BASIC CONCEPTS OF INFLAMMATION-STAGES OF INFLAMMATION-ALL ABOUT GINGIVAL INFLAMMATION-CLINICAL FEATURES AND STAGES OF GINGIVITIS-HOW TO MANAGE-ALL IN ONE-FOR B.D.S LEVEL PROJECTS AND SEMINARS

1. GINGIVAL
INFLAMMATION
BY DR.MOINDRILA HALDER
B.D.S(HONOURS), WBUHS

2. INFLAMMATION
• Definition: local response of living tissues
to injury due to any agent.
• It is the defense reaction of the body in
order to eliminate or limit the spread of
injurious agentremoval of the necrosed
cells and tissues.
• Agents:
Infective,Immunological,Physical,Chemica
l.
• Signs of Inflammation:
RUBOR(redness),TUMOR(swelling),CALOR(
heat),DOLOR(pain) and LOSS OF
FUNCTION.

3. TYPES OF INFLAMMATION
DEPENDING UPON DEFENSE CAPACITY OF HOST AND DURATION OF
RESPONSE:
ACUTE
INFLAMMATION
• Short duration,resolves
quickly,usually followed
by healing.
• FEATURES: accumulation
of fluid and plasma at
affected site,intravascular
activation of
platelets,polymorphonucl
ear
neutrophils(inflammatory
cells).
CHRONIC
INFLAMMATION
• Prolonged process,tissue
destruction occurs,may
be after prolonged acute
inflammation.
• FEATURES: presence of
chronic inflammatory
cells(plasma cells ,
lymphocytes ,
macrophages),granulatio
n tissue formation.

5. CHEMICAL MEDIATORS OF INFLAMMATION :

6. EVENTS IN ACUTE INFLAMMATION:
VASCULAR EVENTS:
• HAEMODYNAMIC
CHANGEStransient
vasoconstriction followed
by progressive
vasodilatationincrease
in local hydrostatic
pressurestasis of
microcirculation causes
raised blood viscosity.
• ALTERED VASCULAR
PERMEABILITYincrease
d.
CELLULAR EVENTS:
• EXUDATION OF
LEUCOCYTES
• PHAGOCYTOSIS

7. CELLULAR EVENT:EXUDATION OF LEUCOCYTES

8. PHAGOCYTOSIS:[STAGES]
1]OPSONISATION OF FOREIGN PARTICLES
2]ENGULFMENT OF FOREIGN PARTICLE
BY PHAGOCYTE
3]INCORPORATION WITHIN THE CELL
AND DEGRANULATION
4]FORMATION OF PHAGOLYSOSOME

9. FATE OF INFLAMMATION

10. FEATURES OF CHRONIC INFLAMMATION:
• MONONUCLEAR CELL INFILTRATION: like phagocytes and
lymphoid cells.These may appear at site of chronic
inflammation .
• TISSUE DESTRUCTION AND NECROSIS: by activated
macrophages [release a variety of biologically active
substances like protease,elastase,collagenase,lipase] etc.
• PROLIFERATIVE CHANGES:necrosis proliferation of small
blood vessels and fibroblastsinflammatory granulation
tissue.

11. INFLAMMATORY CELLS:MORPHOLOGY
AND FUNCTION

12. GIANT CELLS IN INFLAMMATION
• FOREIGN BODY GIANT CELLS:numerous
nuclei,uniform in size and shape.Resemble nuclei
of macrophages which are scattered throughout
the cytoplasm.(LEPROSY,TUBERCULOSIS,CHRONIC
INFECTIVE GRANULOMAS)
• LANGHAN’S GIANT CELLS:nuclei around periphery
in a horshoe or ring pattern or clustered at two
poles of the giant cell.Nuclei are like those of
macrophages and epitheloid
cells.(TUBERCULOSIS,SARCOIDOSIS)
• TOUTON GIANT CELLS:multinucleated,vacuolated
cytoplasm due to lipid content.(XANTHOMA)
• ASCHOFF GIANT CELLS:multinucleated cells
derived from cardiac histiocytes.(RHEUMATIC
NODULE)

13. REGULATION OF INFLAMMATION:
BY HOST MECHANISMS
*ACUTE PHASE REACTANT PROTEINS in plasma such as:
1]Cellular protection factors:plasminogen activator inhibitor.
2]Coagulation proteins:fibrinogen,plasminogen,vonWillebrand factor.
3]Transport proteins:ceruloplasmin,haptoglobulin.
4]Immune agents:serum amyloid A and P component, C reactive
protein.
*GLUCOCORTICOIDS:level increases in infections and trauma.
*FREE CYTOKINE RECEPTORS:presence indicates disease activity.
*ANTI-INFLAMMATORY CHEMICAL MEDIATORS:PGE2 or prostacyclin
have pro as well as anti-inflammatory actions.

14. PARTS OF GINGIVA[DISEASE FREE]

15. GINGIVAL INFLAMMATION
• Inflammation of the gingiva is termed as GINGIVITIS.
• It is associated with the presence of oral micro-organisms
attached to the tooth and perhaps in or near the gingival
sulcus.
• These micro-organisms are capable of synthesizing
products(COLLAGENASE,HYALURONIDASE,PROTEASE,CHON
DROITIN SULFATASE,ENDOTOXIN)damage to epithelial
and connective tissue cells,as well as to intercellular
constituents such as collagen,ground substance and
glycocalyx.
Widening of the spaces between the junctional epithelial
cellsbacteria themselves or their toxins to gain access to the
connective tissue.

