroid hor-

    mone given to restore the euthyroid state

    varies, but for adults, it usually lies between

    0.05 to 0.15 mg (50 to 150 micrograms) of

    levothyroxine or its equivalent daily. Patients

    usually notice an improvement two to three

    weeks after the start of treatment. Reductions

    in weight and puffiness and increases in the

    pulse rate and pulse pressure occur early in

    treatment, but other signs and symptoms

    may take months to resolve. The need for thy-

    roid hormone may decrease slightly with age

    and increase somewhat with stress and

    infection. Inadequate thyroxine-replacement

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  • 144 VOLUME 39 NUMBER 2 FEBRUARY 2008

    QUINTESSENCE INTERNATIONALHuber/Terzhalmy

    therapy is associated with continued clinical

    features of hypothyroidism. Substantial over-

    treatment with thyroxine results in clinical

    manifestations of hyperthyroidism.

    Hyperthyroidism Antithyroid drugs are the cornerstones in the

    management of hyperthyroidism (Table 3). 39,40

    They may be used as primary treatment for

    hyperthyroidism or preparative therapy before

    surgery or radioiodine therapy. Antithyroid

    drugs are usually discontinued or tapered

    after 12 to 18 months of therapy. Lifelong fol-

    low-up is required for patients in remission,

    since spontaneous hypothyroidism may devel-

    op decades later. Iodine or iodide prepara-

    tions may be prescribed as adjunctive therapy

    for short-term benefits and to decrease the

    size and vascularity of the thyroid gland in

    preparation for surgery. Radioactive iodine,

    given orally in the treatment of older patients

    with thyrotoxicosis, accumulates in the storage

    follicles and emits beta rays with a half-life of 5

    days, which destroys a portion of the hyperac-

    tive gland. Beta-adrenergic antagonists may

    be used to suppress some of the symptoms of

    hyperthyroidism, such as tremor, anxiety, and

    tachycardia.

    ORAL MANIFESTATIONSOF THYROID DYSFUNCTION

    With few exceptions, the oral manifestations

    attributable to thyroid dysfunction are neither

    well-established nor consistent and are large-

    ly based on anecdotal case reports. The age

    of onset, severity, and duration of any thyroid

    dysfunction directly affects the likelihood of

    any potential oral manifestations. Thus, the

    presence of associated oral manifestations is

    more likely to occur at either end of the thy-

    roid dysfunction spectrum (ie, extreme

    hypothyroidism or extreme hyperthyroidism).

    HypothyroidismCretinism. The oral complications of undiag-nosed and untreated congenital thyroid hypo-

    function include the characteristic facies of

    cretinism (puffy face, disproportionately large

    Adverse drug Drug Mechanisms of action Indication effects (ADEs)

    Levothyroxin T4 and T3 replacement (T4 is Drug of choice No ADEs at therapeuticconverted to T3 in plasma) dosages

    Hyperthyroidism at overdose

    Liothyronine T3 replacement Used when levothyroxin is notabsorbed adequately

    Liotrix T4 and T3 replacement Used when the conversion of levothyroxin from T4 to T3 is abnormal

    Table 2 Drugs used to treat hypothyroidism

    Adverse drug Drug Mechanisms of action Indication effects (ADEs)

    Methimazole Inhibits the transformation of Long-term thyroxin suppression Agranulocytosis, hepatotoxicity,inorganic iodine to organic or in preparation for surgery urticarial or macular reactions,iodine or 131I therapy arthralgia, sialadenitis (rarely)

    with methimazolePropylthiouracil Inhibits the transformation

    of inorganic iodine to organic iodine and blocks the conversion of T4 to T3

    Iodine or iodide Short term inhibition of Adjunctive therapy to the drugsthyroxin release above and in preparation for

    surgery

    Table 3 Drugs used to treat hyperthyroidism

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  • VOLUME 39 NUMBER 2 FEBRUARY 2008 145

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    cranium, dull expression, flat and broad nose,

    macroglossia, malocclusion, thick everted

    lips, and an open mouth). 41 There are con-

    flicting reports of altered tooth morphology

    (hypoplastic versus unaltered) and eruptive

    patterns (delayed versus normal). 4144

    Myxedema. The principal oral findingassociated with chronic hypothyroidism in

    adults is macroglossia (Fig 1).21,4446 The

    nose, eyelids, and lips may be edematous.

