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Dental Plaque-Induced Gingival Diseases

Angelo Mariotti*
* Ohio State University, Columbus, Ohio.

Gingival diseases are a diverse family of complex and distinct

pathological entities found within the gingiva that are the result
of a variety of etiologies. There are several clinical characteristics common to all gingival diseases and these features include
clinical signs of inflammation, signs and symptoms that are confined to the gingiva, reversibility of the disease by removing the
etiology, the presence of bacterial laden plaque to initiate and/or
exacerbate the severity of the disease and a possible role as a
precursor for attachment loss around teeth. Defining and classifying gingival diseases has not been an easy task. The tools
and methods to identify gingival diseases have varied depending on the criteria used by epidemiologists, researchers, or the
practicing clinician. The classification of gingival disease in this
review relied upon experimental and/or epidemiological human
studies that accurately and reliably assessed an underlying functional derangement that was localized to the gingiva and was
reported in a peer-reviewed journal. The classification of gingival diseases that depends on dental plaque to initiate the disease process(es) has been categorized into two groups. The two
categories of plaque-induced gingival diseases are those affected
by local factors and those that are affected by local factors and
modified by specific systemic factors found in the host. In this
review, the clinical characteristics of gingival disease associated
with plaque, endogenous hormone fluctuations, drugs, systemic
diseases, and malnutrition were investigated. Ann Periodontol
1999;4:7-17.
KEY WORDS
Gingival diseases/etiology; gingival diseases/classification;
dental plaque/adverse effects; risk factors.

t was described almost 3500 years ago

by the Chinese;1 estimates of its prevalence have varied widely;2 its etiology
has been defined3 and yet needs to be
resolved;4,5 it has been the subject of
intense research and benign neglect;6 it
has been described by the type of exudate;6-9 it has been depicted by the location of where it develops and when it
develops;3,6 it has been characterized by
what clinical manifestations it may or
may not exhibit, as well as its bacterial
profile, its association with systemic
infections, and its putative etiologic profiles; but when it cannot be placed into
any category, it has just been called idiopathic.3,6 It can be easily treated yet at
times difficult to manage and impossible to eradicate;10 it has been hyped as
a gateway to more serious conditions11
yet, its clinical significance as a disease
has been questioned.3,6 It has been and
is called gingivitis.
Gingivitis has been defined12 and
refined5 but in many ways our notions
about gingivitis are still emerging. The
evolution of what we know to be gingivitis is the result of how we define a
disease. Definitions of disease, illness,
and health have varied with the times
and continue to evolve. This is due
largely to societys perception of disease,
illness, and health which has been influenced by our expanding scientific
knowledge base as well as our cultural,
social, and individual value judgements.13 Furthermore, philosophical
arguments between ontologists (those
who believe diseases are entities with an
existence of their own) and physiologists
(those who believe diseases are illnesses
that are a unique process in one person
7

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Volume 4 Number 1 December 1999

Table 1.

over time)14 continue to affect how we perceive and

thereby define disease. Therefore the definition of a
disease and its classification are not static or simple.
Despite the continually changing set of pretexts, the
classification of disease is important because it provides a common reference point to define recurring
signs and symptoms that are a significant deviation
from a standard of health and allows for the diagnosis and treatment of the disease.
Defining and classifying gingivitis has not been a
facile assignment for periodontists. That is evident by
the number of different permutations of gingivitis nomenclature that have developed over the years.12,15,16
There is growing acceptance that gingivitis does not
represent a single disease, but rather a spectrum of diseases that are the end result of a variety of different
processes.5 It is true that inflammation of the gingiva
induced by bacteria is the most common form of gingivitis;17 however, this has created a bias toward naming all forms of disease that affect the gingiva, whether
it be atrophy, enlargement, neoplasia, or bacterialinduced inflammation, as a gingivitis.
Defining all the various clinical entities that affect the
gingiva as gingivitis is too restrictive and at times confusing. Unlike the restrictive nomenclature of gingivitis, the term gingival diseases is a more comprehensive and encompassing definition of the different
entities that affect the gingiva. This review will use the
term gingival diseases to describe the pattern of
observable signs and symptoms of different disease
entities that are localized to the gingiva.
The classification of gingival diseases that rely on
dental plaque to initiate the disease process(es) has
been organized into 2 large categories. The 2 categories of plaque-induced gingival diseases are those
that are affected by local factors and those that are
affected by local factors and modified by specific systemic factors found in the host. The modification of
plaque-induced gingival diseases by systemic factors
principally occurs via the endocrine system, hematologic diseases, drugs, or malnutrition.

