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Introduction. The decrease in serum estrogens concentration at menopause disrupts the metabolic balance and leads to visceral obesity, which causes an increase in serum estradiol levels, through aromatase activity. Also, estrogen deficiency is a reason for the development of osteoporosis. The objective of the study was to investigate the serum estradiol levels and changes in bone alpha estrogen receptor expression in an experimental model of osteoporosis. Materials and methods. The study included 20 female Wistar rats at a reproductive age of two months, divided into two groups: group 1 (G1) – 10 ovariectomized rats, and group 2 (G2) -10 rats sham-operated. SPSS 20 software (SPSS, Inc., Chicago, IL, USA) was used for statistical analysis of the results. For the immunohistochemical study, the nonparametric test – Mann Whitney was used, by comparing the median values. Data were presented as mean ± standard deviation, with p

Introduction. Canonical Wnt signaling pathway regulates stromal stem cells (SSCs) differentiation and controls the balance between adipogenesis and osteogenesis. Estrogen deficiency affects Wnt signaling by altering the expression of sclerostin (SCL) and the peroxisome proliferator-activated receptor-∝ coactivator 1-∝(PGC-1∝) in the bone tissue. The objective of the study was to monitor whether there is a feedback mechanism between SCL and PGC-1∝ and to determine the extent of the immunohistochemical staining of PGC-1∝ and SCL in bone tissue of estrogen deficiency-induced osteoporosis in female Wistar rats. Materials and methods. An experiment was performed on 20 female Wistar rats at reproductive age (2 months), divided into 2 groups: in group 1 (G1) 10 animals were ovariectomized (ovx) and in group 2 (G2) 10 of the remaining were sham-operated (sham). Results. We found that the PGC-1∝ in the bone marrow stromal cells was reduced in the group with osteoporosis (G1 – ovariectomized rats), compared to sham-operated control group G2 (p