Stereologic analysis of chronic lymphoid cell infiltrates in human gingiva

Schroeder, Hubert E.; Beer, M. Graf-de

doi:10.1016/0003-9969(76)90018-2

Cited by 30 publications

(16 citation statements)

References 13 publications

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“…Such a picture may reflect the "initial" stage of the pathological process, as Page and Schroeder (1976) suggest, but it may equally reflect a quiescent phase following destructive disease and thus may be a much later or constantly recurring stage in disease progression. When such a lesion is found there is also found a brisk traffic of neutrophils from the capillaries in this area through the junctional epithelium and into the gingival The area of connective tissue underlying pocket and junctional epithelium lining the sulcus is also reported to be characterised by a very marked degree of focal collagen loss, even when the cellular infiltrate is small (Schroeder & Graf-De Beer 1976). A similar reduction in collagen was also reported in the vicinity of the infiltrate in dogs (Schroeder & Attsrom 1979 though here the infiltrate underhes the gingival crest.…”

Section: Gingivitismentioning

confidence: 99%

The role of histopathology in the diagnosis and prognosis of periodontal diseases

et al. 1992

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and Wilton JMA: The role of histopathology in the diagnosis and prognosis of periodontal diseases. J Clin Periodontol 1990; 17: 673-684. Abstract. The histological evaluation of surgical biopsies from affected tissues is a standard way of assessing pathological change and determining treatment in many diseases. In most forms of periodontal disease, however, this approach fmds limited apphcation. Here, we review what uses the histopathological approach has in the study and evaluation of the periodontal diseases. Current understanding of the changes in epithelial anatomy during pocket formation, the cellular composition and dynamics of the inflammatory infiltrate and the mechanisms of bone resorption and repair are reviewed from the perspective of the information available from microscopical investigation, including the uses and potential application of modern immunocytochemical methods to these questions. The usefulness of histological study of biopsy material is reassessed in the light of advances made in immunohistochemical techniques and their application to gingival inflammatory infiltrates and epithelia. Such techniques offer immediately valuable research opportunities with potential for diagnostic applications, noteably the recognition of phases of destructive activity and their differentiation from periods of effective host defence.

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Section: Gingivitismentioning

confidence: 99%

The role of histopathology in the diagnosis and prognosis of periodontal diseases

et al. 1992

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“…At the ultrastructural level the cells identified and counted were small and medium lymphocytes, monocytes and macrophages, polymorphonuclear leucocytes, mast cells, fibroblasts, endothelial cells, transforming B-lymphocytes and plasma cells and transformed T-lymphocytes (Tblasts or immunoblasts). Criteria for identification of all cell types were drawn from published work of, among others, Zucker-Franklin 1969, Vernon-Roberts 1972, Janossy et al 1972, Bessis 1973, Schroeder and Graf-de Beer 1976. By applying rigid criteria for cell identification as summarized in Schroeder anid Munzel-Pedrazzoli (1973) and Gillett et al (1978) and not attempting to identify parts of cells from the cytoplasm alone, it was possible to assign each cell to a specific group.…”

Section: Resuitsmentioning

confidence: 99%

Electron microscope quantitation of inflammatory infiltrates in childhood gingivitis

Longhurst

Gillett

Johnson

1980

J of Periodontal Research

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Quantitation of inflammatory cell infiltrates in gingival connective tissues was carried out on 12 gingival biopsies from the deciduous dentition of 11 children aged 4–8 years. The tissue was prepared for electron microscopy and from ultrathin sections mounted on 200 mesh grids, cells in one third of the grid squares enclosing infiltrated connective tissue were counted. The infiltrate displayed large numbers of small and medium lymphocytes and was moderately vascular. A distinct population of peripherally distributed plasma cells was present and pathologically altered fibroblasts together with marked collagen loss were notable features. Small numbers of macrophages, mast cells and polymorphonuclear neutrophils were recorded but T‐blasts (immunoblasts) were very rarely encountered. The childhood lesions have much in common with the early lesion of adult gingivitis which is considered to be a cell‐mediated immune phenomenon. However, the lack of T‐blasts and rather larger proportion of plasma cells suggest that the lesion of childhood gingivitis represents a position between the early and established phases of gingival disease described in older individuals. A more exact interpretation of these, the earliest stages of human gingival disease should be achieved when the lymphocytes contributing to the childhood infiltrates can be assigned to the T‐ and B‐ cell lines.

