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Exploring the Impact of Catechins on Bone Metabolism: A Comprehensive Review of Current Research and Future Directions - PubMed

  • ️Mon Jan 01 2024

Review

Exploring the Impact of Catechins on Bone Metabolism: A Comprehensive Review of Current Research and Future Directions

Iris Jasmin Santos German et al. Metabolites. 2024.

Abstract

Background/Objectives: Degenerative musculoskeletal diseases represent a global health problem due to the progressive deterioration of affected individuals. As a bioactive compound, catechins have shown osteoprotective properties by stimulating osteoblastic cells and inhibiting bone resorption. Thus, this review aimed to address the mechanism of action of catechins on bone tissue. Methods: The search was applied to PubMed without limitations in date, language, or article type. Fifteen articles matched the topic and objective of this review. Results: EGCG (epigallocatechin gallate) and epicatechin demonstrated action on the osteogenic markers RANKL, TRAP, and NF-κβ and expression of BMPs and ALP, thus improving the bone microarchitecture. Studies on animals showed the action of EGCG in increasing calcium and osteoprotegerin levels, in addition to regulating the transcription factor NF-ATc1 associated with osteoclastogenesis. However, it did not show any effect on osteocalcin and RANK. Regarding human studies, EGCG reduced the risk of fracture in a dose-dependent manner. In periodontal tissue, EGCG reduced IL-6, TNF, and RANKL in vitro and in vivo. Human studies showed a reduction in periodontal pockets, gingival index, and clinical attachment level. The action of EGCG on membranes and hydrogels showed biocompatible and osteoinductive properties on the microenvironment of bone tissue by stimulating the expression of osteogenic growth factors and increasing osteocalcin and alkaline phosphate levels, thus promoting new bone formation. Conclusions: EGCG stimulates cytokines related to osteogenes, increasing bone mineral density, reducing osteoclastogenesis factors, and showing great potential as a therapeutic strategy for reducing the risk of bone fractures.

Keywords: bone diseases; bone metabolism; bone resorption; catechins; osteoblasts.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1

Therapeutic effects of catechins. Catechins maintain a balance in the synthesis and degradation of proteins and reduce oxidative stress by removing excessive free radicals, promoting the protection of vascular endothelial growth factors in the neovascularization process, and increasing neural function and regeneration by stimulating the binding of nerve growth factors and high-affinity receptors such as the tropomyosin kinase A (TrkA) receptor. In glucose metabolism, catechins increase the phosphorylation of PI3K and protein kinase B, in addition to controlling the oxidation of fatty acids in mitochondria. The anticancer effect occurs by inducing apoptosis of tumor cells and reducing the harmful effects of cancer treatment. Catechins stimulate bone formation mainly through suppressing the RANKL/RANK pathway. As scaffolds or as a supplement incorporated into nanoparticles, polyphenols modify the microenvironment by decreasing free radicals and reducing microorganisms and the inflammatory response.

Figure 2
Figure 2

Molecular pathways of ECG, EGCG, EC, and EGC in bone tissue. The main mechanism of action of ECG stimulates the transcription of the osteogenic markers PP1A, TAZ, and Runx2, thus promoting osteogenic differentiation. EGCG increases the production of the bone markers osteocalcin, ALP, and osterix in osteoblasts and inhibits SAPK/JNK by suppressing the HSP2 and TGF-b pathways. EC also promotes osteogenesis by blocking NFATc-1, NF-κβ, and IL-1b, inhibiting the binding of RANKL and RANK, one of the main pathways of osteoclastogenesis. Finally, EGC initiates the depression of TRAP, a marker of bone resorption that promotes osteoclast migration and also degrades osteonectin. Protein phosphatase 1 catalytic subunit alpha: PP1A; runt-related transcription factor 2: RUNX2; transcriptional coactivator with PDZ-binding motif: TAZ; stress-activated protein kinase: SAPK/Jun amino-terminal kinase: JNK; heat shock protein family: Hsp; Transforming growth factor beta: TGF-β; tartrate-resistant acid phosphatase: TRAP; nuclear factor of activated T cells 1: NFATc-1; factor nuclear kappa B: NF-κβ; receptor activator of nuclear factor kappa-Β ligand: RANKL; receptor activator of nuclear factor kappa-Β: RANK.

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References

    1. Häussler B., Gothe H., Göl D., Glaeske G., Pientka L., Felsenberg D. Epidemiology, Treatment and Costs of Osteoporosis in Germany—the BoneEVA Study. Osteoporos. Int. 2007;18:77–84. doi: 10.1007/s00198-006-0206-y. - DOI - PubMed
    1. Ahmadieh H., Arabi A. Vitamins and Bone Health: Beyond Calcium and Vitamin D. Nutr. Rev. 2011;69:584–598. doi: 10.1111/j.1753-4887.2011.00372.x. - DOI - PubMed
    1. Datta H.K., Ng W.F., Walker J.A., Tuck S.P., Varanasi S.S. The Cell Biology of Bone Metabolism. J. Clin. Pathol. 2008;61:577–587. doi: 10.1136/jcp.2007.048868. - DOI - PubMed
    1. Florencio-Silva R., Sasso G.R.D.S., Sasso-Cerri E., Simões M.J., Cerri P.S. Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells. Biomed. Res. Int. 2015;2015:421746. doi: 10.1155/2015/421746. - DOI - PMC - PubMed
    1. Clarke B. Normal Bone Anatomy and Physiology. Clin. J. Am. Soc. Nephrol. 2008;3((Suppl. S3)):S131–S139. doi: 10.2215/CJN.04151206. - DOI - PMC - PubMed

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Grants and funding

This article was supported by the Brazilian National Council for Scientific and Technological Development (CNPq), Brazil [Nº. 140808/2021-3].

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