Halitosis: An etiologic classification, a

treatment approach, and prevention

Dominic P. Lu, B.A., D.D.S., F.A.G.D., F.R.S.H.(Engl.), F.I.C.D.,* Allentown, .Pa.

Halitosis, a condition that causes a severe social handicap to those who suffer from it, has a
multifactorial etiology. Since patients with this condition seek professional consultation from dentists
much more frequently than from physicians, dentists, who treat diseases of the oral cavity, should
have an understanding of the local as well as the systemic factors which cause halitosis. This article
presents an extensive review of the information available, with an etiologic classification of this
condition to help clinicians develop the diagnostic acumen to distinguish one type of halitosis from
another. Once the etiology of this condition is ascertained for the patient who suffers from it,
treatment can be readily rendered.

H alitosis did not become a clinical entity until
1874, when it was described by Howe.’ Recognition
of this condition is simple, but diseaseswhich cause
halitosis may produce distinctly different smells. The
distinct smell which each diseaseproduces may offer
some help in differentiating the etiology of halitosis
if various factors causing this condition are under-
stood.
Halitosis can be divided into the following catego-
ries: (1) halitosis due to local factors of the patholog-
ical origin, (2) halitosis due to local factors of
nonpathological origin, (3) halitosis due to systemic
factors of pathologic origin, (4) halitosis due to
systemic factors of nonpathologic origin, (5) halitosis
due to systemic administration of drugs, and (6)
halitosis due to xerostomia.
HALITOSIS DUE TO LOCAL FACTORS OF
PATHOLOGIC ORIGIN
Halitosis may be caused by local conditions such
as poor oral hygiene, extensive caries, gingivitis,
periodontitis, open contacts allowing food impaction,
Vincent’s disease, hairy or coated tongue, fissured
tongue, excessive smoking, healing extraction
wounds, and necrotic tissues from ulceration.1-7 In
adults, chronic periodontal disease is a major cause
of halitosis. Periodontal pockets produce hydrogen
sulfides which give off an offensive odora; these
pockets encourage trapping of food.),5 Periodontal
*Consultant of Hospital Dentistry, Fairleigh Dickinson University
School of Dentistry, and Attending Teaching Staff, General
Dentistry Residency Programs, Allentown Hospital and Sacred
Heart Hospital.
0030-4220/82/l 10521 + 06$00.60/O @ 1982 The C. V. Mosby Co.
therapy may alleviate halitosis by reducing volatile
sulfur compounds.gHalitosis may also be related to
an increase of gram-negative filamentous organisms,
an increase in pH to 7.2, and the formation of indoles
and amines in the oral cavity.‘ODentigerous cyst with
fistula draining into the oral cavity may also cause
halitosis.” Other conditions which may produce
halitosis include chronic sinusitis with postnasal drip,
rhinitis, lethal granuloma, pharyngitis, tonsillitis,
syphilitic ulcers, cancrum oris, tumors of the nose,
abscess, ulcerogangrenous processes, cancerous
tumors of the trachea and bronchi, chronic fetid
bronchitis, and infectious malignant neoplasms of
the oral and pharyngeal cavities.5*‘2s I3
HALITOSIS DUE TO LOCAL FACTORS OF
NONPATHOLOGIC ORIGIN
Stagnation of saliva associated with food debris
which causesthe halitosisI most often experienced in
the morning is due, in part, to lack of movement of
the cheek and tongue and also to a decrease in the
basal metabolic rate during sleep which leads to a
reduction in salivary flow which inhibits self-cleans-
ing of the oral cavity. I59I7Odor intensity of the breath
increases with age.7 During meals, the chewing
movement involving the tongue, cheek, teeth, and
other structures increases salivary flow; this helps to
remove food debris, which helps to decrease the
intensity of halitosis.15
Excessive smoking, especially cigar smoking, not
only causes fetid breath but also encourages the
hairy tongue condition, which traps food debris and
tobacco odor. It also decreasesthe salivary flow and
further increases the severity of the condition.16-‘9
521
522 Lu
Table I. Systemic diseases capable of producing
halitosis
Disease entity
Diabetes mellitus or
impending diabetic coma
Liver failure (terminal stage)
Acute rhematic fever
Portocaval venous
anastomoses
Lung abscess, tuberculosis,
bronchiectasis
Blood dyscrasias
Liver cirrhosis
Uremia, kidney failure
Toxemia, gastrointestinal
disorder, neuropsychiatric
disorder
Fever, dehydration
macroglobulinemia (with
salivary gland
involvement), Heerfordt’s
syndrome, Miklickz’s
disease, Sjijgren’s
syndrome
Syphillis, exanthematous
disease, granuloma
venereum
Internal hemorrhage
Eosinophilic granuloma,
Letterer-Siwe disease,
Hand-Schiiller-Christian
disease
Scurvy
Wegener’s granulomatosis
Noma developed from
patients who are
debilitated or
undernourished from:
diphtheria, dysentery,
measles, pneumonia,
scarlet fever, tuberculosis,
syphilis
Dentures, particularly if made of vulcanite rather
than acrylic resin, can cause a type of halitosis
known as “denture breath,“15**0 because of the
porous nature of vulcanite which encourages the
accumulation of food debris. Occasionally, endodon-
Oral Surg.
