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346
İ. Dişikırık and M. A. Kanmaz
26.2 History ofHalitosis
The history of halitosis dates back to ancient times. Some sources mention halitosis
in Greek, Roman, and Jewish cultures [9]. Halitosis was accepted as a clinical nding after Howe, one of the pioneers of halitosis research, described this symptom in
1874 [10].
In 1934, Fair and Wells developed a device to measure odor. Later, in 1940 and
1950, Fosdic and his colleagues conducted various studies on the etiology of halitosis using this device [3]. In the 1960s, Tonzetich and his colleagues introduced the
gas chromatography method that measured volatile sulfur compounds (VSCs) in
breath and saliva [11].
26.3 Epidemiology ofHalitosis
In the few studies investigating the prevalence of halitosis in the general population,
this rate varies between 22 and 50% [12]. Miyazaki etal. [13] found this rate to be
28% in Japan’s 18–64years age group. They found no difference in the amount of
VSC between men and women and that age was not a risk factor for increased
VSC.In their study, Liu etal. [14] stated that this rate was 27.5% in the Chinese
population. In their research, Al-Ansari etal. [15] found this rate to be 23.3%.
In their study in Sweden, Soder etal. [16] evaluated lousy breath and periodontal
disease and reported that 2.4% had severe bad breath.
Some studies have found no difference between the incidence and severity of
halitosis between men and women [17, 18].
26.4 Classification ofHalitosis
The most common classication for halitosis is the classication made by Miyazaki
etal. According to this classication, halitosis is categorized as
1. True Halitosis.
2. Pseudo Halitosis.
3. Halitophobia is examined in three categories.
Genuine halitosis is a terrible breath problem easily diagnosed by organoleptic
and chemical means. Pseudohalitosis is a condition in which the patient believes he
has bad breath, even though he does not have bad breath. A state in which the patient
still believes that they have terrible breath despite being treated, whether it is real or
pseudohalitosis, is called Halitophobia [19].
Genuine halitosis is divided into physiological (temporary) and pathological.
Physiological halitosis describes lousy breath due to temporary conditions such as
dry mouth, hunger, stress, and consumption of smelly foods such as garlic and
onions. Bad morning breath is the most common example of temporary halitosis
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
347
because salivary secretion decreases during the night, the washing effect of saliva
decreases, and anaerobes are prevented. VSC production increases, resulting in bad
breath. This condition is not pathological and does not require treatment [9]. Again,
hunger odor is one of the causes of temporary halitosis and occurs due to the decomposition of pancreatic uid in the stomach during fasting.
Pathological halitosis is a condition that causes social problems that do not go
away despite oral hygiene and treatment.
26.5 Halitosis Physiopathology
Oral malodor: Saliva is formed by the proteolytic destruction of organic substances,
such as gingival crevicular uid, interdental plaque, shed epithelial residues, postnasal discharge, and blood, such as glucose, mucin, peptide, and protein, by microorganisms in the mouth, and as a result, the formation of VSC. VSC is the most
common cause of bad breath. These are hydrogen sulde (H2S), methyl mercaptan,
and dimethyl sulde [3]. On the other hand, diamines (putrescine, cadaverine), phenol compounds (indol, skatole, pyridine), short-chain fatty acids (butyric acid, propionic acid, valeric acid), alcohols, alkynes, ketones, and nitrogen-containing
compounds are also among the factors that can cause bad breath [20–22].
The microorganisms responsible for the hydrolysis of peptides and proteins and
the resulting VSC production are gram (−) proteolytic anaerobes [3, 23, 24]. The
bacteria responsible for VSC production are shown in Table26.1 [3, 23, 25].
The most important source region for VSC is the dorsoposterior region of the
tongue [26, 27]. Because this area is the largest surface area of the tongue, the
tongue papillae located here are protected from the proteolytic anaerobes accumulated between the taste buds from the washing effect of saliva, and these anatomical
structures also provide the anaerobic environment necessary for the reproduction of
bacteria. VSC concentration increases as you move from the tip of the tongue to the
root of the tongue.
