A12_IPC_AAP_Annals_553640 6/7/00 8:53 AM Page 65

Ann Periodontol

Necrotizing Ulcerative Gingivitis

Randal W. Rowland*

* University of California San Francisco, San Francisco, California.

Necrotizing periodontal diseases are unique in their clinical pre-

sentation and course. Data suggest that the etiology and patho-
genesis of necrotizing periodontal diseases may also be dis-
tinctive from other periodontal diseases. Necrotizing ulcerative
gingivitis (NUG) is a type of necrotizing periodontal disease in
which the necrosis is limited to the gingival tissues. Three spe-
cific clinical characteristics must be present to diagnose NUG,

N
ecrotizing ulcerative gingivitis
pain (usually of rapid onset) interdental necrosis, and bleeding. (NUG) is unique among the peri-
Epidemiological and prospective clinical studies have found an odontal diseases. It has an acute
altered ability to cope with psychological stress, immunosup- clinical presentation with the distinctive
pression, and tobacco use to be strongly associated with the characteristics of rapid onset of gingival
onset of NUG. Ann Periodontol 1999;4:65-73. pain, interdental gingival necrosis, and
KEY WORDS bleeding. Necrotizing ulcerative gingivi-
tis has been recognized for centuries. It
Gingivitis, necrotizing ulcerative/etiology; gingivitis,
has been known by many names: Vin-
necrotizing ulcerative/pathogenesis; gingivitis, necrotizing
cents disease, fusospirochetal gingivitis,
ulcerative/classification.
trench mouth, acute ulcerative gingivi-
tis, necrotizing gingivitis, and acute
necrotizing ulcerative gingivitis or ANUG,
to name a few.1-6 The onset of NUG is
associated with increased psychological
stress, increased physical demand, and
decreased nutrient intake.1-10 It is not
surprising that early historical documen-
tations of NUG were made in the mili-
tary and especially at times of war. The
first reference to an oral disease distin-
guished by these clinical signs and symp-
toms is credited to the historical war
records of Xenophons troops during the
fourth century BC.11-13 These records
included descriptions of painful decay-
ing tissue between the teeth which
allowed for the distinction between NUG
and scurvy, another common gingival
lesion of that era.13 A NUG-like condition
was also reported in the Roman army of
the first century AD.12 In general, this
clinical description is still in use today in
the diagnosis of NUG. John Hunter first
delineated the clinical differences be-
tween NUG, scurvy, and chronic peri-
odontitis in 1778.12,14 Necrotizing ulcer-
ative gingivitis was commonly found
among the French soldiers in the nine-