November, 1982
tic patients will complain of bad breath due to
leakage of eugenol and creosote placed in the
tooth.
Characteristic of odors
Certain age groups present a characteristic specif-
Acetone, fruity (not ic mouth odor.*OYoung children aged 2 to 5 years
detectah!e in may have a sweet fetid mouth odor due to their tonsil
well-controlled patients) crypts lodging food and bacteria. Vincent’s disease
Sweetish, musty, feculent
“amine” odor resembling
and its odor are most frequently seen in teenagers.
a fresh cadaver, known as Middle-aged men and women tend to suffer more
“fetor hepaticus” severemorning breath odor.8*‘5In addition, there are
Acid, sweet more periodontal problems in this age group. In the
Same as fetor hepaticus but old-age group, most halitosis is due to unclean
characteristically
intermittent in nature for
dentures and putrefaction of stagnated saliva.15
long period of time
HALITOSIS DUE TO SYSTEMIC FACTORS OF
Foul, putrefactive
PATHOLOGIC ORIGIN
Resembling decomposed Diabetes is the best-known example of a systemic
blood of a healing
surgical extraction wound
condition of pathologic origin. While the odor is not
Resembling decayed blood detectable in well-controlled patients, an acetone,
Ammonia or urine sweet, fruity odor could indicate diabetic acidosis or
Varies; poor oral hygiene impending hyperglycemic coma due to the abnormal
intensifies the odor accumulation of ketones in the blood which are
excreted through the respiratory system. The odor of
Odor mainly due to
xerostomia with poor oral ammonia and urine on the breath may well suggest
hygiene and/or toxic uremia or kidney failure. In severehepatic failure the
waste byproducts breath, known as fetor hepaticus, produces a sweet-
accumulated in the body ish, feculent, “amine” odor resembling a fresh cadav-
er. This kind of breath is often followed by hepatic
Fetid coma. Sometimes, such breath is also present in a
patient with extensive portocaval venous anastomo-
sis, but it is, by nature, intermittent for a long period
Decayed blood of time.2’ An acid sweet odor suggests acute rheu-
Fetid breath and unpleasant
matic fever, and a foul putrefactive breath simula-
taste
ting odorous rotting meat is indicative of lung
abscessor bronchiectasis due to dilatation of bronchi
Patients have the typical secreting pus.13,22Other systemic diseases causing
foul breath of persons halitosis include gangrene of the lung and pulmonary
with fusospirochetal
stomatosis
tuberculosis.5 Halitosis can also occur in toxemia,
Necrotic, putrefactive gastrointestinal disorders, or hemorrhage at any level
Extremely foul odor of the gastrointestinal tract; it may be present in
resembling acute neuropsychiatric disorders where the only subjective
necrotizing complaint is “bad breath.“‘*4s’6 While these neuro-
gingivostomatosis, but
psychiatric diseases do produce halitosis to some
much more intense and
fetid degree, it is further intensified by the poor oral
hygiene commonly seenin patients under physical or
mental stress who tend to neglect oral hygiene.
