Naslov
The role of Angiotensin II and 4-Hydroxynonenal on Osteoblast like Cells and Stapes Metabolism

Autori
Rudić, Milan

Vrsta, podvrsta i kategorija rada
Ocjenski radovi, doktorska disertacija

Fakultet
Medicinski fakultet i ECOLE DOCTORALE: PHYSIOLOGIE ET PHYSIOPATHOLOGIE

Mjesto
Zagreb, Pariz

Datum
22.06

Godina
2011

Stranica
192

Mentor
Žarković, Neven ; Bozorg Grayeli, Alexis

Ključne riječi
angiotensin II; 4-hydroxynonenal; osteoblast like cells; oxidative stress

Sažetak
Active phase of otosclerosis is accompanied by signs of inflammation. There are numerous multi nucleated osteoclasts, osteocyte-like cells and proliferating endothelial cells in the pseudo- vascular spaces of the active otosclerotic foci. Mostly, CD8 positive, cytotoxic T lymphocytes and activated osteoclasts with possible cytokine secretion are found in the peripheral zone of active foci. Previous studies have suggested different types of proinflammatory and regulatory cytokines playing a role in the etiopathogenesis of otosclerosis (Sziklai et al., 2009, Karosi et al., 2006). The origin or the triggering factor of this inflammation is not elucidated. Participation of microorganisms such as bacteria, virus, fungi or even mastication trauma has been advocated (Schrauwen et al., 2010 ; Niedermayer et al., 1996). Another issue in the pathophysiology of otosclerosis is the persistent inflammation during several years. In a pathophysiological model proposed for diabetes mellitus type 1, a coxsackie virus is the triggering factor in the destruction of the islets of Langerhans. The inflammation is maintained by an auto-immune reaction which appears secondarily and completes the endocrine tissue destruction (Tirabassi et al., 2010). This model is a possible explanation for the chronic inflammation in otosclerosis considering several reports on autoimmune activity in patients with otosclerosis (Schrauwen et al., 2010). However, autoimmunity is not constantly observed in otosclerosis (Karosi et al., 2010). In order to elucidate other factors which may participate in the maintenance of the inflammation, Ang II was investigated (Imauchi et al. 2008). By inducing or promoting inflammation, Ang II can potentially induce oxidative stress in otosclerosis. Potentially, this stress has dramatic effects on bone remodeling. Reactive oxygen species (ROS) diffusion into the inner ear might also explain inner ear lesions during otosclerosis.

Izvorni jezik
Engleski

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