Efcacy of antiplaque mouthwashes:

A ve-day clinical trial

Muhammad Wasif Haq, BDS
n
Mehwish Batool, BDS
n
Syed Hammad Ahsan, MSc
n
Gaurav Sharma
D
ental plaque (bioflm) forma-
tion is a naturally occurring
process, resulting from bacte-
rial interactions with the acquired
salivary pellicle formed over the sur-
face of the tooth shortly after brush-
ing the tooth. Although the newly
formed plaque lacks any pathogenic
potential due to an insufcient
number of microorganisms pres-
ent, the persistence of dental
plaque allows for multiple bacterial
interactions, resulting in various
pathologies such as gingivitis, caries,
periodontitis, and peri-implantitis.
1,2

Adequate plaque control will not
only contribute toward optimal oral
health, it also will reduce highly
prevalent diseases such as gingivitis,
caries, and periodontitis.
3
For opti-
mal oral hygiene, toothbrushing,
fossing, and using mouthwashes is
recommended. Mouthwashes with
antiplaque agents such as chlorhexi-
dine, fuoride, and cetylpyridinium
chloride are recommended for use
in conjunction with toothbrushing
because rinsing with mouthwashes
in addition to toothbrushing has
been found to impart superior
plaque control compared to tooth-
brushing alone.
4

Chlorhexidine, a bisguanide cat-
ionic molecule with broad-spectrum
antimicrobial activity, is considered
the gold standard in plaque con-
trol.
5
Tis agent, depending on the
concentration, can be bactericidal
or bacteriostatic and exerts more
potent action against Gram-positive
microorganisms than Gram-negative
microorganisms.
6
Chlorhexidine
causes a reduction in salivary pellicle
formation through the inhibition of
bacterial enzyme glucosyl-transferase
needed for bacterial adherence to
tooth structure; it also produces
bacterial cell wall disruption and
cytoplasmic precipitation.
7,8
Recent
studies have shown chlorhexidine to
be an efective inhibitor of matrix
metalloproteinases, proinfamma-
tory cytokines, interleukins, and
salivary cathepsin C, all of which
play an important role in gingivitis
and periodontitis.
9-11
Fluoride is an anionic, anti-
cariogenic agent that helps to
reprecipitate minerals lost during
demineralization and also pro-
motes the formation of larger and
more acid-resistant fuorapatite
crystals. It exerts its antimicrobial
action through the inhibition of
bacterial enzymes such as enolase
and glucosyl-transferase and also
causes inhibition of glucose uptake
and utilization by bacteria.
12,13
As
with chlorhexidine, fuoride has
an inhibitory efect on salivary
cathepsin C and can be bacterio-
static as well as bactericidal to
oral bacteria.
14,15

Cetylpyridinium chloride is a
bactericidal, quartenary ammo-
nium compound that denatures
bacterial proteins, inactivates vari-
ous metabolic enzymes of bacteria,
and damages cell membranes.
16
It
has more potent activity against
Gram-positive organisms than
Gram-negative organisms. Cetyl-
pyridinium chloride also has been
shown to accumulate in dental
plaque, thereby exerting its antimi-
crobial efect for a longer period.
17

Several studies, both in vitro and
The aim of this study was to evaluate and compare the efcacy of
antiplaque mouthwashes. Plaque levels were determined by apply-
ing a plaque-disclosing solution using the Turesky et al modication
of the Quigley Hein plaque index. The control group (n = 6) brushed
twice per day with uoride toothpaste for one minute and rinsed
with water, while the study groups (n = 6) brushed once per day
with uoride toothpaste for one minute, followed by rinsing with
5.0 mL of mouthwash diluted with 10.0 mL of water for 30 seconds.
The control group brushed and rinsed with water twice per day.
The results indicated that cetylpyridinium chloride in
combination with sodium uoride offered maximum plaque
inhibition, followed by chlorhexidine gluconate and sodium
monouorophosphate, while plaque levels increased in the control
group and with the combination of chlorhexidine gluconate
and sodium uoride. The only antiplaque agents to demonstrate
a statistically signicant difference from the control were
cetylpyridinium chloride in combination with sodium uoride, and
chlorhexidine gluconate. Increasing the uoride concentration had
no impact on antiplaque activity.
