This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.

1. Presented by
PRABLEEN ARORA
MDS STUDENT

2. GINGIVAL INFLAMMATION
Inflammation is defined as an observable alteration in tissues associated
with changes in vascular permeability and dilation, often with the
infiltration of leukocytes into affected tissues.
These changes result in erythema, edema, heat, pain and loss of function
which are the cardinal signs of inflammation.
The sequence of events cumulating in clinically apparent gingivitis is
categorized into:
• Initial
•Early
•Established stages
•With periodontitis designated as the Advanced Stage.

3. Microorganisms attached to tooth surface or gingival sulcus
These organisms synthesize collagenase, hyaluronidase, protease, chondroitin
sulfatase, endotoxin
Which cause damage to epithelial, connective tissue cells & intercellular
constituents and also widens the spaces between junctional epithelial cells.
Permit injurious agents derived from bacteria, or bacteria themselves, to gain
access to the connective tissue.
Microbial products activate monocytes/macrophages to produce vasoactive
substances such as prostaglandin E2, interferon, tumor necrosis factor and
interleukin-1.

4.  Loe et al (1965) conducted a study to produce experimental gingivitis
in patients with healthy gingiva by withdrawing all active efforts
directed towards oral cleanliness, and to study the sequence of changes
in the microbial flora and in the gingiva .
 They concluded that clinically normal gingiva resulted in gross
accumulations of soft debris and the development of marginal
gingivitis in all subjects. The time necessary to develop gingivitis
varied from ten to twenty-one days.
 Concurrent bacteriological examinations showed that the number of
microorganisms in the gingival area increased and that distinct changes
in the relative composition of the flora occurred.

5.  In all subjects gram-positive cocci and short rods accounted for
45-60 percent of the microorganisms in the plaque along the buccal
gingiva. The distribution of other bacteria constituting the
remaining 40-55 per cent of the flora, was as follows:
 Gram negative cocci and short rods- 22 %
 Gram positive filaments- 10%
 Fusobacteria -10 %
 Vibrios -6 %
 Spirochetes- 1 %
 Original predominating flora of gram positive cocci and short rods
was reduced 50 – 70 % of the total flora during the first 4-7 days of
plaque formation and remained fairly constant 45- 60 %
throughout the rest of experimental period.
 Gram positive filaments, fusobacteria, gram negative cocci and
small rods were conspicous in the smears after 2-4 days, while
vibrios and spirochetes generally were found a few days later.

6.  First manifestations of gingival inflammation are vascular
changes consisting of dilated capillaries and increased blood
flow.
 These initial inflammatory changes occur in response to
microbial activation of resident leukocytes and the subsequent
stimulation of endothelial cells.
 Clinically, this initial response of the gingiva to bacterial plaque
(subclinical gingivitis) is not apparent.
 Subtle changes can also be detected in the junctional
epithelium and perivascular connective tissue at this
early stage.
 The perivascular connective tissue matrix becomes altered,
and there is exudation and deposition of fibrin in the
affected area.

7.  Also, lymphocytes soon begin to accumulate .
 The increase in the migration of leukocytes and their
accumulation within the gingival sulcus may be correlated
with an increase in the flow of gingival fluid into the sulcus.
 The character and intensity of the host response determine
whether this initial lesion resolves rapidly, with the
restoration of the tissue to a normal state, or evolves into a
chronic inflammatory lesion.
 If the latter occurs, an infiltrate of macrophages and
lymphoid cells appears within a few days.

8. Classic features of acute inflammation can be seen in the connective
tissue beneath the junctional epithelium.
 Changes in blood vessel morphologic features (e.g., widening of small
capillaries or venules) and adherence of neutrophils to vessel walls
(margination) occur within 1 week and sometimes as early as 2 days after
plaque has been allowed to accumulate.
 Leukocytes, mainly polymorphonuclear neutrophils (PMNs), leave the
capillaries by migrating through the walls.
 They can be seen in increased quantities in the connective tissue, the
junctional epithelium, and the gingival sulcus .
 Exudation of fluid from the gingival sulcus and extravascular proteins
are present

9.  The early lesion evolves from the initial lesion within about 1 week after
the beginning of plaque accumulation.
Clinical signs
 Erythema may appear, mainly because of the proliferation of capillaries
and increased formation of capillary loops between rete pegs or ridges .
 Bleeding on probing may also be evident.
 Gingival fluid flow and the numbers of transmigrating leukocytes
reach their maximum between 6 and 12 days after the onset of clinical
gingivitis.
 The amount of collagen destruction increases-- 70% of the collagen is
destroyed around the cellular infiltrate.
 The main fiber groups affected appear to be the circular and
dentogingival fiber assemblies.

