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| CASE REPORT |
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| Year : 2018 | Volume
: 8
| Issue : 1 | Page : 39-46 |
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Oral physician: A portal to systemic health through oral health – A case of hypothyroidism and review of literature
Kavita Nagar, GP Sujatha, C Shubha, Ashok Lingappa
Department of Oral Medicine and Radiology, Bapuji Dental College and Hospital, Davangere, Karnataka, India
| Date of Web Publication | 9-May-2018 |
Correspondence Address:
Dr. Kavita Nagar
Department of Oral Medicine and Radiology, Bapuji Dental College and Hospital, Room No 1, MCC B Block, Davangere - 577 004, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijohs.ijohs_7_18
Hypothyroidism refers to deficiency of thyroid hormones. It is potentially fatal if left untreated. It is more commonly seen in females and can be classified on the basis of age, severity, and etiology. Clinical manifestations of hypothyroidism range from subtle changes to life-threatening condition. The most common features are fatigue, lethargy, cold intolerance, weight gain, puffy face, constipation, change in voice, decreased mental activity, and dry skin. Oral manifestations include over-retained deciduous teeth, macroglossia, anterior open bite, enamel hypoplasia, enamel defects, poor periodontal health, and increased incidence of caries. Oral physicians play an important role in early diagnosis of this condition by identifying various signs and symptoms and thus prevent complications associated with dental treatment of such patients. Here, we are presenting a case of hypothyroidism in a 15-year-old female patient diagnosed by oral physician, highlighting the role of dentists in management of such cases.
Keywords: Enamel hypoplasia, hypothyroidism, impacted teeth, macroglossia, retained deciduous teeth
How to cite this article:
Nagar K, Sujatha G P, Shubha C, Lingappa A. Oral physician: A portal to systemic health through oral health – A case of hypothyroidism and review of literature. Int J Oral Health Sci 2018;8:39-46 |
How to cite this URL:
Nagar K, Sujatha G P, Shubha C, Lingappa A. Oral physician: A portal to systemic health through oral health – A case of hypothyroidism and review of literature. Int J Oral Health Sci [serial online] 2018 [cited 2023 Jun 7];8:39-46. Available from: https://www.ijohsjournal.org/text.asp?2018/8/1/39/232174 |
| Introduction | |  |
The thyroid gland is one of the largest endocrine glands in the body, which plays an important role in growth, development, and metabolism of our body. The two main hormones produced by the thyroid gland are triiodothyronine, or T3, and thyroxine, or T4. Their synthesis and secretion is regulated by hypothalamus-pituitary thyroid axis through thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone. Hypothyroidism refers to the common pathological condition of thyroid hormone deficiency. If untreated, it can lead to serious adverse health effects and ultimately death.
| Case Report | | |
A 15-year–old female patient reported to our department with chief complaint of forwardly placed loose milk teeth in upper front teeth region for 1 year. History of present illness revealed that patient had forwardly placed upper milk teeth, which were loose for 1 year. Mobility of teeth was insidious in onset and had gradually increased to the current state. The patient was born by cesarean operation and had normal milestones. Her milk teeth had erupted on time. Past medical history revealed that patient was a known case of epilepsy – generalized tonic–clonic type for 14 years, was on medication, and currently taking tablet levetiracetam 500 mg twice daily. This was patient's first dental visit. Family history was not significant. Personal history revealed that patient had attained menarche 4 years back and had irregular menstrual