the role of
biomechanics in initiating OA cannot be foreseen in early post-traumatic knee OA patients where
the injury often starts an unfortunate cascade of events, leading to increased cartilage contact stress
and eventually full-blown symptomatic knee OA in susceptible individuals. Numerous efforts are
currently ongoing into the development of disease-modifying drugs for OA, but, so far, results have
been rather disappointing. In many OA cases and trials, we are likely past the point of no return in
the vicious cycle of abnormal contact stress and the pathological response of tissues to this stress, at
least to interrupt it by pharmacological means without correction of the biomechanical problem.
We need to focus our efforts on the early disease process and on prevention. This is where we
can do the most good in the long term to slow down or halt the growing public health concern of
knee OA.