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Osteophyte development during osteoarthritis (OA) : consideration of angiogenesis, mechanical loading and tissue microstructure

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Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
This paper is devoted to modelling and investigation of the effects of mechanical loading, blood vessels development and tissue microstructure in osteoarthritis (OA) – a degenerative joint disease. OA is one of the most common diseases affecting the population, and therefore it is a social and medical problem of utmost importance. It predominantly affects the elderly but also sportsmen, obese people and those with curvature of the spine. Although the phenomenon of OA is not yet fully understood, it is commonly accepted that mechanical aspects are crucial in its evolution [1, 2]. Mechanical overloading leads to chondrocytes apoptosis which increases generation of vascular endothelial growth factors [3] then expansion of angiogenesis and osteophyte onset. A properly formulated mathematical model of cartilage degeneration and osteophytes development can significantly help in understanding the complexity of this process. The presented model reflects the most important aspects of the interactions between mechanical and biological factors, crucial for the phenomenon of OA.
Rocznik
Strony
533--540
Opis fizyczny
Bibliogr. 11 poz., rys.
Twórcy
  • Warsaw University of Technology Faculty of Production Engineering Institute of Mechanics and Printing Department of Construction Engineering and Biomedical Engineering Narbutta 85, 02-524 Warsaw, Poland
autor
  • Warsaw University of Technology Faculty of Production Engineering Institute of Mechanics and Printing Department of Construction Engineering and Biomedical Engineering Narbutta 85, 02-524 Warsaw, Poland
Bibliografia
  • 1. Felson D.T., Osteoarthritis as disease of mechanics, Osteoarthritis and Cartilage, 21(1): 10–15, 2013, doi: 10.1016/j.joca.2012.09.012.
  • 2. Wang T.-M. et al., Loading rates during walking in adolescents with Type II osteonecrosis secondary to pelvic osteotomy, Journal of Orthopedic Research, 2016, doi: 10.1002/jor.23239.
  • 3. D’Lima D.D. et al., Human chondrocyte apoptosis in response to mechanical injury, Osteoarthritis and Cartilage, 9(8): 712–719, 2001, doi: 10.1053/joca.2001.0468.
  • 4. Pfander D. et al., Vascular endothelial growth factor in articular cartilage of healthy and osteoarthritic human knee joints, Annals of Rheumatic Diseases, 60(11): 1070–1073, 2001, doi: 10.1136/ard.60.11.1070.
  • 5. Pufe T. et al., Mechanical overload induces VEGF in cartilage discs via hypoxia-inducible factor, The American Journal of Pathology, 164(1): 185–192, 2004, doi: 10.1016/S0002- 9440(10)63109-4.
  • 6. Monod J., The growth of bacterial cultures, Annual Review of Microbiology, 3: 371–394, 1949, doi: 10.1146/annurev.mi.03.100149.002103.
  • 7. Verhulst P.F., Deuxi`eme memoire sur la loi daccrossement de la population ˇ , M´emoires de l’Acad´emie Royale des Sciences, Des Lettres et des Beaux-Arts de Belgique, 20: 1–32, 1847, http://eudml.org/doc/178976.
  • 8. Lekszycki T., dell’Isola F., A mixture model with evolving mass densities for describing synthesis and resorption phenomena in bones reconstructed with bio-resorbable materials, ZAMM (Journal of Applied Mathematics and Mechanics/Zeitschrift f¨ur Angewandte Mathematik und Mechanik), 92(6): 426–444, 2012, doi: 10.1002/zamm.201100082.
  • 9. COMSOL Multiphysicsr v. 5.2, COMSOL AB, Stockholm, Sweden. www.comsol.com.
  • 10. Hashimot S. et al., Development and regulation of osteophyte formation during experimental osteoarthritis, Osteoarthritis and Cartilage, 10(3): 180–187, 2002, doi: 10.1053/joca.2001.0505.
  • 11. Kamekura S. et al., Osteoarthritis development in novel experimental mouse models induced by knee joint instability, Osteoarthritis and Cartilage, 13(7): 632–641, 2005, doi: 10.1016/j.joca.2005.03.004.
Uwagi
Opracowanie ze środków MNiSW w ramach umowy 812/P-DUN/2016 na działalność upowszechniającą naukę (zadania 2017).
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-616e1810-9c31-45ea-991b-f7819252ed05
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