Abstract
Oxytocin (OT) is involved in breastfeeding and childbirth and appears to play a role in regulating the bone matrix. OT is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and is released in response to numerous stimuli. It also appears to be produced by osteoblasts in the bone marrow, acting as a paracrine–autocrine regulator of bone formation. Osteoarthritis (OA) is a disease of the whole joint. Different tissues involved in OA express OT receptors (OTRs), such as chondrocytes and osteoblasts. This hormone, which levels are reduced in patients with OA, appears to have a stimulatory effect on chondrogenesis. OT involvement in bone biology could occur at both the osteoblast and chondrocyte levels. The relationships between metabolic syndrome, body weight, and OA are well documented, and the possible effects of OT on different parameters of metabolic syndrome, such as diabetes and body weight, are important. In addition, the effects of OT on adipokines and inflammation are also discussed, especially since recent data have shown that low-grade inflammation is also associated with OA. Furthermore, OT also appears to mediate endogenous analgesia in animal and human studies. These observations provide support for the possible interest of OT in OA and its potential therapeutic treatment.
Highlights
Osteoarthritis (OA) is the most common form of arthritis and a leading cause of impaired mobility in the elderly population [1]
The classification of OA into different phenotypes provides another lens to this complex disease and explains its different evolutionary trajectories depending on various etiological factors
Alterations in the expression of different signaling pathway-related molecules, such as the TGF-β superfamily of proteins, Wnt/β-catenin, Notch, and Indian Hedgehog (Ihh) have been shown to contribute to the development and progression of OA by primarily inducing catabolic responses [3,4,5,6,7,8,9,10,11]. Such responses include the upregulation of inflammatory mediators that lead to cartilage extracellular matrix (ECM) degradation via increased expression of matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTs) [12,13,14,15,16]
Summary
Osteoarthritis (OA) is the most common form of arthritis and a leading cause of impaired mobility in the elderly population [1]. Alterations in the expression of different signaling pathway-related molecules, such as the TGF-β superfamily of proteins, Wnt/β-catenin, Notch, and Indian Hedgehog (Ihh) have been shown to contribute to the development and progression of OA by primarily inducing catabolic responses [3,4,5,6,7,8,9,10,11] Such responses include the upregulation of inflammatory mediators that lead to cartilage extracellular matrix (ECM) degradation via increased expression of matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTs) [12,13,14,15,16]. A recent study showed that OT controls chondrocyte matrix degradation through the downregulation of metalloproteinases mRNA expression, strongly supporting the role of OT in the physiopathology of OA [28]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
