Periodontology 2000, Vol. 48, 2008, 66–75
Printed in Singapore. All rights reserved
Halitosis (breath odor)
CRISPIAN SCULLY & JOHN GREENMAN
Humans emit a variety of volatile and nonvolatile
molecules that are influenced by genetics, diet, stress
and disease. Halitosis, from the Latin for breath hal-
itus, is a complaint analogous to body odor (30) and
is used to describe any disagreeable odor in the
breath. Several terms describe and characterize the
different aspects of the problem (Table 1) (37, 47).
Halitosis frequently causes embarrassment, may
affect interpersonal social communication (4) and
has also become an important market for the phar-
macological and cosmetic industries (with millions of
pounds spent annually on medications and over-the-
counter products). Oral malodor may rank behind
only dental caries and periodontal disease as the
reason for patients visiting the dentist, the perception
of halitosis being different in culturally diverse pop-
ulations (38).
The true prevalence of halitosis is unknown and
some reports are difficult to evaluate unless they
specify the classification, terminology and method-
ology used. Currently available epidemiological data
are difficult to evaluate as they are mainly based on
subjective self-estimation of malodor, which is well
known to be limited by inaccuracy and low sensitiv-
ity. However, the available evidence suggests that
halitosis is common and can affect people of all ages.
The prevalence of persistent oral malodor in a recent
Brazilian study was reported to be 15%, was nearly
three times higher in men than in women (regardless
of age) and the risk was slightly more than three
times higher in people over 20 years of age compared
with those aged 20 years or under, controlling for
gender (34). The large majority of studies report that
about 30% of people have halitosis (31, 36, 47) but
some studies estimate that more than 50% of the
population have halitosis (63).
Types of breath odor
Oral malodor is common on awakening (morning
breath), and is transient and rarely of any special
66
 2008 The Authors.
Journal compilation  2008 Blackwell Munksgaard
PERIODONTOLOGY 2000
significance (36, 37, 47, 51, 69), probably resulting
from increased microbial metabolic activity during
sleep that is aggravated by a physiological reduction
in salivary flow, lack of nocturnal physiologic oral
cleansing (e.g. movement of the facial and oral
muscles) and variable oral hygiene procedures prior
to sleep. Starvation can lead to a similar malodor.
These forms of oral malodor can be readily rectified
by eating, oral cleansing and rinsing the mouth with
fresh water (17). Tongue cleansing using a scraper
may help but was found to be unable to prevent
morning oral malodor in the absence of tooth
cleaning in periodontally healthy individuals (21).
Malodor at other times may be the consequence of
lifestyle. Halitosis as a result of the ingestion of cer-
tain food and drinks, such as spices, garlic, onion,
durian, cabbage, cauliflower and radish, or of habits
such as smoking tobacco or drinking alcohol, is
usually transient, often caused by sulfur-containing
volatile agents and is considered to arise both from
intra-oral (food debris) and extra-oral (respiratory)
origins (60). Tobacco smoke contains volatile sulfur
compounds, which are at least partly responsible for
the oral malodor of smokers (57), but tobacco prod-
ucts also predispose to dry mouth and periodontal
disease – further causes of malodor. Alcohol intake
may be a predictor of oral malodor (46). The avoid-
ance of these foods and habits is the best prevention.
Halitosis from oral causes
In about 85% of patients with persistent genuine
halitosis, the odor originates from the mouth (12),
mainly from microorganisms. It is likely that there is
a complex interaction between several oral bacteria
species (mainly gram-negative anerobic flora) be-
cause no single specific bacterial infection has
invariably been associated with halitosis (Box 1). The
bacterium Solobacterium moorei was found to be
present in all subjects with halitosis, but not in any
control subjects, suggesting that some subjects with
halitosis harbor some distinct bacterial species on

