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PubMed1997

Effects of triclosan and triclosan monophosphate on maximum specific growth rates, biomass and hydrolytic enzyme production of Streptococcus sanguis and Capnocytophaga gingivalis in continuous culture.

Dental plaque species, Streptococcus sanguis and Capnocytophaga gingivalis, were grown in continuous culture with progressively increasing concentrations of triclosan or its phosphorylated derivative, triclosan monophosphate (TMP). For both organisms, the maximum specific growth rates decreased with increasing concentrations of triclosan or TMP until complete inhibition of growth occurred, which for S. sanguis was at 20 mg/L and 50 mg/L, and for C. gingivalis was at 10 mg/L and 5 mg/L for triclosan and TMP respectively. For both species, biomass levels remained approximately constant or, in some cases, increased slightly at low levels of triclosan or TMP. However, biomass levels then decreased significantly as the triclosan or TMP concentrations approached lethal levels. For S. sanguis, levels of hydrolytic enzymes (acid phosphatase, leucine aminopeptidase and esterase) generally remained approximately constant or increased with increasing concentrations of triclosan or TMP until close to inhibitory levels where enzyme levels were reduced. The ratio of extracellular soluble enzymes to cell-bound enzymes remained constant or increased slightly with increasing levels of triclosan or TMP. For C. gingivalis, production of hydrolytic enzymes (neutral phosphatase, leucine aminopeptidase and trypsin-like protease) remained constant or were reduced when grown with low levels of triclosan and TMP but in some cases increased with higher levels of agents. The proportion of extracellular soluble activity increased significantly when concentrations of agent neared inhibitory levels. The results taken together show that the physiology of cells is significantly altered and that hydrolytic enzymes are released from the cells when these are grown in the presence of increasing concentrations of triclosan or TMP. Enzyme release is more pronounced in the Gram-negative C. gingivalis and indicates that triclosan or TMP can cause membrane perturbation with subsequent release of membrane-located (S. sanguis) or periplasmic (C. gingivalis) hydrolytic enzymes. S. sanguis was more sensitive to triclosan than TMP while C. gingivalis was more sensitive to TMP. This suggests that, in C. gingivalis, TMP may diffuse into the cell wall more easily than triclosan and then be converted to triclosan by phosphatase activity within the cell wall complex, where it may give rise to high localized concentrations and subsequent cell damage.

Acid Phosphatase↗
PubMed2002

Chemistry and safety of triclosan, and its use as an antimicrobial coating on Coated VICRYL* Plus Antibacterial Suture (coated polyglactin 910 suture with triclosan).

BACKGROUND: The safety of the antimicrobial agent triclosan was reviewed, and the biocompatibility of coated polyglactin 910 suture with triclosan was evaluated. METHODS: Acute single exposure LD(50) values for triclosan were determined in multiple species by several routes of administration. Subacute to chronic toxicity for dermal and oral exposure to triclosan was determined in multiple species in studies of up to one year's duration. Chronic oral toxicity/carcinogenicity potential was determined in 2-year studies in rodents and non-rodents. The genotoxicity potential of triclosan was determined using a battery of standard assays. Reproductive toxicity and teratology studies were conducted in rodents and non-rodents. Immunotoxicity studies in guinea pigs and the repeat-insult patch test in humans were conducted to assess the potential for sensitization reactions. Pharmacokinetic studies were conducted in animals and humans to understand the metabolic profile of triclosan. Preclinical biocompatibility studies conducted on coated polyglactin 910 suture with triclosan included in vitro cytotoxicity, in vivo intracutaneous reactivity, material-mediated pyrogenicity, and intramuscular tissue reaction/absorption studies. RESULTS: The oral LD(50) values for triclosan ranged from 3,750 to 5,000 mg/kg, whereas the LD(50) after subcutaneous injection was >14,600 mg/kg. Safety factors calculated from repeated daily dosing studies ranged from 1,000 to 25,000 times the no-observed-effect levels. There was no evidence of carcinogenic potential in either species, and genotoxicity studies were negative. Reproductive toxicity studies did not reveal any evidence of teratogenic potential. There was no evidence of skin sensitization potential in controlled studies. Pharmacokinetic studies in animals and humans have shown that triclosan is rapidly absorbed, well distributed in the body, metabolized in the liver, and excreted by the kidneys, with no indication of accumulation over time. Biocompatibility studies showed that coated polyglactin 910 suture with triclosan was non-cytotoxic, non-irritating, and not a chemical pyrogen. In addition, an intramuscular implantation study demonstrated a tissue reaction, a healing response, and an absorption profile comparable to current polyglactin 910 suture. CONCLUSION: The extensive toxicology database supporting the safety of triclosan and the biocompatibility studies conducted on coated polyglactin 910 suture with triclosan demonstrate the safety of this suture for clinical use. Considering the clinical relevance of surgical site infections and the relatively low level of triclosan required to inhibit bacterial colonization of the suture, the use of this antimicrobial technology is well suited to this application.

