Osteoarthritis year in review 2018: biomarkers (biochemical markers)

Abstract

The aim of this narrative review is to summarize important findings from biochemical marker studies relevant to osteoarthritis (OA) in the context of new discoveries and clinical and scientific need. Design: We conducted a systematic search of electronic medical databases (Embase, Medline, Web of Science, Cochrane central) between 01-03-2017 and 31-03-2018. The search was restricted to human studies, English language and full text available publications while reviews were excluded. Only papers describing protein based biomarkers measured in human body fluids (blood, urine and synovial fluid (SF)) were included. Of the 992 papers, 86 were reviewed here, with inclusion primarily based on relevance to OA biochemical markers. Results: This review highlights a selection of studies based on their quality and perceived importance to the field mainly including those that 1 evaluate prognostic value of biomarkers for OA progression (i.e., biomarkers reflecting change in composition of joint tissues and biomarkers of inflammation) 2 , help in assessment of intervention efficacy, and 3 are innovative and uncover new candidate biomarkers, or use new approaches in biomarker discovery. Conclusions: Key findings and implications for possible clinical utility of biochemical markers are summarized and discussed. Given the paucity of robust biomarkers within the field, and the heterogeneity of the condition, enormous works are needed for development and validation of novel and clinically applicable biomarkers to reduce the impact of this highly prevalent and debilitating condition.

Pulsed Electromagnetic Field Versus Whole Body Vibration on Cartilage and Subchondral Trabecular Bone in Mice With Knee Osteoarthritis

“…Although loss of articular cartilage is the hallmark pathological feature in OA, disease progression involves early subchondral trabecular bone remodeling resulting in decreased trabecular bone mass and formation of osteophytes at the joint margins [McCann et al, 2017]. Changes in bone remodeling are frequently present early in the OA process [Saberi Hosnijeh et al, 2018]. Therefore, we investigated the subchondral trabecular bone microarchitecture by micro‐CT.…”

“…Several clinical studies showed an elevated level of IL‐1β in synovial fluid, synovial membrane, cartilage, and subchondral trabecular bone layer in patients with OA [Jotanovic et al, 2012; Sohn et al, 2012; Wojdasiewicz et al, 2014]. Animal studies suggested that inhibiting IL‐1β may reduce pain and slow structural progression in OA [Saberi Hosnijeh et al, 2018]. IL‐1β can increase synthesis and release of many proteolytic enzymes that decompose articular cartilage, which include MMPs, mainly stromelysin‐1 (MMP‐3) and collagenase 3 (MMP13).…”

Upregulation of long noncoding TNFSF10 contributes to osteoarthritis progression through the miR‐376‐3p/FGFR1 axis

“…For example, inflammatory cytokines (eg, tumor necrosis factor α) and degradative enzymes (eg, matrix metalloproteinases) are helpful to cartilage degradation . These results suggested that OA had influence on different structures of human joints through multiple causal pathways . Recently, some advances have been made in distinguishing subgroups of patients with distinct pathology .…”

Skeletal stem cell-mediated suppression on inflammatory osteoclastogenesis occurs via concerted action of cell adhesion molecules and osteoprotegerin

“…The process is also accompanied by the expression of osteoclastic genes, including nuclear factor of activated T cells 1 (NF‐ATc1), c‐Fos, c‐Fms, receptor activator of NF‐κB (RANK), dendrocyte expressed seven transmembrane protein (DC‐STAMP), and cathepsin K. Notably, accumulating studies indicate that OCs are involved in the initiation and progression of inflammatory bone diseases, including osteoarthritis . The increase of proinflammatory cytokines, such as interleukin‐1 β (IL‐1β), tumor necrosis factor‐α (TNF‐α), and interleukin‐17A (IL‐17A), in osteoarthritis synovial fluid (OASF) or subchondral bones lead to overactive OC formation and joint damage . Moreover, cell surface molecules in bone stromal cells typically act as pro‐osteoclastic factors .…”

“…[9][10][11] The increase of proinflammatory cytokines, such as interleukin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-17A (IL-17A), in osteoarthritis synovial fluid (OASF) or subchondral bones lead to overactive OC formation and joint damage. [12][13][14] Moreover, cell surface molecules in bone stromal cells typically act as pro-osteoclastic factors. [15][16][17][18] Furthermore, inflammatory osteoclastogenesis was reported to contribute to bone infection-induced osteoporosis.…”