Received: April 20, 2010
Accepted: June 21, 2010
Caries Detection and Prevention
e110 May/June 2011 General Dentistry www.agd.org
in vivo, have evaluated the efcacy
of the antiplaque agents mentioned
above.
18,19
Te simultaneous use of
chlorhexidine with fuoride has been
a matter of debate due to inconclu-
sive results.
20,21
In some studies, this
combination decreased the efcacy
and substantivity of chlorhexidine,
possibly due to inactivation of the
cationic chlorhexidine by anionic
fuoride.
6,22
Because most tooth-
pastes contain sodium fuoride or
sodium monofuorophosphate, the
fuoride in these sources could infu-
ence and interfere with the activity
of chlorhexidine. Variable results on
the efcacy of cetylpyridinium chlo-
ride as an antiplaque agent also have
been reported.
23
Similarly, to the
authors knowledge, very few studies
have evaluated the antiplaque com-
bination of cetylpyridinium chloride
with fuoride.
24,25
Te aim of this study was to
determine and compare the ef-
cacy of mouthwashes containing
chlorhexidine, sodium mono-
fuorophosphate, chlorhexidine in
combination with sodium fuoride,
and cetylpyridinium chloride in
combination with sodium fuoride.
Materials and methods
Te study was conducted at Liaquat
College of Medicine & Dentistry,
Karachi, Pakistan, where approval
was received from the ethical com-
mittee. Tirty patients who attended
the dental outpatient department
were selected for this open-label,
nonrandomized, controlled trial.
Te patients were allocated into
four test groups and one control
group (n = 6). Each participant was
informed of the reason for the study,
and informed consent was obtained.
Participants were chosen for this
study if they were from 1850 years
of age (due to a greater likelihood of
compliance and a lesser likelihood
of co-morbidities and medicine
use) and had complete dentition
through the second molars in all four
quadrants.
Participants were excluded from
this study if any of their teeth
had active dental caries or signs of
periodontal involvement (visible on
clinical examination and probing),
they were taking any medications
or showed signs of systemic disease,
they were undergoing orthodontic
treatment, or they had a prosthetic
appliance.
Following a clinical examination
with a sterilized dental mirror and
probe, participants were instructed
to rinse their mouths with water
repeatedly until it fushed without
color. Two drops of plaque-
disclosing solution (GDK Densell)
were applied to a cotton pellet and
patients were advised to apply the
dye on the labial/buccal and lingual
surfaces of all teeth.
Preregimen plaque levels on the
smooth surfaces of all teeth, exclud-
ing third molars, were estimated by
using the Turesky et al modifcation
of the Quigley-Hein plaque index.
Participants in the test groups were
instructed to brush with fuoride
toothpaste (Close-Up, Church &
Dwight Co., Inc.) once a day for
one minute (30 seconds per jaw).
Next, they rinsed their mouths
for 30 seconds with 5.0 mL of
mouthwash diluted with 10 mL of
water. Te mouthrinses, measuring
cup, and fuoride toothpaste were
provided to each participant for
use during the fve-day trial. Each
mouthwash and its active antimicro-
bial agent(s) are listed in Table 1.
Te plaque scores for every group
were calculated twice: at the time of
examination and upon completion
of the study. Te diference between
the initial and fnal readings was
Table 2. Initial and nal plaque levels and the difference in plaque level
among groups in this study.
Group Initial plaque level Final plaque level Difference
1 11.89 11.0 0.89
2 11.22 10.95 0.27
3 13.37 13.41 -0.04
4 13.36 12.34 1.02
Control 11.61 14.23 -2.62
Table 1. Basic information about the mouthwashes used in this study.