Animals↗
PubMed2005

Fate of triclosan and triclosan-methyl in sewage treatment plants and surface waters.

The fate of triclosan in diverse stages of two sewage treatment processes has been determined. The elimination process differed considerably depending on the technology applied in the respective sewage treatment plant (STP). The plant operating with a two-stage biologic (activated sludge) process removed triclosan more efficiently than the STP with a combination of physical and activated sludge process. The treatment in the aeration basin was the dominant elimination mechanism, whereas the final biologic filter was not very effective. The elimination rates for triclosan were 87% and 95%, respectively. These data were compared with emissions of a multitude of STPs in the river Ruhr catchment area as well as triclosan and its known transformation product, triclosan-methyl, in the river. The concentrations of both compounds were between <3 and 10 ng/L in true surface-water samples for triclosan and between 0.3 and 10 ng/L for triclosan-methyl. The STP effluents held higher concentrations (10 to 600 ng/L triclosan). The ratio of triclosan to triclosan-methyl did not change significantly within the longitudinal profile of the river, but diverse STPs discharging to the river exhibited individual triclosan-to-triclosan-methyl ratios. From the riverine concentration data, in-river elimination rates and half-life were estimated.

Environmental Monitoring↗
PubMed1994

Experiments with triclosan-containing mouthrinses: dose response--and an attempt to locate the receptor site(s) of triclosan in the mouth.

A double-blind cross-over clinical study was performed on eight volunteers to determine the plaque-inhibiting effect of different triclosan- and sodium lauryl sulfate (SLS)-containing mouthrinses. An attempt was also made to locate the binding site(s) of triclosan in the oral cavity. After the volunteers rinsed for four days with solutions of various concentrations of triclosan and/or SLS, plaque deposits were scored according to the Silness and Löe Plaque Index. The study showed that 0.15% and 0.3% concentrations of triclosan yielded a comparable plaque-inhibiting effect in vivo. Furthermore, the 0.1% triclosan with 1.5% SLS exhibited a higher (though not significant) effect than 0.1% triclosan with 0.75% SLS. The mouthrinse containing 0.05% triclosan and 0.25% SLS was as effective as the two mentioned mouthrinses containing 0.1% triclosan. Collectively, the results indicate that triclosan alone has an antiplaque effect, independent of the effect of SLS. Furthermore, the results suggest that the SLS monomers may play a role as carriers of triclosan and that the teeth are not the only binding site of triclosan, since topical application of 0.3% triclosan failed to produce a clinically discernible effect.

Adult↗
PubMed2004

Occurrence of methyl triclosan, a transformation product of the bactericide triclosan, in fish from various lakes in Switzerland.