endogenous hormonal fluctuations, drugs, systemic

diseases, and malnutrition have several essential characteristics in common (Table 1). The universal features of these gingival diseases include clinical signs
of inflammation, signs and symptoms that are confined to the gingiva, reversibility of the diseases by
removing the etiology(ies), the presence of bacterial
laden plaque to initiate and/or exacerbate the severity of the lesion, and a possible role as a precursor to
attachment loss around teeth.
Clinical signs of gingival inflammation involve
enlarged gingival contours due to edema or fibrosis,20,21 color transition to a red and/or bluish-red
hue20,21 elevated sulcular temperature,22,23 bleeding
upon probing,20,24-26 and increased gingival exudate.7,27-29 Clinical signs of gingival inflammation
indicative of a gingival disease must be associated
with stable (i.e., nonchanging) attachment levels on a
periodontium with no loss of attachment or alveolar
bone or on a stable but reduced periodontium.

CLASSIFICATION CRITERIA
FOR GINGIVAL DISEASES
In the past, the tools and methods to identify gingival
diseases have varied due to different criteria needed
by epidemiologists18 or researchers19 or the practicing clinician.20 The methods available for developing
criteria for classifying gingival diseases have involved
patient symptoms; medical and dental histories; the
present health status of the patient; and a clinical
examination that includes the extent, distribution, duration and physical description of lesions affecting the
gingiva, clinical or relative attachment levels, microbiological profiles, and radiographs.
The gingival diseases associated with plaque,

GINGIVAL DISEASES ASSOCIATED

PRIMARILY WITH LOCAL FACTORS
Plaque-Induced Gingivitis (Table 2)
Plaque-induced gingivitis is an inflammation of the gingiva resulting from bacteria located at the gingival
margin. The relationship of plaque to gingival inflammation has often been postulated as the cause for gingivitis, but it was not until the methodical, carefully
reasoned experimental gingivitis studies in humans
that a plaque bacterial etiology was confirmed.24 Epidemiological data have shown plaque-induced gingivitis to be prevalent at all ages of dentate populations30-34 and this disease has been considered to be
the most common form of periodontal disease.17 The

Characteristics Common to All Gingival

Diseases
1 Signs and symptoms that are confined to the gingiva.
2. The presence of dental plaque to initiate and/or exacerbate the
severity of the lesion.
3. Clinical signs of inflammation (enlarged gingival contours due to
edema or fibrosis, color transition to a red and/or bluish-red
hue, elevated sulcular temperature, bleeding upon stimulation,
increased gingival exudate).
4. Clinical signs and symptoms associated with stable attachment
levels on a periodontium with no loss of attachment or on a
stable but reduced periodontium.
5. Reversibility of the disease by removing the etiology(ies).
6. Possible role as a precursor to attachment loss around teeth.

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Table 2.

Table 3.

Characteristics of Plaque-Induced Gingivitis

Characteristics of Plaque-Induced
Gingivitis on a Reduced Periodontium

1. Plaque present at gingival margin

2. Disease begins at the gingival margin
3. Change in gingival color
4. Change in gingival contour
5. Sulcular temperature change
6. Increased gingival exudate
7. Bleeding upon provocation
8. Absence of attachment loss
9. Absence of bone loss
10. Histological changes
11. Reversible with plaque removal

