STAGES OF INFLAMMATION AND ITS HISTOPATHOLOGY

1. ABIRAMI VETRISELVAN

3. DEFINITION
Inflammation is defined as the
local response of living
mammalian tissues to injury
due to any agent.
( HARSH MOHAN )

4. CARDINAL SIGNS OF INFLAMMATION

5. Transient
vasoconstriction
of arterioles
Persistent
progressive
vasodilatation
Local
hydrostatic
pressure
Slowing or
stasis
Leucocytic
margination
The sequence of these changes in as under :-

7. INFLAMMATORY CELLS
 POLYMORPHONUCLEAR
NEUTROPHILS (PMNS)
 EOSINOPHILS
 BASOPHILS
 LYMPHOCYTES
 PLASMA CELLS
 MONONUCLEAR – PHAGOCYTE
SYSTEM
 GIANT CELLS

10. ACUTE VS CHRONIC INFLAMMATION
FEATURES ACUTE CHRONIC
ONSET FAST – MINUTES OR
HOURS
SLOW- DAYS
CELLULAR INFILTRATE MAINLY NEUTROPHILS MONOCYTES,
MACROPHAGES AND
LYMPHOCYTES
TISSSUE INJURY,
FIBROSIS
USUALLY MILD AND
SELF-LIMITED
OFTEN SEVERE AND
PROGRESSIVE
LOCAL AND SYSTEMIC
SIGNS
PROMINENT LESS PROMINENT

11. VASCULAR EVENTS
Alteration in the
microvasculature
(arterioles,
capillaries and
venules ) is the
earliest response
to tissue injury .
These alterations
include :
Haemodynamic
changes
Changes in
vascular
permeability

14. CELLULAR EVENTS

15. 1 2
3

16. The pathologic changes of gingivitis are associated
with the presence of oral microorganisms attached
to the tooth and perhaps in or near the gingival
sulcus.

18. Stage I Gingival Inflammation: The Initial Lesion
•The first manifestations of gingival inflammation are vascular changes that consist of
dilated capillaries and increased blood flow.
•These initial inflammatory changes occur in response to the microbial activation of
resident leukocytes and the subsequent stimulation of endothelial cells.
• Clinically, this initial response of the gingiva to bacterial plaque is not apparent.
•However, these findings are not accompanied by manifestations of tissue damage that
are perceptible at the light microscopic or ultrastructural level; they do not form an
infiltrate, and their presence is not considered to indicate pathologic change

19. Microscopically, some classic features of acute inflammation can be seen in the
connective tissue beneath the junctional epithelium.
Changes in blood vessel morphologic features (e.g., the widening of small
capillaries or venules) and the 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

20. Stage II Gingival Inflammation: The Early Lesion
•The early lesion evolves from the initial lesion within about 1 week after the
beginning of plaque accumulation.
•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.
•clinical signs of erythema may appear, mainly because of the proliferation of
capillaries and the 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

21. •70% of the collagen is destroyed around the cellular infiltrate.
•The main fiber groups that are affected appear to be the circular and
dentogingival fiber assemblies.
•Alterations in blood vessel morphologic features and vascular bed patterns
have also been described.

22. Microscopic examination of the gingiva reveals leukocyte infiltration in the
connective tissue beneath the junctional epithelium, which consists mainly
of lymphocytes (75%, with the majority being T cells) but also includes
some migrating neutrophils as well as macrophages, plasma cells, and mast
cells.
All of the changes seen in the initial lesion continue to intensify with the
early lesion. The junctional epithelium becomes densely infiltrated with
neutrophils

23. Stage III Gingival Inflammation: The Established Lesion
•Over time, the established lesion evolves. It is characterized by a predominance of plasma
cells and B lymphocytes, and it is probably in conjunction with the creation of a small
gingival pocket lined with a pocket epithelium
•With 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
•The result is localized gingival anoxemia, which superimposes a somewhat bluish hue on the
reddened gingiva.
•The extravasation of erythrocytes into the connective tissue and the breakdown of
hemoglobin into its component pigments can also deepen the color of the chronically
inflamed gingiva.

24. •The established lesion can be described as moderately to severely inflamed gingiva.
•The predominance of plasma cells is thought to be a primary characteristic of established
lesions.
•Collagenolytic activity is increased in inflamed gingival tissue by the enzyme collagenase.
•Collagenase is normally present in gingival tissues; it is produced by some oral bacteria
and by PMNs.
•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 convert to progressively
destructive lesions.

25. •A key feature that differentiates established lesions is the increased number of
plasma cells, which become the preponderant inflammatory cell type.
•Plasma cells invade the connective tissue not only immediately below the
junctional epithelium but also deep into the connective tissue, around the blood
vessels, and between the bundles of collagen fibers.
•The junctional epithelium reveals widened intercellular spaces that are filled with
granular cellular debris, including lysosomes derived from disrupted neutrophils,
lymphocytes, and monocytes .

26. Stage IV Gingival Inflammation: The Advanced Lesion
•The extension of the lesion into alveolar bone characterizes the fourth stage,
which is known as the advanced lesion or phase of periodontal breakdown
•Gingivitis will progress to periodontitis only in individuals who are susceptible.
•Patients who had sites with consistent bleeding had 70% more attachment loss as
compared with sites that were not consistently inflamed.

27. •Microscopically, fibrosis of the gingiva is present and there is widespread
manifestation of inflammatory and immunopathologic tissue damage.
• At the advanced stage, the presence of plasma cells dominates the connective
tissue, and neutrophils continue dominating the junctional epithelium.