The bactericide triclosan and methyl triclosan, an environmental transformation product thereof, have been previously detected in lakes and a river in Switzerland. Both compounds are emitted via wastewater treatment plants (WWTPs), with methyl triclosan probably being formed by biological methylation. Passive sampling with semi-permeable membrane devices (SPMDs) showed the presence of methyl triclosan in some lakes, suggesting some potential for bioaccumulation of the compound. In this study, we report the presence of methyl triclosan in fish (white fish, Coregonus sp.; roach, Rutilus rutilus) from various lakes in Switzerland receiving inputs from WWTPs. Identification of the compound was based on mass spectral (MS) evidence including MS/MS data. The concentrations of methyl triclosan in the fish were up to 35 ng g(-1) on a wet weight basis and up to 365 ng g(-1) on a lipid basis with concentrations in a relatively narrow range for fish from the same lake (Thunersee, 4-6 ng g(-1); Zürichsee, 32-62 ng g(-1); Pfäffikersee, 43-56 ng g(-1); Greifensee, 165-365 ng g(-1), lipid basis). No methyl triclosan (<1 ng g(-1), lipid basis) was detected in fish (lake trout, Salmo trutta) from a remote lake in Sweden (Häbberstjärnen) and in fish (roach) from a small lake in Switzerland with no input from WWTPs (Hüttnersee, <2-<5 ng g(-1), lipid basis). The concentrations of methyl triclosan in fish correlated (r2 = 0.85) with the ratio of population in the watershed to water throughflow of the lakes (P/Q ratio), which is considered to be a measure for the domestic burden from WWTPs to a lake. Passive sampling with SPMDs confirmed the presence of methyltriclosan in lakes and a river (Zürichsee and Greifensee; Limmat) but not in a remote mountain lake (Jörisee) and in Hüttnersee. The bioconcentration factor (BCF) of methyl triclosan estimated from the fish data and SPMD-derived water concentrations was in the order of 1-2.6 x 10(5) (lipid basis) and thus in the range of other persistent organic pollutants. SPMDs were found to be reliable for monitoring low concentrations of methyl triclosan in surface water. Methyl triclosan appears to be a suitable marker for WWTP-derived lipophilic contaminants in the aquatic environment and fish.

Animals↗
PubMed2000

Ecological effects of triclosan and triclosan monophosphate on defined mixed cultures of oral species grown in continuous culture.

The effects of triclosan and its phosphorylated derivative, triclosan monophosphate were studied using a continuous culture microcosm model. Two conditions were simulated, a caries-like state (pH 5.5 with artificial saliva plus glucose as growth medium) and a periodontal disease-like state (pH 7.5 with BHI plus yeast extract, haemin and cysteine as growth medium). Both cultures were maintained anaerobically at 37 degrees C at a growth rate of 0.1/h. Steady-state chemostats were pulsed with triclosan or triclosan monophosphate (initial concentrations between 20 and 40 mg/L) and changes in the ecological composition noted after 6 h. The caries-like microcosm steady state was dominated by streptococci, Lactobacillus and Veillonella sp. with low but detectable levels of Neisseria, Actinomyces and Fusobacterium sp. No significant ecological shifts occurred following pulses of either antimicrobial agent; all species were affected to approximately the same degree. The periodontal disease-like microcosm steady state was dominated by streptococci, Fusobacterium, Veillonella, Actinomyces, Prevotella and Porphyromonas sp. with low numbers of Neisseria and Lactobacillus sp. Significant ecological shifts were apparent following pulses of triclosan. The streptococci became the dominant group followed by Fusobacterium sp. For triclosan monophosphate, the streptococci again became dominant although Lactobacillus and Actinomyces were now the main sub-dominant species and Gram-negative anaerobes including Fusobacterium sp. were markedly inhibited. It is concluded that in the periodontal disease state, both triclosan and triclosan monophosphate affected the Gram-negative anaerobes to a greater extent than the Gram-positive groups and that this effect was more marked for triclosan monophosphate.

Anti-Infective Agents, Local↗
PubMed2004

Inhibition of the bacterial enoyl reductase FabI by triclosan: a structure-reactivity analysis of FabI inhibition by triclosan analogues.

To explore the molecular basis for the picomolar affinity of triclosan for FabI, the enoyl reductase enzyme from the type II fatty acid biosynthesis pathway in Escherichia coli, an SAR study has been conducted using a series of triclosan analogues. Triclosan (1) is a slow, tight-binding inhibitor of FabI, interacting specifically with the E.NAD(+) form of the enzyme with a K(1) value of 7 pM. In contrast, 2-phenoxyphenol (2) binds with equal affinity to the E.NAD(+) (K(1) = 0.5 microM) and E.NADH (K(2) = 0.4 microM) forms of the enzyme and lacks the slow-binding step observed for triclosan. Thus, removal of the three triclosan chlorine atoms reduces the affinity of the inhibitor for FabI by 70,000-fold and removes the preference for the E.NAD(+) FabI complex. 5-Chloro-2-phenoxyphenol (3) is a slow, tight-binding inhibitor of FabI and binds to the E.NAD(+) form of the enzyme (K(1) = 1.1 pM) 7-fold more tightly than triclosan. Thus, while the two ring B chlorine atoms are not required for FabI inhibition, replacement of the ring A chlorine increases binding affinity by 450,000-fold. Given this remarkable observation, the SAR study was extended to the 5-fluoro-2-phenoxyphenol (4) and 5-methyl-2-phenoxyphenol (5) analogues to further explore the role of the ring A substituent. While both 4 and 5 are slow, tight-binding inhibitors, they bind substantially less tightly to FabI than triclosan. Compound 4 binds to both E.NAD(+) and E.NADH forms of the enzyme with K(1) and K(2) values of 3.2 and 240 nM, respectively, whereas compound 5 binds exclusively to the E.NADH enzyme complex with a K(2) value of 7.2 nM. Thus, the ring A substituent is absolutely required for slow, tight-binding inhibition. In addition, pK(a) measurements coupled with simple electrostatic calculations suggest that the interaction of the ring A substituent with F203 is a major factor in governing the affinity of analogues 3-5 for the FabI complex containing the oxidized form of the cofactor.

