Adipokine Contribution to the Pathogenesis of Osteoarthritis

Abstract

Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

Polymerized-Type I Collagen Induces a High Quality Cartilage Repair in a Rat Model of Osteoarthritis

“…Recent compelling investigations have attributed the onset of OA to age, female sex, genetic factors, adiposity, obesity, and diet and joint-level factors such as injury, malalignment, and joint biomechanics [2,4]. Latest studies suggest that patients exhibit inflammatory infiltration of synovial tissue membranes [5][6][7][8].…”

“…S100), fibronectin fragments, hyaluronic acid fragments, type II collagen cleavage epitopes, proteoglycan fragments and high-mobility group box; and e) the increased of autophagy and chondroptosis [2,4,[9][10][11].…”

CITED2 mediates the mechanical loading–induced suppression of adipokines in the infrapatellar fat pad

“…Chronic low‐grade inflammation plays a key role in the pathogenesis of osteoarthritis (OA) . Obesity, which emerging evidence implicates as a major risk factor for knee OA, induces a low‐grade systemic inflammatory state characterized by the production of adipokines and proinflammatory cytokines by adipose tissue . The infrapatellar fat pad (IPFP), also known as Hoffa's fat pad, is the main adipose structure within the knee joint, and plays a role in distributing mechanical loads within the articular joint .…”

“…[1][2][3][4] Obesity, which emerging evidence implicates as a major risk factor for knee OA, [5][6][7] induces a low-grade systemic inflammatory state characterized by the production of adipokines and proinflammatory cytokines by adipose tissue. [8][9][10] The infrapatellar fat pad (IPFP), also known as Hoffa's fat pad, is the main adipose structure within the knee joint, 11 and plays a role in distributing mechanical loads within the articular joint. 12 The IPFP has been suggested to be involved in OA pathogenesis [13][14][15][16][17][18] by secreting proinflammatory cytokines (e.g., TNF-␣ and IL-6 14,17,[19][20][21] ) and adipokines (adipose tissue-derived cytokines), 8,22,23 contributing to intra-articular inflammation and pain.…”

“…[8][9][10] The infrapatellar fat pad (IPFP), also known as Hoffa's fat pad, is the main adipose structure within the knee joint, 11 and plays a role in distributing mechanical loads within the articular joint. 12 The IPFP has been suggested to be involved in OA pathogenesis [13][14][15][16][17][18] by secreting proinflammatory cytokines (e.g., TNF-␣ and IL-6 14,17,[19][20][21] ) and adipokines (adipose tissue-derived cytokines), 8,22,23 contributing to intra-articular inflammation and pain. 8 Studies suggest that adipokines, including adipsin, adiponectin, and leptin, play specific roles in the development of OA.…”