Hyaluronic Acid in Rheumatology

Abstract

Hyaluronic acid (HA), also known as hyaluronan, is an anionic glycosaminoglycan widely distributed throughout various tissues of the human body. It stands out from other glycosaminoglycans as it lacks sulfation and can attain considerable size: the average human synovial HA molecule weighs about 7 million Dalton (Da), equivalent to roughly 20,000 disaccharide monomers; although some sources report a lower range of 3–4 million Da. In recent years, HA has garnered significant attention in the field of rheumatology due to its involvement in joint lubrication, cartilage maintenance, and modulation of inflammatory and/or immune responses. This review aims to provide a comprehensive overview of HA’s involvement in rheumatology, covering its physiology, pharmacology, therapeutic applications, and potential future directions for enhancing patient outcomes. Nevertheless, the use of HA therapy in rheumatology remains controversial with conflicting evidence regarding its efficacy and safety. In conclusion, HA represents a promising therapeutic option to improve joint function and alleviate inflammation and pain.

Current Knowledge and Regulatory Framework on the Use of Hyaluronic Acid for Aesthetic Injectable Skin Rejuvenation Treatments

“…Other studies have suggested that the free radical scavenging nature of hyaluronic acid contributes to protection against UVB and UVA radiation, which supports the role of CD44 as a hyaluronic acid receptor in the epidermis [9,10]. The current popularity of hyaluronic acid as an ingredient in cosmetic products and in injectable aesthetic medical devices, alongside emerging research findings on its cellular effects, has instigated further studies [4,[20][21][22][23][24][25][26][27][28].…”

Pain Management Strategies in Osteoarthritis

“…In inflammatory contexts of osteoarthritis (OA) or rheumatoid arthritis (RA), HMWHA is dissipated by reactive oxygen species (ROS), reducing the viscous state and compromising its lubricating and shock absorbing potential [56]. This deterioration leads to impaired joint movement and pain [57]. Additionally, reductions in pain associated with intra-articular HA have been linked to a decreased development of bradykinin, prostaglandin E2, and substance P, along with the direct constraint of nociceptive afferents [58].…”