10.  PMNs that have left the blood vessels in response to chemotactic
stimuli from plaque components travel to the epithelium, cross
the basement lamina, and are found in the epithelium, emerging
in the pocket area.
 PMNs are attracted to bacteria and engulf them in the process of
phagocytosis.
 Different MMPs are responsible for extracellular matrix
remodeling within 7 days of inflammation, which is directly
related to MMP-2 and MMP-9 production and activation.
Microscopic examination :
 Leukocyte infiltration in the connective tissue beneath the
junctional epithelium, consisting mainly of lymphocytes
(75%, with the majority T cells) but also composed of some
migrating neutrophils, as well as macrophages, plasma
cells, and mast cells.

11.  Characterized by a predominance of :
1. Plasma cells and B lymphocytes
2. Creation of a small gingival pocket lined with a pocket
epithelium.
 The B cells found in the established lesion are predominantly of
the immunoglobulin G1 (IgG1) and G3 (IgG3) subclasses.
 In chronic gingivitis, which occurs 2 to 3 weeks after the beginning
of plaque accumulation, the blood vessels become engorged
and congested, venous return is impaired, and the blood
flow becomes sluggish.
RESULTS IN
 Localized gingival anoxemia, which superimposes a somewhat
bluish hue on the reddened gingiva.

12.  Extravasation of erythrocytes into the connective tissue and
breakdown of hemoglobin into its component pigments
Deepen the color of the chronically inflamed gingiva.
The established lesion can be described as moderately to
severely inflamed gingiva.

14. STAGE IV : THE ADVANCED LESION
Extension of the lesion into alveolar bone characterizes a fourth stage known
as the advanced lesion or phase of periodontal breakdown.
Microscopically, there is fibrosis of the gingiva and widespread
manifestations of inflammatory and immunopathologic tissue damage.
In general at this advanced stage, plasma cells continue to dominate the
connective tissues, and neutrophils continue to dominate the junctional
epithelium and gingival crevice.

16. COMPONENTS OF GINGIVAL INFLAMMATION
PREVALENCE
The prevalence of gingivitis is evident worldwide. More than
82% of U.S. adolescents have overt gingivitis and signs of
gingival bleeding. A similar or higher prevalence of gingivitis is
reported for children and adolescents in other parts of the world.
In children on average 6% of sites measured showed bleeding on
probing.

17. Clinical Features of Gingivitis
Characterized by the presence of any of the following clinical signs:
• Redness and sponginess of the gingival tissue
•Bleeding on provocation
•Changes in contour
•Presence of calculus or plaque with no radiographic evidence of crestal
bone loss.
Histologic examination of inflamed gingival tissue reveals
ulcerated epithelium.
•The presence of inflammatory mediators negatively affects epithelial
function as a protective barrier.
• Repair of this ulcerated epithelium depends on the proliferative or
regenerative activity of the epithelial cells.
• Removal of the etiologic agents triggering the gingival breakdown is
essential.

18. COURSE AND DURATION
Acute Gingivitis can occur with sudden onset and short duration
and can be painful .
Recurrent gingivitis reappears after having been eliminated by
treatment or disappearing spontaneously.
Chronic gingivitis is slow in onset and of long duration. It is painless,
unless complicated by acute or subacute exacerbations, and is the
type most often encountered fluctuating disease in which
inflammation persists or resolves and normal areas become
inflamed.

