Gingivitis: An Overall View for Undergraduate

Abstract

Gingivitis is a non-destructive disease that causes inflammation of the gums.

The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial plaque that is attached to tooth surfaces, termed plaque-induced gingivitis.

Gingivitis is reversible with good oral hygiene; however, without treatment, gingivitis can progress to periodontitis, in which the inflammation of the gums results in tissue destruction and bone resorption around the teeth. Periodontitis can ultimately lead to tooth loss.

Full text

Gingivitis: An overall review
for undergraduates
ABSTRACT
Gingivitis is a non-destructive disease that causes
inflammation of the gingiva.
The most common form of gingivitis, and the most
common form of periodontal disease overall, is in
response to bacterial plaque that is attached to tooth
surfaces, termed plaque-induced gingivitis.
Gingivitis is reversible with good oral hygiene;
however, without treatment, gingivitis can progress to
Periodontitis, in which the inflammation of the gums
results in tissue destruction and bone resorption
around the teeth. Periodontitis can ultimately lead to
tooth loss.(1)
INTRODUCTION
The gingiva is a part of the soft tissue lining of the
mouth. It surrounds the teeth and provide a seal
around them. Unlike the soft tissue linings of the
lips and cheeks, most of the gingiva is tightly
bound to the underlying bone which helps resist
the friction of food passing over them. Thus when
healthy, it presents an effective barrier to the
barrage of periodontal insults to deeper tissue.
Healthy gums are usually coral pink in light-
skinned people but may be naturally darker with
melanin pigmentation.
The gingiva is divided anatomically into marginal,
attached, and interdental areas.
1
24 Nov. 2018
Mohammed A. Alawadh.
General Dentist, Qassim University, Qassim, Saudi Arabia
KEYWORDS: Gingival diseases. Classification. Gingival hemorrhage. Gingivitis. Periodontitis. Diabetes
Mellitus. Hypersensitivity. Infections. Medications.
!https://orcid.org/0000-0002-4928-6500

Periodontal disease is a major public health
problem, particularly in low-income settings like
sub-Saharan Africa (2). Aside from irreversible
tooth loss, chronic periodontitis may also increase
the risk of adverse systemic conditions (3), such as
cardiovascular disease (4) and preterm birth;
however for preterm birth, different studies have
reported conflicting results (5).
The association between periodontitis and
systemic disease may be due to both increased
systemic inflammation and to translocation of
bacteria into the bloodstream (6).
Despite its importance, the microbial ecology of
periodontal disease in different oral habitats
remains incompletely understood. Studies of the
oral microbiome in periodontal disease typically
focus on small populations in developed countries
with advanced dental health care systems, which
may not be representative of the natural history of
periodontal disease in the absence of treatment (7).
In periodontal disease, the immune system
responds with inflammation to oral biofilms (8).
After an initial focus on identifying particular
periodontal pathogens (9), it is now widely
accepted that oral bacterial communities undergo a
shift or dysbiosis (10) and that the presence of
particular disease - a s s ociated species may
exacerbate the inflam m ato r y re a cti o n to
commensal bacteria (11). The two main features of
periodontal disease are gingival inflammation
(gingivitis) and the formation of periodontal
pockets (periodontitis).
While it is clear that gingivitis always precedes
periodontitis (12), gingivitis does not always
progress to periodontitis (13), suggesting that these
conditions may not simply represent different
stages of a continuous spectrum of disease. While
there is some evidence that a steady continuous
progression may be expected (14), most models
involve acute bursts of exacerbation and longer
periods of remission (15, 16).
CLINICAL FEATURES
Most cases of gingivitis occur from a lack of
proper or a l h y g i e n e , which leads to the
accumulation of dental plaque and calculus;
however, many other factors can affect the
gingiva’s susceptibility to the oral flora. The
frequency of gingivitis is high in all age groups,
but its true prevalence is difficult to determine
because of the lack of a standardized method of
measurement. Clinically detectable inflammatory
changes of the gingiva begin in childhood and
increase with age. With similar amounts of dental
plaque, the severity of gingivitis is greater in
adults than in prepubertal children. Around the
time of puberty, there is a period of increased
susceptibility to gingivitis (puberty gingivitis),
with the peak prevalence of involvement occurring
between the ages of 9 and 14 years. Between the
ages of 11 and 17 years, the frequency declines;
then a slow increase is seen until the prevalence
approaches 100% in the sixth decade of life.
In most age groups, females demonstrate a lower
frequency of gingivitis than males (although
females have periods of increased susceptibility).
This may be due more to better oral hygiene in
females than to a physiologic difference between
the sexes. In addition to the years of puberty (17).
2
Difference between Periodontitis (Upper image)
and Gingivitis (Lower image).

