Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

Parathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, ost...

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Autores principales:	Yankova I., Shinkov A., Kovatcheva R.
Formato:	article
Lenguaje:	EN
Publicado:	Sciendo 2020
Materias:	parathyroid hormone primary hyperparathyroidism bone turnover th17 osteoclasts rankl Medicine R
Acceso en línea:	https://doaj.org/article/02182e0469224b45bb49328e7d74663e
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spelling	oai:doaj.org-article:02182e0469224b45bb49328e7d74663e2021-12-02T17:55:13ZChanges in Bone Metabolism and Structure in Primary Hyperparathyroidism0324-175010.2478/amb-2020-0050https://doaj.org/article/02182e0469224b45bb49328e7d74663e2020-11-01T00:00:00Zhttps://doi.org/10.2478/amb-2020-0050https://doaj.org/toc/0324-1750Parathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.Yankova I.Shinkov A.Kovatcheva R.Sciendoarticleparathyroid hormoneprimary hyperparathyroidismbone turnoverth17osteoclastsranklMedicineRENActa Medica Bulgarica, Vol 47, Iss 4, Pp 75-80 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	parathyroid hormone primary hyperparathyroidism bone turnover th17 osteoclasts rankl Medicine R
spellingShingle	parathyroid hormone primary hyperparathyroidism bone turnover th17 osteoclasts rankl Medicine R Yankova I. Shinkov A. Kovatcheva R. Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
description	Parathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.
format	article
author	Yankova I. Shinkov A. Kovatcheva R.
author_facet	Yankova I. Shinkov A. Kovatcheva R.
author_sort	Yankova I.
title	Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
title_short	Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
title_full	Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
title_fullStr	Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
title_full_unstemmed	Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism
title_sort	changes in bone metabolism and structure in primary hyperparathyroidism
publisher	Sciendo
publishDate	2020
url	https://doaj.org/article/02182e0469224b45bb49328e7d74663e
work_keys_str_mv	AT yankovai changesinbonemetabolismandstructureinprimaryhyperparathyroidism AT shinkova changesinbonemetabolismandstructureinprimaryhyperparathyroidism AT kovatchevar changesinbonemetabolismandstructureinprimaryhyperparathyroidism
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Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

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