    Caries risk has been variably reported as

    increased, normal, or decreased.41 Impaired

    periodontal health has been reported, but it

    is unclear whether this finding is related to a

    lack of adequate patient compliance with

    hygiene procedures, altered bone metabo-

    lism, or both.41,47 Some patients may experi-

    ence dysgeusia. Salivary gland enlargement,

    especially of the parotid and sublingual

    glands, has been reported.48

    HyperthyroidismChildren with hyperthyroidism may experi-

    ence early loss of deciduous teeth and early

    eruption of the permanent dentition.5,42 Other

    potential findings in either the child or adult

    hyperthyroid patient include tremor of the

    lips and tongue, increased caries risk, accel-

    erated alveolar ridge atrophy, and increased

    incidence of mucosal erosions (burning

    mouth syndrome).5,42 The characteristic

    exophthalmos often observed in Graves dis-

    ease might be striking. Lid retraction with

    exposure of the white sclera above the lim-

    bus produces a characteristic stare.24 Other

    findings include lid lag, proptosis, diplopia,

    and decreased visual acuity.

    PRINCIPLES OF DENTALMANAGEMENT

    GoalsWhen treating patients with thyroid dysfunc-

    tion in the oral healthcare setting, the goals

    are to develop and implement timely preven-

    tive and therapeutic strategies compatible

    with the patients physical and emotional

    ability to undergo and respond to dental

    care, as well as the patients social and psy-

    chological needs and desires.

    Patient assessmentThe first priority for the dental practitioner is

    to obtain a meticulous medical history and

    perform a thorough head and neck examina-

    tion. The presence of signs and symptoms of

    a potential thyroid dysfunction mandate a

    medical consultation for further evaluation.5,24

    Medical historyFor patients with an acknowledged thyroid

    dysfunction, it is essential to assess the

    patients current status and identify potential

    comorbidities, which may necessitate a mod-

    ification to the delivery of dental care.

    Identifiable risk factors for thyroid dysfunc-

    tion from the medical history include previ-

    ous thyroid dysfunction; goiter; surgery or

    radiotherapy of the thyroid gland; diabetes

    mellitus (DM); vitiligo; pernicious anemia;

    leukotrichia; medications such as lithium car-

    bonate and iodine-containing drugs; and a

    family history of diabetes mellitus, pernicious

    anemia, thyroid disease, or primary adrenal

    insufficiency.32 Clinicians should also seek to

    determine the presence or absence of car-

    diovascular diseases (such as angina pec-

    toris, coronary artery disease, arrhythmias,

    and congestive heart failure). There is some

    evidence that patients with hyperlipidemia

    associated with overt hypothyroidism have

    an increased incidence of coronary artery

    disease and associated angina pectoris.38,49

    Furthermore, some patients with hypothy-

    roidism cannot tolerate full replacement

    therapy because of angina pectoris and

    increased incidence of myocardial infarction

    and sudden death.38 There is also evidence

    that patients treated for thyroid disease

    (Graves disease, toxic multinodular goiter,

    Hashimotos thyroiditis) have an increased

    long-term cardiovascular risk despite restora-

    tion of euthyroidism.50

    Functional capacity. Since T4 and T3exert direct inotropic and chronotropic

    effects on cardiac muscle and appear to act

    synergistically with epinephrine, the history

    should also seek to determine the patients

    functional capacity. Functional capacity,

    which is expressed in terms of metabolic

    equivalents (METs), is a measure of an indi-

    viduals ability to perform a spectrum of com-

    mon daily tasks (physical stressors). Cardiac

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  • 146 VOLUME 39 NUMBER 2 FEBRUARY 2008

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    risk in association with noncardiac proce-

    dures is increased in patients unable to meet

    a 4-MET demand during normal daily activi-

    ties. 5153 Four METs is approximately equiva-

    lent to the physiological stress produced by

    doing light yard work (such as raking leaves,

    weeding, or pushing a power mower), paint-

    ing, doing light carpentry, or climbing a flight

    of stairs. The hemodynamic effects of 4

    METs is equivalent to that produced by 0.045

    mg of epinephrine.54

    Physical examinationGeneral appearance. The hypothyroidpatient may present with coarse facial fea-

    tures (thick lips, puffy eyelids, sad expression),

    dry hair, and dry and cold skin. The hyperthy-

    roid patient may manifest tremor, excitability,

    warm and moist skin, and exophthalmos.

    Vital signs. Thyroid hormones appear toact synergistically with epinephrine affecting

    cardiac contractility, vascular tone, and blood

    pressure. As a result of this increased sym-

    pathomimetic activity, heart rate, blood pres-

    sure, and the rate of respiration are increased

    in the hyperthyroid and decreased in the

    hypothyroid patient. Myxedema coma is an

    extreme life-threatening complication of

    hypothyroidism. It is characterized by

    hypoventilation, hypotension, and bradycar-

    dia. A blood pressure of < 90/50 mm Hg is a

    reliable sign of shock. Thyroid storm is the

    extreme manifestation of hyperthyroidism. It

    is characterized by an elevated temperature,

    tachycardia, and high blood pressure. A

    blood pressure in excess of 180/110 mm Hg

    represents a hypertensive crisis. A resting

    pulse rate below 60 or above 100 beats per

    minute in adults, if symptomatic (sweating,

    weakness, dyspnea, and/or chest pain),

    should be considered a cardiac risk in

    association with noncardiac procedures.

