**2.3.1 Blood laboratory markers**

440 Recent Advances in Arthroplasty

prosthesis. Late infections are low-grade infections due to less virulent agents belonging to the normal skin flora (e. g. coagulase-negative staphylococci, *Propionibacterium* species, coryneform bacteria), which are mostly also attained during the operation procedure or are infections which result from hematogenous spreading from remote sites (Cui et al., 2007;

The characteristics of arthroplasty infection reflect a unique pathogenesis which is ultimately marked by two features: biofilm development and manifestation of a

Biofilm-forming bacteria share the ability to colonize foreign implant materials by initial attachment to the surface, followed by agglomeration in multi-cellular layers. During the accumulation process the bacteria excrete matrix substances into which the infectious agents themselves become embedded. Due to alterations in cellular metabolism, regulated by complex signal pathways within the biofilm, the bacteria switch from the planktonic state to a sessile condition in which proliferation rates are extremely low (Costerton et al., 1999;

Infections involving biofilm formation are both difficult to identify and to treat. On one hand, the biofilm matrix provides a substantial barrier to host defense mechanisms and to diffusion of antibiotics. On the other hand, the low proliferation levels of the sessile organisms may dramatically impair their antibiotic susceptibility, especially to bactericidal agents (Jones et al., 2001; Monzon et al., 2002; Stewart & Costerton, 2001), and their

As biofilm formation is a gradual process, this mechanism is the characteristic feature of late, low-grade infections. Implants with an established biofilm are definitely subject to removal although the causative agents are less virulent by themselves than the bacteria

The periprosthetic membrane is the histomorphologic hallmark of joint implant failure. It is a seam of connective tissue which develops at the interface between the bone and the implant in the course of the inflammatory process that leads to septic or aseptic prosthetic loosening. Interestingly, there are four morphologic types which can be linked to different etiologies of inflammation. Of these, the infectious type (type II) is particularly often associated with periprosthetic infection. It is characterized by predominant infiltration with neutrophilic polymorphonuclear leukocytes (Krenn et al., 2011; Morawietz et al., 2006). As the periprosthetic membrane must be removed if the surgical revision procedure is to be successful, it is ideal sample material for characterizing the type of inflammation by histology, thus providing valuable evidence for the underlying cause of implant loosening.

Early periprosthetic infections are mostly associated with typical clinical signs of infectious disease. However, in low-grade (late) infections the clinical symptoms and radiologic signs are often unspecific and therefore not suitable for ruling out aseptic implant failure

Donlan & Costerton, 2002; Donlan, 2005; Gristina & Costerton, 1985).

Hanssen & Osmon, 2002; Virolainen et al., 2002).

cultivation for diagnostic purposes in vitro.

which cause early arthroplasty infections.

**2.3 Inflammation parameters: Utility to detect infections** 

**2.2.2 Periprosthetic membrane** 

**2.2 Pathogenetic aspects** 

periprosthetic membrane.

**2.2.1 Biofilms** 

Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are the parameters most widely used for preoperative evaluation of patients with suspected arthroplasty infection. While sensitivity is mostly high, specificity is limited, especially in patients with systemic inflammatory diseases (e. g., rheumatoid arthritis) (Bottner et al., 2007; Della Valle et al., 2007; Fink et al., 2008; Greidanus et al., 2007; Kamme & Lindberg, 1981). Nevertheless, from the studies with reliable data the AAOS strongly recommends testing of both ESR and CRP in all patients assessed for arthroplasty infection (Della Valle et al., 2010).

Other inflammation markers (interleukin 6, procalcitonin, tumor necrosis factor ) are evaluated increasingly for periprosthetic infections, but at present there seems to be no advantage over CRP testing (Berbari et al., 2010; Bottner et al., 2007; Di Cesare et al., 2005).
