Endocrine - Thyroid Development

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Embryonic origins of the endocrine organs of the neck
Thyroid development cartoon

The boundary endoderm in the floor region forms a pocket (marked by the foramen cecum) that separates from the surface and forms the thyroid. Cells originate on the surface of the floor and descend into mesoderm above aortic sac and into the hypopharyngeal eminence as "cords". These cells continue to descend until they reach their final destination in the neck adjacent to the thyroid cartilage.

This pathway forms a temporary duct (thyroglossal duct). There are abnormalities of incomplete or excessive descent of these thyroid precursor cells. The thyroid is one of the earliest endocrine organs to differentiate and has an important hormonal role in embryonic development. The early bundle of cells then forms the thyroid by first dividing to form 2 lobes separated by a narrow connecting isthmus.

In the first trimester, the developing fetus is initially dependent upon maternal thyroid hormone crossing the placental barrier.[1] Around week 16 (GA week 18) the fetal thyroid becomes active enough to support the fetal requirements for neural development.

  • Maternal thyroid hormone - required for early stages of brain development (Maternal Thyroid recent studies show both high and low thyroid hormone impact)
  • Fetal functions from week 10 - required for neural development, stimulates metabolism (protein, carbohydrate, lipid), reduced/absence = cretinism (see abnormalities)
  • Fetal fully functional 16 - 18 weeks - (GA 18-20 weeks)
  • Hormones - (amino acid derivatives) Thyroxine (T4), Triiodothyronine (T3)

Maternal thyroid function also changes in early pregnancy, through pituitary changes, resulting in thyroid stimulating hormone (TSH) levels decreasing during the transition from pre-pregnancy to early pregnancy.[2] This change in TSH was less predictable in women with thyroid antibodies. Generally maternal TSH and free T4 are maintained within the same range as those in nonpregnant women.

Hyperthyroidism in adults is generally treated with antithyroid drugs (ATDs), some of these drugs have been identified as teratogens during pregnancy. (More? Antithyroid Drugs)

Iodine deficiency disorders (IDD) is the single most common cause of preventable mental retardation and brain damage in the world. Iodine (Greek, ioeides = violet) is required for the synthesis of thyroid hormone, a key regulator of neurological development. IDD causes goiters and decreases the production of hormones vital to growth and development. (More? iodine deficiency)

Endocrine Links: Introduction | BGD Lecture | Science Lecture | Lecture Movie | pineal | hypothalamus‎ | pituitary | thyroid | parathyroid | thymus | pancreas | adrenal | endocrine gonad‎ | endocrine placenta | other tissues | Stage 22 | endocrine abnormalities | Hormones | Category:Endocrine
Historic Embryology - Endocrine  
1903 Islets of Langerhans | 1903 Pig Adrenal | 1904 interstitial Cells | 1908 Pancreas Different Species | 1908 Pituitary | 1908 Pituitary histology | 1911 Rathke's pouch | 1912 Suprarenal Bodies | 1914 Suprarenal Organs | 1915 Pharynx | 1916 Thyroid | 1918 Rabbit Hypophysis | 1920 Adrenal | 1935 Mammalian Hypophysis | 1926 Human Hypophysis | 1927 Adrenal | 1927 Hypophyseal fossa | 1930 Adrenal | 1932 Pineal Gland and Cysts | 1935 Hypophysis | 1935 Pineal | 1937 Pineal | 1935 Parathyroid | 1940 Adrenal | 1941 Thyroid | 1950 Thyroid Parathyroid Thymus | 1957 Adrenal

