Artopt

Huber1.
qxd
12/18/07
2:35 PM
Page 139
Q U I N T E S S E N C E I N T E R N AT I O N A L
Risk stratification and dental management

of the patient with thyroid dysfunction
Michaell 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 intolerance, tremors, increased sweating, frequent bowel movements, and quickened heart
rate. The effect of inadequately treated or undiagnosed hyperthyroidism on the heart carries perioperative risks. To provide competent dental care to patients with thyroid dysfunction, 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
Thyroid activity is controlled by the hypothalamic-pituitary-thyroid axis. Thyroid-releasing

hormone (TRH), secreted by the hypothalamus, induces the secretion of thyroid stimulating hormone (TSH) by the anterior pituitary, which in turn stimulates thyroid hormone synthesis and secretion by the thyroid
gland.13 The thyroid gland is a bilobular
structure that lies on either side of the trachea.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 (thyroxine [T4], triiodothyroxine [T3], and reverse
triiodothyronine [rT3]).1 The enzyme responsible 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. rT3
appears 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 lipoproteins.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
Associate 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.
Endowed 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
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
VOLUME 39
NUMBER 2
FEBRUARY 2008
139
Huber1.qxd
12/18/07
2:35 PM
Page 140
H u b e r / Te r z h a l m y
Ta b l e 1
Common thyroid disorders12
Disorders characterized by euthyroidism

Euthyroid goiter (diffuse, nodular, multinodular)
Benign tumors
Malignant tumors
Differentiated (papillary, follicular)
Undifferentiated (small cell, giant cell)
Medullary
Thyroiditis
Acute
Subacute thyroiditis (de Quervains)
Chronic autoimmune (Hashimotos disease)
Postpartum
Reidels thyroiditis
Disorders characterized by hypothyroidism
With hypothyroidism
Primary hypothyroidism
Chronic autoimmune thyroiditis
Iatrogenic (surgery, 131I [radioiodine] therapy)
Diffuse and nodular goiter
Severe iodine deficiency
Neonatal congenital hypothyroidism
Secondary hypothyroidism
Pituitary hypothyroidism
Tertiary hypothyroidism
Hypothalamic hypothyroidism
Without hypothyroidism
Generalized and peripheral resistance to thyroid
hormones
Transient hypothyroidism (iodine
deficiency/excess, druginduced, postpartum)
Disorders characterized by hyperthyroidism
Glandular hyperfunction
Diffuse hyperthyroid goiter with thyroid associated
ophthalmopathy (Graves disease)
Multinodular hyperthyroid goiter or Plummers
disease
Autonomous nodule
Thyrotoxicosis (without thyroid gland hyperfunction)
Excessive exogenous thyroid hormones
Post-inflammatory or from glandular destruction
Amiodarone induced
Transient hyperthyroidism
ETIOLOGY AND
EPIDEMIOLOGY
T4 serves as a prohormone for the extrathyroidal production of T3, which, in its free form,
accounts for most of the biological activity of
thyroid hormones.6 T3 stimulates RNA polymerase and phosphoprotein kinases and the
synthesis of nuclear proteins, which are
involved in the regulation of growth and