Moreover, emotional upsets that affect digestion and
body chemistry can sometimes influence the
breath.23 In patients suffering from any of the
nonlipid reticuloendotheliosis disorders, such as
eosinophilic granuloma, Letterer-Siwe disease, and
Hand-Schiiller-Christian disease, the chief com-
plaints are halitosis, sore mouth, and unpleasant
Volume 54
Number 5
taste.23 In almost all cases of acute and chronic
scurvy due to vitamin C deficiency, patients have the
typical foul breath of persons with fusospirochetal
stomatitis.‘9 Among patients with macroglobulin-
emia, primary herpes simplex infection, hemophilia,
Von Willebrand’s disease,cryoglobulinemia, aplastic
anemia, polycythemia Vera, agranulocytosis, leuke-
mia, infectious mononucleosis, thrombocytopenic
purpura, and thrombocythemia, halitosis is common
as a result of infection, necrosis, and decomposed
blood from spontaneous bleeding in the oral cavi-
ty.‘3*‘9 Patients who suffer from noma have the
typical, although much more intense, odor and
breath of acute necrotizing gingivostomatitis. Noma
is a rapidly spreading gangrene of the oral and facial
tissues that occurs chiefly in persons who are debili-
tated or undernourished from diphtheria, dysentery,
measles,pneumonia, scarlet fever, syphilis, tubercu-
losis, or blood dyscrasias. Thus noma, although
initiated from and involved mainly in the oral maxil-
lofacial area, may be considered a secondary compli-
cation of systemic disease.19
HALITOSIS DUE TO SYSTEMIC FACTORS OF
NONPATHOLOGIC ORIGIN
Metabolites from ingested foods that are excreted
through the lungs can also causehalitosis. A vegetar-
ian has less tendency to produce halitosis than an
excessive meat eater because there are fewer de-
graded waste byproducts of proteinous substancesin
vegetables. Meat also contains fat, and volatile fatty
acids produced in the gastrointestinal system are
absorbed into the blood and finally excreted in the
breath.‘2+‘51*OS
24It is also known that fad diets result
in acidosis or ketosis and impart an unpleasant odor
to the breath exactly the same as that noted in
impending diabetic coma.23 Garlic, onion, leeks,
alcohol, etc. impart odors to the breath by being
absorbed into the circulatory system and then perme-
ating the air as it is ventilated in the lungs.20*30
Excessive alcohol drinking leads to alteration of the
microbial flora and causes proliferation of odor-
fermenting organisms capable of producing halito-
sis.15This, coupled with liver cirrhosis, produces very
offensive breath. Halitosis is also common following
tonsillectomies.26 Halitosis cannot originate from
gastric contents except in belching or vomiting since
the odor and gas cannot escapewhen the esophagus
is in a normal closed condition.20 When the body
cannot eliminate waste byproducts faster than it
accumulates them, as when the body metabolism
slows or when the body is in an overexhausted
condition and lacks rest, the malodor of metabolic
Halitosis 523
wastes may eventually reach the breath through the
blood system, just as happens in uremia patients,
even if there is adequate oral hygiene. Some patients
with dysmenorrhea suffer from a mousy odor resem-
bling decayed clotted blood.15From time to time one
may experience “hunger odor” with hunger sensa-
tions. It has been suggested that the odor might be
due to putrefaction of pancreatic juices in the stom-
ach during hunger periods and such an odor cannot
be eliminated, even with toothbrushing.‘5*20
HALITOSIS DUE TO SYSTEMIC ADMINISTRATION
OF DRUGS
A common antiangina pectoris drug, isosorbide
dinitrate, is known to cause halitosis.*’ Drugs con-
taining iodine or chloral hydrate can reach the
breath.‘**13 Some antineoplastic agents, antihista-
mines, amphetamines, tranquilizers, diuretics, phe-
nothiamines, and atropine-like drugs tend to dimin-
ish saliva production and, therefore, decrease the
self-cleansing ability of the oral cavity. Antineoplas-
tic drugs, in addition to causi.ng xerostomia, can
cause candidiasis, gingival bleeding, and oral ulcera-
tions; this occurs most often with methotrexate,
actinomycin D, fluorouracil, adriamycin, and bleo-
mycin and is due to the leukopenia these agents
cause.27Patients receiving antineoplastic drugs fre-
quently complain about halitosis due to decomposed
blood from gingival hemorrhage and plaque forma-
tion from dehydration of the oral cavity; these
patients tend to neglect oral hygiene becauseof their
poor prospects for life.