19. DISTRIBUTION
Localized gingivitis is confined to the gingiva of a single tooth or group of
teeth.
Generalized gingivitis involves the entire mouth.
Marginal gingivitis involves the gingival margin and may include a portion of
the contiguous attached gingiva.
Papillary gingivitis involves the interdental papillae and often extends into the
adjacent portion of the gingival margin and the earliest signs of gingivitis often occur
in the papillae.
Diffuse gingivitis affects the gingival margin, the attached gingiva and the
interdental papillae.

20. Localized marginal gingivitis
is confined to one or more of the
marginal gingiva.
Localized diffuse gingivitis
extends from the margin to the
mucobuccal fold in a limited area.
Localized papillary gingivitis
is confined to one or more
interdental spaces in a limited area.

21. Generalized marginal gingivitis
involves the gingival margins in relation
to all the teeth. The interdental papillae
are usually affected .
Generalized diffuse gingivitis involves
the entire gingiva. The alveolar mucosa
and attached gingiva are affected, so the
mucogingival junction is sometimes
obliterated.

22. Bleeding
on probing
Local factors
Systemic
factors
color
In gingivitis
In metallic
pigmentations
consistency
calcified masses
in gingiva
Tooth brushing
contour
Stillmans clefts
McCall festoons
position
Traumatic
lesion
Gingival
recession
Surface
texture

23. EARLIEST SIGNS of gingival inflammation preceding established
gingivitis:
• Increased gingival crevicular fluid rate.
• Bleeding from the gingival sulcus on gentle probing.
GINGIVAL BLEEDING varies in :
• Severity , duration and ease of provocation.
Bleeding on probing is widely used to measure:-
 Disease prevalence and
 Progression,
 To measure outcomes of treatment, and
 To motivate patients with their home care.
GINGIVAL BLEEDING ON BLEEDING ON PROBING

24.  Bleeding on probing detected EARLY DIAGNOSIS
PREVENTION OF MORE ADVANCED GINGIVITIS
 Even though gingival bleeding on probing may not be a good
diagnostic indicator for clinical attachment loss, its absence is an
excellent negative predictor of future attachment loss.
 In addition, the use of bleeding rather than color changes to diagnose
early gingival inflammation is advantageous in that bleeding is a more
objective sign that requires less subjective estimation by the
examiner.

25.  Lang NP et al (J Clin Periodontol 1990) through their studies
following active periodontal therapy concluded that continuous
absence of bleeding on probing is a reliable predictor for the
maintenance of periodontal health.
 Daniel Royzman et al (J Periodontol 2004) studied the effect of
aspirin intake on bleeding on probing in patients with gingivitis.It was
concluded that there was failure to consider the effects of aspirin on
bleeding on probing,but it could impair proper diagnosis and treatment
planning for clinicians.
 Thomas Dietrich et al (J periodontol 2004) studied the effect of
cigarette smoking on gingival bleeding and concluded that smoking
exerts a strong chronic and dose dependent suppressive effect on
gingival bleeding on probing.
 Nair P et al (J Clin periodontol 2003) revealed that there is an
increase in gingival bleeding on probing in patients who quits
smoking.

26.  Anatomic and developmental tooth variation
 Caries
 Frenum pull
 Iatrogenic factors
 Malpositioned teeth
 Mouth breathing
 Overhangs
 Partial dentures
 Lack of attached gingiva
 Recession
 Orthodontic treatment and fixed retainers

27. Most common cause of abnormal gingival bleeding on probing is chronic
inflammation
Provoked by:- 1. Mechanical trauma 2. Biting into solid foods
Chronic and Recurrent Bleeding
Lorencini M et al revealed that in early stages of gingivitis, expression of
cytokines responsible for connective tissue breakdown, matrix
metalloproteinases (MMPs), is ubiquitous.
Different MMPs play a role in this breakdown at different stages (e.g., a decrease
of MMP-14 activity at 7 days of inflammation and an immediate increase in
MMP-2, especially with fibroblastic stimulation).
In addition, MMP-9 expression peaked 5 days after gingivitis occurrence, which
was also regulated by macrophages and neutrophils.
Thus extracellular matrix remodeling was regulated with MMP-2 and -9
production and activation by host inflammatory response.