Group Product name (manufacturer) Active agent
1 Enziclor (Platinum Pharmaceuticals) 0.2% chlorhexidine gluconate
2 Secure (Platinum Pharmaceuticals) 0.05% sodium monouorophosphate
3 Protect (Roomi Enterprises) 0.12% chlorhexidine gluconate and
0.05% sodium uoride
4 Aquafresh (GlaxoSmithKline) 0.05% cetylpyridinium chloride and
0.05% sodium uoride
Control water -
www.agd.org General Dentistry May/June 2011 e111
calculated and is presented in Table
2. Te means and the standard
deviations were calculated at the
completion of the study. Te
confdence interval was set at 95%,
with a level of signifcance of 0.05.
Te ANOVA and Bonferroni tests
calculated the statistically signif-
cant diferences between the study
groups and the control and among
the study groups (Table 3). SPSS
software, version 17, was used for
the analysis.
Results
Te diferences between the initial
and fnal plaque levels are presented
in Table 2. Te P value obtained
from the one-way ANOVA was less
than 0.5 (P = 0.016), indicating a
statistically signifcant diference.
A Bonferroni multiple comparisons
test assessed how much the study
groups difered from each other
and from the control; the results are
presented in Table 3.
Discussion
Controlling plaque and preventing
related diseases still pose a chal-
lenge for contemporary dentists.
Finding an efective means of
controlling plaque formation and
maturation can result in a drastic
decrease in the incidence and
prevalence of plaque-associated
diseases and contribute toward
improving overall patient oral
health. Since few people use dental
foss and many may not be aware of
the proper fossing technique, it is
imperative to recommend mouth-
washes that are equally efcacious
and compatible with dentifrices to
prevent plaque maturation.
26
Tis study evaluated the efcacy
of antiplaque agents in mouth-
washes in combination with the
use of a fuoride-based toothpaste
for fve days. Results indicated that,
when compared to the control, all
study groups caused lesser plaque
formation, refecting the efcacy of
antiplaque agents to various degrees.
Table 3. Results of the Bonferroni test for multiple comparisons among study groups and the control group.
(I) group (J) groups Mean difference (I-J) Standard error Signicance
95% condence interval
Lower bound Upper bound
1 2 0.10833 0.16900 1.000 -0.4119 0.6286
3 0.15500 0.16900 1.000 -0.3652 0.6752
4 -0.02167 0.16900 1.000 -0.5419 0.4986
control 0.55167* 0.16900 0.032 0.0314 1.0719
2 1 -0.10833 0.16900 1.000 -0.6286 0.4119
3 0.04667 0.16900 1.000 -0.4736 0.5669
4 -0.13000 0.16900 1.000 -0.6502 0.3902
control 0.44333 0.16900 0.146 -0.0769 0.9636
3 1 -0.15500 0.16900 1.000 -0.6752 0.3652
2 -0.04667 0.16900 1.000 -0.5669 0.4736
4 -0.17667 0.16900 1.000 -0.6969 0.3436
control 0.39667 0.16900 0.271 -0.1236 0.9169
4 1 0.02167 0.16900 1.000 -0.4986 0.5419
2 0.13000 0.16900 1.000 -0.3902 0.6502
3 0.17667 0.16900 1.000 -0.3436 0.6969
control 0.57333* 0.16900 0.023 0.0531 1.0936
control 1 -0.55167* 0.16900 0.032 -1.0719 -0.0314
2 -0.44333 0.16900 0.146 -0.9636 0.0769
3 -0.39667 0.16900 0.271 -0.9169 0.1236
4 -0.57333* 0.16900 0.023 -1.0936 -0.0531
*The mean difference is signicant at the 0.05 level.
Caries Detection and Prevention Efcacy of antiplaque mouthwashes
e112 May/June 2011 General Dentistry www.agd.org
However, statistically signifcant
diferences compared to the control
group were observed for only
Groups 1 (P = 0.032) and 4 (P =
0.023). Tere were no statistically
signifcant diferences between the
study groups. Group 4 showed the
greatest plaque inhibition, followed
by Groups 1 and 2, while Group 3
and the control displayed increased
levels of plaque.
