Chondrogenic Potential of Dental-Derived Mesenchymal Stromal Cells

Jeyaraman, Naveen; Prajwal, Gollahalli Shivashankar; Jeyaraman, Madhan; Muthu, Sathish; Khanna, Manish

doi:10.3390/osteology1030016

Cited by 2 publications

(1 citation statement)

References 211 publications

(229 reference statements)

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“…Nevertheless, it is important to mention that protocols for isolation and culture of fetal cells are difficult; it is also difficult to direct fetal cells towards chondrogenic differentiation, with a requirement to add additional morphogens to maintain chondrogenic culture conditions. A few other reported MSCs cell sources that offer encouraging prospects include muscle-derived MSCs [ 158 ], human nasal inferior turbinate tissue-derived MSCs (hT-MSCs) [ 197 ], and dental-pulp-derived MSCs [ 198 ].…”

Section: Models To Study Chondrocyte Hypertrophymentioning

confidence: 99%

Chondrocyte Hypertrophy in Osteoarthritis: Mechanistic Studies and Models for the Identification of New Therapeutic Strategies

Chawla

Mainardi

Majumder

et al. 2022

Cells

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Articular cartilage shows limited self-healing ability owing to its low cellularity and avascularity. Untreated cartilage defects display an increased propensity to degenerate, leading to osteoarthritis (OA). During OA progression, articular chondrocytes are subjected to significant alterations in gene expression and phenotype, including a shift towards a hypertrophic-like state (with the expression of collagen type X, matrix metalloproteinases-13, and alkaline phosphatase) analogous to what eventuates during endochondral ossification. Present OA management strategies focus, however, exclusively on cartilage inflammation and degradation. A better understanding of the hypertrophic chondrocyte phenotype in OA might give new insights into its pathogenesis, suggesting potential disease-modifying therapeutic approaches. Recent developments in the field of cellular/molecular biology and tissue engineering proceeded in the direction of contrasting the onset of this hypertrophic phenotype, but knowledge gaps in the cause–effect of these processes are still present. In this review we will highlight the possible advantages and drawbacks of using this approach as a therapeutic strategy while focusing on the experimental models necessary for a better understanding of the phenomenon. Specifically, we will discuss in brief the cellular signaling pathways associated with the onset of a hypertrophic phenotype in chondrocytes during the progression of OA and will analyze in depth the advantages and disadvantages of various models that have been used to mimic it. Afterwards, we will present the strategies developed and proposed to impede chondrocyte hypertrophy and cartilage matrix mineralization/calcification. Finally, we will examine the future perspectives of OA therapeutic strategies.

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Section: Models To Study Chondrocyte Hypertrophymentioning

confidence: 99%