Initial gingivitis in dogs

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

doi:10.1111/j.1600-0765.1975.tb00017.x

Cited by 73 publications

(35 citation statements)

References 15 publications

(9 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…He suggests that this may be a pointless pursuit, mainly since even non-keratinized epithelia may offer resistance to the penetration of many substances (35,38) and 41 (1983) since keratinization of the highly permeable (28,30) junctional epithelium may lead to loss of epithelial attachment to the tooth surface and thus be harmful. Although this latter point may be well taken, it should be kept in mind that in spite of the intensive antibacterial therapy over considerable periods of time in this and other (2, 5 , 32) studies, keratinization of the junctional epithelium in situ has never been reported as a result of antibacterial therapy and may not be readily achieved (30,41).…”

Section: Discussionmentioning

confidence: 95%

Ultrastructural Study of Induced Keratinization in Sulcular Gingival Epithelium in Rhesus Monkeys

Kristoffersen

Caffesse

Nasjleti

et al. 1983

Acta Odontologica Scandinavica

View full text Add to dashboard Cite

Gingival sulcular epithelium--which in primates normally does not keratinize--can be induced to undergo keratinization by prolonged intensive antibacterial therapy. Three months before biopsy the teeth of two adult male rhesus monkeys were scaled and polished, and for 5 days the monkeys were given intravenous injections of 75 mg Achromycin daily. Their teeth were subsequently subjected to daily cleaning and polishing. The presumably in-situ-keratinized sulcular epithelium was examined by transmission electron microscopy. It was also compared with oral gingival epithelium from the same two animals and with oral and sulcular epithelium from a rhesus monkey that had not been exposed to local or systemic antibacterial therapy. The results confirmed earlier histological studies, which have shown that under the conditions described the sulcular epithelium becomes parakeratinized. In addition, several other ultrastructural changes were observed, some of which suggest that the treatment given may result in the formation of a more efficient permeability barrier in the sulcular area. The possible clinical significance of such a barrier is briefly discussed.

show abstract

Section: Discussionmentioning

confidence: 95%

Ultrastructural Study of Induced Keratinization in Sulcular Gingival Epithelium in Rhesus Monkeys

Kristoffersen

Caffesse

Nasjleti

et al. 1983

Acta Odontologica Scandinavica

View full text Add to dashboard Cite

show abstract

“…In inflammatory gingivae, numerous neutrophils and macrophages emigrate into the JE, with increasing signs of inflammation; these cells eventually become the predominant population (Schroeder et al, 1975). The activity of various proteinases (cathepsins B, D, H, and L, collagenase, and elastase) has been shown to increase with the severity of periodontitis (Ishikawa et al, 1972;Kunimatsu et al, 1990).…”

Section: Discussionmentioning

confidence: 96%

Immunocytochemical Localization of Cathepsin D in Rat Junctional Epithelium

Ayasaka

Goto²,

Tsukuba³

et al. 1993

J Dent Res

View full text Add to dashboard Cite

Localization of cathepsin D was studied in the junctional epithelium (JE) of healthy rat gingivae by immuno-light and -electron microscopy, by means of both the avidin-biotin-peroxidase complex method and a colloidal gold IgG method. At the light-microscopic level, cathepsin D was demonstrated in the JE and oral sulcular epithelium (OSE). Cathepsin D immunoreactivity was remarkable in the coronal portion of the JE and decreased toward its apical portion. However, cathepsin D immunoreactivity in the basal cell layer of the JE was negligible or negative. In the OSE, the granular layer was positive for cathepsin D. In the adjacent connective tissue, many macrophage-like cells (not clear at this level) close to the basal cell layer showed strong immunoreactivity. At the electron microscopic level, cathepsin D was found in the primary lysosomes and trans-cisternae of Golgi apparatus in the JE cells. These lysosomes were often fused together or were fused with cathepsin D-negative intracytoplasmic vacuoles to form secondary lysosomes, which indicated that intracellular digestion may have been in progress. However, neutrophils contained few gold particles based on cathepsin D. It is likely that the amounts of cathepsin D contained in the JE cells and macrophages are larger than those of cathepsin D contained in the neutrophils. These findings provided morphological evidence that JE cells have the same endocytotic capacity as macrophages and neutrophils, and that JE cells participate in the intracellular digestion that is carried out by lysosomal enzymes such as cathepsin D. It is suggested, in addition, that maximum intracellular digestion occurs in the coronal portion of the JE.

show abstract

“…Capillary luminal distances (VD in our study) probably decrease and sometimes are completely occluded in DM because of structural alterations in vessel walls. A tendency for vascular thickening secondary to atherosclerotic changes with occlusion of small vessels is regarded as one of the putative factors in luminal distance decrease 16,58,59 . Gül and Özsoy, 60 in an experimental study in rats, examined the thickening of gingival vessels in detail by transmission electron microscopy, and they observed that the lumens had been closed by epithelial cells proliferation in some sections.…”

Section: Discussionmentioning

confidence: 99%