Table 2.

Molecules and pathways involved in degeneration of ECM in TMJ OA.

Main Factors	Pathways	Effect on ECM Degeneration	References
IL-1β, MMP13	–	Aggravation	39
MMP12	–	Aggravation	2
MMP3/8	–	Aggravation	40
MMP1/3/13	ERK	Aggravation	42
RANTES	–	Aggravation	43
SDF-1	–	Aggravation	43,44
Periostin	NF-κB	Aggravation	45
Osteopontin	NF-κB	Aggravation	46
HMGB2	Wnt/β-catenin	Aggravation	47
miR-21-5p	–	Aggravation	48
Estrogen	ERK, NF-κB	Aggravation	49,50
Notch1	NF-κB, Notch	Aggravation	51
Smad3	TGF-β/Smad3 S1P/S1P3	Inhibition	52
TGF-β1	TGF-β1/Smad2	Aggravation	53
LOXL2	NF-κB, ERK, Integrin/FAK	Inhibition	54,55
Lubricin	–	Inhibition	56
COLV	Wnt/β-catenin	Inhibition	57
Axin1	Wnt/β-catenin FGF/ERK1/2	Inhibition	58
FGFR3	Ihh	Inhibition	59
miR-29b	–	Inhibition	60

Abbreviations: IL: interleukin; MMP: matrix metalloproteinase; ADAMTS: a disintegrin and metalloproteinase with thrombospondin motifs; NF-κB: nuclear factor-kappa B; ERK: Extracellular Signal-Regulated Kinase; RANTES: regulated upon activation, normal T cell expressed and presumably secreted; SDF-1: stromal cell-derived factor 1; TβR1: TGF-beta type I receptor; HMGB: high mobility group box; COL: collagen; S1P: sphingosine-1-phosphate; TGF-β: transforming growth factor beta; FAK: focal adhesion kinase; FGF: fibroblast growth factor; FGFR3: fibroblast growth factor receptor type 3.