Bacterial invasion of oral tissues of immunosuppressed rats

Sallay, K; Listgarten, Max A.; Sanavi, F.; Ring, Ian; Nowotny, Alois

doi:10.1128/iai.43.3.1091-1093.1984

Cited by 43 publications

(17 citation statements)

References 4 publications

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“…If the host defenses are severely undermined, for example by the experimental elimination of the PMN population, bacterial invasion of the periodontal tissues and their destruction will be speeded up. In such an extreme case of weakened host defenses, which can be achieved experimentally in some animal systems, septicemia caused by unchecked bacterial invasion of the tissues may lead to rapid death of the host (50,51). The importance of PMNs in periodontal health and disease has been recently reviewed by Miller et al (52) Van Dyke et al (14) and Taichman et al (10).…”

Section: Indirect Toxicitymentioning

confidence: 99%

Nature of periodontal diseases: Pathogenic mechanisms

Listgarten

1987

J of Periodontal Research

185

115

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Section: Indirect Toxicitymentioning

confidence: 99%

Nature of periodontal diseases: Pathogenic mechanisms

Listgarten

1987

J of Periodontal Research

185

115

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“…a micro-organism which has been implicated in the etiology og Juvenile Periodontitis, can attach to the pocket epithelium and invade the periodontal con-nective tissue (Gillett & Johnson 1982). Sallay et al (1982Sallay et al ( . 1984 and Sanavi et al (1985) studied problems associated with bacteria!…”

mentioning

confidence: 99%

Lack of bacterial invasion in experimental periodontitis

Ericsson

Lindhe

Liljenberg

et al. 1987

J Clinic Periodontology

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The present study in the beagle dog was performed to analyze whether micro-organisms from a subgingival microbiota could be translocated into or had the potential to invade the pocket epithelium and the gingival connective tissue during a phase of rapid breakdown of the attachment apparatus. An attempt was also made to assess whether tetracycline therapy suppressed the subgingival microbiota and changed the size and quality of the lesions in the gingival tissue. 5 inbred beagle dogs were used. Throughout the period of experimentation, the animals were fed a soft diet permitting gross accumulation of plaque and calculus. No mechanical plaque control measures were performed during the course of the study. On day 0, a 120-day period of periodontal tissue breakdown was initiated at the right mandibular 3rd and 4th premolars by tying cotton floss ligatures around the neck of these teeth. The process of tissue breakdown at the mandibular left 3rd and 4th premolars was started 30 days later. The ligatures were replaced once every 2 weeks during the subsequent 4-month period. On experimental day 120, the first biopsy was performed and gingival tissue sections prepared for light and electron microscopic assessment of a series of histometric characteristics. On day 120, a 30-day period of tetracycline (per os) administration was initiated. Each dog was given a dose of 500 mg tetracycline twice daily. On day 150, the biopsy procedure was repeated in the mandibular left premolar regions.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…There is however the chnical observation that even in the terminal stages of periodontitis, the investing tissues have retreated in good order while, histologically, there is no inflammation in the underlying, reconstituted transeptal or alveolar crest fibres or the deeper periodontal ligament. To postulate invasion is to deny the slow rate of progress of the disease, even in its relatively severe forms, and to ignore the absence of micro-organisms from all but a minority of parts of ultrathin sections from large numbers of specimens (Liakoni et al 1986, 1987, Sallay et al 1984, Sanavi et al 1985, Saravanamuttu 1987, Vrahopoulos et al 1988, Joachim et al 1989, and to overlook the obvious capacity of plaque metabolites to enter the tissues and stimulate the contained host response. Rare translocation due to minor trauma may result in enhanced bacterial product entry, or, more infrequently, of bacteria.…”

Section: Evasion or Translocation?mentioning

confidence: 99%

Plaque and chronic inflammatory Periodontal disease A question of ecology

Newman

1990

J Clinic Periodontology

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The nature of the relationship between dental plaque and chronic inflammatory periodontal disease (CIPD) remains unclear, although there is no doubt that plaque is the direct cause. Non-specific, specific and exogenous hypotheses have been proposed to explain plaque-host relationships. Current evidence indicates that plaque is part of the natural human microflora, one of many such in nature, and that disruption of oral microbial ecology, due primarily to diet texture changes, leads to gingivitis and periodontitis. These result in increased plaque accumulation, and particularly in increased interdental effective plaque thickness. The latter leads to alterations in plaque ecology, particularly increasing anaerobiosis, with resultant shifts in proportions of its constituent species. These shifts are responsible for the increased counts of, for example, Bacteroides gingivalis, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Wolinella recta, spirochaetes and others, associated with chronic periodontitis in its various forms. Measures to prevent or control chronic periodontitis should aim, not to eliminate plaque, which ignores ecology and would compromise host defence, but to restore the species distribution in plaque to that compatible with health.

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Bacterial invasion of oral tissues of immunosuppressed rats

Cited by 43 publications

References 4 publications

Nature of periodontal diseases: Pathogenic mechanisms

Nature of periodontal diseases: Pathogenic mechanisms

Lack of bacterial invasion in experimental periodontitis

Plaque and chronic inflammatory Periodontal disease A question of ecology

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