Development of temporomandibular joint ankylosis in rats using stem cells and bone graft

Porto, Gabriela Granja; Vasconcelos, Belmiro Cavalcanti do Egito; Fraga, Simone do Nascimento; Castro, Célia Maria Machado Barbosa de; Andrade, Emanuel S. S.

doi:10.1016/j.ijom.2011.07.910

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…However, no bone bridge was seen between the condyle and TMJ fossa. 8 In summary, these studies suggest that MSCs might play an essential role in TMJA bone mass formation.…”

Section: Cellular Studies Of Tmjamentioning

confidence: 74%

“…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%

“…Nevertheless, the MSCs derived from the radiolucent zone and bone marrow exhibited decreased proliferative and osteogenic behavior, 6,7 further explaining the long course of TMJA formation. Interestingly, while establishing an animal model of TMJA, Porto et al 8 reported that application of MSCs induced more bone formation in the damaged area of the TMJ and more severe ankylosis symptoms than application of bone grafts. However, no bone bridge was seen between the condyle and TMJ fossa.…”

Section: Cellular Studies Of Tmjamentioning

confidence: 99%

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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, no bone bridge was seen between the condyle and TMJ fossa. 8 In summary, these studies suggest that MSCs might play an essential role in TMJA bone mass formation.…”

Section: Cellular Studies Of Tmjamentioning

confidence: 74%

Section: Resultsmentioning

confidence: 99%

Section: Cellular Studies Of Tmjamentioning

confidence: 99%

See 1 more Smart Citation

Pathogenesis of traumatic temporomandibular joint ankylosis: a narrative review

Zhang

Xiao

et al. 2020

J Int Med Res

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“…Conducting clinical trials of TMJ bony ankylosis in humans is limited by ethical considerations. Several animal models of TMJ bony ankylosis have been proposed over the last few decades [13][14][15]. Published studies describe injuries to the articular surfaces as procedures to induce TMJ ankylosis [15].…”

Section: Introductionmentioning

confidence: 99%

“…Several animal models of TMJ bony ankylosis have been proposed over the last few decades [13][14][15]. Published studies describe injuries to the articular surfaces as procedures to induce TMJ ankylosis [15]. Large animal models are indispensable, as the size and anatomical structure of their TMJs are comparable to those of human beings [3].…”

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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