Anti-Bacterial Agents↗
PubMed2004

The role of Triclosan in dentifrice formulations, with particular reference to a new 0.3% Triclosan calcium carbonate-based system.

AIM: To discuss the role of Triclosan in dentifrice systems and demonstrate the enhanced efficacy of Triclosan in calcium carbonate-based systems when the level of the antimicrobial agent is raised from 0.2% to 0.3%. Triclosan is the most commonly used antimicrobial agent in oral care products, being compatible with a wide range of ingredients found in toothpaste formulations, whilst having no negative sensory features (e.g. taste, staining) that are associated with some other antimicrobial/anti-plaque agents. Triclosan is a broad spectrum antimicrobial agent, with additional anti-metabolic and anti-inflammatory properties. When delivered to the mouth in oral care products, Triclosan can selectively inhibit Gram negative anaerobic bacteria implicated in gingivitis and periodontal diseases, while leaving species associated with oral health relatively unaffected. Worldwide, attempts have been made to boost delivery/activity of Triclosan, either by use of copolymers or by combination with other agents such as zinc citrate. However, Triclosan has also been shown to maintain clinical efficacy against plaque and gingivitis when present as the sole antimicrobial in toothpaste formulations.

Anti-Infective Agents, Local↗
PubMed2002

Experimental gingivitis studies: effects of triclosan and triclosan-containing dentifrices on dental plaque and gingivitis in three-week randomized controlled clinical trials.

A recently reported six-month gingivitis study demonstrated that in subjects with gingivitis, a triclosan/pyrophosphate dentifrice provided supragingival plaque control. The level of plaque reduction was comparable with that reported for other triclosan-containing dentifrices; however, no reductions in gingivitis were observed for triclosan/pyrophosphate relative to the negative control. One possible explanation of this result is that the Hawthorne effect in the study was too great to allow the detection of a treatment benefit for the triclosan product. In order to further explore the relevance of these results, three independent clinical studies were undertaken utilizing designs based on a 21-day experimental gingivitis model in which Hawthorne effects are minimized, in part due to the absence of toothbrushing. In each model, a pre-study prophylaxis was followed by a three-week period of oral hygiene instruction to establish optimum baseline gingival health in study participants. The studies varied in enrollment; 120, 33 and 32 subjects completed treatment on studies 1, 2, and 3, respectively. In study 1, test articles were dentifrice products (0.28% triclosan/5% pyrophosphate/0.145% sodium fluoride, 0.2% triclosan/0.5% zinc citrate/0.112% sodium fluoride, 0.145% sodium fluoride and 0.15% sodium monofluorophosphate) applied neat and undiluted via a performed tooth shield (that prevents mechanical tooth-brushing at the test sites in the oral cavity) in a partial mouth design. In study 2, test articles were also dentifrice products (0.28% triclosan/5% pyrophosphate/0.243% sodium fluoride, 0.3% triclosan/2% Gantrez copolymer/0.24% sodium fluoride and 0.243% sodium fluoride) but administered to subjects in the form of 1:3 aqueous slurry rinses. Lastly, in study 3, test articles were all mouthrinses (0.12% chlorhexidine, 0.045% triclosan in ethanol plus respective vehicle placebos). Clinical assessments to quantify the test articles' effects on the development of plaque and gingivitis were conducted at baseline (studies 1, 2 and 3), day 7 (studies 2 and 3), day 14 (studies 2 and 3) and day 21 (studies 1, 2 and 3). In study 1, no statistically significant treatment effects were observed between the test articles and controls for plaque or gingivitis development. In study 2, no statistically significant treatment effects were observed at any time point between test products for the development of gingivitis. At days 7 and 14, there were no significant differences between test products and control for plaque development as well. At day 21, the group rinsing with the triclosan/pyrophosphate/sodium fluoride slurry had significantly less plaque accumulation than the group rinsing with the triclosan/copolymer/sodium fluoride slurry (p < 0.05); however, neither of the groups using test products containing triclosan was significantly different for plaque development from the group using the sodium fluoride control test article. In addition, aspartate aminotransferase activity in gingival crevicular fluid was assayed at days 0 and 21; no between-group differences were found at either of these time points, though day 21 AST activities were higher than those at baseline. In study 3, statistically significant treatment differences in plaque regrowth and gingivitis were observed at day 21 for the chlorhexidine rinse versus all other rinses (p < 0.05). No other statistically significant treatment effects were observed between test compounds at any other time points. The results benchmark the anti-plaque and anti-gingivitis benefit for a range of triclosan-based product forms against positive and negative controls in a three different experimental gingivitis models, a design considered predictive of clinical efficacy in longer-term investigations. It is concluded that dentifrice products containing triclosan do not possess sufficient antimicrobial activity to suppress plaque and gingivitis development in the absence of normal oral hygiene, and that relative to chlorhexidine, triclosan itself offers only modest efficacy for the prevention of plaque accumulation and therefore the delayed onset of gingivitis.

