Download Oral Malodor

Halitosis
BY:
Amir A. Kargoshaie
Assistant professor of otorhinolaryngology
Isfahan university of medical sciences
1
Oral Malodor
4 Classes…. 3 Sub-types
• Above Carina (URTI’s)- OZOSTOMIA
• Below Carina (LRTI’s)•
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STOMATODYSODIA
HALITOSIS:
i) Physiological
ii) Pathological
iii) Psychological
FETOR EX ORE/ FETOR ORIS:
Oral Hygiene, Perio, and Decay
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• Breath odor
• the subjective perception after smelling someone’s breath
• pleasant,
• unpleasant,
• or even disturbing, if not repulsive
• . If unpleasant, the terms breath malodor, halitosis, bad
breath, or fetor ex ore can be applied.
• not synonymous with oral malodor. This term is restricted
to halitosis with an origin in the oral cavity.
• three main categories of halitosis:
•
genuine halitosis
• pseudo-halitosis
• halitophobia
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• Genuine halitosis
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when the breath malodor really exists and can be diagnosed
organoleptically or by measurement of the responsible compounds.
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physiologic halitosis
– The transient disturbing odor caused by food intake (e.g., garlic,
onions, and certain spices), smoking, or medication (e.g.,
metronidazole)
do not reveal a health problem and are common examples of
physiologic halitosis.
– The same is true for “morning” bad breath, as habitually
experienced on awakening. This malodor is caused by a decreased
salivary flow and increased putrefaction during the night and
spontaneously disappears after breakfast or after oral hygiene
measures.
pathologic halitosis .
A persistent breath malodor, reflect s some pathology
•
The causes of this will be discussed later
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pseudo-halitosis
. When an obvious breath malodor cannot be perceived, but the patient is
convinced that he or she suffers from it,
halitophobia,
If the patient still believes that there is bad breath after treatment of
genuine halitosis or diagnosis of pseudo-halitosis,
is a recognized psychiatric condition.
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OZOSTOMIA…
above carina
[G. ozo, to smell, + stoma, mouth]
• Obstruction, Nasaldischarge, Tonsillitis,
Tonsoliths, Laryngitis,
• Dysphagia, Voice
problems
• Previous ENT pathology
• Sinusitis, Rhinitis,
Pharyngitis, Foreign
Bodies
• Stagnation and Infection
• Malignancies
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STOMATODYSODIA
…below carina
Tobacco Smokers
Bronchitis
Bronchiectasis
Lung Abscess
Pleuritis
Pneumonia
Blood
Foreign Body
Neoplasia, Mucous
Stagnation/Infection
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HALITOSIS physiological
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Poor hydration
Menstruation
Diet
Constipation
Starvation, Morning
breath
• Habits (Mouth
breathing, thumb
sucking)
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HALITOSIS pathological
• Lungs release blood-borne
catabolic products
• Stomach--Gastritis, Liver
hepatitis, Kidney nephritis
• Pancreas--Diabetes mellitus
(Ketosis)
• Anorexia/Bulimia nervosa
• IgA deficiency
• Xerostomia (Sjogrens,
Radiation therapy, Stress)
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HALITOSIS psychological
• “Halitophobia” not very
accurate term
• Delusional cacosmia
• Psychogenic
dysosmia
• Symptomatic
schizophrenia
• Temporal lobe
epilepsy (Aura)
• Cerebral tumors
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Fetor ex Ore/ Fetor Oris
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From Mouth: Gums &Teeth
Gingivitis/Periodontitis
Percoronitis/Peri-implantitis
Dorsum of tongue
Interdental areas
ANUG/NUG
Post-extraction, Dry socket
Plaque & Calculus Oral
Hygiene, Stagnation areas
• Caries: Tooth decay
• Brushing and Flossing
• Reduced salivary flow
• Faulty fillings, Overhangs
• Dental materials
• Cements: Eugenol,
Cajeput, Creosote, Kri3
• Fixed bridgework, Pontics
• Appliances– Orthodontic,
Prosthodontic
• Denture hygiene
• Oral medicine conditions
• Ulcerations, Abrasions,
Wounds
• Neoplasias
• Hemorrhagic diatheses 12
• Epidemiology
• Breath malodor is a common complaint among the general
population.(as high as 50% in some articles)
• It has a significant socioeconomic impact but
unfortunately has been neglected until recently by
scientists and clinicians
• hardly covered in the medical curricula
• Halitosis can lead to personal discomfort and social
embarrassment, and is still one of the biggest taboos of
society.
