All about gingivitis *definition *classification *Signs and Symptoms: Increased GCF, Gingival Bleeding, Color change, Consistency, Surface texture (STIPPLING), Position of Gingiva, Gingival Contour, Size. Treatment consisits of scaling and root planing. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health

1. GINGIVITIS

3. Index
1. Definition
2. Etiology
3. Types of Gingivitis
(a) Depending on course and duration
(b) Depending on Distribution
(c) Classification of Gingivitis (Page and Schroeder 1976) (Histological
Evaluation)
 Initial,
 Early,
 Established,
 Advanced.

4. Index
4. Clinical Features
 Increased GCF
 Gingival Bleeding
 Color change
 Consistency
 Surface texture (STIPPLING)
 Position of Gingiva
 Gingival Contour
 Size

5. GINGIVITIS
Genco 1990- ‘Gingivitis is inflammation
of the gingiva in which the junctional
epithelium remains attached to the tooth
at its original level.’
This definition infers that gingivitis does
not exist if the tooth has periodontitis

6. GINGIVITIS VERSUS PERIODONTITIS
 Gingivitis is inflammation of the gingiva in
which the junctional epithelium remains
attached to the tooth at its original level.
 Periodontitis is inflammation of the gingiva in
which the junctional epithelium shifts apically
leading to clinical attachment loss.

7. ETIOLOGY

8. In recent classification of periodontal diseases (2017)
Gingivitis has been classified under ‘Periodontal health,
Gingival diseases and conditions’
1. Periodontal health and gingival health (a. Clinical gingival health on
an intact periodontium; b. Clinical gingival health on a reduced
periodontium)
2.Gingivitis: dental biofilm induced
(a. Associated with dental biofilm alone; b. Mediated by systemic or
local risk factors; c. Drug-influenced gingival enlargement)
3. Gingival diseases: non-dental biofilm-induced
(1. Genetic or developmental disorder; 2. Specific infections; 3.
Inflammatory and immune conditions; 4. Reactive processes; 5.
Neoplasms; 6. Endocrine, nutritional and metabolic diseases; 7.
Traumatic lesions; 8.Gingival Pigmentation)

9. Gingivitis: dental biofilm induced
a. Associated with dental biofilm alone
b. Mediated by systemic or local risk factors
i) Systemic risk factors a. Smoking
b. Hyperglycemia
c. Nutritional factors
d. Pharmacological (prescription, non prescription)
e. Sex Steroid hormones
(Puberty, pregnancy, Menstrual cycle, oral contraceptives)
f. Hematological agents
ii) Local risk factors a. Oral dryness
b. Dental plaque biofilm retention factors (prominent restoration margins)
c. Drug-influenced gingival enlargement

10. GINGIVAL DISEASES: NON-DENTAL
BIOFILM-INDUCED
(8 categories)
1. Genetic or developmental disorder
1.1 Hereditary Gingival fibromatosis
2. Specific infections
2.1 Bacterial infections
a) Necrotizing Periodontal disease
b) Neisseria Gonorrhoeae (gonorrhea)
c) Treponema pallidum (syphlis)
d) Mycobacterium tuberculosis (tuberculosis)
e) Streptococcal gingivitis (strains of streptococcus)

11. b.2 Viral origin-
a) Coxsachie virus (Hand foot and mouth disease
b) Herpes simplex virus; HSV1,2 (primary or recurrent)
c) Varicella zoster virus (chicken pox)
d) Molluscum contagiosum
e) Human papilloma virus
b.3 Fungal-
a) Candidiasis
b) Other mycosis (eg. Histoplasmosis, aspergillosis)

12. 3. Inflammatory and immune conditions
3.1 Hypersensitivity reaction-
a) Contact allergy
b) Plasma cell gingivitis
c) Erythema multiforme
3.2 Auto immune diseases of skin and mucous membrane-
a) Pemphigus vulgaris
b) Pemphigoid
c) Lichen Planus
d) Lupus erythematosis

13. 3.3 Granulomatous inflammatory condition-
a) Crohn’s disease
b) Sarcoidosis
4. Reactive processes
4.1 Epulidus
a) Fibrous epulis
b) Calcifying fibroblastic granuloma
c) Pyogenic granuloma
d) Peripheral giant cell granuloma (or central)