Adolescent↗
PubMed2003

The effect of a toothpaste containing 2% zinc citrate and 0.3% Triclosan on bacterial viability and plaque growth in vivo compared to a toothpaste containing 0.3% Triclosan and 2% copolymer.

OBJECTIVE: To compare the antimicrobial efficacy and effect on plaque growth of a new silica-based fluoride toothpaste containing 2% zinc citrate/ 0.3% Triclosan with a silica-based fluoride toothpaste containing 0.3% Triclosan/2% copolymer. METHODS: In Study 1, plaque was collected after one week's use of each toothpaste and assessed for bacterial viability, live/ dead ratio and microbial membrane integrity. In study 2, plaque was measured immediately and 18 hours after a single brushing with the specified toothpastes. RESULTS: The 2% zinc citrate/0.3% Triclosan formulation significantly reduced the total number of viable aerobic and anaerobic bacteria (p = 0.0223 and p = 0.0443 respectively) compared to the 0.3% Triclosan/2% copolymer formulation. Both toothpastes increased the bacterial membrane permeability significantly. However, the proportion of live bacteria for the 2% zinc citrate/0.3% Triclosan product was significantly reduced (p < 0.05). Study 2 showed significantly less plaque growth 18 hours after using the 2% zinc citrate/0.3% Triclosan toothpaste compared to the 0.3% Triclosan/2% copolymer toothpaste (p < 0.01). CONCLUSION: Regular use of a fluoride toothpaste containing 2% zinc citrate and 0.3% Triclosan, significantly reduced the viability of plaque bacteria compared to a fluoride toothpaste containing 0.3% Triclosan/ 2% copolymer 12 hours after brushing. In addition, a clinical plaque growth study confirmed that this anti-microbial efficacy leads to a significant reduction in plaque growth.

Adult↗
PubMed2001

Cross-resistance between triclosan and antibiotics in Pseudomonas aeruginosa is mediated by multidrug efflux pumps: exposure of a susceptible mutant strain to triclosan selects nfxB mutants overexpressing MexCD-OprJ.

Triclosan is an antiseptic frequently added to items as diverse as soaps, lotions, toothpaste, and many commonly used household fabrics and plastics. Although wild-type Pseudomonas aeruginosa expresses the triclosan target enoyl-acyl carrier protein reductase, it is triclosan resistant due to expression of the MexAB-OprM efflux system. Exposure of a susceptible Delta(mexAB-oprM) strain to triclosan selected multidrug-resistant bacteria at high frequencies. These bacteria hyperexpressed the MexCD-OprJ efflux system due to mutations in its regulatory gene, nfxB. The MICs of several drugs for these mutants were increased up to 500-fold, including the MIC of ciprofloxacin, which was increased 94-fold. Whereas the MexEF-OprN efflux system also participated in triclosan efflux, this antimicrobial was not a substrate for MexXY-OprM.

