Hypothyroidism and Bone

Issue: Supplement to issue 3/2017

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

Clinic of Endocrinology and metabolic diseases; University Hospital “Sv. Marina”; Medical University, Varna

Abstract:
Thyroid hormones play a crucial role in skele-tal growth and development, peak bone mass acquisition and maintenance of bone mass. Triiodothyronine (T3) plays a primordial role in the skeletal homeostasis and stimulates osteoblast dif-ferentiation and activity by complex direct actions on TH-receptors and indirect mechanisms, involv-ing diverse growth factors and cytokines. T3 also stimulates osteoclast differentiation and bone resorption, but it still remains unclear whether this effect results from direct action in osteoclasts or indirectly through RANK-RANKL system. There is now evidence that TSH itself acts as a direct regu-lator of bone remodeling through receptors both on osteoblasts and osteoclasts, highlighting the importance of integrity of the hypothalamo-pitu-itary-thyroid axis.

Untreated hypothyroidism in childhood leads to growth retardation, disturbances of endochon-dral ossification, delayed bone age and persistent short stature. Hypothyroidism in adults causes gen-eral hypometabolism. Bone formation processes are slowed in 50%, bone resorption processes – in 40%. The calciuria is reduced, serum concentra-tion of osteocalcin and alkaline phosphatase is decreased, but serum concentration of parathy-roid hormone and vitamin D can be elevated. Along with the reduction of bone turnover, it has been reported that cortical thickness increases, while bone mineral density of trabecular bone is not affected. Nevertheless, population based stud-ies prove that hypothyroidism is related to increased risk of fractures, although their mecha-nism remains unclear.

Impairment of bone quality is believed to occur in association with the reduction of mechanical stim-uli due to lower physical activity and with an increased risk of falls. Thus, increased fracture risk in hypothyroidism is due to bone stiffness and neu-romuscular instability.

Chronic treatment with thyroid hormones influences bone metabolism. Not only suppressive doses of thyroxin leading to subclinical hyperthy-roidism, but also replacement T4 therapy may neg-atively influence BMD. Once replacement therapy is initiated, there is a “catch-up” bone loss that is transient and actually reversed ultimately by new bone formation.

Key words: hypothyroidism, bone, skeletal growth, fracture risk

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