No abstract available.
Embolism, Air ; Magnetic Resonance Imaging

Objectives: Periodontitis-causing microorganisms and their virulence factors can provoke periodontal destruction in the host. This study was aimed at evaluating the distribution of periodontal disease and its relationship with 11 periodontal disease-causing bacteria in the elderly. Methods: Individuals aged 60 years or above were recruited after obtaining informed consent. The clinical attachment loss was measured at studied sites to determine the severity of periodontitis. Further, the stimulated salivary samples were collected and analyzed with real-time polymerase chain reaction to detect 11 strains of periodontitis-causing bacteria. Results: The severity of periodontal disease was proportional to the amount of periodontal diseasecausing bacteria. Porphyromonas gingivalis in the red complex increased from 6.60±5.50 in stage 1 to 5.36±5.39 in stage 2 and 7.19±5.56 in stage 3 (P=0.003). Tannerella forsythia increased from 6.54±4.60 in stage 1 to 7.44±4.56 in stage 2 and 8.49±4.70 in stage 3 (P=0.007). Conclusions The presence of complex bacterial groups and their number of strains were high in participants with severe periodontitis. Controlling periodontitis-related bacteria is important for periodontal health in the elderly.

Background: Multiple system atrophy (MSA) is a sporadic neurodegenerative disease characterized by various combinations of parkinsonism, cerebellar ataxia, autonomic dysfunction and pyramidal signs. Two clinical subtypes are recognized: MSA with predominant cerebellar ataxia (MSA-C) and MSA with predominant parkinsonism (MSA-P). The aim of this study was to compare pathological features between MSA-C and MSA-P. Methods: Two autopsy confirmed cases with MSA were included from the Pusan National University Hospital Brain Bank. Case 1 had been clinically diagnosed as MSA-C and case 2 as MSA-P. The severity of neuronal loss and gliosis as well as the glial and neuronal cytoplasmic inclusions were semiquantitatively assessed in both striatonigral and olivopontocerebellar regions. Based on the grading system, pathological phenotypes of MSA were classified as striatonigral degeneration (SND) predominant (SND type), olivopontocerebellar degeneration (OPC) predominant (OPC type), or equivalent SND and OPC pathology (SND=OPC type). Results: Both cases showed widespread and abundant α-synuclein positive glial cytoplasmic inclusions in association with neurodegenerative changes in striatonigral or olivopontocerebellar structures, leading to the primary pathological diagnosis of MSA. Primary age-related tauopathy was incidentally found but Lewy bodies were not in both cases. The pathological phenotypes of MSA were MSA-OPC type in case 1 and MSA-SND=OPC type in case 2. Conclusions Our data suggest that clinical phenotypes of MSA reflect the pathological characteristics.