Outlines of the Biochemistry of Osteoarthritis

Abstract

Osteoarthritis (OA) is a complex, age dependent disease in which various factors, including metabolic changes, are all major contributors to its onset and progression. Anatomically, OA embraces the whole joint, i.e. articular cartilage, subchondral bone alterations and joint-lining synovial membrane. Correspondingly, OA development involves elaborate interactions of cartilaginous tissue metabolism and maintenance, osteogenesis, mineralization and inflammation of the synovial membrane. Identification of the molecular pathways and individual factors involved in OA etiology, understanding of mechanisms of their action and interaction are necessary conditions for developing the accurate diagnostic and prognostic tools and for providing OA patients effective treatment. There is a major progress in understanding of the molecular mechanisms of OA appearance and progression, which are pointing out to the network of biochemical factors important for normal functioning of the joints and changes leading to OA. The present review summarizes the data on the efficacy of the relevant biochemical factors affecting all the components of the joint and that could be therefore useful targets in treatment of OA. However, despite the dramatic growth of the knowledge concerning the biochemistry of OA and discovery of a number of useful biomarkers the real breakthrough in this area is still not achieved.

The Role of Inflammatory Cytokine and Inflammatory Regulator Protein Related to Severity of Joint Effusion in Osteoarthritis

“…This study was an exploratory study conducted in the context of exploring the role of the inflammatory pathway on joint effusion severity in OA cases. Inflammation is a pathogenesis that is widely believed to play a role related to severity joint effusion in OA [7], [17], [18], [19], [20].…”

Hierarchical, imbalanced pro-inflammatory cytokine networks govern the pathogenesis of chronic arthropathies

“…However, usage of IL-1, TNF, or ADAMTS inhibitors in OA animal models or RCTs has so far revealed inconsistent results 67 . In contrast, applying a TGFb-neutralizing antibody attenuated OA progression in rodent OA models (Table III), underscoring the key role of TGFb in OA-associated cartilage and bone damage 69,70 . In addition, crosstalk between Wnt signaling components and cytokines, such as IL-1b, TNFa, and IL-6 in creating OAassociated RANKL-mediated cartilage and SB destruction has been demonstrated 71 .…”

The Effects Of Cell Cycle Synchronization On The Growth Potential Of Primary Articular Chondrocytes

“…Changes occur on a biochemical level in terms of the structural macromolecules that comprise the tissue [81][82][83]. Advanced stages of OA as well as general tissue degeneration are both associated with a decrease in DNA content (a measure of cellularity) in affected regions of the articular cartilage [83].…”

“…Water content is observed to increase slightly in OA patients, affecting structure of the collagen fibril network-restrained proteoglycans in the ECM [82][83]. Proteoglycan content is reduced in advanced stage OA patients, with significantly decreased levels of aggregation, suggesting increased activity of the proteolytic enzymes [82,83].…”