Table 1. Terminology related to halitosis
Terms used Definition
Halitosis Any disagreeable odor of expired air, regardless of origin
Bad breath Lay term for halitosis
Genuine halitosis Where breath malodor can be verified objectively
Physiologic halitosis, also termed
transient halitosis
e.g. morning breath
Pseudo-halitosis No objective evidence of malodor, but the patient thinks they have it
Halitophobia The patient persists in believing they have halitosis despite firm evidence for the absence of
objective evidence
Box 1. Microorganisms mainly associated with hali-
tosis (listed in alphabetical order)
Centipeda periodontii
Eikenella corrodens
Enterobacteriaceae
Fusobacterium nucleatum subsp. nucleatum
Fusobacterium nucleatum subsp. polymorphum
Fusobacterium nucleatum subsp. vincentii
Fusobacterium periodonticum
Porphyromonas endodontalis
Porphyromonas gingivalis
Prevotella (Bacteroides) melaninogenica
Prevotella intermedia
Bacteroides (Bacteroides) loescheii
Solobacterium moorei
Tannerella forsythia (Bacteroides forsythus)
Treponema denticola
their dorsal tongue (22). The tongue is the location of
many of the organisms implicated.
The odiferous products that cause halitosis arise
from the interaction of microbes with specific sub-
strates, namely the amino acids cysteine, methionine,
tryptophan, arginine and lysine that are biotrans-
formed into hydrogen sulfide, methylmercaptan, in-
dole, putrescine and cadaverine, respectively (20).
These and other amino acids can also be fermented
into short-chain organic acids (e.g. propionate and
butyrate) by many of the anerobic species listed in
Box 1. Although some free amino acids (primary
substrates) can be found in saliva (and gingival
crevicular fluid is a richer source still), the majority of
the immediate substrates are derived from secondary
substrates – proteins and peptides – which are
hydrolysed into primary substrates by the proteolytic
Halitosis (breath odor)
Pathologic halitosis
Subclassified into
• oral malodor (Foetor oris Foetor ex oris) and
• extra-oral
and peptidolytic activities of the microbes. Peptides
include glutathione (derived from desquamating
cells), which many microbial species can use directly,
and proteins may come from food or saliva (en-
trapped within microbial biofilms). Salivary mucins
may also be an important source of primary sub-
strates, but microbial deglycosylation may be a nec-
essary first step prior to full proteolytic digestion (58).
In common with caries and periodontal disease,
two theories of microbial etiology can be proposed: a
Ôspecific theoryÕ (that just a few ÔsingleÕ species are
etiological and capable of causing malodor; their
presence solely will explain malodor) and a Ônon-
specific theoryÕ, which suggests that many species
(most being strict anerobes) have the ability to bio-
transform substrates into volatile compounds or
volatile sulfur compounds and that many groups can
therefore substitute for others; there is no single
causative species. However, there is a relationship
between bacterial numbers on the tongue (as mea-
sured by determining the colony-forming units per
square centimeter) and oral malodor, so it does ap-
pear that the load of microbes per mouth (i.e. the
thickness or aerial density of biofilms) is the most
important feature of chronic oral malodor, rather
than the presence or absence of specific microbial
agents. It is probably the microbial load that best
predicts the total levels of biotransforming enzymes
(and biotransforming microenvironments) found in
the mouth. However, it is clear that anerobes and
anerobic environments are an important feature of
biogenesis (36, 37, 51, 52, 69). These anerobes pro-
duce malodor volatile compounds in many instances,
which include (28) (see Table 2) the following:
• volatile sulfur compounds, mainly methyl mer-
captan and hydrogen sulfide, which are the main
contributors to intra-oral halitosis. The volatile
67
Scully & Greenman