These bacteria found in the subgingival area are signicantly associated with
chronic periodontitis and gingivitis and cause VSC formation in the periodontal
pocket and gingival crevicular uid [28]. The same microorganisms settle on the
tongue dorsum in individuals with a tongue coating. The papillary structure of the
Table 26.1 The bacteria responsible for VSC production
Actinobacillus
actinomycetemcomitans
Actinomyces species Desulfovibrio species Porphyromonas gingivalis
Atopobium parvulum Eikenella corrodens Prevotella species
Atopobium parvulum Eubacterium sulci Solobacterium moorei
Atopobium parvulum Fusobacterium species Tannerella forsythia
Atopobium parvulum Peptostreptococcus micros Treponema denticola
Campylobacter rectus Porphyromonas endodontalis
(Bacteriodes forsythus/Tannerella
forsythensis)
348
tongue dorsum provides the necessary anaerobic environment to reproduce these
microorganisms. The microorganisms multiply here, and the production of VSCs,
which causes bad breath, increases. Amino acids such as cysteine, and methionine,
which are necessary for VSC production and contain sulfur, are found in saliva and
gingival crevicular uid. Research shows that oral malodor may be associated with
gram (−) anaerobic bacteria in the saliva and dorsum of the tongue [28, 29].
There is a close relationship between oral malodor and the amount of saliva.
Factors that reduce the ow rate of saliva may cause halitosis.
In the mechanism of halitosis caused by non-oral causes, volatile sulfur compounds formed from mouth breathing, affecting the salivary glands, and therefore
eliminating the washing effect of saliva play a role. Halitosis can also be seen in
gastroesophageal reux due to the change in the acidity of the oral environment
[30]. In other systemic diseases, bad breath may occur due to changes in the oral
microora due to the medications’ effects.
İ. Dişikırık and M. A. Kanmaz
26.6 Etiology ofHalitosis
We can examine halitosis by dividing it into oral and non-oral causes.
26.6.1 Oral Halitosis (Intraoral Halitosis, Oral Malodor)
Bad breath is related to the condition of the oral cavity. Delanghe etal. [31] reported
that the cause of approximately 87% of halitosis was intraoral. 51% originate from
the tongue, 17% from gingivitis, 15% from periodontitis, and 17% from a mixture
[32]. Oral causes include periodontal diseases, implant diseases, caries, necrotic
dental pulps, mucosal ulcers, faulty restorations, 20-year pericoronitis, lack of salivation, presence of food residues, aphthous sores, dental abscesses, herpetic infections, candidiasis, xerostomia, poor oral hygiene. Causes such as peritonsillar
abscess, mouth breathing, all unpolished surfaces in the mouth, dorsal part of the
tongue being covered with plaque (large surface area of the tongue, papillary structure, and irregular and deeply ssured surface) can be listed as reasons.
26.6.1.1 Periodontal Infections
Bacteria associated with gingivitis and periodontitis are mostly gram (−) bacteria,
and these bacteria are responsible for VSC production. This explains why the VSC
level in the mouth has a positive relationship with the periodontal pocket depth and
why the amount of VSC increases as the number and depth of periodontal pockets
increase [5, 33, 34]. Low oxygen pressure in the deep periodontal pockets causes
the pH there to decrease and an anaerobic environment to form, activating the decarboxylation of amino acids (such as lysine ornithine) to cadaverine and putrescine,
two malodor diamines. This explains that VSC and other molecules may be essential in bad breath in gingivitis or periodontitis infections [35].
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
349
VSC causes thinning of periodontal pockets and mucosal epithelium, thereby
increasing the permeability of the epithelium, and the connective tissue beneath the
epithelium is exposed to bacterial metabolites, thereby accelerating the process of
periodontitis. Also, methyl mercaptan causes connective tissue destruction by
increasing collagenase production, interleukin-1, and cathepsin B production [6].
Additionally, methyl mercaptan affects the cytoskeleton of gingival broblasts.
Methyl mercaptan alters cell proliferation and migration. Based on these data, VSC
plays a role in the pathogenesis of gingivitis and periodontitis.
Tooth decay in children occurs due to the interaction of dietary carbohydrates
with bacteria in the mouth, especially Streptococcus Mutans, on the tooth surface.
Organic acids produced by bacteria fermenting carbohydrates demineralize the
tooth surface, causing tooth decay. This is a signicant cause of bad breath in children. If left unchecked, the decay progresses to the tooth’s inner layers, and the
inammation reaches the alveolar bone, resulting in dental abscesses. The most
effective way to prevent caries is to use uoride water at a rate of 1ppm. In addition,
reducing carbohydrate intake through food is an essential method in caries prevention. Children should start brushing their teeth from the age of three and should be
brought for dental check-ups.
