Identification of tissue‐invading bacteria in human periodontal disease

Saglie, F. R.; Carranza, Fermín A.; Newman, Michael G.; Cheng, Linyin; Lewin, Klaus J.

doi:10.1111/j.1600-0765.1982.tb02024.x

Cited by 166 publications

(91 citation statements)

References 8 publications

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“…In periodontitis, approximately 85% of bacteria are gram negative and among them, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) (formerly known as Actinobacillus actinomycetemcomitans), Tannerella forsythensis (T. forsythensis) (formerly known as Bacteroides forsythu),Porphyromonas gingivalis (P. gingivalis), Treponema denticola (T. denticola), Campylobacter rectus (C. rectus) and Fusobacterium nucleatum (F. nucleatum) are considered important periodontal pathogens [117]. In the periodontal pocket, periodontophatic bacteria occurs close to the soft tissue wall [38] favoring the invasion of epithelial and connective tissue [104] by some bacteria.…”

Section: Periodontal Bacteriamentioning

confidence: 99%

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Kamer¹,

Dasanayake²,

Craig³

et al. 2008

JAD

153

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Abstract. Alzheimer's disease (AD) affects approximately 4.5 million people in the U.S. and this number will increase as the population ages and the life-span increases. Therefore, of paramount importance is identifying mechanisms and factors that affect the risk of developing AD. The etiology and pathogenic mechanisms for AD have not been defined, although inflammation within the brain is thought to play a role. Consistent with this hypothesis, studies suggest that peripheral infections contribute to the inflammatory state of the central nervous system. Periodontitis is a prevalent, persistent peripheral infection associated with gram negative, anaerobic bacteria that are capable of exhibiting localized and systemic infections in the host. This review offers a hypothetical link between periodontitis and AD and will present possible mechanistic links between periodontitis related inflammation and AD. It will review the pathogenesis of periodontitis and the mechanisms by which periodontal infections may affect the onset and progression of AD. Since periodontitis is a treatable condition, it may be a readily modifiable risk factor for AD.

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Section: Periodontal Bacteriamentioning

confidence: 99%

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Kamer¹,

Dasanayake²,

Craig³

et al. 2008

JAD

153

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“…Once established in the oral cavity, A. actinomycetemcomitans has been found inside gingival tissues (11,49) and mucosal epithelium apart from the gingiva (47). The adhesive and invasive nature of A. actinomycetemcomitans has been examined with an in vitro model (35,36,52).…”

mentioning

confidence: 99%

Aae, an Autotransporter Involved in Adhesion of Actinobacillus actinomycetemcomitans to Epithelial Cells

2003

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“…Periodontal diseases are characterized by mixed bacterial infections associated with progressive destruction of the tissue surrounding and supporting the teeth (37,41,46,54,55). Oral spirochetes, including Treponema denticola, are associated with both acute and chronic periodontal diseases and are frequently found in high numbers at diseased sites (3,38,40,60).…”

mentioning

confidence: 99%

“…Oral spirochetes, including Treponema denticola, are associated with both acute and chronic periodontal diseases and are frequently found in high numbers at diseased sites (3,38,40,60). The interaction of periodontal organisms with host tissues is complex, involving mechanisms of adhesion, proteolysis, and evasion and modulation of the immune system (37,39,46,54,55). T. denticola binds to a number of extracellular matrix (ECM) components and other host factors that may mediate binding to gingival tissue (11,18,23).…”

mentioning

confidence: 99%

Sequence analysis, expression, and binding activity of recombinant major outer sheath protein (Msp) of Treponema denticola

1996

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The gene encoding the major outer sheath protein (Msp) of the oral spirochete Treponema denticola ATCC 35405 was cloned, sequenced, and expressed in Escherichia coli. Preliminary sequence analysis showed that the 5 end of the msp gene was not present on the 5.5-kb cloned fragment described in a recent study ( showing the msp transcript to be approximately 1.7 kb was consistent with the identification of a promoter consensus sequence located optimally upstream of msp and a transcription termination signal found downstream of the stop codon. The entire msp sequence was amplified from T. denticola genomic DNA and cloned in E. coli by using a tightly regulated T7 RNA polymerase vector system. Expression of Msp was toxic to E. coli when the entire msp gene was present. High levels of Msp were produced as inclusion bodies when the putative signal peptide sequence was deleted and replaced by a vector-encoded T7 peptide sequence. Recombinant Msp purified to homogeneity from a clone containing the full-length msp gene adhered to immobilized laminin and fibronectin but not to bovine serum albumin. Attachment of recombinant Msp was decreased in the presence of soluble substrate. Attachment of T. denticola to immobilized laminin and fibronectin was increased by pretreatment of the substrate with recombinant Msp. These studies lend further support to the hypothesis that Msp mediates the extracellular matrix binding activity of T. denticola.

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Identification of tissue‐invading bacteria in human periodontal disease

Cited by 166 publications

References 8 publications

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Alzheimer's Disease and Peripheral Infections: The Possible Contribution from Periodontal Infections, Model and Hypothesis

Aae, an Autotransporter Involved in Adhesion of Actinobacillus actinomycetemcomitans to Epithelial Cells

Sequence analysis, expression, and binding activity of recombinant major outer sheath protein (Msp) of Treponema denticola

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