• Almost $1 billion a year is spent in the United States on
deodorant-type mouth (oral) rinses, mints, and related
over-the-counter products to manage bad breath.
• It would be preferable to spend this money on a proper
diagnosis and etiologic care instead of short-term and
even inefficient masking attempts.
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Etiology
In the vast majority, breath malodor originates from the oral cavity. Gingivitis,
periodontitis, and especially tongue coating are the predominant causative factors.
In general, one can identify two pathways for bad breath. The first one involves an
increase of certain metabolites in the blood circulation (e.g., due to a systemic
disease), which will escape via the alveoli of the lungs during breathing (bloodbreath exchange) and it is commonly referred as “extraoral halitosis.” The second
pathway (intraoral halitosis) involves an increase of either the bacterial load or the
amount of substrate for these bacteria at one of the lining surfaces of the
oropharyngeal cavity, the respiratory tract, or the esophagus. All types of
infections, ulcerations, or tumors at one of the previously mentioned areas can thus
lead to bad breath. Studies also suggest that oral malodor is associated with the
total bacterial load of anaerobic bacteria in both saliva and tongue coating.
The most commonly involved bacteria are Porphyromonas gingivalis, Prevotella
intermedia/nigrescens, Aggregatibacter actinomycetemcomitans (previously
Actinobacillus actinomycetemcomitans), Campylobacter rectus, Fusobacterium
nucleatum, Peptostreptococcus micros, Tannerella forsythia, Eubacterium spp, and
spirochetes.
A study conducted by Niles and Gaffar made clear that these gram-negative
species in particular cause an unpleasant smell by the production of sulfur
compounds.
However, because of the large species diversity found in patients with halitosis, it
can be suggested that breath malodor is the result of complex interactions between
several bacterial species. A recent study indicates that some gram-positive
microorganisms, such as Streptococcus salivarius, also contribute to oral malodor
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production by deglycosylating salivary glycoproteins, thus exposing their protein
core to further degradation by gram-negative microorganisms.
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There are few studies that document the prevalence of oral malodor. Moreover, the studies that
exist used different methodologies ranging from self-reported breath malodor to more objective
assessments such as the measurement of the volatile sulfur compounds (VSCs). Because selfreported halitosis correlates weakly with objective measurements and tends to overestimate the
problem, data should be interpreted carefully.
The incidence of halitosis remains poorly documented in most countries. Large-scale studies
have been performed for the Japanese,Swedish,and Chinese populations.
Smaller investigations in Brazilian,Polish,and Israeli habitants have also been reported.
Despite the different approach of each study, if a VSC level of 75 ppb (limit for social
acceptance) is used as a threshold for halitosis, the prevalence reported in the different
populations can be calculated as 23% (late-morning group) and 20% for the Japanese and
Chinese studies, respectively. In line with this, prevalences of 27.5% and 29.8% for the Chinese
and the Israeli groups, respectively, can be calculated when an organoleptic score of at least 2 is
considered as being representative for halitosis. With the same criterion, the calculated
prevalence varied between 11.0% and 29.7% for the different age groups in the Polish
population. In conclusion, independent of the method used to assess oral malodor and
independent of the study population, the results point out that about one in four subjects suffer
from persistent bad breath.
From large-scale inventories in multidisciplinary outpatient clinics for breath odor,
no gender predominance seems to exist for bad breath, although other studies indicate a higher
prevalence in women.
It has also been observed that women seek treatment more often than men.
Age can range from 5 years to more than 80 years. No association was found between
increased age and oral malodor.
Most of the patients had been complaining about breath malodor for several years before
seeking proper advice (recent report of the department involving 2000 patients).
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• A recent large-scale study including 2000 patients with halitosis
complaints showed that for those where bad breath could be
objectively detected, the cause of it was mostly found within the
oral cavity (90%).
• Tongue coating (51%), gingivitis/periodontitis (13%), or a
combination (22%) accounted for the majority of the cases.
• Because a large part of the population has a tongue coating or
gingivitis/periodontitis, there is a risk that an intraoral condition is
too easily considered as the cause while more important
pathologies are overlooked.
