| Author publication year | Animal studies | TMD condition method of inducing TMD | Gene studied | Results | Study limitations |
| Jing [25] 2014 | Mice | Mutant condylar cartilage Conditional Osxknockout (cKO) mice were generated by crossing Osx-loxP mice to Aggrecan-Cre mice. Cre activity induced by Tamoxifen injection | Osx | Defect in coupling chondrogenesis and osteogenesis in cKO mice, calcified cartilage in hypertrophic zone, few signs of endochondral bone formation, disorganized intramembranous bone | NR |
| Ishizuka [26] 2014 | Mice | OA-like changes Mechanical stress | Samp8 | Abnormal condylar organization, condylar degeneration, decreased chondroprogenitor cell proliferation and increased cell death | NR |
| Li [27] 2014 | Mice | Disc Disorder Knock-in mouse line with replacement of mouse Shox2 by the human SHOX coding sequence | Shox2 | Genetic association with congenital articular disc degeneration, suggesting that SHOX2 represents a susceptible locus for OA of the TMJ | NR |
| Jiao [28] 2014 | Mice | Cartilage degradation Green fluorescent protein mice were crossed with Cre mice | Tgfb1 | Abnormalities in the subchondral bone which induced cartilage degradation | Small sample size |
| Inman [29] 2013 | Mice | Syngnathia, agenesis of TMJ Crossbreeding | Foxc1 | Foxc1−/−mutant mice exhibit bilateral fusion of the upper jaw zygomatic complex to the dentary bone (syngnathia) | NR |
| Ricks [30] 2013 | Mice | OA Heterozygous mice (Dmm/+) of a C3H strain were crossed to produce wildtype(+/+) and Dmm/+ mice | Col2a1 | TMJ in Dmm/+ mice displayed premature articular cartilage and greater defects in chondrocyte arrangement, known biomarkers of OA were significantly expressed (P < 0.01) | NR |
| Yasuda [31] 2012 | Mice | Abnormal endochondral ossification and Class 3 dental malocclusion, shortening of cranial base Knock-in mutation in exon 7 of Fgfr3 gene | Fgfr3 | Articular disc fused with temporal bone, articular surface developed fissures, defects in endochondral ossification, abnormal glenoid fossa, defective trabecular bone formation | NR |
| Purcell [32] 2012 | Mice | NR Inactivation of genes Spry1, Spry2 | Spry1 Spry2 | Combined inactivation of Spry1 and Spry2 genes leads to absence of glenoid fossa and overgrowth of lateral pterygoid and temporalis muscles | NR |
| Huang [13] 2011 | Mice | Internal derangement Commercially bred ank/ank mutant mice were purchased | Ank | Fibrous ankylosis, narrower and/or ankylosed superior and inferior synovial cavities filled with fibrous connective tissue throughout the entire joint space | Utilization of 3-to-5 month old mice in this study might be responsible for the absence of erosive changes in the TMJ. |