initial changes from health to plaque-induced gingivitis may not be detectable clinically,35 but as plaqueinduced gingivitis progresses to more advanced forms
of this disease, clinical signs and symptoms become
more obvious. Plaque-induced gingivitis will begin at
the gingival margin and can spread throughout the
remaining gingival unit.
The intensity of the clinical signs and symptoms will
vary among individuals as well as among sites within
a dentition. The common clinical findings of plaqueinduced gingivitis include erythema, edema, bleeding,
sensitivity, tenderness, and enlargement.24,36 The
severity of plaque-induced gingivitis can be influenced
by tooth and root anatomy as well as restorative and
endodontic considerations. Radiographic analysis
and/or probing attachment levels of individuals with
plaque-induced gingivitis will not indicate loss of supporting structures. Histopathologic changes include
proliferation of basal junctional epithelium leading to
apical and lateral cell migration, vasculitis of blood
vessels adjacent to the junctional epithelium, progressive destruction of the collagen fiber network with
changes in collagen types, cytopathologic alteration
of resident fibroblasts, and a progressive inflammatory/immune cellular infiltrate.35 Although the composition of bacterial flora associated with plaqueinduced gingivitis differs from the flora associated with
gingival health, there are no specific bacterial flora that
are pathognomonic for plaque-induced gingivitis.3
Plaque-Induced Gingivitis on a Reduced
Periodontium (Table 3)
Following active periodontal treatment and the resolution of periodontal inflammation in periodontitis, the
periodontal tissue is healthy but with a reduced

1. Resolution of a periodontitis, therefore, pre-existing

attachment loss or bone loss may be present
2. Plaque present at gingival margin
3. Disease begins at the gingival margin
4. Change in gingival color
5. Change in gingival contour
6. Sulcular temperature change
7. Increased gingival exudate
8. Bleeding upon provocation
9. Histological changes
10. Reversible with plaque removal

connective tissue attachment and alveolar bone height.

Plaque-induced gingivitis on a reduced periodontium
is characterized by the return of bacteria-induced
inflammation to the gingival margin on a reduced periodontium with no evidence of progressive attachment
loss (i.e., no indication of active disease). The common clinical findings are the same as plaque-induced
gingivitis except for the presence of pre-existing attachment loss.
GINGIVAL DISEASES ASSOCIATED WITH
ENDOGENOUS SEX STEROID HORMONES
(ENDOCRINOTROPIC GINGIVAL DISEASE)
The homeostasis of the periodontium involves complex, multifactorial relationships that include the
endocrine system.37 Since the initial description in the
nineteenth century of an exaggerated gingival response
during pregnancy,38,39 evidence has accrued to suggest that tissues of the periodontium are modulated
by androgens, estrogens, and progestins. Although all
4 tissues of the human periodontium are regulated by
sex steroid hormones at one time or another, most of
our information about sex hormone-induced effects
has been described in the gingiva of women. These
gender-specific observations are not surprising given
the distinct events (menstrual cycle, pregnancy, etc.)
that affect women and produce observable endocrinotropic phenomena in a periodontal tissue that is readily visible. Although plaque bacteria in conjunction
with steroid hormones are needed to produce the gingival response, the composition of required flora is
not specific; therefore, bacteriological diagnosis of endocrinotropic gingival diseases is not a useful concept.37
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Table 4.

Table 5.

Characteristics of Puberty-Associated
Gingivitis

Characteristics of Menstrual CycleAssociated Gingivitis

1. Plaque present at gingival margin

1. Plaque present at gingival margin

2. Pronounced inflammatory response of gingiva

2. Modest inflammatory response of gingiva prior to ovulation.

3. Must be circumpubertal as designated by Tanner Stage 2 or

greater: (girls, estradiol 26 pmol/L; boys, testosterone
8.7 nmol/L)

3. Must be at ovulatory surge when luteininzing hormone levels

are >25 mIU/ml and/or estradiol levels are >200 pg/ml

4. Change in gingival color

4. Increase in gingival exudate by at least 20% during ovulation

5. Absence of attachment loss

5. Change in gingival contour with possible modification of

gingival size

6. Absence of bone loss

6. Increased gingival exudate

7. Reversible following ovulation

7. Bleeding upon provocation

8. Absence of attachment loss
9. Absence of bone loss
10. Reversible following puberty

Puberty-Associated Gingivitis (Table 4)

