Cortical remodeling during menopause, rheumatoid arthritis, glucocorticoid and bisphosphonate therapy

Bone mass, bone geometry and its changes are based on trabecular and cortical bone remodeling. Whereas the effects of estrogen loss, rheumatoid arthritis (RA), glucocorticoid (GC) and bisphosphonate (BP) on trabecular bone remodeling have been well described, the effects of these conditions on the cortical bone geometry are less known. The present review will report current knowledge on the effects of RA, GC and BP on cortical bone geometry and its clinical relevance. Estrogen deficiency, RA and systemic GC lead to enhanced endosteal bone resorption. While in estrogen deficiency and under GC therapy endosteal resorption is insufficiently compensated by periosteal apposition, RA is associated with some periosteal bone apposition resulting in a maintained load-bearing capacity and stiffness. In contrast, BP treatment leads to filling of endosteal bone cavities at the epiphysis; however, periosteal apposition at the bone shaft seems to be suppressed. In summary, estrogen loss, RA and GC show similar effects on endosteal bone remodeling with an increase in bone resorption, whereas their effect on periosteal bone remodeling may differ. Despite over 50 years of GC therapy and over 25 years of PB therapy, there is still need for better understanding of the skeletal effects of these drugs as well as of inflammatory disease such as RA on cortical bone remodeling.

Cryopreservation and transplantation of ovarian tissue exclusively to postpone menopause: technically possible but endocrinologically doubtful.

Transplantation of cryopreserved ovarian tissue has been shown to induce pregnancies and puberty successfully. Therefore, using cryopreserved ovarian tissue to postpone menopause (tissue hormone therapy [THT]) seems to be an interesting option to avoid conventional menopause hormone therapy (MHT). Pregnancy induction and replacing MHT by THT, however, are completely different topics as different requirements need to be met. First, MHT requires long-lasting and continuous hormone production. It still needs to be proven if the transplanted tissue is active for at least 5 years with a continuous follicle growth to avoid phases with low oestrogen production, which would otherwise cause menopausal symptoms and could reduce the postulated benefit for women's health. Second, the advantage of a physiological hormone production over a non-physiological MHT is still hypothetical. Third, women who have undergone hysterectomies who do not need progesterone for endometrial protection would only require oestrogens, imposing more health benefits (cardiovascular system, mammary gland) than oestrogen and progesterone production or replacement. Therefore, transplanting ovarian tissue exclusively to postpone menopause is endocrinologically doubtful and should only be carried out within clinical trials.

Is Menopause Optimal?

Various theories have been put forward to explain the fact that humans experience menopause while virtually no animals do. This paper aims to investigate one such theory: children provide a savings technology into old age, but as human babies are usually large and have long gestation periods, a substantial risk of death exists for the mother as she bears children. It seems therefore appropriate to impose a stopping rule for fertility. Given an objective (support for old age) and demographics (mortality of mother and children), an optimal age for menopause can be calculated. Using demographic data from populations that have seen little influence from modern medicine, this optimal age is compared to empirical evidence.