Gingival Inflammation :

CLASSIFICATION
:I. According to duration
.It is sudden in onset and of short duration which is painful :Acute gingivitis .1
and is painless, unless complicated ,It is slow in onset and of long duration :Chronic gingivitis .2
.It is the most common type of gingivitis .by acute or subacute exacerbations
:II. According to distribution
Gingivitis confined to the :Localized gingivitis .1
.)Fig. 1( gingiva of a single tooth or group of teeth
.Involves the entire mouth :Generalized gingivitis .2
Involves the gingival margin and may include a portion of the contiguous :Marginal gingivitis .3
.)Fig. 2( attached gingiva
Localized gingivitis in left maxillary anterior region :Fig. 1

Marginal gingivitis :Fig.2

Involves the interdental papillae and often extends into the adjacent :Papillary gingivitis .4
Fig. 3( portion of the gingival margin

Papillary gingivitis :Fig3

Affects the gingival margin, the attached gingiva and the interdental :Diffuse gingivitis .5
.papillae

STAGES OF GINGIVITIS
histopathological stages of Page and Schroeder developed a system to categorize the clinical and
histopathological stages of periodontal inflammatory periodontaldiseases and defined four
periodontal lesion initial, early and established gingival lesions and an advanced changes: The
evidence available at that time largely consisted of animal It is important to note that the .)Fig. 4(
considered to adolescent biopsies. Their description, based on these material, is now and human
Kinane and Lindhe recently classified .be not fully applicable to the normal adult situation
:healthy gingiva into two types
.Super healthy or pristine state, which histologically has little or no inflammatory infiltrate
histologically, has features of Clinically healthy gingiva, which looks similar clinically, but
clinical situations one would normally see the healthy ,an inflammatory infiltrate. In everyday
supervised only in exceptional circumstances, such as in a clinical trial with gingiva type and
pristine gingiva daily cleaning and professional assistance, one would see

