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Biomedical subjects

G C Sornberger

Publications and source records attributed to G C Sornberger.

15 recordsLinked to original sources

An approach to the definition of periodontal disease syndromes by cluster analysis.

Clinical syndromes of 22 untreated patients with advanced destructive periodontal disease were analyzed using cluster analysis. Clinical characteristics coded for each patient included age, sex, measures of gingival inflammation, plaque, suppuration, pocket depth, attachment level, extent and pattern of bone loss, rate of change in pocket depth, and correlation coefficients between certain clinical measurements. Microbiologic features included darkfield enumeration of 10 morphologically distinct forms of organisms which were removed from the three sites showing the most advanced destruction in each patient, as well as viable counts of specific microbial groups from the same teeth using elective and selective media. Serum antibody levels were determined by the ELISA technique to 13 species of subgingival microorganisms. The Gower coefficient was used to estimate similarity between patients and clusters were formed using an average unweighted linkage sort. Three distinct patient clusters were observed with greater than 70% average intra-cluster similarity. One subject did not fall into any of the patient clusters. The features which defined and differentiated the clusters were found to include age of subject, extent and patterns of bone loss, percent of sites showing change in pocket depth and attachment level, percent of small motile rods, intermediate spirochetes and fusiforms and serum IgG levels against Bacteroides gingivalis, Selenomonas sputigena and a Wolinella strain.

Adolescent↗

Patterns of progression and regression of advanced destructive periodontal disease.

Attachment level at two sites on each tooth in 22 untreated subjects with existing periodontal pockets was measured every month for 1 year. Regression analysis was then applied to the data from each periodontal site to determine if statistically significant trends in attachment level change could be detected. 82.8% of the sites monitored did not significantly change during the year. 5.7% of the sites became significantly deeper and 11.5% of the sites became significantly shallower (P less than 0.01) during the period. Among those sites in which pocket depth increased, approximately half exhibited a cyclic deepening followed by spontaneous recovery to their original depth. In 15 of the subjects, sites were found which became significantly deeper while other sites within the same subject became significantly shallower. In six subjects, who might be considered to have an arrested form of periodontal disease, virtually no sites became deeper during the monitoring period whereas 11-36% of their sites became significantly shallower. The results of this investigation suggest that a dynamic condition of disease exacerbation and remission as well as periods of inactivity may be characteristic of periodontal disease.

Adolescent↗

Marijuana, tetrahydrocannabinol, and pulmonary antibacterial defenses.

Although marijuana is now consumed extensively, little is known of its biologic effects on the lung. To study this problem, the intrapulmonary inactivation of an aerosolized challenge of Staphylococcus aureus was quantified in rats exposed to graded amounts of fresh marijuana smoke. Controls inactivated 85.1 percent +/- 0.3 percent of the bacteria six hours after inoculation. Following an in vivo accumulative exposure to smoke from progressively increasing numbers of marijuana cigarettes for periods of ten minutes each hour for five consecutive hours, intrapulmonary bacterial inactivation was impaired in a dose-dependent manner. Evaluation of the effects of parenterally administered delta-9-tetrahydrocannabinol (THC) or of exposure to fresh smoke from THC-extracted marijuana placebo cigarettes indicated that the cytotoxin in marijuana was not related to the primary psychomimetic component. Thus, marijuana smoke is toxic to the lung and impairs the pulmonary antibacterial defense system in a dose-dependent manner.

Animals↗

A morphometric analysis of the male and female tracheal epithelium after experimental exposure to marijuana smoke.

Male and female rats were exposed to marijuana smoke that was generated from nonfiltered marijuana research cigarettes three times each day for 31 +/- 1 consecutive days. Morphometric analyses of the tracheal epithelium were made for the volume density of secretory cells in the trachal epithelium, volume density of glycoprotein in the secretory cells, and number of secretory cells per unit length of the tracheal epithelium. Glycol methacrylate sections of the trachea stained with a combined Alcian Blue and periodic acid-Schiff technique and hematoxylin permitted analysis of not only stained secretory cells and their glycoprotein composition but also unstained secretory cells, providing a complete profile of the total secretory cell population in the tracheal epithelium. Exposure to marijuana smoke resulted in an increase in the volume density of glycoprotein in the secretory cells in association with an increase in the number of stained secretory cells per unit length of epithelium and a shift in the secretory cell mucin production from periodic acid-Schiff-positive to the production of mixtures of periodic acid-Schiff-positive and Alcian Blue-positive glycoproteins. Exposure to marijuana smoke, however, decreased the volume density of total secretory cells and the number of unstained secretory cells. It appears that the increased number of stained secretory cells in marijuana smoke-exposed rats was the result of a conversion from unstained to stained secretory cells. Female rats demonstrated larger relative increases than male rats in the total glycoprotein in secretory cells, in the number of stained secretory cells, and a larger shift in glycoprotein composition after exposure to smoke.

Animals↗

Morphometric analyses of tracheal gland secretion and hypertrophy in male and female rats after experimental exposure to tobacco smoke.

Quantitative morphologic analyses were performed by stereologic methods on the tracheal glands of male and female rats after exposure to tobacco smoke for 30 consecutive days. The female rats were evaluated at 2 stages of their estrous cycle. The upper segment of trachea from each animal was embedded in glycol methacrylate, sectioned, and stained with a combined Alcian blue and periodic acid-Schiff stain for glycoproteins. Exposure to tobacco smoke caused an increase in the relative proportion of gland cells in each sex when expressed in reference to the total tissue within the cartilage ring, and an increase in mucins in the gland by 50% in both sexes. Although the relative proportions of gland cells and lumina were equivalent between the sexes, male rats had a larger quantity of mucin. The volume proportion in the glands of Alcian blue-positive mucin was 80 to 84% greater in males, and periodic acid-Schiff-positive mucin was 18 to 19 per cent greater in males than in females, both in control animals and those exposed to tobacco smoke. This study demonstrated that sexual differences were present in the mucin composition of the tracheal glands of normal male and female rats, that the female glycoproteins varied during the estrous cycle, and that these differences were retained after exposure to tobacco smoke.

