The Polymerisation of Dietary Sugars by Dental Plaque

Critchley, Peter; Wood, Jeanie M.; Saxton, C. A.; Leach, Steve

doi:10.1159/000259506

Cited by 114 publications

(46 citation statements)

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“…Micro-organisms incorporate SA into their cell surface, which helps them evade the innate immune response of the host [4]. Removal of terminal SA (either by neuraminidase (sialidase) enzyme of virulent bacteria or by inherited disorder of host endogenous neuraminidase) from sialylated glycoprotein, could incorporate onto the surface of developing plaque which may play a role in plaque formation and cause destruction of host tissue [5]. SA is present in several acute phase proteins which are known to be associated with periodontitis [6].…”

Section: Introductionmentioning

confidence: 99%

Estimation of Salivary and Serum Total Sialic Acid Levels in Periodontal Health and Disease

Rathod

Khan

Kolte

et al. 2014

JCDR

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Background: Chronic gingivitis and periodontitis are inflammatory diseases. An important function of host sialic acid is to regulate innate immunity. The aim of the study was to assess the concentration of Total sialic acid (TSA) in saliva and serum and also to find out their association if any, in periodontal health and disease. Materials and Methods:A total of 90 subjects were clinically examined and distributed into three groups (n=30) according to the periodontal status namely healthy, chronic gingivitis and chronic periodontitis.Clinical measurements including probing depth, clinical attachment level, gingival index, oral hygeine index were recorded .TSA concentration was determined in saliva and serum of all subjects. Results:In healthy group the mean salivary TSA level was 39.05mg/dl ±6.35(p<0.0001), mean serum TSA level was 49.75 mg/dl ± 4.87 (p<0.0001). In the chronic gingivitis group the mean salivary TSA level was 68.23 mg/dl ± 2.71 (p<0.0001), mean serum TSA level was 65.65 mg/dl ±3.56 (p<0.0001). In the chronic periodontitis group the mean salivary TSA was 81.33 mg/dl ±3.94 (p<0.0001), mean serum TSA level was 75.98 mg/ dl ±3.58 (p<0.0001).

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Section: Introductionmentioning

confidence: 99%

Estimation of Salivary and Serum Total Sialic Acid Levels in Periodontal Health and Disease

Rathod

Khan

Kolte

et al. 2014

JCDR

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“…Gtf-SI, which is bound to a solid surface, synthesizes a mixture of soluble 1,6-bonds and insoluble glucans and acts as the attachment site for bacteria (4,5). Gtf-S produces soluble glucans, which serve as primers for Gtf-I activity (6,7). Fructan is synthesized by Ftf from sucrose and serves as a nutrient source for biofilm cells (8).…”

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confidence: 99%

Raffinose Induces Biofilm Formation by Streptococcus mutans in Low Concentrations of Sucrose by Increasing Production of Extracellular DNA and Fructan

Nagasawa

Sato

Senpuku

2017

Appl Environ Microbiol

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Streptococcus mutans is the primary etiological agent of dental caries and causes tooth decay by forming a firmly attached biofilm on tooth surfaces. Biofilm formation is induced by the presence of sucrose, which is a substrate for the synthesis of extracellular polysaccharides but not in the presence of oligosaccharides. Nonetheless, in this study, we found that raffinose, which is an oligosaccharide with an intestinal regulatory function and antiallergic effect, induced biofilm formation by S. mutans in a mixed culture with sucrose, which was at concentrations less than those required to induce biofilm formation directly. We analyzed the possible mechanism behind the small requirement for sucrose for biofilm formation in the presence of raffinose. Our results suggested that sucrose contributed to an increase in bacterial cell surface hydrophobicity and biofilm formation. Next, we examined how the effects of raffinose interacted with the effects of sucrose for biofilm formation. We showed that the presence of raffinose induced fructan synthesis by fructosyltransferase and aggregated extracellular DNA (eDNA, which is probably genomic DNA released from dead cells) into the biofilm. eDNA seemed to be important for biofilm formation, because the degradation of DNA by DNase I resulted in a significant reduction in biofilm formation. When assessing the role of fructan in biofilm formation, we found that fructan enhanced eDNA-dependent cell aggregation. Therefore, our results show that raffinose and sucrose have cooperative effects and that this induction of biofilm formation depends on supportive elements that mainly consist of eDNA and fructan.IMPORTANCE The sucrose-dependent mechanism of biofilm formation in Streptococcus mutans has been studied extensively. Nonetheless, the effects of carbohydrates other than sucrose are inadequately understood. Our findings concerning raffinose advance the understanding of the mechanism underlying the joint effects of sucrose and other carbohydrates on biofilm formation. Since raffinose has been reported to have positive effects on enterobacterial flora, research on the effects of raffinose on the oral flora are required prior to its use as a beneficial sugar for human health. Here, we showed that raffinose induced biofilm formation by S. mutans in low concentrations of sucrose. The induction of biofilm formation generally generates negative effects on the oral flora. Therefore, we believe that this finding will aid in the development of more effective oral care techniques to maintain oral flora health.

