Osteoarthritis is a skeletal disease characterized by low bone mineral density (BMD) and microarchitectural deterioration, which leads to impaired skeletal strength and increased susceptibility to fracture. Osteoporosis and its associated fractures are a significant cause of morbidity and mortality among older individuals. It has been confirmed that it is highly age dependent and that it is generally slightly more common in females than in males, but it is also becoming clear that some differences in its distribution around the skeleton have taken place over time.
The disease is best defined in terms of anatomic changes in the joints. The earliest changes such as softening and fibrillation of the articular cartilage can only be recognized with certainty by inspection of the bone ends, a procedure only practicable in autopsy studies or animal experiments, but the later changes such as loss of articular cartilage, the development of marginal osteophytes, sclerosis of the subchondral bone, cysts and disorganization of the trabecular pattern of the bone ends are easily demonstrated on radiographs. The preceding definition assumes that osteoarthrosis is a single disease process, but it more likely represents the most common form of articular failure which, like cardiac or renal failure, may result fom a variety of disease processes. Obesity is an important risk factor for initiation and progression of OA. It is accepted that excess body weight may lead to cartilage degeneration by increasing the mechanical forces across weight-bearing joints. However, emerging data suggest that additional metabolic factors released mainly by white adipose tissue may also be responsible for the high prevalence of OA among obese people. Adipocyte-derived molecules ‘‘adipokines’’ have prompt much interest in OA pathophysiological research over the past decade since they play an important role in cartilage and bone homeostasis.
Osteoarthritis (OA) is closely associated with aging. With increasing OA incidence, more senior people are facing heavy financial and social burdens. Recently, it has been realized that age-related changes in other tissues besides articular cartilage may also contribute to OA development. Many factors including senescence-related secretory phenotypes, chondrocytes' low reactivity to growth factors, mitochondrial dysfunction and oxidative stress, and abnormal accumulation of advanced glycation end products (AGEs) may all play key roles in the pathogenesis of age-related OA. Lately, epigenetic regulation of gene expression was recognized for its impact on age-related OA pathogenesis.