FACTORS ASSOCIATED WITH
GINGIVITIS
1. Hormonal changes
2. Stress
3. Poor nutrition
4. Certain medications:
● !Phenytoin
● !Calcium channel blockers
● !Cyclosporine
5. Diabetes mellitus
6. Immune dysfunction
7. Local trauma
8. Dental caries
9. Tooth crowding with overlapping
TYPES OF GINGIVITIS
•Plaque-induced gingivitis
•Necrotizing ulcerative gingivitis (NUG)
•Medication-influenced gingivitis
•Allergic gingivitis
•Specific infection-related gingivitis
•Systemic diseases gingivitis
•Plaque-induced gingivitis
The cause of plaque-induced gingivitis is bacterial
plaque, which acts to initiate the body's host
response. This, in turn, can lead to destruction of
the gingival tissues, which may progress to
des truction of the periodo n tal attachm ent
apparatus (18).
The plaque accumulates in the small gaps between
teeth, in the gingival grooves and in areas known
as plaque traps: locations that serve to accumulate
and maintain plaque. Examples of plaque traps
include bulky and overhanging restorative
margins, claps of removable partial dentures and
calculus that forms on teeth.
Although these accumulations may be tiny, the
bacteria in them produce chemicals, such as
degradative enzymes, and toxins, such as
lipopolysaccharide (LPS, otherwise known as
endotoxin) or lipoteichoic acid (LTA), that
promote an inflammatory response in the gum
tissue.
This inflammation can cause an enlargement of the
gingiva and subsequent formation. Early plaque in
health consists of a relatively simple bacterial
community dominated by Gram-positive cocci and
rods.
As plaque matures and gingivitis develops, the
communities become increasingly complex with
higher proportions of Gram-negative rods,
fusiforms, filaments, spirilla and spirochetes. Later
experimental gingivitis studies, using culture,
provided more information regarding the specific
bacterial species present in plaque.(19)
3
Plaque-induced gingivitis

•Necrotizing ulcerative gingivitis (NUG)
Has a distinctive pattern of gingival pathologic
changes that have been recognized for hundreds of
years. Until recently, the name of this process has
been preceded by the term acute (i.e., ANUG);
however, several investigators have discontinued
the use of this word because there is no chronic
form of the disease.
The infection frequently occurs in the presence of
psy chologic stress. dec reased neu trophilic
chemotaxis and phagocytic response seen in
patients with NUG. Stress-related epinephrine may
result in localized ischemia, which pre- disposes
the gingiva to NUG.
In addition to stress, other factors have been
related to an increased frequency of NUG:
● !Immunosuppression
● !Smoking
● !Local trauma
● !Poor nutritional status
Although the association with bacteria is strong,
controversial research has suggested that viruses
such as cytomegalovirus, Epstein- Barr virus, and
herpes simplex may contribute to the onset and
progression of the process (20, 21).
•Medication-influenced gingivitis
Refers to abnormal growth of the gingival tissues
secondary to the use of systemic medication. The
term is a misnomer because neither the epithelium
nor the cells within the connective tissue exhibit
either hyperplasia or hypertrophy.
The increased gingival size is due to an increased
amount of extracellular matrix, predominantly
collagen. Therefore, several authors designate the
alteration as medication-associated gingival
enlargement.
These designations are further supported by
investigators who have suggested the gingival
changes arise from interference with normal
intracellular collagen degradation.
It is known that gingival collagen constantly
undergoes physiologic remodeling, and the process
must be tightly controlled to maintain a constant
volume of the gingival tissues.
Investigators have suggested that cyclosporine,
phenytoin, and nifedipine are all associated with
calcium deregulation, which disrupts the normal
collagen phagocytosis and remodeling process. If
this is true, then the increased collagen does not
occur from hyperplasia but from impaired collagen
degradation and remodeling. (22, 23, 24)
4
Cyclosporine-related gingival hyperplasia. #
Gingiva is fibrotic and erythematous.
Necrotizing ulcerative gingivitis (NUG).
Gingiva is hemorrhagic with necrosis of the interdental
papillae.

