Injection in temporomandibular joint of rats. Description of technical protocol

Fuentes, Ramón; Veuthey, Carlos; Arias, Ana Reguera; Saravia, Diego; Ottone, Nicolás Ernesto

doi:10.1515/pjvs-2017-0025

Cited by 16 publications

(11 citation statements)

References 8 publications

(26 reference statements)

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“…Inflammation was induced by injection of 50 μ l CFA (Sigma, MO, USA) into the upper compartment of the bilateral TMJ [ 30 ]. The rats in which inflammation was not induced received injections of the same volume of saline.…”

Section: Methodsmentioning

confidence: 99%

C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats

Zhou

Jian

et al. 2022

Journal of Immunology Research

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Background. C-reactive protein (CRP), a biomarker of inflammation, is highly expressed in osteoarthritis- (OA-) related diseases, but its exact role remains unknown. In this study, we evaluated the biological effect of CRP on temporomandibular joint (TMJ) inflammation. Methods. Freund’s complete adjuvant (CFA) was used to induce TMJ inflammation in CRP-knockout (CRP-/-) and control rats. Degenerative changes in the TMJ were compared to elucidate the role of CRP in TMJ inflammation. In addition, inflammatory cytokines, macrophage activation, and osteoclast differentiation were evaluated by real-time quantitative polymerase chain reaction, immunohistochemistry, and tartrate-resistant phosphatase staining to explore the potential regulatory mechanism. Results. Compared to the control, CFA induced TMJ inflammation, which increased systemic and local CRP expression. Furthermore, CRP-/- rats exhibited less severe inflammatory symptoms. The downregulation of proinflammatory cytokines (interleukin- (IL-) 1β and IL-6) and upregulation of the anti-inflammatory cytokine IL-10 were detected in CRP-/- rats, which also exhibited reduced macrophage activation and osteoclast differentiation. Conclusion. These results indicated that controlling the highly elevated levels of CRP during inflammation could modify the cytokine profile, macrophage activation, and osteoclast differentiation, thus, providing beneficial effects for TMJ-OA prevention and treatment.

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Section: Methodsmentioning

confidence: 99%

C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats

Zhou

Jian

et al. 2022

Journal of Immunology Research

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“…The technical procedure of injection into the TMJ of rats has been previously described. 24 As TMJOA developed, the destruction of the surface of the condyles was evaluated using a stereoscopic microscope. Five synovium samples from each group were collected, mixed, and stored in TRIzol for RNA extraction.…”

Section: Methodsmentioning

confidence: 99%

Histone deacetylase inhibitors attenuated interleukin-1β-induced chondrogenesis inhibition in synovium-derived mesenchymal stem cells of the temporomandibular joint

Liao

Sun

Wang

et al. 2022

Bone & Joint Research

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Aims In the repair of condylar cartilage injury, synovium-derived mesenchymal stem cells (SMSCs) migrate to an injured site and differentiate into cartilage. This study aimed to confirm that histone deacetylase (HDAC) inhibitors, which alleviate arthritis, can improve chondrogenesis inhibited by IL-1β, and to explore its mechanism. Methods SMSCs were isolated from synovium specimens of patients undergoing temporomandibular joint (TMJ) surgery. Chondrogenic differentiation potential of SMSCs was evaluated in vitro in the control, IL-1β stimulation, and IL-1β stimulation with HDAC inhibitors groups. The effect of HDAC inhibitors on the synovium and condylar cartilage in a rat TMJ arthritis model was evaluated. Results Interleukin (IL)-1β inhibited the chondrogenic differentiation potential of SMSCs, while the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and panobinostat (LBH589), attenuated inhibition of IL-1β-induced SMSC chondrogenesis. Additionally, SAHA attenuated the destruction of condylar cartilage in rat TMJ arthritis model. IL-6 (p < 0.001) and matrix metalloproteinase 13 (MMP13) (p = 0.006) were significantly upregulated after IL-1β stimulation, while SAHA and LBH589 attenuated IL-6 and MMP13 expression, which was upregulated by IL-1β in vitro. Silencing of IL-6 significantly downregulated MMP13 expression and attenuated IL-1β-induced chondrogenesis inhibition of SMSCs. Conclusion HDAC inhibitors SAHA and LBH589 attenuated chondrogenesis inhibition of SMSC induced by IL-1β in TMJ, and inhibition of IL-6/MMP13 pathway activation contributes to this biological progress. This study provides a theoretical basis for the application of HDAC inhibitors in the treatment of TMJ arthritis. Cite this article: Bone Joint Res 2022;11(1):40–48.

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“…In ammation was induced by injection of 50 μl CFA (Sigma, MO, USA) into the upper compartment of the bilateral TMJ [30]. The rats in which in ammation was not induced received injections of the same volume of saline.…”

Section: Animals and Induction Of Tmj In Ammationmentioning

confidence: 99%

C-Reactive Protein Knock Out Attenuate Temporomandibular Joint Inflammation in Rats

Zhou

Jian

et al. 2021

Preprint

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Background: C-reactive protein (CRP), a biomarker of inflammation, is highly expressed in osteoarthritis (OA)-related diseases, but its exact role remains unknown. In this study, we evaluated the biological effect of CRP on temporomandibular joint (TMJ) inflammation.Methods: Freund’s complete adjuvant (CFA) was used to induce TMJ inflammation in CRP-knockout (CRP-/-) and control rats. Degenerative changes in the TMJ were compared to elucidate the role of CRP in TMJ inflammation. In addition, inflammatory cytokines, macrophage activation and osteoclast differentiation were evaluated by real-time quantitative polymerase chain reaction, immunohistochemistry and tartrate-resistant phosphatase staining to explore the potential regulatory mechanism.Results: Compared to the control, CFA induced TMJ inflammation, which increased systemic and local CRP expression. Furthermore, CRP-/- rats exhibited less severe inflammatory symptoms. The downregulation of proinflammatory cytokines (interleukin (IL)-1β and IL-6) and upregulation of the anti-inflammatory cytokine IL-10 were detected in CRP-/- rats, which also exhibited reduced macrophage activation and osteoclast differentiation.Conclusion: These results indicated that controlling the highly elevated levels of CRP during inflammation could modify the cytokine profile, macrophage activation and osteoclast differentiation, thus providing beneficial effects for TMJ-OA prevention and treatment.

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Injection in temporomandibular joint of rats. Description of technical protocol

Cited by 16 publications

References 8 publications

C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats

C-Reactive Protein Knockout Attenuates Temporomandibular Joint Inflammation in Rats

Histone deacetylase inhibitors attenuated interleukin-1β-induced chondrogenesis inhibition in synovium-derived mesenchymal stem cells of the temporomandibular joint

C-Reactive Protein Knock Out Attenuate Temporomandibular Joint Inflammation in Rats

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