Patients taking amylnitrite by inhalation also
produce an objectionable odor. Phenothiazine, in
addition to causing xerostomia, occasionally causes
black or white hairy tongue which encourages the
lodging of food debris. Dimethyl sulfoxide is pre-
scribed for some patients suffering from muscle pain
or from interstitial cystitis.28 For muscle pain or
spasm this medication is rubbed on the skin and is
absorbed, and about three percent of it is exhaled
through the lungs.28 For interstitial cystitis, it is
administered through intravesical installation. This
chemical, also known as DMSO, has been used to
treat a great variety of ailments, including arthritis,
headache, scleroderma, gout, acne, and brain and
spinal cord trauma. A characteristic of this chemical
is that, although it is colorless and odorless, once it is
absorbedinto the body, it is metabolized and reduced
to dimethyl sulfide, a chemical cousin of allicin,
which is the chemical essenceof garlic; consequently,
a distinct garlic-like odor is given off through the
skin and lungs. Patients usually note the garlic taste
524 Lt.4 Oral Surg.
November, 1982

Table II. Halitosis due to systemic administration of drugs

Drug I Main therapeutic uses I Mechanism

Isordil Angina1 therapy Both intrinsic odor of the drug and

metabolic end products of the drug
Ethyl alcohol Angina1 therapy, sedation Odor of the drug reaches the breath via
Chloral hydrate Hypnotic sedation systemic route; objectional odor of the
Medications containing iodine, such as Mucolytic expectorant drug itself
iodinated glycerol
Amy1 nitrite Angina1 therapy
Antihistamines Allergy, sedation
Antineoplastics Cancer therapy
Diuretics Antihypertension, antiedematic
Phenothiazine and its derivatives Schizophrenia, antiemetics, Due to xerostomia caused by drug
psychosedative
Tranquilizers Sedation
Amphetamines Anorexant analeptic, CNS stimulant
Dimethyl sulfoxide (Rimso-50) Interstitial cystitis, muscle pain Metabolized by being reduced to dimethyl
sulfide

within a few minutes after instillation and it lasts
several hours. The odor on the breath and skin
remains for up to 72 hours.
HALITOSIS DUE TO XEROSTOMIA
In addition to the systemic drug administrations
previously mentioned, other conditions causing
symptoms include mouth breathing, heavy smoking,
aging, Sjiigren’s syndrome, salivary gland aplasia,
Mikulicz’s disease,radiation therapy exceeding 800
rads, macroglobulinemia with salivary gland involve-
ment, Heerfordt’s syndrome, diabetes, menopausein
women, systemic and metabolic diseaseswith high
fever and dehydration, emotional disturbances,
excessive use of condiments, and poor oral
hygiene.15,19x20
TREATMENTAPPROACHANDPREVENTION
Different disease processesproduce different dis-
tinct characteristic mouth odors, as described before,
which can be very valuable in diagnosis. Since the
breath normally consists of odors originating from
both the oral cavity and the lungs, it would be
advisable to differentiate the odor from the lungs
from that of the oral cavity to help identify whether
the odor is from local or systemic factors. The
practitioner may ask the patient to seal the lips
tightly and then forcibly blow through the nostrils.
Odor detected in this way is from systemic fac-
tors.15
To detect odor from the mouth, the patient should
be asked to pinch the nose with the fingers, stop
respiration for a moment with the lips sealed, and
then exhale gently by opening the mouth. The odor
detected this way is from local factors of the oro-
pharyngeal cavity.
One should not solely rely on odors for diagnosis.
