Embree M C, Iwaoka G M, Kong D, Martin B N, Patel R K, Lee A H, Nathan J M, Eisig S B, Safarov A, Koslovsky D A, Koch A, Romanov A, Mao J J
College of Dental Medicine, Columbia University Medical Center, New York, NY, USA.
College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA.
Osteoarthritis Cartilage. 2015 Apr;23(4):629-39. doi: 10.1016/j.joca.2014.12.015. Epub 2015 Jan 5.
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.
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.
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.
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.
颞下颌关节(TMJ)疾病,包括退行性疾病、盘穿孔和异位骨化(HO),临床治疗方法有限。阻碍新疗法发展的一个障碍是,模拟TMJ疾病的动物模型尚未完善。本研究的目的是建立一种用于TMJ软骨退变和盘病变(包括盘穿孔和软组织HO)的动物模型。
对9只新西兰白兔进行单侧TMJ盘穿孔手术,对侧进行假手术。用活检打孔器在兔TMJ盘中制造一个2.5毫米的缺损。在4周、8周和12周后,对TMJ髁突和盘进行宏观和组织学评估。由四名独立观察者根据骨关节炎研究学会国际(OARSI)对兔组织骨关节炎(OA)宏观和组织病理学评分的建议,对髁突进行盲法评分。
与假手术对照组相比,在4周和8周后,实验侧髁突在盘穿孔后出现明显的TMJ髁突软骨退变的组织学证据,包括表面裂隙和番红O染色缺失。在12周时,OARSI评分表明实验侧髁突软骨侵蚀至软骨下骨。最显著的是,8周和12周后,6只兔子在穿孔损伤后TMJ盘内出现HO。
我们首次报道了一种兔TMJ损伤模型,该模型显示了髁突软骨退变和盘骨化,这对于测试潜在TMJ治疗方法的疗效是必不可少的。