Reducing macrophage numbers alleviates temporomandibular joint ankylosis

Zhao, Lu; Xiao, E.; He, Linxin; Duan, Deng-Hui; He, Yang; Chen, Shuo; Zhang, Yi; Gan, Ye‐Hua

doi:10.1007/s00441-019-03087-7

Cited by 7 publications

(10 citation statements)

References 62 publications

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“…The results also suggested that inhibiting the release of inflammatory cytokines in the early stage of bony ankylosis might be a promising approach to prevent its onset or delay its progression. In fact, a recently published study by Zhao et al [ 30 ] supports our findings. They found that large numbers of macrophages infiltrated in the early phase of ankylosis and that reducing macrophage numbers alleviated the progression of ankylosis by inhibiting cartilage formation [ 30 ].…”

Section: Discussionsupporting

confidence: 92%

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Microarray Analysis of Differential Gene Expression Between Traumatic Temporomandibular Joint Fibrous and Bony Ankylosis in a Sheep Model

et al. 2021

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Background The type of traumatic temporomandibular joint (TMJ) ankylosis depends on the degree of severity of TMJ trauma. Here, we performed comprehensive differential molecular profiling between TMJ fibrous and bony ankylosis. Material/Methods Six sheep were used and a bilateral different degree of TMJ trauma was performed to induce fibrous ankylosis in one side and bony ankylosis in the other side. The ankylosed calluses were harvested at days 14 and 28 postoperatively and analyzed by Affymetrix OviGene-1_0-ST microarrays. DAVID was used 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. Ten DEGs, including 7 hub genes from PPI analysis, were confirmed by real-time PCR. Results We found 90 and 323 DEGs at least 2-fold at days 14 and 28, respectively. At day 14, bony ankylosis showed upregulated DEGs, such as TLR8, SYK, NFKBIA, PTPRC, CD86, ITGAM, and ITGAL, indicating a stronger immune and inflammatory response and cell adhesion, while genes associated with anti-adhesion (PRG4) and inhibition of osteoblast differentiation (SFRP1) had higher expression in fibrous ankylosis. At day 28, bony ankylosis showed increased biological process related to new bone formation, while fibrous ankylosis was characterized by a prolonged immune and inflammatory reaction. Conclusions This study provides a differential gene expression profile between TMJ fibrous and bony ankylosis. Further study of these key genes may provide new ideas for future treatment of TMJ bony ankylosis.

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Section: Discussionsupporting

confidence: 92%

“…In fact, a recently published study by Zhao et al [ 30 ] supports our findings. They found that large numbers of macrophages infiltrated in the early phase of ankylosis and that reducing macrophage numbers alleviated the progression of ankylosis by inhibiting cartilage formation [ 30 ].…”

Section: Discussionsupporting

confidence: 92%

Microarray Analysis of Differential Gene Expression Between Traumatic Temporomandibular Joint Fibrous and Bony Ankylosis in a Sheep Model

et al. 2021

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“…Interestingly, once the macrophages were diminished at the time of TMJA model surgery, the severity of ankylosis was alleviated and the ankylosis bone mass formation was limited with reduced cartilage size and decreased expression of cartilage-related genes. 13 Consistent with these studies on fracture healing, macrophage depletion during fracture healing has been shown to reduce callus formation and cartilage size, while macrophage colony-stimulating factor 1 increased the number of macrophages and soft callus formation. [49][50][51] These studies suggest that macrophages might have an essential role in initiating fracture healing and the TMJA process and are closely related to the callus and ankylosis bone mass size.…”

Section: Cellular Studies Of Tmjasupporting

confidence: 66%

“…Nineteen articles that investigated the pathology of traumatic TMJA were finally included. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] These articles were classified into three groups: predisposing factors and etiological factors, cellular studies, and molecular studies (Table 1).…”