head | iodine deficiency | Antithyroid Drugs

Some Recent Findings

Thyroid branching model[3]
  • A branching morphogenesis program governs embryonic growth of the thyroid gland[3] "Here, we show that branching-like morphogenesis is a driving force to attain final size of the embryonic thyroid gland in mice. Sox9, a key factor in branching organ development, distinguishes Nkx2-1+ cells in the thyroid bud from the progenitors that originally form the thyroid placode in anterior endoderm. As lobes develop the thyroid primordial tissue branches several generations. Sox9 and Fgfr2b are co-expressed distally in the branching epithelium prior to folliculogenesis. The thyroid in Fgf10 null mutants has a normal shape but is severely hypoplastic. Absence of Fgf10 leads to defective branching and disorganized angiofollicular units although Sox9/Fgfr2b expression and the ability of cells to differentiate and form nascent follicles are not impaired." SOX | FGF
  • Review - Development of the thyroid gland[4] "Thyroid hormones are crucial for organismal development and homeostasis. ...Here, we review the principal mechanisms involved in thyroid organogenesis and functional differentiation, highlighting how the thyroid forerunner evolved from the endostyle in protochordates to the endocrine gland found in vertebrates. New findings on the specification and fate decisions of thyroid progenitors, and the morphogenesis of precursor cells into hormone-producing follicular units, are also discussed."
  • Thyroid follicle development requires Smad1/Smad5- and endothelial-dependent basement membrane assembly[5] "Thyroid follicles, the functional units of the thyroid gland, are delineated by a monolayer of thyrocytes resting on a continuous basement membrane. Developmental mechanisms whereby follicles are formed by reorganization of a non-structured mass of non-polarized epithelial cells (folliculogenesis) largely unknown. Here we show that assembly of the epithelial basement membrane is critical for folliculogenesis and is controlled by endothelial cell invasion and by BMP-Smad signaling in thyrocytes."
More recent papers  
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.

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  • The displayed list of references do not reflect any editorial selection of material based on content or relevance.
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References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability.

More? References | Discussion Page | Journal Searches | 2019 References | 2020 References

Search term: Thyroid Embryology | http://www.ncbi.nlm.nih.gov/pubmed/?term=thyroglossal+duct thyroglossal duct]

Older papers  
These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.

See also the Discussion Page for other references listed by year and References on this current page.

  • Pyramidal lobe of the thyroid gland and the thyroglossal duct remnant: a study using human fetal sections[6] "To investigate developmental changes in the thyroglossal duct, we observed serial sagittal sections of eight embryos (crown-rump length (CRL) 6-12 mm; approximately 5-6 weeks of gestation) as well as serial horizontal or cross-sections of 70 embryos and fetuses (CRL 15-110 mm; 6-15 weeks). In the sagittal sections, the thyroglossal duct was identified as a small sheet or mass of relatively large cells with vacuolization anterior, superior or inferior to the fourth pharyngeal arch artery. However, we found no continuous duct-like structure that reached the thyroid gland. Thus, previous classical schemes might have overestimated the continuity of the duct. ...Descent of the thyroid gland was not evident after the CRL 20 mm stage (6 weeks): the gland appeared to retain its position at the level of the third-sixth cervical vertebrae."
  • Early thyroid development requires a Tbx1-Fgf8 pathway[7] "The thyroid develops within the pharyngeal apparatus from endodermally-derived cells. ... a Tbx1->Fgf8 pathway in the pharyngeal mesoderm is a key size regulator of mammalian thyroid."
  • Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review.[8] "The World Health Organization (WHO) recently increased their recommended iodine intake during pregnancy from 200 to 250 microg/d and suggested that a median urinary iodine (UI) concentration of 150-249 microg/L indicates adequate iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3-4 d after birth may be a sensitive indicator of even mild iodine deficiency during late pregnancy; a <3% frequency of thyrotropin values >5 mU/L indicates iodine sufficiency."


  • Human Embryology (2nd ed.) Larson
  • The Developing Human: Clinically Oriented Embryology (6th ed.) Moore and Persaud Ch10: p230-233, Ch12: p280-282, Ch13: p319-347
  • Before We Are Born (5th ed.) Moore and Persaud
  • Essentials of Human Embryology Larson
  • Human Embryology Fitzgerald and Fitzgerald Ch24: p166-167
Endocrinology - An Integrated Approach.png Endocrinology - An Integrated Approach Stephen Nussey and Saffron Whitehead

