Low‐intensity pulsed ultrasound protects subchondral bone in rabbit temporomandibular joint osteoarthritis by suppressing TGF‐β1/Smad3 pathway

Yi, Xin; Wu, Lin; Liu, Jie; Qin, Yi‐Xian; Li, Bo; Zhou, Qing

doi:10.1002/jor.24628

Cited by 14 publications

(7 citation statements)

References 42 publications

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“…1,22,23 Intra-articular injection of chemical mediators such as monosodium iodoacetic acid (MIA) and complete Freund's adjuvant (CFA) could mimic the inflammatory response of the TMJ over a short period of time. [24][25][26] Surgical methods have been used to destroy part or all of the disc or cartilage of the condyle. [27][28][29] In addition, since the occurrence of osteoarthritis is closely related to age, 30 aged mice were used in some studies to mimic spontaneous TMJ osteoarthritis.…”

Section: In Vivo Animal Model S and In Vitro Cell Model S Of Tmj Os Teoarthritismentioning

confidence: 99%

“…Similar to other osteoarthritis animal models, gene editing such as overexpression of short stature homeobox 2 (SHOX), transforming growth factor‐β1 (TGF‐β1), and β‐catenin, 18‐21 and inhibiting or knocking out genes such as Discoidin domain receptor 1 (DDR1), small mother against decapentaplegic 3 (SMAD3), and fibroblast growth factor receptor (FGFR3), could lead to the formation of TMJ osteoarthritis 1,22,23 . Intra‐articular injection of chemical mediators such as monosodium iodoacetic acid (MIA) and complete Freund's adjuvant (CFA) could mimic the inflammatory response of the TMJ over a short period of time 24‐26 . Surgical methods have been used to destroy part or all of the disc or cartilage of the condyle 27‐29 .…”

Section: In Vivo Animal Models and In Vitro Cell Models Of Tmj Osteoa...mentioning

confidence: 99%

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Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Guan

et al. 2021

J Cellular Molecular Medi

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Temporomandibular joint (TMJ) osteoarthritis is a common chronic degenerative disease of the TMJ. In order to explore its aetiology and pathological mechanism, many animal models and cell models have been constructed to simulate the pathological process of TMJ osteoarthritis. The main pathological features of TMJ osteoarthritis include chondrocyte death, extracellular matrix (ECM) degradation and subchondral bone remodelling. Chondrocyte apoptosis accelerates the destruction of cartilage. However, autophagy has a protective effect on condylar chondrocytes. Degradation of ECM not only changes the properties of cartilage but also affects the phenotype of chondrocytes. The loss of subchondral bone in the early stages of TMJ osteoarthritis plays an aetiological role in the onset of osteoarthritis. In recent years, increasing evidence has suggested that chondrocyte hypertrophy and endochondral angiogenesis promote TMJ osteoarthritis. Hypertrophic chondrocytes secrete many factors that promote cartilage degeneration. These chondrocytes can further differentiate into osteoblasts and osteocytes and accelerate cartilage ossification. Intrachondral angiogenesis and neoneurogenesis are considered to be important triggers of arthralgia in TMJ osteoarthritis. Many molecular signalling pathways in endochondral osteogenesis are responsible for TMJ osteoarthritis. These latest discoveries in TMJ osteoarthritis have further enhanced the understanding of this disease and contributed to the development of molecular therapies. This paper summarizes recent cognition on the pathogenesis of TMJ osteoarthritis, focusing on the role of chondrocyte hypertrophy degeneration and cartilage angiogenesis.

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Section: In Vivo Animal Model S and In Vitro Cell Model S Of Tmj Os Teoarthritismentioning

confidence: 99%

Section: In Vivo Animal Models and In Vitro Cell Models Of Tmj Osteoa...mentioning

confidence: 99%

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Guan

et al. 2021

J Cellular Molecular Medi

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“…Intra-articular injection models are mainly used to investigate the molecular mechanisms of osteoarthritic pain and screening of preclinical therapies ( Kim et al, 2019 ; Sannajust et al, 2019 ; Yi et al, 2020 ; Rotpenpian et al, 2021 ). Xu et al (2017) suggested that IHH signaling facilitates TMJOA in CFA-induced rats by driving formation of hypertrophic chondrocytes and expression of catabolic enzymes, such as type X collagen, MMP-13, and ADAMTS-5, which may lead to degenerative changes in the articular cartilage.…”

Section: Classification Of Animal Models In Temporomandibular Joint O...mentioning

confidence: 99%

Animal Models of Temporomandibular Joint Osteoarthritis: Classification and Selection

Zhao

Zhou

et al. 2022

Front. Physiol.