Te combination of chlorhexidine
and fuoride was not found to be
efective in reducing plaque levels;
in fact, plaque levels were found to
have increased at the completion
of the study (diferential = 0.04).
Another study also concluded that
the combination of chlorhexidine
and fuoride was unable to contrib-
ute to any signifcant reduction in
bacterial counts.
27

Kohlahi and Soolari suggested
that chlorhexidine forms salts with
two agents in toothpaste, namely
sodium monofuorophosphate and
sodium lauryl sulfate, which could
result in the decreased efcacy of
chlorhexidine.
28
Tey recommended
that 30 minutes to two hours elapse
between the use of a chlorhexidine
mouthwash and brushing with a
fuoride-based toothpaste.
28
Since all
groups in this study used the same
toothpaste, the increase in plaque
levels in Group 3 could refect fuo-
rides role in causing decreased anti-
plaque activity, since Group 3 was
exposed to higher levels of fuoride
from the toothpaste as well as from
the mouthwash.
6,29
Other studies
also have reported the variability of
chlorhexidine results.
30,31

Te synergistic activity observed
in several studies from the simul-
taneous use of both chlorhexidine
and fuoride was not observed in
the current study.
32-34
Many of the
earlier studies involved the use of
varnishes, while the current study
evaluated antiplaque mouthrinses.
Diferent methods of delivering
antiplaque agents could infuence
the outcome. At least one study has
indicated that chlorhexidine varnish
is more efective than chlorhexidine
mouthrinses in reducing the level
of Streptococcus mutans; this may
be due to the longer exposure to
chlorhexidine in varnishes.
35,36

Fluoride also can be inactivated
by its interaction with other
agents. Not only can the efcacy
of chlorhexidine be reduced by the
presence of fuoride, chlorhexidine
can infuence fuorides activ-
ity as well. It has been found
that chlorhexidine and fuoride
have competitive binding on
hydroxyapatite crystals in teeth,
resulting in decreased binding of
fuoride to hydroxyapatite crystals
and rendering fuoride unable to
play its role in the remineralization
of carious teeth.
37,38
However, the
diferences in the current study
between Groups 1 and 3 were not
found to be statistically signifcant
(P = 1.000).
Another fnding obtained from
the current study points to a limited
antiplaque efect for all antiplaque
agents, even after exposure to
increased fuoride. In Group 2,
sodium monofuorophosphate
mouthrinse was used with a
fuoride-based toothpaste; however,
this group still did not demonstrate
the reduction in plaque that was
observed for Groups 1 and 4 (dif-
ferential = 0.27). Tis fnding is
consistent with results obtained from
a similar study.
39
In high-risk caries
patients, antiplaque agents in addi-
tion to fuoride are recommended.
Te maximum plaque inhibitory
efect was observed in Group 4 (dif-
ferential = 1.02). Although multiple
studies have difered considerably
regarding the antiplaque efcacy of
cetylpyridinium chloride, it appears
that this agent in combination with
fuoride could ofer the best anti-
plaque activity.
40,41

Cetylpyridinium chloride facili-
tates better plaque removal when
used in combination with tooth-
brushing.
42
It has been documented
that cetylpyridinium chloride in
combination with sodium fuoride
is more efective in inhibiting plaque
than the combination of chlorhexi-
dine with fuoride.
43
Unfortunately,
very few studies have been carried
out to evaluate the combination
of cetylpyridinium chloride and
fuoride. It is extremely important
that fuoride is included to assist
with the remineralization of dental
structure lost to decay. Group 1 did
not ofer as much plaque inhibition
as Group 4; this could be attributed
to a decrease in the efcacy of
chlorhexidine caused by the fuoride
in the toothpaste. If fuoride is not
inactivated or is negatively infu-
enced by cetylpyridinium chloride,
then this combination could prove
to be equivalent to chlorhexidine.
One major factor limiting the
regular use of antiplaque agents
is their associated side efects.