• Indeed, for a minority of patients (4% in the same recent study),
extraoral causes could be identified, including ear-nose-throat
(ENT) pathologies, systemic diseases (e.g., diabetes), metabolic or
hormonal changes, hepatic or renal insufficiency, bronchial and
pulmonary diseases, or gastroenterologic pathologies.
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• Recently, the presence of Solobacterium moorei, a gram positive
bacterium, has also been linked to oral malodor.
• For oral malodor, the unpleasant smell of the breath mainly originates
from volatile sulphur compounds (VSCs), especially hydrogen sulfide
(H2S), methylmercaptan (CH3SH), and (less significantly) dimethyl
sulfide [(CH3)2S], as first discovered by Tonzetich.
• However, in certain conditions (e.g., when the saliva dries out on the
mucosal surfaces), other compounds in mouth air may also play a role
such as diamines (e.g., putrescine, cadaverine), indole, skatole, and
volatile organic acids like butyric or propionic acid.
•
Most of these compounds result from the proteolytic degradation by
oral microorganisms of peptides present in saliva (sulfurcontaining or
non–sulfur-containing amino acids) ,shed epithelium, food debris,
gingival crevicular fluid (GCF), interdental plaque, postnasal drip, and
blood. In particular, gram negative, anaerobic bacteria possess such
proteolytic activity.
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Proteolytic degradation by
oral microorganisms of
four amino acids (two
containing sulfur and two
not containing sulfur) to
malodorous compounds.
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For the extraoral causes of halitosis, other compounds besides the VSCs
may be involved.
Bad-smelling metabolites can be formed/absorbed at any place in the
body (e.g., the liver, the gut) and transported by the bloodstream to the
lungs. Exhalation of these volatiles in the alveolar air then causes
halitosis, at least when the concentrations of the bad-smelling
metabolites are sufficiently high.
The crevicular fluid reflects the circulating molecules in the blood and can
thus also play a relevant role but due to the small amount probably not a
very dominant one.
The extraoral causes are much more difficult to detect, although they can
sometimes be recognized by a typical odor.
Uncontrolled diabetes mellitus can be associated with a sweet odor of
ketones,
liver disease can be revealed by a sulfur odor,
and kidney failure can be characterized by a fishy odor because of the
presence of dimethylamine and trimethylamine.
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In a special patient category, subjects imagine they have breath malodor;
this is called imaginary breath odor or halitophobia.
The latter has been associated with obsessive-compulsive disorders and
hypochondria. Well-established personality disorder questionnaires (e.g.,
Symptom Checklist 90) allow the clinician to assess the patient’s
tendency for illusional breath malodor.
The presence of a psychologist or psychiatrist at the malodor
consultation can be especially helpful for such patients. Because of the
complexity of this pathology, a malodor consultation is thus preferably
multidisciplinary, combining the knowledge of a periodontologist or
dentist, an ENT specialist, an internist (if necessary), and a psychologist
or psychiatrist. In a recent study of 2000 patients, 16% were diagnosed
with pseudo-halitosis or halitophobia.
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Biological Sources of
Oral Malodor
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BLOOD
NECROSIS
PUS
MUCOUS
BACTERIA
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Oral Malodor
Volatile Sulfur Compounds
• VSC mainly
responsible for stench
• Measure with the
Halimeter®
• VSC’s include
hydrogen sulfide,
methyl mercaptan,
and dimethyl sulfide
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Oral Malodor
CLINICAL Management I
• Full comprehensive Oral
Examination
• Detect, record all gingival
problems
• Gingivitis and Periodontitis
• Scale and Polish: Root
Planing; Pocket elimination
• Restore faulty restorations
• Oral Hygiene PIx<10%
• Recall: re-measure VSC’s
• Outcome analysis:
Results/Proof
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Oral Malodor
CLINICAL Management II
• OHI: Brushing,
Flossing, Gargle, Rinse
• Teeth, Gums, Tongue,
Tonsils, pharynx
• Prosthesis: Hygiene,
Repair, or Replace
• Remove all plaque
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Oral Malodor
CLINICAL Management III
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Floss
Anti-bacterial Paste
Peroxide paste
Bicarbonate of Soda
Paste
• Tongue scraper -Commercial vs Spoon
• Pre-sleep Oral Hygiene
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Intraoral Causes
• Tongue and Tongue Coating.