disease, disorders of the oral mucosa, reduced sali-

Table 2. Odoriferous components that can give rise
to oral malodor
Volatile sulfur compounds Methyl mercaptan
Hydrogen sulfide
Dimethyl sulfide
Diamines Putrescine
Cadaverine
Short-chain fatty acids Butyric acid
Valeric acid
Propionic acid
Indoles Indole
Methyl-indole (skatole)
sulfur compound, dimethyl sulfide, is the main
contributor to extra-oral or blood-borne halitosis
(62) but may also contribute to oral malodor.
• short-chain fatty acids (butyric, valeric and propi-
onic acids).
• polyamines (putrescine and cadaverine).
• acetone, 2-butanone, 2-pentanone and 1-propanol
are common to all volunteers with halitosis and are
present in both alveolar (lung) and mouth air; in-
dole and dimethyl selenide are present in alveolar
air (65, 66).
Most compounds appeared to be (partly) produced
endogenously and ⁄ or in the mouth (65, 66).
Persistent halitosis occurring as a result of intra-
oral causes usually originates from the posterior
dorsum of the tongue and ⁄ or oral ⁄ dental diseases,
including periodontal disease, and can be severe
enough to be considered socially unacceptable (also
known as pathologic halitosis). It is most likely to
occur in patients with conditions that favour the
accumulation of food and bacterial plaque on intra-
oral surfaces (teeth, gingiva and mucosal tissues,
especially the dorsum of the tongue) and the devel-
opment of anerobic ecosystems. Predisposing factors
include poor oral hygiene, gingival and periodontal
vary flow and the wearing of dental appliances
(Table 3) (26, 36, 37, 51, 52, 69).
Prevention of infective processes, improvement of
oral hygiene (including the use of topical antimicro-
bial products, mouthwashes or toothpastes) and
sometimes the use of antimicrobial therapy, if nec-
essary, can usually manage this type of halitosis
(discussed in a later section).
Halitosis from extra-oral causes
Halitosis is less frequently associated with extra-oral
causes (i.e. conditions and diseases that do not affect
primarily the oral cavity). Respiratory disorders (of
the nose, sinuses, tonsils and pharyngeal regions), as
well as diseases of the gastrointestinal system, can
result in the presence of odiforous gases in the air
expelled from the oral cavity and the nose (Table 4)
(10, 36, 37, 40, 69).
Nasal sepsis or foreign bodies, or infection of the
paranasal sinuses or respiratory tract, may be a cause
of halitosis. In children, the insertion of foreign
bodies (such as small toys) into the nose, and sub-
sequent sepsis, is a common cause of halitosis. In
adults, infections in the respiratory tract, such as
tonsillitis, bronchitis, bronchiectasis or other lung
infections, or tumours, may be responsible. The
presence of a tonsillolith represents a 10-fold in-
creased risk of abnormal volatile sulfur compound
halitometry and can be considered as a predictable
factor for abnormal halitometry (40).
Halitosis is a frequent symptom of gastro-esopha-
geal reflux disease and may be considered as an ex-
tra-esophageal manifestation of gastro-esophageal
reflux disease (32, 59). Helicobacter pylori should also
be considered as a possible cause of halitosis (2, 29).
Although some have not found an association be-
tween functional dyspepsia, peptic ulcer disease and

Table 3. Main oral causes of halitosis

Plaque-related gingival and Gingivitis, periodontitis, acute necrotizing ulcerative
periodontal disease gingivitis, pericoronitis, abscesses
Ulceration Systemic disease (inflammatory ⁄ infectious disorders, cutaneous,
gastrointestinal and hematological disease), malignancy,
local causes, aphthae, drugs
Hyposalivation (e.g. from drugs, SjögrenÕs syndrome, radiotherapy, chemotherapy)
Tongue coating Poor hygiene
Wearing dental appliances Poor hygiene
Dental conditions Food packing
Bone diseases Jaw dry sockets, osteomyelitis, osteonecrosis, malignancy