Chlorhexidine is known to cause
brownish staining of the teeth,
restorations, and mucosal surfaces;
this is attributed to its attachment
through the cationic group. Such
stains can be removed only by scal-
ing. For this reason, chlorhexidine
use should be limited to no more
than two weeks, and patients should
be advised to limit their cofee and
tea intake while using the product.
Other side efects of chlorhexidine
include alteration of taste percep-
tion and increased supragingival
calculus.
44
Recent data have shown
chlorhexidine to have other side
efects, such as its cytotoxic efects
on odontoblasts, fbroblasts, and
osteoblasts.
45,46
Cytotoxic efects on
fbroblasts, oral mucosal cells, and
odonotoblast-like cells following
www.agd.org General Dentistry May/June 2011 e113
the use of sodium fuoride also
have been documented.
47,48
Also,
the regular use of cetylpyridinium
chloride has been shown to cause
tooth staining similar to that of
chlorhexidine.
41

Te next research challenges are
to develop antiplaque agents with
reduced or minimum side efects,
limited interactions with other
constituents found in dentifrices
and mouthwashes, and increased
efcacy. In the meantime, it is
prudent to educate patients on all
factors contributing to increased
plaque formation. A very signifcant
factor is limiting the patients sucrose
consumption, which not only can
prove benefcial in reducing plaque
formation, it also would help to
increase the efcacy of antimicrobial
agents, because sucrose intake has
been linked to decreased efcacy of
antimicrobial agents.
49
Te authors
suggest that more clinical trials be
carried out to investigate the interac-
tion of fuoride with chlorhexidine
as well as the combination of cetyl-
pyridinium chloride with fuoride in
hampering plaque growth.
Te present study had certain
limitations, the most important
being the small sample size, which
could have afected the overall
results. Increasing the sample size
could provide more accurate results.
Also, toothbrushing could not be
eliminated during this study, as
restricting the mechanical cleaning
beyond fve days could lead to the
development of gingivitis.
50
A pos-
sible alternative could be to conduct
the study on the teeth of laboratory
animals with a controlled diet,
using antimicrobial isolates. Te
possibilities of noncompliance
among participants and nonuni-
formity of their dietary habits in
diferent groups also could have
infuenced the outcome. Assessing
the microbial growth of plaque
microorganisms and the inhibitory
efect of antiplaque agents through
microscopic analysis could have
provided clearer results.
Conclusion
No synergistic action of chlorhexi-
dine with fuoride was observed
in the current study; instead, the
simultaneous use of chlorhexi-
dine and fuoride was associated
with increased plaque levels. It
seems likely that the efcacy of
chlorhexidine is decreased in the
presence of fuoride. Chlorhexidine
and sodium monofuorophosphate
acted to reduce plaque levels,
although there was no statistical
diference between these agents.
Increasing the fuoride concentra-
tion did not lead to increased
antiplaque activity. Te combina-
tion of cetylpyridinium chloride
and fuoride was most efective at
reducing plaque levels.
Acknowledgements
Te authors would like to thank
the following people for their
unlimited help and support during
this study: Drs. Naheed Najmi,
Asif Hussain, Nadeem Chand, and
Temoor Moghul.
Author information
Drs. Haq and Batool are house of-
cers, Department of Periodontology,
Liaquat College of Medicine & Den-
tistry, Karachi, Pakistan, where Dr.
Ahsan is an assistant professor of oral
pathology. Mr. Sharma is an under-
graduate kinesiology student at San
Diego State University, California.
References
1. Marsh PD. Dental plaque as a biolm and a mi-
crobial communityImplications for health and
disease. BMC Oral Health 2006;6 Suppl 1:S14.
2. Sbordone L, Bortolaia C. Oral microbial biolms
and plaque-related diseases: Microbial communi-
ties and their role in the shift from oral health to
disease.Clin Oral Investig 2003;7(4):181-188.
3. Pihlstrom BL, Michalowicz BS, Johnson NW.
Periodontal diseases. Lancet 2005;366(9499):
1809-1820.
