The Concentration of Lipopolysaccharide on Individual Root Surfaces at Varying Times Following in <i>Vivo</i> Root Planing

McCoy, Sandra A.; Creamer, Howard R.; Kawanami, Masamitsu; Adams, Donald F.

doi:10.1902/jop.1987.58.6.393

Cited by 43 publications

(18 citation statements)

References 14 publications

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“…[18][19][20][21][22][23][24][25][26][27][28][29][30] In vitro studies on the reduction of the biological activities of LPS with mild alkali, sodium dodecylsulphate, and EDTA (ethylene diamine tetraacetic acid) had been previously carried out. [31][32][33] In this study, Er: YAG laser irradiation has been found to be effective for dental hard tissues with little damage to the surrounding structures, except the irradiated areas.…”

Section: Discussionmentioning

confidence: 99%

Effects of Irradiation of an Erbium: YAG Laser on Root Surfaces

Yamaguchi¹,

Kobayashi²,

Osada³

et al. 1997

Journal of Periodontology

152

112

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The application of erbium:yag laser (Er:YAG) irradiation has been investigated for periodontal therapy. The purpose of this study was to evaluate the effects of Er: YAG laser irradiation on root surfaces using a scanning electron microscope (SEM) and to determine the laser's ability to remove lipopolysaccharides (LPS). Infrared spectrophotometry was used to investigate the effects of the laser on LPS applied to root dentin pellets. Premolare extracted for orthodontic reasons were prepared for this study. The crowns were resected below the cemento-enamel junction, longitudinally sectioned, and the contents of the pulp chamber were removed. Then 15 root tips (5X5X1 mm) were classified into 3 groups of 5 each as follows: group 1, tips without any treatment; group 2, planed tips with the cement layers left untouched; and group 3, planed until the dentin surface was disclosed. The center of each specimen was used as the experimental irradiated area and the peripheral area served as a control. The quantity of vapor delivered by Er: YAG laser was highly increased, and the irradiated areas displayed little morphogenetic changes. The lyophilized sample LPS 0111 B4 from E. coli was then mixed with potassium bromide and pressed into a tablet, which was examined at 4,000-650 Kayser. The lyophilized LPS had a peak at 2.94 µ . LPS on the root dentin pellets was cleared away as much as possible by 150 washings in pyrogen-free water using an ultrasonic cleaner. Five µ of 24 EU LPS solution was dropped on the root dentin pellets, which were then irradiated by the Er: YAG laser, and washed using the ultrasonic cleaner in pyrogen-free water. The amount of the extracted LPS solution was determined by spectrophotometer at 405nm. The Er: YAG laser could remove 83.1% of the LPS. This study suggests that Er:YAG laser irradiation might be useful for root conditioning in periodontal therapy. However, clinical testing is necessary to establish what, if any, utility the Er:YAG laser has as a part of periodontal therapy.

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Section: Discussionmentioning

confidence: 99%

Effects of Irradiation of an Erbium: YAG Laser on Root Surfaces

Yamaguchi¹,

Kobayashi²,

Osada³

et al. 1997

Journal of Periodontology

152

112

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“…The innate host response is critical to maintaining a clinically healthy periodontium (18,61), and studies have shown that in healthy individuals a highly orchestrated protective response is found (18,61). P. gingivalis, which resides in close proximity to the gingival epithelial cell surface, releases copious amounts of outer membrane vesicles containing LPS (23,24) which can penetrate periodontal tissue (37,39,53) and have direct inhibitory effects on the highly vascularized tissue adjacent to the tooth root surface. The interruption of endothelial cell responses to LPS is similar to earlier observations (15,35) demonstrating inhibition of IL-8 secretion after invasion of epithelial cells by viable P. gingivalis.…”

Section: Fig 4 Inhibition Of P38 Map Kinase Phosphorylation By P Gmentioning

confidence: 99%

Porphyromonas gingivalisLipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation

