Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target.

Biomaterial-induced tissue responses in patients with total joint replacement are associated with the generation of wear particles, which may lead to chronic inflammation and local bone destruction (periprosthetic osteolysis). Inflammatory reactions associated with wear particles are mediated by several important signaling pathways, the most important of which involves the transcription factor NF-κB. NF-κB activation is essential for macrophage recruitment and maturation, as well as the production of pro-inflammatory cytokines and chemokines such as TNF-α, IL-1β, IL-6 and MCP1.

Co-culture of adipose derived stem cells and chondrocytes with surface modifying proteins induces enhanced cartilage tissue formation.

Objectives: Current treatments for focal cartilage defects include osteochondral allograft transplants-a common treatment for large defects and revisions of previously autografted joints. Allografts with weak osseous regions are usable, since bone remodeling replaces inferior quality bone. However, poor quality chondral surfaces on grafts preclude their use, leading to grafting material shortages.