Relation between renin-angiotensin-aldosterone system and otosclerosis: a genetic association and in vitro study.

Objective/hypothesis: Angiotensin II (Ang II) may be implicated in the regulation of bone remodeling, and its activity is related to several gene polymorphisms including AGT M235T for plasmatic and tissular concentrations of angiotensinogen (AGT), ACE I/D for the angiotensin-converting enzyme activity, and AT(1)R A/C(1166) for the Ang II receptor function. The objective of this study was to investigate the implication of this hormone in otosclerosis.

Study Design: Prospective case-control study.

Glucocorticoids inhibit diastrophic dysplasia sulfate transporter activity in otosclerosis by interleukin-6.

Hypothesis/objective: Otosclerosis is a bone remodeling disorder localized to the otic capsule and associated with inflammation. In vitro, increased activity of the diastrophic dysplasia sulfate transporter (DTDST), which is implicated in bone metabolism, has been reported. Because glucocorticoids modulate the bone turnover and inhibit inflammatory processes, we investigated the effect of dexamethasone (Dex) on interleukin-6 and DTDST in otosclerosis.

Cyclooxygenase-2 regulates the degree of apoptosis by modulating bcl-2 protein in pleomorphic adenoma and mucoepidermoid carcinoma of the parotid gland.

Conclusion: These results suggest that COX-2 and bcl-2 protein were overexpressed and that apoptosis was reduced in MEC compared to PMA, and that COX-2 may regulate the degree of apoptosis by modulating bcl-2 protein in PMA and MEC.

Objective: Cyclooxygenase (COX)-2 plays a crucial role in tumorigenesis and overexpression of COX-2 in vitro accompanied by overexpression of bcl-2 protein has been shown to reduce apoptosis. The purpose of this study was to verify that COX-2 regulates the degree of apoptosis by modulating bcl-2 protein in benign and malignant parotid gland tumors.

Temporal bone density measurements using CT in otosclerosis.

Objective: To assess the bone density around the bony labyrinth in otosclerosis patients and to compare it to that of a control population.

Material And Methods: This was a prospective case-control study. Ten patients with otosclerosis (mean age 42 years; range 24-55 years) and 33 control patients with vestibular schwannoma (mean age 46 years; range 20-71 years) were included.

Acquired atrophy of the long process of the incus.

Various lesions can cause conductive hearing loss in a patient with a normal tympanic membrane. These include congenital ossicular anomaly, otosclerosis, and congenital or acquired ossicular fixation and discontinuity. We had an experience with a patient who presented with a conductive hearing loss in both ears, in which small pieces of the long process of the incus were absent and had been replaced with fibrous tissues in both ears.