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G J Seymour

Publications and source records attributed to G J Seymour.

9 recordsLinked to original sources
PubMed1979

Conversion of a stable T-cell lesion to a progressive B-cell lesion in the pathogenesis of chronic inflammatory periodontal disease: an hypothesis.

Changes in the host's immunological response or, alternatively, changes in the oral microflora have been implicated as possible mechanisms by which a stable lesion of chronic inflammatory periodontal disease may become a progressive lesion leading to tissue destruction and tooth loss. It has recently been established that the progressive lesion in humans can be unequivocally considered as a B-cell response. Circumstantial evidence exists which suggests that the stable lesion is in fact a T-cell-mediated mechanism. An hypothesis is presented to explain the change from a stable to a progressive state in terms of a shift from a predominantly T-cell lesion to one involving large numbers of B-cells. Mechanisms of this shift in cell populations are considered together with a discussion of possible means of preventing such a shift.

Animals↗
PubMed1979

The immunopathogenesis of progressive chronic inflammatory periodontal disease.

Natural, humoral and cellular immune mechanisms have all been implicated in the pathogenesis of chronic inflammatory periodontal disease. However, confusion still exists as to the role played by each of these immunological mechanisms. Recently, characterization of the cell types within the progressive lesion has been established, in which four recognizable zones were described. Immediately subjacent to the epithelium lining the periodontal pocket both polymorphonuclear leukocytes (PMN's) and macrophages were seen, while cells deeper in the tissues had the morphological appearance of lymphocytes. The majority of these lymphocytes had a B-cell phenotype although a few T-cells and macrophages were found. On the advancing front of the lesion the cells had the morphological appearance of plasma cells, the majority of which contained IgG. Other cells found in this region had the morphology of plasma cells yet contained no cytoplasmic immunoglobulin, but they did contain substantial amounts of lysosomal enzymes. Similar cells have previously been described in periodontal disease; their frequent association with fibroblasts may suggest that they are important in the pathogenesis. Deposits of IgG and fibrin were found in the fibrous tissue band surrounding the lesion. These results are reviewed and, although the zones described were not anatomically distinct, by describing the lesion in this way it was possible to establish a convenient model to explain the immunopathogenesis of progressive chronic inflammatory periodontal disease. In this respect, progressive chronic inflammatory periodontal disease in man should be considered as a B-cell lesion.

Animals↗
PubMed1979

The histopathogenesis of acute ulcerative gingivitis.

The present study was a preliminary histological and immunofluorescent investigation of the edge of the ulcer in acute ulcerative gingivitis. The results of this study show that the lesion is dominated by polymorphonuclear leukocytes, with plasma cells present in the deeper parts. The epithelium on the edge shows widening of the intercellular spaces with destruction of the epithelial cells, accompanied by a heavy infiltrate of PMNs. Both IgG and C3 could be demonstrated between these epithelial cells, although the present study could not establish whether this represented immune complex deposition. The histopathogenesis of AUG therefore seems to involve a PMN infiltration of the epithelium, with subsequent destruction of the epithelium, probably due to the release of hydrolytic enzymes. The presence of the PMNs within the epithelium may involve direct bacterial chemotaxis and/or the activation of complement via the classical or alternative pathways.

Acute Disease↗
PubMed1978

Enzyme differentiation of lymphocyte subpopulations in sections of human lymph nodes, tonsils and periodontal disease.

Five enzymes have been studied to differentiate between T and B lymphocytes in sections of human lymph nodes, tonsils and chronic inflammatory periodontal disease. The presence of acid phosphatase, beta-glucuronidase N-acetyl-beta-glucosaminidase, non-specific esterase and fluoride-resistant esterase activity was determined histochemically. The results indicate that cells in the B area of both lymph nodes and tonsils are negative for enzyme activity, while those in the T area show a single intense granule of activity. These enzymes were unable to differentiate between T blasts, B blasts and plasma cells in the sections studied. The majority of the lymphoid cells in the lesions of chronic inflammatory periodontal disease are enzyme-negative and probably of B-cell origin.

B-Lymphocytes↗
PubMed1976

The possible pathogenesis of gingival recession. A histological study of induced recession in the rat.

Stages in the pathogenesis of gingival recession were observed in rats in which pocketing had been induced by replacement of natural incisors with dental implants. Suitable conditions were thus created on the palatal aspect of the implant sockets for recession to occur. The recession process was examined at intervals by taking transverse serial sections. In the epithelial and connective tissues deep to the receding margin, morphological changes were seen which apparently lead to cleft formation and recession. These appeared to be associated with mononuclear cell infiltration of the connective tissue. The study suggests that gingival recession involves a localized inflammatory process which causes breakdown of connective tissue and leads to proliferation of the epithelium into the site of connective tissue destruction. Proliferation of the epithelial cells into the connective tissue brings about a subsidence of the epithelial surface, which is manifest clinically as recession.

Animals↗
PubMedDate not supplied

Cytochemical identification of T and B cells in situ in mouse lymphoid tissue and lymph nodes from the rat, gerbil and cat.

The use of enzymes as markers of T or B cells in tissue sections has been studied in mouse lymphoid tissue and lymph nodes from the gerbil, rat and cat. Lymphocytes in the T-cell areas of murine lymph nodes and spleen contained discrete dots of non-specific esterase and N-acetyl-beta-D-glucosaminidase (beta-glucosaminidase) activity, with weak acid phosphatase activity. Lymphocytes in the B-cell areas lacked this discrete staining. Cortical thymocytes contained slight esterase activity while medullary thymocytes were strongly positive for both esterase and beta-glucosaminidase. Lymphocytes with a T-cell staining pattern were only occasionally seen in lymph nodes from Nude (nu/nu) mice. ATPase staining was restricted to lymphocytes in the B-cell areas; weak 5'-nucleotidase staining was only present in a frew lymphocytes in both T- and B-cell areas. Blast cells stimulated by in vivo injection of ConA or PHA in the mouse showed strong discrete enzyme activity for non-specific esterase and beta-glucosaminidase. Lipopolysaccharide-stimulated blast cells and cells within germinal centres lacked this discrete staining. Comparison of lymph nodes from the gerbil, rat and cat suggested at least on enzymes as a T-cell marker in each species although considerable variation in staining profiles was seen in the different species.

Acid Phosphatase↗