Auswirkungen von Schilddrüsenfehlfunktionen auf den Knochen

Abstract

Interactions between thyroid hormones and the bone are complex and are still not fully understood. During development, thyroid hormone is essential for the recruitment and maturation of bone cells. A deficit of thyroid hormone during pregnancy and in the newborn leads to retardation of the skeleton. Hypothyroidism during later life causes a relevant decrease of bone turnover. Excessive amounts of thyroid hormone induce increased activity of osteoblasts and osteoclasts leading to high bone turnover and a loss of BMD, as the activity of osteoclasts predominates over the activity of osteoblasts. In subclinical hyperthyroidism, premenopausal women show no significant BMD loss, whereas postmenopausal women face a significant BMD loss. Men seem to have a limited, but significant bone loss in subclinical hyperthyroidism. Therapeutic consequences focus on the normalization of thyroid function, which can lead to restoration of BMD and normalization of bone turnover. In particular, patients on long-term suppressive L-thyroxine therapy or anti-thyroid drug medication benefit from additional antiresorptive treatment. This article surveys the complex interactions between thyroid hormones and bone cells and their effects on bone turnover, BMD and fractures according to the different states of thyroid function.