Temperature as a periodontal diagnostic

Kung, R. T. V.; Ochs, B.; Goodson, J. Max

doi:10.1111/j.1600-051x.1990.tb01105.x

Cited by 66 publications

(34 citation statements)

References 8 publications

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“…Thus, HtrA protease activity is important for the ability of bacteria to respond to various stress situations. In the periodontal pocket, P. gingivalis survives various environmental stresses during the progression of periodontal disease (Fedi & Killoy, 1992;Kung et al, 1990;Lindskog et al, 1994;Meyerov et al, 1991). The role of HtrA under different stress conditions has been shown for several bacterial species, although the relevance is not universal among all the species tested.…”

Section: Discussionmentioning

confidence: 99%

“…P. gingivalis is found in subgingival plaque in periodontal pockets that have temperatures higher than normal body temperature and varying levels of oxygen (Fedi & Killoy, 1992;Kung et al, 1990;Lindskog et al, 1994;Mettraux et al, 1984;Meyerov et al, 1991;Tanaka et al, 1998). This is an environment in which the bacteria are frequently stressed and one in which they must compete in order to survive.…”

Section: Introductionmentioning

confidence: 99%

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Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival

et al. 2008

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HtrA is a heat-stress protein that functions both as a chaperone and as a serine protease. HtrA has been shown in several organisms to be involved in responses to stressful environmental conditions and involvement of HtrA in virulence has been reported in pathogenic species. A Porphyromonas gingivalis htrA mutant demonstrated no significant difference to the W83 parent strain when subjected to high temperature and pH values from 3 to 11. However, the htrA mutant showed increased sensitivity to H 2 O 2 . Cell invasion assays indicated that the total interaction (adherence) with KB cells, human coronary artery endothelial cells and gingival epithelial cells (GEC) was the same for both the wild-type and the htrA mutant. However, the htrA mutant showed increased invasion in KB cells and GEC. Microarray experiments indicated that a total of 253 genes were differentially regulated in the htrA mutant, including a group of stress-related genes, which might be responsible for the observed decreased resistance to H 2 O 2 . In animal experiments, a competition assay showed that the htrA mutant did not survive as well as the wild-type. In another in vivo assay, fewer mice infected with the htrA mutant died than mice infected with W83, suggesting that the htrA gene is virulence-related. These data indicate that the htrA gene in P. gingivalis does not relate to stress conditions such as high temperature and pH, but rather to H 2 O 2 stress. The htrA gene also appears to be important for virulence and survival in in vivo animal models.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival

et al. 2008

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“…The probe tip dimensions and shape are similar to those of a Michigan-O probe. Response time for thermal equilibrium from room temperature to 370C was reported to be less than a second, and accuracy of the probe was ± 0.10C (Kung et al, 1990;Niederman and Kent, 1993 Sampling number Figure 1. Depletion of MPO in gingival crevices of subjects before ingesting doughnuts.…”

Section: Measurement Of Subgingival Temperaturementioning

confidence: 99%

Gingival Inflammation Induced by Food and Short-chain Carboxylic Acids

Kashket¹,

Zhang²,

Niederman³

1998

J Dent Res

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Earlier studies in our laboratories demonstrated that particles of a number of snack foods that are retained on the dentition accumulate fermentable sugars and short-chain carboxylic acids (SCCA; acetic, formic, lactic, and propionic) to different degrees. The present study was undertaken to test the hypothesis that the accumulated SCCA can induce a gingival inflammatory response. Five periodontally and medically healthy subjects were given portions of plain doughnuts (high SCCA levels) or oatmeal cookie (low SCCA), or had the SCCA applied directly to the gingival margins of designated teeth. Subjects were given wax to chew, or nothing, as controls. Inflammation was assessed by measurements of subgingival temperature, flow rates of gingival crevicular fluid (GCF), and neutrophil emigration into GCF. Subgingival temperatures of the maxillary gingiva rose by 1.32 +/- 0.30 degrees C (mean +/- SE) 5 min after the subjects consumed the doughnuts and remained elevated for at least 1 hr. These values were significantly higher than those obtained from subjects after ingestion of oatmeal cookies (0.63 +/- 0.17 degree C; p < 0.01), consistent with the low levels of SCCA in the retained cookie particles. Wax chewing elicited a similar response, indicating a masticatory effect on the gingiva. Gingival temperatures in the unchallenged controls remained unchanged. Neutrophil emigration into the GCF was significantly elevated in subjects after doughnut consumption. Rinses with a solution of SCCA, or application of the SCCA to the gingiva, also brought about significant elevations in subgingival temperature and neutrophil emigration. The findings describe the inflammatory effects of food ingestion on the gingiva of healthy human subjects, and support the hypothesis that SCCA in the particles of retained food are at least partly responsible for the observed responses.

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“…Large temperature variations occur when hot and cold foods are consumed. Although the variation is smaller, inflammation at periodontal sites also causes an increase in temperature (Baab et al, 1990;Kung et al, 1990;Fedi and Killoy, 1992). Bacterial products (organic acids and proteases) can influence the pH of the oral cavity.…”

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confidence: 99%

Oral Microbial Heat-shock Proteins and Their Potential Contributions to Infections

Goulhen

Grenier

Mayrand

2003

Critical Reviews in Oral Biology & Medicine

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ABSTRACT:The oral cavity is a complex ecosystem in which several hundred microbial species normally cohabit harmoniously. However, under certain special conditions, the growth of some micro-organisms with a pathogenic potential is promoted, leading to infections such as dental caries, periodontal disease, and stomatitis. The physiology and pathogenic properties of micro-organisms are influenced by modifications in environmental conditions that lead to the synthesis of specific proteins known as the heat-shock proteins (HSPs). HSPs are families of highly conserved proteins whose main role is to allow micro-organisms to survive under stress conditions. HSPs act as molecular chaperones in the assembly and folding of proteins, and as proteases when damaged or toxic proteins have to be degraded. Several pathological functions have been associated with these proteins. Many HSPs of oral micro-organisms, particularly periodontopathogens, have been identified, and some of their properties-including location, cytotoxicity, and amino acid sequence homology with other HSPs-have been reported. Since these proteins are immunodominant antigens in many human pathogens, studies have recently focused on the potential contributions of HSPs to oral diseases. The cytotoxicity of some bacterial HSPs may contribute to tissue destruction, whereas the presence of common epitopes in host proteins and microbial HSPs may lead to autoimmune responses. Here, we review the current knowledge regarding HSPs produced by oral micro-organisms and discuss their possible contributions to the pathogenesis of oral infections.

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Temperature as a periodontal diagnostic

Cited by 66 publications

References 8 publications

Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival

Porphyromonas gingivalis htrA is involved in cellular invasion and in vivo survival

Gingival Inflammation Induced by Food and Short-chain Carboxylic Acids

Oral Microbial Heat-shock Proteins and Their Potential Contributions to Infections

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