Human Beta-Defensin-3 for the Diagnosis of Periprosthetic Joint Infection and Loosening

Abstract

In this study, the difference in expression of human beta-defensin-3 in periprosthetic tissue and cancellous bone was observed in the periprosthetic tissue and cancellous bone of patients in the periprosthetic joint infection group, the aseptic loosening group, and the spacer treatment group as well as the synovial membrane and ilium of the normal control group. Hematoxylin and eosin staining of the synovial tissue showed different levels of neutrophil infiltration in all groups except for the normal control group. Immunofluorescence staining of periprosthetic tissue and cancellous bone showed the most positive cells expressing human beta-defensin-3 and the largest mean optical density in the periprosthetic joint infection group, followed by the aseptic loosening group, the spacer treatment group, and the normal control group, with a significant difference in comparison between the periprosthetic joint infection group and the other 3 groups (P<.01). White blood cell count, erythrocyte sedimentation rate, and C-reactive protein level were highest in the periprosthetic joint infection group, whereas no difference was found between the other 3 groups. Taken together, high levels of human beta-defensin-3 protein expression were found in the periprosthetic tissue and cancellous bone of patients with periprosthetic joint infection and aseptic loosening, but there are differential expressions of human beta-defensin-3, and this may provide a new marker for the differential diagnosis of infection and loosening of the artificial joint.

Antimicrobial peptides in human synovial membrane as (low-grade) periprosthetic joint infection biomarkers

“…However, CRP still plays its role as the most common systemic marker for differentiation between PJI and aseptic loosening with a reported possible diagnostic accuracy up to 84% [ 28 ]. In accordance with this study and others, CRP blood levels can be elevated [ 14 , 21 ]. However, interference with systemic diseases such as other infections, rheumatoid arthritis or gout lowers its specificity remarkably.…”

“…This is in accordance with our previous observations with synovial fluid [14]. Liu et al stated to have more HBD-3-positive cells with immunofluorescence staining of periprosthetic tissue in PJI compared to aseptic loosening or native joints [21]. However, information about the type of PJI (acute vs. low grade) and joints is missing, various CoNS and coagulase-positive staphylococcal pathogens up to three cases with uncultured bacteria have been pooled.…”

“…Systemic biomarkers such as WBC are, in contrast to other infections, generally not useful in safely diagnosing (low-grade) PJI as shown in this study and known from others [14,21]. However, CRP still plays its role as the most common systemic marker for differentiation between PJI and aseptic loosening with a reported possible diagnostic accuracy up to 84% [28].…”

“…Regarding the promising AMPs, LL-37, β-defensin-2 (HBD)-2 and HBD-3 were not detectable in healthy human synovial membranes, but HBD-3 and LL-37 showed significant increase in pyogenic native arthritis [20]. Immunofluorescence staining of periprosthetic tissue stated to have more HBD-3-positive cells in PJI compared to aseptic loosening or native joints [21]. However, here information about the type of PJI (acute vs. low grade) and joints is missing, various coagulase-negative and coagulase-positive staphylococcal pathogens have been pooled.…”

Human beta-defensin-3 producing cells in septic implant loosening

“…Another study used immunofluorescence staining followed by a measurement of the mean optical density of the stained sections. This study reported highest hBD-3 values in septic loosening, and lower values in aseptic loosening, spacer group and normal controls [15]. In the work by Liu and co-workers, formalin-fixed and paraffin embedded tissue sections were analyzed using indirect immunofluorescence staining and fluorescence microscopy, but due to morphological restrictions of the analysis it was difficult to evaluate the cellular origin of hBD-3.…”