St. George's Hospital Medical School, London, UK Oxford: BIOS Scientific Publishers; 2001. ISBN-10: 1-85996-252-1

Copyright © 2001, BIOS Scientific Publishers Limited. Bookshelf

Chapter 3. The thyroid gland

Development Overview

foramen caecum Stage 13 and Stage 22 thyroid development
Foramen Caecum Stage 13 and Stage 22 thyroid development
  • thyroid median endodermal thickening in the floor of pharynx, outpouch – thyroid diverticulum
  • tongue grows, cells descend in neck
  • thyroglossal duct - proximal end at the foramen cecum of tongue thyroglossal duct
  • thyroid diverticulum - hollow then solid, right and left lobes, central isthmus

Thyroid Timeline

  • 24 days - thyroid median endodermal thickening in the floor of pharynx, outpouch – thyroid diverticulum
  • Week 11 - colloid appearance in thyroid follicles, iodine and thyroid hormone (TH) synthesis growth factors (insulin-like, epidermal) stimulates follicular growth

Stage 13

Stage 13 image 058.jpg Stage 13 image 058.jpg

Links: Stage 13 Sections | Carnegie stage 13

Stage 22

Stage 22 image 068.jpg Stage 22 image 166.jpg

Links: Stage 22 Sections | Carnegie stage 22

Thyroid System and Neural Development

Human thyroid system and neural development.jpg

Links: Neural System Development | Iodine Deficiency

Fetal Thyroid Hormone

Endocrine Pituitary-Thyroid Pathway
  • Initial secreted biologically inactivated by modification, late fetal secretion develops brown fat
  • Iodine deficiency- during this period, leads to neurological defects (cretinism)
  • Birth - TSH levels increase, thyroxine (T3) and T4 levels increase to 24 h, then 5-7 days postnatal decline to normal levels

Thyroid Hormone

Thyroid hormone is synthesized in the thyroid gland by the iodination of tyrosines (monoiodotyrosine) and the coupling of iodotyrosines (diiodotyrosine) in the thyroglobulin.


Thyroxine (T4) molecular structure showing iodine positions (red rings).


Triiodothyronine (T3)

Thyroxine (T4) - (Mr 777) majority of thyroid hormone derived from the thyroid gland. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Triiodothyronine (T3) - synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4), though T3 is mainly used by tissues. Derived mainly from peripheral monodeiodination of T4 (at the 5' position of the outer ring of the iodothyronine nucleus).

HPT axis.jpg


A group of enzymes that can modify the thyroid prohormone secreted by the thyroid gland either activating (deiodinase 2) or deactivating (deiodinase 3) thyroid hormone. Their role is thought to regulate the amount of active hormone available locally in a tissue.

Deiodinase 2

  • (Dio2) A deiodinating enzyme that activates thyroid hormone by clipping the 5'-iodine off of the T4 prohormone to create T3, which is the preferred ligand for thyroid receptors. The enzyme has 5'- outer ring (5'-) catalytic activity.

Deiodinase 3

  • (Dio3) A deiodinating enzyme that inactivates thyroid hormone by removing the 5-iodine from either the T4 prohormone or the T3 active hormone. The enzyme has 5- inner ring (5-) catalytic activity.
Thyroid hormone homeostasis.jpg

Thyroid hormone homeostasis

Links: PubChem - T4 | PubChem - T3


Calcitonin is synthesized by parafollicular cells (C cells) interspersed in the connective tissue between the follicles and the blood capillary network.[9]

Maternal Thyroid

Maternal thyroid related changes during pregnancy[10]:

  • stimulation of maternal thyroid gland by elevated levels of human chorionic gonadotropin (hCG)
  • occurs mainly near end of first trimester associated with a transient lowering in serum TSH
  • increase in serum thyroxine-binding globulin levels
  • small decrease in free hormone concentrations (in iodine-sufficient conditions) significantly amplified in iodine restriction or overt iodine deficiency
  • trend toward a slight increase in basal thyrotropin (TSH) values between first trimester and term
  • modifications of the peripheral metabolism of maternal thyroid hormones