68

Table 4. Extra-oral causes of halitosis
Respiratory system Sinusitis
(microbial etiology) Antral malignancy
Cleft palate
Foreign bodies in the nose
Nasal malignancy
Tonsilloliths
Tonsillitis
Pharyngeal malignancy
Lung infections
Bronchitis
Bronchiectasis
Lung malignancy
Gastrointestinal Esophageal diverticulum
tract Gastro-esophageal reflux disease
Malignancy
Metabolic disorders Acetone-like smell in
(blood borne) uncontrolled diabetes
Uremic breath in renal failure
Foetor hepaticus in liver disease
Trimethylaminuria
(fish odor syndrome)
Hypermethioninemia
Cystinosis
Drugs • amphetamines
(blood borne) • chloral hydrate
• cytotoxic agents
• dimethyl sulphoxide
• disulfiram
• nitrates and nitrites
• phenothiazines
• solvent abuse
Psychogenic causes
H. pylori infection with halitosis occurrence or
severity (32), H. pylori has been suggested as a cause,
and can produce volatile sulfur compounds (29).
Furthermore, with some metabolic disorders,
odiferous agents circulating in the bloodstream can
be exhaled, through alveolar gas exchange, into the
breath and cause halitosis (also known as blood-
borne halitosis). The volatile sulfur compound
dimethyl sulfide is the main contributor to extra-oral
or blood-borne halitosis, as the result of a hitherto-
unknown metabolic disorder (62).
Diabetes can give rise to ketone bodies in the
breath. The genetic metabolic disorder trimethyl-
aminuria (fish odor syndrome) is the principal cause
of undiagnosed body odor caused by excessive
blood levels of trimethylamine. Many trimethyl-
Halitosis (breath odor)
aminuria-positive individuals present with oral
symptoms of dysguesia and halitosis, as well as
body odor (66). In trimethylaminuria, trimethyl-
amine is excreted into body fluids and breath,
leading to a persistent oral and body malodor sim-
ilar to that of rotten fish. The causal factor of
excessive free trimethylamine is substrate overload
or reduced enzyme capacity as a result of an
inherited deficiency, liver damage and ⁄ or hormonal
modulation (transient trimethylaminuria). The latter
explains the occurrence of transient body and oral
malodor in some women around the time of men-
struation (56). Hypermethioninemia is another rare
metabolic disorder that can lead to oral malodor.
Cystinosis is a rare autosomal-recessive disorder
characterized by the intralysosomal accumulation of
cystine. Cysteamine removes cystine from the lyso-
some and slows down the progression of the dis-
ease, but one of its adverse effects is halitosis as it is
converted to dimethyl sulfide and methyl mercap-
tan. The expired air of cystinotic patients contains
elevated concentrations of dimethyl sulfide and
methyl mercaptan (3).
More rarely, halitosis can arise as a side effect of
medications containing a dimethyl sulfide structure
that can appear in breath air (33).
Psychogenic or psychosomatic factors may be at
play in some patients. Interestingly, anxiety itself
increases the levels of volatile sulfur compounds (8).
Not all persons who believe they have halitosis
actually have any malodor, and this pseudo-hali-
tosis can be a real clinical dilemma (53). In those in
whom no evidence of halitosis can be detected,
even with objective testing, and in whom the
complaint persists, halitosis may be attributed to a
form of delusion or monosymptomatic hypochon-
driasis (self-halitosis, halitophobia). Such patients
rarely wish to visit a psychological specialist be-
cause they fail to recognize their own psychological
condition and never doubt they have oral malodor.
Other peopleÕs behavior, or perceived behavior,
such as apparently covering the nose or averting
the face, is typically misinterpreted by these pa-
tients as an indication that their breath is indeed
offensive. Such patients may have latent psycho-
somatic illness tendencies and may be mentally
immature. Many of these patients will adopt
behavior to minimize their perceived problem, such
as covering the mouth when talking, avoiding or
keeping a distance from other people, using
chewing gum, mints, mouthwashes or sprays de-
signed to reduce malodor, or excessively cleaning
their tongue or mouth.
69
Scully & Greenman
Diagnosis
It is important to understand whether a given com-
plaint of bad breath is justified and whether the odor
originates in the mouth, nose or elsewhere. A full
history and an oral examination will be required.
The first step in assessment is to determine whe-
ther halitosis is present. This is important as most
individuals are poor judges of their own breath odor
(14). There are three primary measurement methods