4. Feres M, Gursky LC, Faveri M, Tsuzuki CO,
Figueiredo LC. Clinical and microbiological ben-
ets of strict supragingival plaque control as
part of the active phase of periodontal therapy.
J Clin Periodontol 2009;36(10):857-867.
5. De Araujo Nobre M, Capelas C, Alves A, Almeida
T, Carvalho R, Antunes E, Oliveira D, Cardador A,
Malo P. Non-surgical treatment of peri-implant
pathology. Int J Dent Hyg 2006;4(2):84-90.
6. de Freitas CS, Diniz HF, Gomes JB, Sinisterra RD,
Cortes ME. Evaluation of the substantivity of
chlorhexidine in association with sodium uo-
ride in vitro. Pesqui Odontol Bras 2003;17(1):
78-81.
7. Furiga A, Dols-Lafargue M, Heyraud A, Chambat
G, Lonvaud-Funel A, Badet C. Effect of anti-
plaque compounds and mouthrinses on the ac-
tivity of glucosyltransferases from Streptococcus
sobrinus and insoluble glucan production. Oral
Microbiol Immunol 2008;23(5):391-400.
8. Gronroos L, Matto J, Saarela M, Luoma AR,
Luoma H, Jousimies-Somer H, Pyhala L, Asikain-
en S, Alaluusua S. Chlorhexidine susceptibilities
of mutans streptococcal serotypes and ribo-
types. Antimicrob Agents Chemother 1995;
39(4):894-898.
9. Gendron R, Grenier D, Sorsa T, Mayrand D. Inhi-
bition of the activities of matrix metalloprotein-
ases 2, 8, and 9 by chlorhexidine. Clin Diagn
Lab Immunol 1999;6(3):437-439.
10. Sharma S, Saimbi CS, Koirala B, Shukla R. Effect
of various mouthwashes on the levels of inter-
leukin-2 and interferon-gamma in chronic gingi-
vitis. J Clin Pediatr Dent 2008;32(2):111-114.
11. Dabrowska E, Letko M, Roszkowska-Jakimiec W,
Letko R, Sadowski J. Effect of chlorhexidine
mouthrinse on cathepsin C activity in human
saliva. Adv Med Sci 2006;51 Suppl 1:96-99.
12. Guha-Chowdhury N, Clark AG, Sissons CH. Inhi-
bition of puried enolases from oral bacteria by
uoride. Oral Microbiol Immunol 1997;12(2):
91-97.
13. Shani S, Friedman M, Steinberg D. The anticario-
genic effect of amine uorides on Streptococcus
sobrinus and glucosyltransferase in biolms.
Caries Res 2000;34(3):260-267.
14. Dabrowska E, Letko M, Roszkowska-Jakimiec W,
Letko R, Jamiolkowski J. Effect of uoride prepa-
rations on the activity of human salivary cathep-
sin C. Rocz Akad Med Bialymst 2005;50 Suppl
1:160-162.
15. Summit. Fundamentals of operative dentistry. In:
Burgess JO, Xu X. Fluoride releasing materials,
ed. 3. Carol Stream, IL: Quintessence Publishing
Co.; 2006:413-415.
16. Sandt C, Barbeau J, Gagnon MA, Laeur M.
Role of the ammonium group in the diffusion of
quaternary ammonium compounds in Strepto-
coccus mutans biolms. J Antimicrob Chemother
2007;60(6):1281-1287.
17. Marcotte L, Therien-Aubin H, Sandt C, Barbeau
J, Laeur M. Solute size effects on the diffusion
in biolms of Streptococcus mutans. Biofouling
2004;20(4-5):189-201.
Caries Detection and Prevention Efcacy of antiplaque mouthwashes
e114 May/June 2011 General Dentistry www.agd.org
18. Pizzo G, La Cara M, Licata ME, Pizzo I, DAngelo
M. The effects of an essential oil and an amine
uoride/stannous uoride mouthrinse on supra-
gingival plaque regrowth. J Periodontol 2008;
79(7):1177-1183.