26.6.1.2 Tongue Oriented Halitosis
The dorsal surface of the tongue has an irregular structure due to ssures and
mucosal papillae. This distinctive, rough structure creates a suitable environment
for the growth of bacteria [35, 36]. While approximately 25 bacteria can adhere to
a single cell in other parts of the mouth, about 100 bacteria can attach to a single
epithelial cell in the dorsum of the tongue. The irregular dorsal surface structure of
the tongue causes microorganisms in the tongue to escape the washing effect of
saliva and multiply. This tongue dorsum structure also provides low oxygen levels,
driving anaerobic to increase [13]. A coating is formed by accumulating food residues, epithelial residues, and bacteria on the tongue dorsum. This is called tongue
coating. VSC occurs when this tongue coating cannot be removed due to the irregular anatomical structure, which creates bad breath. A high correlation has been
reported between tongue coating and halitosis formation [18, 35, 36]. For this reason, the tongue dorsum is considered the primary source of bad breath [14, 33,
35, 37].
In people with periodontal disease, hydrogen sulde (H2S) and methyl mercaptan (CH3SH) production is predominant in the tongue dorsum [5, 18, 37, 38]. In
people with good oral hygiene and who do not have periodontal disease, the source
of halitosis is usually the tongue dorsum [39].
26.6.1.3 Peritonsillar Abscess
Peritonsillar abscess is one of the most common causes of bad breath in the pediatric
age group. It usually develops after suppurative infection of the tonsils. It occurs due to
the condition in the tonsil spreading to the peritonsillar area by perforating the tonsillar
capsule, often from the upper pole, and the infection may remain there or apply to
neighboring areas along the constrictor muscle. It may be caused by acute tonsillitis,
350
İ. Dişikırık and M. A. Kanmaz
but studies show anaerobes mainly cause it. Peritonsillar abscess is usually unilateral.
There is fever, odynophagia, dysphagia, trismus, and neck lymphadenopathy.
The patient speaks as if there was a hot potato in his mouth. The patient cannot
swallow his saliva due to pain, so his mouth becomes watery, and his breath smells.
In physical examination (FM), the tonsil is pushed downward and medially, and the
uvula is displaced to the opposite side. In the treatment, rst of all, abscess drainage
is performed. The patient is hospitalized if possible, and parenteral antibiotic treatment is started.
Candidiasis, which occurs due to weakening of the immune system seen in
patients with long-term antibiotic use or corticosteroid treatment, chemotherapy or
radiotherapy, and diabetic patients, is also a cause of halitosis in the pediatric age
group and is cured by the use of antifungal drugs. Children with leukemia who
receive radiotherapy and chemotherapy are also more prone to tissue destruction,
infection, and bleeding. In this case, since protein degradation provides a suitable
environment for accumulation of anaerobic bacteria, the production of odor- forming
VSCs increases, and this causes bad breath.
Oroantral stula, abscessed teeth, dental caries, open ulcers, stulas, and papillary losses can also cause halitosis by causing accumulation of food residues and
desquamated tissues.
In cases affecting the oral mucosa, such as herpetic gingivostomatitis, Vincent’s
stomatitis, measles, diphtheria, and herpangina, it is one of the causes of bad breath
by causing tissue destruction, changes in salivary ow, and putrication.
26.7 Paranasal Sinus Diseases
They have a share of 5% in the causes of halitosis in children. These diseases can
cause bad breath (postnasal drip), causing inammation and increased mucus secretion. Nasal obstruction may also lead to mouth breathing and disrupt oral hygiene [10].
Sinusitis is a suppurative infection of the paranasal sinuses and is often a complication of colds and allergic rhinitis. Besides this, sinusitis is high in patients with
cyanotic heart disease, cystic brosis, immunoglobulin deciency, immobile cilia
syndrome, and dental infection. Maxillary ethmoid and sphenoid sinuses are present
at birth. The frontal sinus develops in the rst year of life. The frontal sinuses may
only appear as airy spaces at age 10.
In its etiology, preventing mucociliary ow paves the way for bacterial proliferation. The causative agents are generally pneumococci, H. inuenza, M. catarrhalis,
anaerobic bacteria, and rarely Streptococci and Staphylococci. Sinusitis may develop
as a result of Aspergillus or Zygomycete infections in immunocompromised patients
and patients with neutropenia. The patient may experience mucopurulent rhinorrhea,
cough, snifing, nasal voice, facial swelling, tenderness, headache, and postnasal drip.
