Chondrogenic differentiation of mesenchymal stem cells (MSCs) relies on inductive media of chondrogenic environment. With proper design, a cellular microenvironment mimicking chondrogenic environment might be created to induce chondrogenesis of MSCs. In this study, bone marrow mesenchymal cells (BMSCs) were encapsulated in collagen-based hydrogel, and then enclosed in diffusion-chambers which allow the body fluid to permeate and preclude the host cells to invade. Then, the chamber with the hydrogel-BMSCs composite was implanted in the back of rabbits subcutaneously. The specimens in the chamber were harvested for histological, immunohistochemical, and RT-PCR analyses after 8 weeks. The results showed that cells with the characteristic of chondrocytes were homogenously distributed and the extracellular matrix (ECM) of cartilage has been secreted, indicating the chondrogenic differentiation of BMSCs. As control, nothing was obtained with only BMSCs. Moreover, the expression of collagen type II, indicator of cartilage ECM, was less in tissues with collagen-alginate-hydrogel (CAH) than that with collagen-hydrogel (CH). The results showed that both CH and CAH may induce the chondrogenesis and the induction is materials dependent. From in vitro experiments, TGF-beta is a necessary signal molecule for chondrogenesis, and it was suggested that the material may take in vivo growth factors to trigger chondrogenesis. From the studies, the chondrogenic induction of the hydrogel may be ascribed to that the hydrogel may provide a suitable environment and aggregate the signal molecule for chondrogenesis in vivo. The results would lend valuable reference in clinical for selection of appropriate scaffold for cartilage repair.

Further increased osteogenic differentiation and mineralization of co-cultured PDLSCs under hypoxia were regulated by MEK/ERK and p38 MAPK pathways. And the ECs-mediated paracrine of PGE(2) and VEGF may facilitate the unidirectional PDLSC-EC communication and promote PDLSCs osteogenesis.

In HPDLFs, MDP and LPS activated NLRP3 inflammasome and induced IL-1β secretion. ASC plays an important role in this inflammatory response.

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