Structure of the rat tracheal mucosa after chronic intermittent hypoxia or chronic hyperbaric oxygen therapy.

OBJECTIVE: This paper is aimed at identifying putative morphological changes induced in the rat's tracheal mucosa by chronic hyperbaric oxygen (HBO) treatment or chronic intermittent hypoxia (CIH). STUDY DESIGN: Tracheal samples were obtained from three groups of 11, 12 and 13 adult Wistar rats. The first group was submitted to 20 sessions of 100 min-long HBO treatment; the second group was submitted to eucapnic CIH for 35 days; and the third group was not submitted to any CIH or HBO therapy. METHODS: Four proximal tracheal rings were collected after sacrifice and neck dissection of the animals. The samples were processed for both light microscopy and morphometric analysis. Inflammatory leukocyte infiltration was evaluated by a semiquantitative method. Unpaired t test and Bernoulli distribution were applied to evaluate statistical differences in the data collected from the three groups. RESULTS: Both CIH and HBO promote an increase in the thickness of the epithelium and of the basement membrane of the rat tracheal mucosa, as well as an increment in the number of infiltrating leukocytes, when compared with results seen in the untreated group. In the HBO group there was a significant lack of seromucous glands, as opposed to the results obtained in the CIH group. CONCLUSIONS: Chronic HBO and CIH exposure causes only minor changes in the architecture of the tracheal mucosa of the rat. The respiratory tract of the rat showed a mild inflammatory response when subject to variations of pressure and oxygen content. Apparently these effects do not constitute a critical issue on prescribing HBO treatments and in the management of sleep apnea patients.

Relationship between menopause and periodontal disease: a cross-sectional study in a Portuguese population.

BACKGROUND: Menopause is associated with important systemic and oral changes. Many researchers have tried to evaluate the influence of hormonal changes associated with menopause in the periodontium, however results are contradictory. OBJECTIVE: Evaluate the possible effects of menopause on the severity of periodontal disease and tooth loss, by considering several general, oral and periodontal parameters. METHODS: 102 women with chronic periodontitis, and at least six teeth, were divided into two groups: a study group (SG) consisting of 68 menopausal women and a control group (CG) consisting of 34 premenopausal women. The participants had extensive anamnesis, made by a single senior periodontologist, which collected demographic data, medical and gynaecological history and habits. Additionally, oral and periodontal parameters including: number of teeth, plaque index, presence of calculi, probing depth, bleeding on probing, gingival recession and attachment loss were recorded. The following statistical tests were used: Chi-square, Fisher's t-test for independent samples, non-parametric Wilcoxon-Mann-Whitney, and linear multiple regression. RESULTS: The number of teeth was significantly lower in postmenopausal women (SG 10.8 ± 5.9, CG 6.8 ± 4.6), however, after adjusting for age, smoking and plaque index, the difference was no longer statistically significant (P=0.169). The attachment loss was slightly higher in the study group, although the difference is not significant (SG 4.31 ± 1.08, CG 4.05 ± 1.28). CONCLUSIONS: Menopause does not appear to significantly influence the severity of periodontal disease and tooth loss. Other factors may exert a greater influence on the progression of periodontal disease rather than menopause itself.

Histomorphometric evaluation of the small coronary arteries in rats exposed to industrial noise.

UNLABELLED: Morphological changes induced by industrial noise (IN) have been experimentally observed in several organs. Histological observations of the coronary arteries showed prominent perivascular tissue and fibrosis among IN-exposed rats. The effects on the small arteries are unknown. OBJECTIVE: To evaluate the histomorphometric changes induced by IN on rat heart small arteries. METHODS: Twenty Wistar rats exposed to IN during a maximum period of seven months and 20 age-matched controls were studied. Hearts were transversely sectioned from ventricular apex to atria and a mid-ventricular fragment was selected for analysis. The histological images were obtained with an optical microscope using 400× magnifications. A total of 634 arterial vessels (298 IN-exposed and 336 controls) were selected. The mean lumen-to-vessel wall (L/W) and mean vessel wall-to-perivascular tissue (W/P) ratios were calculated using image J software. RESULTS: There were no differences between exposed and control animals in their L/W ratios (p=0.687) and time variations in this ratio were non-significant (p=0.110). In contrast, exposed animals showed lower W/P ratios than control animals (p<0.001), with significant time variations (p=0.004). CONCLUSIONS: Industrial noise induced an increase in the perivascular tissue of rat small coronary arteries, with significant development of periarterial fibrosis.

Industrial noise and tooth wear - experimental study.