Diagnosis can be easily made with paranasal CT and direct lms. Amoxicillinclavulanic acid, trimethoprim, and Cefaclor are generally effective in treating acute
sinusitis. Complications are treated by drainage and parenteral route.
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
351
26.8 Adenoid Vegetation
Adenoid vegetation is another cause of pediatric halitosis. Adenoids are masses of
normal lymphoid tissue in the nasopharynx. It reaches its maximum size until the
age 3–7, spontaneously regresses, and becomes smaller after puberty. Adenoid
hypertrophy and frequent infections may obstruct the mouth of the Eustachian tube,
thus causing frequent middle ear infections or sinus infections by blocking the posterior sinus ostia. Chronic sinusitis causes constant irritation and hypertrophy of the
adenoid tissue due to chronic inammation and post-nasal discharge.
In addition, allergic reactions also cause adenoid hypertrophy. It most commonly
causes complaints of sleeping with the mouth open, snoring, hearing loss, and halitosis in children.
Adenoids are most often involved during throat infections affecting the lymphoid
tissues in the tonsil and lateral pharyngeal wall. Viral factors such as rhinovirus,
adenovirus, inuenza, and bacterial factors such as Group A Beta-Hemolytic
Streptococci (GABHS) play a role in developing the disease. Various studies have
shown that microorganisms that play a role in tonsil infection also cause adenoiditis
[12]. The treatment is adenoidectomy.
26.9 Chronic Pharyngitis
Factors that irritate are of great importance in the chronicity of pharyngitis.
Predisposing factors include acidic foods, smoking, spicy foods, environmental pollution, mouth breathing due to nasal congestion, and an atopic constitution.
Patients may apply to the ENT clinic complaining of a foreign body feeling in
their throat, a raspy cough, tingling, and bad breath. Treatment is symptomatic in
the acute phase. If there is a granular appearance, treatment can be made with the
Mandel solution. However, the most crucial thing in medicine is the removal of
predisposing factors. Polyps causing nasal obstruction, septal perforation, and adenoid vegetation are other conditions that may cause halitosis in children.
Foreign bodies in the nose or oropharynx can cause infection and lousy odor
secondary to inammation. Many foreign objects may have accidentally gotten into
the nose and remained neglected for a long time. This situation should not be
ignored, especially in children.
26.10 Chronic Tonsillitis
Chronic tonsillitis is a chronic inammation of the tonsils after recurrent acute or
subclinical infections. During acute tonsillitis, if a small abscess focused within the
follicles is not treated adequately, it will continue and cause the next tonsillitis attack.
Again, inammatory rashes within the crypts may cause subclinical infection and
cause acute tonsillitis attacks. The causative agent is mostly gram (+) bacteria. Among
these bacteria, GABHS are the organisms most commonly seen in chronic tonsillitis.
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İ. Dişikırık and M. A. Kanmaz
Although chronic tonsillitis is common between the ages of 6–15, it can be seen at
any age.
As a result of recurrent acute or subclinical infections in chronic tonsillitis, deep
crypts form in the tonsils. Saliva, food, and necrotic waste can ll these crypts. If
natural mechanisms cannot clear these, magma accumulates in the form of tonsil
stones. In this case, halitosis will occur along with chronic inammation [11].
Patients may have complaints such as recurrent sore throat and systemic complaints
such as fever, joint pain, malaise, bad breath, and bad taste in the mouth.
Diagnosis of chronic tonsillitis is made by history and examination. antistreptolysin O (ASO), C-reactive protein (CRP), and sedimentation examination are
requested to investigate GABHS.The denitive treatment for tonsillitis is tonsillectomy if there is an indication. Otherwise, if a bacterial agent is suspected, antibiotic treatment is recommended.
26.11 Tonsillolith
Tonsillolith is the formation of stones within the tonsil tissue. Fibrosis develops due
to recurrent inammation where the crypts are opened. Bacteria and epithelial residues accumulate in these crypts. Calcication occurs by depositing organic salts
such as calcium phosphate or magnesium carbonate. It may cause bad breath and
ulcerations. Complaints of sore throat, foreign body sensation in the back of the
throat and otalgia may occur. Tonsillectomy is indicated in cases with severe clinical complaints that do not resolve with symptomatic treatment. One of the causes of
pediatric halitosis is xerostomia. Xerostomia is a clinical condition we call capitalism or dry mouth syndrome. Many reasons can be listed in its etiology, and we can
summarize them as follows: Aplasia of the salivary gland is an infrequent condition.