Stages of gingivitis :Fig. 4

histopathology of clinically The initial and early lesion descriptions were thought to reflect the
established lesion reflected the histopathology of more early stages of gingivitis, while the
was considered gingivitis. The description of the histopathology of the advanced lesion chronic
.periodontitis to reflect the progression of gingivitis to
Stage I: The Initial Lesion
of plaque accumulation. Initial changes in the development of gingivitis occur after 2 to 4 days
inflammation are vascular changes which include dilation of The first manifestations of gingival
flow. There is capillaries and venules of the dentogingival plexus and increased blood ,arterioles
resulting in exudation of fluids and proteins increase in the permeability of the microvascular bed
lesion enlarges, and gingival crevicular fluid flow increases, noxious into the tissues. As the
crevice. The quantities of substances from microbes will be diluted both in the tissue and the
neutrophils (PMNs) are increased in the connective leukocytes, mainly polymorphonuclear
leukocytes junctional epithelium and the gingival sulcus. The recruitment of tissue, the
to the chemoattractant actions of the (predominantly PMNs) from the tissues to the crevice is due
and products derived from the biofilm (lipopolysaccharide ). )host systems (interleukin-8, C5a
the gingival increase in the migration of leukocytes and their accumulation within Thus, the
gingival fluid into the sulcus. There is little or sulcus is correlated with an increase in the flow of
the junctional epithelium laterally (rete pegs). Collagen depletion within no proliferation of
structures. Exudative and transudative infiltrated area is noted along with an increase in vascular
.in the gingival crevice region fluid and plasma proteins arrive
Stage II: The Early Lesion
removal of plaque. But repaired after the Initial lesion may be transitory and may be quickly
clinical signs of erythema appear. There is after 4 to 7 days of plaque accumulation, the
and increased formation of capillary loops between rete pegs or ridges proliferation of capillaries
lymphocytes) and PMNs are and thus, bleeding on probing is evident. Lymphocytes (mainly T
cells are noted within the lesion. 70% of the predominant at this stage and very few plasma
be around the cellular infiltrate. The main fiber groups affected appear to collagen is destroyed
epithelium develops widened the circular and dentogingival fiber assemblies. The junctional
mainly by neutrophils and small numbers of mononuclear intracellular spaces that are infiltrated
.monocytes cells, especially
Stage III: The Established Lesion
vessels. Venous return is The gingiva gives bluish hue due to engorged and congested blood
Extravasation of red blood cells (RBCs) into the .impaired, and the blood flow becomes sluggish
breakdown of hemoglobin into its component pigments can also deepen connective tissue and
exudation and leukocyte color of the chronically inflamed gingiva. There is increased fluid the
crevice. The established lesion as defined by Page and migration into the tissues and the gingival
apical dominated by plasma cells. Collagen loss continues in both lateral and Schroeder is
in collagen depleted spaces directions as the inflammatory cell infiltrate expands, resulting
then available for leukocytic infiltration. The extending deeper into the tissues which are
the epithelium continues to proliferate and the rete pegs extend deeper into dentogingival
and a barrier to microbial entry. connective tissue in an attempt to maintain epithelial integrity
closely attached to the tooth surface. There is no evidence The junctional epithelium is no longer
epithelium. Within 2 to 4 bone loss at this stage, or of apical migration of junctional of alveolar
accumulation, the gingivitis become established. Migrating weeks after the beginning of plaque
.spaces are found in the junctional epithelium, within widened intercellular leukocytes
Stage IV: Advanced Lesion
cell infiltrate extends This is the final stage called as the advanced lesion. The inflammatory
connective tissue. The advanced lesion has all the laterally and further apically into the
loss occurs, the established lesion but differs importantly in that alveolar bone characteristics of
migrates apically from the fiber damage is extensive and the junctional epithelium
accepted that plasma cells are the dominant cell cementoenamel junction (CEJ). It is generally
.lesion type in the advanced
CLINICAL FEATURES OF GINGIVITIS
Gingival Bleeding
inflammation. Gingival bleeding Gingival bleeding is one of the earliest symptoms of gingival
ease with which it is provoked. Gingival bleeding is mainly varies in severity, duration, and the
epithelium is dilation and engorgement of capillaries. Permeability of the sulcular due to the
substances and widening o intercellular increased by degradation of intercellular cementing
becomes chronic, ulceration of sulcular epithelium takes place. spaces. As the inflammation
being ulcerated and the capillaries are engorged and closer to the surface and epithelium Because
innocuous causes rupture of capillaries and gingival less protective, stimuli that are ordinally
:Etiological factors responsible for gingival bleeding are .bleeding
:Local factors .A
of hard food, gingival burns from hot Aggressive toothbrushing, sharp pieces :Acute bleeding .a
.ulcerative gingivitis food or chemicals and necrotizing
.Chronic gingival inflammation :Chronic bleeding .b
:Systemic factors .B
Vitamin C deficiency and allergy such as Henoch Schnlein purpura :Vascular abnormality .a
.Vitamin K deficiency .b
.Idiopathic thrombocytopenic purpura :Platelet disorder .c
.Uremia, multiple myeloma and postrubella purpura :Deficient platelet thromboplastic factors .d
.Hemophilia, Christmas disease :Coagulation defects .e
.Leukemia :Malignancy .f
.)Salicylates and anticoagulants (dicoumarol, heparin :Drugs .g
Bleeding on probingis easily detectable clinically and :Significance of gingival bleeding
therefore, is of value
is a more objective sign for the early diagnosis and prevention of more advanced gingivitis. It
estimation by the examiner. It appears earlier than other and therefore requires less subjective
based on this of inflammation. Thus, several gingival indices have been developed visual signs
determine whether the lesion is an active or earliest sign. Gingival bleeding on probing helps to
.inactive
Changes in Gingival Color
vascular supply and The normal gingival color is coral pink which is produced mainly by the
become red when there is an increase in modified by overlying keratinized layer. The gingiva
of keratinization. Color changes vary with the intensity of the vascularization and reduction
.inflammation. Initially, there is an increasingly red erythema
:Factors responsible for change in gingival color are
:Color changes associated with local factors .A
:Acute gingivitis .a
NUG- marginal bright red erythema. In severe
The gray .)Fig. 5( acute inflammation, the red color gradually becomes a dull, whitish gray
the adjacent gingiva by a thin, discoloration produced by tissue necrosis is demarcated from
.sharply defined erythematous zone
Herpetic gingivostomatitis: Diffuse
Chemical irritations: Patch like/diffuse
NUG :Fig. 5

the red or bluish red color because of Chronic inflammation intensifies :Chronic gingivitis .b
reduction of keratinization due to epithelial compression by the vascular proliferation and
.inflamed tissue
systemically absorbed metals results from Gingival pigmentation from :Metallic pigmentation .c
metallic sulfides in the subepithelial connective tissue. Gingival perivascular precipitation of
areas of inflammation, where pigmentation is not a result of systemic toxicity. It occurs only in
into the blood vessels permits seepage of the metal the increased permeability of irritated
.surrounding tissue
Bismuth pigmentation Black line
Arsenic pigmentation Black
Mercury pigmentation Black line
)Lead pigmentation Bluish red, deep blue o gray (Burtonian line
Silver pigmentation Voilet marginal line
:Color changes associated with systemic factors .B
:a. Endogenous factors
Addisons disease Increased Melanin pigmentation
Peutz-Jeghers syndrome Increased Melanin pigmentation
Albrights syndrome Increased Melanin pigmentation
Jaundice Yellowish color due to deposti of bilirubin
Hemochromatosis Bluish gray due to depostion of Iron
Diabetes
Pregnancy
Blood dyscrasias
Hyperthyroidism
DrugsChloroquine (slate gray), Minocycline (brown), Chlorpromazine, Zidovudine,
.Ketoconazole, Methyldopa and Busulphan
:Exogenous factors .b
Tobacco/smokingGrayish color due toincreased melanin pigmentation
)Fig. 6( Amalgam Localized bluish black areas
.Coloring agents in food, lozenges and betel

