98%
921
2 minutes
20
Treatment of osteoarthritic patients requires the development of morphologically and mechanically complex hyaline cartilage at the injury site. A tissue engineering approach toward differentiating mesenchymal stem cells into articular chondrocytes has been developed to overcome the drawbacks of conventional therapeutic and surgical procedures. To imitate the native micro and macro environment of articular chondrocytes, cell culture parameters such as oxygen concentration, mechanical stress, scaffold design, and growth factor signalling cascade regulation must be addressed. This review aims to illuminate the path toward developing tissue engineering approaches, accommodating these various parameters and the role these parameters play in regulating chondrogenesis for better articular cartilage development to treat osteoarthritis effectively.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2217/rme-2023-0017 | DOI Listing |
J Vis Exp
August 2025
Laboratory of Regenerative Medicine in Sports Science, School of Physical Education and Sports Science, South China Normal University; Bone and Joint Research Team of Degeneration and Injury, Guangdong Provincial Academy of Chinese Medical Sciences;
Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease triggered by trauma or intense mechanical stress, leading to joint cartilage degeneration and functional impairment. Prostaglandin E2 (PGE2) contributes significantly to cartilage degradation following mechanical injury by activating its receptor, Prostaglandin E receptor 4 (EP4), on chondrocyte membranes. The homeostasis of articular cartilage primarily relies on the dynamic balance between cartilage degradation and repair, a process finely regulated by chondrocytes.
View Article and Find Full Text PDFJ Extracell Vesicles
September 2025
Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Osteoarthritis (OA), the prevalent debilitating joint disorder, is accelerated by dysregulated intercellular crosstalk, yet the role of fibroblast-like synoviocyte (FLS)-derived extracellular vesicles and particles (EVPs) in disease progression remains to be elucidated. Here, integrative analysis of clinical specimens, animal models, and publicly available datasets revealed significant alterations in exosomal pathways within OA synovium. Proteomic profiling revealed distinct molecular signatures in EVPs derived from inflammatory and senescent FLSs, reflecting the pathophysiological status of their parent cells.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Rehabilitation Medicine, Second Xiangya Hospital, Central South University, Changsha 410011.
Objectives: Osteoarthritis (OA) is one of the most common chronic degenerative diseases, with chondrocyte apoptosis and extracellular matrix (ECM) degradation as the major pathological changes. The mechanical stimulation can attenuate chondrocyte apoptosis and promote ECM synthesis, but the underlying molecular mechanisms remain unclear. This study aims to investigate the role of primary cilia (PC) in mediating the effects of mechanical stimulation on OA progression.
View Article and Find Full Text PDFACS Nano
September 2025
School of Medicine, Nankai University, Tianjin 300071, China.
In situ articular cartilage (AC) regeneration is a meticulously coordinated process. Microfracture has been the most extensive clinical approach in AC repair, but it faces challenges such as matrix degradation, generation, and remodeling within a local inflammatory microenvironment. So far, it remains a challenge to establish a multistage regulatory framework for coordinating these cellular events, particularly the immune response and chondrocyte proliferation in microfracture-mediated AC repair microenvironments, which is crucial for promoting AC regeneration quality.
View Article and Find Full Text PDFJ Adv Res
September 2025
State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi International Joint Research Center for Oral Diseases, Department of Oral Anatomy and Physiology and TMD, School of Stomatology, The Fourth Military Medical Univ
Introduction: Aberrant biomechanical force-induced chondrocyte adipogenesis is involved in the development of temporomandibular joint osteoarthritis (TMJ OA). Growth differentiation factor 11 (GDF11) has been implicated in this process. However, whether mechanosensitive histone deacetylase 3 (HDAC3) regulates GDF11 signaling in the context of TMJ OA remains to be elucidated.
View Article and Find Full Text PDF