Osteoarthritis
Osteoarthritis (OA), the most common form of arthritis, is characterized by degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation, subchondral bone remodeling, and inflammation of the synovial membrane. This dise
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Introduction to Osteoarthritis
Pathophysiology of Osteoarthritis
Osteoarthritis (OA) is the most common form of arthritis, affecting 13.9 % of US adults aged 25 and older, totaling 26.9 million [1]. OA is characterized by degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation (bony projections along the joint margin), subchondral bone remodeling, and inflammation of the synovial membrane. Other tissues of the joint including the muscles and ligaments are also altered during the OA process. OA can be triggered by external factors such as trauma and endogenous predisposing factors including age, genetics, and high body mass index. It results in pain, reduced quality of life, and disability necessitating joint replacement in end-stage disease. Important advances have been made in understanding its pathological processes, and promising new disease-modifying OA drugs (DMOADs) are being developed that will slow the progression of the disease and improve the current symptomatic treatment.
OA is a multifactorial disease resulting in the failure of the articular tissues to maintain a homeostatic balance between matrix synthesis and degradation. An initial phase of cartilage remodeling is characterized by edema, followed by degradation and loss of this tissue. These alterations are associated with synovial inflammation and subchondral bone remodeling (Fig. 1). In cartilage, there is only one type of cell, the chondrocyte, which is responsible for the maintenance of this tissue’s extracellular matrix (ECM, see chapter “Overview” under part “Joints”). Early during the OA process, increased biomechanical stress and/or biochemical stimuli can activate the anabolic function of chondrocytes to repair early cartilage damage. Over time, this anabolic attempt fails and leads to an imbalance favoring degradation. This degradation will induce a vicious circle, in which the degradative fragments of ECM proteins (e.g., fibronectin and collagen) induce synovial membrane inflammation, which in turn will produce catabolic and inflammatory factors [2, 3], thus aggravating the OA process. Increasing evidence suggests that in OA there is a cross talk between the cartilage, synovial membrane, and subchondral bone, which sustains the catabolic process [4, 5]. Synovial inflammation, which is suggested to be secondary to the release of cartilage products into the synovial fluid, and subchondral bone remodeling by its release of soluble mediators, affects the cartilage by sustaining its degradation. The
C. Roubille • J. Martel-Pelletier • J.-P. Pelletier (*) Osteoarthritis Research Unit, University of Montreal Hospital Research Centre (CRCHUM), 900 Saint-Denis, Tour Viger, Montreal, QC H2X 0A9, Canada e-mail: [email protected]; [email protected]; [email protected]
E. Lammert, M. Zeeb (eds.), Metabolism of Human Diseases, DOI 10.1007/978-3-7091-0715-7_18, © Springer-Verlag Wien 2014
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Endogenous predisposition to OA
External risk factors Trauma Overload
Age G
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