Articular cartilage is an avascular, aneural and alymphatic connective tissue (which determines its very poor self-recovery ability) lining the bone ends of diarthrodial joints
[1]. Combined with excellent load-bearing capacities, this cushion of articular cartilage, especially the outer surface of cartilage, provides extremely low friction with a friction coefficient as low as 10
−3 under a wide range of physiological pressures (even up to 100 atm) to maintain daily movements during a person’s lifetime
[2][3][4]. Recently, researchers noticed that the increase of cartilage friction plays a determining role in initiating the most common degenerative joint disability disease, that is osteoarthritis (OA), which is mainly characterized by the progressive but irreversible degradation of articular cartilage
[5][6][7][8][9]. Briefly, aging-related changes or lesions usually lead to the compromisation of the outer surface of cartilage, which subsequently causes an increase of the friction coefficient. Chondrocytes, as the only cell type in cartilage, in return, up-regulate the secretion of the cartilage-degrading enzymes, such as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) to degrade the type II collagen and aggrecan (the main components of cartilage matrix), respectively. Moreover, the cartilage degradation fragments are phagocytosed cells (such as macrophage and synovial fibroblasts) to inflame the synovium, promoting the production of MMPs and ADMATS to break down cartilage and deteriorate lubrication
[10][11][12][13][14][15]. In this way, a positive feedback loop is formed due to the mutually reinforcing effect of increased friction and secretion of degradation enzymes, resulting in the progressive till total degradation of articular cartilage. Early, moderate, and late stages of OA can be classified mainly based on the degree of cartilage degradation. It is thought the breakdown of the type II collagen network initiates the point where the OA is considered irreversible
[16][17]. Is it possible to modify and prevent the disease at its early stage especially considering the role of cartilage lubrication?
Among the population over 60 years old, 9.6% of men and 18.0% of women have OA symptoms, which made OA a serious global disease defined by the Osteoarthritis Research Society International in 2016
[18]. Cell-based therapies or cartilage tissue engineering for cartilage repair or regeneration have made significant advances recently
[19][20], such as the adhesive peptide-based 3D scaffolds for cell culture
[21], however, considerable efforts are still required for the tribological properties and durability of the neocartilage before clinical translation. Currently, the main nonsurgical options for OA treatment before the end of OA include using analgesics, anti-inflammatory drugs (such as acetaminophen), inhibitors (such as cyclooxygenase), or articular injection of hyaluronan and corticosteroids
[22][23]. However, these nonsurgical options usually are highly controversial due to the nonuniversal effects when compared to that in state-of-the-art placebo-controlled
[24][25]. Therefore, it is highly important to shed light on the remarkable lubrication of cartilage and the correlation between lubrication and cartilage regeneration, with the aim to improve the understanding of OA and encourage the development of approaches to alleviating and even treating it.