Cartilage Wound Healing: An Overview

Silver, Frederick H.; Glasgold, Alvin I.

doi:10.1016/s0030-6665(20)30463-1

Cited by 72 publications

(12 citation statements)

References 56 publications

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“…1 The self-healing capacity of articular cartilage is minimal because of the lack of endogenous cell sources, vasculature for nutrient supply, 2 and scar tissue formation. 3 Osteoarthritis (OA) develops after damage to the articular cartilage and the inability to achieve full-thickness hyaline cartilage repair. 4 Cell-based tissue engineering such as autologous chondrocyte implantation (ACI) and matrix autologous chondrocyte implantation (MACI) has demonstrated promising clinical results.…”

Section: Introductionmentioning

confidence: 99%

Influence of Cellular Microenvironment on Human Articular Chondrocyte Cell Signaling

et al. 2020

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Objective Alteration of the cellular microenvironment may influence the intra- and intercellular communication and contribute to cartilage injury and repair. The purpose of this study was to investigate how matrix elasticity/stiffness affects chondrogenic activities, including cell survival, phenotypic expression, and the release of both pro- and anti-inflammatory cytokines. Design Human articular chondrocytes (HACs) cultured on traditional 2-dimensional (2D) plastic surfaces were compared with those cultured within 3D hydrogel matrices of varying stiffness. Chondrogenic proliferation, differentiation, and the expression of pro- and anti-inflammatory cytokines were evaluated. Both interleukin-1-beta (IL-1β) and human synovial fluid–derived cells (hSFCs) were introduced to study the effects of matrix stiffness on chondrocyte response. Results Cells demonstrated the most robust chondrogenic differentiation and secreted the least pro-inflammatory cytokines when the matrix stiffness was close to their native microenvironment. The IL-1β effects were attenuated when HACs were co-cultured with hSFCs. Conclusion Modifying the matrix stiffness to mimic the native cartilage microenvironment not only optimized chondrogenic expression but also was essential for the regulation of physiological homeostasis. This study proposed a new toolkit to study cell-molecule, cell-cell, and cell-matrix influence on cartilage physiology.

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Section: Introductionmentioning

confidence: 99%

Influence of Cellular Microenvironment on Human Articular Chondrocyte Cell Signaling

et al. 2020

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“…Virtually every person at some point in their life suffers skin damage, and tissue repair occurs effectively. If the tissue repair process is not appropriately terminated, however, excessive deposition of ECM occurs resulting in the deposition of excessive scar tissue (Silver and Glasgold, 1995). These scars are generally limited in their nature; however, although relatively rare, progressive, pathologic, fatal scarring (fibrotic) disorders can occur.…”

mentioning

confidence: 99%

Insights Into the Molecular Mechanism of Chronic Fibrosis: The Role of Connective Tissue Growth Factor in Scleroderma

Leask

Denton

Abraham

2004

Journal of Investigative Dermatology

124

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Connective tissue growth factor (CCN2), a member of the CCN family of proteins, is a cysteine-rich matricellular protein. Connective tissue growth factor is not normally expressed in dermal fibroblasts unless induced. The most potent inducer of connective tissue growth factor thus far identified is transforming growth factor beta. Connective tissue growth factor, however, is constitutively overexpressed by fibroblasts present in skin fibrotic lesions, including scleroderma. The overexpression of connective tissue growth factor present in fibrotic lesions contributes to the phenotype of scleroderma in that connective tissue growth factor promotes matrix deposition, and fibroblast adhesion and proliferation. In animal models, whereas either transforming growth factor beta or connective tissue growth factor alone produce only a transient fibrotic response, connective tissue growth factor and transforming growth factor beta act together to promote sustained fibrosis. Thus the constitutive overexpression of connective tissue growth factor by fibroblasts present in fibrotic lesions would be expected to contribute directly to chronic, persistent fibrosis. This review discusses recent information regarding insights into connective tissue growth factor biology and, using scleroderma as a model system, the part connective tissue growth factor might play in fibrotic disease.

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“…The cartilage healing process after fracture in general involves an equilibrium between the deposition of type I collagen (scar tissue) and expression of type II collagen (repair). Small full-thickness cartilage defects are mainly replaced by brocartilage, whereas partial-thickness defects heal through the deposition of brous scar tissue 39 . Full-thickness cartilage fractures were induced in our current rat model.…”

Section: Discussionmentioning

confidence: 99%

Serial Histological Changes in the Cartilaginous Eustachian Tube in the Rat Following Balloon Dilation

Kim

Kang

Ryu

et al. 2021

Preprint

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Although balloon dilation has shown promising results in the treatment of dilatory Eustachian tube (ET) dysfunction, the histological effects of ET balloon dilation (ETBD) remain unclear. We evaluated this in a rat model. The left ET of 20 Wistar rats was dilated with a balloon catheter and the right ET was used as a control. Five rats were sacrificed immediately after ETBD, at 1, 4 and 12 weeks after the procedure for histological examination. The epithelial cells, presence of squamous metaplasia, and the proportion of the goblet cells in the epithelium; the vascular structures and dimensions of the submucosa; and presence of cartilage fracture and the area of the ET lumen were evaluated and compared between the groups. Desquamation of nearly all epithelial cells and the fracture of tubal cartilages were observed immediately after ETBD. At 1-week post-ETBD, the ciliated epithelial cells started to recover with squamous metaplasia and epithelial hyperplasia. The goblet cells recovered by 4 weeks post-ETBD and epithelial hyperplasia decreased but was still present at 12 weeks post-ETBD. The depth of the submucosa increased and neovascularization in this region was observed at 1-week post-ETBD and persisted up to 12 weeks post-ETBD. The lumen of the cartilaginous ET increased immediately after ETBD but decreased at 1-week post-ETBD. The cartilaginous ET lumen recovered to the normal value at 4 weeks post-ETBD. This study is the first to describe the serial histological changes to the cartilaginous ET after ETBD and helps our understanding of the histological changes that occur after an ETBD intervention for intractable ET dysfunction.

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Cartilage Wound Healing: An Overview

Cited by 72 publications

References 56 publications

Influence of Cellular Microenvironment on Human Articular Chondrocyte Cell Signaling

Influence of Cellular Microenvironment on Human Articular Chondrocyte Cell Signaling

Insights Into the Molecular Mechanism of Chronic Fibrosis: The Role of Connective Tissue Growth Factor in Scleroderma

Serial Histological Changes in the Cartilaginous Eustachian Tube in the Rat Following Balloon Dilation

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