Secondary Osteoporosis in Thyrotoxicosis

Issue: Supplement to issue 3/2017

Author: Dimitrova, Radina S., Boyadzhieva, Mila B., Hristozov, Kiril H., Siderova, Mira V.

Clinic of Endocrinology, University Hospital “Sv. Marina”, Medical University, Varna

Abstract:
Тhyroid hormones are essential for normal skeletal development, linear bone growth, peak bone mass formation and maintenance of normal bone structure and strength.

Thyrotoxicosis causes acceleration of bone remodelling and is one of the main risk factors for secondary osteoporosis with increased bone turnover in elderly. Not only overt but also subclin-ical forms of thyrotoxicosis, including prolonged suppresive levothyroxine treatment, reduce bone mineral density (BMD) and increase fracture risk, especially in postmenopausal women.

Furthermore, studies among euthyroid sub-jects demonstrated a lower BMD and increased risk of fractures in low-normal thyrotropin (TSH). The normal duration of the remodelling cycle is about 200 days, while in thyrotoxicosis it is reduced by half, and in each cycle 9,6% of miner-alised bone is lost. Osteoclastic bone resorption is more pronounced in cortical than in trabecular bone. Triiodothyronine (T3) mediates bone resorp-tion mainly by its alfa receptors (TRa), both direct-ly through effects on the osteoclasts, and indirect-ly activating the osteoblasts. Thyrotropin defficien-cy is suggested as another risk factor for develop-ing osteoporosis. TSH affects bone metabolism through the receptors (TSHR) on the osteoclast and osteoblast precursors. Normalization of thy-roid function reduces bone turnover and increases BMD, but even after treatment it is possible that bone density does not reach its initial level. Previous hyperthyroidism remains a risk factor for hip fractures and for increased mortality in older people.

Key words: thyrotoxicosis, TSH, thyroid hormones, bone

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