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Updated: Jul 3, 2026

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Interleukin-1 and transforming growth factor-beta 1 as crucial factors in osteoarthritic cartilage metabolism
Jean-Pierre Pujol1, Christos Chadjichristos, Florence Legendre
1Laboratory of Connective Tissue Biochemistry, Faculty of Medicine, Caen Cedex, France. jean-pierre.pujol@unicaen.fr
Abstract:
In osteoarthritis (OA), interleukin-1 (IL-1) stimulates the expression of metalloproteinases and aggrecanases, which induce cartilage degradation. IL-1 is also capable of reducing the production of cartilage-specific macromolecules, including type II collagen, through modulation of the transcription factors Sp1 and Sp3. Conversely, Transforming growth factor-beta (TGF-beta) counteracts with most of the IL-1 deleterious effects and contributes to cartilage homeostasis. However, OA chondrocytes progressively loose the expression of TGF-beta type II receptor and become insensitive to the factor. This downregulation is also driven by IL-1. This review provides insights into the molecular mechanisms that underly the interplay between IL-1 and TGF-beta in OA cartilage metabolism and enlightens the central role of Sp1 and Sp3 transcription factors in the matrix pathological alterations.
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