Maternal thyroid hormone crosses the placenta possibly by 3 transport protein family mechanisms[1]

  1. thyoorganic anion-transporting polypeptide
  2. L-type amino acid transporter
  3. monocarboxylate transporter

Maternal Thyroid Function
Pregnancy Time Thyrotropin (TSH) mIU/L Free Thyroxine (FT4) pmol/L
9-12 weeks 0.18 - 2.99 11 - 19.2
second trimester 0.11 - 3.98 10.5 - 18.2
third trimester 0.48 - 4.71 9.0 - 16.1
Total T4 (TT4) reference interval after 19 weeks GA was 77 - 186 nmol/L.

Data[11] - 95th percentile reference

A study has identified an association of maternal thyroid function during early pregnancy with child brain morphology and IQ[12]

  • Maternal levels of free T4 during pregnancy correlate with their offspring's IQ, cortex volume and grey matter volume

• Both the upper and lower limits of normal maternal levels of free T4 during pregnancy are associated with reduced child IQ, as well as decreased child cortex and grey matter volume • Maternal levels of TSH during pregnancy are not associated with child IQ or child brain morphology

In the placenta, the inner ring placental deiodinase inactivates most of the maternal T4 to reverse T3 (rT3). During fetal development to term, up to 30% of the fetal thyroid hormones are of maternal origin.


Thyroid hormone homeostasis and disruptors.[13]

There are structural anatomical variations and thyroid under and over development, there are a number of abnormalities associated with the persistence of the embryological path of thyroid cell descent, the thyroglossal duct.

In addition there are abnormalities due to low iodine environmental conditions of growth and development. This has subsequent effects upon neural and renal development.

Lingual thyroid gland

The failure of thyroid descent.

Ectopic thyroid - lingual 01.jpg sublingual, suprahyoid and subhyoid sublingual and suprahyoid
Ectopic thyroid - lingual[14] Sublingual, suprahyoid and subhyoid[15] Sublingual and suprahyoid[15]

Thyroglossal Cyst

The persistence of the thyroglossal duct.

Thyroglossal fistula

The partial degeneration of the thyroglossal duct.

Abnormal development of the thyroid

Incomplete or excessive descent.

Pyramidal Lobe

Thyroid pyramidal lobe

This additional lobe is formed from the isthmus (50% of people) attached to hyoid bone distal end of thryoglossal duct.

Agenesis of Isthmus

Thyroid agenesis of isthmus[16] An absence of the isthmus with the lateral lobes positioned independently on either side of the trachea. The normal isthmus measures about 1.25 cm transversely as well as vertically and is located anterior to the second and third tracheal cartilages.[16]

Congenital Hypothyroidism

Infant with congenital hypothyroidism[17]
Human thyroid system and neural development

Occurs approximately 1 in 3000 births, associated with neurological abnormalities. This abnormality can occur through either dysgenesis or agenesis of the thyroid gland development or abnormal thyroid hormone production. The condition can be classified as a permanent and transient form.

American Academy of Pediatrics 2006 - Update of newborn screening and therapy for congenital hypothyroidism[18] "Unrecognized congenital hypothyroidism leads to mental retardation. Newborn screening and thyroid therapy started within 2 weeks of age can normalize cognitive development. The primary thyroid-stimulating hormone screening has become standard in many parts of the world. However, newborn thyroid screening is not yet universal in some countries. Initial dosage of 10 to 15 microg/kg levothyroxine is recommended. The goals of thyroid hormone therapy should be to maintain frequent evaluations of total thyroxine or free thyroxine in the upper half of the reference range during the first 3 years of life and to normalize the serum thyroid-stimulating hormone concentration to ensure optimal thyroid hormone dosage and compliance. Improvements in screening and therapy have led to improved developmental outcomes in adults with congenital hypothyroidism who are now in their 20s and 30s. Thyroid hormone regimens used today are more aggressive in targeting early correction of thyroid-stimulating hormone than were those used 20 or even 10 years ago. Thus, newborn infants with congenital hypothyroidism today may have an even better intellectual and neurologic prognosis."