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“…In recent years, new concepts for the pathogenesis of periodontal diseases have been formulated (Page & Schroeder 1976). Based on qualitative as well as on morphometric point-counting procedures used for stereologic analysis of the gingival and periodontal tissues (Schroeder & Graf-de Beer 1976, Schroeder, Munzel-Pedrazzoli & Page 1973, 5 different states ranging from health to advanced disease of the periodontium have been proposed: 1) the healthy periodontium characterized by a dense connective tissue with tightly packed collagenous fibers containing only a few leukocytes, and a few layers of junctionai epithelial cells, 2) the initial lesion triggered by a 2-to 4-d plaque accumulation and characterized by a limited, predominantly perivascular loss of collagen, an increase in the number of leukocytes, primarily PMN's, and a conversion of the most coronal part of the sulcular and junctionai epithelia into pocket epithelium, 3) the early lesion appearing at the site of the initial lesion 4 to 10 d following plaque accumulation, with a more pronounced loss of collagen, a connective tissue dominated by lymphocytes and a proliferation of the basal cells of the junctionai epithelium, 4) the established lesion caused by 2 to 3 wk of plaque accumulation, with a further loss of collagen, a predominance of plasma cells within the connective tissue and the formation of numerous epithelial rete pegs, and 5) the advanced lesion characterized by the persistence of the features of the established lesion associated with the loss of connective tissue fiber attachment concomitant with an apical migration of the junctionai epithelium, and the extension of the cellular infiltrate into the underlying connective tissue, and by alveolar bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Comparison between histological and clinical parameters during human experimental gingivitis

Brecx

Schlegel

Gehr

et al. 1987

J of Periodontal Research

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The purpose of this investigation was to study stereologically the histopathologic alterations occurring during a human experimental gingivitis, and to establish a relationship between clinical parameters and histologic findings. Eight dental students volunteered for the study. After a prophylaxis they performed optimal oral hygiene for 3‐4 weeks to reach mean plaque and gingival indices approaching zero. They then abandoned all oral hygiene procedures for a period of 21 days. At d 0, 4, 7, 14 and 21, Plaque Index (PII), Gingival Index (GI) and Gingival Exudate Flow Rate (GEFR) were assessed, and a buccal biopsy of their gingiva was taken. Point counting procedures were performed at 2 different levels of magnification to estimate the volume densities of epithelium, infiltrated and non‐infiltrated connective tissue, and collagen. The percentages of polymorphonuclear neutrophilic granulocytes, lymphocytes, plasma cells, macrophages and fibroblasts were estimated by counting the number of profiles of these cells in the connective tissue area close to the apical end of the junctional epithelium. The histological picture during the entire experiment was one of an early lesion (Page & Schroeder 1976). The clinically healthy gingiva did not correspond to a histologically healthy gingiva containing only a few inflammatory cells, probably because the 3‐4 wk of perfect oral hygiene were not sufficient to generate histological health. Furthermore, no chronic inflammation of the gingiva, as characterized by a predominance of plasma cells, was observed after 3 wk without oral hygiene. Thus, more than 3 wk of no oral hygiene are necessary to obtain an established gingival lesion. With increasing gingivitis scores between GI = 0 and GI = 2 there was a significant increase in the percentages of lymphocytes and a significant decrease in the percentages of fibroblasts. With increasing GEFR similar trends in percentages were observed for lymphocytes and fibroblasts. It was concluded that GI scores and GEFR reflect histologic changes in tissue and, hence, are valid indicators of gingivitis development.

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Stereologic analysis of chronic lymphoid cell infiltrates in human gingiva

Cited by 30 publications

References 13 publications

The role of histopathology in the diagnosis and prognosis of periodontal diseases

The role of histopathology in the diagnosis and prognosis of periodontal diseases

Electron microscope quantitation of inflammatory infiltrates in childhood gingivitis

Comparison between histological and clinical parameters during human experimental gingivitis

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