of halitosis. Organoleptic measurement and gas
chromatography are very reliable methods, but clin-
ically are not very easily implemented. The use of
organoleptic measurement is suggested as the Ôgold
standardÕ. Gas chromatography is the preferable
method if precise measurements of specific gases are
required. Sulfide monitoring is an easily used meth-
od, but has the limitation that important odors are
not detected. The scientific and practical value of
additional or alternative measurement methods,
such as the BANA (benzoyl–arginine–naphthyl–
amide) test, chemical sensors, the salivary incubation
test, quantifying b-galactosidase activity, ammonia
monitoring, the ninhydrin method and the poly-
merase chain reaction, have yet to be fully estab-
lished (5, 6).
Assessment is thus usually based upon organo-
leptic assessment of exhaled air, namely the clinician
sniffs the air exhaled from the mouth and nose and
subjectively defines the presence or absence of mal-
odor (13). Smelling both nose and mouth air is
important as malodor detectable from the nose alone
(asking the patient to breathe while the mouth is
closed) is likely to come from the nose or the sinuses,
or from respiratory or gastrointestinal tracts.
For purposes of fine quantification (for example in
clinical trials of the efficacy of antimalodor com-
pounds) it has been suggested that organoleptic
assessments should be performed by two or more
different examiners (68) and that both the human
subject and the examiners should follow some
instructions in order to obtain more reliable results.
(69). However, unless halitosis is borderline between
detectable and nondetectable, then providing the
clinician has full smell acuity, only one judge should
suffice for an individual patient. As a general rule
in clinical practice, it is advisable that the patient
abstains from eating odiferous foods for 48 h before
the assessment and that both the patient and the
examiner refrain from drinking coffee, tea or juice,
smoking and using scented cosmetics before the
assessment (69).
70
More objective measurements of halitosis are
available but they are rarely used in routine clinical
practice as they are expensive and time-consuming.
Some centers are able to undertake objective mea-
surements of the volatile sulfur compounds using a
halimeter (Interscan Corp., Chatsworth, CA), a por-
table sulfide monitor. However, this machine cannot
differentiate between the different types of sulfides
and cannot detect other classes of volatile com-
pounds.
Gas chromatography is considered by many to be
the method of choice for differentiating and quanti-
fying the volatile sulfur compound and (especially if
it runs with a Mass Spectrometry Detector) can also
distinguish other classes of compound (e.g. indole).
Traditional laboratory gas chromatography or gas
chromatography–mass spectrometry are cumber-
some, need inert column carrier gas (gas cylinders of
nitrogen or helium) and require technicians or
specialists with adequate training, and are thus clin-
ically impractical. (66). However, a newly developed
portable gas chromatograph (OralChromaTM, Abi-
medical, Abilit Corp., Osaka, Japan) has now been
described (61), which does not use a special carrier
gas (using air instead) and is highly sensitive yet
relatively low cost compared with a standard gas
chromatograph.
Likewise, secondary tests associating measure-
ments with oral malodor (e.g. detection of likely
causative bacteria and ⁄ or microbial enzymatic
activity) fall outside the routine clinical assessment of
halitosis.
Examination of the oral flora, for example using the
BANA test or dark-field microscopy, can be helpful, at
least for patient education.
Assay for the major glycosidic enzyme (b-galacto-
sidase) in saliva, which deglycosylates oral mucins,
leading to their subsequent proteolysis and putre-
faction, may also be useful (58).
If no malodor can be found during the initial
examination, the assessment for halitosis should be
repeated on two or three different days.
Thereafter, if halitosis is still not present, the pa-
tient can be considered to be affected by imaginary
(pseudo-halitosis) - a diagnosis that can be supported
by established questionnaires (69). Experienced and
intuitive clinicians are well placed to suspect imagi-
nary (pseudo-halitosis) at an early stage of the
assessment. In general, obsessive behavior, depres-
sion, phobic anxiety, paranoid ideation, reduced so-
cial interactions and the wrong interpretation of
peopleÕs actions as an indication that their breath is
offensive (e.g. opening windows, covering their nose),