Amino Acid Sequence↗
PubMed2000

Clinical evidence for the lack of triclosan accumulation from daily use in dentifrices.

PURPOSE: To demonstrate through clinical pharmacokinetic studies that triclosan does not accumulate in blood or plasma in human subjects who regularly use triclosan-containing dentifrice. MATERIALS AND METHODS: Three clinical pharmacokinetic studies were conducted to assess the blood or plasma levels of triclosan following toothbrushing with dentifrice formulations containing triclosan. In Study 1, both a single-dose and a multiple-dose phase were conducted. In the single-dose phase, subjects brushed one time with 1.25 g dentifrice containing 0.3% triclosan (3.75 mg triclosan dose) and ingested all of the dentifrice. Blood samples were collected at multiple time points from pre-dose to 72 hrs post-dose and analyzed for total triclosan levels. In the multiple-dose phase, these same subjects brushed three times daily as in the single-dose phase. This pattern was followed for 12 consecutive days. Blood samples were taken for triclosan analysis at multiple time points up to 48 hrs after the first dose of day 12. Study 2 was a parallel, open-labeled clinical study to compare triclosan blood levels from twice daily brushing with 1 gm of dentifrice containing 0.2% triclosan to twice daily ingestion of 20 ml of a 0.01% triclosan aqueous solution over a period of 21 days. Blood samples were taken for triclosan analysis at baseline and at 4 hrs after the morning dose on days 7, 14, and 21. Study 3 was a parallel, double-blind, 12-wk brushing study with dentifrice containing 0.2% triclosan or a matching placebo. Blood samples were taken for triclosan analysis at baseline and at 3 and 12 wks at 4 hrs after the morning dose. RESULTS: In the single-dose study, Triclosan was absorbed into the systemic circulation with a T(1/2) of the terminal plasma concentration ranging between 6-63 hrs. The mean AUC(0-inf) after a single dose was found to be 2,809 ng x hr/ml. After 12 days of three times daily toothbrushing and ingestion of the dental slurry, the mean triclosan plasma concentration was 352 ng/ml in the steady state period, and the mean AUC in a 24-hr period (AUC24) was found to be 8,460 ng x hr/ml. This AUC24 was normalized for the number of brushings for comparison to the AUC(0-inf) after a single brushing. There was no significant (P = 0.93) difference between these AUC values suggesting a complete elimination of daily triclosan dose and no increase in the triclosan level during repeated brushing/ingestion. In the two other dentifrice studies, the triclosan blood concentration appeared to reach a steady state level by day 7 and was maintained at the steady state level (14 to 21 ng/ml) for up to 12 wks. These results support the conclusion that the elimination of a daily triclosan dose is complete and no accumulation of triclosan was observed even after three times daily toothbrushing with 1.25 g dentifrice containing 0.3% triclosan and full ingestion of the dentifrice.

Anti-Infective Agents, Local↗
PubMed1996

Hydrolysis of triclosan monophosphate by dental plaque and selected species of oral micro-organisms.

Triclosan monophosphate is a phosphorylated derivative of the antimicrobial agent, triclosan. In comparison with triclosan, it is highly soluble in aqueous solutions. It is hypothesized that, within the oral environment, triclosan monophosphate (which may be devoid of antimicrobial activity) will be hydrolyzed into triclosan by the action of microbial phosphatases. The liberated triclosan may then exert antimicrobial activity. To test this hypothesis, we designed experiments to measure the phosphatase activity of plaque and selected species of oral micro-organisms and to demonstrate hydrolysis of triclosan monophosphate. Tests comparing the minimal inhibitory concentration and minimal bactericidal concentration of triclosan and triclosan monophosphate were also undertaken. Dental plaque and the majority of the bacterial strains tested showed phosphatase activity against p-nitrophenyl phosphate which peaked below neutral pH (acid phosphatases) or above neutral pH (alkaline phosphatases). Dental plaque showed the highest levels of alkaline phosphatase (optimum at pH 9.0) and relatively high levels of acid phosphatase (optimum at pH 6.0 to 6.5). Dental plaque and selected species of micro-organisms were all capable of hydrolyzing triclosan monophosphate, albeit at different rates. The minimal inhibitory concentration and minimal bactericidal concentration values for triclosan monophosphate against eight bacterial strains were always considerably higher than the corresponding values for triclosan. Addition of triclosan monophosphate to an established culture (ca. 10(9) cfu/mL) of Capnocytophaga gingivalis growing continuously showed that triclosan monophosphate was rapidly hydrolyzed into triclosan with concomitant loss of total bacterial viability. It is therefore likely that triclosan monophosphate will be broken down into triclosan within the oral environment with concomitant antimicrobial activity.