19. Featherstone JD. The science and practice of
caries prevention. J Am Dent Assoc 2000;
131(7):887-899.
20. Altenburger MJ, Klasser M, Schirrmeister JF,
Hellwig E. Remineralisation of carious enamel
lesions after application of a CHX/F-mouthrinse
compared with sole CHX- and placebo-applica-
tion. Oral Health Prev Dent 2006;4(4):255-263.
21. Mendieta C, Vallcorba N, Binney A, Addy M.
Comparison of 2 chlorhexidine mouthwashes
on plaque regrowth in vivo and dietary staining
in vitro. J Clin Periodontol 1994;21(4):296-300.
22. Duarte AR, Peres MA, Vieira RS, Ramos-Jorge
ML, Modesto A. Effectiveness of two mouth
rinses solutions in arresting caries lesions: A
short-term clinical trial. Oral Health Prev Dent
2008;6(3):231-238.
23. Gunsolley JC. A meta-analysis of six-month
studies of antiplaque and antigingivitis agents. J
Am Dent Assoc 2006;137(12):1649-1657.
24. White DJ, Barker ML, Klukowska M. In vivo anti-
plaque efcacy of combined antimicrobial denti-
frice and rinse hygiene regimens. Am J Dent
2008;21(3):189-196.
25. Zimmer S, Kolbe C, Kaiser G, Krage T, Ommer-
born M, Barthel C. Clinical efcacy of ossing
versus use of antimicrobial rinses. J Periodontol
2006;77(8):1380-1385.
26. Knishkowy B, Sgan-Cohen HD. Oral health prac-
tices among adolescents: A study from family
practice clinics in Israel. Int J Adolesc Med
Health 2005;17(2):99-104.
27. Roldan S, Herrera D, Santa-Cruz I, OConnor A,
Gonzalez I, Sanz M. Comparative effects of dif-
ferent chlorhexidine mouth-rinse formulations
on volatile sulphur compounds and salivary bac-
terial counts. J Clin Periodontol 2004;31(12):
1128-1134.
28. Kolahi J, Soolari A. Rinsing with chlorhexidine
gluconate solution after brushing and ossing
teeth: A systematic review of effectiveness.
Quintessence Int 2006;37(8):605-612.
29. Bascones A, Morante S, Mateos L, Mata M, Pob-
let J. Inuence of additional active ingredients
on the effectiveness of non-alcoholic chlorhexi-
dine mouthwashes: A randomized controlled
trial. J Periodontol 2005;76(9):1469-1475.
30. Forgie AH, Paterson M, Pine CM, Pitts NB, Nu-
gent ZJ. A randomized controlled trial of the
caries-preventive efcacy of a chlorhexidine-
containing varnish in high-caries-risk adoles-
cents. Caries Res 2000;34:432-439.
31. Featherstone JD. Delivery challenges for uoride,
chlorhexidine and xylitol. BMC Oral Health 2006;
6 Suppl 1:S8.
32. de Amorim RG, Leal SC, Bezerra AC, de Amorim
FP, de Toledo OA. Association of chlorhexidine
and uoride for plaque control and white spot
lesion remineralization in primary dentition. Int J
Paediatr Dent 2008;18(6):446-451.
33. Jayaprakash K, Veeresha KL, Hiremath SS. A com-
parative study of two mouthrinses on plaque and
gingivitis in school children in the age group of
13-16 years in Bangalore city. J Indian Soc Pedod
Prev Dent 2007;25(3):126-129.
34. Autio-Gold J. The role of chlorhexidine in caries
prevention. Oper Dent 2008;33(6):710-716.
35. Newbrun E. Topical uorides in caries preven-
tion and management: A North American per-
spective. J Dent Educ 2001;65(10):1078-1083.
36. Torres-Lagares D, Infante-Cossio P, Gutierrez-
Perez JL, Romero-Ruiz MM, Garcia-Calderon M,
Serrera-Figallo MA. Intra-alveolar chlorhexidine
gel for the prevention of dry socket in mandibu-
lar third molar surgery. A pilot study. Med Oral
Patol Oral Cir Bucal 2006;11(2):E179-E184.
