Pathogenesis and Bone Resorption in Acquired Cholesteatoma: Current Knowledge and Future Prospectives

Cholesteatoma is a cystic non tumorous lesion of the temporal bone that has the ability to destroy nearby structures by its power to cause bone resorption and as a result, fatal complications prevail. We aimed to conduct a comprehensive review for pathogenesis of acquired cholesteatoma, bone resorption mechanisms, and offer a future vision of this serious disease. We have reviewed different theories for pathogenesis of acquired cholesteatoma including the most relevant and updated ones with special emphasis on the mechanisms of bone resorption through Medline/PubMed research using the keywords ‘aetiopathogenesis, bone resorption, acquired cholesteatoma, temporal bone, and cytokines.’ In order to strengthen our study, we searched the reference lists of identified reviews. Cholesteatoma is a subject of debate among otolaryngologists since it was prescribed firstly. Over many decades, several theories were postulated for aetiopathogenesis of cholesteatoma with a tendency to follow more than one theory to explain the proper nature of that disease. Until now, the mechanism of bone resorption has yet to be more clarified. In the last century, a leap has occurred in the field of biomolecular cholesteatoma research which improved our knowledge about its pathophysiology and bone destructive mechanism. However, surgery is still the only available treatment. We conclude that discovery of new therapeutic choices for cholesteatoma other than surgery by the use of anti-growth, anti-proliferative, apoptotic agents as well as medications that antagonize osteoclastogenesis should be the main concern in the future clinical and experimental research work. Also, searching for predictors of the aggressiveness of cholesteatoma can affect the timing of intervention and prevent occurrence of complications.

Serum antioxidant and pro-oxidant trace elements: relationship with oxidative stress in children with chronic renal failure on regular hemodialysis

There is a good evidence indicating that uremia, in general, is associated with enhanced oxidative stress and treatment of uremic patients with hemodialysis [HD] or peritoneal dialysis [PD] has been suggested to particularly contribute to oxidative stress and reduced antioxidant levels in those patients. Also uremic patients have abnormalities in trace elements which maybe caused by the uremia itself and/or enhanced or modified by the dialysis procedures. The aim of this study was to evaluate the oxidative stress imbalance and its relationship to the trace elements in children with chronic renal failure [CRF] on regular HD. This study was conducted on 36 children with CRF on regular HD and in 25 age and sex matched normal control children. Thiobarbituric acid [TBARS], total antioxidant [TAO], and hydrogen peroxide [H[2] O[2]] were measured by colorimetric assays. Trace elements [selenium [Se[+2]], zinc[zn[+2]], copper [Cu[+2]], manganese [Mn[+2]], lead [Pb[+2]] and cadmium [Cd[+2]] were measured by atom absorption/flame emission spectrophotometry. The results showed that the serum concentrations of TBARS, H[2]O[2], Cd and Pb were significantly higher in the studied cases [2.498 +/- 0.29, 2.967 +/- 0.414, 21.74 +/- 2.37 and 38.01 +/- 4.18 respectively] than in the controls [1.649 +/- 0.093, 0.311 +/- 0.032, 5.83 +/- 0.68 and 12.67 +/- 0.85 respectively] P<0.05 and P<0.001 for the others. The serum concentration of TAO, selenium, zinc and copper were significantly lower in the studied cases [1.379 +/- 0.017, 2.411 +/- 0.138, 91.07 +/- 2.979 and 84.89 +/- 3.145 respectively] than in the controls [2.049 +/- 0.014, 4.012 +/- 0.203, 128.7 +/- 4.924 and 128.7 +/- 3.904 respectively] [P<0.001 for each]. A significantly positive correlations were found between serum levels of cadmium and TBARS and between serum levels of selenium and TAO [r=0.359 P<0.05, and r=0.398, P<0.05 respectively]. Also a significant negative correlation was found between serum levels of zinc and serum level of TBARS [r=-0.392 P<0.05]. Our data suggest an enhanced oxidative stress and significant changes in trace elements in end stage renal disease [ESRD] patients undergoing HD. Also there is a significant relationship between the oxygen stress imbalance and the changes in the trace elements in these patients