The female sex hormone oestrogen plays an important role in the structural stability of bones. To date, however, it had been unclear exactly which cells were involved in the hormone’s protective function in preventing changes in bone density. Researchers at Vetmeduni Vienna were able to show for the first time that oestrogen uses a certain cell type as a “mediator” for its beneficial effects on bone. When oestrogen binds to these so-called “bone lining cells”, which cover the bone surfaces, it regulates the expression of a protein called RANKL in these cells. Oestrogen deficiency leads to uncontrolled expression of RANKL, which can trigger pathological changes in the bones. The results were published in Scientific Reports.
The most important female sex hormone, oestrogen, plays a crucial role in the regulation of bone mass. Oestrogen deficiency is known to be a major cause of postmenopausal osteoporosis, or bone weakness. Skeletal stability and pathological skeletal changes thus depend directly on the hormone’s availability and its interaction with the bone cells.
Until now, however, the actual target cells responsible for mediating the effect of oestrogen on bone had still been unknown. Researchers at Vetmeduni Vienna have now demonstrated that bone lining cells act as “gatekeepers” for the hormone. By binding to these cells, oestrogen controls the expression of RANKL, an important factor in bone turnover and remodelling.
Oestrogen uses a certain cell type to mediate its effect on bone density
The development of bone structure depends on a complex system of hormones and proteins. One important component is the signalling molecule RANKL. It influences the development of special cells, the so-called osteoclasts that are responsible for bone resorption. A lack of oestrogen or the corresponding cell receptors where it can bind results in the overproduction of RANKL, which triggers a variety of pathological bone changes.
Several studies confirm oestrogen’s role in regulating RANKL production and thus in protecting skeletal integrity. “Which cells it must bind to in order to have this effect, however, had been a matter of debate,” says study director Reinhold Erben from the Unit of Physiology, Pathophysiology and Experimental Endocrinology. “We were now able to confirm that oestrogen’s effect on bone occurs primarily through binding to the bone lining cells.”
The bone lining cells cover the bone surfaces and contact other bone cells, such as the osteocytes that reside inside the bones, through cell-to-cell contact. They had been suspected of being involved in the regulation of bone resorption through the osteoclasts. The fact that the bone lining cells, as target cells for oestrogen, play a role in bone maintenance confirms this suspicion.