The Spondyloepiphyseal Dysplasia Congenita homozygous Mutant: A Model for the Mechanism of Osteoarthritis

Authors

David Macdonald, Brigham Young University
Dr. Robert Seegmiller, Brigham Young University

Keywords

spondeloepipheseal dysplasia congenita, sedc, Col2A1, mutation

College

Life Sciences

Department

Physiology and Developmental Biology

Abstract

Articular cartilage is a hard-wearing and specialized form of hyaline cartilage which allows for an almost frictionless surface during joint movement (Ofek et al. 2008). These unique characteristics are primarily due to chondrocyte secretions, and the composition and properties of the extracellular matrix (ECM) (Buckwalter and Mankin 1998). Chondrocytes play a crucial role in cartilage durability because of their extracellular secretions (Knudson and Knudson 2001). Being immotile, chondrocytes depend greatly upon the equilibrium of the ECM for protection, integrity, and regulation (Aszodi et al. 2003). The ECM is composed primarily of type II collagen, glycoproteins, water and aggrecan proteoglycan (Hollander et al.1994).

Recommended Citation

Macdonald, David and Seegmiller, Dr. Robert (2013) "The Spondyloepiphyseal Dysplasia Congenita homozygous Mutant: A Model for the Mechanism of Osteoarthritis," Journal of Undergraduate Research: Vol. 2013: Iss. 1, Article 1519.
Available at: https://scholarsarchive.byu.edu/jur/vol2013/iss1/1519