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Otic Capsule (otic + capsule)
Selected AbstractsOsteoprotegerin in the Inner Ear May Inhibit Bone Remodeling in the Otic Capsule,THE LARYNGOSCOPE, Issue 1 2005Andreas F. Zehnder MD Abstract Objectives: To elucidate factors that may be responsible for the inhibition of remodeling of bone within the otic capsule. Methods: Expression of osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (RANK), and RANK ligand (RANKL) were assayed in samples of bone obtained from the otic capsule, calvarium, and femur, and from the soft tissue within the cochlea using semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in mice. Immunostaining was used for histologic localization of the gene products. An enzyme-linked immunosorbent assay (ELISA) was used to quantify the amount of OPG within perilymph, serum, and cerebrospinal fluid. The micro-anatomy of the interface between the otic capsule and the fluid spaces of the cochlea was investigated by brightfield and phase-contrast microscopy and by three-dimensional reconstruction in the mouse and human. Results: OPG, a powerful inhibitor of bone remodeling, was expressed at extremely high levels within the soft tissue of the cochlea and was present in the perilymph at very high concentrations. The OPG produced within the inner ear may diffuse into the surrounding otic capsule, where it may be responsible for inhibition of bone turnover. Our anatomic studies revealed an extensive system of interconnected canaliculi within the otic capsule that had direct openings into the fluid spaces of the inner ear, thus providing a possible anatomic route for the diffusion of OPG from the inner ear into the surrounding bone. Conclusion: OPG, a potent inhibitor of osteoclast formation and function, is expressed at high levels within the inner ear and is secreted into the perilymph and the surrounding bone and may serve to inhibit active bone remodeling within the otic capsule, especially immediately adjacent to the cochlea. By this means, the cochlear soft tissue may control the nature of the surrounding petrous bone. [source] Prenatal growth and development of the modern human labyrinthJOURNAL OF ANATOMY, Issue 2 2004Nathan Jeffery Abstract The modern human bony labyrinth is morphologically distinct from that of all other primates, showing derived features linked with vestibular function and the overall shape of the cranial base. However, little is known of how this unique morphology emerges prenatally. This study examines in detail the developing fetal human labyrinth, both to document this basic aspect of cranial biology, and more specifically, to gain insight into the ontogenetic basis of its phylogenetically derived morphology. Forty-one post-mortem human fetuses, ranging from 9 to 29 weeks gestation, were investigated with high-resolution magnetic resonance imaging. Quantitative analyses of the labyrinthine morphology revealed a number of interesting age-related trends. In addition, our findings show that: (1) the prenatal labyrinth attains an adult equivalent size between 17 and 19 weeks gestation; (2) within the period investigated, shape changes to all or most of the labyrinth cease after the 17,19-week size maturation point or after the otic capsule ossifies; (3) fetal cochlea development correlates with the surrounding petrosal morphology, but not with the midline basicranium; (4) gestational age-related rotations of the ampullae and cochlea relative to the lateral canal, and posterior canal torsion are similar to documented phylogenetic trends whereas other trends remain distinct. Findings are discussed in terms of the ontogenetic processes and mechanisms that most likely led, in part, to the emergence of the phylogenetically derived adult modern human labyrinth. [source] The etiology of otosclerosis: A combination of genes and environment,THE LARYNGOSCOPE, Issue 6 2010Isabelle Schrauwen MSc Abstract Otosclerosis is a common form of hearing loss characterized by abnormal bone remodeling in the otic capsule. It is a complex genetic disease, caused by a combination of genetic and environmental factors. During the past decade, several attempts have been made to identify factors for otosclerosis. This review provides an overview of the current understanding of the etiology of otosclerosis and describes the genetic and environmental factors that have been implicated in the disease. Environmental factors include fluoride and viral factors, particularly measles. Genetic association studies for otosclerosis have reported several associations of genetic variants that