37. Ben-Yaakov D, Friedman M, Hirschfeld Z, Geda-
lia I. Fluoride enhancement of chlorhexidine up-
take by hydroxyapatite and enamel powders. J
Oral Rehabil 1984;11(1):65-70.
38. Ullsfoss BN, Ogaard B, Arends J, Ruben J, Rolla
G, Afseth J. Effect of a combined chlorhexidine
and NaF mouthrinse: An in vivo human caries
model study. Scand J Dent Res 1994;102(2):
109-112.
39. Casals E, Boukpessi T, McQueen CM, Eversole
SL, Faller RV. Anticaries potential of commercial
dentifrices as determined by uoridation and
remineralization efciency. J Contemp Dent
Pract 2007;8(7):1-10.
40. Pizzo G, Guiglia R, Imburgia M, Pizzo I,
DAngelo M, Giuliana G. The effects of antimi-
crobial sprays and mouthrinses on supragingival
plaque regrowth: A comparative study. J Perio-
dontol 2006;77(2):248-256.
41. Sheen S, Addy M. An in vitro evaluation of the
availability of cetylpyridinium chloride and
chlorhexidine in some commercially available
mouthrinse products. Br Dent J 2003;194(4):
207-210.
42. Kozak KM, Gibb R, Dunavent J, White DJ. Efca-
cy of a high bioavailable cetylpyridinium chlo-
ride mouthrinse over a 24-hour period: A plaque
imaging study. Am J Dent 2005;18 Spec
No:18A-23A.
43. Santos S, Herrera D, Lopez E, OConnor A, Gon-
zalez I, Sanz M. A randomized clinical trial on
the short-term clinical and microbiological ef-
fects of the adjunctive use of a 0.05% chlorhex-
idine mouth rinse for patients in supportive
periodontal care. J Clin Periodontol 2004;31
(1):45-51.
44. Eley BM. Antibacterial agents in the control of
supragingival plaqueA review. Br Dent J 1999;
186(6):286-296.
45. de Souza LB, de Aquino SG, de Souza PP, He-
bling J, Costa CA. Cytotoxic effects of different
concentrations of chlorhexidine. Am J Dent 2007;
20(6):400-404.
46. Giannelli M, Chellini F, Margheri M, Tonelli P,
Tani A. Effect of chlorhexidine digluconate on
different cell types: a molecular and ultrastruc-
tural investigation. Toxicol In Vitro 2008;22(2):
308-317.
47. Jeng JH, Hsieh CC, Lan WH, Chang MC, Lin SK,
Hahn LJ, Kuo MY. Cytotoxicity of sodium uoride
on human oral mucosal broblasts and its mech-
anisms. Cell Biol Toxicol 1998;14(6):383-389.
48. He LF, Chen JG. DNA damage, apoptosis and
cell cycle changes induced by uoride in rat oral
mucosal cells and hepatocytes. World J Gastro-
enterol 2006;12(7):1144-1148.
49. Kreth J, Zhu L, Merritt J, Shi W, Qi F. Role of su-
crose in the tness of Streptococcus mutans.
Oral Microbiol Immunol 2008;23(3):213-219.
50. Mitchell DA, Mitchell L. Oxford handbook of
clinical dentistry. In: Mitchell DA, Mitchell L.
Periodontology, ed. 4. London: Oxford University
Press;2005:202.
Manufacturers
Church & Dwight Co., Inc., Princeton, NJ
800.524.1328, www.churchdwight.com
GDK Densell, Buenos Aires, Argentina
054.11.4962.1212, www.densell.com.ar
GlaxoSmithKline, Research Triangle Park, NC
888.825.5249, www.gsk.com
Platinum Pharmaceuticals, Karachi, Pakistan
92.21.4750.1123, www.platinumpharma.net
Roomi Enterprises, Karachi, Pakistan
92.21.1110.16023, www.roomi.com.pk
www.agd.org General Dentistry May/June 2011 e115
COMMENT