Abstract
Traumatic injuries of the knee joint result in a wide variety of pathomechanisms, which contribute to the development of so-called posttraumatic osteoarthritis (PTOA). These pathogenetic processes include oxidative stress, excessive expression of catabolic enzymes, release of damage-associated molecular patterns (DAMPs), and synovial inflammation. The present review focuses on the underlying pathomechanisms of PTOA and in particular the behavior and fate of the surviving chondrocytes, comprising chondrocyte metabolism, regulated cell death, and phenotypical changes comprising hypertrophy and senescence. Moreover, possible therapeutic strategies, such as chondroanabolic stimulation, anti-oxidative and anti-inflammatory treatment, as well as novel therapeutic targets are discussed.
Highlights
Osteoarthritis (OA) is considered to be the most prevalent joint disease worldwide
Synovial inflammation is relevant after joint injuries as the central initiating event of so called posttraumatic osteoarthritis (PTOA), a special form of OA, which accounts for about 10% of the overall knee OA incidence [10,11]
There is a sudden release of extracellular matrix (ECM)-derived debris, in particular fibronectin [84], and intracellular alarmins, i.e., nucleic acids, high mobility group box 1 (HMGB1) and S100A8/9 [85]. These so-called damage-associated molecular patterns (DAMPs) induce intracellular signaling pathways via pattern recognition receptors (PRRs), including toll-like receptors 2 and 4 (TLR 2/4) and receptor for advanced glycation end products (RAGE), which are expressed on the cell surface of chondrocytes and synovial cells [86]
Summary
Osteoarthritis (OA) is considered to be the most prevalent joint disease worldwide. In general, OA might occur in all synovial joints, from the mandibular joint to the foot joints this review will mainly focus on the most commonly affected joint, the knee [1]. An increased metabolic activity of chondrocytes has been observed in early OA, concerning the biosynthesis of ECM components [30,31,32] and catabolic enzymes [33] This might explain the finding of Catterall et al who demonstrated that collagen and non-collagenous proteins in cartilage of patients suffering from knee OA were about 30 years ‘younger’ on a biological scale as compared to non-OA cartilage [34]. Overall, both ECM components as well as the majority of catabolic enzymes are derived from chondrocytes in a well-regulated manner, creating a fine-tuned and fragile homeostasis. Before proceeding to the consequences of traumatic injuries and subsequent cartilage degeneration, the section will first focus on the chondroanabolism
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