Temporomandibular joint trauma and disability assessment - A longitudinal exploratory study

Author(s):  
Cristina Figueiredo ◽  
Américo Afonso ◽  
Francisco Caramelo ◽  
Corte-Real Ana
2021 ◽  
Author(s):  
Mai-Ning Jiao ◽  
Tong-Mei Zhang ◽  
Kun Yang ◽  
Zhao-Yuan Xu ◽  
Guan-Meng Zhang ◽  
...  

Abstract Background: Traumatic haemarthrosis was hypothesized to be the etiology of temporomandibular joint (TMJ) ankylosis. Here, taking haematoma absorbance as a control, we aimed to reveal the molecular mechanisms involved in haematoma organizing into ankylosis using transcriptome microarray profiles.Material/Methods: Disk removal was performed to building haematoma absorbance (HA) in one side of TMJ, while removal of disk and articular fibrous layers was performed to induced TMJ ankylosis through haematoma organization (HO) in the contralateral side in a sheep model. Haematoma tissues harvested at days 1, 4 and 7 postoperatively were examined by histology, and analyzed by Affymetrix OviGene-1_0-ST microarrays. The DAVID were recruited to perform the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis for the different expression genes (DEGs). The DEGs were also typed into protein–protein interaction (PPI) networks to get the interaction data. Six significant genes screened from PPI analysis, were confirmed by real-time PCR.Results: We found 268, 223 and 17 DEGs at least 2-fold at days 1, 4 and 7, respectively. At day 1, genes promoting collagen ossification (POSTN, BGN, LUM, SPARC), cell proliferation (TGF-β), and osteogenic differentiation of mesenchymal stem cells (BMP-2) were up-regulated in the HO side. At day 4, several genes involved in angiogenesis (KDR, FIT1, TEK) shower higher expression in the HO side. While HA was characterized by a continuous immune and inflammatory reaction.Conclusions: Our results provide a comprehensive understanding of the role of haematoma in the onset and progress of TMJ ankylosis. Further study of key genes may provide new ideas for future treatment of the disease.


1983 ◽  
Vol 16 (3) ◽  
pp. 549-562 ◽  
Author(s):  
Albert Hohmann ◽  
Kent Wilson ◽  
C. Randall Nelms

2020 ◽  
Vol 36 (6) ◽  
pp. 624-631
Author(s):  
Cristina Paiva Figueiredo ◽  
Helena M. Teixeira ◽  
Américo Santos Afonso ◽  
Ana Corte‐Real

2019 ◽  
Vol 27 (2) ◽  
pp. 99-106 ◽  
Author(s):  
Shravan Kumar Renapurkar ◽  
Robert A. Strauss

2014 ◽  
Vol 26 (5) ◽  
pp. 439-445 ◽  
Author(s):  
Adrian F DeAngelis ◽  
Roland A Barrowman ◽  
Richard Harrod ◽  
Alf L Nastri

2021 ◽  
pp. 209-217
Author(s):  
Darpan Bhargava ◽  
Yogesh Sharma ◽  
Preeti Gurjar

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