14. 5. Neoplasms
5.1 Premalignant
a) Leukoplakia
b) Erythroplakia
5.2 Malignant
a) Squamous cell carcinoma
b) Leukemia
c) Lymphoma

15. 6. Endocrine, nutritional and metabolic diseases
6.1 Vitamin deficiency
a) Vitamin C deficiency (Scurvy)
7. Traumatic lesions
7.1 Physical and mechanical insults
a) Frictional Keratosis
b) Tooth brushing induced gingival abrasions
c) Factitious injury (self harm)

16. 7.2 Chemical insults
a) Etching
b) Chlorhexidine
c) Acetyl salicylic acid
d) Cocaine
e) Hydrogen peroxide
f) Dentifrice detergent
g) Paraformaldehyde/ calcium hydroxide
7.3 Thermal insults
a) Burn of mucosa

17. 8. Gingival pigmentation
a) Melanoplakia
b) Smoker’s melanosis
c) Drug induced pigmentation
(antimalarial; minocycline)
d) Amalgam tattoo

18. TYPES OF
GINGIVITIS

19.  Depending on course and
duration
i) Acute gingivitis
ii) Subacute gingivitis
iii) Chronic gingivitis
iv) Recurrent gingivitis

20. DEPENDING ON COURSE AND DURATION
 Acute gingivitis: Sudden onset, short duration and can be
painful.
 Subacute: Less severe phase of acute condition.
 Recurrent gingivitis: Reappears after treatment or after
disappearing spontaneously.
 Chronic gingivitis: Slow onset, long duration, usually
painless. The most commonly occurring gingival condition.

21.  Depending on Distribution
i) Localized gingivitis
- Localized papillary gingivitis
- Localized marginal gingivitis
- Localized diffuse gingivitis
ii) Generalized gingivitis
- Generalized marginal gingivitis
- Generalized diffuse gingivitis

22. DEPENDING ON THE DISTRIBUTION
 If gingivitis is involving a single tooth or group of teeth it is called
localized gingivitis, while generalized gingivitis involves entire
mouth.
 According to distribution, gingivitis can be marginal, papillary or
diffuse
 Papillary, marginal and diffuse gingivitis can occur as localized or
generalized conditions.

23.  Depending on Distribution
 Marginal gingivitis: that involves the gingival
margin.
 Papillary gingivitis: involves interdental papilla
extending into gingival margin.
 Diffuse gingivitis: involves interdental papilla,
gingival margin and attached gingiva. Normally
it occurs in patients having some systemic
diseases.

24. THE DIAGNOSIS OF GINGIVITIS
SHOULD BE:
 Localized marginal/papillary/diffuse chronic/acute
gingivitis
 Generalized marginal/papillary/diffuse chronic/acute
gingivitis

25. CLASSIFICATION OF
GINGIVITIS
(PAGE AND
SCHROEDER 1976)

26. HISTOLOGIC DEVELOPMENT OF THE
GINGIVAL LESION
The pathogenesis of human periodontitis was first
documented in detail by Page and Schroeder in 1976
 Initial,
 Early,
 Established,
 Advanced

27. CLINICAL CONDITION HISTOPATHOLOGIC CONDITION
 Pristine gingiva Histologic perfection
 Normal health gingiva Initial lesion of Page & Schroeder (PMNs)
 Early gingivitis Early lesion of Page & Schroeder
(mainly T lymphocytes)
 Established gingivitis Established lesion with no bone loss and
epithelial migration (plasma cell density
between 10% and 30% of leukocyte infiltrate)
 Periodontics Advanced lesion with bone loss and
epithelial migration from the cementoenamel
junction (plasma cell density > 50%)

28. HEALTHY GINGIVA
 Super healthy or ‘‘pristine’’ state- histologically has
little or no inflammatory infiltrate. It occurs in ideal
conditions.
 ‘‘Clinically healthy’’ gingiva- looks similar clinically,
but histologically has features of some
inflammatory infiltrate. It is the healthy gingiva we
see clinically in everyday situations. (Initial Lesion)

29. STAGE I :THE INITIAL LESION
 First manifestations are vascular
changes:
‘vasodilatation, increased blood flow,
increased vascular permeability’
 Clinically not apparent: subclinical
gingivitis

30.  MICROSCOPICALLY- Widening of small capillaries
or venules, adherence of neutrophils (PMNs) to
vessel walls (margination) occur within 1 week and
sometimes as early as 2 days after plaque
accumulation
 PMNs leave the capillaries by migrating through the
walls. From the connective tissue, they move
through the junctional epithelium to the gingival
sulcus to kill microbes

31.  Increased vascular permeability causes the exudation of
fluid (plasma) from the gingival sulcus. This leads to
increased Gingival crevicular fluid (GCF) flow
 Increased GCF flow is the first sign of gingivitis, though it is
not visible as its amount is very less.

