Formation of synovial joints and articular cartilage

Moskalewski, Stanisław; Hyc, Anna; Jankowska‐Steifer, Ewa; Osiecka-Iwan, Anna

doi:10.5603/fm.2013.0031

Cited by 9 publications

(7 citation statements)

References 64 publications

(86 reference statements)

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“…[39][40][41] Following joint specification, cavitation results in the separation and subsequent formation of two distinct articular surfaces, synovium, and surrounding joint structures (e.g., the assorted ligaments that connect bone to bone). 42 This transition, once thought to be solely controlled by molecular signaling pathways, is in fact partly regulated by muscle contraction. A number of studies using chick paralysis models revealed that muscle activity is necessary for joint specification.…”

Section: Joint Developmentmentioning

confidence: 99%

Mechanobiology of limb musculoskeletal development

Arvind

Huang

2017

Annals of the New York Academy of Sciences

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While there has been considerable progress in identifying molecular regulators of musculoskeletal development, the role of physical forces in regulating induction, differentiation, and patterning events is less well understood. Here, we highlight recent findings in this area, focusing primarily on model systems that test the mechanical regulation of skeletal and tendon development in the limb. We also discuss a few of the key signaling pathways and mechanisms that have been implicated in mechanotransduction and highlight current gaps in knowledge and opportunities for further research in the field.

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Section: Joint Developmentmentioning

confidence: 99%

Mechanobiology of limb musculoskeletal development

Arvind

Huang

2017

Annals of the New York Academy of Sciences

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“…WNT/β-catenin stimulates the growth plate chondrocytes in chondrogenesis (33,34). Moreover, β-catenin has major effects in the differentiation of MSCs to chondroblast and osteoblast and proliferation of these cells in osteogenesis (14,15,40,41,42). Tamamura claims that β-catenin levels have an important role in skeletogenesis.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of chondrogenesis and osteogenesis via Wnt/β-Catenin, S100 immunoexpression and histomorphometry in fetal rats following maternal uterine artery ligation

et al. 2020

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The aim of this study is to investigate the effects of intrauterine growth retardation depending on maternal uterine artery ligation model, Wnt/β-catenin and S100 expression immunohistochemistry and histomorphometrically on growth plate and bone tissue of fetal rats. Materials and Methods: Maternal rats were randomly divided into 3 groups (n=5). No surgery or anesthesia were applied in control group. Bilaterally the maternal uterine arteries were ligated on gestational day 18 in experimental group. Although all surgical procedures were performed in sham group, the uterine artery ligation were not made. Fetuses were taken on gestational day 20, thicknesses of growth plate and zones, trabecular number and thickness and cortical thickness were evaluated with the histomorphometrically in samples from left proximal tibia. The expressions of βcatenin and S100 immunohistochemically were evaluated in the growth plate. Results: Thicknesses of growth plate (p<0.01), proliferation zone (p<0.05) and degeneration zone (p<0.01) were measured significantly thinner in experimental group than the others and thicknesses of hypertrophic zones were lesser than the control and sham group, but the results were not statistically significant (p>0.05). Also trabecular numbers were lower (p<0.01) and trabecular thickness were also thinner (p<0.05) in experimental group. Expression of β-catenin was declined and S100 expression was increased in experimental group. Conclusion: We conclude that maternal uterine artery ligation, leads to shortness of growth plate and degenerated bone architecture because of Wnt/β-catenin signaling pathway.

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“…During the vertebrate limb development, the limb mesenchyme cells form an intermediate cartilage scaffold first, which then develops into the growth plate and is replaced by bone [1]. Although Ihh plays a critical role during endochondral ossification and synovial joint formation [5,6], its role from the mesenchyme cells to the earlier stages of chondrogenesis and growth plate formation is unclear. To do so, we ablated Ihh in the mesenchyme cells.…”

Section: Discussionmentioning

confidence: 99%

“…The Hh homologous proteins in mammals are Sonic hedgehog, Indian hedgehog (Ihh), and Desert hedgehog, which all share the same signaling pathway [1]. Ihh, which is synthesized and expressed primarily in prehypertrophic chondrocytes of growth plate, has an essential function in cartilage development, endochondral bone formation [3], and synovial joint formation [4,5]. The main function of Ihh is to regulate chondrocyte hypertrophy and differentiation during endochondral ossification [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Indian Hedgehog Deletion on Mesenchyme Cells: Inducing Intermediate Cartilage Scaffold Ossification to Cause Growth Plate and Phalange Joint Absence, Short Limb, and Dwarfish Phenotypes

Sun

Wei

et al. 2018

Stem Cells and Development

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The endochondral ossification plays a critical role in vertebrate limb development and skeletal homeostasis, where limb mesenchyme cells form an intermediate cartilage scaffold that develops into growth plates and then replaced by bone. Although Indian hedgehog (Ihh) is known to control the hypertrophic differentiation process of chondrocytes, its role from the mesenchyme cells to the early stages of chondrogenesis is unclear. To define the function of Ihh in the mesenchymal cell's early stages of chondrogenesis, we specifically delete Ihh in Prx1-expressed mesenchyme cells at E9.5 using Prx1-Cre;Ihh;Rosa26 mice. We found that deleting Ihh in the mesenchyme cells results in an early and quick ossification of the intermediate cartilage scaffold, causing the growth plate and phalange joint absence, short limbs, and dwarfishness. The green fluorescent protein (GFP)-positive cells derived from deleted Ihh mesenchyme cells overlap with von Kossa- and osteocalcin-positive staining area. These deleted Ihh/GFP-positive cells isolated from Prx1-Cre;Ihh;Rosa26 newborn mice had osteogenic differentiation by showing a positive Alizarin red and von Kossa staining, as well as an enhanced Col1a1, osteocalcin, and Runx2 expression. Our findings demonstrate that deleting Ihh in mesenchyme cells during early limb development promotes intermediate cartilage scaffold ossification, which prevents growth plate formation that causes phalange joint absence, short limb, and dwarfish phenotype.

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Formation of synovial joints and articular cartilage

Abstract: (Folia Morphol 2013; 72, 3: 181-187)

Cited by 9 publications

References 64 publications

Mechanobiology of limb musculoskeletal development

Mechanobiology of limb musculoskeletal development

Evaluation of chondrogenesis and osteogenesis via Wnt/β-Catenin, S100 immunoexpression and histomorphometry in fetal rats following maternal uterine artery ligation

The Effects of Indian Hedgehog Deletion on Mesenchyme Cells: Inducing Intermediate Cartilage Scaffold Ossification to Cause Growth Plate and Phalange Joint Absence, Short Limb, and Dwarfish Phenotypes

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