• The dorsal tongue mucosa, with an area of 25 cm , shows a very
irregular surface topography.
• The posterior part exhibits a number of oval cryptolymphatic units,
which roughen the surface of this area. The anterior part is even
rougher because of the high number of papillae: the filiform papillae
with a core of 0.5 mm in length, a central crater and uplifted borders;
the fungiform papillae, 0.5 to 0.8 mm in length; the foliate papillae,
located at the edge of the tongue, separated by deep folds; and the
vallate papillae, 1 mm in height and 2 to 3 mm in diameter. These
innumerable depressions in the tongue surface are ideal niches for
bacterial adhesion and growth, sheltered from cleaning actions.
• Moreover, desquamated cells and food remnants also remain trapped
in these retention sites and consequently can be putrefied by the
bacteria.
• A fissurated tongue (deep fissures on dorsum, also called scrotal
tongue or lingua plicata) and a hairy tongue (lingua villosa) have an
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even rougher surface
• The accumulation of food remnants intermingled with exfoliated
cells and bacteria forms a coating on the tongue dorsum. The latter
cannot be easily removed because of the retention offered by the
irregular surface of the tongue dorsum .
• As such, the two factors essential for putrefaction are united.
Several investigators have identified the dorsal posterior surface of
the tongue as the primary source of breath malodor.
• Indeed, high correlations have been reported between tongue
coating and odor formation.
• Both in healthy individuals and periodontitis patients with or
without complaints of oral halitosis, a significant positive
correlation was found between the presence or amount of tongue
coating and levels of VSCs and/or organoleptic scores of the
mouth odor.
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In a group of 2000 patients visiting a multidisciplinary halitosis clinic, significant correlations were
found between the organoleptic scores and tongue coating (R = 0.52; p < 0.001).
In another study,it was also observed that the amount of tongue coating was significantly greater in the
halitosis-positive group compared to the halitosis-negative group.
Morita and Wang found that the volume of tongue coating and the percentile of sites with bleeding on
probing, were significantly associated with oral malodor.
In 1992, Yaegaki and Sanada demonstrated that, even in patients with periodontal disease, 60% of the
VSCs were produced from the tongue surface.
Recent research showed that the strongest determinant for the presence of tongue coating is
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suboptimal oral hygiene. Other influencing factors were: periodontal status, presence of a denture,
smoking, and dietary habits.
Different clinical pictures of heavily coated tongues
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Periodontal Infections.
A relationship between periodontitis and oral malodor has been shown.
However, not all patients with gingivitis and/or periodontitis complain about
bad breath, and there is some disagreement in the literature as to what extent
oral malodor and periodontal disease are related.
Bacteria associated with gingivitis and periodontitis are indeed able to
produce VSCs.
Several studies have shown that the VSC levels in the mouth correlate
positively with the depth of periodontal pockets (the deeper the pocket, the
more bacteria, particularly anaerobic species) and that the amount of VSCs in
breath increases with the number, depth, and bleeding tendency of the
periodontal pockets.
It is important to realize that VSCs aggravate the periodontitis process by, for
example, increasing the permeability of the pocket and mucosal epithelium and
therefore exposing the underlying connective tissues of the periodontium to
bacterial metabolites. Moreover, methylmercaptan enhances interstitial collagenase
production, interleukin-1 (IL-1) production by mononuclear cells, and cathepsin B
production, thus further mediating connective tissue breakdown.
It was also shown that human gingival fibroblasts developed an affected
cytoskeleton when exposed to methylmercaptan.
The same gas alters cell proliferation and migration. VSCs are also known to
impede wound healing. Thus, when periodontal surgery is planned, especially the
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insertion of implants, clinicians should recognize this pathologic role of VSCs.
• Some studies, however, have shown that when the presence of
tongue coating is taken into account, the correlation between
periodontitis and oral malodor is much lower, indicating that
tongue coating remains a key factor for halitosis. The prevalence of
tongue coating is six times higher in patients with periodontitis,
and the same bacterial species associated with periodontal disease
can also be found in large numbers on the dorsum of the tongue,
particularly when tongue coating is present.
• The reported association between periodontitis and oral malodor
may thus primarily be due to the effects of periodontal disease on
tongue coating. And may explain why other articles did not find a
correlation.
