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Notes: Anaerobic Gram-negative bacteria dominate in periodontitis locations, while Gram-positive bacteria characterize healthy sites. A well-established Gram-positive flora might therefore inhibit the colonization of Gram-negative pathogens. The purpose of the present investigation was to examine whether endogenous S. sanguis could prevent, or reduce, periodontal bone loss in rats infected with a virulent P. gingivalisstrain. Sixty specific pathogen-free Wistar rats were divided into 6 groups. Doxycycline was administered in the drinking water for 2 weeks to the groups A, B, C, and D to suppress the preexisting microflora in the mouth. Rats in groups A and C were subsequently inoculated with an 5. sanguis strain, isolated from one of the rats, once a day for 5 d. Infection with P. gingivalis 381 was then carried out for 5 d in groups A, B, and E. Group F was not treated with doxycycline nor infected with bacteria and served as untreated control. Six weeks after the P. gingivalis inoculation, the rats were killed. Periodontal bone levels were assessed radiographically and morphometrically, and serum antibody against P. gingivalis 381 was determined by a fluorescence immunoassay. Periodontal bone support, determined radiographically, was reduced in group B (doxycycline-treated, P. gingivalis-inoculated) compared with the other groups. In contrast, the morphometric determination showed no differences between the groups. In group B antibody levels against two different P. gingivalis 381 cell surface antigens were significantly elevated. The data indicated that the preinoculation of an endogenous S. sanguis strain protected against a reduction of the radiographically assessed periodontal bone support induced by P. gingivalis 381. and similarly prevented an elevation of the total serum antibody response to P. gingivalis 381.

Notes: The article deals with the use of glucocorticosteroids in the treatment of the oral manifestations of Systemic Lupus Erythematosus (SLE), Disecid Lupus Erythematosus (DLE), Rheumatoid Arthritis (RA) in the temporomandibular joint, Pemphigus Vulgaris, Pemphigoid, Erythema Multiforme Exudativum (EME), Lichen Plaints (LP), and Recurrent Aphthous Ulcerations (RAU). The benefit from steroids is discussed on the basis of current knowledge of etiology and pathogenesis of the various disorders. All of them are characterized by inflammation which appears secondary to a hypersensitivity reaction against autocomponents. Glucocorticoids do not interfere with the primary disease mechanisms. But it is concluded from the literature, that because of anti-inflammatory and immunosuppressive effects of the hormones, it seems reasonable to profit from steroids as palliatives in acute phases of the diseases and/or as long-term suppressors of the general host defense.

Notes: Tetracyclines have been widely used as adjuncts in periodontal therapy due to the antimicrobial efficacy of these drugs. Recently, their ability to inhibit host-derived matrix metalloproteinases (collagenase and gelatinase) and bone resorption in organ culture has also been invoked as a therapeutic rationale. The current study was undertaken to determine whether tetracyclines can inhibit alveolar bone loss in vivo due to a non-antimicrobial action of these drugs. Experimental periodontitis was induced by inoculating adult, male Sprague-Dawley rats with P. gingivalis (strain 381) following kanamycin/ampicillin pretreatment. Doxycycline, non-antimicrobial chemically-modified tetracycline (CMT-1) and vehicle alone were administered daily to 3 infected groups of rats (n=6 rats per group; each group housed in a sterilized inflatable isolator) beginning 10 days after P. gingivalis inoculation. The control group (n = 6; non-infected rats) received only vehicle. After 5 weeks of daily drug administration by gastric intubation, the experiment was terminated and blood samples were taken from each animal to determine antibody levels against P. gingivalis. Plaque samples were collected from each group of animals before and after P. gingivalis inoculation and at the end of the experiment for microbiological examination. The jaws were removed from each rat, defleshed and then analyzed morphometrically and radiographically to assess bone loss. Serum antibody levels against P. gingivalis were significantly elevated in the 3 infected groups compared to the non-infected controls. This, together with the microbiologic findings, indicated that these groups of rats were infected with P. gingivalis. Significantly greater bone loss was observed in the untreated P. gingivalis-infected group compared to the controls based on both morphometric and radiographic measurements. Oral administration of doxycycline or CMT-1 to the P. gingivalis-infected rats completely inhibited this bone loss. As expected, CMT-1 did not exhibit an antimicrobial effect against P. gingivalis. Therefore, this study indicates that tetracyclines can inhibit alveolar bone loss in vivo by a mechanism which is independent of the antimicrobial efficacy of these drugs.

Notes: Summary Fetal rat neocortex grafted into lesion cavities made in the newborn rat neocortex can exchange multiple axonal connections with the host brain. Most previous studies demonstrating efferent transplant-tohost brain connections have used fluorescent retrograde tracers injected into the host brain (Castro et al. 1985, 1987; Floeter and Jones 1984; O'Leary and Stanfield 1989). Other studies have used anterograde axonal tracing with either tritium-labelled amino acids impregnating the transplant and its efferents (Floeter and Jones 1985) or horseradish peroxidase injected into the transplants (Chang et al. 1984, 1986). In the present study we used the anterograde axonal tracer Phaseolus vulgaris — leucoagglutinin (PHA-L) to examine in detail the course and termination of the efferent neocortical graft fibers. Twenty-six newborn rats had the right frontal cortex forepaw area removed by vacuum aspiration, while anesthetized by hypothermia. A piece of fetal frontal cortex 14–16 embryonic days old (E14–16) was immediately thereafter placed in the lesion, and the recipient rats allowed to survive for 5–7 months. At this time the rats were reoperated under sodium pentobarbital (Nembutal) anesthesia and the transplants iontophoretically injected with PHA-L. Two weeks later the animals were again anesthetized, perfused, and processed for PHA-L immunocytochemistry and routine histology. Analysis of acetylcholinesterase- (AChE) and Nissl-stained sections showed graft survival in 19 of the 26 animals used in this study. When these 19 brains were processed for PHA-L immunocytochemistry, 5 of them were found with certainty to have the PHA-L injection confined to the transplant. Based on these cases PHA-L-reactive fibers arising from labelled transplant neurons were traced into the ipsilateral host neocortex adjacent to the transplant and found to project through the subcortical white matter to the ipsilateral parietal neocortical area 1, and claustrum. Callosal fibers were traced to the contralateral frontal neocortical forelimb and parietal areas. Transplant fibers were also observed to descend through the caudate putamen in the dispersed fiber bundles of the internal capsule to distribute as terminal branches and varicose fibers within the mesencephalic periaqueductal gray, red nucleus, deep mesencephalic nucleus, and intermediate gray of the superior colliculus, as well as in the pontine gray. Similar fibers and terminations were present in the caudate putamen, the reticular, ventrobasal, centrolateral, posterior, and parafascicular thalamic nuclei. On the side contralateral to the transplant, fewer fibers were observed in the caudate putamen, the ventrobasal, centrolateral, and posterior thalamic nuclei, as well as more caudally in the deep mesencephalic nucleus and the intermediate gray of the superior colliculus. Our findings demonstrate that homotopic grafts of fetal rat frontal neocortex can project to the developing host brain in a manner which for most projections corresponds to the normal rat neocortical parietal area 1–2 and forelimb area. The density of these transplant-to-host projections is, however, less than in the normal rat corticofugal pathways.