32. STAGE II : THE EARLY LESION
 Clinical signs of erythema (redness) appear owing
to proliferation of capillaries and increased
formation of capillary loops.
 Bleeding on probing evident. It is the second sign of
gingivitis but first objective (visible by patient) sign.

33. MICROSCOPICALLY
 Microscopic examination of the gingiva
reveals a leukocyte infiltration in connective
tissue below the epithelium, consisting of
mainly lymphocytes (75%, with majority of
them T cells) and less of neutrophils,
macrophages, plasma cells and mast cells.
 All the changes seen in initial lesion continue
to intensify.

34.  The junctional epithelium becomes densely
infiltrated with neutrophils, as does the
gingival sulcus.
 The junctional epithelium may begin to show
development of rete pegs and ridges to
increase the surface area of attachment.

35.  Increased amount of collagen destruction (>70%)
 Circular and dento-gingival groups of gingival fibers
are most severely affected
 Fibroblast show reduced collagen production

36. STAGE III : THE ESTABLISHED
LESION
 It is a chronic stage of gingivitis.
 Blood vessels become engorged and congested,
venous return is impaired and blood flow becomes
sluggish. Stasis of blood leads to breakdown of
hemoglobin leading to bluish hue

37.  Microscopically
 Plasma cells (10-30%) are the predominant inflammatory cell type
 The junctional epithelium reveals widened intercellular spaces filled with
granular cellular debris, including lysosomes derived from disrupted
PMNs, lymphocytes and monocytes. The lysosomes contain acid
hydrolases that can destroy its tissue components.
 The junctional epithelium develops rete pegs or ridges that protrude into
the connective tissue and the basal lamina is destroyed in some areas.

38.  Collagen fibers are destroyed around the
infiltrate of inflammatory cells(disrupted plasma
cells, PMNs, lymphocytes, monocytes and mast
cells)
 Upto this stage, gingivitis is reversible

39. STAGE IV : THE ADVANCED LESION
 Extension of the lesion into alveolar bone
 Phase of periodontal breakdown
 Gingivitis will progress to this stage
(periodontitis) only in individuals who are
susceptible.

40. STAGE IV : THE ADVANCED LESION
 Irreversible stage
 Predominance of plasma cells > 50%
 Junctional epithelium infiltrated by increasing number
of PMNs, unable to hold itself as lysosomes derived
from disrupted PMNs contain acid hydrolases that
can destroy its tissue component attachments to
tooth, leading to its apical movement causing clinical
attachment loss (Periodontitis)

41. Stage Time
(days)
Blood
vessels
Junctional/
sulcular
epithelium
Predomi
nant
Immune
cells
collagen Clinical
findings
I. Initial
lesion
2-4 Vascular
dilation
vasculitis
Infiltrated
by PMNs
PMNs Perivascula
r loss
Gingival
fluid
flow
II. Early
lesion
4-7 Vascular
proliferation
Same as
stage I
Rete peg
formation
Atrophic
areas
lymphoc
ytes
Increased
loss around
infiltrate
Erythe
ma
Bleedin
g on
probing

42. Stage Time
(days)
Blood
vessels
Junctional/
sulcular
epithelium
Predom
inant
immune
cells
collagen Clinical
findings
III.
Establish
ed lesion
14-21 Same as
stage II,
plus blood
stasis
Same as
stage II but
more
advanced
Plasma
cells
Continued
loss
Change
s in
color,
size,
texture,
etc.

43. BIOCHEMICAL
CHANGES

44. BIOCHEMICAL CHANGES IN CHRONIC GINGIVITIS
• acid and alkaline phosphatase,
• ß-glucuronidase,
• ß-glucosidase,
• ß-galactosidase,
• esterases,
• aminopeptidase and
• cytochrome oxidase.
• Neutral mucopolysaccharide levels are decreased,
presumably as a result of degradation of the ground
substance.