can be warning signs of pseudo-halitosis (24, 36, 47).
However, these factors, alone, are insufficient to
categorize a patient under the label of pseudo-hali-
tosis, as this remains a diagnosis of exclusion.
Management
The management of halitosis depends largely on the
cause.
Avoiding smoking, drugs and foods that might be
responsible for halitosis is sensible. In addition,
chewing gum, parsley, mint, cloves or fennel seeds,
and the use of proprietary Ôfresh breathÕ preparations,
may help. Cosmetic nonpharmacological methods,
such as chewing gums, mints, flavored sprays, and
some mouth rinses, however, merely provide a
competing and temporary smell that may mask the
unfavourable odor. (36).
In the large majority of patients, treatment is pri-
marily directed towards reducing the accumulation
of food debris and malodor-producing oral bacteria.
This is usually achieved via treating oral ⁄ dental
diseases, improving oral hygiene and reducing the
tongue coating. A combination of treatments typi-
cally helps (15, 37, 43, 49–52).
Regular meals are important, as is dental prophy-
laxis, and the patient should use appropriate regular
oral hygiene procedures, which include regular tooth
cleaning (brushing and interdental flossing) and the
use of antimicrobial toothpastes and ⁄ or mouth-
washes. Generally, it is recommended that mouth-
washes should be used two or three times daily for at
least 30 s. A multitude of oral healthcare and phar-
maceutical products is available over the counter,
testimony to the extent of the perceived, or indeed
real, problem of halitosis. The effectiveness of active
ingredients in oral healthcare products is dependent
on their concentration and, above a certain concen-
tration the ingredients can have unpleasant side ef-
fects (5, 6).
Mouthwashes containing chlorhexidine gluconate,
ceptylpyridinium chloride or triclosan, a two-phase
oil:water mouthwash, may be beneficial (27, 41–43,
50). Good short-term results have been reported with
chlorhexidine, essential oils and ceptylpyridinium
chloride for up to 2 or 3 h. Metal ions and oxidizing
agents, such as hydrogen peroxide, chlorine dioxide
and iminium chloride, can actively neutralize volatile
sulfur compounds. Zinc seems to be an effective and
safe metal at concentrations of at least 1%: at pres-
ent, a combination of low concentrations of zinc and
chlorhexidine seems to be the most efficient way to
Halitosis (breath odor)
remove the volatile sulfur compound that causes bad
breath (64). Other products are available, such as
those containing chlorine dioxide, and alpha ionone,
but the evidence demonstrating their efficacy is cur-
rently weak.
Toothpastes containing triclosan and a copolymer
(Colgate Total Toothpaste) provide effective control
of breath odor at 12 h after brushing the teeth (35,
55). There is significant, immediate antimalodor
activity also for a 0.454% stabilized SnF2 sodium
hexametaphosphate dentifrice (16).
If oral malodor persists, the tongue may be the
source of odor and hence gentle and regular tongue
cleaning is indicated (11). This is aimed at dislodging
trapped food, cells and bacteria from between the
filiform papillae, thus decreasing the concentration
of volatile sulfur compounds. Tongue cleaning
should be carried out at night (because if done early
during the day may induce retching) using a tongue
scraper or a hard toothbrush and cold water, but no
toothpaste. There is weak and unreliable evidence
showing a small, but statistically significant, differ-
ence in the reduction of volatile sulfur compound
levels when tongue scrapers or cleaners, rather than
toothbrushes, are used to reduce halitosis in adults
(36). There is no high-level evidence comparing
mechanical cleaning with other forms of tongue
cleaning. The benefits of tongue scraping seem to be
only short term (36).
The results of a range of treatments have been
outlined elsewhere (5) but in Table 5 we show a
comparison of various oral malodor therapies or
treatments made on the basis of objective reduction
of volatile sulfur compound or component gases (by
gas chromatography, halimeter or sensor) in com-
parison with appropriate controls (trials of >10
subjects).
In recalcitrant cases, the specialist empirically may
use a 1-week course of metronidazole (200 mg three
times daily) in an effort to eliminate unidentified
anerobic infections; metronidazole may reduce ton-
gue microbiota and odor levels (23).
Halitosis as a result of extra-oral causes is managed
through the treatment of the underlying cause (see
Table 1). Medical help may be required to manage
patients with a systemic background to their com-
plaint. Triple-drug eradication therapy in patients
with functional dyspepsia and H. pylori infection has
resulted in sustained resolution of halitosis during
long-term follow-up in the majority (25). Pseudo-
halitosis almost always requires referral for clinical
psychologist management. In extreme instances,
patients become socially isolated, may have their
71
72
Table 5. Comparison of various oral malodor therapies or treatments made on the basis of reduction of volatile sulfur compounds (VSC) or component gases (by
gas chromatography, halimeter or sensor) in comparison with appropriate controls (trials of n > 10 subjects)
Category of treatments Volunteers Comments Outcomes Instrument used to Statistical Reference
per group measure VSC or gas significance
of reduction
Scully & Greenman

