Submitted to: Osteoporosis International
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/11/2010
Publication Date: 1/7/2011
Publication URL: http://handle.nal.usda.gov/10113/58082
Citation: Shen, C., Yeh, J.K., Samathanam, C., Cao, J.J., Stoecker, B.J., Dagda, R.Y., Chyu, M., Dunn, D.M., Wang, J. 2011. Green tea polyphenols attenuate deterioration of bone microarchitecture in female rats with systemic chronic inflammation. Osteoporosis International. 22:327-337. Interpretive Summary: Bone loss occurs in patients with different types of chronic inflammation and with increased oxidative stress. Green tea, the most popular beverage in the world, has antioxidant and anti-inflammatory properties and may be beneficial to bone health. We evaluated whether green tea polyphenols (green tea bioactive components) can restore bone microstructure in an animal model of chronic inflammation (lipopolysaccharide implantation). Forty female rats were assigned to 4 groups. Rats were either implanted with or without slow-release lipopolysaccharide pellets and supplemented with or without green tea polyphenols in drinking water for 12 weeks. Bone structure and quality were evaluated using hitomorphometric and micro-computed tomographic methods. Lipopolysaccharide implantation decreased trabecular bone volume, thickness, and bone formation while increased osteoclast number and surface in proximal tibia. Green tea polyphenols improved the strength of femur and suppressed TNF-alpha expression in proximal tibia. We conclude that green tea can prevent bone loss induced by chronic inflammation by suppressing TNF-alpha expression. Our findings suggest that green tea polyphenols may have a beneficial role in bone health in patients with chronic inflammation.
Technical Abstract: Introduction: Our previous study demonstrated that green tea polyphenols (GTP) benefit bone health in female rats with chronic inflammation, because of GTP’s antioxidant capacity. The current study further evaluates whether GTP can restore bone microstructure along with related mechanism in rats with chronic inflammation. Methods: A 12-week study was performed based on a 2 (placebo vs. lipopolysaccharide, LPS)×2 [no GTP vs. 0.5% GTP (w/v) in drinking water) factorial design. 40 female rats (3-month-old)were assigned to 4 groups (n=10/group): placebo (P), LPS implantation (L), P+0.5% GTP (PG), and LPS+0.5% GTP (LG). Efficacy was evaluated by examining changes in tibial and femoral microarchitecture using histomorphometric and micro-computed tomographic analyses respectively, as well as that in bone quality using 3-point bending test. In addition, a possible mechanistic profile was studied by assessing the difference in expression of tumor necrosis factor-a (TNF-a) in tibia using immunohistochemistry. Results: LPS administration decreased trabecular volume, thickness, bone formation, and osteoclast number in proximal tibia, while increased eroded surface in endocortical tibial shafts. GTP supplementation increased trabecular volume and number in both femur and tibia, as well as periosteal mineralized surface in endocortical tibial shafts, while decreased trabecular separation in proximal tibia and eroded surface in endocortical tibial shafts. There is an interaction between LPS and GTP in trabecular number, separation, bone formation, and osteoclast number in proximal tibia, and trabecular thickness and number in femur. Supplementation of GTP in drinking water significantly improved the strength of femur, as shown in higher level of maximum force and yield point force by 3-point bending test. In addition, GTP supplementation suppressed the expression of TNF-a in tibia induced by LPS. Conclusion: We concluded that GTP supplementation mitigated deterioration of bone microarchitecture and improved bone integrity in female rats with chronic inflammation by suppressing bone erosion and modulating cancellous and endocortical bone compartments, resulting in a larger net bone volume. Such a protective role of GTP may, in part, be attributed to a suppression of pro-inflammatory cytokine mediator, TNF-a.