Congenital Hypothyroidism Classification

Classification Etiology
Primary Thyroid dysgenesis (developmental anomaly)

Thyroid dyshormonogenesis (impaired hormone production)

Resistance to TSH binding or signaling

Central Isolated TSH deficiency

Thyrotropin-releasing hormone deficiency

Thyrotropin-releasing hormone resistance

Deficiency in pituitary development transcription factors

Peripheral Resistance to thyroid hormone

Abnormalities of thyroid hormone transport

Syndromic Pendred syndrome

Bamforth-Lazarus syndrome

Ectodermal dysplasia


Kocher - Deber - Semilange syndrome

Benign chorea - hypothyroidism


Obesity - colitis

Transient Maternal intake of antithyroid drugs

Transplacental passage of maternal TSH receptor blocking antibodies

Maternal and neonatal iodine deficiency or excess

Heterozygous mutations of THOX2 or DUOXA2

Congenital hepatic hemangioma/hemangioendothelioma

Based on Table 3 from review on congenital hypothyroidism.[17]

genital - hypothyroidism can also impact upon male genital development, by inhibiting testicular growth, through a delay of Sertoli cell differentiation and proliferation.

Iodine Deficiency

Iodine deficiency disorder (IDD) is the single most common cause of preventable mental retardation and brain damage in the world (More? Abnormal Development - Iodine Deficiency). It is required for synthesis of thyroid hormone, which in turn regulates aspects of neural development.


1.6 billion people are at risk IDD affects 50 million children 100,000 cretins are born every year It causes goiters and decreases the production of hormones vital to growth and development. Children with IDD can grow up stunted, apathetic, mentally retarded and incapable of normal movement, speech or hearing. IDD in pregnant women cause miscarriage, stillbirth and mentally retarded children.

A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly. In areas of endemic iodine deficiency, where soil and therefore crops and grazing animals do not provide sufficient dietary iodine to the populace, food fortification and supplementation have proven highly successful and sustainable interventions.

Iodized salt programs and iodized oil supplements are the most common tools in the fight against IDD.

(Data: ICCIDD)

Prolonged intake of large amounts (excess) of iodide can increase the incidence of goiter and/or hypothyroidism in humans. African Congo appears to be the only country that appears to have a dietary excess.

Links: Iodine Deficiency

Maternal Abnormalities

Thyroid uptake scans .jpg

Thyroid uptake scan images of normal and abnormal thyroids (A) Normal

(B) Graves disease: diffuse increased uptake in both thyroid lobes.

(C) Toxic multinodular goiter (TMNG): "hot" and "cold" areas of uneven uptake.

(D) Toxic adenoma: increased uptake in a single nodule with suppression of the surrounding thyroid.

(E) Thyroiditis: decreased or absent uptake.

Thyroid uptake scans image[19] Maternal Graves Disease - "The dose of anti-thyroid drug usually needs to be decreased during pregnancy, and often Graves disease remits completely and the medication can be withdrawn. This is probably due to the overall immunosuppressive effect of pregnancy."

Graves' disease in mothers can cause thyrotoxic fetus - may have increased fetal motility and develop a range of abnormalities including: goitre, tachycardia, heart failure associated hydrops, growth retardation, craniosynostosis and accelerated bone maturation.

Maternal Hashimoto's Thyroiditis (common autoimmune thyroid disease) usually no consequences on fetal thyroid, even if antibodies (anti-TPO and anti-Tg) found in the newborn due to transplacental passage.

maternal hypothyroxinemia

Links: NIH Genes & Disease - Chapter 41 - Endocrine | EPA (USA) - Radiation Technetium

Environmental Thyroid Disruptors

Thyroid hormone homeostasis and disruptors.[13]

There are several environmental compounds (chemicals) that are suspected of being thyroid disruptors including:

  • halogenated phenolic compounds (3,3',5,5'-tetrabromobisphenol A, 3,3',5,5'-tetrachlorobisphenol A, 4-hydroxy-2',3,4',5,6'-pentachlorobiphenyl)
  • phenol compounds (pentachlorophenol, 2,4,6-triiodophenol)

They have been demonstrated to induce partial agonistic and/or complex competitive/uncompetitive antagonistic responces in cell culture.