•Specific infection-related gingivitis
๏Bacterial infections:
Bacterial infections can affect patients with and
without immunodefi c i e n cy . N e is s er ia
gonorrhoeae, Treponema pallidum, streptococci,
Mycobacterium chelonae, are the most common
bacterial infections that give rise to gingival
lesions.
They can manifest as fiery red, edematous, and
painful ulcerations, asymptomatic chancres,
mucous patches or atypical non-ulcerated, highly
inflamed gingiva.(25)
๏Viral infections:
The most common viral infections are herpes
simplex virus type1(HSV-1) and 2 (HSV-2) and
varicella-zoster virus.
HSV is the most common viral infection of the
oral/facial area. It has two subtypes: type 1, which
affects the oral cavity; and type 2, which affects
the genitals. Primary herpetic gingivo-stomatitis is
most commonly observed in children from 7
months to 4 years of age but can also be found in
adolescents or young adults. Children are often
infected with HSV by their own parents if these
have recurrent herpes lesions.
The primary infection may be asymptomatic but
can manifest as severe gingivostomatitis, in which
the gingiva are painful, inflamed and ulcerated.
Fever and lymphadenopathy are classic features
and affected individuals experience difficulty in
chewing. (26)
๏Fungal infections:
Gingival inflammation can also be caused by
fungal infections such as candidosis, linear
gingival erythema, and histoplasmosis. (27)
•Allergic gingivitis
A distinctive pattern of gingival inflammation,
plasma cell gingivitis, was brought to the attention
of health care practitioners during the late 1960s
and early 1970s. A rash of cases occurred during
that time, and most appear to have been related to
a hypersensitivity to a component of chewing gum.
Since that time, the number of cases has dwindled,
but similar gingival alterations are reported
occasionally. (28)
Although the association with chewing gum has
decreased, allergy still is responsible for many
reported cases. A brand of herbal toothpaste, a
specific type of mint candy, and peppers used for
cooking have all been implicated in more recent
reports.
The list of allergens appears to be variable, and a
thorough evaluation often is required to rule out an
allergic cause. (29)
5

•Systemic diseases gingivitis
O t h e r s y s t e m i c d i s e a s e s w i t h g i n g i v al
manifestations include gastrointestinal diseases
(e.g., Crohn´s disease), leukemia, and diabetes
mellitus.
Crohn´s disease
An inflammatory disease of the intestines that can
involve any part of the gastrointestinal tract,
causing a wide variety of symptoms. It primarily
causes abdominal pain, diarrhea (which may be
bloody if the inflammation is severe), vomiting, or
weight loss.
The oral lesions in Crohn´s disease are similar to
those of the gastrointestinal tract, including large
ulcerations. The oral lesions are sometimes the
fir s t si gn s of t h e di se a se . Typ i ca l or a l
manifestations are folds in the labial or buccal
sides of the sulcus.(30)
Leukemia
A malignant hematological disorder characterized
by an abnormal increase in white blood cells.
Oral manifestations have been reported in patients
with acute monocytic leukemia, chronic myeloid
leukemia, acute lymphocytic leukemia, and
chr oni c lym p ho c yt i c leu kem ia. G ing i va l
infiltration is the initial presenting complication in
5% of acute monocytic leukemia cases.(31)
Diabetes mellitus
Diabetes mellitus is characterized by disorders in
i n s u l i n p r o d u c t i o n , t h e m e t a b o l i s m o f
carbohydrates, fats, and proteins and in the
functioning and structure of blood vessels.
Patients with type I diabetes are at greater risk of
developing gingivitis. Both children and adults
with poor metabolic control show a greater
tendency towards more severe gingivitis.
The prevalence of gingivitis in children and
adolescents with diabetes is nearly twice that
observed in children and adolescents without this
disease. The association between diabetes and
gingivitis in children and adolescents is so widely
accepted that diabetes mellitus– associated
gingivitis appears as a specific entity in the most
recent classification of periodontal diseases. Adults
with type II diabetes may show higher rates of
gingival inflammation versus adults without
diabetes.
Almost 64% of diabetics are estimated to have
gingival inflammation, in comparison to 50% of
non-diabetics.(32)
6