    Respiratory rates less than 10 or greater that

    20 breaths per minute may indicate respira-

    tory distress.

    Head and neck examination. Everypatient should be clinically screened for a

    thyroid abnormality as part of the routine

    head and neck examination.5,37,42 Normal thy-

    roid tissue is often difficult to distinguish in

    the relaxed neck; however, having the patient

    extend the neck to one side allows for easier

    palpation of the thyroid lobule on the opposite

    side. The thyroid gland should be assessed

    for textural consistency, overall size, presence

    of growths, and tenderness. 5,37 The presence

    of multinodularity of similar consistency is

    most consistent with a benign goiter, while

    the presence of a midline mass that moves

    up with protrusion of the tongue is likely to be

    a thyroglossal duct cyst.37

    Treatment strategiesAs noted earlier, both hypothyroidism and

    hyperthyroidism adversely affect cardiac

    function. Thyroid dysfunction may also be

    associated with DM and adrenal disease

    (autoimmune polyglandular syndrome, type 2).

    Consequently, treatment strategies for a

    patient with thyroid dysfunction (Table 4)

    should take into consideration the patients

    overall health as reflected by the patients

    medical history and vital signs. The dental

    management of patients with cardiovascular

    diseases, DM, and adrenal dysfunction

    has been extensively reviewed in recent

    publications. 5560

    The hypothyroid patientThere are no randomized, prospective studies

    in dentistry or medicine looking at surgical

    outcomes in hypothyroid patients versus

    controls. However, two retrospective case-

    matched controls can provide some guid-

    ance with relevance to dentistry. In one study,

    researchers reviewed anesthetic and surgical

    outcomes in 59 hypothyroid patients and 59

    paired euthyroid controls.61 There were no dif-

    ferences between the groups in perioperative

    complications, surgical outcome, or length of

    hospital stay. There were also no differences

    in outcome among subsets of hypothyroid

    patients as determined by thyroxine levels;

    however, only a few patients were severely

    hypothyroid. The authors concluded that

    there was no evidence to justify deferring nec-

    essary surgery in patients with mild to moder-

    ate hypothyroidism and not enough evidence

    to make recommendations for patients with

    severe hypothyroidism. A severe hypothyroid

    patient is one with myxedema characterized

    by delayed mentation, pericardial effusions,

    heart failure, or very low levels of thyroxine.62

    In the second study, investigators looked

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  • VOLUME 39 NUMBER 2 FEBRUARY 2008 147

    QUINTESSENCE INTERNATIONALHuber/Terzhalmy

    at perioperative complications in 40 hypothy-

    roid patients compared with 80 matched con-

    trols. 63 Hypothyroid patients had more intra-

    operative hypotension in noncardiac surgery,

    but there were no differences between the

    groups in perioperative arrhythmias or dura-

    tion of hospitalization.

    The use of local anesthetic agents andanalgesics. A review of the literature revealedno adverse effects associated with epineph-

    rine infusion in patients with hypothyroidism

    without significant cardiovascular disease.58

    Well-controlled, medically supervised patients

    on thyroid replacement and patients with mild

    to moderate symptoms of hypothyroidism

    may safely undergo routine dental care under

    local anesthesia. However, patients with

    hypothyroidism are hyperreactive to central

    nervous system depressants (opioid anal-

    gesics, anxiolytic agents), which should there-

    fore be administered judiciously.5

    The hyperthyroid patientT4 and T3 exert direct inotropic and chrono-

    tropic effects on cardiac muscle. Left ventricu-

    lar ejection fraction may not increase normally

    during physiological stress, and increased

    cardiac output may limit cardiac reserves dur-

    ing surgery in the hyperthyroid patient.65

    Consequently, the effect of inadequately treat-

    ed or undiagnosed hyperthyroidism on the

    heart carries perioperative risks. If hyperthy-

    roidism is suspected, because of either med-

    ical history or clinical signs and symptoms, the

    patient should be referred for evaluation by an

    internist or endocrinologist. Once medical

    treatment has been instituted and the patient

    is euthyroid, there is no contraindication to

    dental treatment.

