Search

Continuous eruption in response to attrition has been reported for different tooth groups in preindustrial remains. However, no full intra-arch and inter-arch comparison of eruption has been undertaken. The position of the gingival margin, which is unknown in skeletal dentitions, is important in assessing periodontal disease and also in establishing whether root exposure occurred as continuous eruption progressed. The apical margin of supragingival calculus (SGC) provides a marker of the original gingival crest and could be used to study loss of attachment in dental remains. Thirty nine Irish pre-industrial dentitions were examined for continuous eruption, and 17 for the position of the gingival margin. To score attrition an index was devised. The apical border of supragingival calculus represented the gingival margin. Cemento-enamel junction (CEJ) to alveolar crest (AC) and SGC-AC measurements were recorded at six sites on teeth. Intra-arch analyses indicated no differences for the rate of continuous eruption between tooth groups. Inter-arch comparison revealed that the degree of eruption was greater in the mandible than in the maxilla (p 3 mm occurred at 1.8 per cent of sites. The distance of SGC-AC followed a distinct pattern with tooth type. Proximal CEJ-AC values were less than buccal-lingual levels (p < 0.001), suggesting that periodontal disease was not a major feature of the dentitions examined. It is concluded that in the dentitions examined: (i) continuous eruption was greater in the mandible; (ii) chronic periodontitis with pocketing and loss of proximal AC was not a significant finding; (iii) the position of the gingival margin was maintained at a relatively stable relationship with the AC, which would have resulted in root exposure as attrition progressed. These observations indicate that caution is required when interpreting evidence of attachment loss as an indicator of periodontal disease in pre-industrial remains and contemporary populations exhibiting high rates of functional attrition.

The lipid composition of the "mucous barrier" of rat stomach was investigated. Cellular mucus of the mucous cells from gastric epithelium and surface mucus from gastric mucosa were obtained by perfusion in vivo of Ghosh-Lai rat stomachs with 2 M NaCl. Lipids extracted from dialyzed and lyophilized 2 M NaCl perfusates and 0.9% NaCl (saline) controls were quantitatively separated into single components by means of two-dimensional thin layer chromatography and compared. Significant differences in the level of cholesterol esters, di- and triglycerides, and glycolipids were found. Three to 4 times greater quantities of cholesterol esters and di- and triglycerides, and 2 to 6 times greater quantities of glycolipids were found in 2 M NaCl perfusates as compared to saline controls. The glycolipid fraction consisted of neutral and acidic glyceroglucolipids and was devoid of glycosphingolipids. The phospholipids constituted the smallest portion of the lipids present in 2 M NaCl and saline perfusates and were 2 times higher in 2 M NaCl. These data indicate that mucous barrier in addition to mucins contains considerable quantities of lipids of which glyceroglucolipids are the most prominent components.

In order to determine the possible effects of the circulating intrinsic factor antibodies (IFA) on gastric morphology and secretory function, four groups of 12 rats each received intravenous injection daily for 8 to 12 weeks of immunoglobulin G (IgG) fractions separated on DEAE-cellulose columns from various sources: (1) sera of patients with pernicious anemia, containing both IFA and parietal cell antibodies (PCA), (2) sera from patients with atrophic gastritis, containing parietal cell antibody only, and (3) and (4) sera of rabbits immunized with semipurified human or rat intrinsic factor (IF). In addition three control groups of 12 rats each received intravenous injections daily for 8 to 12 weeks of either (5) saline or (6) and (7) IgG processed from human or rabbit normal sera. Still another group of 12 rats (8) did not receive any injections whatsoever for the same duration of time. One-third of the rats were intubated biweekly after histamine stimulation and the hourly outputs of CHl pepsin, and IF were determined. At conclusion of the experiments, rats were killed, the mucosal surface and thickness of the mucosa were measured, and parietal cell and peptic cell masses were counted. The control groups showed either progressive growth of the cellular mass in gastric mucosa and increase of the HCl, pepsin, and IF outputs, or no significant changes. In contrast, rats injected with IgG containing IFA to human or rat IF showed a statistically significant thinning of the gastric mucosa, reduction of peptic cells, which are known to secret IF in this species, and corresponding decreases in the ouputs of pepsin and IF. These became reduced by about 50% from initial values, and by 62 or 75%, respectively, when compared to rats injected with normal human or rabbit IgG's. In rats injected with IgG's from pernicious anemia sera, which contained both IFA and PCA, the outputs of IF, pepsin, and HCl decreased signigicantly, as well as the peptic and parietal cell masses. The rats injected with PCA only demonstrated thinning of the gastric mucosa, reduction of parietal cell mass, and a significant decrease of the HCl output. These findings imply an active role of the circulating gastric.

One hundred fifty alcoholic men and women and 150 age and sex-matched nonalcoholic controls (after exclusion of pernicious anemia and cancer of the stomach) were evaluated for the presence of parietal cell antibodies (PCA). Blocking and binding intrinsic factor antibodies (IFA) were determined in the PCA positive sera. The prevalence and age and sex distribution of PCA in the alcoholics and nonalcoholics was identical. In alcoholics above the age of 60 years, the incidence of PCA, although higher than in those of the younger age group was similar to that in the nonalcoholics of the same age group (in men 6.3 percent and 7.3 percent and in women 7.5 percent and 10.0 percent respectively). Antral gastritis of moderate or severe degree was the frequent lesion in alcoholics. This form of gastritis was not associated with any significant increase in the incidence of PCA. No patients with sera positive for IFA were detected among the 22 PCA positive patients. There is no evidence for humoral derangement of the gastric autoimmunity in chronic alcoholics.

Gastric mucosal damage was produced in 130 mice by forced ingestion of alcohol, followed by restraint in the cold. Animals were killed at intervals from six hours to 27 days following the stress. Linear hemorrhagic erosions and diffuse hemorrhagic patches were found grossly, predominantly in the glandular portion of the stomach, in about 75% of the animals 6 to 24 hours after stress. At later time intervals, the linear mucosal depressions persisted; these became progressively less prominent with time but substantial numbers were still readily discernible three weeks after injury. Microscopical examination of the fresh lesions showed a variable amount of mucosal necrosis and acute inflammation. Epithelial regeneration became prominent after three days and persisted for several weeks. The first regenerating epithelial cells were primitive, cuboidal elements followed by mucous cells, parietal cells, and zymogen cells, in that order. The morphological features and evolution of the lesions were similar to that described in human stress ulcers.

In an attempt to localize intrinsic factor in the human parietal cell, and to study its intracellular union with the intrinsic factor antibody and complement, intrinsic factor antibody was separated from coexisting parietal cell antibody in pernicious anaemia sera by gel filtration. Intrinsic factor antibody of both `binding' and `blocking' type was also produced in rabbits by immunization with semi-purified human intrinsic factor–[57Co]B12 complex.