Clinical therapy alone

POHC and n = 923 Post-treatment assessments following 98% of population showed Halimetry NA 39
mouthwash (clinic) visits to bad breath clinic reductions of VSC from
>180p.p.b. to <180
POHC n = 37 Two-year study; test group received 60% reduction in CH3SH when Electronic P < 0.05 1
POHC every week including tongue measured using an electronic
cleaning. Control group (n = 30) did not sensor sensitive to CH3SH
POHC (clinic) n = 92 Before vs. after clinical treatment at 80% reduction in VSC Gas chromatography P < 0.0001 61
bad breath clinic
Short-term (0-8h) effects (single use)
Tongue cleaning n = 30 Three-hour, randomized crossover 42% reduction in VSC immediately Halimetry P < 0.001 54
study (three groups) after treatment and still significantly
reduced for up to 25 minutes
thereafter
Zn2 + mouthrinse n = 62 Three-hour, parallel-study (three 70-80% reduction of VSC at 1, 2 Gas chromatography P < 0.05 48
groups, Zn2 + vs. controls and 3h
Zn2 + (toothpaste) n = 11 Three-hour, crossover study; five Between 40 and 70% reduction for Gas chromatography P < 0.05 7
treatments (+ 1-week washout periods) both H2S and CH3SH in the Zn
(silica base dentrifice with 2% Zn) pastes compared with controls at 1,
2 and 3 h post-treatment
ClO2 (mouthwash) n = 16 96-h parallel study with two groups: test 21% and 19% reduction in VSC at Halimetry P < 0.01 18
(ClO2 at 0.1%) and control (water; 2 h and 4 h respectively
n = 15)
Two-phase rinse n = 19 One-day, parallel study with three For two-phase rinse, 38% reduction Halimetry P < 0.05 45
(essential oils groups (two-phase mouthwash, in VSC at 8–10 h compared with P < 0.05
plus aqueous CPC) CHX and placebo) placebo.
Chlorhexidine For CHX, 50% reduction in VSC at
gluconate (0.2%) 8–10 h compared with placebo
Mouthrinses n = 12 A six-step double-blind, crossover, For CHX (0.12%), a 63% reduction Halimetry P = 0.01 9
CHX (0.4%) randomized study on morning breath in VSC. P = 0.001
CHX (0.05%) in volunteers with healthy For CHX (0.2%), a 70% reduction in
Triclosan (0.03%) periodontium (who refrained VSC. For other agents, reductions in
CPC (0.05%) from mechanical plaque control VSC were not statistically
during 4-day periods). significant.
 Halitosis (breath odor)

teeth extracted and occasionally commit suicide.

CH3SH, methyl mercaptan; CHX, chlorhexidine; ClO2, chlorine dioxide; CPC, cetylpyridinium chloride; GC, gas chromatography; H2 S, hydrogen sulfide; POHC, professional oral healthcare; Sn, stannous; VSC, volatile sulfur
Reference
However, patients often refuse to acknowledge that
they may have a psychological problem. Therefore,

19

67
the involvement of a third party (e.g. a confidant such
as a close family member or a trusted friend) in the
management may provide the patient with additional
of reduction
significance
Statistical

psychological support to consider the problem in a

P < 0.05

P < 0.01
more objective manner (44).

References

Exclusions: trials that have fewer than 11 subjects; those that only use organoleptic or hedonic methods; and those where subjects have known inflammatory periodontal disease.
measure VSC or gas
Instrument used to

1. Adachi M, Ishihara K, Abe S, Okuda K, Ishikawa T. Effect of

professional oral health care on the elderly living in nursing
homes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
Halimetry

Halimetry

2002: 94: 191–195.

2. Adler I, Denninghoff VC, Alvarez MI, Avagnina A, Yoshida
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