Puberty is the complex process of sexual maturation
resulting in an individual capable of reproduction. It is
not a single episode but rather a phase of endocrinological events that produces changes in physical
appearance and behavior of adolescents. The incidence and severity of gingivitis in adolescents are influenced by a variety of factors, including plaque levels,
dental caries, mouth breathing, crowding of the teeth,
and tooth eruption;32 however, the dramatic rise in
steroid hormone levels during puberty in both sexes
has a transient effect on the inflammatory status of
the gingiva.37 A number of studies have demonstrated
an increase in gingival inflammation in circumpubertal age individuals of both sexes without a concomitant increase in plaque levels.40-42 Although pubertyassociated gingivitis has many of the clinical features
of plaque-induced gingivitis, it is the propensity to
develop frank signs of gingival inflammation in the
presence of relatively small amounts of plaque during
the circumpubertal period that distinguish this disease.
Menstrual Cycle-Associated Gingivitis (Table 5)
Following menarche, there is a periodicity of estrogen
and progesterone secretion that is an important component for continued ovulation until the menopause.
This rhythm of sex steroid hormone secretion over a
25- to 30-day period is described as the menstrual
cycle. During the menstrual cycle, significant and
observable inflammatory changes in the gingiva have
been documented. A case of gingivitis intermenstrualis, which consisted of bright red hemorrhagic lesions
of the interdental papilla, was identified prior to
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Volume 4 Number 1 December 1999

menses.43 Notwithstanding this case report, the cases

of overt gingival changes that fluctuate in conjunction
with the menstrual cycle are infrequent.37 The more
common gingival inflammatory changes involve less
dramatic signs of inflammation in the gingiva during
ovulation. More specifically, gingival exudate has been
shown to increase at least 20% during ovulation in over
75% of women tested.44 Since these changes in crevicular fluid flow are not observable unless measured with
an electronic micro-moisture meter, most women with
gingival inflammation induced by the menstrual cycle
will present with a very mild form of the disease.
Pregnancy-Associated Gingivitis (Table 6)
Some of the most remarkable endocrine and oral alterations accompany pregnancy due to the prominent
increase in plasma hormone levels over several
months. During pregnancy, the prevalence and severTable 6.

Characteristics of Pregnancy-Associated
Gingivitis
1. Plaque present at gingival margin
2. Pronounced inflammatory response of gingiva
3. Onset is in pregnant women (2nd or 3rd trimester)
4. Change in gingival color
5. Change in gingival contour
6. Increase in gingival exudate
7. Bleeding upon provocation
8. Absence of attachment loss
9. Absence of bone loss
10. Reversible at parturition

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ity of gingivitis has been reported to be elevated and

unrelated to the amount of plaque present.44-47 Both
longitudinal and cross-sectional studies have found the
prevalence and severity of the gingival inflammation
significantly higher in the pregnant versus the postpartum patient even though plaque scores remained
the same between the 2 groups.44,45 Furthermore, gingival probing depths are deeper,44,45,48 bleeding on
probing or toothbrushing is increased,47,48 and gingival crevicular fluid flow is elevated44 in pregnant
women. The features of pregnancy-associated gingivitis are similar to plaque-induced gingivitis, except
for the propensity to develop frank signs of gingival
inflammation in the presence of relatively little plaque
during pregnancy.
Pregnancy-Associated Pyogenic Granuloma
(Pregnancy Tumor) (Table 7)
Described over a century ago,49 the pregnancy tumor
has been referred to by an extraordinary number of
names including epulis angiomatosa, epulis telangiectaticum, lobular capillary hemangioma, granuloma
gravidarum, pyogenic granuloma, Crocker-Hartzell disease, hemangiomatous granuloma, and nodular gingival hyperplasia.50 A pregnancy-associated pyogenic
granuloma is not a tumor but an exaggerated inflammatory response during pregnancy to an irritation
resulting in a solitary polyploid capillary hemangioma
which can easily bleed upon mild provocation.50 Pregnancy-associated pyogenic granulomas present clinically as a painless protuberant, mushroom-like, exophytic mass that is attached by a sessile or pedunculated
base from the gingival margin or more commonly from
an interproximal space.50 The pregnancy-associated
pyogenic granuloma has been reported to occur in
0.5% to 5.0% of pregnant women.51-54 It is more common in the maxilla50 and may develop as early as the

