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. 2023 Apr 18;18(3):959–971. doi: 10.1016/j.jds.2023.04.002

Table 5.

Molecules and pathways involved in other biological behaviors in TMJ OA.

Main Factors Pathways Effects References
Netrin-1 Osteoclast activation 74
Wnt5a/Ror2 JNK, Ca2+/NFAT Osteoclast activation 75
TGF-β/TβRI TGFβ/Smad2,3 Osteoclast activation 76
VEGF Osteoclast activation 77
Sema 4D, Plexin B1 Osteoclast activation Osteoblast inhibition 78
miR-29b Wnt5a Osteoclast inhibition 60
miR-26b Wnt/β-catenin Osteoblast activation 79
FGF1, EGF + IL-1β, TNF-α MAPK/ERK FLS activity inhibition 80
Dnmt3b Wnt/β-catenin Stem/progenitor cells differentiation regulation 81
CaSR Chondrocyte terminal differentiation acceleration 82
PTH1R Ihh Chondrocyte terminal differentiation inhibition 83
COL VI Chondrocyte differentiation regulation 84
Lubricin (Prg4) Ihh, BMP Ectopic chondrogenesis inhibition 85

Abbreviations: Ror2: eceptor tyrosine kinase-like orphan receptor 2; JNK: c-Jun N-terminal kinase; NFAT: Nuclear factor of activated T cells; TGF-β: transforming growth factor beta; TβR1: TGF-beta type I receptor; COL: collagen; VEGF: vascular endothelial growth factor; MMP: matrix metalloproteinase; VEGF: vascular endothelial growth factor; FGF: fibroblast growth factor; EGF: epidermal growth factor; Dnmt3b: DNA methylation 3b; CaSR: calcium-sensing receptor; PTH1R: parathyroid hormone type 1 receptor.