As observed by post hoc analysis.Boro et al. European Journal
As observed by post hoc analysis.Boro et al. European Journal of Medical Research (2014) 19:Page 6 ofTable 6 Comparison of clinical parameters analyzed and particular genotypes of the -197G > A IL-17 polymorphism in women with osteoporosisParameter/genotype T-score Z-score Body mass (kg) Height (cm) Body mass index (kg/m2) Age Birth weight Reproductive years Age of menarche Last menstrual period age* Number of pregnancies Years after menopause* BMD L2 4 (g/cm2) BMD L2 4 YA ( )* BMD L2 4 AM ( )* GG -2.93 ?0.73 -1.50 ?0.66 64.11 ?8.13 163.61 ?4.89 25.92 ?3.62 60.07 ?7.90 3192.68 ?493.06 37.28 ?4.88 13.68 ?1.52 47.6 ?4.82 1.95 ?1.09 10.31 ?5.78 0.84 ?0.06 59.93 ?6.02 69.73 ?6.82 GA -3.30 ?0.67 -1.62 ?0.50 60.07 ?9.22 160.77 ?4.90 23.30 ?4.11 50.32 ?8.18 3062.23 ?443.24 35.62 ?5.39 13.59 ?1.84 50.78 ?5.00 1.93 ?1.14 12.37 ?6.33 0.084 ?0.04 76.32 ?6.90 74.56 ?6.14 AA -2.97 ?0.75 -1.40 ?0.72 59.68 ?8.47 157.82 ?5.13 22.61 ?3.73 52.13 ?8.36 2878.24 ?506.06 34.02 ?4.93 12.87 ?1.97 50.32 ?4.36 1.99 ?1.31 12.85 ?6.04 0.082 ?0.06 70.23 ?6.93 80.88 ?7.*P < 0.05 ?significance of bold entries was observed by post hoc analysis.It has been known for some years that IL-17 and cytokines involved in the production of Th17 lymphocytes, among other IL-23 and IL-21, have an important role in the pathogenesis of rheumatoid arthritis. Today it is known that interleukin 17 is produced not only by the Th17 lymphocytes but also other cell types, including macrophages, neutrophils and mast cells [2]. Interleukin 17 shows strong pro-destructive properties. It stimulates the epithelial, endothelial and fibroblastic cells to release proinflammatory cytokines and connective tissue degrading metalloproteinases [21,22]. Mice in which the IL-17 was neutralized or in which the expression was stopped by means of genetic engineering showed PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27797473 a milder course of bone and joint disease. Therefore, clinical studies are being performed to use antibodies neutralizing this cytokine [2]. Patients suffering from joint and bone disorders show enhanced osteoclastogenesis and activity of osteoclasts along with impaired bone remodeling [23]. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26024392 It is known that osseous tissue erosion follows two routes: from the marrow cavity, effecting in osteoporosis, and from the joint cavity, leading to bone erosion. In normal conditions, RANKL occurs in osteoblasts, whereas under pathological conditions, the sources are other cells. The major reason for bone resorption is the excess of cytokines (including IL-17), promoting osteoclastogenesis through RANKL induction, accompanied by deficiency of cytokines hampering such process [10]. On the other hand, IL-17 not only enhances production of osteoclasts, as initiated by RANKL, but is also capable of inducing such process independently [11].Conclusions Our results suggest that the -197G > A polymorphism of the IL-17 gene may be considered as a genetic factor of postmenopausal osteoporosis. This polymorphism can have the influence on bone mineral density and T-score value in young women and postmenopausal women.Abbreviations AM: age matched; BMD: bone mineral density; BMI: body mass index; CI: confidence interval; DXA: dual energy X-ray absorptiometry; HRT: hormonal replacement therapy; IFN-: interferon gamma; IL: interleukin; MMP-1: ARRY-334543 web matrix metalloproteinase-1; NF-B: nuclear factor kappa-light-chain-enhancer of activated B cells; OR: odds ratios; PCR: polymerase chain reaction; RANK: receptor activator of nuclear factor B; RANKL: receptor activator for nuc.