• Other relevant malodorous pathologic manifestations of the
periodontium are pericoronitis (the soft tissue “cap” being
retentive for microorganisms and debris), major recurrent oral
ulcerations, herpetic gingivitis, and necrotizing
gingivitis/periodontitis. Microbiologic observations indicate that
ulcers infected with gramnegative anaerobes (i.e., Prevotella and
Porphyromonas species) are significantly more malodorous than
noninfected ulcers.
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Dental Pathologies
• . Possible causes within the dentition are deep carious
lesions with food impaction and putrefaction, extraction
wounds filled with a blood clot, and purulent discharge
leading to important putrefaction. The same applies to
interdental food impaction in large interdental areas and
crowding of teeth favor food entrapment and accumulation
of debris. Acrylic dentures, especially when kept
continuously in the mouth at night or not regularly cleaned,
can also produce a typical smell. The denture surface
facing the gingiva is porous and retentive for bacteria,
yeasts, and debris, which are compounds needed for
putrefaction.
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Dry Mouth.
• Saliva has an important cleaning function in the oral cavity.
Patients with xerostomia often present with large amounts
of plaque on teeth and an extensive tongue coating. The
increased microbial load and the escape of VSCs when
saliva is drying up explain the strong breath malodor.
• Several studies link stress with VSC levels, but it is not clear
whether this can simply be explained by a reduction of salivary
flow.
• Other causes of xerostomia are medication,
• alcohol abuse,
• Sjögren syndrome (a common autoimmune rheumatic disease),
• and diabetes.
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Extraoral Causes
• Ear-Nose-Throat. During chronic or purulent
tonsillitis, the
• deep crypts of the tonsils accumulate debris and
bacteria, especially periopathogens, resulting in
putrefaction. In the crypts, even calculus (e.g.,
subgingivally) can be formed (tonsilloliths or tonsil
stones). Other examples include acute pharyngitis (viral
or bacterial) and postnasal drip. The latter is a rather
common condition, which is perceived by patients as a
liquid flow in the throat, originating from the nasal cavity.
• It is often associated with chronic sinusitis or
regurgitation esophagitis, in which the acidic content of
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the stomach reaches the nasopharynx and causes
mucositis. Ozena (caused by Klebsiella ozaenae) is a
• Bronchi and Lungs. Pulmonary causes
include chronic bronchitis, bronchiectasis
(infection of standing mucus secretion in
cystic dilations through walls of
bronchioles), pneumonia, pulmonary
abscesses, bronchial carcinoma, and
carcinoma of the lung.
• The relevance of an early diagnosis is evident.
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• Gastrointestinal Tract. In contrast to the common public opinion, even
among medical physicians, gastrointestinal pathologies are rarely
responsible for bad breath.
• The following pathologies might be responsible for less than 1% of malodor
cases:
• A Zenker diverticulum (a hernia in the esophageal wall, allowing accumulation of food and
debris and thus putrefaction) can cause a significant breath odor because it is not
separated from the oral cavity by any sphincter.
• • A gastric diaphragmatic hernia (the fundus of the stomach protrudes through the
diaphragm with relative sphincter insufficiency, allowing gases to escape or contents to
flow back in the esophagus) can cause reflux of the gastric contents up to the
oropharynx. This is sometimes combined with ructus, in which air from the stomach
suddenly regurgitates.
• • Regurgitation esophagitis (ulceration of the mucosal lining of the esophagus by acidic
stomach contents flowing back because of an improper function of the sphincter).
• • Intestinal gas production: Some gases (e.g., dimethyl sulfide) are absorbed but not
metabolized by the intestinal endothelium and thus transported by the blood. These
gases can then be exhaled through the lungs.
• There is some disagreement in the literature whether Helicobacter pylori infection is
associated with halitosis.
•
In a recent paper, H. pylori was shown to produce hydrogen sulfide and
methylmercaptan, which suggests that this microorganism can contribute to the
development of halitosis.
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•
Tangerman et alfound no association between halitosis and H. pylori infection.
• Liver. Patients with various degrees of hepatocellular
failure and/ or portosystemic shunting of blood may
acquire a sweet, musty, or even slightly fecal aroma of
the breath, termed fetor hepaticus, which has been
mainly attributed to the accumulation of dimethyl
sulfide.
• Moreover, if the metabolizing function of the liver fails, the
concentration of certain metabolites, normally processed in
the liver, will increase and they will enter the systemic
circulation again and will be exhaled.