first trimester,50 ultimately regressing or completely

disappearing following parturition.51
GINGIVAL DISEASES ASSOCIATED
WITH MEDICATIONS
(DRUG-INFLUENCED GINGIVAL DISEASES)
Prior to the twentieth century, only a few chemicals
(e.g., alcohol, ether, morphine, digitalis, quinine, iron,
iodine, mercury, diphtheria antitoxin, and smallpox
vaccine) were employed to cure, alleviate, diagnose,
treat, or prevent human ailments. In the past century,
particularly since World War II, the development and
use of chemicals for the improvement of mankind has
been breathtaking. This astonishing array of drugs has
led to the alleviation of human afflictions as well as to
the creation of new maladies that affect the gingiva.
Drug-Influenced Gingival Enlargement (Table 8)
The esthetically disfiguring overgrowth of gingiva is a
significant untoward outcome principally associated
with an anticonvulsant (e.g., phenytoin), an immunosuppressant (e.g., cyclosporine A), and calcium channel blockers (e.g., nifedipine, verapamil, diltiazem,
sodium valproate).4,55 The common clinical characteristics of drug-influenced gingival enlargements
include a variation in the interpatient or intrapatient
pattern of enlargement (i.e., genetic predisposition),4,55
Table 8.

Characteristics of Drug-Influenced
Gingival Enlargement
1. Variation in interpatient and intrapatient pattern
2. Predilection for anterior gingiva
3. Higher prevalence in children
4. Onset within 3 months

Table 7.

5. Change in gingival contour leading to modification of gingival

size

Characteristics of PregnancyAssociated Pyogenic Granuloma

6. Enlargement first observed at the interdental papilla

7. Change in gingival color

1. Plaque present at gingival margin

8. Increased gingival exudate

2. Pronounced inflammatory response of gingiva

9. Bleeding upon provocation

3. Can occur anytime during pregnancy

4. More common in maxilla
5. More common interproximally
6. Sessile or pedunculated protuberant mass
7. Not a neoplasm; has histologic appearance of a pyogenic
granuloma
8. Regresses following parturition

10. Found in gingiva with or without bone loss but is not

associated with attachment loss
11. Pronounced inflammatory response of gingiva in relation to
the plaque present
12. Reductions in dental plaque can limit the severity of lesion
13. Must be using phenytoin, cyclosporine A, or certain calcium
channel blockers; the plasma concentrations to induce the
lesion have not been clearly defined in humans
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a tendency to occur more often in anterior gingiva,4,55

