Periodontal disease is associated with increased gut colonization of pathogenic Haemophilus parainfluenzae in patients with Crohn's disease.

Intestinal colonization of the oral bacterium Haemophilus parainfluenzae has been associated with Crohn's disease (CD) severity and progression. This study examines the role of periodontal disease (PD) as a modifier for colonization of H. parainfluenzae in patients with CD and explores the mechanisms behind H. parainfluenzae-mediated intestinal inflammation. Fifty subjects with and without CD were evaluated for the presence of PD, and their oral and fecal microbiomes were characterized. PD is associated with increased levels of H. parainfluenzae strains in subjects with CD. Oral inoculation of H. parainfluenzae elicits strain-dependent intestinal inflammation in murine models of inflammatory bowel disease, which is associated with increased intestinal interferon-γ (IFN-γ)+ CD4+ T cells and disruption of the host hypusination pathway. In summary, this study establishes a strain-specific pathogenic role of H. parainfluenzae in intestinal inflammation and highlights the potential effect of PD on intestinal colonization by pathogenic H. parainfluenzae strains in patients with CD.

Porphyromonas gingivalis indirectly elicits intestinal inflammation by altering the gut microbiota and disrupting epithelial barrier function through IL9-producing CD4+ T cells.

Recent epidemiological studies have shown that inflammatory bowel disease is associated with periodontal disease. The oral-gut microbiota axis is a potential mechanism intersecting the two diseases. Porphyromonas gingivalis is currently considered a keystone oral pathogen involved in periodontal disease pathogenesis and disease progression. Recent studies have shown that oral ingestion of P. gingivalis leads to intestinal inflammation. However, the molecular underpinnings of P. gingivalis-mediated gut inflammation have remained elusive. In this study, we show that the oral administration of P. gingivalis indeed leads to ileal inflammation and alteration in gut microbiota with significant reduction in bacterial alpha diversity despite the absence of P. gingivalis in the lower gastrointestinal tract. Utilizing an antibiotic-conditioned mouse model, cecal microbiota transfer experiments were performed to demonstrate that P. gingivalis-induced dysbiotic gut microbiota is sufficient to reproduce gut pathology. Furthermore, we observed a significant expansion in small intestinal lamina propria IL9+ CD4+ T cells, which was negatively correlated with both bacterial and fungal alpha diversity, signifying that P. gingivalis-mediated intestinal inflammation may be due to the subsequent loss of gut microbial diversity. Finally, we detected changes in gene expression related to gut epithelial barrier function, showing the potential downstream effect of intestinal IL9+ CD4+ T-cell induction. This study for the first time showed the mechanism behind P. gingivalis-mediated intestinal inflammation where P. gingivalis indirectly induces intestinal IL9+ CD4+ T cells and inflammation by altering the gut microbiota. Understanding the mechanism of P. gingivalis-mediated intestinal inflammation may lead to the development of novel therapeutic approaches to alleviate the morbidity from inflammatory bowel disease patients with periodontal disease.

Comparison of Munich Chronotype Questionnaire (MCTQ) and Morningness-Eveningness Questionnaire (MEQ) Czech version.

A chronotype is a designation for individual preference of times for different activities in humans. In chronobiological research, it can be measured in many ways, including subjective questionnaires. The most frequently used questionnaires for determining the chronotype are Morningness-Eveningness Questionnaire (MEQ) and Munich Chronotype Questionnaire (MCTQ). Many studies from around the world have already reported metric properties of the MEQ and MCTQ and their relationship in different languages. In this study, we created the Czech version of the MCTQ and examined its relationship with the Czech version of MEQ, including socio-demographic effects. We also examined the ability of the MCTQ to identify chronotypes and cutoffs for their determination. In total, 2703 people (1964 females, 739 males, 18-75 years of age) were screened by the MEQ, MCTQ and reported on age, sex and self-declared body mass index (BMI). We found a significant relationship (p < .001) between MEQ and MCTQ (MSFsc score, used as a chronotype indicator). No significant sex differences in MEQ and in MSFsc were found, but the relationship between age and MSFsc (mid-sleep on free days corrected for sleep debt on weekdays) (p < .001), MEQ (p < .001), social jet-lag (SJL, p < .001) and BMI (p < .001) were found. The SJL was related to MSFsc (p < .001), MEQ (p < .001) and BMI (p < .05). The optimal cutoff value of MSFsc to identify morning and evening chronotype was 3.35 and 4.6, respectively. The results of this study support the mutual substitutability of the Czech version of MEQ and MCTQ.

The relationship between adolescent obesity and pelvis dimensions in adulthood: a retrospective longitudinal study.

BACKGROUND: The effect of fat tissue on a developing individual is fundamentally different from the effect on an adult. Several changes caused by obesity during sexual maturation have an irreversible and severe negative effect (lower fertility, reduced final height, type 2 diabetes mellitus) even for those who have subsequently lost weight. Our study was focused on monitoring the skeletal structure substantially influenced by sex hormones-the pelvis. The adult pelvis is strongly sexually dimorphic, which is not the case for the juvenile pelvis; skeletal differences between sexes are not so prominent and start to manifest with the onset of puberty. Evidence from animal models and case studies of treatment of gender dysphoria suggests that estrogens have a stimulatory effect on the growth plates present on the pelvis, leading to morphological change. Male obesity, especially in puberty, is connected with hypogonadism, manifesting in low levels of testosterone, and high levels of estrogens. The goal of our study was to evaluate the influence of obesity during adolescence on the morphology of the adult pelvis in the context of androgen and estrogen status. SAMPLE AND METHODS: Our sample consists of 238 individuals (144 females, 94 males) observed after an 8 year follow-up (mean age during enrollment 15.2 years, follow-up 23.3 years). Anthropometry and body composition using bioimpedance analysis (BIA) were obtained. During the follow-up, saliva samples from male participants were also collected to estimate testosterone and estradiol levels using the salivary ELISA kit (Salimetrics LLC, State College, PA, USA). RESULTS: The body fat (percentage of body fat estimated using BIA) was strongly positively associated with relative pelvic breadths in adulthood (males r = 0.64; females r = 0.56, both with p < 0.001). Adulthood pelvic breadth was a highly sensitive (0.81) and specific (0.74) retrospective marker of obesity during adolescence. The complex regression model (with reduction of dimensionality) including testosterone, estradiol to testosterone ratio and body fat (adolescent and adulthood) was able to describe 54.8% variability of pelvic breadth among males. DISCUSSION: We observed that adults with a history of obesity from adolescence tend to have a wider dimension of the bony pelvis in adulthood. Based on the parameters of the adult pelvis, the history of obesity can be determined with satisfactory sensitivity and specificity (<70%). One of the explanations for this observation can be the influence of relatively elevated estrogens levels connected with excessive adiposity leading to a wider pelvis. However, the biomechanical stress connected with elevated body mass also has to be considered, as does the influence of physical activity and gait pattern on the skeletal build.

Colonic squamous cell carcinoma in ulcerative colitis: Report of a case and review of the literature.

Squamous cell carcinoma (SCC) is a rare neoplasm in the colorectum. A case of SCC rising from an area of squamous metaplasia in the rectum is presented in a patient with long-standing ulcerative colitis and perianal warts. This is the first report in the literature describing the evolution of squamous metaplasia in the colonic mucosa into invasive carcinoma over time. Related literature on colorectal SCC and squamous metaplasia, and their relationships with inflammatory bowel disease and human papilloma virus, is reviewed.