M.

RAZICK NISHADH
History
Classification
Signs of gingivitis
Stages of gingivitis
Gingival bleeding
Color changes of gingiva
Change in consistency
Change in surface texture
Change in position
Change in contour
Universal features of gingival diseases
 The development of gingivitis has
been extensively studied in a model system
referred to as experimental gingivitis and initially
described by Herald Loe and coworkers in 1965.
This study established the fact that there is a
relationship between gingivitis and bacterial
plaque.
NORMAL GINGIVA GINGIVITIS
 Depending on course and duration gingivitis
can be classified into the following types.
 Acute: Characterized by sudden onset and
short duration and can be painful
 Recurrent: Reappears after being eliminated
by treatment
 Chronic: Slow in onset and of long duration.
It is painless unless complicated.
 Localized : Is confined to the gingiva of a single tooth or
group of teeth

 Generalized : Involves the entire mouth

 Marginal : Involves the gingival margin and may

include a portion of contiguous attached
gingiva.

 Papillary: Papillae are involved more frequently

than gingival margin

 Diffuse: Affects gingival margin, attached gingiva and the

interdental papilla.
 The degree of gingival enlargemnt caan
be scored as follows
 Grade 0: No signs of enlargement

 Grade 1: Enlargement confined to interdental

papilla
 Grade 2: Enlargement involves papilla and

marginal gingiva
 Grade 3: Enlargement covers three quarters or

more of the crown

Stage Time Blood Junctional Immune collagen Clinical
vessels And cells feature
sulcular
epithelium
I. Initial 2-4 Vascular Infiltration PMNs Perivasc Increased
dilation and by ular loss GCF
vasculitis PMNs
2. Early 4-7 Vascular Same as lymphoc Increase Erythema
proliferation stage 1, ytes d loss Bleeding
atrophic around on
areas infiltrate probing

3.Establis 14-21 Same as Same as Plasma Continu- Changes

hed stage 2 plus stage 2 but cells ed loss in
stasis of more color,size
blood advanced , texture
etc
 Gingivitis can be characterized by
the following signs.
Redness and sponginess of the gingiva.
Bleeding on provocation
Changes in contour
Presence of calculus or plaque with no
radiographic evidence of crestal bone loss.
 Two of the earliest signs of gingival
disease includes
1.Increased GCF production
2.Bleeding on probing
Advantages:
 Appears earlier than color change
 Its an objective sign
 Indicates an inflammatory lesion in both the
epithelium and the connective tissue
 Its a good negative predictor of future attachment loss
Earliest clinical sign of gingival disease
 Gingival bleeding caused by local factors
Contributing factors to local plaque
retention.
 Bleeding associated with systemic changes.

 Modifying factors in gingival bleeding.

 These factors cause plaque retention and
contributed to the development of gingivitis
1.anatomic and developmental tooth
variations.
2.Dental caries.
3.Frenum pull
4.Iatrogenic causes
5.Malpositioned teeth
6.Mouth breathing
7.overhangs
8.Partial dentures
9.Lack of attached gingiva
10.Recession
 LACK OF ATTACHED
DENTAL CARIES GINGIVA
FRENUM PULL MALPOSITION OF TOOTH
 The most common cause of abnormal
gingival bleeding is chronic marginal
gingivitis.The ease with which bleeding is
provoked and its duration depends on the
severity of inflammation and the associated tissue
changes.The cause of gingival bleeding is
attributed to the following changes.
 Dilation and engorgement of the capillaries
and increased capillary permeability.
 The epithelium in relation to the connective
tissue papillae is relatively thinned out.
Commonest cause of gingival bleeding
 Stimuli which are normally innocuous
cause a rupture of the engorged capillaries.

