German Iris Jasmin Santos, Barbalho Sandra Maria, Andreo Jesus Carlos, Zutin Tereza Lais Menegucci, Laurindo Lucas Fornari, Rodrigues Victória Dogani, Araújo Adriano Cressoni, Guiguer Elen Landgraf, Direito Rosa, Pomini Karina Torres, Shinohara André Luis
Department of Biological Sciences (Anatomy), School of Dentistry of Bauru, University of São Paulo, (FOB-USP), Alameda Doutor Octávio Pinheiro Brisolla, 9-75, Bauru 17012-901, Brazil.
Postgraduate Program in Structural and Functional Interactions in Rehabilitation, University of Marilia (UNIMAR), Marília 17525-902, Brazil.
Metabolites. 2024 Oct 18;14(10):560. doi: 10.3390/metabo14100560.
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. The search was applied to PubMed without limitations in date, language, or article type. Fifteen articles matched the topic and objective of this review. 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. 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.
由于受影响个体的病情逐渐恶化，退行性肌肉骨骼疾病成为一个全球性的健康问题。作为一种生物活性化合物，儿茶素通过刺激成骨细胞和抑制骨吸收表现出骨保护特性。因此，本综述旨在探讨儿茶素对骨组织的作用机制。检索了PubMed，检索日期、语言或文章类型均无限制。有15篇文章符合本综述的主题和目标。表没食子儿茶素没食子酸酯（EGCG）和表儿茶素对成骨标志物RANKL、TRAP和NF-κβ以及骨形态发生蛋白（BMPs）和碱性磷酸酶（ALP）的表达有作用，从而改善骨微结构。动物研究表明，EGCG除了调节与破骨细胞生成相关的转录因子NF-ATc1外，还具有增加钙和骨保护素水平的作用。然而，它对骨钙素和RANK没有任何影响。关于人体研究，EGCG以剂量依赖的方式降低了骨折风险。在牙周组织中，EGCG在体外和体内均降低了IL-6、TNF和RANKL。人体研究表明牙周袋、牙龈指数和临床附着水平有所降低。EGCG对膜和水凝胶的作用通过刺激成骨生长因子的表达以及增加骨钙素和碱性磷酸酶水平，在骨组织微环境中表现出生物相容性和骨诱导特性，从而促进新骨形成。EGCG刺激与成骨相关的细胞因子，增加骨密度，减少破骨细胞生成因子，作为降低骨折风险的治疗策略具有巨大潜力。
