Aging does not change the compressive stiffness of mandibular condylar cartilage in horses

Mirahmadi, Fereshteh; Koolstra, J.H.; Fazaeli, Sepanta; Lobbezoo, Frank; Lenthe, G. Harry van; Snabel, Jessica; Stoop, Reinout; Arbabi, Vahid; Weinans, Harrie; Everts, Vincent

doi:10.1016/j.joca.2018.08.007

Cited by 5 publications

(2 citation statements)

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“…Proteoglycan plays an important role in the transport of solute and nutrients transport. Age-related changes in cartilage affect the diffusion of nutrients in cartilage [ 118 ]. Deposition of calcium-containing crystals, primarily calcium pyrophosphate and basic calcium phosphate (BCP), is a major alteration in aged cartilage.…”

Section: Age-related Changes In the Ecm Composition And Characteristicsmentioning

confidence: 99%

How are Aging and Osteoarthritis Related?

Wakale,

Wu,

Sonar

et al. 2023

Aging and disease

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Osteoarthritis is the most prevalent degenerative joint disease and one of the leading causes of physical impairment in the world's aging population. The human lifespan has significantly increased as a result of scientific and technological advancements. According to estimates, the world's elderly population will increase by 20% by 2050. Aging and age-related changes are discussed in this review in relation to the development of OA. We specifically discussed the cellular and molecular changes that occur in the chondrocytes during aging and how these changes may make synovial joints more susceptible to OA development. These changes include chondrocyte senescence, mitochondrial dysfunction, epigenetic modifications, and decreased growth factor response. The age-associated changes occur not only in the chondrocytes but also in the matrix, subchondral bone, and synovium. This review aims to provide an overview of the interplay between chondrocytes and matrix and how age-related changes affect the normal function of cartilage and contribute to OA development. Understanding the alterations that affect the function of chondrocytes will emerge new possibilities for prospective therapeutic options for the treatment of OA.

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Section: Age-related Changes In the Ecm Composition And Characteristicsmentioning

confidence: 99%

How are Aging and Osteoarthritis Related?

Wakale,

Wu,

Sonar

et al. 2023

Aging and disease

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show abstract

“… 1 - 3 Much like skin, tendon, and bones, articular cartilage thickness and cellularity decrease with age as a result of a homeostatic imbalance that contributes to an increased risk of osteoarthritis (OA). 4 , 5 With age, degenerative processes exceed anabolic activity in cartilage, leading to a loss of hyaline cartilage ECM components and a decrease in the number of functional chondrocytes, eventually manifesting in symptomatic OA. 4 , 6 Age is the leading risk factor for primary OA 7 and cartilage thickness is highly correlated with disease severity and progression to joint replacement surgery.…”

Section: Introductionmentioning

confidence: 99%

Adeno-Associated Virus-Delivered Fibroblast Growth Factor 18 Gene Therapy Promotes Cartilage Anabolism

Hollander

Goraltchouk²,

Rawal

et al. 2023

CARTILAGE

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Objective To determine the characterization of chondrogenic properties of adeno-associated virus type 2 (AAV2)-delivered hFGF18, via analysis of effects on primary human chondrocyte proliferation, gene expression, and in vivo cartilage thickness changes in the tibia and meniscus. Design Chondrogenic properties of AAV2-FGF18 were compared with recombinant human FGF18 (rhFGF18) in vitro relative to phosphate-buffered saline (PBS) and AAV2-GFP negative controls. Transcriptome analysis was performed using RNA-seq on primary human chondrocytes treated with rhFGF18 and AAV2-FGF18, relative to PBS. Durability of gene expression was assessed using AAV2-nLuc and in vivo imaging. Chondrogenesis was evaluated by measuring weight-normalized thickness in the tibial plateau and the white zone of the anterior horn of the medial meniscus in Sprague-Dawley rats. Results AAV2-FGF18 elicits chondrogenesis by promoting proliferation and upregulation of hyaline cartilage–associated genes, including COL2A1 and HAS2, while downregulating fibrocartilage-associated COL1A1. This activity translates to statistically significant, dose-dependent increases in cartilage thickness in vivo within the area of the tibial plateau, following a single intra-articular injection of the AAV2-FGF18 or a regimen of 6 twice-weekly injections of rhFGF18 protein relative to AAV2-GFP. In addition, we observed AAV2-FGF18-induced and rhFGF18-induced increases in cartilage thickness of the anterior horn of the medial meniscus. Finally, the single-injection AAV2-delivered hFGF18 offers a potential safety advantage over the multi-injection protein treatment as evidenced by reduced joint swelling over the study period. Conclusion AAV2-delivered hFGF18 represents a promising strategy for the restoration of hyaline cartilage by promoting extracellular matrix production, chondrocyte proliferation, and increasing articular and meniscal cartilage thickness in vivo after a single intra-articular injection.

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Diffusion of charged and uncharged contrast agents in equine mandibular condylar cartilage is not affected by an increased level of sugar-induced collagen crosslinking

Mirahmadi

Koolstra

Fazaeli

et al. 2019

Journal of the Mechanical Behavior of Biomedical Materials

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Aging does not change the compressive stiffness of mandibular condylar cartilage in horses

Abstract: Our data demonstrated that aging was not necessarily reflected in the biophysical properties of TMJ condylar cartilage. The combination of the changes happening due to aging resulted in different diffusive properties, depending on the nature of the solution.

Cited by 5 publications

References 50 publications

How are Aging and Osteoarthritis Related?

How are Aging and Osteoarthritis Related?

Adeno-Associated Virus-Delivered Fibroblast Growth Factor 18 Gene Therapy Promotes Cartilage Anabolism

Diffusion of charged and uncharged contrast agents in equine mandibular condylar cartilage is not affected by an increased level of sugar-induced collagen crosslinking

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