Parathyroid gland

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Parathyroid glands
Parathyroid es.svg
Diagram showing the thyroid in front of the thyroid cartilage surrounding the trachea. The four green shaded areas represent the parathyroid glands, positioned behind the thyroid gland.
Illu thyroid parathyroid.jpg
Thyroid and parathyroid.
Latin glandula parathyreoidea inferior, glandula parathyreoidea superior
Gray's p.1271
System Endocrine
Artery superior thyroid artery, inferior thyroid artery,
Vein superior thyroid vein, middle thyroid vein, inferior thyroid vein,
Nerve middle cervical ganglion, inferior cervical ganglion
Lymph pretracheal, prelaryngeal, jugulo-diagastric,and lympahtics of thymus
Precursor neural crest mesenchyme and third and fourth pharyngeal pouch endoderm
MeSH Parathyroid+Glands

The parathyroid glands share a similar blood supply, venous drainage, and lymphatic drainage to the thyroid glands. The glands are derived from the third and fourth brachial arches, with the superior glands arising from the fourth arch, and the inferior glands arising form the third arch. This is a result of an artefact of embryological development, whereby the inferior glands are dragged down alongside the third brachial arch.

Hyperparathyroidism and hypoparathyroidism, characterised by alterations in the blood calcium levels and bone metabolism, are states of surplus or insufficient parathyroid function.


The parathyroid glands are two pairs of glands positioned behind the outer wings of the thyroid. There are typically four parathyroid glands. The two parathyroid glands on each side which are positioned higher are called the superior parathyroid glands, while the lower two are called the inferior parathyroid glands. The parathyroid glands usually weigh between 25 mg and 40 mg in humans. These glands are not visible or palpable during extraoral examination of a patient.[1]

Blood supply[edit]

The blood supply, drainage, and lymphatic drainage of the parathyroid glands are equivalent to the thyroid gland.[2]:918

The superior parathyroid glands receive their blood from the superior thyroid arteries, which are direct branches from the common carotid arteries. The inferior parathyroid glands receive a variable blood supply, from either the ascending branch of the inferior thyroid arteries or the thyroid ima artery. The inferior thyroid artery arises from the subclavian arteries.[2]:917–918

The parathyroid artery drains into the superior and, middle and inferior thyroid veins. The superior and middle veins drain into the jugular vein and the inferior thyroid vein drains into the brachiocephalic veins.[2]:918

Lymphatic drainage[edit]

Lymphatic vessels from the parathyroid glands drain into deep cervical lymph nodes and paratracheal lymph nodes.[2]:918


The parathyroid glands are variable in number: three or more small glands, about the size of a grain of rice, can be located on the posterior surface of the thyroid gland.[3] Occasionally, some individuals may have six, eight, or even more parathyroid glands.[1] Additionally, the glands may not only be located on the back of the thyroid, but also within the thyroid gland itself or in the chest or even the thymus.[3]


The parathyroid glands are named for their proximity to the thyroid but serve a completely different role than the thyroid gland. The parathyroid glands are quite easily recognizable from the thyroid as they have densely packed cells, in contrast with the follicle structure of the thyroid.[4] Two unique types of cells as present in the parathyroid gland:

  • Chief cells, which synthesise and release parathyroid hormone. These cells are small, and appear dark when loaded with parathyroid hormone, and clear when the hormone has been secreted, or in their resting state.[5] :337
  • Oxyphil cells, which are lighter in appearance and increase with age, of unknown function.[5] :337


The parathyroid glands originate from the interaction of neural crest mesenchyme and third and fourth branchial pouch endoderm.[3] The inferior glands develop from the third pouch, and the superior pair from the fourth pouch. During embryological development, the third pouch migrates downwards, dragging the inferior glands with it. The superior pair are not dragged downwards by the fourth pouch to the same degree. Consequently, the inferior glands develop in a position above the superior glands, but their positions are ultimately reversed. The glands are named after their final, not embryological, positions.[6] :377–378

Parathyroid development is regulated by a number of genes, including those coding for several transcription factors.[7] [a]


The major function of the parathyroid glands is to maintain the body's calcium and phosphate levels within a very narrow range, so that the nervous and muscular systems can function properly. The parathyroid glands do this by secreting parathyroid hormone.[5] :336

Parathyroid hormone (PTH, also known as parathormone) is a small protein that takes part in the control of calcium and phosphate homeostasis, as well as bone physiology. Parathyroid hormone has effects antagonistic to those of calcitonin.[8] :985–988

  • Calcium. PTH increases blood calcium levels by stimulating osteoclasts to break down bone and release calcium. PTH also increases gastrointestinal calcium absorption by activating vitamin D, and promotes calcium conservation (reabsorption) by the kidneys.[8] :985–988
  • Phosphate. PTH is the major regulator of serum phosphate concentrations via actions on the kidney. It is an inhibitor of proximal tubular reabsorption of phosphorus. Through activation of Vitamin D the absorption of Phosphate is increased.[8] :985–988

