Pregnancy and lactation, a challenge for the skeleton

Abstract

In this review we discuss skeletal adaptations to the demanding situation of pregnancy and lactation. Calcium demands are increased during pregnancy and lactation, and this is effectuated by a complex series of hormonal changes. The changes in bone structure at the tissue and whole bone level observed during pregnancy and lactation appear to largely recover over time. The magnitude of the changes observed during lactation may relate to the volume and duration of breastfeeding and return to regular menses. Studies examining long-term consequences of pregnancy and lactation suggest that there are small, site-specific benefits to bone density and that bone geometry may also be affected. Pregnancy- and lactation-induced osteoporosis (PLO) is a rare disease for which the pathophysiological mechanism is as yet incompletely known; here, we discuss and speculate on the possible roles of genetics, oxytocin, sympathetic tone and bone marrow fat. Finally, we discuss fracture healing during pregnancy and lactation and the effects of estrogen on this process.

Figure 1

Proposed model for the control of osteoclastogenesis and resorptive function of osteoclast (OCs) during adaptations of the skeleton to the demanding situations of pregnancy and lactation. Parathyroid hormone-related protein (PTHrP), synthesized in the placenta, breast tissue, parathyroid glands and the uterus, is the main actor of increased bone resorption. The increased production of oxytocin (OT) from the posterior pituitary stimulates osteoclastogenesis by acting on the osteoclast precursor (preOCs). The over-activity of the sympathetic nervous system (SNS), which increases release of neurotransmitters such as norepinephrine, stimulates bone resorption through an enhanced RANKL secretion by osteoblasts (OBs). In the bone marrow adipose tissue (BMAT), adipocytes undergo lipolysis to provide fatty acids as an energy source for the increased bone resorption.