influence the risk of disease, mainly involving bone remodeling pathways, although their individual risk contributions are small. Rare monogenic forms of otosclerosis also exist, which are caused by a mutation in a single gene leading to a clear familial segregation of the disease. Linkage analysis of large otosclerosis families has led to the identification of seven loci, and recently evidence was found that T cell receptor beta is a gene responsible for familial otosclerosis, suggesting an underlying immunological pathway. However, this might also represent an autoimmune process, a hypothesis that is supported by other data as well. In conclusion, a variety of pathways have been identified to be involved in the development of otosclerosis, showing that distinct mechanisms involving both genetic and environmental risk factors can influence and contribute to a similar disease outcome. [source] Glucocorticoids Inhibit Diastrophic Dysplasia Sulfate Transporter Activity in Otosclerosis by Interleukin-6THE LARYNGOSCOPE, Issue 9 2006Yutaka Imauchi MD Abstract 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 sulf/te 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. Study Design: The authors conducted a prospective, case,control study. Materials and Methods: Primary cell cultures were obtained from stapes and external auditory canals in otosclerosis (n = 21) and control patients (n = 18). Assays with [3H]Dex evaluated specific binding sites in otosclerotic and control stapes. The effects of Dex (10,9 to 10,6 M) and RU486 (10,7 M), a glucocorticoid antagonist, were studied on DTDST activity by sulfate uptake. IL-6 secretion was measured in culture media before and after Dex (10,7 M, 24 hours). The effect of IL-6 (10,7 M, 24 hours) was assessed on DTDST activity in control stapes. Results: The number of specific Dex-binding sites was similar in all stapedial cultures. Dex inhibited DTDST activity (19.4 ± 1.02 vs. 29.4 ± 3.94 pmol/,g prot/5 minutes) only in otosclerotic stapes. This effect was dose-dependent, antagonized by RU 486 and only observed 24 hours after Dex exposure. Interleukin (IL)-6 stimulated DTDST activity in normal stapes, whereas Dex inhibited IL-6 production only in otosclerotic stapes. Conclusion: Dex inhibits the DTDST activity, at least in part, through a reduction of IL-6 secretion only in otosclerotic cells. This effect is mediated through the glucocorticoid receptors and may lead to the reduction of bone turnover. [source] Quantification of Angiogenesis in Otosclerosis,THE LARYNGOSCOPE, Issue 5 2005Robert W. Jyung MD Abstract Objectives/Hypothesis: The determinants of clinical versus histologic otosclerosis are unknown, but angiogenesis is associated with active disease. We hypothesized that quantification of angiogenesis in otosclerotic human temporal bones could reveal significant differences between clinical and histologic cases. Study Design: We reviewed all otosclerosis specimens meeting criteria from the temporal bone collection of the Massachusetts Eye and Ear Infirmary and 10 normal controls. Methods: Digital images were taken at predilection sites, followed by computer-assisted analysis. Canalicular area (CA), the aggregate of vascular spaces within bone, microvessel density (MVD), area, and depth were the main measures. Evidence of a direct connection between local vessels and the vasculature of the otosclerotic focus was also recorded for each specimen. Results: The average area (mm2) and depth (number of sections containing otosclerosis) of clinical lesions was significantly greater than histologic lesions. Total microvessel counts were significantly greater in clinical versus histologic lesions, and both clinical and histologic lesions contained significantly greater numbers of microvessels than the normal otic capsule. CA was also significantly higher in clinical lesions. MVD was slightly but not significantly higher in clinical lesions. Importantly, a direct connection between named vessels and the otosclerotic vasculature was significantly more frequent in clinical lesions. Conclusions: Computer-assisted quantification revealed significantly greater measures of angiogenesis in clinical versus histologic otosclerosis. Direct connection to adjacent vessels may support angiogenesis in this disease. Sustained angiogenesis may be an important determinant of clinical otosclerosis. [source] Osteoprotegerin in the Inner Ear May Inhibit Bone Remodeling in the Otic Capsule,THE LARYNGOSCOPE, Issue 1 2005Andreas F. Zehnder MD Abstract Objectives: To elucidate factors that may be responsible for the inhibition of remodeling