2 Journal of Aging Research Ligament instability loss of proprioception Meniscus (micro)trauma Muscle atrophy/sarcopenia Synovitis/eﬀusion Cartilage damage/chondrocyte apoptosis Subchondral osteosclerosis/ bone stiﬀness Osteoporosis Figure 1: Osteoarthritis as a whole joint disease in the elderly. the surrounding soft tissue. Similarly, the penetration of synovial ﬂuid into the subchondral space after microfracture of the subchondral bone plate can induce an inﬂammatory response. The exact reason for the inﬂamed status of the OA joint remains unclear. Overuse can lead to an activation of oste- oblasts but also mast cells. Subsequently, other immune cells of the innate or adaptive immune system are attracted. Crystals, for example, in calcium pyrophosphate disease, a typical bystander in OA can activate the inﬂammasome lead- ing to interleukin-1 activation [8]. On the other hand, during aging the immune system is less capable to resolve inﬂammation in general. In other words, not only the initiation of inﬂammation, but also the lack of inﬂammation might be involved in OA, notably in the aged individual. Notwithstanding, mechanical dysfunction is still regard- ed as key player in OA pathogenesis, predominantly in weight bearing joints. This is also referred as “continuous loading theory.” Apart from the aforementioned molecular impair- ment of cartilage, also the musculature is involved in stabi- lization and therefore protection of the joint. Muscle atrophy is well recognized in OA pathogenesis [9]. In the elder- ly, muscle atrophy is highly prevalent; this can be caused by sarcopenia in general, lack of physical training, malnutrition or arthrogenic muscle inhibition as a direct consequence of OA. Finally, aging leads to a reduced regenerative capacity, for example, shown by the reduced levels of stem cells in connective tissue in the elderly. The elderly enters a catabolic state, where a presenescent cell state leads to subsequent loss of connective tissue homeostasis. In this paper we give an overview of age-related structural and functional changes occurring in the course of OA. 2. Changes in Gait Biomechanics in OA Changes in the joint biomechanics of patients suﬀering from OA have been shown in various studies. Gait analyses showed that patients with OA in the medial compartment of the knee walk with a more extended knee at heel strike [10]. Additionally, the external knee adduction moment has been identiﬁed as an important factor in medial knee OA [10–12]. The peak knee adduction moment has been shown to increase with increasing varus malalignment [12] and with increasing radiographic disease severity [10, 11]. Although the knee adduction moment has been identiﬁed as a risk factor for disease progression [11], there is also evidence that in early stages of OA, patients are able to reduce the knee adduction moment by moving the trunk laterally [10]. However, to achieve this, suﬃcient hip abduction muscle strength is needed to balance the external hip adduction moment.