development; thermoregulation and calorigenesis; the metabolism of carbohydrates, proteins, and lipids; and oxygen consumption.1
Thyroid hormones also appear to act synergistically with epinephrine to enhance
glycogenolysis and hyperglycemia and
enhance tissue sensitivity to catecholamines.
Yet, there appears to be a paradoxical
inverse relationship between circulating norepinephrine and thyroid hormone levels.710
While the myocardial effects of excess thyroid hormone mimic a hyperadrenergic state,
the levels of circulating catecholamines, in
these scenarios, are actually low or normal. It
is postulated that the increased sympathomimetic 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 norepinephrine (possibly through 1-adrenergic and/or
2-adrenergic receptor modulation) and
enhanced acetylcholine-induced vasodilatation.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 thyroid disorders (Graves disease, Hashimotos
thyroiditis, postpartum thyroid dysfunction,
and painless sporadic thyroiditis) represent
autoimmune phenomenas.13,14 In addition to
genetic predisposition, numerous environmental factors, such as low birth weight, iodine
deficiency or excess, selenium deficiency, the
use of oral contraceptives and other medications, stress, allergy, smoking, ionizing radiation, and bacterial or viral infection, have been
postulated to contribute to etiopathogenesis of
autoimmune thyroid disease.14
140
VOLUME 39
NUMBER 2
FEBRUARY 2008
Huber1.qxd
12/18/07
2:35 PM
Page 141
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% hyperplastic nodules, 15% adenomas, and less
than 1% cysts).16 In 2006, an estimated
30,180 cases of thyroid carcinoma were diagnosed in the United States (7,590 men and
22,590 women).17 Thyroid carcinoma is most
frequently papillary (81%), followed by follicular and Hrthle-cell (14%), medullary (3%),
and anaplastic (2%) forms.16
Fig 1 Myxedema is characterized by coarse facial

features,accented by thick lips,macroglossia,puffy eyelids, dry hair and skin, and a lethargic sad expression.
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 hyperthyroidism may evolve into a life-threatening
medical emergency.
Hypothyroidism
Hypothyroidism 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.
Cretinism
Congenital hypothyroidism occurs at an overall 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 hypothyroidism (cretinism) is a recognized cause of

mental retardation. The clinical manifestations of hypothyroidism are difficult to recognize 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.
Myxedema
Myxedema 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), cardiovascular abnormalities (including slow pulse
rate, hypotension, cardiomegaly, low-amplitude 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-
VOLUME 39
NUMBER 2
FEBRUARY 2008
141
Huber1.qxd
12/18/07
2:35 PM
Page 142
Figs 2 and 3 Common signs and symptoms of

hyperthyroidism include a goiter and exophthalmos
often associated with symptoms of a gritty sensation, light sensitivity, increased tearing, double
vision, and a feeling of retroocular pressure.
served.8,20 It is postulated to be a consequence of the deposition of mucopolysaccharides 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 patterns.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 elevated levels of aspartate transaminase, alanine
transaminase, lactate dehydrogenase, creatinine, and cholesterol.5
Myxedema coma is an extreme life-threatening complication of hypothyroidism.
Typically, the patient is elderly and has a history 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 supplementation.26 The patient manifests worsening alveolar hypoventilation, hypothermia,
bradycardia and decreased cardiac contractility, hyponatremia and decreased glomerular filtration, and rarely coma.27 Management
requires prompt administration of thyroid
hormone and supportive measures (ie, ventilatory support, fluid restoration, glucose
administration, and glucocorticoid adminis-
tration) to stabilize and reverse the downward spiral. Mortality rates of 20% to 60%
have been reported. 27
Hyperthyroidism
Hyperthyroidism 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 thyrotoxicosis 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 manifest 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 associated 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 levels 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
Huber1.qxd
12/18/07
2:35 PM
Page 143
Thyroid storm is the extreme manifestation of hyperthyroidism. Its uncommon and

occurs most frequently in patients with
Graves disease, toxic adenomas, toxic
multinodular goiters, and hypersecretory thyroid carcinoma.26 Predisposing factors
include infection, nonthyroid trauma, psychosis, parturition, myocardial infarction,
intake of radioiodine and high doses of
iodine-containing compounds, thyroid trauma, the discontinuation of antithyroid drug
therapy, and the recent institution of amiodarone therapy.25 Cardinal clinical findings
include fever (greater than 101.3F), tachycardia, 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
Adult Hypo- or Hyperthyroidism