of bone within the otic capsule. Methods: Expression of osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (RANK), and RANK ligand (RANKL) were assayed in samples of bone obtained from the otic capsule, calvarium, and femur, and from the soft tissue within the cochlea using semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in mice. Immunostaining was used for histologic localization of the gene products. An enzyme-linked immunosorbent assay (ELISA) was used to quantify the amount of OPG within perilymph, serum, and cerebrospinal fluid. The micro-anatomy of the interface between the otic capsule and the fluid spaces of the cochlea was investigated by brightfield and phase-contrast microscopy and by three-dimensional reconstruction in the mouse and human. Results: OPG, a powerful inhibitor of bone remodeling, was expressed at extremely high levels within the soft tissue of the cochlea and was present in the perilymph at very high concentrations. The OPG produced within the inner ear may diffuse into the surrounding otic capsule, where it may be responsible for inhibition of bone turnover. Our anatomic studies revealed an extensive system of interconnected canaliculi within the otic capsule that had direct openings into the fluid spaces of the inner ear, thus providing a possible anatomic route for the diffusion of OPG from the inner ear into the surrounding bone. Conclusion: OPG, a potent inhibitor of osteoclast formation and function, is expressed at high levels within the inner ear and is secreted into the perilymph and the surrounding bone and may serve to inhibit active bone remodeling within the otic capsule, especially immediately adjacent to the cochlea. By this means, the cochlear soft tissue may control the nature of the surrounding petrous bone. [source] Genetic variants in RELN are associated with otosclerosis in a non-European population from TunisiaANNALS OF HUMAN GENETICS, Issue 5 2010Ayda Khalfallah Summary Otosclerosis is a common form of conductive hearing loss, caused by an abnormal bone remodelling in the otic capsule. Both environmental and genetic factors have been implicated in the etiology of this disease. A recent genome wide association study identified two regions associated with otosclerosis, one on chr7q22.1, located in the RELN gene, and one on chr11q13.1. A second study in four European populations has replicated the association of the RELN gene with otosclerosis. To investigate the association of these loci with otosclerosis in a non-European population, we tested 11 SNPs from the two regions in 149 unrelated Tunisian patients and 152 controls. Four SNPs were significantly associated with otosclerosis. Three SNPs are located in the RELN region and the last one is located in the region on chromosome 11. We also observed a significant interaction with gender for rs3914132. This suggests an influence of sex on the association of RELN with otosclerosis. A meta-analysis showed that the disease-associated alleles in the Tunisian sample are the same as in all previously reported associations. Our study provides additional evidence implicating RELN in the development of otosclerosis. Additional functional studies should determine the role of RELN in the physiopathology of this disease. [source] A new articulated hybodontoid from Late Permian of northwestern ChinaACTA ZOOLOGICA, Issue 2009N.-Z. Wang Abstract A new genus and species of hybodontoid elasmobranchs, Gansuselache tungshengi, is described on the basis of an articulated skeleton from the Fangshankou Formation (Late Permian) of the Mazongshan Mountain of Gansu Province, northwestern China. All dermal skeletons including dorsal fin-spines, cephalic spines, dermal denticles and one tooth are well preserved in their natural position. It is a shark of about 490 mm total length with a fusiform body. The braincase has large, downturned postorbital processes and otic capsules, no postorbital articulation, long palatoquadrate and large triangular Meckel's cartilage. It bears two dorsal fins and two pairs of heteromorphic cephalic spines. The tooth is of low-crowned, multicuspid type; the elongate tooth crown has stout crown shoulder and well-developed, rounded labial peg; the cusp and cusplets are moderately tumid, and have a few strong and curved folds; the tooth root is higher on the labial face than the lingual face. The dermal denticle is placoid scale-like, with its crown surface ornamented with some parallel ridges. Gansuselache, the first articulated hybodontiform from Asia, also represents the first complete hybodontiform from the Permian. [source] | ||||||||||