<abstract xmlns="http://www.w3.org/1999/xhtml">

<p>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.</p>
</abstract>

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.

Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

Department of Endocrinology, Medical Faculty

Acta Medica Bulgarica

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

{"article-title":"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...

Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

Publié en ligne: 24 nov. 2020

Pages: 75 - 80

Reçu: 20 nov. 2020

Accepté: 23 nov. 2020

DOI: https://doi.org/10.2478/amb-2020-0050

Mots clés
Parathyroid hormone, primary hyperparathyroidism, bone turnover, Th17, osteoclasts, RANKL

© 2020 I. Yankova et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism

Publié en ligne: 24 nov. 2020

Pages: 75 - 80

Reçu: 20 nov. 2020

Accepté: 23 nov. 2020

DOI: https://doi.org/10.2478/amb-2020-0050

Mots clésParathyroid hormone, primary hyperparathyroidism, bone turnover, Th17, osteoclasts, RANKL

© 2020 I. Yankova et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

Mots clés
Parathyroid hormone, primary hyperparathyroidism, bone turnover, Th17, osteoclasts, RANKL