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.
Highlights
Osteoarthritis (OA) is the most common form of chronic joint disease and a major cause of pain and disability in the adult population, affecting females more than males and disabling nearly 27 million of adults in USA [1, 2]
Synovitis might be associated with reduced immunostaining for markers specific to sensory nerves, when angiogenesis and stromal hyperplasia outstrip the capacity for nerve growth [72]; we demonstrated that synovial membrane of end-stage OA patients displays an increase of vascularization compared with healthy synovium [19]
Sensory nerve fibers permeability leading distributed to plasma and frequently extravasation and edema associated with blood vessels
Summary
Osteoarthritis (OA) is the most common form of chronic joint disease and a major cause of pain and disability (typical clinical OA features) in the adult population, affecting females more than males and disabling nearly 27 million of adults in USA [1, 2]. The main target-joint is the knee with a global prevalence of 3.8% [2]. OA was ranked as the 11th highest contributor to global disability and 38th highest in disability-adjusted life year in 2010 [3]. Being a progressive condition, it leads to functional decline and loss of quality of life, with important and huge impact on healthcare and social costs [5]. OA determines a significantly high economic burden due to the increase of both direct (healthcare visits and total joint replacements) and indirect costs (productivity losses and cares) [6]. Knee OA (KO) is considered as a whole joint disease that involves cartilage and the meniscus [7], the subchondral bone [8], the synovial membrane [9], and the infrapatellar fat pad (IFP) that are stricken [10]
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