Advanced Search

Home > Journals > Minerva Endocrinologica > Past Issues > Minerva Endocrinologica 2005 December;30(4) > Minerva Endocrinologica 2005 December;30(4):237-46



A Journal on Endocrine System Diseases

Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,118

Frequency: Quarterly

ISSN 0391-1977

Online ISSN 1827-1634


Minerva Endocrinologica 2005 December;30(4):237-46


Effects of thyroid status on bone metabolism: a primary role for thyroid stimulating hormone or thyroid hormone?

Galliford T. M., Murphy E.,Williams A. J., Bassett J. H. D., Williams G. R.

Thyroid hormones are essential for normal skeletal growth and the maintenance of bone mass in adulthood, although their mechanism of action in bone is poorly understood. Hypothyroidism causes impaired bone formation and growth retardation whereas thyrotoxicosis results in accelerated growth, advanced bone age and decreased bone mass. Adults with thyrotoxicosis or a suppressed thyroid stimulating hormone (TSH) from any cause have an increased risk of osteoporotic fracture. Conventionally, bone loss in thyrotoxicosis has been regarded as a direct consequence of thyroid hormone excess acting locally on bone. Recently, however, it has been proposed that TSH may be a direct negative regulator of bone turnover acting via the TSH receptor on both osteoblasts and osteoclasts. Thus, TSH deficiency could be partly responsible for the skeletal loss seen in thyrotoxicosis. Here we provide an overview of the molecular actions of thyroid hormone in bone and discuss in detail the current evidence relating to a possible role for TSH in bone metabolism.

language: English

Full text temporarily not available online. Contact us  REPRINTS

top of page