28. Vessel wall contracts
blood flow diminishes
Platelet adhere to the edges of the tissue
Fibrous clot formed, which contracts and results
in approximation of the edges of the injured area.
The severity of the bleeding and the ease of its provocation depends on the intensity
of the inflammation.
After the vessels are damaged and ruptured, interrelated mechanisms induce
hemostasis.

29. Histopathologic alterations that result in abnormal gingival bleeding
include:-
Dilation and engorgement of the capillaries and thinning or
ulceration of the sulcular epithelium. Because the capillaries are
engorged and closer to the surface, and the thinned, degenerated
epithelium is less protective, stimuli that are normally innocuous
cause rupture of the capillaries and gingival bleeding.
Sites that bleed on probing have a greater area of inflamed
connective tissue than the sites that do not bleed.

30.  Laceration of the gingiva by toothbrush bristles or by sharp pieces
of hard food.
 Gingival burns from hot foods or chemicals.
 Spontaneous bleeding or bleeding on slight provocation can occur
in acute necrotizing ulcerative gingivitis.

31. Gingival Bleeding Associated with Systemic
Changes
In some systemic disorders, gingival hemorrhage occurs spontaneously
or after irritation and is excessive and difficult to control.
 Systemic disorders have the common feature of a hemostatic
mechanism failure and result in abnormal bleeding in
• The skin
• Internal organs
• Other tissues, including the oral mucosa.
 Hemorrhagic disorders in which abnormal gingival bleeding is
encountered include :-

32.  Vascular abnormalities:
Vitamin C deficiency or
Allergy, e.g., Schonlein-Henoch purpura,
 Platelet disorders
Thrombocytopenic purpura,
 Hypoprothrombinemia
(Vitamin K deficiency),
 Other coagulation defects
 Hemophilia,
 Leukemia,
 Christmas disease,
 Deficient platelet thromboplastic factor (PF3) resulting from uremia,
 Multiple myeloma and Post rubella purpura
In addition, in women, long-term depression-related stress exposure may increase
concentrations of interleukin-6 (IL-6) in gingival crevicular fluid and may worsen
periodontal conditions with elevated gingival inflammation and increased pocket
depths.

33. In addition, changes in androgenic hormones have long been established as
significant modifying factors in gingivitis, especially among adolescents.
Effects of fluctuating estrogen/progesterone levels on the periodontium,
starting as early as puberty.
Among pathologic endocrine changes, diabetes is an endocrine condition with a
well-characterized effect on gingivitis.
In diabetes, marked inflammation affects both the epithelial and connective
tissues, which leads to degeneration of the dermal papilla, increase in the number
of inflammatory cells, destruction of reticulin fibers, and accumulation of dense
collagen fibers that causes fibrosis.
Several medications have also been found to have adverse effects on the gingiva.
• Anticonvulsants
• Antihypertensive
• Calcium channel blockers
• Immunosuppressant drugs
Aspirin’s effect on bleeding during a routine dental examination should be
considered to avoid false-positive readings, which could result in an inaccurate
patient diagnosis.
GINGIVAL
ENLARGEMENT
secondarily
GINGIVAL
BLEEDING

34. The color of the gingiva is determined by several factors, including
:
 the number and size of blood vessels,
 epithelial thickness,
 quantity of keratinization,
 pigments within the epithelium .
Color Changes in Chronic Gingivitis:
 Change in color is an important clinical sign of gingival disease.
 The normal gingival color is "coral pink" and is produced by the
tissue's vascularity and modified by the overlying epithelial
layers.

35.  The color becomes pale when vascularization is reduced (in association with
fibrosis of the corium) or epithelial keratinization increases. The gingiva
becomes redder when there is increase in vascularisation and decrese in
degree of epithelial keratinization.
 The changes start in the interdental papillae and gingival margin and spread
to the attached gingiva.
 Chronic inflammation intensifies red or bluish red color due to vascular
proliferation and reduction of keratinization owing to epithelial compression
by inflamed tissue. Venous stasis will add a bluish hue.
 Originally a light red, the color changes through various shades of red,
reddish blue and deep blue with increasing chronicity of inflammatory
process.