65
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Necrotizing Ulcerative Gingivitis
teenth century. Hirsch added secondary findings to the
clinical presentation of NUG in 1886 and Bergeron
described both acute and chronic forms of the disease
in 1895.12
Although its clinical signs are easy to identify, much
is still not understood regarding the etiology and patho-
genesis of NUG. For example, with such a profound
bacterial mass and concomitant inflammation, why is
NUG usually self-limited to the interdental and marginal
gingiva? Does NUG in the immunocompromised host
(e.g., acquired immune deficiency syndrome [AIDS])
progress to include much of the periodontium result-
ing in severe loss of clinical attachment and bone?
Does NUG in extremely nutritionally deficient children
(e.g., Kwashiorkor) progress to include the external
structures of the face sometimes leading to death? The
literature concerning the clinical diagnosis, pathogenic
mechanisms, and progression of NUG is often in con-
flict. The purpose of this paper is to critically review
data that exist in relation to NUG as a clinical diagnosis.
A comprehensive understanding of NUG will assist in
clinical diagnosis and delivery of appropriate therapy
for this infrequent, yet clinically significant, periodon-
tal condition.
DEFINING CHARACTERISTICS OF NUG
Clinical Presentation
Necrotizing ulcerative gingivitis is different from the
other periodontal diseases, in that it presents with inter-
dental gingival necrosis as often described by punched
out ulcerated papillae, gingival bleeding, and pain.1-6
Interproximal gingival necrosis is easy to detect. How-
ever, tooth shape, size, and alignment may alter the
form of papillae. Consequently, these factors must be
considered when assessing interdental papillae. It is
possible for inexperienced clinicians to misclassify
papillae as necrotic when in fact the papillae are
blunted due to the presence of a diastema and inflamed
due to bacterial plaque. Loss of attachment and bone
in NUG are infrequent findings, but can occur after
multiple recurrences of the disease. Gingival bleeding
associated with NUG is probably the least distinctive
of the clinical signs of NUG, since it is a frequent find-
ing in other periodontal diseases. However in other
periodontal diseases, a substantial stimulus such as
tooth brushing or periodontal probing is required to
elicit bleeding. In comparison, gingival bleeding in NUG
occurs with little or no provocation. Pain is the hallmark
of NUG. The quality of pain in NUG is intense and
results in patients seeking treatment. Typical gingivi-
tis and periodontitis are not associated with severe gin-
gival pain. Periodontal abscesses and herpetic infec-
tions are painful but can be easily distinguished from
NUG. If any of the 3 criteria (interproximal necrosis,
bleeding, and pain) are absent, a diagnosis of NUG
cannot be made. Other signs and symptoms that have
66
Volume 4 Number 1 December 1999
been reported to occur in NUG include lym-
phadenopathy, fetor ex ore, fever, and malaise.15-17
However, none of these are pathognomonic since they
frequently occur in many other forms of periodontal
disease. Lymphadenopathy is an infrequent finding in
NUG. Its presence is probably related to the severity
of the disease since it is usually observed in severe,
advanced cases.3,18 The strong malodor (fetor ex ore)
that has often been associated with NUG is not always
noted4,18 and may be associated with many other oral
diseases such as chronic periodontitis. While there are
reports that fever and malaise are common clinical
features of NUG,1,16 most clinical studies have indi-
cated that their presence may suggest primary her-
petic gingivostomatitis or mononucleosis.2,4,19,20 If one
compares the features that are unique to NUG to those
that are common, it is easy to distinguish NUG clini-
cally from other gingival and periodontal diseases.
It has been suggested that there are acute and
chronic forms of NUG.21,22 Patients presenting with
NUG are indeed often susceptible to future recur-
rences.1-6,23 However, the historical terminology of
chronic should be considered a misidentification of
a recurrence of disease. In addition, the rapid onset
of NUG has led many, especially in the United States,
to refer to NUG as ANUG. The term acute in ANUG
is a clinical descriptive term and should not be used
as a diagnostic classification. As there is no chronic
form of NUG, it is also best to consider ANUG a mis-
nomer.
Necrotizing ulcerative gingivitis is diagnosed at the
onset of specific clinical signs and symptoms.5,6,24
Episodes of NUG will usually resolve within a few days
after receiving adequate treatment. Such response is
extraordinary among plaque-associated periodontal
diseases. Furthermore, unlike other forms of peri-
odontal infection, NUG primarily affects the interden-
tal and marginal soft tissue with little osseous involve-
ment. It may be superimposed upon periodontitis and
complicate the diagnosis.2,6 Some reports indicate that
NUG is associated with attachment loss. In a study of
13 patients with a history of NUG, it was found that
mean probing attachment loss in the interdental crater
sites were significantly greater than the mean for all
other sites. The presence of interdental craters was
assumed to be the previous sites of NUG. An associ-
ation between NUG and attachment loss was made in
this report.25 Attachment loss has also been noted
upon recurrences of NUG.17 Such findings have led
some to support the surgical treatment of any resid-
ual interdental soft tissue craters.2,3,17
Even if clinical attachment loss is associated with
NUG, it is obvious that this disease presents with a
different response to therapy than other forms of peri-
odontal disease. Resolution is quick upon removing
the bacterial challenge.2,20,23,26 In addition, it has been
