Abstract
The pathogenesis of posttraumatic osteoarthritis (PTOA) remains unrevealed. We speculate that cartilage crack caused by joint trauma will induce local abnormal tensile stress, leading to change in extracellular matrix (ECM) expression of chondrocytes, cartilage degeneration, and initiation of osteoarthritis. Finite element model was used to examine whether the local tensile stress could be produced around the crack. Cell experiments were conducted to test the effect of tensile strain on chondrocyte ECM expression. Animal tests in rabbits were carried out to examine the change around the cartilage crack. The results indicated that the local tensile stress was generated around the crack and varied with the crack angles. The maximum principal tensile stress was 0.59 MPa around the 45° crack, and no tensile stress was found at 90°. 10% tensile strain could significantly promote type I collagen mRNA expression and inhibit type II collagen and aggrecan (the proteoglycan core protein) mRNA expression. Type I collagen was detected around the 45° crack region in the cartilage with no change in type II collagen and proteoglycan. We conclude that the local tensile stress produced around the cartilage crack can cause the change in cartilage matrix expression which might lead to cartilage degeneration and initiation of osteoarthritis. This study provides biomechanical-based insight into the pathogenesis of PTOA and potentially new intervention in prevention and treatment of PTOA.
Highlights
Posttraumatic osteoarthritis (PTOA) is a common orthopedic disease that may occur after joint trauma
The finite element calculation indicated that cartilage crack could induce local tensile stress and the stress distribution around the crack changed significantly along with crack angles (Figure 3)
Chondrocyte test in vitro showed that 10% tensile strain increased the expression of COL1A1 by 41.9% and 41.2%, respectively, compared with the control group (P = 0.009) and 5% tensile strain (P = 0.006)
Summary
Posttraumatic osteoarthritis (PTOA) is a common orthopedic disease that may occur after joint trauma. Type II collagen fibers are arranged crosswise to form a network structure in which proteoglycans and other molecules are firmly bound together [9]. This sponge-like structure provides cartilage with the most important properties of withstanding the compression applied to joints during daily activities [10]. Type I collagen is the main component in bone, ligament, and tendon, which has enormous tensile strength needed in these structures [11] This implies that a tensile stress environment may exist when osteoarthritis occurs causing the alteration of chondrocyte phenotype
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