Table 1.
Molecules and pathways involved in inflammatory responses in TMJ OA.
| Main Factors | Pathways | Effect on Inflammation | References |
|---|---|---|---|
| CRP | – | Aggravation | 4 |
| IL-17a | NF-κB, PI3K/Akt | Aggravation | 6 |
| IL-1β |
|
Aggravation | 7, 8, 9,13 |
| COX2 | – | Aggravation | 10 |
| PGE2 | – | Aggravation | 11 |
| MIP-3 | MAPK, NF-κB | Aggravation | 12 |
| HMGB1 | – | Aggravation | 14 |
| TLR4/MyD88 | NF-κB p38 MAPK | Aggravation | 15,16 |
| HDAC(10) | NF-κB | Aggravation | 17,18 |
| BRD4 | – | Aggravation | 19 |
| LncRNA HOTAIR | – | Aggravation | 20 |
| LncRNA AK094629 | MAPK | Aggravation | 21 |
| miR-1246 | Wnt/β-catenin | Aggravation | 22 |
| hsa_circ_0000448 | – | Aggravation | 23 |
| Connexin 43 | – | Aggravation | 24 |
| Leptin | JAK/STAT3, PI3K/Akt, p38 MAPK | Aggravation | 25 |
| Estrogen | NF-κB | Aggravation | 26,27 |
| SDF-1 | – | Aggravation | 28 |
| Dkk-1 | Wnt/β-catenin NF-κB |
Aggravation | 29 |
| p38 MAPK | p38 MAPK | Aggravation | 30 |
| IL-37 | ERK, JNK, NF-κB, p38 | Inhibition | 31,32 |
| miR-146-5p | – | Inhibition | 33 |
| Progesterone (P4) | NF-κB | Inhibition | 34 |
| Bmal1 | MAPK/ERK | Inhibition | 35 |
| 15d-PGJ2 | – | Inhibition | 36 |
| p21 | – | Inhibition | 37 |
Abbreviations: CRP: C-reaction protein; IL: interleukin; NF-κB: nuclear factor-kappa B; PI3K: phosphoinositide-3 kinase; Akt: protein kinase B; iNOS: inducible nitric oxide synthase; MMP: matrix metalloproteinase; Pin1: peptidyl-prolyl cis-trans isomerase NIMA-interacting 1; HMGB: high mobility group box; TLR: toll-like receptor; SDF-1: stromal cell-derived factor 1; MAPK: mitogen-activated protein kinases; JAK: Janus kinase; STAT3: signal transducer and activator of transcription 3; ERK: Extracellular Signal-Regulated Kinase; JNK: c-Jun N-terminal kinase.