36.  The color changes may be marginal, diffuse or patch like, depending on the
underlying acute condition.
 In acute necrotizing ulcerative gingivitis, - marginal;
 In herpetic gingivostomatitis, - diffuse;
 In acute reactions to chemical irritation, - patch like or diffuse.
 Color changes vary with the intensity of the inflammation.
 In all instances there is an initial bright red erythema. If the condition does
not worsen, this is the only color change until gingiva reverts back to
normal.
 In severe acute inflammation, the red color changes to shiny slate gray,
which gradually becomes a dull whitish gray. The gray discoloration is
caused by tissue necrosis.
COLOR CHANGES IN ACUTE DISEASES

37.  Heavy metals (bismuth, arsenic, mercury, lead and silver) absorbed
systemically from therapeutic use or occupational or household
environments may discolor the gingiva and other areas of the oral
mucosa.
 Metals produce a black or bluish line in the gingiva that follows the
contour of the margin .
 The pigmentation may also appear as isolated black blotches involving
the interdental marginal and attached gingiva.
 Lead - bluish red or deep blue linear pigmentation of the gingival
margin (Burtonian line)
 Exposure to silver a violet line accompanied by a diffuse bluish grey
discoloration in throughout the oral mucosa (Argyria)

38.  Gingival pigmentation from systemically absorbed metals results from
perivascular precipitation of metallic sulfides in the subepithelial
connective tissue.
 Gingival pigmentation is not a result of systemic toxicity. It occurs
only in areas of inflammation, where the increased permeability of
irritated blood vessels permits seepage of the metal into the
surrounding tissue.

39. Bismuth gingivitis . Linear black
discoloration of the gingiva in a patient
receiving bismuth therapy.
Discoloration of the gingiva
caused by embedded metal
particles (amalgam).
Gingival pigmentation from systemically absorbed metals results from perivascular
precipitation of metallic sulfides in the subepithelial connective tissue.
Gingival pigmentation is not a result of systemic toxicity. It occurs only in areas of
inflammation, where the increased permeability of irritated blood vessels permits
seepage of the metal into the surrounding tissue.

40.  Endogenous oral pigmentations can be caused by melanin, bilirubin, or iron.
 Diseases that increase melanin pigmentation include the following:
•Addison’s disease
• Peutz-Jeghers syndrome
• Albright’s syndrome and Von Recklinghausen’s disease.
 Skin and mucous membranes can also be stained by bile pigments.
 The deposition of iron in hemochromatosis - blue-gray pigmentation.
 Exogenous factors - atmospheric irritants, such as coal and metal dust, and
coloring agents in food or lozenges.
 Tobacco causes hyperkeratosis of the gingiva and also may induce a
significant increase in melanin pigmentation of the oral mucosa.
 Localized bluish black areas of pigment are often caused by amalgam
implanted in the mucosa

41.  Both chronic and acute inflammations produce changes in the
normal firm and resilient consistency of the gingiva.
 In chronic gingivitis, both destructive (edematous) and reparative
(fibrotic) changes. coexist, and the consistency of the gingiva is
determined by their relative predominance.
 Calcified Masses in the Gingiva.
 Calcified microscopic masses may be found in the gingiva. They
can occur alone or in groups and vary in size, location, shape, and
structure.
 Such masses may be calcified material removed from the tooth and
traumatically displaced into the gingiva during scaling,root
remnants, cementum fragments, or cementicles.

42. Toothbrushing
 Toothbrushing has various effects of the consistency of the gingiva
such as promoting keratinization of the oral epithelium, enhancing
capillary gingival circulation, and thickening alveolar bone.
 Horiuchi M et al found Toothbrushing to increase the proliferative
activity of the junctional basal cells in dog gingiva by 2.5 times
compared with using a scaler.
 These findings may indicate that toothbrushing causes an increased
turnover rate and desquamation of the junctional epithelial surfaces.
This process may repair small breaks in the junctional epithelium and
prevent direct access to the underlying tissue by periodontal pathogens.

