Inhibition of notch signaling pathway temporally postpones the cartilage degradation progress of temporomandibular joint arthritis in mice. Issue 7 (July 2018)

• Record Type: Journal Article
• Authors: Luo, Xueting; Jiang, Yangmei; Bi, Ruiye; Jiang, Nan; Zhu, Songsong
• Is Part Of: Journal of cranio-maxillofacial surgery. Volume 46:Issue 7(2018)
• Page Start: 1132
• Page End: 1138
• Publication Date: 2018-07
• Subjects: Notch signal pathway -- Temporomandibular joint -- Osteoarthritis -- Articular cartilage; Skull -- Surgery -- Periodicals; Maxilla -- Surgery -- Periodicals; Face -- Surgery -- Periodicals; Surgery, Plastic -- Periodicals; Maxilla -- surgery -- Periodicals; Face -- surgery -- Periodicals; Skull -- surgery -- Periodicals; Oral Surgical Procedures -- Periodicals; Reconstructive Surgical Procedures -- Periodicals; Surgery, Plastic -- Periodicals; Surgery, Oral -- Periodicals; Electronic journals; 617.514
• DOI: 10.1016/j.jcms.2018.04.026
• Languages: English
• ISSNs: 1010-5182

Abstract

Abstract: Purpose: The aim of this study is to explore the role of Notch signaling pathway in the initiation and progression of temporomandibular joint osteoarthritis (TMJOA). Methods: 48 mice were divided into DAPT-TMJOA, Control-TMJOA and Control-Sham groups. Animals received discectomy/Sham surgery in their right TMJ, following the DAPT/saline intra-articular injections every week. Mice were sacrificed at 1/4/8 weeks post-surgery. Safranin-O and H&E staining were performed on the TMJ sections for the modified Mankin's score. qPCR and immunohistochemistry were used to evaluate Notch1, Jagged1 and Hes5 expressions. Results: The mRNA expressions of Notch1, Jagged1 and Hes5 were significantly increased in Control-TMJOA group compared with Control-Sham group. Immunostaining revealed a dramatic elevation of Notch1, Jagged1 and Hes5 signals distributed in the cartilage at 1 and 4 weeks after discectomy. However, the increased number of those immuno-positive cells turned down at 8 weeks after surgery. DAPT treatment partially rescued the elevated mRNA expression and immuno-positive cell numbers of Notch1, Jagged1 and Hes5. More importantly, the cartilage destruction during TMJOA was delayed by DAPT treatment, analyzed by modified Mankin's score. Conclusion: Notch signaling participates in the onset and development of TMJOA. Inhibiting Notch signaling activation by DAPT can partially delay the progress of TMJOA. Highlights: In our study, the results of the current study indicated the following: In the TMJOA mouse model, Notch signaling pathway was rapidly increased, and was consistently active during the development of cartilage degradation during TMJOA. After blocking Notch signaling by DAPT, the progression of cartilage damage occurred later than in the control group. The cartilage degradation progress was postponed but not inhibited by DAPT treatment, suggesting that blocking Notch signaling pathway can partially delay the progress of cartilage degradation in TMJOA mice.