Animals↗

Effects of experimental marijuana and tobacco smoke inhalation on alveolar macrophages. A comparative stereologic study.

Male rats were exposed for 30 consecutive days to whole smoke from either marijuana or tobacco cigarettes. At the end of this period, anesthetized animals from the two smoke-exposed groups together with their age-matched, nonexposed controls underwent bronchopulmonary lavage, and the free lung cells obtained were fixed and collected for light and electron microscopy. Measurements made on 1-micrometer. sections indicated slight, but statistically nonsignificant, shifts in the frequency distributions of alveolar macrophage profile diameters after both exposure regimens. Stereologic techniques were used to study the subcellular morphology of alveolar macrophages from the three groups of animals. Statistically significant changes were found in cells from tobacco-exposed animals in the volume densities of mitochondria, lipid inclusions, lysosomes, remaining cytoplasm, and the surface to volume ratio of the cell. In contrast, only two parameters in the cells from marijuana-exposed animals were found to have changed significantly, with a 3-fold increase in the volume density of lipid inclusions and a slight reduction in the volume density of the remaining cytoplasm. Possible reasons for the differences in the response of the cells in the two smoke-exposed groups are discussed.

Animals↗

Differential response in the male and female tracheal epithelium following exposure to tobacco smoke.

Histochemical quantification of goblet cells and measurements of the epithelial thickness were made in the trachea of male and female rats exposed to fresh whole tobacco smoke for 30 consecutive days. Exposure to tobacco smoke resulted in an increase in the total goblet cell count in both sexes, with the female rats differentially responding to a greater degree than the male rats. There was a shift from PAS-positive to alcian blue-positive goblet cells, an increase in the number of both "large" and "small" goblet cells, and an increase in the epithelial thickness. PAS-positive "small" cells, the major glycoprotein-reactive cell in the rat tracheal epithelium, increased in the female rats but showed no increase in the male rats. On the other hand, male rats contained a substantially higher proportion of alcian blue-positive cells than did female rats, both before and after exposure to the smoke. The significance of these observations in relation to the prevalence of chronic bronchitis in human smokers is discussed.

Animals↗

A method for the collection of alveolar macrophages for microscopy.

A method is described for the collection and fixation for microscopy of samples of alveolar macrophages harvested by bronchopulmonary lavage. The cell pellicles thus obtained were analyzed by light microscopy by measurement of cell profile diameters. Statistical comparison indicated that no gradient in profile size was present across individual pellicles; they were therefore suitable for random sampling. Mean profile diameters and size distributions were compared for the individual populations of alveolar macrophages.

Animals↗

The stereology of pulmonary alveolar macrophages after prolonged experimental exposure to tobacco smoke.

Morphometric analysis was performed on alveolar macrophages obtained by bronchopulmonary lavage of rats exposed to tobacco smoke for periods up to 60 consecutive days. Smoke dosage levels were adjusted so as to be comparable to those of human smokers. Size distributions were obtained for the lavaged macrophage populations of treated and age-matched control animals following 30 and 60 days of smoke exposure. Electron microscopic stereology was used to quantitate alterations in the ultrastructure of the same macrophage preparations. Several significant changes were observed in macrophage morphology following exposure to tobacco smoke, with an estimated mean cell volume more than twice that of controls following 60 days of smoking. After 30 and 60 days of exposure there was a 10- and 16-fold increase, respectively, in the volume density of cytoplasmic lipid inclusions. The surface to volume ratio of the cells and the lysosomal volume density were reduced in macrophages from smoke-exposed animals. A possible relationship between the incidence of lysosomes and the accumulation of cytoplasmic lipid in treated cells is discussed.

Animals↗

The effect of chronic exposure to tobacco smoke on the antibacterial defenses of the lung.

To evaluate the effects of cigarette smoking on the host defenses of the lung, male CD rats were exposed to fresh whole smoke for up to 60 consecutive days. Intrapulmonary deposition of smoke and animal exposure levels, quantified with decachlorobiphenyl and other smoke tracers, indicated a daily cigarette exposure equivalent to approximately a pack and a half per day in man. Pulmonary alveolar macrophage function in situ was quantified by the inactivation of an aerosolized challenge of Staphylococcus aureus six hours after inoculation. Controls (n=120) inactivated 88.8+/-0.64% of the staphylococci. Exposure to whole smoke did not impair intrapulmonary antistaphylococcal defenses, with inactivation rates of 89.8+/-0.97% (n=49) and 89.1+/-0.46% (n=74) at 30 and 60 days, respectively. Inactivation distribution frequency analysis in controls revealed that 7% of animals had inactivation values greater than two standard deviations from the mean. With prolonged exposure mean with less skewing towards the abnormal. Alveolar macrophages harvested from smoked animals were comparable in viability and in vitro antistaphylococcal activity to controls, appeared to be metabolically activated and had specific stereologic ultrastructural alterations. These studies indicate that chronic exposure to tobacco smoke does not impair, and in fact may stimulate, the host defenses of the lung, as evaluated by in vivo and in vitro pulmonary alveolar macrophage function.

Animals↗