Abstract

Osteoarthritis (OA) is a type of degenerative joint disease where the balance between the degradation and the regeneration of articular cartilage is impaired, which leads to its progressive loss. This disease is the most common chronic musculoskeletal disease that leads to premature motor disability. Risk factors for developing OA include age, obesity, sex, past traumas and arthritis, genetic factors, diet and ethnicity. Typical OA symptoms are arthralgia, restriction of movement, cracking and secondary inflammatory lesions. In recent years, the underlying causes of this disease include chondrocyte death by apoptosis, necrosis or combinations of these types of cell death. Apoptosis, called programmed cell death, has clear morphological features, and is a highly regulated process. Apoptosis is involved in maintaining homeostasis; however, its severity is observed in many pathological conditions. Articular cartilage chondrocyte death by apoptosis disrupts the proper maintenance of cartilage structure by reducing cell density. Chondrocyte apoptosis causes mechanical damage, manifested by increased synthesis of free oxygen radicals and disturbance of the integrity of the extracellular matrix. An increasing amount of reports regarding the potential pharmacological substances that have been used as inhibitors of apoptosis have improved the quality of life in OA patients. This article presents the current state of knowledge on apoptosis and apoptotic death of chondrocytes in the course of osteoarthritis.

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