Vessel wall rupture Hemostasis vessel wall

contracts blood flow diminished platelets
adhere to the edges clot is formed
But the clot gets dislodged and bleeding
occurs by the slightest of stimuli
 Acute episodes of gingival bleeding occurs during
 Trauma
 Acute gingival diseases e.g. ANUG
Spontaneous or bleeding on slightest provocation occurs in
ANUG due to the exposure of the engorged connective tissue by
desquamation of necrotic surface epithelium.
 Systemic influences affect gingival bleeding by
exaggerating the tendency towards bleeding associated with local
irritation and by initiating spontaneous hemorrhage.
 Vitamin c deficiency
 Schonlein –Henoch purpura
 Hypoprothrombinemia
 Hemophilia
 Leukemia
 Christmas disease
 Deficient platelet thromboplastic factor
 Hormonal replacement therapy
 Oral contraceptive pills
 The following factors have been
identified as significant modifying factors in
gingival bleeding.
 Androgenic hormones
 Diabetes mellitus
 Calcium channel blockers
 Immunosuppresant drugs
 Aspirine
 The normal color of gingiva is described
as “coral pink” and is produced by the tissue
vascularity and modified by overlying
epithelium. Color changes can be observed
during
 Chronic inflammation
 Acute inflammation
 Metallic pigmentation
 Color changes associated with systemic
factors.
 Chronic inflammation intesifies red or
bluish red color because of vascular proliferation
and reduction of keratinisation.
The changes start in the interdental
papilla and gingival margin and then spread to
the attached gingiva.
Venous stasis will contribute to a bluish
hue.
 Color changes is acute inflammation
differ in both nature and distribution from
those in chronic gingivitis.
 It may be marginal ,diffuse or plaque like
depending on the underlying acute condition.
ANUG- marginal
Herpetic gingivostomatitis- Diffuse
Acute chemical reactions-Patchlike or
diffuse
CHRONIC
INFLAMMATION ACUTE INLAMMATION
 Heavy metals such as bismuth
,asenic,mercury,lead and silver absorbed
systemically can discolor the gingiva .
 This occurs due to the perivascular
precipitation of mettalic sufides in the
subepithelial connective tissue.
 It occurs only in areas of gingival
inflammation due to the increased permeability
of the blood vessels
 Increased melanin pigmentation can be seen in
conditions like
Addisons disease
Peutz-Jeghers syndrome
Mccune albright syndrome
Neurofibromatosis
 Bile pigments can impart a yellowish colour to the
oral mucosa.
 Deposition of iron in hemochromatosis can cause
blue grey pigmentation of the oral mucosa.
 PEUTZ-JEGHERS
ADDISON’S DISEASE SYNDROME
 Inflammatory conditions can produce a change
in the normal firm and resilient consistency of
the gingiva
 Both destructive(edematous) and reparative
( fibrotic) changes coexist and the consistency
ofthe gingiva is detrmined by their relative
predominance
Clinical change
In chronic gingivitis
 Soggy puffiness that pits on
pressure
 Marked softness and friability
 Firm and leathery consistency
Microscopic feature
Infiltration by fluids and cells of
inflammatory exudate
Degeneration of connective tissue and
eppithelium,change in epithelium
connective tissue relation
Fibrosis and epithelial proliferation
Clinical change
Acute gingivitis
 Diffuse puffiness and softening
 Sloughing of epithelium
 Vesicle formation
Microscopic feature
Diffuse edema of acute inflammatory
origin
Necrosis with formation of
pseudomembrane
Intercellular and intracellular edema
 Calcified microscopic masses maybe found in
the gingiva
 Such masses may be calcified material removed
from the tooth and traumatically displaced into
the ginfiva.
 Chronic inflammation and fibrosis can occur in
relation to these masses
 The surface of gingiva normally
exhibits depressions and elevations giving the
tissue an orange peel appearance referred to as
stippling.
 In chronic inflammation surface is
either smooth and shiny or firm and nodular
depending depending weather the changes are
exudative or fibrotic.
 Smooth surface texture is produced by
epithelial atrophy in atrophic gingivitis.
 Peeling of the surface occurs in desquamative
gingivitis
 Hyperkeratosis results in leathery texture.
 Changes in the positions of the gingival margin
results from
Traumatic injuries
gingival recession
 Gingival recession:

