Dike N. Kalu

TL;DR: Ovariectomy induced bone loss in the rat and postmenopausal bone loss share many similar characteristics, including: increased rate of bone turnover with resorption exceeding formation; and initial rapid phase of bone loss followed by a much slower phase.

TL;DR: The aged rat model of ovarian hormone deficiency bone loss qualifies for serious consideration as a practical convenient cost-effective animal model for exploring aspects of the pathogenesis and treatment of postmenopausal bone loss.

TL;DR: It is demonstrated that intermittent administration of PTH prevents ovariectomy‐induced bone loss and augments cancellous and cortical bone formation in sexually mature ovariectomized rats, compatible with the view that intermittentadministered PTH increases bone mass, in part by stimulating the proliferation and differentiation of osteoblast progenitors while inhibiting osteoclast proliferation.

TL;DR: The low to very high doses of estradiol used in this study decreased the progression of the bone loss due to ovariectomy by suppression of the rate of bone turnover that involved the depression of both osteoclastic resorption and osteoblastic bone formation.

TL;DR: Findings support the concept of increased sensitivity of bone to PTH in ovarian hormone deficiency osteopenia, but the decrease in serum Ca in ovariectomized rats indicates that other factors may be involved as well.