Podium Presentation Osteoarthritis

18.2.8 - Modulation of the inflammatory osteoarthritis environment in presence of MSCs from bone marrow and adipose tissue: an in vitro study

Presentation Number
18.2.8
Presentation Topic
Osteoarthritis
Lecture Time
15:18 - 15:27
Session Type
Free Papers
Corresponding Author
  • F. Veronesi (Bologna, IT)
Authors
  • F. Veronesi (Bologna, IT)
  • S. Pagani (Bologna, IT)
  • G. Filardo (Bologna, IT)
  • M. Fini (Bologna, IT)
Disclosure
No Significant Commercial Relationship

Abstract

Purpose

Osteoarthritis (OA) is a degenerative and inflammatory joint disease, due to the high levels of pro-inflammatory cytokines and catabolic enzymes. The scarce regenerative capacity of cartilage and the limited outcome of the therapies are increasing the interest in mesenchymal stem cells (MSCs). Furthermore, in literature it is yet observed that platelet-rich plasma (PRP), thanks to its regenerative and anti-inflammatory abilities, is a recommended treatment for OA, as well as being a low-cost biological and not invasive remedy. This study investigates the chondrogenic ability of MSCs from adipose tissue (ADSCs) and bone marrow (BMSCs) in an OA-like microenvironment; evaluates the anti-inflammatory and regenerative roles of blood autologous protein solution (APS), enriched of anti-inflammatory cytokines and growth factors.

Methods and Materials

BMSC and ADSC micromasses, stimulated with interleukin (IL)1β and tumor necrosis factor (TNF)α or synovial fluid from OA patients, were cultured for 4 weeks in presence or absence of APS conditioned medium (CM). Their differentiation toward chondrogenic lineage was evaluated with histology, immunohistochemistry, histomorphometry and molecular biology approaches.

Results

ADSCs and BMSCs were well organized in compact micromasses, with a more abundant matrix in ADSCs and cellularity in BMSCs (Figure 1). Gene expression of SOX9 and ACAN decreased in presence of inflammatory factors and did not recover with CM (in ADSC and BMSC). Conversely, the addition of CM reduced Metalloproteinases (MMP13), collagen (COL1a1), COLL X and COLL I in ADSCs and BMSCs. COL2a1 and MMP13 were respectively more and less expressed in ADSCs than in BMSCs in all culture conditions. Moreover, CM appeared to have more effect in cells treated with IL1β and TNFα than those treated with synovial fluid.

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Conclusion

From these preliminary results it seems that both ADSCs and BMSCs might contribute to cartilage regeneration in a joint affected by OA and that APS might be useful in this regard.

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