MANAGEMENT
Gingivitis can be prevented through regular oral
hygiene that includes daily brushing and flossing.
(33) Hydrogen peroxide, saline, alcohol, or
chlor h e xidin e m o uthwa s h es may als o b e
employed. In a 2004 clinical study, the beneficial
effect of hydrogen peroxide on gingivitis has been
highlighted.(34) The use of oscillation-type brushes
might reduce the risk of gingivitis compared to
manual brushing.(35)
Rigorous plaque control programs along with
periodontal scaling and curettage also have proved
to be helpful, although according to the American
Dental Association, periodontal scaling and root
planing are considered as a treatment for
periodontal disease, not as a preventive treatment
for periodontal disease.(36) In a 1997 review of
effectiveness data, the U.S. Food and Drug
Administration (FDA) found clear evidence
showing that toothpaste containing triclosan was
effective in preventing gingivitis.(37)
TREATMENT AND PROGNOSIS
Although periodontitis always is preceded by
gingivitis, most areas of gingivitis remain stable
for years, and the number of affected sites that
convert to periodontitis is small. In spite of this,
optimal gingival health should be the goal of all
clinicians and their patients. In a 26-year study of a
cohort receiving state-of-the-art dental care, the
prevalence of localized tooth loss increased 46
times in areas associated with gingiva that
consistently bled on probing during routine
examinations. Even when attachment loss is not
evident and the alterations appear restricted to the
gingival soft tissues, proactive interventions are
recommended to eliminate these areas of persistent
pathosis during the early stages of disease.
Treatment of gingivitis consists of elimination (if
possible) of any known cause of increased
susceptibility and improvement in oral hygiene to
decrease the dental plaque responsible for the
inflammatory alterations. Most self-administered
plaque control programs are ineffective unless
periodic professional reinforcement also is
provided. (17)
The discussion of periodontitis presents a further
discussion of dental plaque and its relationship to
gingival inflammation. Research has shown that
few individuals have the physical skills and
motivation necessary to obtain and maintain
ultimate oral hygiene.
Mechanical removal of dental plaque can be aided
by the use of numerous chemical agents, such as
mouth rinses with chlorhexidine or essential oils,
or dentifrices containing triclosan with 2.0%
Gantrez copolymer. In this vein, studies have
evaluated the addition of these chemo-preventative
agents to typical oral hygiene efforts and shown a
statistically significant positive response to these
products in controlling plaque and gingivitis.
On occasion, hyperplastic and fibrotic gingiva may
have to be re-contoured surgically to allow total
resolution of the pathosis after improved hygiene.
If the gingivitis does not resolve after improved
plaque control and elimination of obvious
contributing factors, then the patient should be
evaluated for underlying systemic disorders that
could be contributing to the process. (38)
CONCLUSION
Gingivitis can have multiple origins and can be the
manifestation of a wide range of systemic diseases.
Gingival tissue inflammation is one of the most
common lesions encountered in the clinical setting
and may be the first symptom in many types of
disease. Gingivitis may therefore have important
diagnostic relevance, and it is vital for clinicians to
be aware of its different possible causes to ensure a
correct diagnosis and treatment.
7

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