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Osteoarthritis (OA) is the result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, the extracellular matrix, and subchondral bone. It involves the entire joint, including the articular cartilage, subchondral bone, pericapsular muscles, capsule, and synovium.
The condition leads to loss of cartilage, sclerosis and eburnation of the subchondral bone, osteophytes, and subchondral cysts. It is clinically characterised by joint pain, stiffness, and functional limitation.2 There are currently no treatments that have demonstrated the ability to modify disease progression. Current treatments for OA are focused on the relief of pain symptoms and other physical treatments aiming to improve function – that is, physiotherapy and rehabilitation.
It is our ambition to stop the progression of Osteoarthritis.
We therefore see a need for:
All forms of OA are characterised by a loss of cartilage and there is a bidirectional interplay between cartilage, bone and synovial fluid. Examples of some of the symptoms that these changes lead to include pain, stiffness, swelling and weakness.3
Currently, just in the US, 30 million people are affected by OA.4 In 2013, OA was the single most common cause of disability in older adults globally, and the World health Organization predicts by 2050, 40 million people will be severely disabled by OA.1 Risk factors for OA can be grouped in 3 factors: systemic (age, gender and ethnicity), local joint (previous damage) and extrinsic (obesity and sport activities).3
Two of the main pharmacological management approaches are currently non-steroidal anti-inflammatory drugs and opioids.3 Unfortunately, in severe cases of OA, the only treatment option becomes joint replacement. This is highlighted by 98% of initial knee replacements in the UK being caused by OA.5