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Review
. 2009 Jul;29(7):437-56.
doi: 10.1016/j.nutres.2009.06.008.

Green tea and bone metabolism

Affiliations
Review

Green tea and bone metabolism

Chwan-Li Shen et al. Nutr Res. 2009 Jul.

Erratum in

  • Nutr Res. 2009 Sep;29(9):684

Abstract

Osteoporosis is a major health problem in both elderly women and men. Epidemiological evidence has shown an association between tea consumption and the prevention of age-related bone loss in elderly women and men. Ingestion of green tea and green tea bioactive compounds may be beneficial in mitigating bone loss of this population and decreasing their risk of osteoporotic fractures. This review describes the effect of green tea or its bioactive components on bone health, with an emphasis on (i) the prevalence and etiology of osteoporosis; (ii) the role of oxidative stress and antioxidants in osteoporosis; (iii) green tea composition and bioavailability; (iv) the effects of green tea and its active components on osteogenesis, osteoblastogenesis, and osteoclastogenesis from human epidemiological, animal, as well as cell culture studies; (v) possible mechanisms explaining the osteoprotective effects of green tea bioactive compounds; (vi) other bioactive components in tea that benefit bone health; and (vii) a summary and future direction of green tea and bone health research and the translational aspects. In general, tea and its bioactive components might decrease the risk of fracture by improving bone mineral density and supporting osteoblastic activities while suppressing osteoclastic activities.

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Figures

Figure 1
Figure 1
Possible actions (stimulatory or inhibitory) of green tea bioactive component (EGCG) in osteoblasts (OB) and osteoclasts (OC). Green tea bioactive components appear to promote bone formation by decreasing oxidative stress (ROS) and pro-inflammatory mediators (TNF-α, COX-2), and by increasing OB activity and survival (HSP27, TGFβ, Runx2, Wnt), resulting in enhanced mineralization (Runx2, osteocalcin, osterix, ALP). Green tea bioactive components suppress bone resorption by inhibiting OC formation (MMP) via increasing OC apoptosis (caspases, Fenton) that results in suppressing osteoclastogenesis. In addition, EC is involved in stimulating osteoblastogenesis, while T-cells and DC are involved in suppressing osteoclastogenesis.

References

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