cycle. Her bowel and bladder movements were normal. She had gained weight and was lethargic. Her scholastic performance had also decreased. On general physical examination, she was well oriented to time, place, and person and showed no signs of pallor, icterus, or cyanosis. Her weight was 65 kg and height was 155 cm with body mass index (BMI) calculated to be 27.08, which was suggestive of overweight. She had dry and rough skin. Her vital signs were normal. On extraoral examination, a solitary swelling was seen on anterior lower part of the neck in the midline region, roughly oval in shape, about 7 cm in diameter with diffuse borders, smooth overlying skin, and normal surrounding skin [Figure 1]. On palpation, no local rise in temperature, nontender, firm in consistency, and moved on swallowing. No bruit was heard on auscultation. Mouth opening and temporomandibular joint (TMJ) movements were normal. Intraoral soft-tissue examination revealed no abnormality. Gingiva was pink in color with diffuse melanin pigmentation, firm and resilient except in the region of maxillary and mandibular anterior teeth where marginal and interdental gingiva was erythematous and enlarged, soft in consistency, and bleeding on probing was present. On hard-tissue examination [Figure 2], permanent teeth present were 11, 12, 16, 17, 21, 22, 26, 27, 31, 32, 36, 41, 42, and 46. 13, 14, 15, 23, 24, 25, 33, 34, 35, 43, 44, and 45 were clinically missing. Over-retained 52, 53, 54, 55, 62, 63, 64, 65, 71, 72, 73, 74, 75, 82, 83, 84, and 85 were present. 52, 62, 71, 72, and 82 were labially placed and 52 and 62 showed mobility. | Figure 1: (a) Profile of the patient. (b) Swelling on anterior lower part of the neck in midline region
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 | Figure 2: Intraoral photographs depicting over-retained deciduous teeth and clinically missing multiple permanent teeth
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Based on history and clinical examination, a provisional diagnosis of over-retained deciduous teeth was given. For swelling in anterior lower part of the neck, provisional diagnosis of the enlarged thyroid gland was given. For over-retained deciduous teeth, following were given as differential diagnosis – congenitally missing permanent successors, multiple impacted permanent teeth, and hypothyroidism. The patient was advised the following investigations: orthopantomogram (OPG), complete hemogram, and thyroid hormone assay.
OPG [Figure 3] revealed mixed dentition in the maxilla and mandible with over-retained 52, 53, 54, 55, 62, 63, 64, 65, 71, 72, 73, 74, 75, 82, 83, 84, and 85 and impacted 13, 14, 15, 23, 24, 25, 33, 34, 35, 43, 44, and 45. No root resorption of deciduous teeth was evident. All permanent impacted teeth had normal follicular space, and root formation was completed. | Figure 3: Orthopantomogram showing over-retained deciduous teeth and multiple impacted permanent teeth
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Complete hemogram was within normal range. Thyroid function assay revealed normal T3 and T4. TSH levels were increased (100 μIU/ml) and antithyroglobulin antibody titer was increased (655.17 IU/ml). Correlating the history and clinical examination with investigation results, a final diagnosis of over-retained deciduous teeth secondary to hypothyroidism (Hashimoto's thyroiditis) was given. Her parents were informed about her systemic condition which she required immediate attention, and the patient was referred to the endocrinologist wherein she was prescribed tablet levothyroxine 100 g once daily. Regarding dental treatment, she was advised to undergo oral prophylaxis and extraction of 52 and 62, after the attainment of normal thyroid assay. The patient was kept under regular follow-up. However, the patient was followed up only for few months after which the patient had not reported despite constant efforts.