    The use of local anesthetic agents andanalgesics. The use of local anestheticagent containing a vasoconstrictor in

    patients with high concentrations of T4 and

    T3 is an area of concern.5,24,42,66 Thyroid hor-

    mones appear to act synergistically with epi-

    nephrine by increasing tissue sensitivity to

    catecholamines and possibly up-regulating

    adrenergic receptors. An additional problem

    associated with the use of local anesthetic

    agents containing epinephrine is related to

    the treatment of hyperthyroid symptoms with

    a nonselective !-adrenergic antagonist. 5,67

    However, these concerns must be balanced

    against the value of a vasoconstrictor in

    Euthyroid patient OR patient with mild to moderate thyroid dysfunction AND/OR minor clinical predictors(advanced age, atrial fibrillation, history of stroke) OR intermediate clinical predictors (stable angina pectoris, pre-vious myocardial infarction [MI], compensated heart failure renal insufficiency) of cardiovascular risk

    Blood pressure less than 180/110 mm Hg; normal pulse pressure, rate and rhythm; functional capacity greaterthan 4 METsComprehensive dental careRoutine referral for medical management and risk factor modification

    Blood pressure less than 180/110 mm Hg; normal pulse pressure, rate and rhythm; BUT functional capacityless than 4 METs Appropriate limited dental care*Routine referral for medical management and risk factor modification

    Blood pressure greater than 180/110 mm Hg OR systolic blood pressure less than 90 mm Hg AND/OR abnor-mal pulse pressure, rate, or rhythm Appropriate emergency dental care**If patient is symptomatic, immediate referral for medical management and risk factor modification If patient is asymptomatic, routine referral for medical management and risk factor modification

    Patient with severe hypothyroidism OR thyrotoxicosis AND/OR major clinical predictors (unstable coronary syn-drome, decompensated heart failure, severe valvular disease, significant arrhythmias) of cardiovascular risk

    Appropriate emergency dental care**Immediate referral for medical management and risk factor modification

    * Limited office care may include dental prophylaxis, restorative procedures, simple periodontal and endodontic procedures, androutine extractions.** Emergency office care under local anesthesia without a vasoconstrictor should be based on firm evidence that the benefitsachieved by therapeutic intervention outweigh the risk of complications associated with the patient's diabetic or cardiovascularstatus and may include activities related to pain relief, the treatment of infection (including simple incision and drainage), and theinduction of hemostasis (avoid the use of epinephrine to control local bleeding).

    Table 4 Dental management of the patient with thyroid dysfunction

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  • 148 VOLUME 39 NUMBER 2 FEBRUARY 2008

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    inducing profound local anesthesia, which is

    essential in reducing the physiologic stress

    associated with pain. For the patient with

    overt evidence of hyperthyroidism, the use of

    vasoconstrictors should be avoided. For all

    other scenarios, the cautious use of vaso-

    constrictors, based on the patients function-

    al capacity, should be considered. For those

    patients whose functional capacity is equal

    to or greater than 4 METs, 4.5 mL of a local

    anesthetic agent with epinephrine 1:100,000

    (or equivalent) can be administered safely.

    Furthermore, combination analgesics con-

    taining acetylsalicylic acid (ASA) are con-

    traindicated in patients with hyperthyroidism

    because ASA interferes with the protein bind-

    ing of T4 and T3, thereby increasing their free

    form, and can lead to thyrotoxicosis.

    Preventive strategiesSome patients with hyperthyroidism may be

    treated with 131I (radioiodine) for the short-

    term inhibition of thyroxin release. Salivary

    glands are known to concentrate iodide

    selectively (up to 24% of administered 131I is

    lost through the saliva). To reduce the poten-

    tial for 131I-induced sialadenitis, it is recom-

    mend that measures be taken to increase

    salivation and thus accelerate the flow of 131I

    through the glandular parenchyma.59 These

    patients may benefit from simple measures

    such as eating carrots or celery or chewing

    sugarless or xylitol-containing gums. How-

    ever, pilocarpine hydrochloride (Salagen,

    MGI Pharma) and cevimeline hydrochloride

    (Evoxac, Daiichi Pharmaceuticals), both mus-

    carinic agonists, may more predictably

    increase salivary activity. The use of the

    radioprotectant agent amifostine has also

    been advocated. The patient who manifests

    residual salivary gland damage should be

    managed in a manner similar to that estab-

    lished for the patient who has received thera-

    peutic head and neck radiotherapy. 60

    CONCLUSIONS

    When treating patients with thyroid dysfunc-

    tion in the oral healthcare setting, the goals

    are to develop and implement timely preven-

    tive and therapeutic strategies compatible

    with the patients physical and emotional

    ability to undergo and respond to dental

    care. There is no evidence to justify deferring

    necessary dental procedures in patients with

    mild to moderate hypothyroidism. However,

    T4 and T3 exert direct inotropic and

    chronotropic effects on cardiac muscle. Left

    ventricular ejection fraction may not increase

    normally during physiological stress, and

    increased cardiac output may limit cardiac

    reserves during stressful procedures in the

    hyperthyroid patient. The effect of inade-

    quately treated or undiagnosed hyperthy-

    roidism on the heart may carry perioperative

    risks in the oral healthcare setting.

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