UNLABELLED: Tooth wear is a complex multifactorial process that involves the loss of hard dental tissue. Parafunctional habits have been mentioned as a self-destructive process caused by stress, which results in hyperactivity of masticatory muscles. Stress manifests itself through teeth grinding, leading to progressive teeth wear. The effects of continuous exposure to industrial noise, a "stressor" agent, cannot be ignored and its effects on the teeth must be evaluated. AIMS: The aim of this study was to ascertain the effects of industrial noise on dental wear over time, by identifying and quantifying crown area loss. MATERIAL AND METHODS: 39 Wistar rats were used. Thirty rats were divided in 3 experimental groups of 10 animals each. Animals were exposed to industrial noise, rich in LFN components, for 1, 4 and 7 months, with an average weekly exposure of 40 hours (8h/day, 5 days/week with the weekends in silence). The remaining 9 animals were kept in silence. The areas of the three main cusps of the molars were measured under light microscopy. STATISTICAL ANALYSIS USED: A two-way ANOVA model was applied at significance level of 5%. RESULTS: The average area of the molar cusps was significantly different between exposed and non-exposed animals. The most remarkable differences occurred between month 1 and 4. The total crown loss from month 1 to month 7 was 17.3% in the control group, and 46.5% in the exposed group, and the differences between these variations were significant (p<0.001). CONCLUSIONS: Our data suggest that industrial noise is an important factor in the pathogenesis of tooth wear.

Structure of the rat nasal mucosa after acute and chronic hyperbaric oxygen therapy.

OBJECTIVE: We aimed at the identification of putative morphologic changes induced in the rat nasal mucosa by acute or chronic hyperbaric oxygen (HBO2) treatment. STUDY DESIGN: Nasal samples were obtained from three groups of eight adult Wistar rats. The first group was submitted to 30 daily sessions of 100-minute-long HBO2 treatments at 2.5 ATA, the second group to a single 485-minute-long HBO2 session following the U.S. Navy Table 6 extended twice at 2.8 and 1.9 ATA, and the third group was composed of rats not submitted to any HBO2 therapy. METHODS: Samples of anterior portion of the lower nasal turbinates (concha nasalis ventralis) were collected after sacrifice and head dissection of the animals. The samples were processed for light and electron microscopy and for morphometric analysis. Inflammatory leukocyte infiltration was evaluated by a semiquantitative method. Non-parametric ANOVA was applied to evaluate statistical differences between leukocyte infiltration, and ANOVA one-way was used to evaluate the thickness of epithelium and basement membrane from samples of HBO2-treated rats and untreated rats. RESULTS: Samples of the turbinate mucosa of the rats submitted to chronic HBO2 treatment showed a significant increase in the thickness of the epithelium and a mild enhancement in the number of infiltrating leukocytes when compared with data from samples from untreated rats or from rats submitted to a single HBO2 treatment. CONCLUSIONS: Chronic HBO2 treatment causes only minor changes in the architecture of the nasal mucosa of the rat; they reflect a mild inflammatory response of the respiratory tract to the increase in pressure and in oxygen content induced by HBO2. No significant morphological changes were observed after a single HBO2 treatment.

Chronic hyperbaric oxygen therapy and the human nasal mucosa: increased thickness of epithelium basement membrane and moderate neutrophilic infiltration.

OBJECTIVE: We aimed to identify potential morphologic changes induced in the nasal mucosa by hyperbaric oxygen (HBO) treatment. STUDY DESIGN: Biopsies were obtained from two groups of 9 individuals: the first group had a diagnosis of tinnitus and was submitted to 15 sessions of 100 min-long HBO treatments, and the latter group consisted of healthy volunteers not submitted to HBO therapy. METHODS: Small biopsies of the anterior portion of the lower nasal turbinate were collected with the help of a Hartmann forceps under direct visual inspection. The samples were processed for light microscopy and morphometric analysis. Inflammatory infiltration (neutrophils and lymphocytes) was evaluated by a semiquantitative method. Unpaired t test and Bernoulli distribution were applied to evaluate statistical differences between data from the two groups of samples. RESULTS: Samples of the turbinate mucosa of the HBO-treated group showed a significant increase in the thickness of the epithelial basement membrane and a moderate enhancement in infiltrating neutrophils when compared with the samples from the control group. CONCLUSIONS: Chronic HBO treatment causes only minor changes in the architecture of the nasal mucosa that may represent the response of the respiratory tract to the increase in pressure and in oxygen content induced by this type of therapy.

Noise-induced gastric lesions: a light and scanning electron microscopy study of the alterations of the rat gastric mucosa induced by low frequency noise.

INTRODUCTION: Exposure to low frequency noise (LFN) can lead to vibroacoustic disease (VAD), recognized as a systemic disease with lesions in a broad spectrum of organs. Although gastrointestinal complaints are common among individuals exposed to noise, only few studies tried to evaluate the digestive lesions. The authors performed this study in order to investigate gastric lesions in an animal model of VAD. MATERIAL AND METHODS: Adult Wistar rats were exposed to continuous LFN. After five weeks they were sacrificed. The stomachs were studied by light microscopy and scanning electron microscopy, and compared with stomachs of animals kept in silence. RESULTS: Superficial erosions were present in the noise-exposed animals. Massive cell death of the gastric epithelium was observed, both by light and electron microscopy. DISCUSSION: The erosions, reflecting cellular degeneration and death, occurred without inflammation, similar to what has been observed in other LFN-exposed organs.