Transient Anabolic effects of Synovium in early post-traumat
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Osteoarthritis (OA) is a serious joint disease with no disease-modifying medical treatment. The aim of this study was to investigate the effects of synovial pathology due to post-traumatic OA (PTOA) on articular chondrocyte physiology.

A novel joint tissue co-culture system was developed and validated by researchers to model the biological interactions between synovium and articular chondrocytes. Whole-joint synovial tissue from a surgical rat model of PTOA vs sham and surgical-naive controls was co-cultured with adult primary articular chondrocytes (n = 4-5) in a co-culture system. The effects of PTOA synovium on chondrocyte anabolic, inflammatory, and catabolic gene expression, as well as sulfated glycosaminoglycan (sGAG) secretion and aggrecan synthesis, were investigated, and the results from early and late stages of PTOA development, were compared.

--Synovial injury by arthrotomy (sham surgery) alone decreased primary chondrocyte expression of genes including Col2a1(0.36±0.15-fold) and Acan (0.41±0.28-fold).

--Early PTOA synovium rescued the suppression of Acan, induced increased sGAG secretion (3.94±0.44 microg/mL vs surgery-naive 2.41±0.55 and sham 2.92±0.73 microg/mL controls), and upregulated Mmp3 (3.73±2.62-fold) and Prg4 (4.93±4.29-fold). These effects were lost with later stage PTOA synovium.

To summarize, early PTOA synovium causes transient anabolic responses in articular chondrocytes rather than pro-inflammatory responses that must be inhibited. These findings indicate that the PTOA synovium plays at least a partially protective role, and that the loss of these protective effects may lead to the progression of PTOA.