Serum TSH concentrations represent the
most reliable indicator of thyroid status.26 The
American Thyroid Association recommends
that all patients obtain a serum TSH determination at age 35 and every 5 years thereafter.32 In general, results demonstrating a
high TSH and low free T4 (FT4) are indicative
of hypothyroidism, while results demonstrating 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 antibody testing (antithyroglobulin antibody
[TgAb], anti-TPO antibody [TPOAb], antithyroid 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), follicular neoplasm, and multinodular goiter.36,37
PRINCIPLES OF MEDICAL
MANAGEMENT
Patients with a suspected thyroid disorder

should undergo a thorough physical evaluation, including an exhaustive medical history,
physical examination, and appropriate laboratory 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 sensitivity/specificity of available tests, can challenge the diagnostic acumen of even the
most experienced clinician.
Cretinism
Mandatory screening of TSH levels in newborns allows for the early identification of congenital hypothyroidism and the prompt institution of management strategies aimed at reducing neurological impairment (cretinism).30,31
Hypothyroidism
With early detection and medical management, permanent mental retardation may be
avoided in the young. Purified or synthetic
thyroid preparations are available for replacement 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 hormone 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 thyroid hormone may decrease slightly with age
and increase somewhat with stress and
infection. Inadequate thyroxine-replacement
VOLUME 39
NUMBER 2
FEBRUARY 2008
143
Huber1.qxd
12/18/07
2:35 PM
Page 144
Ta b l e 2
Drug
Drugs used to treat hypothyroidism

Mechanisms of action
Adverse drug
effects (ADEs)
Indication
Levothyroxin
T4 and T3 replacement (T4 is

converted to T3 in plasma)
Drug of choice
Liothyronine
T3 replacement
Liotrix
T4 and T3 replacement
Used when levothyroxin is not

absorbed adequately
Used when the conversion of
levothyroxin from T4 to T3 is abnormal
Ta b l e 3
Drug
Methimazole
No ADEs at therapeutic
dosages
Hyperthyroidism at
overdose
Drugs used to treat hyperthyroidism

Mechanisms of action
Inhibits the transformation of

inorganic iodine to organic
iodine
Adverse drug
effects (ADEs)
Indication
Long-term thyroxin suppression

or in preparation for surgery
or 131I therapy
Agranulocytosis, hepatotoxicity,
urticarial or macular reactions,
arthralgia, sialadenitis (rarely)
with methimazole
Propylthiouracil 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 drugs
thyroxin release
above and in preparation for
surgery
therapy is associated with continued clinical

features of hypothyroidism. Substantial overtreatment with thyroxine results in clinical
manifestations of hyperthyroidism.
hyperthyroidism, such as tremor, anxiety, and

tachycardia.
Hyperthyroidism
ORAL MANIFESTATIONS
OF THYROID
DYSFUNCTION
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 follow-up is required for patients in remission,
since spontaneous hypothyroidism may develop decades later. Iodine or iodide preparations 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 hyperactive gland. Beta-adrenergic antagonists may
be used to suppress some of the symptoms of
With few exceptions, the oral manifestations

attributable to thyroid dysfunction are neither
well-established nor consistent and are largely 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 thyroid dysfunction spectrum (ie, extreme
hypothyroidism or extreme hyperthyroidism).
Hypothyroidism
Cretinism. The oral complications of undiagnosed and untreated congenital thyroid hypofunction include the characteristic facies of
cretinism (puffy face, disproportionately large
144
VOLUME 39
NUMBER 2
FEBRUARY 2008
Huber1.qxd
12/18/07
2:35 PM
Page 145
cranium, dull expression, flat and broad nose,

