**5.2 Radiographic analysis**

302 Recent Advances in Arthroplasty

(Lee et al., 2005). ROS production may exceed physiological protection mechanisms and can

CoCr alloys have higher corrosion rate compared to titanium and titanium alloys and release toxic Co and Cr ions. Furthermore, Co ions mediate oxidative stress and could

It proves that elevated oxidative stress in the setting of aseptic loosening is a local phenomenon. Recent studies showed that increased levels of Co and Cr ions are not connected with elevation of the level of oxidative stress in the blood of patients (Antoniou et

Excessive amounts of ROS are toxic to the organism and cells have specific protection mechanisms against oxidative stress. In ROS deactivation, superoxide dismutase (SOD), catalase and gluthatione (GSH-GSSG) system play central role. In one of the most important systems, glutathione peroxidases detoxifies peroxides with GSH acting as an electron donor in the reduction reaction, producing GSSG as an end product (Townsend et al., 2003). Hence, the balance between reduced (GSH) and oxidized gluthatione (GSSG) is very important for protection against oxidative stress. A deficiency of GSH puts the cell at risk for oxidative damage. It is not surprising that an imbalance of protection mechanisms against oxidative stress is observed in wide range of pathologies including inflammatory and

Elevated oxidative stress was associated with low bone mineral density (Ozgocmen et al., 2007, Basu et al., 2001) and gene polymorphisms in antioxidant enzymes were also associated with low bone mineral density (Mlakar et al., 2010). Further research elucidated oxidative stress as a potential modulator of osteogenesis in different skeletal diseases (Liu et al., 2010). ROS have been involved in osteoporosis by causing cellular death and by inhibiting osteoblast proliferation and stimulating osteoclast differentiation (Hamel et al., 2008, Weitzmann & Pacifici, 2006). It was proven that H2O2 inhibits osteoblast proliferation time- and dose-dependently (Li et al., 2009) and that decreasing oxidative stress normalizes bone formation and bone mass in mice (Rached et al., 2010). Although extensively studied (Bai et al., 2005, Basu et al., 2001, Mody et al., 2001, Rached et al., 2010)., the mechanisms of action of ROS on bone formation are not completely understood. (Bai et al., 2005, Basu et al.,

In two studies, we investigated 58 total hip arthroplasties revised for aseptic loosening or high rate of wear of the polyethylene (40 hips) and osteolysis (12 hips) in order to clarify the

Between August 1999 and October 2002, periprosthetic tissues were consecutively obtained at revision of 40 primary THAs at the Department of Orthopedic Surgery, Medical University of Graz. Group I consisted of 8 men and 20 women, with mean age 66 years (range, 32–88 years) at the time of revision. The mean interval between primary THA and revision was 126 months (range, 11–320 months). In Group II, there were three men and nine women with mean age 69 years (range, 54–84 years). In this group, the

increase up to eight times oxidative stress in the cell (Limbach et al., 2007).

**4.1 Response to oxidative stress - oxidative stress and bone** 

thus be referred to as oxidative stress (Tsaryk, 2009).

al., 2008, Tkaczyk et al., 2010).

degenerative disorders with tissue fibrosis.

2001, Mody et al., 2001, Rached et al., 2010).

involvement of ROS in the process of aseptic loosening.

**5. Material and methods** 

**5.1 Patients** 

Prostheses fixation was graded according to the criteria of Engh et al. (Engh et al., 1989) for the cementless and Harris & Penenberg (Harris & Penenberg, 1987) for the cemented components. Osteolysis was graded according to Paprosky (Paprosky & Burnett, 2002). Annual polyethylene wear was measured as described by Livermore et al. (Livermore et al., 1990) and corrected for magnification.