A12_IPC_AAP_Annals_553640 6/7/00 8:53 AM Page 67
Ann Periodontol
reported that even with conservative treatment, regen-
eration of the affected interdental sites is possible.27
Using periodic scaling, root planing, and antimicrobial
rinses, this study showed that the disease process was
not only halted, but that regeneration of the necrotic
papillae was possible.27 In contrast, longitudinal stud-
ies involving similar therapeutic regimens in the main-
tenance of post-therapy periodontitis sites found sta-
bilization, but not necessarily regeneration, of the lost
periodontium.28 The clinical presentation, course, and
response to therapy for NUG are specific among the
periodontal diseases and support a unique clinical dis-
ease category.
Etiology
Necrotizing ulcerative gingivitis is an infectious dis-
ease. Dramatic resolution of signs and symptoms can
be affected by reduction of the microbial plaque either
by antibiotic therapy,3,26,29 mechanical debride-
ment,2,17,20 or both.1,5,6,27 A specific infectious dis-
ease should be associated with a specific etiology. The
bacterial etiology of NUG provides one of our strongest
examples of a primary bacterial etiology in a peri-
odontal disease.30 This bacterial etiology was first
proposed by Plaut in 189431 and Vincent in 1896.32
Working independently, they both reported that
fusiform-spirochete bacterial flora were associated with
the lesions of necrotizing ulcerative gingivitis. Even
though fusiforms and spirochetes are commonly found
in patients who do not have NUG,33 it does appear
that these and perhaps other bacteria play a major
role in the pathogenesis of NUG. First, electron micro-
scopic studies of gingival biopsies from NUG patients
have provided some of the most well known findings
in support of bacterial invasion in a periodontal disease.
In a classic electron microscopic investigation in 1965,
four zones associated with the gingival lesion of NUG
were identified.34
1. Bacterial zone: composed of a large mass of bac-
teria with varying morphotypes, including some spiro-
chetes.
2. Neutrophil rich zone: underlies the bacterial zone,
contains many leukocytes with neutrophils predomi-
nating. Bacteria, including many spirochetes, are
located between the cells.
3. Necrotic zone: characterized by disintegrating
cells and many spirochetes (large and intermediate)
and other bacteria that appear to be fusiforms.
4. Spirochetal infiltration zone: tissue elements
appear well preserved but are infiltrated by spirochetes,
both large and intermediate in size. No other bacteria
were observed.
Essentially the same findings were reported in
another study 2 years later.35 A later study also found
cocci and rods in addition to the spirochetes, within the
adjacent non-necrotic connective tissue region.36 The
Rowland
neutrophil rich, necrotic, and spirochetal infiltration
zones are unique to NUG. The histologic appearance
of NUG is different from other gingival and periodontal
diseases,37-39 but it is complex and may be mislead-
ing, as cells associated with chronic lesions such as
lymphocytes may be present also. These are probably
due in part to a preexisting established gingivitis.39
Microbial studies have also characterized the gen-
era and species of the cultivable flora in NUG.24,40 In
one study, the cultivable flora and microscopic findings
were evaluated on the same plaque samples.40 It was
reported that both the cultivable and microscopic flora
had what the authors identified as constant and vari-
able components. The constant cultivable flora con-
sisted of a limited number of predominant organisms,
B. melaninogenicus ssp. intermedius, now known as
Prevotella intermedia, and Fusobacterium sp. Micro-
scopically, Treponema and Selenomonas sp. comprised
the constant flora. The concept of a predominant con-
stant flora suggests an association of these flora with
the disease. As with other periodontal diseases how-
ever, this association does not necessarily demonstrate
an etiologic role for these bacteria in the initiation of
NUG. Attempts to satisfy Kochs postulates by trans-
fer of the disease from one animal to another have
been attempted. When inoculated subcutaneously into
the groin of guinea pigs, scrapings from lesions of NUG
have produced fusospirochetal infections.41 It was also
possible to pass this infection from animal to animal
by the same route. Skin abscesses have been pro-
duced in guinea pigs by injecting pure cultures of T.
vincentii and T. buccalis separately and in combina-
tion with other oral isolates.42 However, several differ-
ent organisms singly or in combination have been
demonstrated to be capable of producing similar
lesions.43 Using a steroid-induced immunosuppression
in the beagle dog, it has been possible to transmit NUG
from animal to animal.44-48 Some histologic differ-
ences were noted in the dog model compared to the
earlier studies of human specimens; however, spiro-
chetes were seen penetrating normal epithelium, which
may suggest that spirochetes were involved in the ini-
tiation of the pathogenesis in NUG.48 In other forms of
periodontal disease, spirochetes are involved in
advanced gingivitis and periodontitis lesions but are
not associated with sites of early periodontitis or gin-
gival health.24,49,50 Studies of the bacterial etiology of
NUG indicate that NUG is different from other peri-
odontal diseases.
For many years, NUG was considered a communi-
cable disease. A diagnosis of NUG often required a
report to community health departments in a similar
fashion as a venereal disease. A particularly insight-
ful discussion of the data in regards to the communi-
cability of NUG led the American Dental Association
to conclude that NUG was not communicable.51
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Necrotizing Ulcerative Gingivitis
Predisposing Factors
Psychological stress. Development of NUG is closely
