In vitro Implant Debris-Induced Inflammatory Responses Between Monocytes and Osteoclasts
thesisposted on 21.02.2013 by Jessica Yadav
In order to distinguish essays and pre-prints from academic theses, we have a separate category. These are often much longer text based documents than a paper.
Aseptic failure of joint replacement is attributed to implant debris induced osteolysis, or local resorption of bone surrounding the implant. Monocytes and osteoclasts, when in presence of implant debris (metal particles and ions), release pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6, which in turn facilitate osteolysis. The degree to which metal implant debris affects monocytes/macrophages versus osteoclasts directly is unknown. We investigated monocyte versus osteoclast responses to metal implant debris (particles and ions) to determine the relative inflammatory and osteoclastogenic effects of metal debris on each cell type (e.g. released IL-1β and TNF-α). Our results show that osteoclasts have a highly reduced inflammatory response, than monocytes, in terms of the amount of cytokine released, indicating that as monocytes differentiate into osteoclasts, they lose some monocyte characteristics and functionalities and become more role-specific. Specifically for monocytes, over 10,000 pg/ml of IL-1β is secreted and less than 5000 pg/ml of TNF-α is produced. For osteoclasts, the number reduce to less than 150 pg/ml for IL-1β and less than 600 pg/ml for osteoclasts. Osteoclast precursors challenged by supernatants from activated monocytes and osteoclasts challenged directly exhibit relatively the same amount of TRAP positivity, but greater than negative controls.