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Adipose Tissue-Derived Adult Stem Cells
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Laura Aust, Lyndon Cooper, Blythe Devlin, Tracey du Laney, Sandra Foster, Jeffrey M. Gimble, Farshid Guilak, Yuan Di C. Halvorsen, Kevin Hicok, Amy Kloster, Henry E. Rice, Anindita Sen, Robert W. Storms, William O. Wilkison
Articular cartilage is the thin layer of deformable, load-bearing material that lines the bony ends of all diarthrodial joints. The primary functions of cartilage are to support and distribute forces generated during joint loading and to provide lubricating surfaces to prevent wear or degradation of the joint. Cartilage is a metabolically active tissue with relatively slow state of turnover by a sparse population of specialized cells, chondrocytes. Cartilage has limited capacity for intrinsic repair, and even minor lesions or injuries may lead to progressive damage and joint degeneration. Chondral or osteochondral lesions may be a significant source of pain and loss of function and rarely heal spontaneously. The poor repair capability of cartilage is often attributed to the lack of blood supply to the affected area or due to the lack of a source of un-differentiated cells that can promote repair.40,41 Recently, a cell based cartilage repair product became available for clinical application. The Carticel (Genzyme, Cambridge MA) procedure involves the isolation and amplification of autologous chondrocytes and subsequent reimplantation into the defect, which is covered by a flap of autologous periosteal tissue.42 Other potential sources of cell therapy include chondrocytes isolated from elastic cartilage,43 bone marrow derived mesenchymal stem cells (MSC),44,45 and ADAS cells.18,46,47
Osteoarthritis
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
David Musnick, Richard D. Batson
OA progresses when tissue regeneration cannot keep pace with the rate of cartilage loss. Joint damage may occur when the biomaterial properties of the articular cartilage are inadequate or the load on the joint is excessive. Contributing factors related to the development or progression of OA in a particular joint are: traumatic injury including sprains and contusion, joint malalignment, prolonged myofascial tightness, ligament laxity with joint hypermobility, prolonged muscle recruitment weakness in muscles stabilizing or moving the joint, genetic predisposition, obesity, aging, gender, hormone issues and nutritional factors. Additional insult on the total joint load can come from the extra weight burden associated with obesity and certain physical activities such as high-impact sports. Recent scientific literature suggests that, in addition to the extra weight burden associated with obesity, inflamed adipose tissue and dyslipidemia associated with obesity can contribute to OA.
Articular Cartilage
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Tim S. Waters, Nima Heidari, George Bentley
The main functions of articular cartilage are joint lubrication (allowing movement between opposing surfaces with the minimum of friction and wear) and shock absorption (distributing joint loads and therefore reducing the stresses experienced). Articular cartilage has a very low coefficient of friction (0.002), 30 times smoother than most modern joint replacements. This coefficient of friction can be lowered further by fluid-film formation, elastic deformation of articular cartilage, synovial fluid and efflux of fluid from cartilage. The coefficient of friction can be increased by fibrillation of articular cartilage.
A novel knee joint model in FEBio with inhomogeneous fibril-reinforced biphasic cartilage simulating tissue mechanical responses during gait: data from the osteoarthritis initiative
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Alexander Paz, Gustavo A. Orozco, Petri Tanska, José J. García, Rami K. Korhonen, Mika E. Mononen
Articular cartilage is a highly specialized tissue covering bone ends in diarthrodial joints. The mechanical capabilities of cartilage emerge from its biphasic composition and unique fibril-reinforced structure (Mow et al. 1992). The solid phase consists of non-fibrillar and fibrillar parts. The former is mainly responsible for the equilibrium response, while the latter contributes strongly to fluid pressurization and tensile strength, affecting mainly the dynamic and instantaneous stiffness of the tissue (Soulhat et al. 1999). In addition, collagen fibril orientation affects the zone-specific mechanical response of cartilage in joints (Huang et al. 2005). In particular, in-plane strains along the cartilage surfaces are sensitive to the split-line patterns, and out-of-plane stresses, strains, and fluid pressures to the depth-dependent structure (Mononen et al. 2012; Li et al. 2016).
Regulatory T Cells in Bioactive Peptides-Induced Oral Tolerance; a Two-Edged Sword Related to the Risk of Chronic Diseases: A Systematic Review
Published in Nutrition and Cancer, 2021
Meisam Barati, Masoumeh Jabbari, Hamid Nickho, Mojgan Esparvarinha, Amirreza Javadi Mamaghani, Hasan Majdi, Anwar Fathollahi, Sayed Hossein Davoodi
OA is a deteriorating disease of articular cartilage and subchondral bones. In the recent decades, the growing bodies of evidences indicate the important role of the immune system in the pathogenesis of this disease (53, 54). Collagen IX, Fibromodulin and Hyaluronan, the cartilage specific antigens, release due to the primary injury of articular cartilage caused by mechanical factors. These antigens can play as triggers for immune response activation in susceptible persons (55–58). Immune cells including macrophages, T cells and B cells infiltrate into the joint tissue and chemokines and cytokines release to the synovial fluid from various cell types in the joint. Complement system also activates and collectively, the inflammatory milieu induces production of cartilage degrading factors mostly from chondrocytes. These processes result in more and more damage to the articular cartilage. Based on the evidences from recent studies, it has been shown that there are substantial inflammatory components in the pathogenesis and development of OA (59–61).
Compressive stress relaxation behavior of articular cartilage and its effects on fluid pressure and solid displacement due to non-Newtonian flow
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
In the mammalian musculoskeletal system, an essential biological activity is a locomotion which is possible because the body is capable of moving with diarthrodial joints, e.g. ankle, knee, hip, etc. Simon et al. (1981) showed with experimental results that during normal gait, these joints transmit very heavy loads, one to four times body weight. Articular cartilage is a smooth layer of soft white tissue, which covers the bony ends in diarthrodial and synovial joints. Cartilage provides the joints with mechanical functions such as shock absorption, load-bearing, and wears resistance for seven or eight decades (Mankin 1982). These functional biomechanical characteristics are due to the multiphasic nature of this tissue (Linn and Sokoloff 1965; Mankin and Thrasher 1975; Maroudas 1979; Mow et al. 1980; Lai et al. 1991; Mow and Huiskes 2005).