macroglossia, malocclusion, thick everted
lips, and an open mouth). 41 There are conflicting reports of altered tooth morphology
(hypoplastic versus unaltered) and eruptive
patterns (delayed versus normal). 4144
Myxedema. The principal oral finding
associated 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 metabolism, or both.41,47 Some patients may experience dysgeusia. Salivary gland enlargement,
especially of the parotid and sublingual
glands, has been reported.48
Hyperthyroidism
Children with hyperthyroidism may experience 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, accelerated alveolar ridge atrophy, and increased
incidence of mucosal erosions (burning
mouth syndrome).5,42 The characteristic
exophthalmos often observed in Graves disease might be striking. Lid retraction with
exposure of the white sclera above the limbus produces a characteristic stare.24 Other
findings include lid lag, proptosis, diplopia,
and decreased visual acuity.
PRINCIPLES OF DENTAL
MANAGEMENT
Goals
When treating patients with thyroid dysfunction in the oral healthcare setting, the goals
are to develop and implement timely preventive 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 psychological needs and desires.
Patient assessment
The first priority for the dental practitioner is
to obtain a meticulous medical history and
perform a thorough head and neck examination. The presence of signs and symptoms of
a potential thyroid dysfunction mandate a
medical consultation for further evaluation.5,24
Medical history
For patients with an acknowledged thyroid
dysfunction, it is essential to assess the
patients current status and identify potential
comorbidities, which may necessitate a modification to the delivery of dental care.
Identifiable risk factors for thyroid dysfunction from the medical history include previous thyroid dysfunction; goiter; surgery or
radiotherapy of the thyroid gland; diabetes
mellitus (DM); vitiligo; pernicious anemia;
leukotrichia; medications such as lithium carbonate 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 cardiovascular diseases (such as angina pectoris, 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 hypothyroidism 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 restoration of euthyroidism.50
Functional capacity. Since T4 and T3
exert 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 individuals ability to perform a spectrum of common daily tasks (physical stressors). Cardiac
VOLUME 39
NUMBER 2
FEBRUARY 2008
145
Huber1.qxd
12/18/07
2:35 PM
Page 146
risk in association with noncardiac procedures is increased in patients unable to meet

a 4-MET demand during normal daily activities. 5153 Four METs is approximately equivalent to the physiological stress produced by
doing light yard work (such as raking leaves,
weeding, or pushing a power mower), painting, 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 examination
General appearance. The hypothyroid
patient may present with coarse facial features (thick lips, puffy eyelids, sad expression),
dry hair, and dry and cold skin. The hyperthyroid patient may manifest tremor, excitability,
warm and moist skin, and exophthalmos.
Vital signs. Thyroid hormones appear to
act synergistically with epinephrine affecting
cardiac contractility, vascular tone, and blood
pressure. As a result of this increased sympathomimetic activity, heart rate, blood pressure, 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 bradycardia. 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 respiratory distress.
Head and neck examination. Every
patient should be clinically screened for a
thyroid abnormality as part of the routine
head and neck examination.5,37,42 Normal thyroid 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 strategies
As 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 patient

There are no randomized, prospective studies
in dentistry or medicine looking at surgical
outcomes in hypothyroid patients versus
controls. However, two retrospective casematched controls can provide some guidance 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 differences 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 necessary surgery in patients with mild to moderate 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
146
VOLUME 39
NUMBER 2
FEBRUARY 2008
Huber1.qxd
12/18/07
2:35 PM
Page 147
Ta b l e 4
Dental management of the patient with thyroid dysfunction
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, previous 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 greater
than 4 METs
Comprehensive dental care
Routine referral for medical management and risk factor modification
Blood pressure less than 180/110 mm Hg; normal pulse pressure, rate and rhythm; BUT functional capacity
less 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 abnormal 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 syndrome, 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, and
routine extractions.
** Emergency office care under local anesthesia without a vasoconstrictor should be based on firm evidence that the benefits
achieved by therapeutic intervention outweigh the risk of complications associated with the patient's diabetic or cardiovascular
status and may include activities related to pain relief, the treatment of infection (including simple incision and drainage), and the
induction of hemostasis (avoid the use of epinephrine to control local bleeding).
at perioperative complications in 40 hypothyroid patients compared with 80 matched controls. 63 Hypothyroid patients had more intraoperative hypotension in noncardiac surgery,
but there were no differences between the
groups in perioperative arrhythmias or duration of hospitalization.
The use of local anesthetic agents and
analgesics. A review of the literature revealed
no adverse effects associated with epinephrine 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 analgesics, anxiolytic agents), which should therefore be administered judiciously.5
The hyperthyroid patient

