Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1980-5-14
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
D
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0300-9777
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-65
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed-meshheading:119837-Animals, pubmed-meshheading:119837-Antibodies, Bacterial, pubmed-meshheading:119837-Antibody-Dependent Cell Cytotoxicity, pubmed-meshheading:119837-B-Lymphocytes, pubmed-meshheading:119837-Chemotaxis, Leukocyte, pubmed-meshheading:119837-Chronic Disease, pubmed-meshheading:119837-Complement Activation, pubmed-meshheading:119837-Gingivitis, pubmed-meshheading:119837-Humans, pubmed-meshheading:119837-Immunity, Cellular, pubmed-meshheading:119837-Immunoglobulins, pubmed-meshheading:119837-Leukocyte Migration-Inhibitory Factors, pubmed-meshheading:119837-Macrophages, pubmed-meshheading:119837-Major Histocompatibility Complex, pubmed-meshheading:119837-Models, Biological, pubmed-meshheading:119837-Neutrophils, pubmed-meshheading:119837-Periodontitis, pubmed-meshheading:119837-Phagocytosis, pubmed-meshheading:119837-T-Lymphocytes
pubmed:year
1979
pubmed:articleTitle
The immunopathogenesis of progressive chronic inflammatory periodontal disease.
pubmed:publicationType
Journal Article, Review