After 9 years, the patient again reported to us with chief complaint of pain in the right lower back tooth region for 1 week. History of presenting illness revealed that the patient presented with 1 week history of pain in the right lower back tooth region. Pain was insidious in onset, moderate in intensity, intermittent in nature, throbbing type, localized, aggravated on chewing food, and used to relieve on its own. Her medical history was known. The patient had undergone removal of her lower front teeth 3 years back from a private clinic as they had become loose after she fell during an epileptic attack. The patient had irregular menstrual cycle and gave history of poor performance in school, history of weight gain, tiredness, and hair loss. On general physical examination, the patient was well oriented to time, place, and person. No signs of pallor, icterus, and cyanosis were present. All vitals were normal. Her weight was 81.4 kg, height was 162 cm [Figure 4]a, and BMI was calculated to be 31.06, which was indicative of obesity. The patient had dry and rough skin and fissured feet [Figure 4]b,[Figure 4]c,[Figure 4]d]. Extraoral examination revealed that the profile was convex and lips were competent. Submandibular lymph nodes were palpable bilaterally – solitary, oval in shape, about 1 cm in size, firm in consistency, mobile, and tender on the right side. Mouth opening was normal, and TMJ movements were normal. | Figure 4: (a) Photograph of the patient. (b-d) Photographs of hand and feet showing dry and rough skin
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Intraoral examination of soft tissues revealed that labial mucosa, buccal mucosa, frenal attachments, vestibule, palate, and floor of mouth were normal. The tongue was slightly enlarged; indentations were evident on the right lateral border of the tongue. Gingiva was pink in color with diffuse melanin pigmentation and was normal except erythematous and enlarged marginal and interdental gingiva in relation to maxillary and mandibular teeth, soft, and edematous and showed bleeding on probing. Intraoral hard tissue examination [Figure 5] revealed that teeth present were 11, 12, 16, 17, 21, 22, 26, 27, 36, 37, 46, and 47, over-retained 53, 54, 55, 63, 64, 65, 74, 75, 84, 85; clinically missing 13, 14, 15, 23, 24, 25, 31, 32, 33, 34, 35, 41, 42, 43, 44, 45 Class I caries 37, 47; tender on percussion 47, spacing evident between 21 and 22, retroclined 11, 21, proclined 12, 22, Angle's class II molar relationship bilaterally. Generalized stains were evident. Based on history and clinical examination, following provisional diagnoses were given – chronic apical periodontitis in relation to 47, over-retained deciduous teeth in relation to 53, 54, 55, 63, 64, 65, 74, 75, 84, 85 secondary to hypothyroidism, chronic reversible pulpitis in relation to 37, Angle's Class II division 2 malocclusion, and Kennedy Class IV in relation to 31, 32, 41, 42. Intraoral periapical radiograph (IOPA) in relation to 47, digital OPG, lateral cephalogram in occlusion, and thyroid function tests were advised. | Figure 5: Intraoral photographs depicting over-retained deciduous teeth and clinically missing multiple permanent teeth
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IOPA in relation to 47 [Figure 6]a revealed loss of lamina dura and widening of periodontal ligament space at apical third of roots. Alveolar crest could not be assessed. Radiolucency was seen on occlusal aspect of crown involving enamel, dentin, and pulp. Impacted 48 was also evident. OPG [Figure 6]b reveals mixed dentition in the maxilla and mandible. Teeth present were 11, 12, 13, 14, 15, 16, 17, 18, 21, 22, 23, 24, 25, 26, 27, 28, 33, 34, 35, 36, 37, 38, 43, 44, 45, 46, 47, and 48. Over-retained 53, 54, 55, 63, 64, 65, 74, 75, 84, and 85 were evident and 31, 32, 41, and 42 were missing. 13, 14, 15, 23, 24, 25, 33, 34, 35, 43, 44, and 45 were impacted. Tooth bud in relation to 18, 28, 38, and 48 were evident. Radiolucency involving enamel, dentin, and pulp on occlusal surface of crown in relation to 47 and involving enamel and dentin on occlusal surface of crown in relation to 47 was seen. No root resorption of deciduous teeth was still evident. All permanent impacted teeth had decreased follicular space, and root formation was completed with apical closure. Lateral cephalogram [Figure 6]c revealed prominent sella turcica. (The size of sella turcica ranges from 4 to 12 mm for the vertical and 5 to 16 mm for the anteroposterior dimension.) ANB angle was increased suggesting skeletal Class II malocclusion. | Figure 6: (a) Intraoral periapical radiograph in relation to 47. (b) Lateral cephalogram. (c) Orthopantomogram
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Thyroid function assay revealed normal T3 and T4. TSH levels were increased (15.57 μIU/ml). The provisional diagnosis was confirmed. The patient was referred to endocrinologist for medical evaluation as her TSH levels were high. Symptomatic treatment was rendered as the patient was prescribed antibiotics and analgesics. The following dental treatment plans were advised after the control of hypothyroidism – oral prophylaxis, root canal treatment in relation to 47, restoration in relation to 37, orthodontic treatment for malocclusion, and replacement of missing teeth. The patient is still under follow-up.
