The knee is one of the most common joints affected by osteoarthritis (OA), frequently with clinical presentation by middle age or even earlier. Accumulating evidence supports that knee OA progression is often driven by biomechanical forces, and the pathological response of tissues to such forces leads to structural joint deterioration, knee symptoms and reduced function. Well-known biomechanical risk factors for progression include joint malalignment and meniscal tear. The high risk of OA after knee injury demonstrates the critical role of biomechanical factors also in incident disease in susceptible individuals. However, our knowledge of the contributing biomechanical mechanisms in the development of early disease and their order of significance is limited. Part of the problem is our current lack of understanding of early-stage OA, when it starts and how to define it.
Osteoarthritis (OA) is an increasingly important health concern in most developed countries and is, according to the World Health Organization (WHO), among the top 10 conditions in Europe with respect to burden on the society . The knee joint, which is highly load bearing, is one of the most commonly affected sites, and the disease often presents by middle age or even earlier. However, our understanding of early knee OA is limited. We often fail to recognise the disease until irreversible morphological joint changes have occurred, for example, loss of joint cartilage and meniscal maceration and extrusion indicated by the loss of joint space on plain radiographs and osteophyte growth. In reality, OA is a long and slow continuum of joint changes and symptoms that has no clear-cut onset. Most studies, including large epidemiological studies, define incident OA as the development of radiographic changes. However, as radiographic OA are late-stage changes of the disease, we need to consider the fact that we, by this definition, are often looking for risk factors for OA progression rather than true initiation. The recognition of truer incident disease would require modern molecular imaging techniques, which are not feasible in large epidemiological studies .
There is steadily accumulating evidence that progression of knee OA is often driven by biomechanical forces, and the pathological response of tissues to such forces leads to further joint deterioration, symptoms and reduced function. So far, trying to slow down the disease using pharmacological treatment without addressing any underlying biomechanical problem has been disappointing. In addition, an inherent risk of the individual by genetic or other predisposition is often needed because not all individuals with unfavourable biomechanics develop knee OA ( Fig. 1 ). This review provides a brief overview through the eyes of a clinical epidemiologist of our current understanding of key concepts of the importance of joint biomechanics in the initiation and progression of knee OA with a focus on the role of knee injury.