Collagen Supplementation for Joint Health: The Link between Composition and Scientific Knowledge

Abstract

Osteoarthritis (OA) is the most common joint disease, generating pain, disability, and socioeconomic costs worldwide. Currently there are no approved disease-modifying drugs for OA, and safety concerns have been identified with the chronic use of symptomatic drugs. In this context, nutritional supplements and nutraceuticals have emerged as potential alternatives. Among them, collagen is being a focus of particular interest, but under the same term different types of collagens coexist with different structures, compositions, and origins, leading to different properties and potential effects. The aim of this narrative review is to generally describe the main types of collagens currently available in marketplace, focusing on those related to joint health, describing their mechanism of action, preclinical, and clinical evidence. Native and hydrolyzed collagen are the most studied collagen types for joint health. Native collagen has a specific immune-mediated mechanism that requires the recognition of its epitopes to inhibit inflammation and tissue catabolism at articular level. Hydrolyzed collagen may contain biologically active peptides that are able to reach joint tissues and exert chondroprotective effects. Although there are preclinical and clinical studies showing the safety and efficacy of food ingredients containing both types of collagens, available research suggests a clear link between collagen chemical structure and mechanism of action.

Therapeutic Effect of Enzymatic Hydrolyzed Cervi Cornu Collagen Np-2007 and Application in Osteoarthritis

“…Actually, collagen include insoluble undenatured native collagens, soluble native collagens, denatured collagens (gelatins), collagen hydrolysates, and collagen peptides. Each product is obtained through specific manufacturing processes, resulting in variations in structure, composition, and properties [25]. Collagen hydrolysates, formed through chemical or enzymatic hydrolysis, lack the triple helix structure and consist of amino acids and peptides.…”

Difficult-to-treat osteoarthritis – justification for multimodal treatment tactics

“…Появляющийся в процессе тканевой деструкции растворимый нативный коллаген (фрагменты массой до 300 kDa, несущие соответствующий эпитоп) может восприниматься макрофагами как чужеродный и вызывать активацию Т-хелперов с последующим развитием клеточной и гуморальной аутоиммунной реакции, направленной на компоненты скелетно-мышечной системы. Этот механизм входит в число причин развития воспаления, связанного со старением (Inflammaging), и играет важную роль в поддержании «низкоинтенсивного» хронического воспаления при ОА [56,57].…”

“…Этот белок как носитель потенциально важной антигенной структуры захватывается дендритными клетками лимфоидной ткани, ассоциированной с кишечником (GALT). Здесь он становится объектом «тренировки» иммунной системы (формирования иммунной толерантности), в ходе которой образуется соответствующий клон Т-регуляторных клеток, способных подавлять Т-хелперы и Т-киллеры и выделять ряд противовоспалительных субстанций, таких как ИЛ10 и трансформирующий фактор роста β. Тем самым фрагменты коллагена, образующиеся при повреждении соединительной ткани, перестают быть «мишенью» для аутоиммунной реакции и больше не поддерживают хроническое воспаление при ОА [56,58].…”

Osteoarthritis 2050 projections and its multiple mitigation challenges

“…In particular, small diverse samples, rather than large scale robust studies that can enable definitive answers to important genetic and epigenetic correlates of osteoarthritis and what should its prevention look like, fail however to often situate the condition in the context of the local overall joint environment and forces acting or failing to act optimally on the joint. 17 Other reported perspectives include genetic based therapies and explanatory factors, [18][19][20] aspects of biomaterial development to treat osteoarthritis, 21,22 such as collagen chondro protection 23,24 and various lubricants 25 but few specifically account for the origin of the disease that is clearly quite diverse, 1 and may include vulnerability to excess stress as well as abnormal stress reactions that might be remediable, but may not be addressed by focal solutions or those that are not actionable or clearly understood. 26 In addition, biological cell based therapies that do not account for the overall environment of the damaged joint are also likely to prove suboptimal at best in clinical terms, no matter how carefully these are construed in the lab or tested on non-human samples.…”