a higher prevalence in younger age groups,56-58 onset
within 3 months of use4,59-61 that is usually first
observed in the papilla,4 and, although it can be found
in a periodontium with or without bone loss, it is not
associated with attachment loss or tooth mortality.4,55
Finally, all of these drugs produce clinical lesions and
histological characteristics that are indistinguishable
from one another.4,55
The first description of a drug causing an enlargement of the gingiva was reported in 1939 and was
associated with the use of phenytoin.62 Phenytoin,
which is used on a chronic regimen for the control of
epileptic seizures, exhibits unwanted gingival enlargements in approximately 50% of patients using this
agent.63 The role of dental plaque on the incidence of
phenytoin-induced gingival enlargement has long been
debated. Controlled clinical studies have begun to
answer this issue. Institution of oral hygiene measures
have been shown to reduce the severity of gingival
enlargement in patients using phenytoin64-66 and
scrupulous oral hygiene can limit the severity of the
gingival enlargements but plaque removal is not able
to prevent development of the lesion.67 Animal studies have confirmed the finding that the presence of
plaque is not necessary for the induction of this lesion
but does play an important role in the severity of the
lesion.68 At the light microscopic level, the histologic
appearance of phenytoin-influenced gingival enlargement is difficult to differentiate from normal gingival
tissue.48
Calcium channel blockers are a class of drugs that
exert effects principally at voltage-gated Ca2+ channels
located in the plasma membrane and are commonly
prescribed as antihypertensive, antiarrhythmic, and
antianginal agents. In 1984, calcium channel blockers
were first linked to gingival enlargements69 and since
then numerous reports have confirmed the untoward
effects of these agents on the gingiva.4,55 Similar to
phenytoin, not all patients taking calcium channel
blockers develop gingival enlargements, but unlike
phenytoin the prevalence of gingival lesions associated with these drugs is lower and has been estimated
to be approximately 20%.70 The influence of plaque on
the induction of gingival enlargements in humans by
calcium channel blockers has not been elucidated;4
however, it does appear that the severity of the lesion
is affected by the oral hygiene of the patient.70 Animal studies have shown that thorough and frequent
plaque removal could prevent or reverse gingival enlargements associated with calcium channel blockers.71
Cyclosporine A is a powerful immunoregulating drug
used primarily in the prevention of organ transplant
rejection.61 The clinical features of cyclosporine influenced gingival enlargement were first described in
198357 and cyclosporine appears to affect between
12

Volume 4 Number 1 December 1999

25% to 30% of the patients taking this medication.4,72

The relationship between plaque-induced gingival
inflammation and the onset and severity of cyclosporine
influenced gingival enlargement has not been conclusively demonstrated. Several human studies have
reported that plaque accumulation can affect the severity of the lesion73-75 but it has not been documented
if cyclosporine enlargements can develop in the
absence of gingival inflammation. Using an animal
model to study the effects of cyclosporine and plaque
on gingival enlargements, rigorous oral hygiene has
been found to reduce but not eliminate the magnitude
of the gingival mass.76
Oral Contraceptive-Associated Gingivitis (Table 9)
Oral contraceptive agents are one of the most widely
utilized class of drugs in the world. Clinical studies
have recorded gingival changes that developed in premenopausal women as a result of the use of oral contraceptive agents. Several case reports described gingival enlargement induced by oral contraceptives in
otherwise healthy females with no history of gingival
overgrowth.77-79 In all cases, the increased gingival
mass was reversed when oral contraceptive use was
discontinued or the dosage reduced. Additional clinical studies have demonstrated that women using hormonal contraceptive drugs have a higher incidence of
gingival inflammation in comparison to women who
do not use these agents.80-82 Although not as thoroughly documented, long-term use of oral contraceptives has also been associated with changes in periodontal attachment levels.83 The features of gingivitis
associated with oral contraceptives in premenopausal
women are similar to plaque-induced gingivitis, except
for the propensity to develop frank signs of gingival
inflammation in the presence of relatively little plaque
in women taking these hormones. It is well documented
that current oral contraceptive concentrations are much
lower than the original doses that were reported in
Table 9.

Characteristics of Oral ContraceptiveAssociated Gingivitis

1. Plaque present at gingival margin
2. Pronounced inflammatory response of gingiva
3. Change in gingival color
4. Change in gingival contour with possible modification of gingival
size
5. Increased gingival exudate
6. Bleeding upon provocation
7. Reversible following discontinuation of oral contraceptives

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these early clinical studies; however, it is not known if

present oral contraceptive formulations can induce
clinical changes similar to those previously described.37
Paradoxically, estrogen supplementation in postmenopausal women has been associated with reduced
gingival inflammation (i.e., a reduced number of gingival sites that bled upon mild provocation) when compared to age-matched controls.84

Table 11.