associated with specific predisposing secondary fac-
tors such as psychological stress, immune suppres-
sion, smoking, malnutrition, pre-existing gingivitis, and
tissue trauma. Acute psychological stress in particu-
lar appears to be associated with the onset of NUG.7
It is well documented that the prevalence of NUG in
the military increases under conditions which produce
high levels of acute stress4,19,22,52 and in drug addicts
during periods of drug withdrawal.8 Additionally, it is
not uncommon to have outbreaks of NUG among col-
lege students during examinations.9
During periods of psychological stress, oral hygiene
measures may decrease, nutrition may become inad-
equate, tobacco smoking may increase, and immune
function may be suppressed. Stressful life events may
lead to an activation of the hypothalamic-pituitary-
adrenal axis, resulting in an elevation of serum and
urine corticosteroid levels.53 Increases in urinary lev-
els of 17 hydroxycorticosteroid (17-OHCS) have been
associated with psychological stress. Accordingly, sig-
nificantly higher levels of urinary 17-OHCS have been
reported in NUG patients when compared with levels
measured after resolution of the disease.54 Another
study reported significantly higher levels of urinary
cortisol in NUG patients in comparison to control sub-
jects.55 Increased corticosteroid levels may play sev-
eral roles in the development of NUG such as immuno-
suppression.
Immunosuppression. Increased cortisol levels have
been associated with a depression of polymorphonu-
clear leukocyte (PMN) function.56 Depressed PMN
function as measured by chemotactic, phagocytic, and
bactericidal abilities has been reported in NUG
patients.57-59 In addition, altered lymphocyte function
has been reported in NUG and will be discussed
below.57,60,61 Further evidence to support the rela-
tionship of immune suppression via increased levels of
corticosteroids was demonstrated by the transfer of
NUG in the beagle dog after pretreatment with steroids
as previously discussed.44-48 Furthermore, it has also
been suggested that elevated steroid levels may pro-
vide essential nutrients for specific bacterial growth
(Prevotella intermedia).40,62
Studies of immune responses in NUG have found, for
the most part, a lack of protective functions. One of
the earliest studies found no differences in antibody
levels to Fusobacterium fusiforme, B. melaninogeni-
cus, and Borrelia vincentii of NUG patients compared
to control subjects.63 A follow-up study using a dif-
ferent methodology from the same laboratory looked
at the immune response to Actinomyces viscosus, F.
fusiforme, Veillonella alcalescens, and B. melanino-
genicus. They also found no differences in serum anti-
body levels between patients and control subjects. This
68
Volume 4 Number 1 December 1999
was true on the first day of attendance and up to one
month after the disease started.64 In another study,
saliva was assayed for all 5 classes of immunoglobu-
lins as well as secretory IgA. A decrease in total
immunoglobulin levels but an increase in secretory
IgA was found in NUG subjects when compared to the
control subjects.65 Another study of the humoral
response reported a depressed total serum IgG and
increased total serum IgM concentrations in patients
with NUG and patients with recurrent NUG compared
to the control subjects.66 Taken together, these early
reports provide interesting findings. The onset of NUG
is associated with a large microbial plaque load. Fur-
thermore an established or pre-existing gingivitis is
considered necessary for the onset of NUG. Therefore
these early studies of the immune response indicate
that a lack of protective antibodies may be involved
in the development of NUG.
In contrast to these early studies, two more recent
investigations of antibody response have reported con-
flicting findings.24,67 Both studies used specific bacte-
rial strains and measured antibody levels by an enzyme-
linked immunosorbent assay. One study found
significantly higher IgG and IgM levels to an interme-
diate size spirochete and higher IgG levels to B. inter-
medius (P. intermedia) in NUG subjects compared to
healthy and gingivitis subjects.67 Examination of the
results, however, indicated that significantly higher IgG
titers were present against only 1 of 2 P. intermedia
strains tested. In addition, the source for the interme-
diate size spirochete in this study was reported to have
been deep periodontal pockets. The other study was
carefully controlled for confounding factors: plaque lev-
els, age, race, gender, and socio-economic status. In
this study, a depressed IgG and IgM response in NUG
subjects compared to control subjects was reported for
4 isolates of P. intermedia (2 from NUG patients, 2 from
control subjects). In addition, no differences in IgG lev-
els to spirochetes isolated from NUG subjects or con-
trol subjects, or IgM levels to the spirochetes from NUG
individuals were found.24 It is arguable that antibody lev-
els, both non-specific and specific, are either similar
or depressed in NUG patients compared to control sub-
jects. However, lymphocyte function as measured by
mitogenic response is severely depressed in NUG.57,60,61
It is apparent that regardless of the mechanisms
involved, a general immune suppression (PMN function,
antibody response, and lymphocyte mitogenesis) is
associated with the onset of NUG.
Thus, it is not surprising that NUG has been asso-
ciated with infection by human immunodeficiency virus
(HIV) and acquired immune deficiency syndrome
(AIDS).6,7,60 Moreover, it has been reported that NUG
may be the first sign of HIV infection.60 Several con-
troversies regarding the association of HIV disease and
NUG exist. Early in the AIDS epidemic, atypical forms
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Ann Periodontol
of gingivitis and periodontitis were reported to be asso-
