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

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.