The news that gum disease may be linked to Alzheimer’s disease is being widely reported, with headlines such as “Gum disease can lead to dementia” in The Sun and “Brushing your teeth reduces risk of dementia” in the Daily Mirror.
While there are many good reasons to brush and floss your teeth regularly, the science behind these stories is not as conclusive as the headlines suggest.
The research in question only involved 20 people. It found that substances on the surface of the bacterium known to cause gum disease (lipopolysaccharides) were present in the brain tissue of 4 out of 10 recently deceased people who had Alzheimer’s. The bacteria was not found in the brain tissue of people who did not have the disease, however.
The study’s authors suggest that the presence of gum bacteria lipopolysaccharides in the brain may cause inflammation. This in turn could trigger a cascade of biological reactions that may be linked to the brain damage associated with Alzheimer’s disease.
However, studying just 20 people rarely produces conclusive results that can point to the cause of a disease.
The definitive headlines are therefore not justified. With such a small sample size, the association between lipopolysaccharides and Alzheimer’s could have been pure coincidence.
Nonetheless, this study highlights that Alzheimer’s disease, while common, is still poorly understood.
Where did the story come from?
The study was carried out by researchers from the University of Central Lancashire, the University of Florida, and the Barts and The London School of Medicine and Dentistry.
It was funded by the UK Medical Research Council, Alzheimer’s Research UK and the Alzheimer’s Association through the Brains for Dementia Research initiative, as well as by the National Institute for Health Research.
The study was published in the peer-reviewed Journal of Alzheimer’s Disease.
The thrust of the media reporting was that a clear link had been found between gum disease bacteria and Alzheimer’s. This overegged the underlying research, which only suggested a potential link and could not provide firm conclusions based on results from just 20 people.
What kind of research was this?
This was a laboratory study that aimed to establish a link between gum disease and Alzheimer’s disease. It specifically aimed to identify the gum disease bacteria that may be present in the brains of people with Alzheimer’s.
Alzheimer’s disease is the most common cause of dementia. Dementia is a group of symptoms associated with a decline in the way a person’s brain functions, affecting their memory and behaviour.
Gum disease can be caused by bacteria lodging in the gums. The bacteria provoke a long-term inflammatory response where the body launches an immune attack to remove them. But this immune response can also damage the teeth, gums and supporting tissues, and doesn’t always get rid of the bacteria.
Gum disease bacteria can enter the bloodstream during chewing, tooth brushing or dental procedures. Once in the blood, bacteria can then reach other parts of the body and provoke similar inflammation in their new site.
Past research has linked gum disease bacteria to other diseases, including diabetes, renal disease and Alzheimer’s disease. The researchers wanted to further investigate whether gum disease bacteria is linked to Alzheimer’s on the basis of this previous research.
What did the research involve?
The researchers used human brain tissue from 10 recently deceased people with diagnosed Alzheimer’s and 10 people without (the control group). The people with and without the disease were matched so the person’s age at death and time to post-mortem were similar.
Brain tissue was removed during the post-mortem and was frozen and dissected for further examination. Time to post-mortem in the group with Alzheimer’s ranged from four to 12 hours and was longer in the age-matched controls at 16 to 43 hours.
Researchers studied the dissected brain tissue for signs that traces of gum disease bacteria were present in the brain tissue of people with Alzheimer’s. They compared these samples with those taken from people who had not been diagnosed with the condition.
They tested how laboratory-grown cells that support brain nerve cells (astrocytes) absorbed and interacted with substances on the surface of gum disease bacteria (lipopolysaccharides). The researchers also looked at whether similar patterns were seen in the brain tissue from people.
What were the basic results?
The main results were:
- the laboratory-grown brain cell support cells absorbed lipopolysaccharides from the surface of the gum bacteria P. gingivalis
- the same pattern of absorption was observed in 4 out of the 10 brain tissue samples taken from people diagnosed with Alzheimer’s, but was not present in any of the 10 brain tissue samples from people without Alzheimer’s
How did the researchers interpret the results?
The observation that the brain tissue had absorbed some of the gum bacteria lipopolysaccharides was interpreted as meaning that this could potentially provoke an immune reaction in the brain.
This in turn could lead either directly or indirectly (through a cascade of other processes) to the degradation of brain cell function seen in people diagnosed with Alzheimer’s.
The researchers’ main interpretation was that, “demonstration of a known chronic oral pathogen-related virulence factor (lipopolysaccharides) reaching the human brains suggests an inflammatory role in the existing Alzheimer’s disease pathology”.
This was a hypothesis generated by the study results and was not studied directly. Further research involving a much larger sample size is needed to add weight to the hypothesis.
This laboratory study showed that gum disease bacteria lipopolysaccharides were found in the brain tissue of 4 out of 10 recently deceased people diagnosed with Alzheimer’s, and 0 out of 10 people without the condition.
This provides some, very limited, evidence to support the theory that in some people with Alzheimer’s, the bacteria responsible for gum disease may be playing a role in the disease.
However, given the limited number of people involved, the difference may have arisen by chance and may not be generalisable to most people with Alzheimer’s. For instance, if more people were recruited to the study, some gum disease bacteria might have been found in the control group, which would lessen the differences between the groups.
A similar study involving a greater number of people in both groups is needed to confirm this study’s results. This would help better establish how many people with Alzheimer’s have signs of gum disease-related bacteria in their brain tissue. This research suggests that a minority (4 out of 10) showed signs of the bacteria, so the majority may not be affected by this.
A further limitation is that the researchers were unable to study whether the presence of the gum disease bacterial lipopolysaccharides in the brain tissue actually caused an inflammatory response that contributed to Alzheimer’s disease, as speculated. This wasn’t possible using the frozen tissue samples from recently deceased individuals.
Given these limitations, this study does not show that “brushing your teeth reduces [the] risk of dementia” or that “gum disease can lead to dementia”, as the media headlines report. This is an exaggeration and simplification of the research involved.
However, the research does highlight that there is plenty more to be understood about the causes of Alzheimer’s and the potential role gum disease bacteria and inflammation plays in this process.