Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

Abstract

Osteoarthritis (OA) is the most common form of joint disease and a major cause of pain and disability in the adult population. Interestingly, there are patients with symptomatic OA displaying pain, while patients with asymptomatic OA that do not experience pain but show radiographic signs of joint damage. Pain is a complex experience integrating sensory, affective, and cognitive processes related to several peripheral and central nociceptive factors besides inflammation. During the last years, the role of infrapatellar fat pad (IFP), other than the synovial membrane, has been investigated as a potential source of pain in OA. Interestingly, new findings suggest that IFP and synovial membrane might act as a functional unit in OA pathogenesis and pain. The present review discuss the role of IFP and synovial membrane in the development of OA, with a particular focus on pain onset and the possible involved mediators that may play a role in OA pathology and pain mechanisms. Inflammation of IFP and synovial membrane may drive peripheral and central sensitization in KOA. Since sensitization is associated with pain severity in knee OA and may potentially contribute to the transition from acute to chronic, persistent pain in knee OA, preventing sensitization would be a potentially effective and novel means of preventing worsening of pain in knee OA.

Extraction and identification of synovial tissue-derived exosomes by different separation techniques

“…Synovial inflammation, as one of the typical pathological features of OA, plays an important role in the development of OA [2,[5][6][7]11]. However, as of now, any article has been published on how to extract and identify exosomes in synovial tissue.…”

“…However, as of now, any article has been published on how to extract and identify exosomes in synovial tissue. Importantly, more and more researchers consider the synovial membrane and intra-articular fat pad as an anatomical unit in OA pathogenesis and pain, and inflammation of synovial membrane in the knee joint may play a central role in OA and affect not only cartilage but also intra-articular fat pad [7,29,30]. Moreover, previous team studies have shown that synovial inflammation may affect articular cartilage damage through the innate immune system, aggravating the course of OA [11].…”

“…For many years, cartilage damage has been considered to be the main pathogenesis of OA. However, with the deepening of research, the important role of soft tissues around the joints such as synovial tissues and fat pad in the pathogenesis of OA has been recognized more and more [2,[5][6][7]. Recent studies have pointed out that synovial inflammation is a precursor to radiological OA [8], has a significant positive correlation with OA symptoms [9], and further aggravates cartilage damage [10].…”

Signaling of the Purinergic System in the Joint

“…The synovial tissue is a two cell layers thick membrane containing mainly two kinds of cell populations: synovial tissue macrophages (type A cells) and fibroblast-like synoviocytes (type B cells) (Falconer et al, 2018). Infiltration of lymphocytes, mild in OA and extensive in RA, leads to tissue hyperplasia contributing to inflammation, neovascularization, cartilage degradation, and pain sensitization (Mor et al, 2005;Asif Amin et al, 2017;Belluzzi et al, 2019). Activated synovial fibroblasts are involved in cartilage damage, particularly in RA subjects, via production of IL-6, IL-8, and TNF-a.…”

Dietary Saturated Fatty Acids Modulate Pain Behaviour in Trauma-Induced Osteoarthritis in Rats

“…The characteristic features of OA include degradation of the cartilage and sclerosis of subchondral bone, with increased synovial inflammation playing a major role in the degenerative bone disease [1,3,4]. Pro-inflammatory mediators may be released by the infrapatellar fat pad to stimulate proliferation of inflammatory cells in the synovial membrane, driving peripheral and central sensitisation in knee osteoarthritis [5]. The major symptom of OA is pain, which eventually leads to disability with increasing disease progression [6].…”