BY Amir A Kargoshaie Assistant professor of otorhinolaryngology Isfahan university of medical sciences 1 Oral Malodor 4 Classes 3 Subtypes Above Carina URTIs OZOSTOMIA Below Carina LRTIs ID: 145011
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Slide1
Halitosis
BY:Amir A. KargoshaieAssistant professor of otorhinolaryngologyIsfahan university of medical sciences
1Slide2
Oral Malodor 4 Classes…. 3 Sub-types
Above Carina (URTI’s)- OZOSTOMIABelow Carina (LRTI’s)- STOMATODYSODIAHALITOSIS:
i) Physiological ii) Pathological iii) Psychological
FETOR EX ORE/ FETOR ORIS:
Oral Hygiene, Perio, and Decay
2Slide3
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
3Slide4
4Slide5
Genuine halitosis when the breath malodor really exists and can be diagnosed
organoleptically or by measurement of the responsible compounds. 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
5Slide6
. 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.
pseudo-halitosis
6Slide7
OZOSTOMIA… above carina
Obstruction, Nasal- discharge, Tonsillitis, Tonsoliths, Laryngitis, Dysphagia, Voice problemsPrevious ENT pathology
Sinusitis, Rhinitis, Pharyngitis, Foreign BodiesStagnation and InfectionMalignancies
[G. ozo, to smell, + stoma, mouth]
7Slide8
STOMATODYSODIA…below carina
Tobacco SmokersBronchitisBronchiectasisLung AbscessPleuritisPneumoniaBlood
Foreign BodyNeoplasia, Mucous Stagnation/Infection
8Slide9
HALITOSIS physiological
Poor hydrationMenstruationDiet ConstipationStarvation, Morning breath
Habits (Mouth breathing, thumb sucking)
9Slide10
HALITOSIS pathological
Lungs release blood-borne catabolic productsStomach--Gastritis, Liver hepatitis, Kidney nephritisPancreas--Diabetes mellitus (Ketosis)Anorexia/Bulimia nervosaIgA deficiencyXerostomia (Sjogrens, Radiation therapy, Stress)
10Slide11
HALITOSIS psychological
“Halitophobia” not very accurate termDelusional cacosmiaPsychogenic dysosmiaSymptomatic schizophreniaTemporal lobe epilepsy (Aura)Cerebral tumors
11Slide12
Fetor ex Ore/ Fetor Oris
From Mouth: Gums &TeethGingivitis/PeriodontitisPercoronitis/Peri-implantitisDorsum of tongueInterdental areas
ANUG/NUGPost-extraction, Dry socketPlaque & Calculus Oral Hygiene, Stagnation areas
Caries: Tooth decay
Brushing and Flossing
Reduced salivary flow
Faulty fillings, Overhangs
Dental materialsCements: Eugenol, Cajeput, Creosote, Kri3
Fixed bridgework, Pontics
Appliances– Orthodontic, Prosthodontic
Denture hygiene
Oral medicine conditions
Ulcerations, Abrasions, Wounds
Neoplasias
Hemorrhagic diatheses
12Slide13
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.
13Slide14
14
EtiologyIn 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 (blood-breath 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 production by deglycosylating salivary glycoproteins, thus exposing their protein core to further degradation by gram-negative microorganisms
.Slide15
15
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 self-reported 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
).Slide16
16
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
.Slide17
17
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
.Slide18
18
Proteolytic
degradation by oral microorganisms of four amino acids (two containing sulfur and two not containing sulfur) to malodorous compounds. Slide19
19
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
.Slide20
20
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
.Slide21
Biological Sources of Oral Malodor
BLOODNECROSISPUSMUCOUSBACTERIA
21Slide22
Oral Malodor Volatile Sulfur Compounds
VSC mainly responsible for stenchMeasure with the Halimeter®
VSC’s include hydrogen sulfide, methyl mercaptan, and dimethyl sulfide
22Slide23
Oral Malodor CLINICAL Management I
Full comprehensive Oral ExaminationDetect, record all gingival problemsGingivitis and PeriodontitisScale and Polish: Root Planing; Pocket elimination
Restore faulty restorationsOral Hygiene PIx<10%Recall: re-measure VSC’s
Outcome analysis: Results/Proof
23Slide24
Oral Malodor CLINICAL Management II
OHI: Brushing, Flossing, Gargle, RinseTeeth, Gums, Tongue, Tonsils, pharynxProsthesis: Hygiene, Repair, or ReplaceRemove all plaque
24Slide25
Oral Malodor CLINICAL Management III
FlossAnti-bacterial PastePeroxide pasteBicarbonate of Soda Paste
Tongue scraper --Commercial vs Spoon Pre-sleep Oral Hygiene
25Slide26
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 even rougher
surface
26Slide27
27
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
.
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 suboptimal oral hygiene. Other influencing factors were: periodontal status, presence of a denture, smoking, and dietary habits.Slide28
Different
clinical pictures of heavily coated tongues 28Slide29
29
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 insertion of implants, clinicians should recognize this pathologic role of VSCs
.Slide30
30
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.
6Slide31
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.
31Slide32
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
.
32Slide33
Extraoral
CausesEar-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 the stomach reaches the
nasopharynx
and causes
mucositis
.
Ozena
(caused by
Klebsiella
ozaenae
) is a rare atrophic condition of the nasal mucosa, with the appearance of crusts that causes a very strong breath malodor. Finally, a foreign body in a nasal or sinus cavity can cause local irritation, ulceration, and subsequent putrefaction (e.g., children and mentally handicapped persons tend to put objects such as peas or wet paper in the nose).
111
33Slide34
34
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.Slide35
35
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
.
Tangerman
et
alfound
no association between halitosis and
H. pylori infection
.Slide36
36
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
.Slide37
37
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 Kingdom
.Slide38
38
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).
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.
40Slide39
39Slide40
40Slide41
41Slide42
Oral Malodor CLINICAL Management VI
Rectify URT and LRTTreat systemic disease Diabetes, Hypertension, CCFOral Health: Teeth and Gum problems cause >90% cases of oral malodorKeep records
Record on VAS scalesNote measures of VSCEducate the patient
42Slide43
OM CLINICAL Management VIIOral Irrigation A
Medicinal MouthwashShort-term for specific effectAssociated risksExamples: 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.
Physiolo
gical
Daily use
Long temMinimal side effects if anyPhysiological substances: Examples: Salt, Bicarbonate of soda, Urea crystals
Fluoride rinse: correct physiological concentration 1ppm
43Slide44
OM CLINICAL Management VIII Saline Mouthwash & Gargle
PREPARATION:NaCl common Table SaltHypertonic solutions: stir one teaspoonful of salt in about 300ml water.Salt should remain at base of glass=Saturated solution
hypertonicFreshly prepared for each use.Not costly; available
MODE OF ACTION
Hypertonicity dehydrates bacteria
bacteriostatic initialthen bacteriocidal
Edema: Swollen Cells are reduced
Saline debridement of tonsillar crypts
Washes and irrigates mucous membranes; mucolytic
Slows inflammation
44Slide45
Oral Malodor Clinics
Part of Practice: NOT isolatedMust have accurate clinical measuring devices--Halimeter® (VSC’s ppb)Must have ALL oral therapeutic back-up
Refer and COMMUNICATEClinical Protocol: Quote fees Examinations, Radiographs, Bacteriology, Histopathology, Periodontics, Endodontics, Restorative, Prosthodontics, Otolaryngology, Psychological referrals
Written Report Mandatory
45