Flavonoids: Classification, Function, and Molecular Mechanisms Involved in Bone Remodelling

Abstract

Flavonoids are polyphenolic compounds spotted in various fruits, vegetables, barks, tea plants, and stems and many more natural commodities. They have a multitude of applications through their anti-inflammatory, anti-oxidative, anti-carcinogenic properties, along with the ability to assist in the stimulation of bone formation. Bone, a rigid connective body tissue made up of cells embedded in a mineralised matrix is maintained by an assemblage of pathways assisting osteoblastogenesis and osteoclastogenesis. These have a significant impact on a plethora of bone diseases. The homeostasis between osteoblast and osteoclast formation decides the integrity and structure of the bone. The flavonoids discussed here are quercetin, kaempferol, icariin, myricetin, naringin, daidzein, luteolin, genistein, hesperidin, apigenin and several other flavonoids. The effects these flavonoids have on the mitogen activated protein kinase (MAPK), nuclear factor kappa β (NF-kβ), Wnt/β-catenin and bone morphogenetic protein 2/SMAD (BMP2/SMAD) signalling pathways, and apoptotic pathways lead to impacts on bone remodelling. In addition, these polyphenols regulate angiogenesis, decrease the levels of inflammatory cytokines and play a crucial role in scavenging reactive oxygen species (ROS). Considering these important effects of flavonoids, they may be regarded as a promising agent in treating bone-related ailments in the future.

Bone remodeling serum markers in children with systemic lupus erythematosus

“…Bone remodeling is a dynamic equilibrium biological process of the interaction between osteoblast and osteoclast. When the balance of bone remodeling is disturbed, and bone resorption exceeds bone formation, it results in conditions like bone loss and osteoporosis [ 2 ].…”

“…Many childhood chronic diseases have impact on bone health, such as type 1 diabetes mellitus [ 3 ], chronic kidney disease [ 4 ], rheumatic arthritis [ 2 ], and SLE [ 1 ], involving bone remodeling degeneration. GC can contribute to bone deterioration through the suppression of bone formation and osteoclast activity.…”

“…Glucocorticoid (GC) and inflammatory mediators could impact bone remodeling by OPG/RANKL/RANK signal system [ 2 ]. There have been few studies on the interactions of the OPG/RANK/RANKL system in children with lupus.…”

Research on the Mechanism of Kaempferol for Treating Senile Osteoporosis by Network Pharmacology and Molecular Docking

“…KP also suppresses the production of nitric oxide that triggers the activation of TNF- α , thereby inhibiting inflammatory response [ 51 ]. There is growing evidence for the role of kaempferol in attenuating inflammatory response mediated by NF- к B, indicating its protective effects on bone loss in postmenopausal osteoporosis by blocking TNF- α -induced nuclear translocation of the NF- к B subunit p65 from the cytoplasm to the nucleus [ 52 ]. And KP could suppress age-related NF- к B activation by inhibition of NF- к B subunit p65 translocation so as to restrain inflammatory response [ 53 ].…”

Purple tea water extract blocks RANKL-induced osteoclastogenesis through modulation of Akt/GSK3β and Blimp1-Irf8 pathways

“…1 and Table 1. Notably, EGCG, quercetin, myricetin, kaempferol, and chlorogenic acid have been reported to attenuate osteoclast differentiation, [17][18][19] prompting us to speculate that PTE may suppress osteoclastogenic activities.…”