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Temporomandibular joint osteoarthritis (TMJOA) is a common degenerative joint disease that can cause severe pain and dysfunction. It has a serious impact on the quality of lives of patients. Since mechanism underlying the pathogenesis of TMJOA is not fully understood, the development of effective tools for early diagnosis and disease-modifying therapies has been hindered. Animal models play a key role in understanding the pathological process of diseases and evaluating new therapeutic interventions. Although some similarities in disease processes between animals and humans are known, no one animal model is sufficient for studying all characteristics of TMJOA, as each model has different translatability to human clinical conditions. For the past 4 decades, TMJOA animal models have been studied by numerous researchers and can be broadly divided into induced, naturally occurring, and genetically modified models. The induced models can be divided into invasive models (intra-articular injection and surgical induction) or non-invasive models (mechanical loading, high-fat diet, and sleep deprivation). Different types of animal models simulate different pathological expressions of TMJOA and have their unique characteristics. Currently, mice, rats, and rabbits are commonly used in the study of TMJOA. This review sought to provide a general description of current experimental models of TMJOA and assist researchers in selecting the most appropriate models for different kinds of research.

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“…Yet, A Kanaguchi Arita induced TMJ‐OA with low‐dose mono‐iodoacetate injections and found that LIPUS group showed significantly higher bone mineral density 15 . Other researchers reported that LIPUS could improve the trabecular microstructure of subchondral bone and suppress abnormal subchondral bone resorption and activation of TGF‐β1/Smad3 pathway in TMJ‐OA induced by type II collagenase induction 16 . As mentioned above, previous studies on TMJ‐OA models were considerably heterogeneous, even if they were assessing one certain therapeutic intervention.…”

Section: Introductionmentioning

confidence: 99%

“…15 Other researchers reported that LIPUS could improve the trabecular microstructure of subchondral bone and suppress abnormal subchondral bone resorption and activation of TGF-β1/Smad3 pathway in TMJ-OA induced by type II collagenase induction. 16 As mentioned above, previous studies on TMJ-OA models were considerably heterogeneous, even if they were assessing one certain therapeutic intervention. Due to the use of different animal models and different effect measures, the relevance and comparability of different studies have been greatly affected.…”

Section: Introductionmentioning

confidence: 99%

Comparison and applicability of three induction methods of temporomandibular joint osteoarthritis in murine models

Yuan

Zhou

et al. 2021

J of Oral Rehabilitation

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Background: Temporomandibular joint osteoarthritis (TMJ-OA) causes severe symptoms such as chewing difficulties, acute pain and even maxillofacial deformity.However, there is hardly any effective disease-curing strategy because of uncertainty in aetiology. Animal model is an excellent tool to investigate the mechanism, prevention and treatment on diseases. Currently, although several TMJ-OA animal models have been established, there are almost no comparative studies on different models, which poses a great challenge for selecting suitable models.Objective: To compare three TMJ-OA induction methods and assess their applicability considering pathological changes in the cartilage, subchondral bone, osteoclasts, and synovium.Methods: Murine models were employed and followed for 3 and 6 weeks after experimental procedures (surgery, injection, crossbite). The TMJ changes were evaluated by Safranin-O/Fast green staining, immunofluorescence staining, micro-CT, TRAP staining, and HE staining. Results:In the Surgery group, a pronounced drop in bone volume fraction was observed. In the Injection group, chondrocytes were mostly disordered or arranged in clusters and a substantial increase in the OARSI score and osteoclasts was found.The OARSI score and osteoclasts also increased significantly in the Crossbite group, although to a lower extent compared with injection. Conclusion:Osteoarthritis-like changes were observed in all models. Concerning the applicability of the different induction methods, surgery might be an important resource for the assessment of post-traumatic TMJ-OA and subchondral bone changes in early stages. Injection induces a severe end-stage osteoarthritis in a short time and provides model basis for advanced TMJ-OA. Crossbite might be more reasonable model to explore the pathogenesis mechanism of temporomandibular arthritis due to occlusal disorders.

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Low‐intensity pulsed ultrasound protects subchondral bone in rabbit temporomandibular joint osteoarthritis by suppressing TGF‐β1/Smad3 pathway

Cited by 14 publications

References 42 publications

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Animal Models of Temporomandibular Joint Osteoarthritis: Classification and Selection

Comparison and applicability of three induction methods of temporomandibular joint osteoarthritis in murine models

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