Abstract
Osteoporosis is the second most common disease only secondary to cardiovascular disease, with the risk of fracture increasing with age. Osteoporosis is caused by an imbalance between osteoblastogenesis and osteoclastogenesis processes. Osteoclastogenesis may be enhanced, osteoblastogenesis may be reduced, or both may be evident. Inflammation and high reactive oxygen enhance osteoclastogenesis while reducing osteoblastogenesis by inducing osteoblast apoptosis and suppressing osteoblastic proliferation and differentiation. Catechins, the main polyphenols found in green tea with potent anti-oxidant and anti-inflammatory properties, can counteract the deleterious effects of the imbalance of osteoblastogenesis and osteoclastogenesis caused by osteoporosis. Green tea catechins can attenuate osteoclastogenesis by enhancing apoptosis of osteoclasts, hampering osteoclastogenesis, and prohibiting bone resorption in vitro. Catechin effects can be directly exerted on pre-osteoclasts/osteoclasts or indirectly exerted via the modulation of mesenchymal stem cells (MSCs)/stromal cell regulation of pre-osteoclasts through activation of the nuclear factor kB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system. Catechins also can enhance osteoblastogenesis by enhancing osteogenic differentiation of MSCs and increasing osteoblastic survival, proliferation, differentiation, and mineralization. The in vitro effects of catechins on osteogenesis have been confirmed in several animal models, as well as in epidemiological observational studies on human subjects. Even though randomized control trials have not shown that catechins provide anti-fracture efficacy, safety data in the trials are promising. A large-scale, placebo-controlled, long-term randomized trial with a tea regimen intervention of optimal duration is required to determine anti-fracture efficacy.
Highlights
The canonical Wnt signaling is the main pathway regulating osteoblastogenesis, including osteoblastic differentiation, proliferation, maturation, and activity
epigallocatechin gallate (EGCG) treatments: ↑ apoptotic cell death of osteoclast-like multinucleated cells, whereas osteoblasts affected the Fenton reaction primarily involved in EGCG-induced osteoclastic cell death
EGCG treatments: ↓ ET-1-induced IL-6 synthesis ↔ ET-1-induced phosphorylation of p38 MAP kinase ↓ phosphorylation of p44/p42 MAP kinase and 12-O-tetradecanoylphorbol 13-acetate (TPA), a direct activator of PKC induced by ET-1
Summary
Osteoporosis is a disease that causes reduced bone density and quality. Bones become fragile and more porous, and as a result the risk of fracture is greatly increased. Bone mineral density (BMD) and quality decide bone strength. Bone quality is determined by bone architecture, turnover, damage accumulation, matrix mineralization, and collagen composition [1]. One in two women and one in three men aged greater than 60 years will have an osteoporosis-related fragility fracture that may increase the monetary burden by USD131.5 billion by 2050 [3,4,5]. Bone has dynamic turnover through a remodeling process controlled by osteoclasts, osteoblasts, and osteocytes. An imbalance of regulatory factors is closely associated with osteoporosis. An imbalance between osteoclastogenesis (bone resorption) and osteoblastogenesis (bone formation) during remodeling, which causes enhanced bone resorption with or without decline in bone formation, remains the main cause of osteoporosis [8]
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