Characteristics of Leukemia-Associated
Gingivitis
1. Pronounced inflammatory response of gingiva in relation to the
plaque present; however, plaque is not a prerequisite for oral
lesions
2. Gingival lesions are primarily found in acute leukemias

GINGIVAL DISEASES ASSOCIATED

WITH SYSTEMIC DISEASES
Diabetes Mellitus-Associated Gingivitis
(Endocrinotropic Gingival Diseases) (Table 10)
Diabetes mellitus is a chronic systemic disease characterized by disorders in insulin production, metabolism
of carbohydrate, fat, and protein, and the structure and
function of blood vessels. Diabetes mellitus most commonly appears as one of two recognized clinical pictures: Type 1 diabetes mellitus (insulin-dependent diabetes mellitus or juvenile onset) and Type 2 diabetes
mellitus (non-insulin dependent diabetes mellitus or
adult onset). Diabetes mellitus-associated gingivitis is
a consistent feature found in children with poorly controlled Type 1 diabetes mellitus.85-87 The features of
gingivitis associated with diabetes mellitus are similar
to plaque-induced gingivitis, except that the level of
diabetic control is more of an important aspect than
plaque control in the severity of the gingival inflammation.85-87 In adults with diabetes mellitus it is much
more difficult to detect the effects of this endocrine disease on gingival diseases since most studies have eval-

Table 10.

Characteristics of Diabetes MellitusAssociated Gingivitis

1. Plaque present at gingival margin
2. Pronounced inflammatory response of gingiva
3. Change in gingival color
4. Change in gingival contour
5. Increased gingival exudate
6. Bleeding upon provocation
7. Most commonly associated in children with poorly controlled
Type 1 diabetes mellitus
8. Absence of bone loss
9. Absence of attachment loss
10. Reversible with control of diabetic state
11. Reduction of dental plaque can limit severity of lesion

3. Change in gingival color

4. Change in gingival contour with possible modification of gingival
size
5. Enlargement first observed at the interdental papilla
6. Bleeding upon provocation (may be one of the initial oral signs)
7. Reductions in dental plaque can limit the severity of lesion

uated gingival inflammation in association with attachment loss.88

Leukemia-Associated Gingivitis (Hematologic
Gingival Diseases) (Table 11)
Leukemia is a progressive, malignant hematologic disorder that is characterized by an abnormal proliferation and development of leukocytes and precursors of
leukocytes in the blood and bone marrow. Leukemia
is classified on the duration (acute or chronic) and the
type of cell involved (myeloid or lymphoid) and the
number of cells in the blood (leukemic or aleukemic).
Oral manifestations have primarily been described in
acute leukemias and consist of cervical adenopathy,
petechiae, and mucosal ulcers as well as gingival
inflammation and enlargement.89 Signs of inflammation in the gingiva include swollen, glazed, and spongy
tissues which are red to deep purple in appearance.90
Gingival bleeding is a common sign in patients with
leukemia and is the initial oral sign and/or symptom
in 17.7% and 4.4% of patients with acute and chronic
leukemias, respectively.89 Gingival enlargement has
also been reported, initially beginning at the interdental papilla followed by marginal and attached gingiva.90
Although local irritants can predispose and exacerbate
the gingival response in leukemia, they are not prerequisites for lesions to form in the oral cavity.90
GINGIVAL DISEASES ASSOCIATED
WITH MALNUTRITION
It is known that malnourished individuals have a compromised host defense system that may affect the individuals susceptibility to infection.91,92 This has led to
the hypothesis that nutritional deficiencies can significantly exacerbate the response of the gingiva to plaque
bacteria. On this basis, some individuals have assumed
a major role for nutritional deficiencies and imbalances
in the development and progression of periodontal dis13