Bisphenol A - monomer used to manufacture polycarbonate plastic, possibly disrupts thyroid hormone function and affects neocortical development (accelerating neuronal differentiation/migration). (More? EHP - Bisphenol A Need for a New Risk Assessment)


Mouse (E14.5) Titf1 gene expression[20]
  • Thyroid Transcriptor Factors (TTF) - TTF-1, TTF-2, PAX-8
  • Fetal hypothyroidism from low levels of these transcription factors- Pit-1, Prop-1, LHX-3
  • Thyrotropin-releasing hormone (TRH)
  • Thyroid-stimulating hormone (TSH)

Mouse thyroid Hes1 model.jpg

Mouse thyroid Hes1 model[21]

Thyroid Images

Adult Histology



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Online Textbooks

Endocrinology: An Integrated Approach Nussey, S.S. and Whitehead, S.A. Oxford, UK: BIOS Scientific Publishers, Ltd; 2001. table of Contents

NIH Genes & Disease Chapter 41 - Endocrine

Developmental Biology (6th ed) Gilbert, Scott F. Sunderland (MA): Sinauer Associates, Inc.; c2000.

Molecular Biology of the Cell (4th Edn) Alberts, Bruce; Johnson, Alexander; Lewis, Julian; Raff, Martin; Roberts, Keith; Walter, Peter. New York: Garland Publishing; 2002.

Health Services/Technology Assessment Text (HSTAT) Bethesda (MD): National Library of Medicine (US), 2003 Oct. Thyroid Gland search Results


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Chan SY, Vasilopoulou E & Kilby MD. (2009). The role of the placenta in thyroid hormone delivery to the fetus. Nat Clin Pract Endocrinol Metab , 5, 45-54. PMID: 19079273 DOI.

Postiglione MP, Parlato R, Rodriguez-Mallon A, Rosica A, Mithbaokar P, Maresca M, Marians RC, Davies TF, Zannini MS, De Felice M & Di Lauro R. (2002). Role of the thyroid-stimulating hormone receptor signaling in development and differentiation of the thyroid gland. Proc. Natl. Acad. Sci. U.S.A. , 99, 15462-7. PMID: 12432093 DOI.

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De Felice M, Postiglione MP & Di Lauro R. (2004). Minireview: thyrotropin receptor signaling in development and differentiation of the thyroid gland: insights from mouse models and human diseases. Endocrinology , 145, 4062-7. PMID: 15231702 DOI.

Grüters A, Biebermann H & Krude H. (2003). Neonatal thyroid disorders. Horm. Res. , 59 Suppl 1, 24-9. PMID: 12566717 DOI.


Abu-Khudir R, Paquette J, Lefort A, Libert F, Chanoine JP, Vassart G & Deladoëy J. (2010). Transcriptome, methylome and genomic variations analysis of ectopic thyroid glands. PLoS ONE , 5, e13420. PMID: 20976176 DOI.

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Iskaros J, Pickard M, Evans I, Sinha A, Hardiman P & Ekins R. (2000). Thyroid hormone receptor gene expression in first trimester human fetal brain. J. Clin. Endocrinol. Metab. , 85, 2620-3. PMID: 10902817 DOI.

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Pages where the terms "Historic" (textbooks, papers, people, recommendations) appear on this site, and sections within pages where this disclaimer appears, indicate that the content and scientific understanding are specific to the time of publication. This means that while some scientific descriptions are still accurate, the terminology and interpretation of the developmental mechanisms reflect the understanding at the time of original publication and those of the preceding periods, these terms, interpretations and recommendations may not reflect our current scientific understanding.     (More? Embryology History | Historic Embryology Papers)


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Cite this page: Hill, M.A. (2024, June 21) Embryology Endocrine - Thyroid Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Endocrine_-_Thyroid_Development

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© Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G