| Discussion | | |
Hypothyroidism is a clinical disease state occurring when insufficient thyroid hormone is available to tissue sites of action.[1] The extent of the disease is determined by the severity of deficiency of the thyroid hormones and length of time the deficiency is present. The overall prevalence of hypothyroidism was 10.95%. Inland cities showed a higher prevalence of hypothyroidism as compared to coastal cities. A significantly higher proportion of females (15.86%) as compared to males (5.02%) and older (13.11%) as compared to younger (7.53%) adults were diagnosed with hypothyroidism. In addition, 8.02% patients were diagnosed to have subclinical hypothyroidism (SH).[2] There is a high prevalence of hypothyroidism (13.13%), majority being subclinical in pregnant women during the first trimester in India.[3]
Hypothyroidism can occur as a congenital or acquired condition. Hypothyroidism can be classified by the patient's age at onset as occurring in infants, juveniles, and adults; based on severity as overt/clinical or mild/subclinical. Based on its etiology, it can be primary or secondary hypothyroidism. The causes of hypothyroidism are listed in [Table 1].
The initial manifestations of hypothyroidism are very subtle and may not be evident clinically. The onset of hypothyroidism is more insidious and progression is much slower. [Table 2] lists the various clinical features of hypothyroidism.
Congenital hypothyroidism (CH) is defined as thyroid hormone deficiency present at birth. It is classified into permanent and transient CH. In India, the incidence of CH is thought to be much higher nearly 1:1000 although published reports have been limited and have been done before the availability of diagnostic methods such as nuclear scans for detection of thyroid gland which have increased the precision of the diagnosis. The female to male ratio is about 2:1.[4] The clinical features of CH are often subtle, and many newborn infants remain undiagnosed at birth. This is due in part to passage of maternal thyroid hormone across the placenta. This is measured in umbilical cord serum to be 25–50 percent of normal. Symptoms of CH are a hoarse cry and constipation, prolonged jaundice, lethargy, feeding difficulty and constipation, umbilical hernia, macroglossia and cold or mottled skin, wide posterior fontanel, palpable goiter, a puffy face, flat nasal bridge, and hypotonia with delayed reflexes.[5]
The onset of hypothyroidism in older children and adults is characterized by a dull expression; puffy eyelids; alopecia of the outer third of the eyebrows; palmar yellowing; dry, rough skin; dry, brittle, and coarse hair; increased size of the tongue; slowing of physical and mental activity; slurred, hoarse speech; anemia; constipation; increased sensitivity to cold; increased capillary fragility; weight gain; muscle weakness; and deafness.[6]
Myxedema coma is a rare life-threatening clinical condition in patients with longstanding severe untreated hypothyroidism, in whom adaptive mechanisms fail to maintain homeostasis. The mortality rates may be as high as 25%–60% even with best possible treatment. As the disease is rare and unrecognized, only a few case reports and case series have been reported in the literature. At present, there are over 300 cases reported in literature. The incidence of myxedema crisis is about 0.22 million per year, and epidemiology of myxedema crisis follows the same pattern as in hypothyroidism and is more common in women and elderly.[7]
SH is biochemically defined as a serum TSH concentration above the statistically defined upper limit of the reference range when serum-free thyroxine (fT4) concentration is within its reference range. It can be further classified into mild and severe SH based on the concentration of TSH.[8] Nonthyroidal causes include diabetes mellitus, cystic fibrosis, celiac disease, and chronic renal failure. The clinical presentation varies widely, ranging from no manifestations to clear signs or symptoms of hypothyroidism.
