Postmenopausal osteoporosis represents an interaction between estrogen scarcity and augmented immune reactivity. T cells are the IL-17 source, while its receptor is expressed on fibroblasts, osteoblasts, chondrocytes, macrophages, dendritic, as well as on endothelial, and most parenchymal cells . IL-17 is one of contributor of bone deterioration in long-established auto-immune inflammatory disorders associated with bone loss including psoriasis, rheumatoid arthritis, systemic sclerosis, and systemic lupus erythematosus [6, 9, 15].
This study aimed to evaluate the levels of IL-17 and estrogen in relation to bone mineral density and risk of fracture in postmenopausal women with and without osteoporosis.
In the present study, IL-17 levels were significantly higher and estradiol levels were significantly lower in the osteoporotic group compared to the non-osteoporotic group (P value ≤ 0.01).
Our results agree with Molnar et al. [16, 17] who investigated serum IL-17A, rank ligand, OPG levels and (BMDs) in 18 pre- and 72 postmenopausal women and reported that IL-17A were elevated in osteoporotic women than in osteopenic ones. They also conveyed the connection between estrogen deficiency and elevated IL-17 level in post-menopausal females.
Same results were also reported by AL-Tai  who evaluated IL-17 in 84 postmenopausal females and concluded that serum IL-17 was significantly high-up in osteoporotic postmenopausal when compared to healthy postmenopausal women. Furthermore, Zhao et al.  reported higher serum concentrations of IL-17, with increased IL-17-producing CD4+ T cells, as well as mRNA levels of IL-17 in CD4+ T cells in osteoporotic postmenopausal women than postmenopausal healthy controls. Similarly, Waliullah et al.  also conveyed a higher level of IL-17 in post-menopausal females with estrogen deficiency.
This is because E2 preserves bone by boosting osteoclasts apoptosis attributed by increased assembly of TGF-β. In an estrogen shortage, the osteoclasts are enhanced by amplified action of proinflammatory cytokines, as IL-1, IL-6, IL-17, and TNF-α, which are adversely operated by estrogen . IL-17 bone loss effect is triggered through RANK ligand-mediated osteoclastogenesis, to generate MCSF and RANKL in osteoblasts and mesenchymal stem cells to boost the growth of bone-resorbing osteoclasts from monocyte/macrophage precursors. Moreover, Th17 cells (RANKL-expressing T cells) reinforce osteoclastogenesis .
De Selm et al.  observed that blocking IL-17 signaling prevents estrogen deficiency-mediated osteoporosis by inhibiting osteoclastogenesis in an animal model. Additionally, there was an upsurge in IL-17A producing T helper 17 cells in BM after ovariectomy of mice, and on providing them with neutralizing IL-17 antibodies; bone loss was no longer deteriorating. While another study established that mice missing the core IL-17 receptor (IL-17RA) or its downstream effector protein, Act1, were guarded from the skeletal impacts of ovariectomy .
In our study, IL-17was inversely correlated to estrogen level and had a highly significant statistical negative correlation with bone mineral density (DEXA score) as well as a highly significant positive one with FRAX index. These results are in harmony with Molnar et al. , Zhang et al. , and Waliullah et al. , who stated that serum IL-17A levels were higher in postmenopausal patients with osteoporosis, with a significant negative correlation between IL-17A levels and BMD further highlighting the influential role of IL-17 in the pathogenesis of postmenopausal OP.
On performing ROC statistical analysis, IL-17 serum level was able to diagnose osteoporosis at a cutoff level of > 80 pg/mL with 100% sensitivity, 100% specificity, 100% PPV, and 100% NPV. To our limited knowledge, this is the earliest study to investigate the diagnostic performance of IL-17 using ROC curve to discriminate osteoporotic from non-osteoporotic postmenopausal females.
In the present study, DEXA score diagnosed osteoporosis at a cutoff level of ≤ 0.875, with 100% sensitivity, 100% specificity, 100% PPV, and 100% NPV and an AUC of 1.0.
As for the FRAX, it can be used to diagnose osteoporosis at a cutoff level of > 0.4, with 93.33% sensitivity, 80% specificity, 82.4% PPV, and 92.3% NPV and an AUC of 0.92.
Kripa et al.  in their study evaluate various screening tools in determining the risk of osteoporosis in 2000 postmenopausal women concluded that the performance of FRAX® was suboptimal as it was devised to foresee fractures not osteoporosis. They found that at a cutoff level of ≥ 0.7%, AUC of 0.736, FRAX® had a sensitivity of 72.7% and an acceptable specificity 60.5%. Thus, the utilization of straightforward evaluating methods for the spotting of osteoporosis helps in the early distinguishing of women in danger of fracture.