Amalgam tattoo :Fig. 6

Changes in Gingival Contour

Interdental papilla is .Normally the contour of marginal gingiva is scalloped and knife-edged
in posterior region it is tent - shaped, filling the pointed and pyramidal in anterior region whereas
diseased conditions related to gingival area. The various
:contour are
.Marginal gingiva may be rounded or rolled :Acute and chronic gingivitis .a
.Papilla may be bulbous :Gingival enlargement .b
identations which extend from and into These are apostrophe shaped :Stillmans clefts .c
.)Fig. 7( surface, most frequently on the labial or buccal surfaces gingival margin along the root
gingiva and remainder of The marginsof the cleft are rolled underneath the linear gap in the
It was originally described by Stillman, .)Fig. 8( edge gingival margin is blunt instead of knife
direction or compound result of occlusal trauma. It may be simple cleavage in a single as a
.cleavage in more than one direction
enlargement of the marginal gingiva with the McCalls festoons are the :McCalls festoons .d
like gingival prominence in relation to canine and premolar facial formation of life-saver
named after John Opple These are semilunar enlargements .)Figs 9 and 10( surfaces mostly
.occlusal traumatism to be an etiologic factor McCall who along with Paul R Stillman, believed
.NUG: Papillae may be cratered .e
Gingival clefts :Fig. 7

Stillman's clefts :Fig. 8

McCalls festoons in relation to canine and premolars :Fig. 9

McCalls festoons :Fig. 10

Changes in Gingival Consistency

chronic gingivitis, there is In acute gingivitis, there is puffiness and softening of the gingiva. In
firm, leathery consistency. Both destructive (edematous) soggy puffiness that pits on pressure or
the gingival fibrotic) changes coexist in chronic gingivitis and the consistency of( and reparative
is seen in the following conditions: is determined by their relative predominance. Gingival lump
gingivitis, fibroepithelial polyp and malignant conditions erupting third molars, pregnancy
.)Kaposis sarcoma, Lymphoma ,(Carcinoma
Changes in the Surface Texture of Gingiva
:Conditions in which there is change in the surface texture of gingiva are
atrophic ,)Fig. 11( Loss of stippling (smooth, shiny surface) is seen in chronic gingivitis .A
.gingivitis and chronic desquamative gingivitis
.Leathery texture is seen in hyperkeratosis .B
.)Fig. 12( Nodular surface is seen in drug induced gingival overgrowth .C

Loss of stippling producing smooth, shiny surface in mandibular anterior region :Fig. 11

Nodular surface seen in drug induced gingival enlargement :Fig. 12

Changes in the Position of the Gingiva

CEJ, at or slightly below In fully erupted tooth, position of gingival margin is 1 - 2 mm above
is at the CEJ. The actual position is the level of the enamel contour. The junctional epithelium
the crest of attachment on the tooth, whereas the apparent position is the level of the epithelial
Actual position is not directly visible but .the gingival margin which is seen by direct observation
.probing can be determined by
When the gingiva enlarges, the gingival margin may be high on the enamel, :Enlargement .A
.)Fig. 13( partly or nearly covering the anatomic crown
shift in the position of the gingiva. It is exposure of the root surface by an apical :Recession .B
determined by the actual position of the gingiva, not its apparent The severity of recession is
.)Fig. 14( position

Idiopathic hyperplastic gingival enlargement :Fig. 13

Localized recession around malposed incisor and canine :Fig. 14

:The characteristics of plaque-induced gingivitis (Mariotti, 1999) are
Plaque present in relation to gingival margin
Disease begins at the gingival margin
Change in gingival color
Change in gingival contour
Sulcular temperature change
Increased gingival exudates
Bleeding upon provocation
Absence of attachment and bone loss
Histological changes including an inflammatory lesion
Reversible with plaque removal
POINTS TO PONDER
gingival margin are Gingival conditions/diseases that mainly involve interdental papilla and
gingivitis, linear gingival erythema and drug induced gingival abscess, necrotizing ulcerative
gingival
.enlargement
stomatitis, aphthae, self-injury, Gingival ulcers are usually seen in NUG, herpes simplex virus
dermatoses, systemic diseases (hematological disorders, ,malignant neoplasms, drugs
.)syphilis, herpes virus, HIV ,tuberculosis
enlargement, diffuse smooth and ,Gingival changes seen in mouth-breathers are erythema, edema
.area affecting mainly maxillary anterior region shiny surface in the exposed gingival
erythroplasia, hemangiomas, ,Gingival red lesions are usually seen in desquamative gingivitis
sarcoidosis, Wegeners granulomatosis ,orofacial granulomatosis, Crohns disease