A good medical history and laboratory tests should
be obtained and used for early referral for medical
treatment. Dietary habits, such as drinking and
smoking, should be noted as well. Since most halito-
sis is causedby local factors, the elimination of these
factors should be the first step in the treatment
approach, especially when the medical history is
essentially negative. The eradication of periodontal
pockets, improvement of oral hygiene, restoration of
carious lesions and open contacts between the teeth,
prophylaxis through thorough polishing and scaling,
extractions of unrestorable teeth, and correction of
any other defects that could minimize the accumula-
tion and putrefaction of food debris, stagnation of
saliva, and degradation of breakdown of protein
byproducts would solve most casesof halitosis. It has
been found that thorough prophylaxis could render
odors from the oral cavity unobjectionable for at
least 2 hours.‘8 Denture wearers should keep their
dentures clean by brushing and soaking them in
cleansing and disinfecting solution. Many persons
with halitosis rely on gum chewing or mint sucking
as a solution to the problem. Sucking mints will
increase saliva flow, thereby facilitating the removal
of food debris to some extent, as well as reducing
stagnation and putrefaction of saliva. Gum chewing,
because of its involvement with the chewing move-
ment of mastication muscles, cheek, and tongue and
the increase of salivary flow, does aid in the removal
and reduction of food debris; it also increases the
cleansing function of the oral cavity. However, it
does not solve the underlying factors causing halito-
sis. Mouthwashes, fragrant dentrifices, and mint oral
deodorizing sprays will only mask the odor of the
breath temporarily, and commercial mouth rinses
Volume 54
Number 5
should not be used too frequently as they have a
tendency to dry the mucosa and alter the delicate
balance of oral microflora. Application of topical
antibiotics for the treatment of halitosis has been
investigated in several studies, mainly with aureomy-
tin and vancomycin. These antibiotics have been
found to be effective in reducing the inflammation of
gingival tissues and offensive odor,3o,3*but their use
should be carefully monitored by the practitioner.
Vancomycin, although it is a potent bactericidal
agent which is effective in preventing microbial
plaque formation,32 should not be used indiscrimi-
nately because prolonged use could lead to hearing
loss and kidney and liver impairment.33 Prolonged
use of Aureomycin, without proper supervision,
could lead to candidiasis, glossitis, and xerostomia,
and the use of deteriorated Aureomycin, which is
improperly stored or outdated, could lead to the
development of reversible “Fanconi-like” syn-
drome,34 which is similar to congenital aplastic
anemia.
When all previously described measuresfor elimi-
nating oral factors as the cause of halitosis fail to
improve the condition in a relatively short period of
time, systemic disease or local factors other than
those of the oral cavity should be suspected.Labora-
tory tests, complete blood count, urinalysis, etc.
should be performed and medical consultation
sought.
Almost everyone experiences morning breath,
mostly becauseof the offending odor of methylmer-
captan and hydrogen sulfide9 which have accumu-
lated in the mouth. While concentrations below 0.5
mg. for the former and 1.5 mg. for the latter are
acceptable, concentrations have been found to
exceed this amount in the early-morning mouth air
of 50 percent of adults in a study.35The tongue was
the principal site of these compounds which can be
effectively reduced by tongue- and toothbrushing
following eating. Even those who suffered from
severe morning breath malodor due to unusual high
concentrations of these compounds could still be
controlled by eating followed by brushing of the
tongue and teeth and by rinsing with a mouthwash.20
In fact, the tongue, one of the main focuses of
microorganisms in the mouth,36-38 should be included
as a necessary part of routine home oral hygiene
procedures,3gs 4oespecially in those with hairy tongue
and fissured tongue. Outgrowth of black or white
hairy tongue due to phenothiazine intake usually
disappears after discontinuation of this drug.27
Those patients in whom halitosis is due to xerosto-
mia could use sodium carboxymethyl cellulose to
moisten the oral cavity without any untoward reac-
Halitosis 525
tions.27If the cause is due to systemic administration
of a drug by a physician, then medical consultation is
essential. In fact, even if the cause of halitosis is a
systemic drug, meticulous oral hygiene can keep the
halitosis minimal. Generally speaking, halitosis
caused by local factors of pathologic origin and local
factors of nonpathologic origin usually ceasesonce
the pathologic condition is treated and satisfactory
oral hygiene is observed. Halitosis from a systemic
factor of pathologic origin, however, is more intense
and persistent unless the systemic diseaseis treated.
Halitosis from a systemic factor of nonpathologic
origin is usually transient in nature and usually
ceases once its cause is found and corrected; for
example, halitosis improves when dietary habits, are
changed, and patients who have gallbladder dysfunc-
tion with impaired digestion of fats could improve a
halitosis condition simply by reducing their intake of
dairy products.20,41
CONCLUSION
Although halitosis has a multifactorial etiology,
local factors play the major role in most casescaused
by bacteria and substancescontaining or capable of
producing hydrogen sulfide, dimethyl sulfide, meth-
ylmercaptan, and diemethyl disulfide.42s46 Any mea-
sures that reduce these bacteria and substanceswill
eliminate most causesof halitosis. Nevertheless, the
practitioner should consider all factors, particularly
systemic ones, when rendering treatment.