Section: Resultsmentioning

confidence: 99%

Pathogenesis of traumatic temporomandibular joint ankylosis: a narrative review

Zhang

Xiao

et al. 2020

J Int Med Res

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Objective To comprehensively review the literature and summarize the results from human and animal studies related to the possible causes and pathogenesis of traumatic temporomandibular joint ankylosis (TMJA). Materials and Methods The Google Scholar, Embase, and Web of Science databases were used to search for articles related to traumatic TMJA from 2011 to 2020. All articles were screened according to the inclusion and exclusion criteria, collected, and analyzed. Results Nineteen relevant articles were collected. These articles were classified into three groups: predisposing and etiological factors, cellular studies, and molecular studies. Conclusion The pathological mechanisms are similar between TMJA and nonunion hypertrophy. Aberrant structural and etiological factors as well as disordered cellular and molecular mechanisms might contribute to TMJA formation. Although preclinical and clinical data have provided new evidence on the pathogenesis of traumatic TMJA, the molecular mechanisms and biological events require further exploration.

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“…However, commercially available biological and molecular assays for goats or sheep are currently limited owing to the lack of antibodies for these species [20][21][22], thus the pathogenesis and pathophysiology of TMJ bony ankylosis in large animal models are not possible to determine [22]. Therefore, TMJ bony ankylosis research on small animal models including rabbits [23][24][25], rats [15,26], and mice [14,27], are more conducive for molecular biology research. Traumatic TMJ bony ankylosis was stimulated using rabbits as small animal models, but the microstructure change of TMJ in rabbit models cannot be continuously and dynamically observed by Micro-CT [24].…”

Section: Introductionmentioning

confidence: 99%

Traumatic temporomandibular joint bony ankylosis in growing rats

Wang

Xue

et al. 2022

BMC Oral Health

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Background The pathogenesis of traumatic temporomandibular joint (TMJ) bony ankylosis remains unknown. This study aimed to explore the pathogenesis of traumatic TMJ bony ankylosis in a rat model. Methods Twenty-four 3-week-old male Sprague–Dawley rats were used in this study. Excision of the whole disc, the fibrocartilage damage of the condyle and glenoid fossa, and narrowed joint space were performed in the left TMJ of the operation group to induce TMJ bony ankylosis (experimental side). The right TMJ underwent a sham operation (sham side). The control group did not undergo any operations. At 1, 4, and 8 weeks postoperatively, rats of the operation group were sacrificed and TMJ complexes were evaluated by gross observation, Micro-CT, histological examinations, and immunofluorescence microscopy. Total RNA of TMJ complexes in the operation group were analyzed using RNA-seq. Results Gross observations revealed TMJ bony ankylosis on the experimental side. Micro-CT analysis demonstrated that compared to the sham side, the experimental side showed a larger volume of growth, and a considerable calcified bone callus formation in the narrowed joint space and on the rougher articular surfaces. Histological examinations indicated that endochondral ossification was observed on the experimental side, but not on the sham side. RNA-seq analysis and immunofluorescence revealed that Matrix metallopeptidase 13 (MMP13) and Runt-related transcription factor 2 (RUNX2) genes of endochondral ossification were significantly more downregulated on the experimental side than on the sham side. The primary pathways related to endochondral ossification were Parathyroid hormone synthesis, secretion and action, Relaxin signaling pathway, and IL-17 signaling pathway. Conclusions The present study provided an innovative and reliable rat model of TMJ bony ankylosis by compound trauma and narrowed joint space. Furthermore, we demonstrated the downregulation of MMP13 and RUNX2 in the process of endochondral ossification in TMJ bony ankylosis.

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Reducing macrophage numbers alleviates temporomandibular joint ankylosis

Cited by 7 publications

References 62 publications

Microarray Analysis of Differential Gene Expression Between Traumatic Temporomandibular Joint Fibrous and Bony Ankylosis in a Sheep Model

Microarray Analysis of Differential Gene Expression Between Traumatic Temporomandibular Joint Fibrous and Bony Ankylosis in a Sheep Model

Pathogenesis of traumatic temporomandibular joint ankylosis: a narrative review

Traumatic temporomandibular joint bony ankylosis in growing rats

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