Fig. 1: Non-canonical activation of NF-κB pathway and RANKL-based osteoclastogenesis around dental implants. | BDJ Open

Fig. 1: Non-canonical activation of NF-κB pathway and RANKL-based osteoclastogenesis around dental implants.

From: Signaling pathways of dental implants’ osseointegration: a narrative review on two of the most relevant; NF-κB and Wnt pathways

Fig. 1

A, B Summarizes the role of RANKL-based activation of NF-κB in osteoclatogenesis. A Diagrammatic representation of a dental implant surrounded by alveolar bone during early inflammatory osseointegration events. At the implant bone interface, (a) osteocytes, (b) activated T cells and (c) osteoblasts secrete receptor activator of nuclear factor kappa-B ligand (RANKL) responsible for osteoclasts differentiation from haematopoietic lineage cells such as (d) macrophages. RANKL attaches to its receptor (RANK) on the cell membrane and activates the alternative NF-κB pathway inside the cell leading to its maturation into an (e) osteoclast. Created with BioRender.com. B Activation of receptor activator of NF-κB (RANK) at the cell membrane leads to the activation of α subunit of IκB kinase complex (IKKα) by the NF-κB-inducing kinase (NIK). The IKKα phosphorylates p100, the precursor protein of NF-κB2 (p52) leading to polyubiquitination of p100 and its proteasomal processing to mature p52. The noncanonical NF-κB activation does not involve degradation of the inhibitory molecule IκBα that was attached to p100 before its activation. Processing and maturation of P52 is followed by nuclear translocation of noncanonical NF-κB complex p52/RelB and transcriptional activation of target genes. Created with BioRender.com.

Back to article page