Polyethylene wear rate and osteolysis: Critical threshold versus continuous dose-response relationship

Abstract

We studied the relationship between polyethylene wear and osteolysis in 230 subjects after cemented Charnley total hip arthroplasty in order to examine the validity of the wear rate threshold concept. Polyethylene wear measured using image analysis (EBRA) software was compared in 1 1 5 subjects with osteolysis versus 115 control subjects that were individually matched for age, sex, and follow up period. Subjects with osteolysis had almost twice the mean annual wear rate versus the controls. The incidence of osteolysis increased in a linear manner with each quintile increase in wear rate throughout the range 0.01-0.54 mm/year. The odds-ratio for osteolysis approximately doubled with each quintile increase in wear rate above the middle quintile (wear rate 0.08-0.1 1 m d year), and decreased at a similar rate with each quintile decrease in wear rate below the middle quintile. Our data suggests that the association of osteolysis with polyethylene wear rate represents a continuous dose-response relationship and does not support the concept of a discrete critical wear rate threshold above which the risk of osteolysis is disproportionately increased.

Acetabular Components in Total Hip Arthroplasty: Is There Evidence That Cementless Fixation Is Better?

“…The regression was modeled as a function of (n, N 2 n) with use of the quasibinomial family to account for the high variation in the pooled binary data among the studies. Three types of models were used: (1) a simple model that considered only the type of acetabular component fixation as a predictor and 169 16,2013 was most directly comparable with the meta-analysis results; (2) an ageadjusted model that considered the fixation type, whether the mean age was at least fifty-five years, and the interaction of fixation type with age; and (3) a full model that expanded on the age-adjusted model by adding the percentage of female patients, the preoperative diagnosis, the mean duration of follow-up, whether the study was prospective or retrospective, and the interaction of age with all of these terms. We did not adjust for the year of publication because many recent publications were actually updated reports of previous cohorts at longer follow-up, and adjusting for the year of publication would therefore not have helped to track the secular trends in practice over time.…”

“…The goal was to eliminate cement as a fixation modality, as bone cement was thought to be the principal cause of pelvic osteolysis. The latter hypothesis was refuted when long-term studies demonstrated that extensive osteolysis could also occur with cementless components and that greater wear and more extensive osteolysis were observed with cementless porous-coated cups 15,16 . It has subsequently become apparent that polyethylene wear and expansion of the effective joint space by hydrostatic fluid flow, rather than ''cement disease,'' are the major causes of pelvic osteolysis 9,17 .…”

Do Genetic Susceptibility, Toll-like Receptors, and Pathogen-associated Molecular Patterns Modulate the Effects of Wear?

“…For example, increased wear of the UHMWPE acetabular cups correlates with an increased rate of osteolysis [44,55,111]. However, those studies also showed that other factors modulate the biologic response to wear particles.…”

Expression profiling reveals alternative macrophage activation and impaired osteogenesis in periprosthetic osteolysis

“…[1][2][3] Several lines of evidence suggest that interaction of prosthetic wear particles with cells at the periprosthetic margin contributes to osteolysis and implant failure. For instance, osteolysis is correlated with higher wear rates, 4,5 abundant wear particles are associated with periprosthetic tissues recovered during revision surgery, [6][7][8] and implantation of wear debris can trigger osteolysis in animal models. [9][10][11][12][13][14] A common theme which has emerged is that a critical initiating event in wear debris action is activation of pro-inflammatory cytokine signaling within periprosthetic macrophages, which in turn leads to an imbalance in the levels of the key osteoclastogenesis regulators RANKL and OPG.…”