45. CLINICAL
FEATURES

46. CLINICAL
CHARACTERISTICS
5 cardinal signs of inflammation:
 redness (rubor)
 swelling (tumor)
 heat (calor)
 pain (dolor)
 loss of function (functio laesa).

47. CLINICAL
CHARACTERISTICS
There are 3 other signs with potential
diagnostic value:
 bleeding on probing
 suppuration
 gingival exudate (increase in GCF) and
ulceration.
All cases of gingivitis must have one or
more of these 9 clinical signs of
inflammation.

48. CLINICAL FINDINGS
Normal gingiva Gingivitis
Color Pale pink
(melanin pigmentation
common in certain groups)
Reddish/ Bluish red
Size Papillary gingiva
fills interdental
spaces; marginal
gingiva forms knife
edge with tooth
surface; sulcus
depth<3mm
Swelling both coronally and
buccolingually; false pocket
formation

49. CLINICAL FINDINGS
Normal gingiva Gingivitis
Shape
Surface Texture
Scalloped- troughs
in marginal areas
rise to peaks in
interdental areas
Stippling present
Edema which blunts the marginal
and papillary tissues leads to loss of
knife edge margins
Stippling absent
Consistency Firm, Resilient Soft; pressure induced pitting due to
edema
Tendency to
bleed
No bleeding on
probing
Bleeding on probing

50. 1. INCREASED GCF
 Increase in GCF is first clinical sign of gingivitis but is
not visible by naked eye, so not a objective sign
 Increased vascular permeability causes the
exudation of fluid (plasma) from the gingival sulcus.
This leads to increased Gingival crevicular fluid
(GCF) flow
 Observed in ‘Initial Lesion’ as discussed

51. 2. GINGIVAL BLEEDING
 Gingival Bleeding on Probing is the
second sign of gingivitis, but it is the
first visual sign of gingivitis
 Observed in ‘Early Lesion’ as
discussed

52. GINGIVAL BLEEDING
 SIGNIFICANCE
 Earliest visual sign of inflammation
 Appear earlier than color change or any other visual signs of inflammation.
 More objective sign (seen by patient)
 The severity and ease with which bleeding can be provoked indicates the
intensity of the inflammation. Also its presence indicates that disease is
active at that site

53. GINGIVAL BLEEDING
 Can occur in three conditions
1. Chronic inflammation (eg. Accumulation of plaque)
(CHRONIC BLEEDING)
2. Acute conditions (ACUTE BLEEDING)
3. Due to systemic diseases (GINGIVAL BLEEDING DUE TO
SYSTEMIC CONDITIONS)

54. 1. Chronic and Recurrent
Bleeding
 Lang et al demonstrated that any
force greater than 0.25 N may
evoke bleeding in an healthy sites
with an intact periodontium. Thus
the probing force should be ≤0.25N

55. 2. Acute Bleeding
 Occur spontaneously by injury or in acute
gingival disease like acute necrotizing ulcerative
gingivitis
 Laceration of the gingiva by toothbrush bristles
during aggressive tooth brushing or by sharp
pieces of hard food.
 Gingival burns from hot foods or chemicals

56. 3. In some systemic disorders, gingival bleeding
occurs spontaneously or after irritation and is
excessive and difficult to control.
Hemorrhagic disorders
•Vascular abnormalities
•Vitamin C deficiency
•Schonlein-Henoch purpura
•Platelet disorders
•Thrombocytopenic purpura
•Hypoprothrombinemia
•Deficient platelet
thromboplastic factor
•Coagulation defects
•Hemophilia
•leukemia
•Christmas disease
Drugs
• Salicylates
• Anticoagualnts
• NSAIDS
Menstrual
cycle
• Abnormal
gingival
bleeding may
also occur
during cyclic
episodes of
menstrual
cycle.

57. HISTOLOGIC FINDINGS
In the epithelium:
 Thinning and micro-ulcerations of the sulcular epithelium.
 Thinning of the epithelium occurs due to the toxic substances released
by plaque bacteria that destroys the intercellular junctions.
 Micro-ulcerations are due to bacteria trying to gain entry into the
connective tissue by breaking through the epithelium and/or in response
to inflammation.
 The neutrophils from the connective tissue cross the epithelial barrier to
reach the site of infection, in doing so they also cause ulceration in
sulcular epithelium

58. HISTOLOGIC FINDINGS
In the connective tissue
 Dilation, and engorgement of the capillaries
 Capillaries are engorged and closer to the
sulcular epithelium which is already thinned and
less protective, stimuli that are otherwise
innocuous can cause rupture of the capillaries
which may result in gingival bleeding

59. 3. COLOR CHANGES
THIRD SIGN OF GINGIVITIS
Color Changes in Chronic Gingivitis.
 Red or bluish red color due to vascular
proliferation and decreased keratinization or
thinning of epithelium
 Venous stasis (that occur due to chronicity ie.
long duration of infection) contribute to bluish
hue.
 The changes start in the interdental papillae
spread to gingival margin and then to the
attached gingiva.

