Event Title

Peri-Implant Osteolysis Effects on Local and Remote Tissues

Session Number

Project ID: BIO 11

Advisor(s)

Dr. Meghan Moran; Rush University Medical Center

Discipline

Biology

Start Date

22-4-2020 8:50 AM

End Date

22-4-2020 9:05 AM

Abstract

Aseptic osteolysis is bone loss triggered by wear particle-induced inflammation and is one of the main causes for implant loosening after primary joint replacement surgery. It is known that wear particles travel from the joint to remote tissues including the liver, spleen and lymph nodes. Previously, we showed in a rat model that loss of implant fixation (a measure of implant loosening) and decreased peri-implant bone results in alterations in the gut microbiome and liver. The current study aimed to determine if a local immune response is associated with these pro-inflammatory remote system alterations. Briefly, rats underwent implant placement surgery and some rats were intra-articularly administered vehicle, lipopolysaccharide (LPS) doped polyethylene (PE) particles, or CoCr particles for 6 weeks. Intact knee joints were harvested and fixed for immunohistochemistry on select immune cell markers: CD68, (macrophages) MPO, (neutrophils) CD3, (T-cells) and CD20 (B-cells). CD68 positive cells were present in the synovium of LPS-PE and CoCr treated knees, but not vehicle-treated knees. MPO was only present in the synovium of CoCr-treated, but not in LPS-PE-treated knees. CD3 and CD20 results were inconclusive. Our results suggest that local immune reaction is critically associated with systemic inflammation we reported in the liver and gut.

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Apr 22nd, 8:50 AM Apr 22nd, 9:05 AM

Peri-Implant Osteolysis Effects on Local and Remote Tissues

Aseptic osteolysis is bone loss triggered by wear particle-induced inflammation and is one of the main causes for implant loosening after primary joint replacement surgery. It is known that wear particles travel from the joint to remote tissues including the liver, spleen and lymph nodes. Previously, we showed in a rat model that loss of implant fixation (a measure of implant loosening) and decreased peri-implant bone results in alterations in the gut microbiome and liver. The current study aimed to determine if a local immune response is associated with these pro-inflammatory remote system alterations. Briefly, rats underwent implant placement surgery and some rats were intra-articularly administered vehicle, lipopolysaccharide (LPS) doped polyethylene (PE) particles, or CoCr particles for 6 weeks. Intact knee joints were harvested and fixed for immunohistochemistry on select immune cell markers: CD68, (macrophages) MPO, (neutrophils) CD3, (T-cells) and CD20 (B-cells). CD68 positive cells were present in the synovium of LPS-PE and CoCr treated knees, but not vehicle-treated knees. MPO was only present in the synovium of CoCr-treated, but not in LPS-PE-treated knees. CD3 and CD20 results were inconclusive. Our results suggest that local immune reaction is critically associated with systemic inflammation we reported in the liver and gut.