Stroke is a leading cause of death and disability globally. In Australia, there are 60,000 new cases of stroke every year and it is estimated that over 250,000 people are presently living with the effects of stroke. The global burden of stroke is estimated at 33 million people who are chronically disabled following stroke.
Adult human DPSC are ideal for treatment after stroke as they have the potential to become neurons. We have previously demonstrated in rats that DPSC injected into the brain 24 hours after a stroke can improve neurological function. We are now evaluating whether intravenous administration of DPSC can also have a positive effect on brain function. We are also investigating whether these same improvements in disability occur when DPSC are administered later, in the chronic phase of stroke.
A major aim of our group is to consider autologous therapy, in which DPSC from one’s own teeth may be used to treat one after stroke. This is a much safer option as the cells are not likely to be rejected. Given that 80% of stroke patients are over 55 years of age, it is important that the neurogenic potential (ability to become neurons) of DPSC from older teeth is investigated. We have conducted a comparison of the neurogenic potential of DPSC isolated from the teeth of patients from a range of ages, demonstrating that DPSC from older teeth are as capable of generating neurons as DPSC from younger teeth.
Following our positive pre-clinical studies, we are developing the first clinical trial of autologous DPSC therapy in chronic stroke patients: The open study of dental pulp stem cell therapy in humans, or TOOTH stroke study. This trial aims to test the safety and efficacy of autologous DPSC treatment and has the potential to improve the quality of life of patients living with stroke disability.
We have demonstrated that an intra-cerebral injection of DPSC results in an improvement in brain function in a rat model of stroke. However, we have found, as have others, that few stem cells survive long-term in the brain and the idea that improvement is due to neural cell replacement is highly unlikely. There are a number of possible mechanisms of action which may underlie how DPSC improve brain function, which we are investigating:
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