60. COLOR CHANGES
THIRD SIGN OF GINGIVITIS
Color Changes in Acute Gingivitis.
 Marginal, diffuse or patch like depending on the
underlying acute condition.
 In initial stage: Red erythema. If the condition
does not worsen, it reverts to normal.
 In severe acute inflammation: Red color
gradually becomes dull, whitish gray due to
tissue necrosis

61. COLOR CHANGES
Color Changes Associated with
Systemic Factors
Endogenous Factors: melanin, bilirubin, or iron.
 Increase melanin pigmentation in: Addison's disease,
Peutz-jeghers syndrome, Albright‘s syndrome
Exogenous factors:
 atmospheric irritants such as coal/metal dust and coloring
agents in food/ lozenges.
 Tobacco causes hyperkeratosis of the gingiva and
increase in melanin pigmentation of oral mucosa.
 Localized bluish black areas of pigment due to amalgam
implanted in the mucosa during restoration (amalgam
tatoo)

62. COLOR CHANGES
Metallic Pigmentation
 Occurs in patients working in metal industry as they
contain metal in their blood. (It is not toxicity and normal
condition)
 Occur only in inflamed gingiva and disappears after
scaling and root planing.
 In inflammation due to increase in vascular permeability,
plasma comes out along with metal in it. These metals form
metallic sulphides in peri vascular areas giving color to
gingiva

63. Metallic Pigmentation
 When inflammation subsides, vascular permeability
decreases and the discoloration disappears. So treatment
in these patients is only scaling and root planing
 This is different from tattooing produced by the
accidental embedding of amalgam or other metal
fragments.

64. 4. CONSISTENCY
 Normal : Firm & resilient. Resiliency is the property in which when we
press the gingiva, it comes back to its original position.
 Gingivitis : Soft & edematous with necrosis in acute gingivitis
Firm & leathery in chronic mainly in smokers because
of vasoconstriction caused by nicotine.
Normal Finding: Chronic inflammation (fibrosis) with overlying acute
inflammation (edematous/swollen gingiva) due to plaque accumulation

65. CHANGES IN THE CONSISTENCY OF GINGIVA
Clinical changes
Chronic gingivitis
1. Soggy puffiness that pits
on pressure
2. Marked softness and friability,
with ready fragmentation
and pinpoint surfaces
of redness with probe
and desquamation.
3. Firm, leathery consistency.
Loss of resiliency.
Underlying microscopic features
1. Infiltration of connective tissue by fluid (due to
increased vascular permeability) and cells of
inflammatory exudates.
2. Degeneration of connective tissue and
epithelium by microbial infiltration, toxins and
inflammatory exudates;
Engorged edematous connective tissue, thinning of
epithelium, leucocyte invasion, epithelial rete pegs are
elongated to connective tissue.
Fibrosis and epithelial proliferation due to long
standing chronic inflammation.

66. CHANGES IN THE CONSISTENCY OF GINGIVA
Clinical changes
Acute gingivitis
1. Diffuse puffiness and softening.
2. Sloughing of grayish, flake like
particles of debris adhering to
eroded surface.
3. Vesicle formation
Underlying microscopic features
1. Diffuse edema by acute inflammatory
cells
2. Necrosis by formation of pseudo
membrane (consisting of bacteria,
polymorphonuclear leucocytes, and
degenerated epithelial cells) in fibrous
meshwork.
3. Intercellular and intracellular edema with

67. 5. CHANGES IN SURFACE
TEXTURE OF GINGIVA
Loss of surface stippling - early sign of gingivitis
In inflammation - Surface is
 either smooth and shiny (in edematous gingiva) (Acute)
 or firm and nodular (in fibrotic gingiva) (Chronic)
In Chronic Desquamative gingivitis - Peeling of the surface occurs
Hyperkeratosis - Leathery texture,
Drug-induced gingival overgrowth - Nodular surface.

