M C Embree1, G M Iwaoka2, D Kong3, B N Martin4, R K Patel5, A H Lee6, J M Nathan7, S B Eisig8, A Safarov9, D A Koslovsky10, A Koch11, A Romanov12, J J Mao13. 1. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: mce2123@cumc.columbia.edu. 2. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: giwaoka@u.rochester.edu. 3. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: dankon101@gmail.com. 4. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: bnm2107@cumc.columbia.edu. 5. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: rkp2118@cumc.columbia.edu. 6. College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA. Electronic address: al2658@cumc.columbia.edu. 7. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: jmn2156@cumc.columbia.edu. 8. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: sbe2002@columbia.edu. 9. Institute of Comparative Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: as2159@cumc.columbia.edu. 10. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: dak2019@cumc.columbia.edu. 11. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: ak2045@cumc.columbia.edu. 12. Institute of Comparative Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: ar2772@cumc.columbia.edu. 13. College of Dental Medicine, Columbia University Medical Center, New York, NY, USA. Electronic address: jm2654@cumc.columbia.edu.
Abstract
OBJECTIVE: There are limited clinical treatments for temporomandibular joint (TMJ) pathologies, including degenerative disease, disc perforation and heterotopic ossification (HO). One barrier hindering the development of new therapies is that animal models recapitulating TMJ diseases are poorly established. The objective of this study was to develop an animal model for TMJ cartilage degeneration and disc pathology, including disc perforation and soft tissue HO. METHODS: New Zealand white rabbits (n = 9 rabbits) underwent unilateral TMJ disc perforation surgery and sham surgery on the contralateral side. A 2.5 mm defect was created using a punch biopsy in rabbit TMJ disc. The TMJ condyles and discs were evaluated macroscopically and histologically after 4, 8 and 12 weeks. Condyles were blindly scored by four independent observers using OARSI recommendations for macroscopic and histopathological scoring of osteoarthritis (OA) in rabbit tissues. RESULTS: Histological evidence of TMJ condylar cartilage degeneration was apparent in experimental condyles following disc perforation relative to sham controls after 4 and 8 weeks, including surface fissures and loss of Safranin O staining. At 12 weeks, OARSI scores indicated experimental condylar cartilage erosion into the subchondral bone. Most strikingly, HO occurred within the TMJ disc upon perforation injury in six rabbits after 8 and 12 weeks. CONCLUSION: We report for the first time a rabbit TMJ injury model that demonstrates condylar cartilage degeneration and disc ossification, which is indispensible for testing the efficacy of potential TMJ therapies.
OBJECTIVE: There are limited clinical treatments for temporomandibular joint (TMJ) pathologies, including degenerative disease, disc perforation and heterotopic ossification (HO). One barrier hindering the development of new therapies is that animal models recapitulating TMJ diseases are poorly established. The objective of this study was to develop an animal model for TMJ cartilage degeneration and disc pathology, including disc perforation and soft tissue HO. METHODS: New Zealand white rabbits (n = 9 rabbits) underwent unilateral TMJ disc perforation surgery and sham surgery on the contralateral side. A 2.5 mm defect was created using a punch biopsy in rabbit TMJ disc. The TMJ condyles and discs were evaluated macroscopically and histologically after 4, 8 and 12 weeks. Condyles were blindly scored by four independent observers using OARSI recommendations for macroscopic and histopathological scoring of osteoarthritis (OA) in rabbit tissues. RESULTS: Histological evidence of TMJ condylar cartilage degeneration was apparent in experimental condyles following disc perforation relative to sham controls after 4 and 8 weeks, including surface fissures and loss of Safranin O staining. At 12 weeks, OARSI scores indicated experimental condylar cartilage erosion into the subchondral bone. Most strikingly, HO occurred within the TMJ disc upon perforation injury in six rabbits after 8 and 12 weeks. CONCLUSION: We report for the first time a rabbit TMJ injury model that demonstrates condylar cartilage degeneration and disc ossification, which is indispensible for testing the efficacy of potential TMJ therapies.
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