Abstract
Osteoarthritis (OA) is a progressive degenerative disease that affects all synovial joints, causing the disability of the main locomotor diarthrodial joints. OA pathogenesis is caused by a complex interplay between a number of genetic and environmental risk factors, involved in the early onset and progression of this chronic inflammatory joint disease. Uncovering the underlying immunological and genetic mechanisms will enable an insight into OA pathophysiology and lead to novel and integrative approaches in the treatment of OA patients, together with a reduction of the disease risk, or a delay of its onset in susceptible patients.
Highlights
Osteoarthritis (OA) is the most common chronic inflammatory joint disease that leads to chronic conditions and disabilities as a result of various pathological changes, including synovial inflammation, cartilage degradation, subchondral bone alterations, and impairment of the supporting musculature
The elevated levels of IL-6 are manifested by abundant infiltration of T-cells in the synovial tissues of OA patients, enhanced production of matrix-degrading enzymes, and inhibition of the extracellular matrix (ECM) constituent synthesis [28]
The IL-6 single nucleotide polymorphisms (SNPs) rs1800795 was linked to hip and knee OA susceptibility and severity [38,39], while another IL-6 polymorphism rs1800796
Summary
Osteoarthritis (OA) is the most common chronic inflammatory joint disease that leads to chronic conditions and disabilities as a result of various pathological changes, including synovial inflammation, cartilage degradation, subchondral bone alterations, and impairment of the supporting musculature. The prevalence and incidence of OA increase with age and are higher among women, and the prevalence is significantly rising among postmenopausal women [2] This degenerative disease predominantly involves weight-bearing joints of lower extremities (the hip, knee, and ankle), exposed to constant and excessive mechanical loading. 80% of OA patients have a reduced range of joints’ motion, while 25% of patients have impaired quality of life due to limitations in activity, pain, deformity, and swelling [3] The complex interactions between a number of genetic and environmental risk factors, including developmental disorders, obesity, metabolic factors and prior joint injuries, contribute to OA initiation and progression (Figure 1) [4]. The genetic background of OA has complex origins and effects, and many studies show conflicting results
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