44. The surface of normal gingiva usually exhibits numerous small
depressions and elevations, giving the tissue an orange-peel appearance
referred as stippling.
In chronic inflammation the gingival surface is either smooth and
shiny or firm and nodular, depending on whether the dominant
changes are exudative or fibrotic.
Smooth surface texture is also produced by epithelial atrophy in atrophic
gingivitis, and peeling of the surface occurs in chronic desquamative
gingivitis.
Hyperkeratosis results in a leathery texture, and drug-induced gingival
overgrowth produces a nodular surface.

45. TRAUMATIC LESIONS
 One of the unique features of the most recent gingival disease
classification is the recognition of non-plaque induced traumatic
gingival lesions as distinct gingival conditions.
Traumatic lesions, whether chemical, physical, or thermal, are among
the most common lesions in the mouth:-
 Chemical injuries - aspirin, hydrogen peroxide, silver nitrate,
phenol, and endodontic materials.
 Physical injuries - lip, oral, and tongue piercing, which can result in
gingival recession.
 Thermal injuries - hot drinks and foods.

46.  Recession is the exposure of the root suface by an apical shift in the
position of gingiva
 The actual position is the level of the coronal end of the epithelial
attachment of the tooth.
 The apparent position is the level of the crest of gingival margin
 The severity of the recession is determined by the actual position of the
gingiva, not its apparent position.

47. The total amount of recession is the sum of the
apparent position and actual position.

48. Etiologic factors implicated in gingival recession :
-Faulty tooth brushing technique
-Tooth malposition
-Friction from soft tissues
-Gingival inflammation
-Abnormal frenum attachment

49.  Susceptibility to recession is also influenced by the
 position of teeth in the arch,
 the root-bone angle,
 mesiodistal curvature of the tooth surface.
 On rotated, tilted, or facially displaced teeth, the bony plate is thinned or
reduced in height. Pressure from mastication or moderate toothbrushing
damages the unsupported gingiva and produces recession.
Clinical Significance
 Exposed root surfaces are susceptible to caries.
 Abrasion or erosion of the cementum – dentinal sensitivity.
 Hyperemia of the pulp and associated symptoms.
 Interproximal recession creates oral hygiene problems and resulting plaque
accumulation.

50.  Changes in gingival contour are primarily associated with gingival enlargement,
but such changes may also occur in other conditions.
 Of historical interest are the descriptions of indentations of the gingival margin
referred to as Stillman's clefts and the McCall festoons.
 Stillman's clefts: The term "Stillman's clefts" has been used to describe a
specific type of gingival recession consisting of a narrow, triangular shaped
gingival recession.
 McCall festoons: The term "McCall festoons" has been
used to describe a rolled, thickened band of gingiva usually
seen adjacent to the cuspids when recession approaches
the mucogingival junction.

51.  Originally described by Stillman and considered to be the result
of occlusal trauma
 These clefts were subsequently described by Box as pathologic
pockets in which the ulcerative process had extended to the facial
surface of the gingiva.
 The clefts may repair spontaneously or persist as surface lesions
of deep periodontal pockets that penetrate into the supporting
tissues.

52. The clefts are divided into
 simple clefts: in which cleavage occurs in a single direction
(the most common type), and
 compound clefts: in which cleavage occurs in more than one
direction.
The clefts vary in length from a slight break in the gingival
margin to a depth of 5 to 6 mm or more.

55.  Carranza’s Clinical Periodontology, 11th edition by Newman, Takei, Klokkevold
and Carranza.
 Niklaus P. Lang, Rolf Adier, Andreas Joss and Sture Nyman (J Clin Periodontol
1990; 17: 714-721)
 Jasim M.Atbandar ,Albert Kingman, L.Jackson Brown and Harald Loe (J Clin
Periodontol 1998: 25: 231-237)
 Richard Amato, Jack Caton, Alan Poison and Mark Espeland (J. Periodontol
February, 1986)
 Jasim M. Albandar, L. Jackson Brown, Janet A. Brunelle and Harald Löe(J
Periodontol October 1996)
 Thomas Dietrich , Jean Pierre Bernimoulin, Robert J Glynn ( J Periodontol 2004
: 75 :16-22)
 Daniel Royzman, Luica Recio, Rachel L Badovinac , Joseph Fiorellini, Max
Goodson, Howard Howell , Nadeem Karimbux (J Periodontol 2004 ;75 :679-
684 )