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 surgery in the hyperthyroid patient.65
Consequently, the effect of inadequately treated or undiagnosed hyperthyroidism on the
heart carries perioperative risks. If hyperthyroidism is suspected, because of either medical 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 and
analgesics. The use of local anesthetic
agent containing a vasoconstrictor in
patients with high concentrations of T4 and
T3 is an area of concern.5,24,42,66 Thyroid hormones appear to act synergistically with epinephrine 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
VOLUME 39
NUMBER 2
FEBRUARY 2008
147
Huber1.qxd
12/18/07
2:35 PM
Page 148
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 vasoconstrictors, based on the patients functional 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 containing acetylsalicylic acid (ASA) are contraindicated in patients with hyperthyroidism
because ASA interferes with the protein binding of T4 and T3, thereby increasing their free
form, and can lead to thyrotoxicosis.
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
Preventive strategies
REFERENCES
Some patients with hyperthyroidism may be

treated with 131I (radioiodine) for the shortterm 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 potential for 131I-induced sialadenitis, it is recommend 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. However, pilocarpine hydrochloride (Salagen,
MGI Pharma) and cevimeline hydrochloride
(Evoxac, Daiichi Pharmaceuticals), both muscarinic 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 established for the patient who has received therapeutic head and neck radiotherapy. 60
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 inadequately treated or undiagnosed hyperthyroidism on the heart may carry perioperative
risks in the oral healthcare setting.
1. Genuth SM. The thyroid gland. In Berne RM, Levy

MN, Koeppen BM, Stanton BA (eds). Physiology, ed
5. St. Louis, Mosby, 2004: 860882.
2. Greenwood M, Meechan JG. General medicine and
surgery for dental practitioners. Part 6: The
endocrine system. Br Dent J 2003;195:129133.
3. Pimentel L, Hansen KN.Thyroid disease in the emergency department: A clinical and laboratory review.
J Emerg Med 2005;28:201209.
4. De Felice M, Di Lauro R. Thyroid development and
its disorders: Genetics and molecular mechanisms.
Endocr Rev 2004;25:722746.
5. Pinto A, Glick M. Management of patients with thyroid disease: Oral health considerations. J Am Dent
Assoc 2002;133:849858.
6. Baloch Z, Carayon P, Conte-Devoix B, et al. Laboratory medicine practice guidelines. Laboratory
support for the diagnosis and monitoring of thyroid disease. Thyroid 2003;13:3126.
7. Carvalho-Bianco SD, Kim BW, Zhang JX, et al.
Chronic cardiac-specific thyrotoxicosis increases
myocardial beta-adrenergic responsiveness. Mol
Endocrinol 2004;18:18401849.
8. Levey GS, Klein I. Catecholamine-thyroid hormone
interactions and the cardiovascular manifestation
of hyperthyroidism. Am J Med 1990;88:642646.
9. Napoli R, Biondi B, Guardasole V, et al. Impact of
hyperthyroidism and its correction on vascular
reactivity
in
humans.
Circulation
2001;104:
30763080.
CONCLUSIONS
10. Ziegler MG, Morrissey EC, Marshall LF. Catecholamines and thyroid hormones in traumatic injury.
When treating patients with thyroid dysfunction in the oral healthcare setting, the goals
are to develop and implement timely preven-
Crit Care Med 1990;18:253258.
148
VOLUME 39
NUMBER 2
FEBRUARY 2008
Huber1.qxd
12/18/07
2:35 PM
Page 149
11. McAllister RM, Grossenburg VD, Delp MD, Laughlin
32. Ladenson PW, Singer PA, Ain KB, et al. American
MH. Effects of hyperthyroidism on vascular contrac-
Thyroid Association guidelines for detection of thy-
tile and relaxation responses. Am J Physiol 1998;
roid
274:E946E953.
160:15731575.
12. Monaco
F. Classification
of
thyroid
dysfunction.
Arch
Intern
Med
2000;
disease:
33. Kane LA, Gharib H. Thyroid testing A clinical
Suggestions for a revision. J Clin Endocrinol Metab
approach. In Braverman LE (ed). Diseases of the
2003;88:14281432.
Thyroid, ed 2. Totowa: Humana Press, 2003: 3953.
13. Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N
34. Carpi A, Nicolini A, Sagripanti A, Righi C, Fabris FM,
Engl J Med 2003;348:26462655.
Di Coscio G. Large-needle aspiration biopsy for the
14. Prummel MF, Strieder T, Wiersinga WM. The environ-
preoperative selection of palpable thyroid nodules
ment and autoimmune thyroid disease. Eur J
diagnosed by fine-needle aspiration as a microfol-
Endocrinol 2004;150:605618.
licular nodule or suspected cancer. Am J Clin Pathol

