2. Inflammation of
the gums (gingiva)
is gingivitis.

3.  Oral micro organisms produce certain
enzymes→ damage tissues→ widening
spaces → activate monocytes→
production of PGE2, TNF, INF, IL-1.
 IL-1β alter gingival fibroblasts
properties & block apoptosis.
 Normal human gingiva contain
inflammatory cells consisting
predominantly of T cells, with very few B
cells or plasma cells.

4. Stages of gingivitis
STAGE 1
The initial lesion
STAGE 2
Early lesion
STAGE 3
Established lesion
STAGE 4
Advanced lesion

5. Initial lesion → early lesion → established → advanced

6. The initial lesion
The 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
.

7.  Microscopically changes of acute
inflammation →in C.T beneath
junctional epithelium.
 Margination occur within 1 week or
sometimes 2 days after plaque
accumulation.
 Diapedesis ,emigration and
exudation & deposition of fibrin

8. PROGRESSION TO STAGE 2
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.

9. 70%
collagen
destroy
around
infiltrate
erythema
Circular &
dentogingival
fibers
Proliferati
on of
capillaries
Leukocytes
number
maximum
Early gingivitis
Gingival
fluid flow
increase
6-12 days
after
clinical
gingivitis
Bleeding on probing

10. Early lesion
The early lesion
evolves from the
initial lesion within
about 1 week.
Clinically, the early
lesion may appear as
early gingivitis, and
it overlaps with and
evolves from the
initial lesion with no
clear-cut dividing
line.

11. Microscopic changes
Leukocyte infiltration in C.T. beneath
junctional epithelium consisting of
Lymphocytes(75% T-cells)
neutrophils
Plasma cells
Macrophages
Mast cells
Development of rete pegs and ridges in
junctional epithelium.

12. Fibroblasts
show
Cytotoxic
alterations
↓Capacity
for collagen

13. Collagen degradation is related to
matrix metalloproteins (MMPs).
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.

14. Established
lesion
• Gingival anoxemia
• Engorged &
congested blood
vessels → impaired
venous return →
bluish hue
• Breakdown of Hb
(extravasated
RBCs)

15. Microscopic changes
Predominance of
plasma cells & B
lymphocytes(Ig
G1 & IgG3)
Widened
intercellular
spaces with
granular
cellular debris
i.e. lysosomes
of neutrophils
monocytes
and
lymphocytes
Hydrolases
destroy
tissue
component
s (collagen)
around
PMNs,
monocytes,
lymphocytes,
mast cells &
plasma cells
Protruding
rete pegs
into C.T.
basal lamina
destroyed in
some areas

16. Amount of
collagen
destruction
∞
No. of
inflammatory
cells

17. Increased levels of following in chronically
inflamed gingiva because of degradation of
ground substance
i. acid and alkaline phosphatase
ii. β-glucuronidase
iii. β-glucosidase
iv.β-galactosidase
v. Esterases
vi.Aminopeptidase
vii. cytochrome oxidase
Neutral mucopolysaccharide levels are decreased

18. Progression to stage 4
Established lesions of two types appear to exist;
some remain stable and do not progress for
months or years and others seem to become
more active and to convert to progressively
destructive lesions. Also, the established lesions
appear to be reversible in that the sequence of
events occurring in the tissues as a result of
successful periodontal therapy vice versa.

19. Advanced
lesion
Extension of the lesion into alveolar bone
characterizes a fourth stage known as
the advanced lesion.
Microscopically, there is fibrosis of the gingiva
and widespread manifestations of inflammatory
and immunopathologic tissue damage. At the
advanced stage, plasma cell presence dominates
connective tissue and neutrophils continue
dominating the junctional epithelium.

20. Patients with gingivitis showed significantly
more plaque accumulation, higher IL-1β, and
lower IL-8 concentrations at 28 days.
Gingivitis will progress to periodontitis only
in individuals who are susceptible
Teeth with non inflamed sites consistently
had a 50-year survival rate of 99.5%,
whereas teeth with consistently inflamed
gingiva had a 63.4% survival rate over 50
years.

22. STAGE
TIME BLOOD
JUNCTIONAL
DAYS VESSELS &
SULCULAR
EPI
PREDOMINANT
IMMUNE CELLS
COLLAGEN
CLINICAL
FINDINGS
1.
2-4
Initial
Lesion
Vascular Infiltration
Dilation By PMNs
&
vasculitis
PMNs
Perivascular Gingival
loss
fluid loss
2.
Early
lesion
Vascular as stage 1
Prolifera Rete pegs
tion
atrophic
areas
Lymphocytes
↑loss
around
infiltrate
Erythema
Bleeding
on probing
3.
14-21 Same as As stage 2
Establi
stage 2 + more
shed
blood
advanced
lesion
stasis
Plasma cells
Continued
loss
Changes in
color
size
Texture
4.
28-so Infiltrate More
Advan on
reaching progression
ced
bone
lesion
Plasma cells
In C.T
PMNs in
junctional epi
fibrosis
Bone
destructio
n
4-7