ciated with HIV infection.68 The gingivitis was described
as a distinct erythematous band of the marginal gin-
giva with either diffuse or punctate erythema of the
attached gingiva with little dental plaque. It was named
HIV-associated gingivitis (HIV-G).68 Spontaneous bleed-
ing was often present in HIV-G. Unlike conventional
gingivitis, it was reported that HIV-G did not respond
to oral hygiene measures. It may be due at least in
part to a candidal infection.69 These early studies from
San Francisco also reported a progression from HIV-
G to NUG to a necrotizing ulcerative periodontitis.68 In
1993, HIV-G was renamed as linear gingival erythema
(LGE) by a collaboration of the EC-Clearinghouse on
Oral Problems related to HIV infection and the WHO
Collaboration Centre on Oral Manifestations of the
Immunodeficiency Virus.69
The distinct periodontitis in the San Francisco HIV-
infected population was described as an ANUG type
of lesion (i.e., NUG) superimposed upon a rapidly pro-
gressing periodontitis; a lesion in which severe loss of
attachment and bone was noted. Patients presenting
with this disease did not have a history of NUG in these
areas.68 The authors referred to this disease as HIV-
associated periodontitis (HIV-P). HIV-associated peri-
odontitis was subsequently renamed as necrotizing
ulcerative periodontitis or NUP.69 Necrotizing stomati-
tis (NS) occurs when the necrosis extends into the
mucosa and bone outside the periodontium.68,69
Through the years NUP in HIV-infected patients has
been either misinterpreted as NUG or as a NUG-like
lesion, which quickly progressed to a necrosis of
bone.70-72 This has occurred in spite of the original
report and subsequent attempts to clearly define these
entities.73-75 It is important to note that these early
findings were generated from essentially non-medically
treated HIV-infected patients. In a sense the actual dis-
ease process of NUG and NUP could be studied. Stud-
ies of the bacterial etiology of NUP (HIV-P) found the
flora to be different from adult periodontitis76 and the
same as adult periodontitis.77 Both studies however
found the flora to be different from that associated with
NUG.40 The issue of periodontal disease in HIV-infected
individuals has become much more complex than war-
ranted.78 There have been attempts to address this
problem. One approach is to clearly define small clin-
ical differences for use in clinical studies of periodon-
tal disease.79 This approach is time consuming, but
would be useful in specific situations; e.g., assessment
of disease progression and treatment outcomes. Oth-
ers have sought to broadly group clinical findings.69,80
Such an approach would be applicable for use in epi-
demiologic studies of oral manifestations but would
lack sensitivity for identification of periodontal diseases
such as NUG and NUP. Excellent reviews of periodontal
diseases in HIV infection have been written by peri-
Rowland
odontists and others experienced with this area of HIV
manifestations.73-75,81,82
Malnutrition. Malnutrition also has been reported to
be a predisposing factor in the onset of NUG.1-6 Necro-
tizing ulcerative gingivitis is considered to be a dis-
ease of young adults in Europe and the United States.
In contrast, NUG occurs in very young children in
developing countries.83-89 The development of NUG
in children appears to be related to poor nutritional
status especially in protein intake83,84 and secondary
to viral infections such as measles.85 Necrotizing ulcer-
ative gingivitis, which occurs in malnourished children,
especially after viral and protozoal infections, may also
progress to a fulminating disfiguring and often lethal
infection known as noma.1-6 Noma has been known
by other names such as cancrum oris in Africa, and
dzo-ma-gan in China. Dzo-ma-gan, which translates as
running horse gangrene, is a historical name and is
a reference to the rapid progression noma exhibits.5,90
While it is generally accepted that NUG will progress
to noma in the compromised patient,1-6 a review of
the literature finds only rare cases that clearly began
as NUG and progressed to noma.88 Moreover, reports
purported to document the progression of NUG to
noma contain photographs of initial presentation that
appear to indicate that patients had more than inter-
proximal gingival necrosis. These included cellulitis of
the external facial structures, advanced lesions involv-
ing the entire periodontium (necrotizing ulcerative peri-
odontitis), or lesions extending past the periodontium
into surrounding bone (necrotizing stomatitis).83-89
While it may seem appropriate to consider noma as
an extension of NUG, this is not well documented. A
recent study indicates that noma is associated with
elevated cortisol levels and reduced levels of zinc and
amino acids in children previously infected with
measles or herpesviruses in consort with F. necropho-
rum infection.91 This finding is in agreement with ear-
lier studies that reported the association of viral infec-
tions with the development of noma.83,86 The
underlying mechanisms of the pathogenesis of noma,
however, still need to be identified.
Other Predisposing Factors. Tobacco smoking,
pre-existing gingivitis, and trauma have been reported
as predisposing factors in NUG also. Tobacco smok-
ing in particular is associated with the onset of
NUG.10,92-94 An earlier report suggested an associa-
tion between NUG and venereal disease.95
SYSTEMIC DETERMINANTS UNKNOWN
The majority of patients with NUG will still present with
systemic determinants unknown. In other words, the
clinician will make a presumption of the etiologic and
pathogenic mechanisms that are ongoing based upon
the identification of predisposing factors. A smaller
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Necrotizing Ulcerative Gingivitis Volume 4 Number 1 December 1999

