3D bioprinting is a promising approach for the repair of cartilage tissue after damage due to injury or disease; however, the design of 3D printed scaffolds has been limited by the availability of bioinks with requisite printability, cytocompatibility, and bioactivity. To address this, we developed an approach termed in situ crosslinking that permits the printing of non-viscous, photocrosslinkable bioinks via the direct-curing of the bioink with light through a photopermeable capillary prior to deposition. Using a norbornene-modified hyaluronic acid (NorHA) macromer as a representative bioink and our understanding of thiol-ene curing kinetics with visible light, we varied the printing parameters (e.g., capillary length, flow rate, light intensity) to identify printing conditions that were optimal for the ink. The printing process was cytocompatible, with high cell viability and homogenous distribution of mesenchymal stromal cells (MSCs) observed throughout printed constructs. Over 56 days of culture in chondrogenic media, printed constructs increased in compressive moduli, biochemical content (i.e., sulfated glycosaminoglycans, collagen), and histological staining of matrix associated with cartilage tissue. This generalizable printing approach may be used towards the repair of focal defects in articular cartilage or broadly towards widespread biomedical applications across a range of photocrosslinkable bioinks that can now be printed.
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http://dx.doi.org/10.1038/s41598-019-56117-3 | DOI Listing |
J Tissue Eng
January 2025
Department of Sports Medicine and Joint Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Bone marrow stimulation treatment by bone marrow stromal cells (BMSCs) released from the bone medullary cavity and differentiated into cartilage via microfracture surgery is a frequently employed technique for treating articular cartilage injuries, yet the treatment presents a main drawback of poor cartilage regeneration in the elderly. Prior research indicated that aging could decrease the stemness capacity of BMSCs, thus we made a hypothesis that increasing old BMSCs (OBMSCs) stemness might improve the results of microfracture in the elderly. First, we investigated the correlation between microfracture outcomes and BMSCs stemness using clinical data and animal experiments.
View Article and Find Full Text PDFFront Pharmacol
December 2024
College of Pharmacy, Jinan University, Guangzhou, China.
Bone homeostasis encompasses two interrelated aspects: bone remodeling and cartilage metabolism. Disruption of bone homeostasis can lead to the development of metabolic bone diseases such as osteoporosis and osteoarthritis. The maintenance of bone homeostasis is a complex process that does not solely rely on the functions of the bone tissue itself.
View Article and Find Full Text PDFCytotechnology
February 2025
Department of Sports Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, 261 Datong Road, Yuexiu District, Guangzhou, 510105 Guangdong China.
Unlabelled: Cartilage and joint damage can lead to cartilage degeneration. Bone marrow mesenchymal stem cells (BMSCs) have the potential to address cartilage damage. Hence, this study probed the mechanism of BMSC-extracellular matrix (BMSC-ECM) in promoting damaged chondrocyte repair by regulating the Notch1/RBPJ pathway.
View Article and Find Full Text PDFOsteoarthritis, a major global cause of pain and disability, is driven by the irreversible degradation of hyaline cartilage in joints. Cartilage tissue engineering presents a promising therapeutic avenue, but success hinges on replicating the native physiological environment to guide cellular behavior and generate tissue constructs that mimic natural cartilage. Although electrical stimulation has been shown to enhance chondrogenesis and extracellular matrix production in 2D cultures, the mechanisms underlying these effects remain poorly understood, particularly in 3D models.
View Article and Find Full Text PDFAm J Sports Med
January 2025
Department of Orthopaedics, Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, Rhode Island, USA.
Background: Meniscal injuries that fail to heal instigate catabolic changes in the knee's microenvironment, posing a high risk for developing posttraumatic osteoarthritis (PTOA). Previous research has suggested that human cartilage-derived progenitor cells (hCPCs) can stimulate meniscal repair in a manner that depends on stromal cell-derived factor 1 (SDF-1) pathway activity.
Hypothesis: Overexpressing the SDF-1 receptor CXCR4 in hCPCs will increase cell trafficking and further improve the repair efficacy of meniscal injuries.
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