Osteoblast role in osteoarthritis pathogenesis

Abstract

Even if osteoarthritis pathogenesis is still poorly understood, numerous evidences suggest that osteoblasts dysregulation plays a key role in osteoarthritis pathogenesis. An abnormal expression of OPG and RANKL has been described in osteoarthritis osteoblasts, which is responsible for abnormal bone remodeling and decreased mineralization. Alterations in genes expression are involved in dysregulation of osteoblast function, bone remodeling, and mineralization, leading to osteoarthritis development. Moreover, osteoblasts produce numerous transcription factors, growth factors, and other proteic molecules which are involved in osteoarthritis pathogenesis.

Nanoscale Analysis of Randall’s Plaques by Electron Energy Loss Spectromicroscopy: Insight in Early Biomineral Formation in Human Kidney

“…43 Several studies have suggested during the last few years that an osteoblast-like mechanism is responsible for pathological calcifications found in blood vessels and cartilage, and for those related to cancer. 3,22,23 Interestingly, MVs have been described for the pathological calcifications associated with e.g. ostheoarthritis, atherosclerosis, arteriosclerosis and tumors.…”

“…Interestingly, some of these calcifications present similarities to the structures reported in 6 physiological bone 17,21 or pathological biominerals. 3,22,23 Our study provides information for understanding the physico-chemical processes involved in the formation of pathological calcifications. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60…”

Down-regulation of protease-activated receptor 2 ameliorated osteoarthritis in rats through regulation of MAPK/NF-κB signaling pathwayin vivoandin vitro

“…Advanced OA can involve the entire joint tissue such as synovium, cartilage and subchondral bone, among that, the destruction of cartilage tissues is an important process in the pathogenesis of OA, and is the main feature of pathological changes of OA [35,36]. Further, unbalanced metabolism and synthesis of cartilage tissues can lead to cartilage wear, matrix loss and chondrocyte death in the course of OA [37].…”

Cell-molecular interactions at the border of articular cartilage and subchondral bone

“…Присутність остеобластів («low osteoarthritic osteoblasts») із низькою «артрозною» імунологічною активністю (підвищена експресія RANKL на фоні пригнічення рівня OPG, PGE 2 , IL-6 на ранніх стадіях розвитку захворювання) пов'язують із посиленням резорбції кісткової тканини та формуванням зон зниженої мінеральної щільності. Наявність остеобластів із високою «артрозною» імунологічною активністю («high osteoarthritic osteoblasts») та посиленою індукцією рівня OPG, PGE 2 та IL-6 пов'язують із підвищенням кісткоутворення, тобто формуванням ділянок склерозу [36].…”