Innervation disorders of the salivary glands and many drugs can affect this innervation: antidepressants, antihistamines, diuretics, ganglion blockers, and parasympatholytic agents. Recurrent parotitis, defects in the histological structure of the
salivary glands, the scarcity or absence of acinar cells, and the irreversible changes
caused by radiotherapy to the salivary glands in the gland parenchyma tissue may
also result. Xerostomia can be seen in some metabolic diseases, diabetes mellitus
(DM), dehydration, and chronic renal failure syndrome. In addition, in cases such as
liver disorders and systemic lupus erythematosus (SLE). Tooth decay, halitosis, and
periodontitis are common pathologies in children with xerostomia. Treatment of
xerostomia is directed toward the cause. Saliva secretion can be increased by treating metabolic diseases, especially dehydration. If it is related to the medications
used, medication use is terminated. The mouth and teeth are cleaned with an antiseptic mouthwash at least twice daily.
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
353
26.12 Non-Oral Halitosis
The prevalence of bad breath due to non-oral causes is 13%. 4% of these originate
from ear-nose-throat, 3% from oral and ear-nose-throat, and 1% from the digestive
system [12]. Zenker’s diverticulum, helicobacter pylori, gastritis, gastroesophageal
reux, and malabsorption syndromes can be mentioned regarding the digestive system. In the study by Delanghe etal. [31], ear-nose-throat problems were stated as the
reason for halitosis in only 5–8% of the patients. Non-oral causes are generally systemic diseases (DM, kidney failure increases the uric acid level, causing an ammonium-like odor in the breath) foods. Vegetarians have less halitosis than a person who
eats a lot of meat. Because the degradation products of protein substances in vegetables are very low. Meat usually contains fat, and the volatile fatty acids formed are
absorbed through the veins and excreted in the breath. Bad smell occurs when substances such as garlic, onion, leek, alcohol, etc., are rst absorbed in the circulatory
system and then released from the lungs as air. In addition, upper respiratory tract
diseases, pathological or physiological disorders in the nose and sinuses, tonsils,
pharynx and digestive organs, vitamin and mineral deciency (vitamin A, vitamin
B12, and iron or zinc deciency), diabetic ketoacidosis, liver failure, renal failure,
uremia, radiation therapy, some lung diseases, Von Willebrand disease, Helicobacter
pylori (bad breath disappeared in around 60% of cases after treatment by increasing
VSC), aplastic anemia, leukemia, bleeding diseases such as thrombocytopenia, diphtheria, measles, pneumonia, syphilis, eosinophilic granuloma and Lettere diseases
such as Siwe, high fever, precipitation of drugs, hunger, and stress can be shown (as
they cause dryness in the mouth) [40–43]. At the same time, psychological factors
such as anxiety and depression and some personality traits such as stress are risk factors for subjective halitosis [44]. Some parasites and their larvae (Ascaris lymbricoides, Trichuris trichura) pass through the lungs and cause infection. Parasitosis
increases the amount of gas in the intestine. In a study conducted in the USA, the
parasitic infestation rate in children with halitosis was 19% [45]. In another study,
halitosis disappeared in 64% of 28 children with parasitosis with mebendazole treatment [46]. Trimethylaminuria (sh odor syndrome), a genetic metabolic disorder,
causes an excessive increase in trimethylamine levels in the blood and lousy odor in
the body. Hypermethioninemia is another metabolic disorder that causes oral halitosis. Cystinosis is a rare autosomal recessive disease characterized by intralysosomal
cystine accumulation, and these patients’ methionine levels in the blood and urine
are very high. In infants, sleepiness is manifested by symptoms of distinctive urine,
sweat and breath odor, bleeding tendency, and hypoglycemia.
26.13 Gastroesophageal Reflux
Gastroesophageal reux, one of the causes of bad breath in children, is a common
condition in babies up to 1-year-old. Single or several factors may be responsible at
the same time. Factors such as decreased lower esophageal sphincter pressure,
insufcient relaxation of this sphincter, large hiatus hernia, and delayed gastric
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İ. Dişikırık and M. A. Kanmaz
emptying play a role. Babies have regurgitation, vomiting, and irritability. In older
children and teenagers, regurgitation causes retrosternal inammation, dysphagia,
or severe asthma. Barium radiography is performed for diagnosis, but the result is
expected in 30% of children. The most accurate results are obtained from studies in
which 24-h esophageal pH is measured.