Clinical significance[edit]

Parathyroid disease is conventionally divided into states where the parathyroid is overactive (hyperparathyroidism), and states where the parathyroid is underactive (hypoparathyroidism). Both states are characterised by their symptoms, which relate to the excess or deficiency of parathyroid hormone.[9]:766–767


Hyperparathyroidism is the state in which there is excess parathyroid hormone circulating. This may cause bone pain and tenderness, due to increased bone reabsorption. Due to increased circulating calcium, there may be other symptoms associated with hypercalcemia, most commonly dehydration. Hyperparathyroidism is most commonly caused by a benign proliferation of Chief cells, and rarely MEN syndrome. This is known as primary hyperparathyroidism.[9] :766–767

Renal disease may also lead to hyperparathyroidism. When too much calcium is lost, there is a compensation by the parathyroid, and parathyroid hormone is released. The glands hypertrophy to synthesise more parathyroid hormone. This is also known as secondary hyperparathyroidism. If this situation exists for a prolonged period of time, the parathyroid tissue may become unresponsive to the blood calcium levels, and begin to autonomously release parathyroid hormone. This is known as tertiary hyperparathyroidism.[10] :98–114

Hyperparathyroidism is generally managed by surgical removal of the parathyroid glands.[9]:767


The state of decreased parathyroid activity is known as hypoparathyroidism. This is most commonly associated with damage to the glands or their blood supply during thyroid surgery, although it may also be associated with rarer genetic syndromes such as DiGeorge syndrome or an autosomal dominant syndrome. Hypoparathyroidism will also occur after surgical removal of the parathyoid glands.[9]:768

Occasionally, an individual's tissues are resistant to the effects of parathyroid hormone. This is known as pseudohypoparathyroidism, as although the parathyroid glands are fully functional, the hormone itself is not able too function, resulting in a decrease in blood calcium levels. Pseudohypoparathyroidism is often associated with the genetic condition Albright's hereditary osteodystrophy. Pseudopseudohypoparathyroidism, one of the longest words in the English language, is used to describe an individual possesses with Albright's hereditary osteodystrophy but with normal parathyroid hormone and serum calcium levels.[9]:768

Hypoparathyroidism may present with symptoms associated with decreased calcium, and is generally treated with Vitamin D analogues.[9]:768


The parathyroid glands were first discovered in the Indian Rhinoceros by Richard Owen in 1852.[11] In his description of the neck anatomy, Owen referred to the glands as "a small compact yellow glandular body attached to the thyroid at the point where the veins emerged". The glands were first discovered in humans by Ivar Viktor Sandström (1852–1889), a Swedish medical student, in 1880 at Uppsala University.[12] Unaware of Owen's description, he described the glands in his monograph "On a New Gland in Man and Fellow Animals" as the "glandulae parathyroidae", noting its existence in dogs, cats, rabbits, oxen, horses and humans.[13][14] For several years, Sandström's description received little attention, until more was known about their relationship with Rickets and muscular tetani.[15] Due to a hereditary mental illness, at age 37 Sandstrom committed suicide.[16]

Physiologist Eugene Gley first documented the putative function of the glands in 1891, noting the connection between their removal and the development of muscular tetani. William J. MacCallum in 1908, investigating tumours of the parathyroid, proposed their role in calcium metabolism.[14] He noted that "Tetany occurs spontaneously in many forms and may also be produced by the destruction of the parathyroid glands".[17]

The first successful removal of the parathyroid may have been carried out in 1928 by medical doctor Isaac Y Olch, whose intern had noticed elevated calcium levels in an elderly patient with muscle weakness. Prior to this surgery, patients with removed parathyroid glands typically died from muscular tetani.[14]

Parathyroid hormone was isolated in 1923 by Adolph M. Hanson and 1925 by James B. Collip. Studies of parathyroid hormone levels by Roger Guillemin, Andrew Schally and Rosalyn Sussman Yalow that lead to the development of immunoassays capable of measuring body substances led to a Nobel Prize in 1977.[12][14]

In other animals[edit]

Parathyroid glands are found in all adult tetrapods, although they vary in their number, and in their exact position. Mammals typically have four parathyroids, while other groups typically have six. The removal of parathyroid glands in animals produces a condition resembling acute poisoning and irregular muscle contractions.[18]

Fish do not possess parathyroid glands, however several species have been found to express parathyroid hormone. The fact that developmental genes genes and calcium-sensing receptors in fish gills is similar to those within the parathyroid glands of birds and mammals. This has been suggested used to suggest that the tetrapod glands may have been evolutionarily derived from these fish gills.[7][19]

Additional images[edit]

See also[edit]

This article uses anatomical terminology; for an overview, see anatomical terminology.


