Chronic oral infection: An emerging risk factor of cerebral small vessel disease.

Chronic oral infections (gingivitis/periodontitis) have been associated with age-related diseases such as diabetes, coronary heart disease, and acute ischemic stroke. In addition, imaging surrogates of cerebrovascular ischemia beyond acute ischemic stroke (i.e., silent strokes and brain white matter hyperintensities) may also be associated with chronic oral infections. The pathology underlying lacunar strokes and brain white matter hyperintensities (WMH) relates to small vessel disease in the brain. In this review, we highlight recent progress in exploring potential associations of oral infections with cerebral small vessel disease and its surrogates (silent strokes, white matter hyperintensities) and clinical sequelae (i.e., vascular dementia). Recent evidence suggests that periodontitis aggravates cerebral small vessel disease and increases lacunar stroke risk. Moreover, periodontitis interacts with Alzheimer's disease to increase the severity of clinical dementia and to accelerate its manifestations. The results suggest that periodontitis may be an emerging risk factor of small vessel disease-associated cerebrovascular disorders and that the risk increase may be mediated by the systemic inflammation resulting from chronic oral infections. Large cohort studies employing state-of-the-art magnetic resonance techniques to identify specific cerebral pathologies as a function of time, oral health status, and systemic inflammation are needed to further substantiate the hypothesis.

[A case of Binswanger disease with numerous diffuse plaques in the neocortex].

A case of Binswanger disease with numerous diffuse plaques in the neocortex was reported. This male patient had a previous history of hypertension and myocardial infarction. From the age of 60, he developed dysarthria, bradykinesia, marche à petit pas and falling down. Neurological examination at his first admission disclosed muscular rigidity and increased jaw and deep tendon reflexes, but dementia was not found. Brain CT showed moderate brain atrophy and EEG consisted of slow wave dysrhythmia. He was diagnosed of Parkinsonism and treatment started without effects. During his second admission for the treatment of myocardial infarction, at the age of 64, delirium developed. Progressive dementia began and finally he was confined to bed. From the age of 69, spontaneous speech became almost lost. Contracture of the extremities, increased deep tendon reflexes and force grasping were noted. Brain CT showed symmetrical low attenuation in the frontal and parietal white matter with moderate dilatation of the lateral ventricles. At the age of 70, he died of general prostration about ten years after the initial symptoms. Neuropathological findings: Macroscopic findings: The brain weighed 1300 g. Atherosclerotic changes of the large arteries at the base of the brain were moderate. Coronal sections of the brain showed moderate enlargement of the lateral ventricles with multiple small lacunes in the basal ganglia. Microscopic findings: Bilateral diffuse demyelination of the white matter with sparing of the U-fibers was noted. Holzer stain revealed fibrillary gliosis in the left parietal and occipital white matter. Marked adventitial fibrosis of the deep white matter arteries and terminal stages of hyalinosis of the perforating arteries were found. Basal ganglia showed status lacunaris. Bilateral pyramidal tracts were atrophic secondly.(ABSTRACT TRUNCATED AT 250 WORDS)