Abstract
BackgroundStroke is a major cause of disability and mortality. Poorer outcome after stroke is associated with concomitant inflammatory and infectious disease. Periodontitis is a chronic inflammatory disease of the dental supporting structures and is a prominent risk factor for many systemic disorders, including cardiovascular disease and stroke. While epidemiological studies suggest that periodontitis increases the likelihood of stroke, its impact on stroke severity is poorly understood. Here, we sought to determine the contribution of periodontitis to acute stroke pathology.MethodsWe characterized a murine ligature model of periodontitis for inflammatory responses that could potentially impact stroke outcome. We applied this model and then subjected mice to either transient or permanent middle cerebral artery occlusion. We also enhanced the periodontitis model with repeated intravenous administration of a periodontal-specific lipopolysaccharide to better mimic the clinical condition.ResultsLigature-induced periodontitis caused bone loss, bacterial growth, and increased local inflammatory cell trafficking. Systemically, periodontitis increased circulating levels of pro-inflammatory cytokines, and primed bone marrow monocytes to produce elevated tumour necrosis factor-alpha (TNFα). Despite these changes, periodontitis alone or in tandem with repeated lipopolysaccharide challenge did not alter infarct volume, blood–brain barrier breakdown, or systemic inflammation after experimental stroke.ConclusionsOur data show that despite elevated systemic inflammation in periodontitis, oral inflammatory disease does not impact acute stroke pathology in terms of severity, determined primarily by infarct volume. This indicates that, at least in this experimental paradigm, periodontitis alone does not alter acute outcome after cerebral ischemia.
Highlights
Stroke is a considerable cause of mortality and the leading cause of neurological disability, with poststroke sequelae negatively impacting long-term mental and physical health.[1]
Placement of ligatures around the second maxillary molars provides a reservoir for bacterial growth and prevents habitual cleaning, culminating in profound bone loss within an acute timeframe
Robust bone loss was observed in the PD mice predominantly at sites around the second molar (Figure 1(b))
Summary
Stroke is a considerable cause of mortality and the leading cause of neurological disability, with poststroke sequelae negatively impacting long-term mental and physical health.[1] Despite a high prevalence and growing incidence, current stroke treatments are limited to reperfusion strategies that, though effective in some patients, are not widely applicable. Lack of alternative stroke treatments is due to a number of reasons, one of which is an under-appreciation of the role that co-morbidities play in stroke etiology and prognosis.[2] It is clear that pre-existing conditions, often with inflammatory pathogeneses, are major determinants of stroke-induced damage in both humans and rodent models. Stroke is a major cause of disability and mortality. Periodontitis is a chronic inflammatory disease of the dental supporting structures and is a prominent risk factor for many systemic disorders, including cardiovascular disease and stroke. We sought to determine the contribution of periodontitis to acute stroke pathology
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