Although the moderate thermal stimulation of articular cartilage exerts chondroprotective effects, it is difficult to effectively heat deep articular cartilage with conventional methods. Photosensitizers increase the ambient temperature using near-infrared (NIR) radiation, which has high tissue permeability. We hypothesized that the intra-articular administration of photosensitizers and NIR irradiation would exert a greater heating effect on articular cartilage. We aimed to evaluate the heating effect of this method on cultured chondrocytes and rat knee cartilage. In vitro, we irradiated a photosensitizer-containing medium with NIR and measured changes in the medium temperature, cytotoxicity, and gene expression of heat shock protein () and aggrecan (). In vivo, the knee joints of rats treated with photosensitizers were irradiated with NIR, and changes in intra-articular temperature and gene expression were measured, alongside histological analysis. The results showed that the medium and intra-articular temperature were raised to approximately 40 °C with no apparent disruption to articular cartilage or the immunohistochemically enhanced staining of HSP70 in chondrocytes. The gene expression of and was increased in both cultured and articular cartilage. In summary, this method can safely heat joints and enhance cartilage metabolism by inducing HSP70 expression in articular cartilage. It presents a new hyperthermia therapy with effective cartilage protection.
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http://dx.doi.org/10.3390/ijms25126728 | DOI Listing |
J Physiol
December 2024
Center for Muscle Biology, University of Kentucky, Lexington, KY, USA.
Knee osteoarthritis contributes substantially to worldwide disability. Post-traumatic osteoarthritis (PTOA) develops secondary to joint injury, such as ligament rupture, and there is increasing evidence suggesting a key role for inflammation in the aetiology of PTOA and associated functional deficits. Colony stimulating factor 1 receptor (CSF1-R) has been implicated in the pathogenesis of musculoskeletal degeneration following anterior cruciate ligament (ACL) injury.
View Article and Find Full Text PDFMicrob Pathog
December 2024
Department of Rheumatism and Immunology, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), No.4, Renmin Road, Shibei District, Qingdao, 266033, China.
Rheumatoid arthritis (RA) is an autoimmune condition that predominantly affects synovial joints, manifesting with joint swelling, pain, and stiffness. In advanced stages, unchecked inflammation can inflict damage on bone and cartilage, resulting in disabilities and deformities of the joints. Additionally, systemic and extra-articular complications may arise due to the consequences of uncontrolled inflammation.
View Article and Find Full Text PDFJ Nanobiotechnology
December 2024
Department of Joint Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, 250021, People's Republic of China.
Osteoarthritis (OA) is the most common disease in aging joints and has characteristics of cartilage destruction and inflammation. It is currently considered a metabolic disease, and the CH25H-CYP7B1-RORα axis of cholesterol metabolism in chondrocytes plays a crucial catabolic regulatory role in its pathogenesis. Targeting of this axis in chondrocytes may provide a therapeutic approach for OA treatment.
View Article and Find Full Text PDFJ Anat
December 2024
Human Anatomy Resource Centre, Education Directorate, University of Liverpool, Liverpool, UK.
Ochronotic pigmentation of connective tissue is the central pathological process in the rare metabolic disease alkaptonuria (AKU). Tissue pigmentation in AKU occurs due to unmetabolised homogentisic acid (HGA) in the circulation, caused by an enzyme deficiency in the liver. Ochronotic pigmentation, derived from HGA, has previously been reported and described in large joints obtained from arthroplasty surgeries, which typically have advanced disease.
View Article and Find Full Text PDFOsteoarthritis Cartilage
December 2024
Department of Biomedical Engineering, Vanderbilt University, Nashville, TN, 37212, USA; Center for Bone Biology, Vanderbilt University, Nashville, TN 37212, USA; Center for Stem Cell Biology, Vanderbilt University, Nashville, TN, 37212, USA. Electronic address:
Objective: Investigational cell therapies have been developed as disease-modifying agents for the treatment of osteoarthritis (OA), including those that inducibly respond to inflammatory factors driving OA progression. However, dysregulated inflammatory cascades do not specifically signify the presence of OA. Here, we deploy a synthetic receptor platform that regulates cell behaviors in an arthritis-specific fashion to confine transgene expression to sites of cartilage degeneration.
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