Particle disease: Biologic mechanisms of periprosthetic osteolysis in total hip arthroplasty

Abstract

Numerous studies provide detailed insight into the triggering and amplification mechanisms of the inflammatory response associated with prosthetic wear particles, promoting final dominance of bone resorption over bone formation in multiple bone multicellular units around an implant. In fact, inflammation is a highly regulated process tightly linked to simultaneous stimulation of tissue protective and regenerative mechanisms in order to prevent collateral damage of periprosthetic tissues. A variety of cytokines, chemokines, hormones and specific cell populations, including macrophages, dendritic and stem cells, attempt to balance tissue architecture and minimize inflammation. Based on this fact, we postulate that the local tissue homeostatic mechanisms more effectively regulate the pro-inflammatory/pro-osteolytic cells/pathways in patients with none/mild periprosthetic osteolysis (PPOL) than in patients with severe PPOL. In this line of thinking, ‘particle disease theory’ can be understood, at least partially, in terms of the failure of local tissue homeostatic mechanisms. As a result, we envision focusing current research on homeostatic mechanisms in addition to traditional efforts to elucidate details of pro-inflammatory/pro-osteolytic pathways. We believe this approach could open new avenues for research and potential therapeutic strategies.

Probiotics protect mice from CoCrMo particles-induced osteolysis

“…4 Wear debris that is generated from implant components plays a key role in aseptic loosening. 5 Wear particles are responsible for the activation of macrophages, which subsequently release various proinflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin (IL)-6 and IL-1β. These inflammatory cytokines can increase osteoclast formation and activate osteoclast activity.…”

Long-term survival of the uncemented Balgrist total hip replacement cup

“…A major factor of aseptic loosening is particle disease that is triggered and perpetuated predominantly by particle load associated with wear of bearing surfaces and corrosion [38]. In this line, there is evidence that bearing surfaces strongly predict the fate of a THA [39,40].…”

A novel nano-copper-bearing stainless steel with reduced Cu2+ release only inducing transient foreign body reaction via affecting the activity of NF-κB and Caspase 3

“…The FBR responses to orthopedic implant materials is often characterized by persistent and severe inflammatory reaction and increased tissue apoptosis, with the specific processes as follows: cytokines, chemokines, and other pro-inflammatory molecules are released at the implant interface by polymorphonuclear leukocytes, macrophages, activated fibroblasts, and other cells, thereby disturbing normal homeostatic mechanisms. 25 Even worse, if this process continues without resolution, it results in chronic inflammation and osteolysis, jeopardizing the long-term stability of the implant. 26 Therefore, we believe that an effective new implant material should have good biocompatibility with lower FBR induction.…”