A primary canine and an impacted permanent canine with infection potentially induced an intracranial abscess.

Intracranial abscess is a rare but life-threatening disease. There have been no reports on intracranial abscess induced by the residual primary tooth and the impacted successive permanent tooth with infection. We report on an interesting case of a 29-year-old man suffering from an epidural abscess, potentially caused by an infection of the residual primary maxillary right canine and the impacted permanent maxillary right canine. The patient recovered completely after prolonged antibiotic treatment and extraction of both of the suspected teeth. Fusobacterium sp. was isolated from the culture of a peripheral blood sample. This case alerts us to realize that the lack of suitable and timely intervention in oral conditions might produce a harmful effect on general health.

Invasive Streptococcus mutans induces inflammatory cytokine production in human aortic endothelial cells via regulation of intracellular toll-like receptor 2 and nucleotide-binding oligomerization domain 2.

Streptococcus mutans, the primary etiologic agent of dental caries, can gain access to the bloodstream and has been associated with cardiovascular disease. However, the roles of S. mutans in inflammation in cardiovascular disease remain unclear. The aim of this study was to examine cytokine production induced by S. mutans in human aortic endothelial cells (HAECs) and to evaluate the participation of toll-like receptors (TLRs) and cytoplasmic nucleotide-binding oligomerization domain (NOD) -like receptors in HAECs. Cytokine production by HAECs was determined using enzyme-linked immunosorbent assays, and the expression of TLRs and NOD-like receptors was evaluated by real-time polymerase chain reaction, flow cytometry and immunocytochemistry. The involvement of TLR2 and NOD2 in cytokine production by invaded HAECs was examined using RNA interference. The invasion efficiencies of S. mutans strains were evaluated by means of antibiotic protection assays. Five of six strains of S. mutans of various serotypes induced interleukin-6, interleukin-8 and monocyte chemoattractant protein-1 production by HAECs. All S. mutans strains upregulated TLR2 and NOD2 mRNA levels in HAECs. Streptococcus mutans Xc upregulated the intracellular TLR2 and NOD2 protein levels in HAECs. Silencing of the TLR2 and NOD2 genes in HAECs invaded by S. mutans Xc led to a reduction in interleukin-6, interleukin-8 and monocyte chemoattractant protein-1 production. Cytokine production induced by invasive S. mutans via intracellular TLR2 and NOD2 in HAECs may be associated with inflammation in cardiovascular disease.

Immunocytochemical localization of cathepsin D in rat junctional epithelium.

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.

Immunohistochemical study of nerve fibres with substance P- or calcitonin gene-related peptide-like immunoreactivity in the junctional epithelium of developing rats.

The beginning of innervation in the junctional epithelium of maxillary first molars was examined in gingival tissues from 19 to 32-day-old rats. Substance P- or calcitonin gene-related peptide (CGRP)-like immunoreactivity was demonstrated by the avidin-biotin peroxidase complex method. In 19-day-old rats, nerve fibres with substance P- or CGRP-like immunoreactivity were seen in the connective tissue and oral epithelium, but not in the reduced enamel epithelium, which would be transformed into the junctional epithelium. In 21-day-old rats, the fibres with substance P- or CGRP-like immunoreactivity formed a plexus in the oral sulcular epithelium and thin varicose fibres were seen for the first time entering the adjacent reduced enamel epithelium. These fibres also penetrated the middle portion of the reduced enamel epithelium, but did not reach the cuboidal reduced ameloblasts. More nerve fibres had CGRP-like immunoreactivity than substance P-like immunoreactivity. In 23-day-old rats, many fibres with both immunoreactivities were seen in the basal layers of the junctional epithelium, but only a few were seen in its superficial layers. In 28-32-day-old rats, numerous fibres with both immunoreactivities were distributed in the whole junctional epithelium and showed a similar pattern of innervation. For all immunoreactive fibres, the density in the middle portion in the junctional epithelium was the highest. The nerve plexus was formed in the basal layers and some fibres with a varicose appearance were found in the superficial layers.

Immunohistochemical evidence for the presence of nerve fibres with substance P- or calcitonin gene-related peptide-like immunoreactivity in the proliferating epithelium in the developing teeth of rats.

By immunohistochemistry using the avidin-biotin peroxidase complex method, nerve fibres with substance P- or calcitonin gene-related peptide (CGRP)-like immunoreactivity (IR) were examined in the dental lamina, cells external to the reduced ameloblasts and oral epithelium in the developing upper first molars of postnatal rats. At birth, very few varicosities with substance P- or CGRP-IR were found in the dental lamina over the mesial cusp of the dental germ. In 5-day-old rats, nerve fibres with substance P- or CGRP-IR in the dental lamina over the mesial cusp gradually increased in number. In 7-day-old rats, over the mesial portion of the dental germ, the oral half of the dental lamina began to thicken on the buccopalatal side, in which many nerve fibres with substance P- or CGRP-IR were observed. A few nerve fibres began to penetrate the cells external to the reduced ameloblasts over the middle buccal cusp. In 10-day-old rats, the oral epithelium over the mesial cusp gradually thickened, and nerve fibres with substance P- or CGRP-IR were found especially in its basal layer. In 13-15-day-old rats, a great many nerve fibres with substance P- or CGRP-IR were distributed all over the fused, thickened dental lamina and cells external to the reduced ameloblasts proliferated over the middle and distal cusps. Nerve fibres with substance P- or CGRP-IR formed a plexus in the thickened oral epithelium, which spread to the mesiopalatal end of the mesial cusp.(ABSTRACT TRUNCATED AT 250 WORDS)

Streptococcus anginosus l-cysteine desulfhydrase gene expression is associated with abscess formation in BALB/c mice.

Streptococcus anginosus, an anginosus group bacterium, is frequently isolated from odontogenic abscesses, and is the oral bacterium that is primarily responsible for producing hydrogen sulfide from l-cysteine through the action of its l-cysteine desulfhydrase (ßC-S lyase) enzyme. However, the relationship between its production of hydrogen sulfide and abscess formation has not been investigated. To elucidate the etiological role of hydrogen sulfide in abscess formation, we initially measured, using specific primers, expression of the lcd gene, which encodes ßC-S lyase, in the pus of abscesses that formed in BALB/c mice following subcutaneous injection of S. anginosus into the dorsa. Expression of lcd was >15-fold higher when l-cysteine was present than when it was absent. A mouse virulence assay revealed that the mean diameter of abscesses caused by S. anginosus FW73 plus l-cysteine was greater than that of abscesses caused by S. anginosus FW73 in the absence of l-cysteine. These findings demonstrate that the lcd gene of S. anginosus is upregulated in mouse abscesses and that hydrogen sulfide, the product of a reaction catalyzed by ßC-S lyase, plays an etiological role in odontogenic abscess formation.