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

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 f...

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Vydáno v:Journal of cellular and molecular medicine Ročník 25; číslo 11; s. 4902 - 4911
Hlavní autoři: Li, Baochao, Guan, Guangzhao, Mei, Li, Jiao, Kai, Li, Huang
Médium: Journal Article
Jazyk:angličtina
Vydáno: England John Wiley & Sons, Inc 01.06.2021
John Wiley and Sons Inc
Témata:
Angiogenesis
Animal models
Apoptosis
Arthralgia
Arthritis
Autophagy
Bone remodeling
bone remodelling
Cartilage
cartilage degeneration
Cartilage diseases
Cell culture
chondrocyte hypertrophy
Chondrocytes
Cognition
Collagen
Cytokines
Degeneration
Degenerative diseases
Endoplasmic reticulum
Extracellular matrix
Growth factors
Hypertrophy
Kinases
Mineralization
Nitric oxide
Ossification
Osteoarthritis
Osteocytes
Osteogenesis
Pathogenesis
Phagocytosis
Phenotypes
Review
Reviews
Signal transduction
Subchondral bone
Temporomandibular joint
Tumor necrosis factor-TNF
bone remodelling
cartilage degeneration
temporomandibular joint
angiogenesis
osteoarthritis
chondrocyte hypertrophy
ISSN:1582-1838, 1582-4934, 1582-4934
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Popis
Shrnutí: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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ISSN:1582-1838
1582-4934
1582-4934
DOI:10.1111/jcmm.16514