68. STIPPLING
ALSO CALLED AS ‘ORANGE PEEL APPEARANCE’
Microscopically it is seen as elevations and depressions of gingiva
due to connective tissue papilla and epithelial rete pegs at interface of
epithelium and connective tissue.
EXAMINATION
It is seen clearly with naked eye after drying the gingiva with cotton to
minimize refraction of light caused by salivary layer. And its better to
visualize in sunlight than in dental chair light.

69. STIPPLING
In inflammation, due to increased vascular
permeability, plasma comes out of blood
vessels and gets collected in connective
tissue. The resulting edema in connective
tissue flattens the junction (epithelium and
connective tissue) leading to disappearance
of stippling.

70. STIPPLING
 Presence of stippling is more important than its
absence.
 Its presence always means healthy gingiva
 But its absence does not always means
inflammation. Because it is absent in children
below five years and disappears in old age

71. 6. CHANGES IN THE POSITION
OF GINGIVA
 Recession is the change in position of gingiva. It is exposure of the root surface
by an apical shift in the position of the gingiva.
Position of the gingiva can be actual or apparent.
Actual position is the level of epithelial attachment (junctional epithelium) on the
tooth i.e., from the cemento-enamel junction to the probable depth of the pocket.
Apparent position is the level of crest of the gingival margin i.e., from the cemento-
enamel junction to the gingival margin.

72. CLINICAL SIGNIFICANCE
Exposed root surfaces are susceptible to
•Caries.
•Abrasion or erosion causing increased sensitivity
•Hyperemia of the pulp (Pulpitis)
•Plaque accumulation.

73. 7. CHANGES IN GINGIVAL CONTOUR
Normal : Marginal gingiva: scalloped and knife edged,
Interdental papilla in anterior region: pyramidal; posteriorly: tent-shaped
Factors affecting contour:
- Shape of teeth
- Alignment in the arch
- Location & size of proximal contact
Disease : Marginal gingiva: rounded or rolled
Interdental papilla: blunt and flat.

74.  Scalloped and knife edged margin makes
the gingiva self cleansing as during
chewing, food gets deflected away from
the margins of gingiva and keep it plaque
free
 Rounded or rolled margins cause plaque
accumulation into the margins, causing
gingivitis

75.  Other changes in gingival contour Stillman's
clefts and McCall festoons (life preserver-
shaped enlargement of the margin).

76.  Stillman's clefts: It is apostrophe (triangular) shaped indentations extending
from and into the gingival margins. Occurs on facial surface of one or two
teeth. It causes gingival recession exposing the cementum of root surface.
When it reaches the mucogingival junction, the apical end becomes inflamed
due to difficulty in maintaining plaque control. Gingival margin is blunt instead
of knife edge
 Etiology : First described by Stillman to be caused by trauma from occlusion.
But later Box described it as pathologic pockets in which ulcerative process
has extended to the facial surface of gingiva.
 Treatment include Gingivoplasty or Gingivectomy if it is shallow and narrow.
But if it is wide then Lateral pedicle or Connective tissue graft is required to
cover the recession defect.

77.  McCall festoons are life preserver- shaped
enlargement of the margin of gingiva. Occurs mainly
on buccal surface of incisors and premolars.
 Described by John Oppie McCall in1922.
 Thought to be due to trauma from occlusion. But now
it is considered to be associated with inflammation of
marginal gingiva due to accumulation of plaque.

78. 8. SIZE
 Sum total of cellular & intercellular elements.
 Increases during gingival inflammation.

79. Scoring of gingival enlargement (increased size)
Grade 0: No signs of gingival enlargement
Grade I: Enlargement confined to interdental
papilla
Grade II: Enlargement involves papilla and
marginal gingiva.
Grade III: Enlargement covers three
quarters or more of the crown

80. COMPONENTS OF
GINGIVAL INFLAMMATION
 Thus the two components are
 the acute inflammatory component, with
vasodilation, edema, and polymorphonuclear
(PMNs) infiltration
 Long standing inflammation leads to chronic
inflammatory component, with B andT lymphocytes
and capillary proliferation with fibrosis.

81.  The more inflamed a gingival
unit appears clinically, the better
the chances of therapeutic
measures resulting in a return to
normal gingival health