One of the difficulties associated with commercial layer production is the development
of osteoporosis in hens late in the production cycle. In light of this fact and because
of hens' unique requirements for Ca, many studies have focused on the regulation of
Ca and the role of estrogen in this process. The time course of estrogen synthesis
over the productive life of hens has been well documented; increased circulating estrogen
accompanies the onset of sexual maturity while decreases signal a decline in egg production
prior to a molt. Numbers of estrogen receptors decrease with age in numerous tissues.
The parallel changes in calcium-regulating proteins, primarily Calbindin D28K, and
in the ability of duodenal cells to transport Ca, are thought to occur as a result
of the changes in estrogen, and are also reversible by the molt process. In addition
to the traditional model of estrogen action, evidence now exists for a possible nongenomic
action of estrogen via membrane-bound receptors, demonstrated by extremely rapid surges
of ionized Ca in chicken granulosa cells in response to 17beta-estradiol. Estrogen
receptors have also been discovered in duodenal tissue, and tamoxifen, which binds
to the estrogen receptor, has been shown to cause a rapid increase in Ca transport
in the duodenum. In addition, recent evidence also suggests that mineralization of
bone per se may not explain entirely the etiology of osteoporosis in the hen but that
changes in the collagen matrix may contribute through decreases in bone elasticity.
Taken together, these studies suggest that changes in estrogen synthesis and estrogen
receptor populations may underlie the age-related changes in avian bone. As with postmenopausal
women, dietary Ca and vitamin D are of limited benefit as remedies for osteoporosis
in the hen.