Virulence of major periodontal pathogens and lack of humoral immune protection in a rat model of periodontal disease

Oral Diseases (2010) 16 , 686–695 Objective: This study was designed to test the hypothesis that periodontal pathogens Tannerella forsythia and Porphyromonas gingivalis are synergistic in terms of virulence potential using a model of mixed‐microbial infection in rats. Materials and methods: Three groups of rats were infected orally with either T. forsythia or P. gingivalis in mono‐bacterial infections or as mixed‐microbial infections for 12 weeks and a sham‐infected group were used as a control. This study examined bacterial infection, inflammation, immunity, and alveolar bone loss changes with disease progression. Results: Tannerella forsythia and P. gingivalis genomic DNA was detected in microbial samples from infected rats by PCR indicating their colonization in the rat oral cavity. Primary infection induced significantly high IgG, IgG2b, IgG1, and IgG2a antibody levels indicating activation of mixed Th1 and Th2 immune responses. Rats infected with the mixed‐microbial consortium exhibited significantly increased palatal horizontal and interproximal alveolar bone loss. Histological examinations indicated significant hyperplasia of the gingival epithelium with moderate inflammatory infiltration and apical migration of junctional epithelium. The results observed differ compared to uninfected controls. Conclusion: Our results indicated that T. forsythia and P. gingivalis exhibit virulence, but not virulence synergy, resulting in the immuno‐inflammatory responses and lack of humoral immune protection during periodontitis in rats.     

Lung findings on high-resolution computed tomography in idiopathic ankylosing spondylitis--correlation with clinical findings, pulmonary function testing and plain radiography

Previous studies on the association of ankylosing spondylitis and abnormalities of the lung parenchyma have been based largely on plain radiography and pulmonary function testing. This study, although uncontrolled, is the first to use high-resolution computed tomography to examine the entire lung parenchyma in ankylosing spondylitis patients, and to correlate the findings with clinical assessment, plain radiography and pulmonary function testing. The study population comprised 26 patients meeting the New York criteria for idiopathic ankylosing spondylitis who attended the out-patient department at our institution. High-resolution computed tomography examination revealed abnormalities in 19 patients (70%): these included interstitial lung disease (n = 4), bronchiectasis (n = 6), emphysema (n = 4), apical fibrosis (n = 2), mycetoma (n = 1) and non-specific interstitial lung disease (n = 12). Plain radiography was abnormal in only four patients and failed to identify any patient with interstitial lung disease. All patients with interstitial lung disease on high-resolution computed tomography had respiratory symptoms and three of the four had evidence of a restrictive process on pulmonary function testing. This study raises, for the first time, the possible association between interstitial lung disease and ankylosing spondylitis, and highlights the use of high-resolution computed tomography in detecting such disease in ankylosing spondylitis patients.      

Radiation-induced red cell damage: role of reactive oxygen species

BACKGROUND: Cellular blood components are irradiated to prevent graft- versus-host disease in transfusion recipients at risk for this syndrome. Because gamma radiation can result in the production of reactive oxygen species, the role of reactive oxygen species was investigated in radiation-induced red cell damage. STUDY DESIGN AND METHODS: Whole blood from normal donors was exposed to various doses of t-butyl hydroperoxide (0-1 mM) and/or to gamma-radiation (0-50 Gy). Oxidative damage was assessed by the extent of lipid peroxidation (measured by thiobarbituric acid-reactive substances [TBARS]) and hemoglobin oxidation. Fresh blood was divided into three parts-one initially irradiated and stored, another stored with portions irradiated weekly, and a third stored without irradiation. TBARS and hemoglobin oxidation were measured weekly. RESULTS: As expected, t- butyl hydroperoxide induced TBARS formation and hemoglobin oxidation in a dose-dependent fashion. The gamma-radiation not only increased hemoglobin oxidation and TBARS formation, but also enhanced the t-butyl hydroperoxide effect on red cells. Red cell storage increased TBARS generation and hemoglobin oxidation in a time-dependent fashion. When radiation was administered either initially or after weekly storage, TBARS production and hemoglobin oxidation were increased over that measured in unirradiated paired controls. CONCLUSION: Gamma radiation at clinically used doses increases lipid peroxidation and hemoglobin oxidation in human red cells. The effect of gamma-radiation is accentuated by blood storage and induces damage independent of time of storage.