Osteoarthritis
Abstract
Osteoarthritis (OA) is characterized by degeneration of articular cartilage, limited intraarticular inflammation with synovitis, and changes in peri‐articular and subchondral bone. Multiple factors are involved in the pathogenesis of OA, including mechanical influences, the effects of aging on cartilage matrix composition and structure, and genetic factors. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines, and other inflammatory mediators by chondrocytes, research has focused on the chondrocyte as the cellular mediator of OA pathogenesis. The other cells and tissues of the joint, including the synovium and subchondral bone, also contribute to pathogenesis. The adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the original cartilage matrix architecture. It may attempt to recapitulate phenotypes of early stages of cartilage development, but the precise zonal variations of the original cartilage cannot be replicated. Current pharmacological interventions that address chronic pain are insufficient, and no proven structure‐modifying therapy is available. Cartilage tissue engineering with or without gene therapy is the subject of intense investigation. There are multiple animal models of OA, but there is no single model that faithfully replicates the human disease. This review will focus on questions currently under study that may lead to better understanding of mechanisms of OA pathogenesis and elucidation of effective strategies for therapy, with emphasis on mechanisms that affect the function of chondrocytes and interactions with surrounding tissues. J. Cell. Physiol. 213:626–634. © 2007 Wiley‐Liss, Inc.
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Osteoarthritis is a highly prevalent type of arthritis characterized by synovitis and degeneration of articular cartilage and subchondral bone in joints of the hands, knees, hips, and spine.
“Osteoarthritis is a highly prevalent type of arthritis characterized by synovitis, and degeneration of both articular cartilage and subchondral bone in the joints of the hands, knees, hips, and spine (Goldring and Goldring, 2007).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Goldring and Goldring, 2007
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- Authors
- Goldring, M. B., & Goldring, S. R.
- Affiliations
- Hospital for Special Surgery (US)
- Corresponding author
- Goldring, Mary B.
- ORCID
- Goldring, Mary B.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2007-09-04
- Volume
- 213
- Issue
- 3
- Pages
- 626-634
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- OpenAlex
- W4232900352
- Cited by
- 1,179
- References
- 102
- Citations by year
- 2026: 31 · 2025: 33 · 2024: 45 · 2023: 41 · 2022: 50 · 2021: 65 · 2020: 64 · 2019: 79 · 2018: 61 · 2017: 72 · 2016: 82 · 2015: 79 · 2014: 77 · 2013: 71 · 2012: 74
- FWCI
- 7.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Arthritis Foundation
- National Institutes of Health (5r01ar045378-04)
- National Institute on Aging (R01AG022021)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01-AR 45378)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Health Sciences › Medicine › Surgery › Hip disorders and treatments
- Keywords
- osteoarthritis, articular cartilage degeneration, chondrocytes, chondrocyte proliferation, cartilage matrix turnover, synovitis, subchondral bone, chondrogenesis, gene therapy, cartilage tissue engineering, animal models of osteoarthritis, chronic pain, cytokines and growth factors
- MeSH terms
- Animals, Cartilage Diseases, Cartilage, Articular, Forecasting, Humans, Models, Biological, Osteoarthritis, Genetic Therapy, Chondrocytes, Matrix Metalloproteinases, Tissue Engineering
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