Skeletal deterioration following ovarian failure: can some features be a direct consequence of estrogen loss while others are more related to physical inactivity?

Abstract

Findings on experimental animals show that ovarian failure is accompanied by a decrease in motor activity. As mechanical loading has a vital role in the maintenance of skeletal health, our aim was to determine to what extent this decrease in motor activity contributes to ovariectomy-induced bone loss. Thirty-two female Wistar rats were ovariectomized or sham-operated and housed in standard cages or with access to running wheels for 36 weeks with their running distance monitored. Markers of bone turnover were assayed in the serum, and bone geometry, trabecular and cortical bone microarchitecture, mineralization degree, and biomechanical properties were assessed in the femur. Differences between groups were determined by one-way ANOVA. Although reduced motor activity and sex steroid deficiency both resulted in decreases in trabecular bone volume, trabecular number decreases were mostly associated with sex steroid deficiency, whereas trabecular thickness decreases were mostly associated with sedentary behavior. Cortical bone appeared to be more sensitive to variations in motor activity, whereas bone turnover rate and bone tissue mineralization degree seemed to be primarily affected by sex steroid deficiency, even though they were further aggravated by sedentary behavior. Increases in femur length were mostly a consequence of sex steroid deficiency, whereas femoral neck length was also influenced by sedentary behavior. Differences in mechanical properties resulted mostly from differences in physical activity. Both the direct effect of sex steroid deficiency and the indirect effect of motor activity changes are implicated in bone loss following ovariectomy.

Osteokines and Bone Markers at Rest and following Plyometric Exercise in Pre- and Postmenopausal Women

“…The higher PINP/CTXI ratio in the premenopausal group, although it did not reach significance, is consistent with a recent study reporting no differences in CTXI but significantly lower PINP/CTXI ratio in postmenopausal women with low bone mineral density compared to those with normal bone mineral density [ 9 ]. In addition, the significant correlation between the PINP/CTXI ratio and estrogen ( r = 0.58, p = 0.002) supports previous studies suggesting that the decline in circulating estrogen postmenopause leads to a negative change in the balance of bone remodeling [ 3 , 4 ].…”

“…Following menopause, women experience an accelerated decline in bone mass caused by the uncoupling of the bone resorption-formation cycle, when the rate of bone formation by the osteoblasts does not match the rate of resorption by the osteoclasts [ 1 , 2 ]. This uncoupling is due to the decline in circulating estrogen, which influences the balance of bone remodeling [ 3 , 4 ]. The changes in bone remodeling that occur with menopause are reflected in increased circulating bone resorption markers like c-terminal crosslinking telopeptides of type I collagen (CTXI) and procollagen type I amino-terminal propeptide (PINP) [ 5 , 6 ].…”

Collagen-chitosan-hydroxyapatite composite scaffolds for bone repair in ovariectomized rats

“…The risk of osteoporosis is also increased in the case of ovariectomy since female gonadal hormones such as estrogen participate in bone growth and mineralization 37 , 38 . Therefore, the aim of the present study was to evaluate the osteoregenerative capacity of collagen/chitosan/hydroxyapatite-based scaffolds, prepared by two different methods of hydroxyapatite incorporation, in order to determine the ideal material for grafting of defects in healthy bone and fragile bone due to gonadal hormone deficiency.…”

The Effect of Porphyromonas Gingivalis Infection on Menopause to the Mechanical Strength of the Mandible and Femur

“…Selain itu, perubahan hormonal juga menyebabkan aktivitas osteoklas meningkat, sehingga proses resorbsi tulang lebih tinggi dari pada aposisi. Hal ini akan mengakibatkan penurunan densitas mineral tulang dan meningkatkan porositas tulang 17.…”