Chondral defects of the knee are prevalent and often encountered during arthroscopic procedures. Despite the limited healing potential of chondral defects, several treatment options have been proposed. However, microfracture, osteochondral autograft (or allograft) transfer, autologous chondrocyte implantation, and matrix-induced autologous chondrocyte implantation are all associated with their respective shortcomings. As such, the optimal treatment for chondral defects of the knee remains unclear. Recently, many authors have advocated treating chondral defects with biological therapies and scaffold-based treatments. Bone marrow aspirate concentrate, a cell-based injection, has gained particular attention because of its differentiation capacity and potential role in tissue regeneration. In addition, scaffold cartilage treatments have emerged and reached clinical practice. BioCartilage is one form of scaffold, which consists of extracellular matrix, and has been claimed to promote the regeneration of hyaline-like cartilage. This article presents our technique of arthroscopic chondral defect repair using BMAC and BioCartilage.

Macrophages are phagocytic cells that play a key role in host immune response and clearance of microbial pathogens. Porphyromonas gingivalis is an oral pathogen associated with the development of periodontitis. Escape from macrophage phagocytosis was tested by infecting THP-1-derived human macrophages and RAW 264.7 mouse macrophages with strains of P. gingivalis W83 and 33277 as well as Streptococcus gordonii DL1 and Escherichia coli OP50 at MOI = 100. CFU counts for all intracellular bacteria were determined. Then, infected macrophages were cultured in media without antibiotics to allow for escape and escaping bacteria were quantified by CFU counting. P. gingivalis W83 displayed over 60% of the bacterial escape from the total amount of intracellular CFUs, significantly higher compared to all other bacteria strains. In addition, bacterial escape and re-entry were also tested and P. gingivalis W83, once again, showed the highest numbers of CFUs able to exit and re-enter macrophages. Lastly, the function of the PG0717 gene of P. gingivalis W83 was tested on escape but found not related to this activity. Altogether, our results suggest that P. gingivalis W83 is able to significantly avoid macrophage phagocytosis. We propose this ability is likely linked to the chronic nature of periodontitis.

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