Anti-Infective Agents, Local↗
PubMed2000

Buccal absorption of triclosan following topical mouthrinse application.

PURPOSE: To determine clinically the buccal absorption and plaque retention of triclosan from a mouthrinse containing 0.03% triclosan. MATERIALS AND METHODS: 15 ml of the triclosan oral rinse (N=9) or placebo mouthrinse (N=12) was used twice daily for 21 days in humans. Blood, dental plaque and the expectorated oral rinse were collected prior to, during the treatment period at given intervals, and 8 days after the treatment. Dental plaque and blood samples were collected 1 hr and 4 hr after the morning rinse, respectively. The oral retention of triclosan was calculated by subtracting the amount of triclosan recovered in the expectorate from the triclosan dose applied (4.50 mg) in the mouthrinse. Plasma samples were analyzed for free triclosan (the parent molecule) and its glucuronide and sulfate conjugates, whereas dental plaque was analyzed only for total triclosan. RESULTS: No significant treatment-related adverse effects were observed during the clinical phase of the study. The average daily oral retention of triclosan was calculated to be 0.660 mg, which is 7.33% of the triclosan dose applied (2 x 4.50 mg). Plaque contained an average 20.5-46.4 microg of triclosan per g of plaque collected. At various sampling times, mean plasma concentrations were: no detectable triclosan, 63.8-86.3 microg/ml of triclosan glucuronide and 8.23-18.0 ng/ml of triclosan sulfate. The mean total triclosan plasma concentration ranged from 74.5 to 94.2 microg/ml with plateau concentrations reached after 2 days of dosing. Eight days after the last treatment the triclosan plasma concentration returned to baseline levels (< 2 ng/ml).

Absorption↗
PubMed2000

Triclosan and antibiotic resistance in Staphylococcus aureus.

Triclosan (2,4,4'-trichloro-2'-hydroxydiphenyl ether) is an antimicrobial agent used in hygiene products, plastics and kitchenware, and for treating methicillin-resistant Staphylococcus aureus (MRSA) outbreaks. S. aureus strains with low-level resistance to triclosan have emerged. It has been claimed that strains with decreased susceptibility to biocides may also be less susceptible to antibiotics. We tested the susceptibility of S. aureus clinical isolates to triclosan and several antibiotics. Triclosan MICs ranged between 0.025 and 1 mg/L. Some, but not all, strains were resistant to several antibiotics and showed low-level triclosan resistance. S. aureus mutants with enhanced resistance to triclosan (< or =1 mg/L) were isolated. In several cases this resistance was stably inherited in the absence of triclosan. These mutants were not more resistant than the parent strain to several antibiotics. Changes in triclosan MICs associated with the acquisition of a plasmid encoding mupirocin resistance were not observed, suggesting that the triclosan/mupirocin co-resistance seen in a previous study was not the result of a single resistance gene or separate genes on the same plasmid. The continuous exposure of a triclosan-sensitive S. aureus strain to sub-MIC concentrations of triclosan for 1 month did not result in decreased susceptibility to triclosan or to several antibiotics tested. Triclosan-induced potassium leakage and bactericidal effects on a triclosan-sensitive strain, a resistant strain and a strain selected for increased resistance were compared with those of non-growing organisms, exponentially growing organisms and organisms in the stationary phase. No significant differences between the strains were observed under these conditions despite their different MICs. Biocides have multiple target sites and so MICs often do not correlate with bactericidal activities. The ability of S. aureus to develop resistance to triclosan and the current view that triclosan may have a specific target in Escherichia coli, namely enoyl reductase, underline the need for more research on the mechanisms of action and resistance.

Anti-Infective Agents, Local↗
PubMed2002

Occurrence and environmental behavior of the bactericide triclosan and its methyl derivative in surface waters and in wastewater.

