Researchers from King’s College London (KCL) and the University of Helsinki, Finland, have identified a link between gum disease and young-onset stroke in patients.

The study revealed that severe gum disease, otherwise known as periodontitis, is a risk factor in cryptogenic ischaemic stroke (CIS) patients.

A stroke, which occurs when the blood supply to the brain is cut off, is currently the second-leading cause of death globally.

Responsible for over seven million new strokes each year, ischaemic strokes represent over 62% of all incident strokes, while a cryptogenic stroke, a stroke that has no identifiable cause, represents up to 40% of all ischaemic strokes that have been increasing in younger populations.

Periodontitis is a serious inflammatory gum infection caused by bacteria growing under the gumline, which damages the soft tissue around the teeth.

“With the infection sending bacteria around the bloodstream from the mouth to other parts of the body, the long-term presence of this has the potential to shape our health well beyond the mouth,” explained Dr Svetislav Zaric, clinical lecturer, periodontology, KCL Centre for Host-microbiome Interactions.

Patients who had experienced CIS took part in clinical and radiographic oral examinations as part of a case-controlled study, which demonstrated that CIS was associated with high periodontal inflammation.

In addition, the study revealed that stroke severity increased with the severity of periodontitis and showed a link between invasive dental procedures, “which may have direct causality with CIS through bacteraemia,” said Zaric.

He added that, in an effort to reduce the risk of stroke, including CIS, “dental care and regular visits to the dentist may help reduce the risk of stroke related to oral health”.

Previous studies have already highlighted that people with gum disease are more likely to experience a stroke; however, further studies are needed to “estimate the favourable effect of oral health on CIS incidence,” added Zaric.

The serious condition is responsible for approximately 11 million deaths worldwide every year.

Researchers from the Wellcome Sanger Institute, the University of Oxford and collaborators have revealed that genetic makeup could help determine the best treatment options for sepsis patients.

Findings from the study could potentially lead to the development of targeted therapies to treat the condition.

Responsible for 11 million deaths globally every year, sepsis is a serious condition in which the body responds improperly to an infection, causing the organs to work poorly.

Depending on patients’ immune responses, which can be difficult to identify based on symptoms alone, treatment for sepsis can vary.

Built on previous studies that identified different subgroups of patients with sepsis, researchers analysed data from the UK Genomic Advances in Sepsis study, involving 1,400 sepsis patients due to community-acquired pneumonia and faecal peritonitis, to investigate the impact of genetic variants that regulate expression of quantitative trait loci (eQTLs), a type of gene expression.

After finding that genetic variation in groups of patients is associated with differences in immune response during sepsis, the team identified key genetic regulators in each group, helping to describe what biological networks, cells and mechanisms are involved in each response.

In doing so, different patient responses provide additional information for developing treatments that work with the immune system, offering a personalised medicine approach to treating sepsis.

In addition, the University of Oxford is developing rapid tests that identify different subtypes of sepsis to quickly show who would benefit from targeted treatments.

Researchers plan to further investigate the immune response to find targeted treatments for each immune response or different stages of it, helping to design rapid tests, organise clinical trials and develop targeted treatments to treat sepsis more quickly.

Dr Katie Burnham, first author from the Wellcome Sanger Institute, commented: “Our study is the next step towards being able to treat sepsis based on someone’s genetics and their particular immune response, instead of their symptoms, which can vary greatly from person to person.”