Arthritis

     Osteoarthritis (OA) is the most common joint disorder and the major cause of disability in the adult population. The pathophysiology of the disease is characterized by progressive loss of articular cartilage, cartilage calcification, osteophyte formation, subchondral bone remodeling, and mild to moderate inflammation of the synovial lining. 

    Symptoms include joint pain, tenderness, stiffness, inflammation, and creaking of the joints. Conventional treatment is focused on pain reduction using NSAIDs, local injections of glucocorticoid or hyaluronan, and joint replacement surgery in severe cases such as bone-on-bone conditions.    Although cartilage destruction is the hallmark of OA disease, changes in the periarticular tissues, including the subchondral bone, ligaments, tendons, menisci, and synovial membrane is also involved.  Simple ‘wear and tear’ due to excessive use as the underlined cause of osteoarthritis is somewhat of an outdated explanation for the role of mechanical overload/injury in osteoarthritis development.   The chondrocyte is the single cell of the cartilage that is responsible for developing and maintaining the cartilage matrix.  It synthesizes and secretes the collagen which is the back bone of the cartilage matrix and the proteoglycan which functions as the cushion of the joint.  When there is cartilage damage, the chondrocyte will synthesize new molecules to repair the damage.  However, if there is too much damage, it will work in a disruptive way.  Cartilage homeostasis is carefully balanced by metabolic and catabolic pathways to maintain the extracellular matrix structure and function throughout the articular cartilage zones. Mechanical overloading, age-associated changes in chondrocyte function, and disturbed cytokine activities may all initiate extracellular matrix degradation and contribute to the onset and progression of articular cartilage deterioration resulting in osteoarthritis.  Joint inflammation due to joint trauma, mechanical overload and overuse results in the remolding of the subchondral bone, upregulation of matrix-degrading enzymes and chondrocyte phenotypic changes which lead to the development and progression of osteoarthritis.  

   The joint injury can cause changes in the periarticular tissues which destabilizes the joint thus causing mechanical stress to the cartilage tissue.  These periarticular tissues include subchondral bone, ligaments, tendons, menisci, and synovial membrane.  Other factors that influence the disease process are those that can cause joint inflammation or mechanical overload such as aging, genetic predisposition, abnormal biomechanics, obesity, and comorbidities such as cardiovascular disease, metabolic syndrome, and diabetes.    Cartilage Matrix Micro-Cracks and Joint Pain  The earliest changes in the development of osteoarthritis is the loss of negatively charged polysaccharide molecules in the cartilage which results in increased water content and swelling of the cartilage matrix.   Swelling of the cartilage matrix causes microcracks in the superficial zone.  As the disease progresses, exfoliation of fragments of cartilage and deep fissures extending into the deeper cartilage layers lead to exposure of the underlying zones of calcified cartilage and subchondral bone.    

 

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