Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats

Long, Hui-Qing; Tian, Pengfei; Guan, Yu-Xin; Liu, Lingxia; Wu, Xiuping; Li, Bing

doi:10.1007/s10735-019-09840-0

Cited by 13 publications

(18 citation statements)

References 39 publications

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“…23 Ihh transmits information to the nucleus through the Ihh-Smo-Gli signalling pathway. 15,77 The pathway ultimately induces chondrocyte hypertrophy via Runt-related transcription factor 2 (Runx2), a transcription factor that directly regulates the expression of Col X and MMP13. 76,77,82,83 In addition, an increased intracellular calcium concentration can promote chondrocyte hypertrophy through calcium-sensing receptor (CaSR) in the endoplasmic reticulum.…”

Section: Chondrocyte Hypertrophy In Tmj Osteoarthritismentioning

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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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: Chondrocyte Hypertrophy In Tmj Osteoarthritismentioning

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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“…Third, the role(s) that altered Ihh signaling and associated pathways, such as primary cilia components, play in the degenerative changes that accompany osteoarthritis are not fully understood in the TMJ or synovial joints [25,69,98,99,115,116]. For example, it has been observed that activation of Hh signaling leads to the induction of ectopic chondrocyte hypertrophy in degenerative articular cartilage [28,115,117]. Further, numerous studies have demonstrated that several signaling pathways, including TGFβ, BMP, IGF-1, and FGF, are up-regulated during osteophyte formation in synovial joints [93][94][95][96][97].…”

Section: Perspectivesmentioning

confidence: 99%

The Roles of Indian Hedgehog Signaling in TMJ Formation

Bechtold

Kurio

Nah

et al. 2019

IJMS

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The temporomandibular joint (TMJ) is an intricate structure composed of the mandibular condyle, articular disc, and glenoid fossa in the temporal bone. Apical condylar cartilage is classified as a secondary cartilage, is fibrocartilaginous in nature, and is structurally distinct from growth plate and articular cartilage in long bones. Condylar cartilage is organized in distinct cellular layers that include a superficial layer that produces lubricants, a polymorphic/progenitor layer that contains stem/progenitor cells, and underlying layers of flattened and hypertrophic chondrocytes. Uniquely, progenitor cells reside near the articular surface, proliferate, undergo chondrogenesis, and mature into hypertrophic chondrocytes. During the past decades, there has been a growing interest in the molecular mechanisms by which the TMJ develops and acquires its unique structural and functional features. Indian hedgehog (Ihh), which regulates skeletal development including synovial joint formation, also plays pivotal roles in TMJ development and postnatal maintenance. This review provides a description of the many important recent advances in Hedgehog (Hh) signaling in TMJ biology. These include studies that used conventional approaches and those that analyzed the phenotype of tissue-specific mouse mutants lacking Ihh or associated molecules. The recent advances in understanding the molecular mechanism regulating TMJ development are impressive and these findings will have major implications for future translational medicine tools to repair and regenerate TMJ congenital anomalies and acquired diseases, such as degenerative damage in TMJ osteoarthritic conditions.

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“…These cells could be resident SSC‐like cells or could be responding to local Hedgehog signaling. Indian Hedgehog (Ihh) positive cells are also found at the cartilage‐bone interface (Long et al, 2019). Beyond its basic function in stimulating the expression of parathyroid hormone‐related peptide (PTHrP) (Kindblom et al, 2002; Vortkamp et al, 1996), Ihh is reported to promote chondrocyte hypertrophy and matrix mineralization directly.…”

Section: Discussionmentioning

confidence: 99%

Identification of distinct subpopulations of Gli1‐lineage cells in the mouse mandible

2023

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The human skeletal system has two developmental origins: mesoderm, which gives rise to non-craniofacial bones such as the vertebral column and appendicular skeleton, and neural crest, which contributes to most of the craniofacial bones (Olsen et al., 2000).There are also two distinct ossification programs. Most of the noncraniofacial bones are formed by endochondral ossification while most of the craniofacial bones are formed by intramembranous ossification. During endochondral ossification, a cartilaginous template

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Expression of Ihh signaling pathway in condylar cartilage after bite-raising in adult rats

Cited by 13 publications

References 39 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

The Roles of Indian Hedgehog Signaling in TMJ Formation

Identification of distinct subpopulations of Gli1‐lineage cells in the mouse mandible

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