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eases. Unfortunately, this has also led to spurious

claims about the value and role of nutrition in periodontal diseases. At this time, the precise role of nutrition in the initiation or progression of periodontal diseases remains to be elucidated. In animal studies,
vitamin A deficiency,93 ariboflavinosis,94 vitamin B
complex and niacin deficiency,95 and starvation96 have
all been shown to affect gingival tissues. Currently,
there is a paucity of information available regarding the
effects of a specific, single nutritional deficiency on
human periodontal tissues. The studies that have
attempted to investigate the relationship of nutrition
to periodontal disease have examined the periodontal
status of individuals in developed and developing countries and have failed to show a relationship between
periodontal disease and nutrition.97-99
Perhaps of all the nutritional deficiencies, the clinical description of severe vitamin C deficiency or scurvy
has been one of the earliest documented in the oral
cavity.100 Even though scurvy is unusual in areas with
an adequate food supply, certain populations on
restricted diets (e.g., infants from low socioeconomic
families, the institutionalized elderly, and alcoholics)
are at risk of developing this condition.101 The classic
clinical signs of scurvy that have been depicted in textbooks describe the gingiva as being bright red, swollen,
ulcerated, and susceptible to hemorrhage.102,103 This
clinical picture has not been reproduced in the few
human, clinical studies that are available for review
on avitaminosis C. In these reports of acute ascorbic
acid deficiency, the gingival lesions were described as
bulbous,104 spongy,104,105 hemorrhagic,106 swollen,104
and erythematous.104 During early phases of experimental ascorbic acid deficiency, modest increases in
gingival inflammation and bleeding upon provocation
in the gingiva that were independent of plaque levels
have been reported.107 Although there is no dispute
about the necessity of dietary ascorbic acid for periodontal health, in the absence of frank scurvy, the
effect of declining ascorbic acid levels on the gingiva
can be difficult to detect clinically108 and when it is
detected usually has characteristics that are similar to
plaque-induced gingivitis described in Table 2.
CONCLUSIONS RELATED TO GINGIVAL
DISEASES INDUCED BY PLAQUE
Gingival diseases are a diverse family of complex and
distinct pathological entities that are the result of a variety of processes. Although these periodontal diseases
are limited to the gingiva, the inflammatory response
initiated in gingival diseases appears to be a prerequisite condition for destruction of connective tissue attachment apical to the cemento-enamel junction.11,109 The
classification of gingival diseases is, therefore, an important first step in defining the disease(s) which may lead
to more serious periodontal ailments.
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In this review, the classification of plaque-induced

gingival diseases required the presence of dental
plaque coupled with clinical signs and symptoms of
gingival inflammation in a stable periodontium. Without a doubt, there were a significant number of gingival conditions described in the literature as plaqueinduced gingival diseases; however, not all of these
observations were classified as gingival diseases in
this paper. To be considered as a plaque-induced gingival disease, a peer-reviewed journal must have
reported an experimental and/or epidemiological
human study that accurately and reliably assessed an
underlying functional derangement that was localized
to the gingiva. Therefore, conditions which had a nonspecific response in the oral cavity or ailments which
were primarily described from case studies or maladies that could not be clinically evaluated accurately
or reliably with current diagnostic tools were not seriously considered. It must be noted that even when
these minimal criteria were set for disease classification, limitations in the experimental designs and collected data from articles in peer-reviewed journals
placed boundaries on the manner by which gingival
diseases could be accurately and reliably identified.
It has long been argued that the fundamental nature
of disease can never be established because of the
continued social, cultural, and scientific evolution of
mankind.110 This is a humbling thought but it also
contains an exciting premise for periodontology that is
predicated on a dynamic and interactive foundation of
knowledge. Therefore, as a result of shifting circumstances represented by the patient; the health care
provider; the basic, clinical, and/or public health scientist; society at large; and the disease itself, periodontists must continue to refine the classification of
gingival disease by expanding the periodontal knowledge base and coupling these data with evolving social
and cultural norms. Consequently, to produce oral
health, dentistry must continually examine the basic
nature of periodontal disease by seeking new knowledge; evaluating what we believe is important in our
society, in our dental specialty, and in ourselves;
acknowledging our limitations; and contemplating the
significance of data, definitions, and classifications.
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Send reprint requests to: Dr. Angelo Mariotti, Ohio State University School of Dentistry, 305 West 12th St., P.O. Box 193,
Columbus, OH 43210. Fax: 614/292-4612; e-mail: mariotti.
3@osu.edu

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