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.
Keywords: Adipokines, articular cartilage, inflammation, mineralization, subchondral bone, synovitis, Osteoarthritis (OA), subchondral bone alterations, joint-lining synovial membrane, OA etiology, biochemical factors, biomarkers, multifactorial etiology, metabolic factors, genetic polymorphisms, extracellular matrix, proteoglycans (PG), hyaluronic acid (HA), chondrocytes, anabolic, catabolic, regulatory mediators, osteoarthritis, obesity (OB), chondrocyte's metabolism, joints' mineralization (chondrocalcinosis), calcium pyrophosphate dehydrate, arthroplasty, pro-inflammatory cytokines, innate immune system, IL-1β, transforming growth factor (TGF)-β, nitric oxide synthetase (iNOS), low-frictional material, proteolytic enzymes, macromolecules, type II collagen, COMP, fibronectin, endogenous matrix, hypertrophic chondrocyte, chondroprogenitor splice variant, COL10A1, MMP-13, MMP-9, OA lesions, mitogen-activated protein kinase (MAPK), ADAMTS-5 activity, Retinoic acid, synovial membrane, osteoarthritic joints, pro-inflammatory, ECM degradation, anti-inflammatory effect, Articular Cartilage Calcification, CPPD deposition, extracellular pyrophosphate (ePPi) ions, ankylosis gene (ANKH), TNAP, ENPP1 genes, bone morphogenetic proteins (BMPs), BMP2, GDF5, transglutaminase, chondrocyte hypertrophy, Obesity, obese gene (ob), adiponectin, adipocytokine, resistin, Subchondral Bone Changes, ADAMTS5, cartilage tissue remodeling, C-telopeptide, osteoprotegerin (OPG), anti-inflammatory drugs, osteoclast differentiation, Synovium Inflammation, Immunohistochemical, lymphocytes, macrophages, antigen-driven immune response, therapeutic intervention, prognostic, efficacy, Collagen, Type II collagen (CII), CII biomarkers, (TIINE), Coll2-1/4N1, Coll2-1/4N2, (CTX-II), HELIX-II, C-propeptide, hypertrophic OA, osteophytes, hemophilic arthropathy, PIIANP synthesis, Cartilage Oligomeric Matrix Protein (COMP), II (Col2CTx), BMI, Human Glycoprotein, Cartilage 39 (YKL-40), Bone Sialoprotein (BSP), circulating IL-6, therapeutical targets, Advanced glycation endproduct, Collagenase type II, Chondroitin sulfate