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• Kidney. Kidney insufficiency, primarily caused by chronic
glomerulonephritis, will lead to an increase of the amines
dimethylamine and trimethylamine, which causes a typical
fishy odor of the breath.
• Systemic Metabolic Disorders. Uncontrolled diabetes
mellitus results in the accumulation of ketones, which have
a sweet smell, like the odor of rotten apples. Insulin
resistance leads to an increase of triglycerides and free
fatty acids and ketones (such as acetone, acetoacetate,
and hydroxybutyrate) are formed during lipolysis.
• Trimethylaminuria. Trimethylaminuria is a hereditary
metabolic disorder that leads to a typical fishy odor of the
breath, urine, sweat, and other bodily secretions.
Trimethylaminuria is an enzymatic defect that prevents the
transformation of trimethylamine to trimethylaminoxide,
resulting in abnormal amounts of this molecule. The
prevalence is unknown but approaches 1% in the United
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Kingdom.
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Hormonal Causes. At certain moments during the menstrual cycle, a typical
breath odor can develop; partners are often well aware of this odor. Evidence
also indicates that VSC levels in the expired air are increased twofold to
fourfold around the day of ovulation and in the perimenstrual period. Increases
in VSCs are smaller in midfollicular phases.
In a study by Kleinberg and Codipilly, aqueous solutions of oral odoriferous
volatiles were placed on the skin of the back of the hand.
• Afterwards, odor scores were given (organoleptic score, cfr. supra). The
results are shown in Table 52-2. All metabolites caused an explicit odor, which
decreased in intensity over time. Some molecules disappeared very fast (e.g.,
hydrogen sulfide and methylmercaptan), whereas others produced a bad smell
for a longer period of time (e.g., indole and skatole, for 10 minutes and longer).
•
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The olfactory response, rated by an organoleptic scale, follows an exponential
curve when correlated with the concentration of different gases. In other
words, when the concentrations of the molecules were compared to their
organoleptic outcome, an optimal fit was only obtained when the
concentrations of the gases were transformed to log values. The latter implies
that all types of breath “measurements” (gas chromatography [GC], portable
breath analyzers [e.g., Halimeter]) require log transformation to be comparable
with organoleptic scores.
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Oral Malodor
CLINICAL Management VI
• Rectify URT and LRT
• Treat systemic disease
Diabetes, Hypertension,
CCF
• Oral Health: Teeth and
Gum problems cause
>90% cases of oral
malodor
• Keep records
• Record on VAS scales
• Note measures of VSC
• Educate the patient
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OM CLINICAL Management VII
Oral
Irrigation
A
• Medicinal
Mouthwash
• Short-term for specific effect
• Associated risks
• Examples: Peridex
(Chlorhexidine gluconate);
Phenol Based with oils
(Listerine); Cetyl-pyridinium Cl
(Cepacol) Chlorine dioxide,
herbal remedies, etc.
• Side effects: staining, taste
changes, toxicity, overgrowth
of bacteria, fungi etc.
• Physiological
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Daily use
Long tem
Minimal side effects if any
Physiological substances:
Examples: Salt, Bicarbonate
of soda, Urea crystals
• Fluoride rinse: correct
physiological concentration
1ppm
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OM CLINICAL Management
VIII Saline Mouthwash &
Gargle
• PREPARATION:
• NaCl common Table Salt
• Hypertonic solutions: stir
one teaspoonful of salt in
about 300ml water.
• Salt should remain at
base of glass=Saturated
solutionhypertonic
• Freshly prepared for each
use.
• Not costly; available
• MODE OF ACTION
• Hypertonicity dehydrates
bacteria bacteriostatic
initialthen bacteriocidal
• Edema: Swollen Cells are
reduced
• Saline debridement of
tonsillar crypts
• Washes and irrigates
mucous membranes;
mucolytic
• Slows inflammation
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Oral Malodor Clinics
• Part of Practice: NOT
isolated
• Must have accurate clinical
measuring devices-Halimeter® (VSC’s ppb)
• Must have ALL oral
therapeutic back-up
• Refer and COMMUNICATE
• Clinical Protocol: Quote fees
• Examinations, Radiographs,
Bacteriology, Histopathology,
Periodontics, Endodontics,
Restorative, Prosthodontics,
Otolaryngology,
Psychological referrals
• Written Report Mandatory
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