Hypothyroidism during pregnancy has an adverse effect on both mother and child. The risk of abortion, gestational hypertension, anemia, abruptio placenta, and postpartum hemorrhage is increased. Children who are born to mothers with hypothyroidism, have increased risk of impairment in IQ scores, neuropsychological developmental and learning abilities.[9]
Oral manifestations of hypothyroidism are facial myxedema, thick lips, large protruding tongue (macroglossia), malocclusion, delayed eruption of teeth, enamel hypoplasia, compromised periodontal health, increased incidence of caries, and change in taste/dysgeusia. The deposition of mucopolysaccharides or glycosaminoglycans, like hyaluronic acid, in the subcutaneous tissues and connective tissue causes puffiness of face and enlarged tongue. This enlarged tongue causes the flaring of anterior teeth leading to anterior open bite.[10] Mucopolysaccharides in the mucous gel surrounding the enamel organ act as a binding material between it and the surrounding connective tissue. As a result of lack of depolymerization, tooth retention occurs. After depolymerization, the passage of the teeth is eased.[11]
Diagnosis of hypothyroidism is given based on the clinical features and confirmed by evaluation of the thyroid function tests. Radiographs are taken to assess the effect of thyroid on the skeleton including teeth and jaws [Table 3]. Differential diagnosis for hypothyroidism includes hypopituitarism and genetic disorders such as Down's syndrome and familial dwarfism. For adults with myxedema, Cushing syndrome can be considered as differential diagnosis.
Thyroid hormone mediates growth and development of skeleton. The classic findings of hypothyroidism in bone are all described in CH, where the thyroid hormone is inadequate before the formation of epiphysis. However, the effects of low thyroid hormone levels on a growing skeleton after formation of epiphysis is less defined.[12]
The resorption of the roots of deciduous teeth is not evident, and root completion and apical closure of permanent teeth may occur depending on the age of the patient. In longstanding cases, the follicular spaces of permanent teeth may decrease in size, and teeth may be shifted toward the inferior border of the mandible.
The thyroid function tests are used to assess the levels of thyroid hormones and the medical control of the disease. The etiology of the disease can be evaluated. TSH is considered more sensitive than T4 levels. Radioactive iodine uptake can also be done. Thyroid deficiency can cause hyperlipidemia, hypoglycemia, and alterations in cardiac activity; therefore, lipid profile, serum glucose, and electrocardiogram should also be considered.
The goals of management of hypothyroidism are to restore euthyroid state, prevent developmental delay, and prevent irreversible damage to nervous system. In general, for hypothyroidism, levothyroxine sodium, or l-thyroxine, replacement is the first drug of choice. The replacement therapy is required lifelong. The appropriate initiating dose should be around 1.6 micrograms per kilogram. An extra dose may be required during pregnancy or when taken concurrently with intake of rifampin and some anticonvulsant medications. Careful monitoring by the physician is required because of the possibility of causing iatrogenic hyperthyroidism with uncontrolled therapy. Thyroid function tests are performed at six weeks after treatment is initiated. Effectiveness of therapy is measured by a sensitive TSH assay, in which an elevated value indicates insufficient treatment. TSH and FT4 levels should be followed for a period of 6 – 12 months, once the dosage of l-thyroxin has been stabilized.[13]
Regular communication of dentist with endocrinologist is a critical component of safe and optimal treatment of thyroid patients. Communication must be bidirectional. The endocrinologist must be apprised of oral manifestations of the disease, and dentists must be updated on thyroid control medications to help them to maintain patient's oral health.[10]
The dentist plays an important role in detecting thyroid abnormalities. The dentist may be the first one to identify signs and symptoms of thyroid disorders and thus, can aid in its early diagnosis. Furthermore, the dentist can avoid possible dental complications resulting from treating patients with the thyroid disorders.
Modifications of dental treatment should be done for treating patients with thyroid disease. The presence of excess subcutaneous mucopolysaccharides may decrease the ability of small blood vessels to constrict when cut and may result in increased bleeding from infiltrated tissues including mucosa and skin. Local pressure for an extended time will probably control the bleeding from the small vessels adequately.[14] The patient with hypothyroidism may have delayed wound healing due to decreased metabolic activity in fibroblasts. Delayed wound healing may be associated with an increased risk for infection because of the longer exposure of the unhealed tissue to pathogenic organisms. These patients are susceptible to cardiovascular disease from arteriosclerosis and elevated low-density lipoprotein.
