ECE2011 Poster Presentations Bone/calcium/Vitamin D (58 abstracts)
1Department of Biochemistry, University of Medicine and Pharmacy Victor Babes, Timisoara, Romania; 2Department of Endocrinology, University of Medicine and Pharmacy Victor Babes, Timisoara, Romania; 3Department of Physiology, University of Medicine and Pharmacy Victor Babes, Timisoara, Romania; 4Department of Immunology, University of Medicine and Pharmacy Victor Babes, Timisoara, Romania.
Aim: The aim of this study was to assess the implications of TRACP-5b (bone tartrate-resistant acid phosphatase izoform-5b), BAP (bone alkaline phophatase) BGP (bone Gla protein) and E2(estradiol) in bone remodelling process, in osteoporotic postmenopausal women.
Material and method: The study comprised two groups of women with postmenopausal osteoporosis (with different degrees of estrogenic deprivation): group I (n=48, estrogenic deprivation <15 years) and group II (n=26, over 15 years of estrogenic deprivation), compared to a control group (n=20, postmenopausal women without osteoporosis). Serum levels of the above mentioned bone markers were measured by ELISA technique.
Results: The levels of TRACP-5b were significantly higher in postmenopausal osteoporosis (group I: 4.21±1.18 U/l, P<0.001, group II: 4.57±1.41 U/l, P<0.001) versus control group (2.45±1.070 U/l), demonstrating osteoclastogenesis activation.
BAP levels were increased in postmenopausal osteoporosis (group I: 13.76±0.6 μg/l, P<0.001, respectively group II: 11.88±0.38 μg/l, P<0.001) versus control group (8.68±0.44 μg/l), showing osteoblastic activation.
Serum BGP levels in postmenopausal osteoporosis were increased in group I (20.12±0.87 ng/ml, P<0.03), attesting osteoblastic activation and decreased in group II (15.12±1.55 ng/ml, P<0.05) versus control group (16.22±1.62 ng/ml), secondary to osteoblastic apoptosis stimulation.
Estradiol levels were significantly lower in both study groups as compared to control cases (group I: 28.3±1.81 pg/ml, P<0.004 and group II: 19.66±1.23 pg/ml, P<0.002). Estradiol levels correlated with low bone mineral density (in group I: spine BMD=0.639±0.051 g/cm2, P<0.0003 and femoral BMD=0.653±0.042 g/cm2, P<0.0002; in group II: spine BMD=0.563±0.012 g/cm2, P<0.0002, respectively femoral BMD=0.577±0.015 g/cm2, P<0.0001) versus control group (spine BMD=0.773±0.141 g/cm2 and femoral BMD=0.785±0.128 g/cm2).
Conclusion: This imbalance of bone markers reflects a decreased bone formation and an increased bone resorbtion. This will lead to bone demineralization and osteoporotic bone microfractures.