Very little has been written about differential
diagnosis of halitosis based on the characteristics of
the odors produced by different systemic diseases.
This article presents a referential aid for the clinician
who wishes to develop the diagnostic acumen to
distinguish one type of halitosis from another by
classifying the etiologic factors which causehalitosis.
Once the factors of a given case of halitosis and its
distinct odor are ascertained, proper treatment can
be readily rendered and prevention achieved.
REFERENCES
I. Howe, J. W.: The Breath and the Diseases Which Give It a
Fetid Odor, New York, 1874, D. Appleton and Co.
2. Massler, M., et al.: Fetor Ex Ore: A Review, ORAL SURG. 4:
110-125, 1951.
3. Hine, M. K.: Halitosis, J. Am. Dent. Assoc. 55: 37-46,
1957.
4. Reilly, E. B.: Halitosis, N. Z. Dent. J. 59: 129-132, 1963.
5. Glickman, I.: Clinical Periodontology, ed. 4, Philadelphia,
1972, W. B. Saunders Company, p. 401.
6. Berg, M., Burrill, D. Y., and Fosdick, L. S.: Chemical Studies
in Periodontal Disease. III. Putrefaction of Salivary Proteins,
J. Dent. Res. 25: 231-246, 1946.
7. Sulser, G. I., Brening, R. H., and Fosdick, L. S.: Some
Conditions That Affect the Odor Concentration of the
Breath, J. Dent. Res. 18: 355-359, 1939.
8. Horowitz, A., and Folke, L.: Hydrogen Sulfide in the Gingival
526 Lu
Environment, IADR Program and Abstracts, 1972, No.
39.
9. Larson, B. T., and Widmark, G.: A Gas Chromatographic
Method for Analysis of Volatiles in Human Breath and
Saliva, Acta Pharm. Suet. 6: 479, 1969.
10. McNamara, T. F., Alexander, J. F., and Lee, M.: The Role of
Microorganisms in the Production of Oral malodor, ORAL
SURG. 34: 41, 1972.
11. Lavasko, J., and Fast, T.: Halitosis Resulting From a Dentig-
erous Cyst, J. Indiana Dent. Assoc. 46: 521-522, 1967.
12. Spouge, J. D.: Halitosis-A Review of Its Causes and
Treatment, Dent. Pratt. 14: 307-317, 1964.
13. Burket, L. W.: Oral Medicine, Diagnosis and Treatment, ed.
7, Philadelphia, 1977, J. B. Lippincott Company, chaps, 7,
19.
14. Allen, H. J.: Fetor in the Breath, Welch’s Monthly 1: 257,
1896.
15. Swenson, H. M.: Halitosis: A Brief Review, Indiana Univer-
sity School of Dentistry Alumini Bulletin, Fall, 1979, pp.
33-34.
16. Krupp, M. A., and Chatton, M. J.: Current Medical Diagno-
sis and Treatment, Los Altos, Calif. 1978, Lange Medical
Publisher, p. 335.
17. Tonzetich, J.: Production and Origin of Oral Malodor: A
Review of Mechanisms and Methods of Analysis, J. Peri-
odont. 48: 13-20, 1977.
18. Morris, P. P., and Read, R. R.: Halitosis: Variations in Mouth
and Total Breath Odor Intensity Resulting From Prophylaxis
and Antisepsis, J. Dent. Res. 28: 324-333, 1949.
19. Shaffer, W. G., Hine, M. K., and Levy, B. M.: Textbook of
Oral Pathology, ed. 3, Philadelphia, 1974, W. B. Saunders
Company, chap. 1, pp. 271, 527, 537, chap. 4.
20. Massler, M.: Fetor Ex Ore: Halitosis: The Compendium of
Continuing Education in Dentistry, University ofPennsylva-
nia vol. II, No. 2, March/Auril. 1981.
21. Houston, J. C., Joiner, d. L., and Trounce, J. R.: A Short
Textbook of Medicine, London, 1966, The English Universi-
ties Press, Ltd., p. 84.
22. McCarthy, F. M.: Vital Signs-The Six Minute Warnings, J.
Am. Dent. Assoc. 100: 682, 1980.