Psychological Stress and Anxiety

Pre-Existing Gingivitis

Increased Corticosteroid Production

Immunosuppression

Increased Bacteria Growth and Invasion

Viral Infection Immunosuppression

Necrotizing Ulcerative Gingivitis

HIV Infection Deficient Nutrition

Candida Infection Viral Infections

Protozoal Infections

Linear Gingival Erythema

Noma

Necrotizing
Ulcerative
Periodontitis

Necrotizing
Stomatitis

Figure 1. Necrotizing ulcerative gingivitis: possible etiological mechanisms and sequelae.

percentage of NUG cases will be attributable to sys-
temic determinants known; e.g., immunosuppression
secondary to HIV infection.
SUMMARY
Necrotizing ulcerative gingivitis is a distinct painful
infectious disease primarily of the interdental and mar-
ginal gingiva. These clinical signs and symptoms of
NUG will usually resolve within a few days after receiv-
ing adequate treatment; however, patients remain at
risk for recurrences of disease. As with other plaque-
associated periodontal diseases, opportunistic bacte-
ria are the primary etiologic agents in NUG. There are
also non-specific predisposing factors for the devel-
opment of NUG: acute psychological stress, tobacco
smoke, and pre-existing gingivitis. From this review
of the literature it is evident that the predominant fac-
tor in the development of NUG is immunosuppression.
Furthermore, immunosuppression may be associated
with all of the predisposing factors.
The epidemiology and etiology of NUG have inter-
ested the research community for many years. Sev-
eral excellent reviews are available for reference.1,15,96
While this interest has led to an extensive body of
knowledge in regards to NUG, there is still much
not known. It has been proposed by many that NUG
may progress to involve the periodontium (NUP) and
surrounding oral tissues (necrotizing stomatitis and
noma) depending upon the health status of the
patient. While the clinical presentation of NUG may
be modified by the systemic health status of the
patient, it has a unique presentation, etiology, and
pathogenesis and warrants a separate disease classi-
fication. Figure 1 depicts the various interactions
thought to occur in NUG.
REFERENCES
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Periodontol 1986;57:141-150.

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2. Goldhaber P, Giddon DB. Present concepts concerning
the etiology and treatment of acute necrotizing ulcera-
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3. Shinn DL. Vincents disease and its treatment. In: Fine-
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4. Grupe HE, Wilder LS. Observations of necrotizing gin-
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5. Armitage GC. Acute periodontal lesions. In: Biologic
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7. Moulton R, Ewen S, Thieman W. Emotional factors in
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1952;5:833-860.
8. Davis RK, Baer PN. Necrotic ulcerative gingivitis in drug
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two cases Oral Surg Surg Oral Med Oral Pathol 1971;31:
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9. Giddon DB, Zackin SJ, Goldhaber P. Acute necrotizing
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10. Stevens AW Jr., Cogen RB, Cohen-Cole S, Freeman A.
Demographic and clinical data associated with acute
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11. Prinz H, Greenbaum SS. In: Diseases of the Mouth and
Their Treatment. Philadelphia: Lea & Febinger; 1935:153-
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12. Hirschfeld I, Beube F, Siegel EH. The history of Vin-
cents infection. J Periodontol 1940;11:89-98.
13. Pickard HM. Historical aspects of Vincents disease. Proc
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