Posted by: Footler PJ17 MAR 2011
Sensorineural hearing loss, which often appears in infancy and childhood, is caused by defects within the brain, in the eighth cranial nerve or in the inner ear. In most cases hearing loss is due to abnormalities in the function of hair cells in the organ of Corti in the cochlea and is thought to have a genetic cause. A hearing aid or cochlear implant may have to be fitted to help prevent cognitive difficulties and speech or language problems.
The human cochlea has only a limited ability to regenerate itself. However, Sharon Oleskevich and a team from the hearing research group at the University of New South Wales in Australia recently demonstrated that stem cells transplanted from the nasal cavity into the cochlea could replace damaged cells and enhance the survival of existing cells. This could prevent the condition from developing further.
The technique was demonstrated in mice that displayed a similar loss of hearing function following infancy and used a particular type of adult stem cell related to mesenchymal stem cells. Mesenchymal stem cells can differentiate into a variety of cell types and are able to migrate to sites of injury in animals.
They have been shown to provide factors that enhance the health and function of many other types of cells and thus contribute to the regeneration of tissues such as bone, muscle, ligaments, tendon and cartilage.
These nasal stem cells have the ability to regenerate throughout life and can be collected with relative ease. As they have a huge potential for repairing cells in other parts of the body they are considered ideal candidates for tissue engineering.
When tested a month after the cells had been injected into the cochlea, the transplanted mice had a significantly lower hearing threshold level (the lowest level to which the brain responds) than those in a control group.
As the mesenchymal cells did not integrate into the cochlea it seems likely that the beneficial effects were due to the release of factors which preserve the function of the endogenous cells.