2000;113:872877.
15. Thyroid Foundation of America. Available at http://

www.tsh.org. Accessed March 21, 2006.
35. Carpi A, Nicolini A, Righi C, Romani R, Di Coscio G.

Large needle aspiration biopsy results of palpable
16. Utiger RD. The multiplicity of thyroid nodules and
thyroid nodules diagnosed by fine-needle aspira-
carcinomas. N Engl J Med 2005;352:23762378.
tion as a microfollicular nodule with atypical cells or

17. American Cancer Society. Cancer facts and figures
suspected
2006. Atlanta: American Cancer Society, 2006.

18. Grters A, Krude H, Biebermann H. Molecular genet-
cancer.
Biomed
Pharmacother
2004;58:351355.
36. Sherman SI. Thyroid carcinoma. Lancet 2003;
ic defects in congenital hypothyroidism. Eur J
361:501511.
Endocrinol 2004;151:U39U44.
37. Singer PA, Cooper DS, Daniels GH, et al. Treatment
19. Vanderpump MP, Tunbridge WM. Epidemiology and
guidelines for patients with thyroid nodules and
prevention of clinical and subclinical hypothy-
well-differentiated thyroid cancer. Arch Intern Med
roidism. Thyroid 2002;12:839847.
1996;156:21652172.
20. Mosby EL, Hiatt WR. Diagnosis of hypothyroidism
38. Toft AD. Thyroxine therapy. N Engl J Med 1994;331:
after a surgical complication. J Oral Surg 1975;33:
174180.
380383.
39. Cooper DS. Antithyroid drugs. N Eng J Med 2005;
21. Lucente FE. Endocrine problems in otolaryngology.
352:905917.
Ann Otal Rhinol Laryngol 1973;82:131137.

40. Franklyn JA. The management of hyperthyroidism.
22. Orr WC, Males JL, Imes NK. Myxedema and obstruc-
N Engl J Med 1994;330:17311738.
tive sleep apnea. Am J Med 1981;70:10611066.

41. Buckman N. Oral manifestation of cretinism; report
23. Rosenow F, McCarthy V, Caruso AC. Sleep apnoea in
of a case. Oral Surg Oral Med Oral Pathol 1957;
endocrine diseases. J Sleep Res 1998;7:311.

24. Sherman RG, Lasseter DH. Pharmacologic manage-
10:938947.
42. Herrmann HJ 2nd, Myall RW. Observations on the
ment of patients with disease of the endocrine sys-
significance of the thyroid gland to the dentist.
tem. Dent Clin North Am 1996;40:727752.

25. Savage MW, Mah PM, Weetman AP, Newell-Price J.
Spec Care Dentist 1983;3:1316.

43. Israel H, Fierro-Benitez R, Garces J. Skeletal and den-
Endocrine emergencies. Postgrad Med J 2004;80:
tal development in endemic goitre and cretinism
506515.
areas of Ecuador. J Trop Med Hyg 1969;72:105113.
26. Sarlis NJ, Gourgiotis L. Thyroid emergencies. Rev
44. Levin HL. Some dental aspects of endocrine dis-
Endocr Metab Disord 2003;4:129136.
eases. Oral Surg Oral Med Oral Pathol 1965;19:
27. Fliers E, Wiersinga WM. Myxedema coma. Rev

Endocr Metab Disord 2003;4:137141.
466477.
45. Silverman S Jr. Oral changes in metabolic disease.
28. Prabhakar BS, Bahn RS, Smith TJ. Current perspective on the pathogenesis of Graves disease and
Postgrad Med 1971;49:106110.