Patients who have hypothyroidism are sensitive to central nervous system depressants and barbiturates, so these medications should be used sparingly.[15] It has been found that recent exposure to a surgical antiseptic that includes iodine (such as povidone) can increase the risk of thyroiditis or hypothyroidism. Patients with underlying thyroid antibodies and a tendency toward autoimmunity appear to be at more risk.[16]
Drug interactions of l-thyroxine include increased metabolism due to phenytoin, rifampicin, and carbamazepine, as well as impaired absorption with iron sulfate, sucralfate, and aluminum hydroxide. When l-thyroxine is used, it increases the effects of warfarin sodium and because of its gluconeogenic effects, the use of oral hypoglycemic agents must be increased. Concomitant use of tricyclic antidepressants elevates l-thyroxine levels.[17]
When the patients with CH or cretinism seek dental treatment, the first step should always be behavior management to attain a cooperation from the patient. Such patients require oral hygiene maintenance and restoration of carious teeth, fissure sealants, fluoride application, extraction of teeth with poor prognosis, and removable space maintainer as per patient's need.[18]
Anterior open bite and skeletal malocclusion are commonly seen in these patients and therefore, require orthodontic treatment. It should be kept in mind that these patients may have a lack of response to functional appliances, and root resorption can occur during orthodontic tooth movements as the bone turnover rate in patients with hypothyroidism is low.[19] Moreover, the enlarged tongue may interfere with the dental treatment. Partial glossectomy can be done depending on the severity of interference.
Maintenance of oral hygiene is very crucial for these patients as they are more susceptible to periodontitis. If left untreated, the prognosis will be poor. Hypothyroidism can be found associated with diabetes mellitus; the synergistic effect of both diseases can further deteriorate the preexisting periodontal condition.
Before carrying out any surgical procedure in these patients, physician's consultation should be made regarding the cardiovascular status of the patient. Antibiotic prophylaxis should be provided. Local anesthesia with epinephrine is not a contraindication but should be used cautiously.
Due to increased incidence of caries and enamel defects, these patients require periodic assessment of their oral health. While doing any dental restorative procedure, it should be focused that patients are not lethargic as it indicates uncontrolled state and poses a risk for patients (for example, patient can aspirate dental materials).
Hypothyroidism decreases recruitment, maturation, and activity of bone cells, possibly by reducing circulating levels of insulin-like growth factor-1; this suppresses bone formation as well as resorption. Fracture healing is therefore inhibited. From this information, one may deduce that hypothyroid states lead to greater failures in implant osseointegration. Poor soft-tissue healing and bone loss after loading of implants can occur. However, in a controlled patient, hypothyroidism fails to influence implant survival.[20]
The awareness about the neonatal screening for hypothyroidism should be made in general public. Regular monitoring of health should be done for pregnant women. Assessment of periodontal health and enamel defects should be done using various indices during screening programs.
| Conclusion | | |
Oral physicians play an important role in identifying the various signs and symptoms of hypothyroidism and thus can help in early diagnosis of the condition. For this, the oral health care professional should be familiar with the oral and systemic manifestations of thyroid disease, so he or she can identify any complication and assess the level to which the condition is controlled. If a suspicion of thyroid disease arises for an undiagnosed patient, all elective dental treatment should be put on hold until a complete medical evaluation is performed. Patients with history of thyroid diseases should be carefully evaluated to determine the level of medical management. Dental treatment modifications may be necessary for dental patients who are under medical management and follow-up for a thyroid condition even if there are no comorbid conditions. Stress reduction, awareness of drug side effects or interactions, and vigilance for appearance of signs or symptoms of hormone deficiency are among the responsibilities of the oral health-care provider.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2], [Table 3]
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