Recession is the exposure of the

root surface by the apical migration of the
position of the gingiva.
 Recession refers to the position of the gingiva
and not its condition.
The severity of recession is determined by the
actual position and not the apparent position
of the gingiva
 Actual position : Level of the coronal end of the
epithelial attachment
 Apparent position : Level of crest of the
gingival margin
 Faulty tooth brushing technique
 Tooth malposition

 Friction from soft tissues

 Gingival inflammation

 Abnormal frenum attachment

Exposed root surfaces are susceptible to

caries .Abrasion and erosion of the cementum
exposes the dentinal surface thereby leading to
sensitivity . Hyperemia of pulp and associated
symptoms may also result.
 Changes in gingival contour are seen in
Gingival enlargement
Stillman’s clefts
McCall Festoons
 Increase in size of the gingiva is common feature
of gingival disease.Accepted curret terminology is
gingival enlargement or gingival overgrowth.It can be
classified according to etiologic factors and pathological
changes as follows.
 Inflammatory enlargement

 Drug induced enlargement

 Enlargements associated with systemic diseases

 Neoplastic enlargements

 False enlargements
 Chronic inflammatory changes are much more
common . In addition inflammatory enlargements usually
are a secondary complication of any other type of
enlargement resulting in a combined enlargement.

Etiology: Chronic inflammatory gingival enlargement is

caused by prolonged exposure to dental plaque.
 Gingival enlargement in mouth breathing
Gingivitis and gingival
enlargement are seen in mouth breathers . The
gingiva appears red and edematous with diffuse
surface shininess of the exposed area . The
maxilllary anterior region is the common site of
such involvement . Its harmful effect is attributed
to irritation from surface dehydration.
CHRONIC INFLAMMATORY MOUTH BREATHING
ENLARGEMENT INDUCED ENLARGEMENT
 Acute inflammation:
Acute inflammatory changes
occur when bacteria are carried deep into the
tissue when a foreign substance is embedded
forcefully into the gingiva.
Gingival abscess
Periodontal abscess
 Drugs associated with enlargement
a) Anticonvulsants
b) Immunosuppressants
c) Calcium channel blockers
 Enlargements associated with systemic diseases or
conditions
Conditioned enlargement
a) Pregnancy
b) Puberty
c) Vitamin c deficiency
d) Plasma cell gingivitis
e) Pyogenic granuloma
 Systemic diseases causing gingival enlargement
a) Leukemia

b) Granulomatous disease

 Neoplastic enlargements

a) Benign tumors

b) Malignant tumors

 False enlargements
PHENYTOIN GINGIVAL
ENLARGMENT VITAMIN C DEFICIENCY
 Stillman’s clefts:
Specific type of gingival
recession consisting of a narrow ,triangular
shaped gingival recession.
 McCall’s festoon:

Term used to describe a rolled

thickened margin of gingiva usually seen adjacent
to the cuspids when recession approaches the
mucogingival junction.
STILLMAN’S CLEFT MCCALL'S FESTOON
Parameter Normal Gingiva Gingivitis
Color Coral pink Red/bluish
Contour Scalloped outline that Edema blunts marginal
envelops the teeth tissues leading to loss of
knife edge adaptation
Consistency Firm and resilient Tissue is soft and
edematous
Bleeding on probing Negative positive
Gingival exudate Minimal Significantly increased
Sulcular temperature ~34 c Slightly increased
Clinical finding Histological correlation
Gingival Ulceration of sulcular epithelium and engorged capillaries
bleeding reaching the surface
Redness Hyperemia with dilation and engorgement of capillaries
swelling Infiltration of connective tissue by fluid and
inflammmatory exudate
Loss of gingival Inflammation with destruction of gingival fibre apparatus
tone
Loss of stippling Edema
Gingival pocket Inflammation with ulceration of sulcular epitheliun
 Signs and symptoms confined to the gingiva
 Presence of dental plaque to initiate and/or
exacerbate the severity of the lesion
 Clinical signs of inflammation
 Clinical signs and symptoms associated with
stable attachment levels on a stable
periodontium with no loss of attachment
 Reversibility of disease
 Possible role as precursor to attachment loss
around teeth