46. Wittmann AL. Macroglossia in acromegaly and
ophthalmopathy. Endocr Rev 2003;24:802835.
hypothyroidism.Virchows Arch A Pathol Anat Histol
29. Greenspan SL, Greenspan FS. The effect of thyroid

hormones on skeletal integrity. Ann Intern Med
1977;373:353360.
47. Young ER. The thyroid gland and the dental practi-
1999;130:750758.
tioner. J Can Dent Assoc 1989;55:903907.
30. Rovet J, Daneman D. Congenital hypothyroidism: A
48. Fulop M. Pouting sublinguals: Enlarged salivary
review of current diagnostic and treatment prac-
glands in myxoedema. Lancet 1989;8662:550551.
tices in relation to neurophysiologic outcome.

49. Toft AD, Boon NA. General cardiology: Thyroid dis-
Paediatr Drugs 2003;5:141149.
ease and the heart. Heart 2000;84:455460.

31. Forrest D. The developing brain and maternal thyroid hormones: Finding the links. Endocrinology
50. Nyirenda MJ et al. Thyroid disease and increased

cardiovascular risk. Thyroid 2005;15:718724.
2004;145:40344036.
51. Bruce RA. Exercise testing for evaluation of ventricular function. N Eng J Med 1977;296:671675.
VOLUME 39
NUMBER 2
FEBRUARY 2008
149
Huber1.qxd
12/18/07
2:35 PM
Page 150
52. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA

guideline update for perioperative cardiovascular
59. Mandel SJ, Mandel L. Radioactive iodine and the

salivary glands. Thyroid 2003;13:265271.
evaluation for noncardiac surgeryexecutive
60. Huber MA, Terzhalmy GT. The head and neck radi-
summary: A report of the American College of
ation oncology patient. Quintessence Int 2003;34:
Cardi-ology/American Heart Association Task

Force on Practice Guidelines (Committee to
Update the 1996 Guidelines on Perioperative
Cardiovascular Evaluation for Noncardiac Surgery).
J Am Coll Cardiol 2002;39:542553.
693717.
61. Weinberg AD, Brennan MD, Gorman CA, Marsh HM,
OFallon WM. Outcome of anesthesia and surgery
in hypothyroid patients. Arch Intern Med 1983;
143:893897.
53. Kenney WL, ed. ACSAMs Guidelines for exercise

testing and prescription. 5th ed. Baltimore: Williams
and Wilkins,1995.
62. Bennett-Guerrero E, Kramer DC, Schwinn DA. Effect

of chronic and acute thyroid hormone reduction on
perioperative outcome. Anesth Analg 1997;85:
54. Niwa H, Satoh Y, Matsuura H. Cardiovascular

responses to epinephrine-containing local anesthetics for dental use: A comparison of hemodynamic responses to infiltration anesthesia and
3036.
63. Ladenson PW, Levin AA, Ridgeway EC, Daniels GH.
Complications of surgery in hypothyroid patients.
Am J Med 1984;77:261266.
ergometric-stress testing. Oral Surg Oral Med Oral

64. Johnson AB, Webber J, Mansell P, Gallan I, Allison SP,
Pathol Oral Radiol Endod 2000;90:171181.
Macdonald
55. Huber MA, Terzhalmy GT. Risk stratification and
dental management of the patient with adrenal
dysfunction. Quintessence Int 2007;38:325338.
I.
Cardiovascular
and
metabolic
responses to adrenaline infusion in patients with

short-term hypothyroidism. Clin Endocrinol 1995;
43:747751.
56. Miley DD, Terzhalmy GT. The patient with diabetes

mellitus: Etiology, epidemiology, principles of med-
65. Klein I, Ojamaa K. Thyroid hormone and cardiovascular system. N Engl J Med 2001;344:501509.
ical management, oral disease burden, and principles of dental management. Quintessence Int
66. Prusse R, Goulet JP, Turcotte JY. Contraindications

to vasoconstrictors in dentistry: Part II. Hyper-
2005;36:779795.
thyroidism, diabetes, sulfite sensitivity, cortico57. Steinhauer T, Bsoul SA, Terzhalmy GT. Risk stratification and dental management of the patient with
dependent asthma, and pheochromocytoma. Oral

Surg Oral Med Oral Pathol 1992;74:687691.
cardiovascular diseases. Part I: Etiology, epidemiology,
and
principles
of
dental
management.
67. Mito RS, Yagiela JA. Hypertensive response to levonordefrin in a patient receiving propranolol:
Quintessence Int 2005;36:119137.
Report of a case. J Am Dent Assoc 1988;116:5557.