The bactericide triclosan and methyl triclosan, an environmental transformation product thereof, were detected in lakes and in a river in Switzerland at concentrations of up to 74 and 2 ng L(-1), respectively. Both compounds were emitted via wastewater treatment plants (WWTPs), with methyl triclosan probably being formed by biological methylation. A regional mass balance for a lake (Greifensee) indicated significant removal of triclosan by processes other than flushing. Laboratory experiments showed that triclosan in the dissociated form was rapidly decomposed in lake water when exposed to sunlight (half-life less than 1 h in August at 47 degrees latitude). Methyl triclosan and nondissociated triclosan, however, were relatively stable toward photodegradation. Modeling these experimental data for the situation of lake Greifensee indicated that photodegradation can account for the elimination of triclosan from the lake and suggested a seasonal dependence of the concentrations (lower in summer, higher in winter), consistent with observed concentrations. Although emissions of methyl triclosan from WWTPs were only approximately 2% relative to those of triclosan, its predicted concentration relative to triclosan in the epilimnion of the lake increases to 30% in summer. Passive sampling with semipermeable membrane devices (SPMDs) indicated the presence of methyl triclosan in lakes with inputs from anthropogenic sources but not in a remote mountain lake. Surprisingly, no parent triclosan was observed in the SPMDs from these lakes. Methyl triclosan appears to be preferentially accumulated in SPMDs under the conditions in these lakes, leading to concentrations comparable to those of persistent chlorinated organic pollutants.

Anti-Infective Agents, Local↗
PubMed1994

Significance of choice of solvents for the clinical effect of triclosan-containing mouthrinses.

The aim of this study was to investigate the plaque-inhibiting effect of triclosan. It is known that triclosan and sodium lauryl sulfate (SLS) have a marked inhibitory effect. However, since SLS has a plaque-reducing effect in itself, the relative importance of triclosan and the surfactant is undecided. Twelve dental students participated in the trial, during which oral hygiene was suspended for 4-day periods when the different mouthrinses were used twice daily. The following mouthrinses were used: A, water (negative control); B, 0.2% chlorhexidine acetate (CHX) (positive control); C, 0.3% triclosan in water-free propylene glycol (PG); D, 0.3% triclosan with 1.5% SLS in PG; E, 0.15% triclosan in PG; F, 0.075% triclosan in PG; G, 0.3% triclosan in diluted PG (1:8 in water) with 1.5% SLS; and H, 0.3% triclosan in 0.5% sodium carbonate. The results showed that triclosan dissolved in the organic solvent PG had a significant plaque-inhibiting effect, whereas, dissolved in alkali, it had a negligible effect. The addition of SLS to PG somewhat reduced the antiplaque activity, and the aqueous solution of triclosan had markedly less effect. Lower concentrations of triclosan exhibited less clinical effect than higher concentrations. It can be concluded that triclosan alone, dissolved in a suitable solvent, has an antiplaque effect. The study confirmed the hypothesis that the nature of the detergent or organic solvent used to dissolve triclosan affects its clinical effect markedly.

Adult↗
PubMed1999

Effect of cyclodextrins and polymers on triclosan availability and substantivity in toothpastes in vivo.

The aqueous solubility of triclosan is only about 10 microg/mL. This very low solubility can hamper its biological activity in the oral cavity, which could explain the mixed clinical results obtained from triclosan toothpaste trials. Triclosan availability in a silica-based toothpaste was improved through cyclodextrin solubilization. The triclosan in vivo availability was optimized through a series of phase-solubility studies and triclosan release studies. It was found that in toothpastes, natural beta-cyclodextrin (betaCD) was just as good a solubilizer as the more water-soluble betaCD derivatives. Furthermore, the amount of cyclodextrin could be reduced by as much as 60% through the addition of a small amount of carboxymethylcellulose (CMC), without affecting triclosan release from the toothpaste. Optimally, cyclodextrins resulted in an almost 3-fold enhancement of triclosan availability compared to an identical toothpaste containing no cyclodextrin. In vivo studies in humans showed that replacing triclosan with triclosan/betaCD in the toothpaste resulted in only moderate improvement in triclosan substantivity. However, replacing triclosan with triclosan/betaCD/CMC complex resulted in significant improvement in triclosan substantivity. Furthermore, the in vivo studies showed that replacing free triclosan with triclosan/betaCD/CMC complex resulted in an almost 3-fold increase in initial triclosan concentration in saliva after brushing and about 2-fold increase in duration of activity.

Adult↗