  1. ^ Namely the co-activator Eya-1, the homeobox transcription factor Six-1, and the transcription factor Gcm-2 [7]


  1. ^ a b Illustrated Anatomy of the Head and Neck, Fehrenbach and Herring, Elsevier, 2012, p. 159
  2. ^ a b c d Drake, Richard L.; Vogl, Wayne; Tibbitts, Adam W.M. Mitchell ; illustrations by Richard; Richardson, Paul (2005). Gray's anatomy for students. Philadelphia: Elsevier/Churchill Livingstone. ISBN 978-0-8089-2306-0. 
  3. ^ a b c Williams, S. Jacob ; dissections by David J. Hinchcliffe ; photography by Mick A. Turton ; illustrated by Amanda (2007). Human anatomy : a clinically-orientated approach (New ed. ed.). Edinburgh: Churchill Livingstone. ISBN 978-0-443-10373-5. 
  4. ^ Lappas D, Noussios G, Anagnostis P, Adamidou F, Chatzigeorgiou A, Skandalakis P (September 2012). "Location, number and morphology of parathyroid glands: results from a large anatomical series". Anat Sci Int 87 (3): 160–4. doi:10.1007/s12565-012-0142-1. PMID 22689148. 
  5. ^ a b c d Deakin, Barbara Young ... [et al.] ; drawings by Philip J. (2006). Wheater's functional histology : a text and colour atlas (5th ed. ed.). [Edinburgh?]: Churchill Livingstone/Elsevier. ISBN 978-0-443-06850-8. 
  6. ^ Larsen, William J. (2001). Human embryology (3. ed. ed.). Philadelphia, Pa.: Churchill Livingstone. ISBN 0-443-06583-7. 
  7. ^ a b c Zajac, Jeffrey D; Danks, Janine A (July 2008). "The development of the parathyroid gland: from fish to human". Current Opinion in Nephrology and Hypertension 17 (4): 353–356. doi:10.1097/MNH.0b013e328304651c. 
  8. ^ a b c Hall, Arthur C. Guyton, John E. (2005). Textbook of medical physiology (11th ed. ed.). Philadelphia: W.B. Saunders. ISBN 978-0-7216-0240-0. 
  9. ^ a b c d e f Britton, the editors Nicki R. Colledge, Brian R. Walker, Stuart H. Ralston ; illustated by Robert (2010). Davidson's principles and practice of medicine. (21st ed. ed.). Edinburgh: Churchill Livingstone/Elsevier. ISBN 978-0-7020-3084-0. 
  10. ^ Staren, [ed. by] Richard A. Prinz; Edgar D. (2000). Endocrine surgery. Georgetown, Tex.: Landes Bioscience. ISBN 978-1-57059-574-5. 
  11. ^ Cave, A.J.E. (1953). "Richard Owen and the discovery of the parathyroid glands". In E. Ashworth Underwood. Science, Medicine and History. Essays on the Evolution of Scientific Thought and Medical Practice 2. Oxford University Press. pp. 217–222. Retrieved 2009-07-20. 
  12. ^ a b Eknoyan G (November 1995). "A history of the parathyroid glands". Am. J. Kidney Dis. 26 (5): 801–7. doi:10.1016/0272-6386(95)90447-6. PMID 7485136. 
  13. ^ "On a New Gland in Man and Several Mammals (Glandulæ Parathyreoideæ)". Journal of the American Medical Association 111 (2): 197. 9 July 1938. doi:10.1001/jama.1938.02790280087037. 
  14. ^ a b c d DuBose, Joseph; Ragsdale, Timothy; Morvant, Jason (January 2005). ""Bodies so tiny": The history of parathyroid surgery". Current Surgery 62 (1): 91–95. doi:10.1016/j.cursur.2004.07.012. 
  15. ^ Carney, JA (1996 Sep). "The glandulae parathyroideae of Ivar Sandström. Contributions from two continents.". The American journal of surgical pathology 20 (9): 1123–44. PMID 8764749. 
  16. ^ "The glands of Owen". Journal of the Royal Society of Medicine 97 (10): 494–495. 
  17. ^ Maccallum, WG; Voegtlin, C (1909 Jan 9). "ON THE RELATION OF TETANY TO THE PARATHYROID GLANDS AND TO CALCIUM METABOLISM.". The Journal of experimental medicine 11 (1): 118–51. PMID 19867238. 
  18. ^ W. T. COUNCILMAN (1913). "One". Disease and Its Causes. United States: New York Henry Holt and Company London Williams and Norgate The University Press, Cambridge, U.S.A. 
  19. ^ Okabe, M.; Graham, A. (10 December 2004). "The origin of the parathyroid gland". Proceedings of the National Academy of Sciences 101 (51): 17716–17719. doi:10.1073/pnas.0406116101. 

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