58. Steinhauer T, Bsoul SA, Terzhalmy GT. Risk stratification and dental management of the patient with
cardiovascular diseases. Part II: Oral disease burden
and principles of dental management. Quintessence
Int 2005;36:209227.
150
VOLUME 39
NUMBER 2
FEBRUARY 2008

Artopt

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Artopt

Uploaded by

Copyright:

Available Formats

Huber1.

Risk stratification and dental management

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

Thyroid activity is controlled by the hypothalamic-pituitary-thyroid axis. Thyroid-releasing

appears to have no biologic function.5 Once

Associate Professor and Head, Division of Oral Medicine,

Endowed Professor in Clinical Dentistry, Dental School, and

Correspondence: Dr Michaell A. Huber, Division of Oral

Common thyroid disorders12

Disorders characterized by euthyroidism

involved in the regulation of growth and

The actual prevalence of thyroid disorders

Fig 1 Myxedema is characterized by coarse facial

mode of inheritance.19 Congenital hypothyroidism (cretinism) is a recognized cause of

Figs 2 and 3 Common signs and symptoms of

Thyroid storm is the extreme manifestation of hyperthyroidism. Its uncommon and

Adult Hypo- or Hyperthyroidism

Patients with a suspected thyroid disorder

Drugs used to treat hypothyroidism

T4 and T3 replacement (T4 is

Used when levothyroxin is not

Drugs used to treat hyperthyroidism

Inhibits the transformation of

Long-term thyroxin suppression

Propylthiouracil Inhibits the transformation

therapy is associated with continued clinical

hyperthyroidism, such as tremor, anxiety, and

Antithyroid drugs are the cornerstones in the

With few exceptions, the oral manifestations

cranium, dull expression, flat and broad nose,

risk in association with noncardiac procedures is increased in patients unable to meet

palpation of the thyroid lobule on the opposite

The hypothyroid patient

Dental management of the patient with thyroid dysfunction

The hyperthyroid patient

inducing profound local anesthesia, which is

tive and therapeutic strategies compatible

Some patients with hyperthyroidism may be

chronotropic effects on cardiac muscle. Left

1. Genuth SM. The thyroid gland. In Berne RM, Levy

Crit Care Med 1990;18:253258.

11. McAllister RM, Grossenburg VD, Delp MD, Laughlin

32. Ladenson PW, Singer PA, Ain KB, et al. American

MH. Effects of hyperthyroidism on vascular contrac-

Thyroid Association guidelines for detection of thy-

tile and relaxation responses. Am J Physiol 1998;

33. Kane LA, Gharib H. Thyroid testing A clinical

Suggestions for a revision. J Clin Endocrinol Metab

approach. In Braverman LE (ed). Diseases of the

Thyroid, ed 2. Totowa: Humana Press, 2003: 3953.

13. Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N

34. Carpi A, Nicolini A, Sagripanti A, Righi C, Fabris FM,

Engl J Med 2003;348:26462655.

Di Coscio G. Large-needle aspiration biopsy for the

14. Prummel MF, Strieder T, Wiersinga WM. The environ-

preoperative selection of palpable thyroid nodules

ment and autoimmune thyroid disease. Eur J

diagnosed by fine-needle aspiration as a microfol-

licular nodule or suspected cancer. Am J Clin Pathol

15. Thyroid Foundation of America. Available at http://

35. Carpi A, Nicolini A, Righi C, Romani R, Di Coscio G.

16. Utiger RD. The multiplicity of thyroid nodules and

thyroid nodules diagnosed by fine-needle aspira-