Detection of Mycoplasma pneumoniae-DNA within diseased gingiva by in situ hybridization using a biotin-labeled probe.

Isolation of Mycoplasma pneumoniae was accomplished in gingival biopsies of four patients exhibiting chronic inflammatory periodontal disease using in situ hybridization with biotin-labeled DNA probes. The distribution of the M. pneumoniae organisms was mainly cytoplasmic and evenly spread around the nuclei of connective tissue cells. Controls of nondisease sites in the same patients showed no infection with M. pneumoniae. Since M. pneumoniae is the only Mycoplasma known to be pathogenic, their role in the pathogenesis of periodontal disease needs further study.

Mycoplasma in periodontal disease. Isolation in juvenile periodontitis.

Mycoplasma have been identified in one case of juvenile periodontitis by size, morphology, hemadsorption and cultural techniques. These microorganisms were found on the surface of the tooth, on the surface of pocket epithelium and invading the gingival epithelium and adjacent connective tissue. These observations suggest the need for further studies on the role of Mycoplasma in the pathogenesis of advanced periodontal infections. The role of Mycoplasma in periodontal disease is discussed.

Scanning and transmission electron microscopic study of tissue-invading microorganisms in localized juvenile periodontitis.

This transmission and scanning electron microscope study documents the invasion of microorganisms into the gingiva and along resorbing alveolar bone surfaces in a 15-year-old patient with localized juvenile periodontitis. The invading bacteria were mainly Gram-negative fusiform, coccobacilli and spirochetes. Microorganisms identified as Mycoplasma were also found to invade in some areas. Polymorphonuclear neutrophils (PMNs) were seen in association with the bacteria. The majority of bacteria were covered by PMNs and enclosed by the phagocyte but did not appear to lie within phagosomes. High numbers of PMNs were found in the gingival connective tissue inflammatory infiltrate and in the pocket epithelium. Invasion into the gingiva and alveolar bone by bacteria and Mycoplasma in localized juvenile periodontitis may be importance in the therapy of this infection.

A scanning electron microscopic study of leukocytes and their interaction with bacteria in human periodontitis.

Shape, size, topographical relationships, surface morphology, phagocytosis and locomotion were used to identify and study leukocytes in human cases of periodontitis. These cells were described in the following locations: in peripheral blood vessels adjacent to the pocket epithelium; gingival connective tissue; basement lamina; sectioned pocket epithelium; surface of pocket epithelium; junctional epithelium; and cementum surface. The interaction of leukocytes and bacteria was documented in the phases of recognition, attachment and engulfment of bacteria. Morphologic data suggesting the process of degranulation was also presented.

Bacterial invasion of gingiva in advanced periodontitis in humans.

Using scanning electron microscopy, bacteria were found invading the epithelial wall of deep periodontal pockets in five out of eight cases. In one case, bacteria had reached the connective tissue. The following bacterial morphotypes were identified: cocci, short rods, filaments and spirochetes. A corncob-like formation with a few scattered spirochetes was found in one case between the junctional epithelial cells. Numerous cocci, rods and filaments were found in intercellular spaces of the epithelium in the lateral wall of the pocket and accumulating on the epithelial side of the basement lamina. Bacterial invasion of gingival tissue may have important pathogenic and therapeutic implications.

A scanning electron microscopic study of the relationship between the most apically located subgingival plaque and the epithelial attachment.

Twelve teeth with chronic periodontitis were extracted and examined in the scanning electron microscope. Subgingival plaque in deep pockets was usually covered by a surface coating, which was absent in the apical part. The apical plaque displayed an organized structure, although varying form one tooth to another. The microorganisms were sometimes overlapping the epithelial cell remnants. Coccal forms were seldom found, but on a morphologic basis, rod-like, filamentous, spiral and branching forms were identified. Both bacteria and spirochetes seemed to have the capacity to invade the epithelial remnants on the tooth surface. The epithelium in direct contact with the microorganimsm showed a widening of the intercellular spaces and a change in surface morphology. This was in contrast to cell layers more distant from the plaque, which appeared normal and homogeneous. Similar reactions were also seen in gingival epithelial-like cell cultures infected with plaque of human origin.

Plaque-free zones on human teeth in periodontitis.

The surface morphology of the pocket area of extracted, periodontally involved, human teeth was studied with steromicroscope. A plaque-free zone was found to be present in all specimens. The width of the plaque-free zone was found to decrease as the pocket depth and loss of attachment increase.

The zone of completely and partially destructed periodontal fibres in pathological pockets.

The morphology, the width and the appearance frequency of the zone completely and partially destructed periodontal fibres on human teeth were studied in the stereomicroscope. This zone was present between the most apical border of identifiable, epithelial attachment remnants and the most coronal intact periodontal fibres, and consisted of only a few fibres without any specific orientation. The mean width of the zone was 0.43 mm, and the appearance frequency almost 100%. The results of the comparison between clinical and laboratory pocket depths indicated that the pocket depths measured in the laboratory were always less deep than those recorded clinically. There seemed to be a relationship between these findings and the presence of a zone of completely and partially destructed periodontal fibres.