Bone fractures, tendon tears and insertional tendinopathies
The number of individuals aged 50 years or more at high risk of fracture worldwide in 2010 was estimated at 158 million and is set to double by 2040.
Between 5% and 15% of all fractures result in impaired healing or non-union, increasing to 40% for risk patients such as diabetes, advancing age, osteoporosis, etc.).
We look at a large market for non- or delayed union.
As mentioned before, potential targets include Achilles tendon and rotator cuff tears, humeral headfractures, as well as tibia fractures and delayed or non-unions in general. These pathologies represent some of the most frequent orthopaedic indications worldwide.
The healing time for these injuries is extensive and often results in unsatisfactory repair, in part due to the overall low regenerative capacity of tendons or immunological constraints for bone tissue.
Rotator cuff tears are the most common cause of shoulder disability Rotator cuff tendons are possibly the most commonly diseased tendons in the human body. The total prevalence of rotator cuff tears is estimated to be around 10 and 25%. A novel therapeutic approach to significantly improve treatment outcomes is urgently needed
Spinal cord injury
Physical trauma to the spinal cord results in vascular disruption that, in turn, causes blood-spinal cord barrier rupture leading to hemorrhage and ischemia, followed by rampant local cell death.
As subsequent edema and inflammation occur, neuronal and glial necrosis and apoptosis spread well beyond the initial site of impact, ultimately resolving into a cavity surrounded by glial/fibrotic scarring. The glial scar, which stabilizes the spread of secondary injury, also acts as a chronic, physical, and chemo-entrapping barrier that prevents axonal regeneration.
Early intervention after acute spinal cord injury can reduce cavitation and glial scarring, but requires a readily available pharmaceutical agent that can be administered in an allogeneic fashion.
It is now well-established that the wound healing process has substantial deleterious effects on the fidelity and reliability of implanted sensors and electrodes.
While overall results are promising, chronically implanted sensors and electrodes frequently and unpredictably experience component failure or complications arising from the wound healing response. The wound healing process begins as soon as the electrodes are inserted, inevitably disrupting the blood–brain barrier. Breaching of the blood–brain barrier leads to hemostasis and the initial stages of inflammation that are typical of those seen in all vascularized tissue.
The simultaneous treatment to suppress scar formation following electrode implant is an appropriate approach to improve the outcome of cochlea implantation.
Germany alone lists 30.000 carriers of a cochlear implant with an annual increase of 2 -3.000 patients.