23. Lamb, L. E.: Physician’s Column, House Call: Bad Breath,
Call Chronicle, Allentown, Pa., April 6, 1976.
24. Crohn, B. B., and Drossd, R.: Halitosis, J.A.M.A. 117: 2242,
1941.
25. Blakenhorn, M. A., and Richards, C. E.: Garlic Breath Odor,
J.A.M.A. 107: 409-410, 1936.
26. Hollander, A. K.: Office Practice of Otolaryngology, Phila-
delphia, 1965, F. A. Davis Company, p. 428.
27. Holroyd, S. V.: Clinical Pharmacology in Dental Practice, ed.
2, St. Louis, 1978, The C. V. Mosby Company, pp. 69, 297,
chap. 18, pp. 307-308, 315.
28. O’Reilly, R. A., and Motley, C. H.: Breath Odor After
Disulfiram, J.A.M.A. 238: 2600, 1977.
29. Physician’s Desk Reference: ed. 35, P-V-Tussin, 1981, Medi-
cal Economics Co. p. 1451.
Oral Surg.
November. 1982
30. Roth, L. H.: Aureomycin in Overcoming Oral Odors, West
Va. Dent. J. 2598-105, 1951.
31. Mitchell, D. F.: Topical Antibiotic Maintenance of Oral
Health, J. Oral Ther. 4~83-92, 1951.
32. Scopp, I. W.: Treatment of Oral Lesions With Topically
Applied Vancomycin Hydrochloride, ORAL SURG. 24: 703-
706, 1967.
33. Physician’s Desk Reference: Vancomycin Hydrochloride, ed.
35, 1981, Medical Economics Co., p. 1098.
34. Cleveland, W. W., et al: Acquired Fanconi Syndrome Follow-
ing Degraded Tetracycline, J. Pediatr. 66~333-342, 1965.
35. Tonzetich, J., and Ng, S. K.: Reduction of Malodor by Oral
Cleansing Procedures, ORAL SURG. 42: 172-181, 1976:
36. Gibbons. R. J.. Kapsimalis. B.. and Secranskv, S. S.: The
Source of Salivary Bacteria, Arch. Oral Biol. 9: 100, 1964.
37. Krasse, B. 0.: The Proportional Distribution of Streptococcus
Salivarius and Strepococci in Various Parts of the Mouth,
Odontol. Rev. 5: 203, 1954.
38. Gordon, D. F., Jr., and Gibbons, R. J.: Studies of the
Predominant Cultivatable Micro-Organisms From the
Human Tongue, Arch. Oral Biol. 11:627, 1966.
39. Gilmore, E. L., Gross, A., and Whitley, R.: Effect of Tongue
Brushing on Plaque Formed In Vitro, J. Periodontol. 43~418,
1972.
40. Gilmore, E. L., Gross, A., and Whitley, R.: Effect of Tongue
Brushing on Plaque Bacteria, ORAL SURG. 36: 201, 1973.
41. Strohmeyer, G.: Functional Disorders of the Gastrointestinal
Tract, Laber. Magen. Darm. 8: 117-182, 1978.
42. Mitchell, D. F., and Holmes, L. A.: Topical Antibiotic
Control of Dentinogingival Plaque, J. Periodontol. 36~202,
1965.
43. Amoore, J. E., and Venstrom, D.: Correlations Between
Stereo-Chemical Assessments and Organoleptic Analysis
Odorous Compounds, in Hayashi, T., editor: Olfaction and
Taste. II. Oxford, 1967, Oxford Symposium Publications
Division, Pergamon Press, Inc. pp. 3-16.
44. Richter, V. J., and Tonzetich, J.: The Application of Instru-
mental Technique for the Evaluation of Odoriferous Volatiles
From Saliva and Breath, Arch. Oral Biol. 9: 47-53, 1964.
45. Tonzetich, J.. and Richter, V. J.: Evaluation of Volatile
Odoriferous Components of Saliva, Arch. Oral Biol. 9: 39-45,
1964.
46. Kaizu, T., Tsunoda, M., Aoki, H., and Kimura K.: Analysis of
Volatile Sulfur Compounds in Mouth Air by Gas Chromatog-
raphy, Bull. Tokyo Dent. U. 19: 43-52, 1978.
Reprint requests to:
Dr. Dominic P. Lu
Northwestern Medical Center
New Tripoli, Pa. 18066