Darveau¹,

Arbabi

Garcia

et al. 2002

Infect Immun

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Lipopolysaccharide (LPS) is a key inflammatory mediator. It has been proposed to function as an important molecule that alerts the host of potential bacterial infection. Although highly conserved, LPS contains important structural differences among different bacterial species that can significantly alter host responses. For example, LPS obtained from Porphyromonas gingivalis, an etiologic agent for periodontitis, evokes a highly unusual host cell response. Human monocytes respond to this LPS by the secretion of a variety of different inflammatory mediators, while endothelial cells do not. In addition, P. gingivalis LPS inhibits endothelial cell expression of E-selectin and interleukin 8 (IL-8) induced by other bacteria. In this report the ability of P. gingivalis LPS to activate p38 mitogen-activated protein (MAP) kinase was investigated. It was found that p38 MAP kinase activation occurred in response to P. gingivalis LPS in human monocytes. In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4). In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli-induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4. These data demonstrate that P. gingivalis LPS activates the LPS-associated p38 MAP kinase in monocytes and that it can be an antagonist for E. coli LPS activation of p38 MAP kinase in endothelial and CHO cells. These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization.The innate host defense system protects mammalian hosts against microbial infection through an orchestrated response to the presence of nonself components (31, 32). Lipopolysaccharide (LPS), a component of the gram-negative bacterial cell wall, is a key structure recognized by a variety of different innate host defense proteins, allowing the host to "sense" a potential bacterial infection (8,62). LPS is evolutionarily an ideal target, since it is a conserved structure found on a wide variety of pathogenic bacteria and is sufficiently different from host components to allow a safe selective response (38). However, there are important structural differences in LPS composition between different bacterial species, such as fatty acid acyl chain composition and charge, which can significantly affect the host response (33,36,42,49,64). Different binding affinities for LPS binding protein and CD14 may only partly explain the lowered inflammatory response to some LPS species that has been observed (14), consistent with the notion that the major role of LPS binding protein and CD14 is to concentrate LPS at host cell surfaces (65). Recently it has been demonstrated that cell surface Toll-like receptor (TLR) proteins participate in the ability of the host to discriminate different LPS structural f...

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“…This bacterium releases copious amounts of outer membrane vesicles containing LPS (19,20), which can penetrate periodontal tissue (38,39,50) and thus participate in the destructive innate host response associated with disease. The potential contribution of P. gingivalis LPS to the disease process is not clear, however, due to complex innate host responses to this cell wall component (4).…”

mentioning

confidence: 99%

Porphyromonas gingivalis Lipopolysaccharide Contains Multiple Lipid A Species That Functionally Interact with Both Toll-Like Receptors 2 and 4

Darveau¹,

Pham²,

Lemley³

et al. 2004

Infect Immun

456

553

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The innate host response to lipopolysaccharide (LPS) obtained from Porphyromonas gingivalis is unusual in that different studies have reported that it can be an agonist for Toll-like receptor 2 (TLR2) as well as an antagonist or agonist for TLR4. In this report it is shown that P. gingivalis LPS is highly heterogeneous, containing more lipid A species than previously described. In addition, purification of LPS can preferentially fractionate these lipid A species. It is shown that an LPS preparation enriched for lipid A species at m/z 1,435 and 1,450 activates human and mouse TLR2, TLR2 plus TLR1, and TLR4 in transiently transfected HEK 293 cells coexpressing membrane-associated CD14. The HEK cell experiments further demonstrated that cofactor MD-2 was required for functional engagement of TLR4 but not of TLR2 nor TLR2 plus TLR1. In addition, serum-soluble CD14 effectively transferred P. gingivalis LPS to TLR2 plus TLR1, but poorly to TLR4. Importantly, bone marrow cells obtained from TLR2؊/؊ and TLR4 ؊/؊ mice also responded to P. gingivalis LPS in a manor consistent with the HEK results, demonstrating that P. gingivalis LPS can utilize both TLR2 and TLR4. No response was observed from bone marrow cells obtained from TLR2 and TLR4 double-knockout mice, demonstrating that P. gingivalis LPS activation occurred exclusively through either TLR2 or TLR4. Although the biological significance of the different lipid A species found in P. gingivalis LPS preparations is not currently understood, it is proposed that the presence of multiple lipid A species contributes to cell activation through both TLR2 and TLR4.

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The Concentration of Lipopolysaccharide on Individual Root Surfaces at Varying Times Following in Vivo Root Planing

Cited by 43 publications

References 14 publications

Effects of Irradiation of an Erbium: YAG Laser on Root Surfaces

Effects of Irradiation of an Erbium: YAG Laser on Root Surfaces

Porphyromonas gingivalisLipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation

Porphyromonas gingivalis Lipopolysaccharide Contains Multiple Lipid A Species That Functionally Interact with Both Toll-Like Receptors 2 and 4

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