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“…The biofilm known as dental plaque is composed of bacteria embedded in a matrix of glucan and fructan polysaccharide [Critchley et al, 1967[Critchley et al, , 1968Hotz et al, 1972]. The glucan is a polymer of glucose synthesized from dietary sucrose and possibly additional oligosaccharides, by glucosyltransferase enzymes (Gtf, EC 2.4.1.5) produced by oral streptococci [Hamada and Slade, 1980;Loesche, 1986;Vacca-Smith et al, 1996a, b].…”

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Studies Concerning the Glucosyltransferase of <i>Streptococcus sanguis</i>

et al. 2000

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We have shown in previous studies that the glucosyltransferase (Gtf) enzymes of Streptococcus mutans have distinct properties when adsorbed to a surface. In the present study, we compared the activity of Gtf from Streptococcus sanguis, designated GtfSs, in solution and on the surface of saliva–coated hydroxyapatite (sHA) beads, and determined the ability of its product glucan to support the adherence of oral microorganisms. Gtf from S. sanguis 804 NCTC 10904 was purified from culture supernatant fluids by means of hydroxyapatite chromatography. Enzyme and the substrate were prepared in buffers at pH values from 3.5 to 7.5. Maximum activity of GtfSs occurred between pH 5.5 and pH 6.5, whether in solution or adsorbed onto a surface. The solubilized and insolubilized enzymes showed highest activity at 40°C; activity was reduced by 50(±2)% at 20 and 30°C. The enzyme did not form glucans in either phase at 10 or 60°C. The K_m, determined from Lineweaver–Burk plots, for the enzyme in solution was 4.3(±0.4) mmol/l sucrose, and the K_m for the enzyme on sHA beads was 5.0(±1.0) mmol/l sucrose. The ability of the GtfSs glucan synthesized on the surface of sHA beads to support the adherence of oral bacteria was investigated. ³H–thymidine–labeled bacteria (S. mutans GS–5, S. sobrinus 6715, S. sobrinus 6716, S. sanguis 10904, Actinomyces viscosus OMZ105E, A. viscosus 2085, and A. viscosus 2086) were incubated with sHA beads coated with GtfSs glucan. S. mutans GS–5 displayed the highest level of binding numerically. These results show that the GtfSs of S. sanguis is active on sHA beads, that the pH optimum for activity on a surface differs slightly from that in solution, and that its product glucan can support the adherence of oral microorganisms.

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The Polymerisation of Dietary Sugars by Dental Plaque

Cited by 114 publications

References 1 publication

Estimation of Salivary and Serum Total Sialic Acid Levels in Periodontal Health and Disease

Estimation of Salivary and Serum Total Sialic Acid Levels in Periodontal Health and Disease

Raffinose Induces Biofilm Formation by Streptococcus mutans in Low Concentrations of Sucrose by Increasing Production of Extracellular DNA and Fructan

Studies Concerning the Glucosyltransferase of <i>Streptococcus sanguis</i>

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