Reux stops spontaneously when babies reach 18 months. If it persists and
causes esophagitis, H2 blockers, antacids, and sucralfate suspensions can be given.
Surgical intervention is required in cases of recurrent pneumonia, severe esophagitis, severe apnea, and failure to respond to 4–6weeks of drug therapy.
26.14 Diagnosis
The methods used to diagnose halitosis can be divided into two groups: direct and
indirect.
Direct methods:
1. Organoleptic.
2. Sulfur monitoring.
3. Gas chromatography.
Indirect method:
1. Indirect methods are based on detecting the microorganisms that produce VSC
or evaluating the products produced by these microorganisms invitro. Indirect
methods include bacterial culture, smear, and enzyme studies [2].
26.14.1 Organoleptic Measurement
Patients exhale through a 2.5cm diameter tube placed in their mouth, approximately 10cm away from the nose of the physician performing the measurement
[47]. In addition, in this method, the patient licks his wrist, waits for the licked area
to dry, and smells it. Before organoleptic evaluation, patients should avoid antibiotics for 3 weeks before the procedure. It is necessary to avoid smoking, alcohol
consumption, onion, garlic, and spicy foods 12h before the process, and oral care
procedures and consumption of food and beverages 2h before the system [48]. A
plastic spoon is placed on the tongue’s surface to evaluate whether the odor originates from the tongue. Scraping is done with the tester, and the evaluation is made
at a distance of 5cm from the nose of the person doing the test.
This test is evaluated as follows: 0=no odor, 1=hardly detectable odor, 2=slight
but detectable odor, 3=medium odor, 4= strong bad odor, and 5=extreme bad
odor [49]. Organoleptic evaluation is the reference in the diagnosis of halitosis [50].
Gas chromatography and portable sulte monitors can evaluate bad breath more
objectively. Oho et al. [51] found a signicant correlation between the results
obtained by organoleptic testing, gas chromatography, and sulte monitoring. Gas
26 Halitosis DuetoPediatric Ear, Nose, andThroat Field Infections
355
chromatography is based on separating gases with different molecular weights and
boiling points in an environment. It is a method based on measuring the concentration of VSCs in oral air. This method is quite expensive and requires experienced
personnel [3, 34, 52, 53]. For this reason, it is used mainly for research purposes
(Table26.2).
26.14.2 Sulfur Monitoring
A portable monitor that can measure oral volatile sulfur compounds (VSC) evaluates VSC concentrations together but does not provide information on their types.
VSC measurement in the mouth is done as follows: A pipette is placed in the
patient’s mouth and he is asked to breathe through the nose by keeping his mouth
closed. As a result of the electrochemical reactions between the VCS compounds in
the breath, an electric current is generated proportional to the amount of VCS.This
value is expressed numerically as ppb (parts per billion) [17, 55].
In some studies, the relationship between the organoleptic method and sulfur
measurements was evaluated, and while organoleptic evaluation gave high scores in
patients, sulfur measurements were found to be normal in patients. This is because
substances or compounds that cause bad breath other than VSC (volatile short-chain
fatty acids, polyamines, alcohols, phenyl compounds, alkanes, ketones, and nitrogen compounds) cannot naturally be detected by the sulfur monitor [21, 56, 57].
26.14.2.1 Indirect Methods
A different strategy in determining bad breath is the detection of VSC-producing
microorganisms or their enzymes. Proteolytic obligate gram-negative anaerobes
found in the subgingival plaque and tongue dorsum can be detected by the BANA
test. BANA is a synthetic trypsin substrate that can be hydrolyzed by VSC-producing
oral anaerobic bacteria [2]. When this strip is treated with saliva, if there is a VSCproducing microorganism in the saliva, the BANA molecule on the strip turns into
β-naphthylamide and appears in blue. The BANA test is a practical and easy-to-use
method. Still, its disadvantage is that it cannot identify different types of bacteria
that do not produce VSCs responsible for halitosis [21, 58, 59]. Some studies have
shown that while there is a statistically signicant relationship between BANA
scores and organoleptic measurements, it has a weak relationship with sulfur monitoring measurements [2].
Table 26.2 14 volatile
sulfur compounds identied
(VSB) [54]
Acetone 2-Butanone
2-Pentanone Indole
Skatole Dimethyl selenide
1-propanol Dimethyl sulde
Dimethyl disulde Dimethyl trisulde
Allyl methyl sulde Carbon disulde
Hydrogen sulde Methyl mercaptan