16. NORMAL GINGIVA
HISTOPATHOLOGY
MARGINAL
GINGIVITIS

17. PRISTINE GINGIVA : A STATE OF SUPER HEALTH WHERE
NORMAL GINGIVA IS FREE FROM SIGNIFICANT
ACCUMULATION OF INFLAMMATORY CELLS[AAP]

20. STAGES OF GINGIVITIS
• STAGE I : THE INITIAL LESION
• STAGE II : THE EARLY LESION
• STAGE III : THE ESTABLISHED LESION
• STAGE IV : THE ADVANCED LESION

21. STAGE I : THE INITIAL LESION
2-4 DAYS
• Vascular changes dilated capillaries and increased
blood flow.
• Initial inflammatory changes due to microbial activation
of resident leukocytes and stimulation of endothelial
cells.
• Changes in junctional epithelium and perivascular
connective tissue:
• 1]Loss of perivascular collagen.
2]Exudation and deposition of fibrin in affected area.
3]Presence of PMNs.
• Increase in the flow of gingival fluid into the sulcus.
• Character and intensity of host response chronic
inflammatory lesion with appearance of infiltrate of
macrophages and lymphoid cells within a few days.

22. STAGE II : THE EARLY LESION
4-7 DAYS
• Evolves after 1 week from the initial lesion.
• Clinical signs : ERYTHEMA[proliferation of
capillaries and increased formation of capillary
loops between rete pegs].
• Evidence of bleeding on probing.
• Increase in gingival fluid flow and number of
trans migrating leukocytes[also T lymphocytes].
• Amount of collagen destruction increases which
is related to Matrix Metalloproteins(MMP-2 and
MMP-9 production and activation)
• Fibroblasts show decreased capacity for collagen.

23. STAGE III : THE ESTABLISHED LESION
14-21 DAYS
• Predominance of plasma cells and B lymphocyte.
Localised gingival anoxmia[impaired venous return](bluish hue on the
reddened gingiva).
• Lesion is moderately to severely inflamed.
• Increased collagenolytic activity.
• Elevated levels of acid and alkaline phosphatase, cytochrome
oxidase,beta-glucuronidase,etc.
• May be reversed by successful periodontal therapy[plasma cells]

24. STAGE IV : THE ADVANCED LESION
• Extension of the lesion into the alveolar
bone.
• Phase of periodontal breakdown[bone
loss].
• All types of inflammatory cells.
• More plaque accumulation, higher IL-
1beta and lower IL-8 concentration at 28
days.
• Gingivitis progresses to periodontitis in
individuals who are susceptible.

25. CLINICAL FEATURES
OF GINGIVITIS

27. COURSE,DURATION AND TYPES
• MAY OCCUR WITH SUDDEN ONSET AND SHORT DURATION.
• Recurrent gingivitis may reappear.
• Chronic gingivitis is slow in onset and of long duration.
• Gingivitis may be LOCALISED(confined to a single tooth or group of teeth) OR
GENERALISED(involves whole mouth).
• MARGINAL(involves gingival margin and may include a portion of contiguous
attached gingiva), PAPILLARY(involves interdental papilla and extends to adjacent
portion of gingival margin), DIFFUSE(gingival margin+attached gingiva+interdental
papilla).

28. THE CHANGES IN GINGIVA DURING
INFLAMMATION CAN BE STUDIED
UNDER THE FOLLOWING HEADINGS:
• COLOR
• CONTOUR
• CONSISTENCY
• SIZE
• SHAPE
• SURFACE TEXTURE
• POSITION

29. COLOR CHANGES IN THE GINGIVA:
• Change in color of gingiva is an important clinical
sign of gingival disease.
• Normal color is “coral pink” produced by tissue
vascularity and modified by overlying epithelial
layers.
• Color changes vary with the intensity of
inflammation.
• Changes start in the interdental papillae and
gingival margin and spread to the attached gingiva.
• Tissue necrosis may produce a gray discoloration
in the gingiva.
• Endogenous oral pigmentation is caused by
melanin(systemic diseases like Addison’s
disease),bilirubin or iron.

30. CHANGES IN GINGIVAL CONTOUR:
Normally the gingiva has a festooned pattern that is lost due to inflammation.
Marginal gingiva is knife edged.
Primarily associated with inflammatory enlargement.
CHRONIC ENLARGEMENT :
• Etiologyprolonged exposure to
dental plaque(poor oral
hygiene,improper
restoration,anatomic
abnormalities).Also mouth
breathing.
• Clinical features :
1]slight ballooning of interdental
papilla and marginal gingiva.
2]generalised or localised.
3]a discrete sessile or pedunculated
mass.
4]slow growing and painless unless
complicated by acute infection.
5]lesions are soft and friable with a
smooth, shiny surface and bleed
easily.
ACUTE ENLARGEMENT :
• Etiologyresults from
bacteria carried deep into the
tissues when a forein
substance is forcefully
embedded in gingiva.
• Clinical features:
1]lesion is confined in gingiva.
2]generally known as gingival abscess
which is localised,painful,rapidly
expanding and has a sudden onset.
3]initially red swelling but within 24 to 48
hours it becomes fluctuant with a surface
orifice that may express purulent exudate.
4]adjacent teeth sensitive to percussion.

32. CHANGES IN CONSISTENCY OF THE
GINGIVA:
Normal consistency of gingiva is firm and resilient.
CHRONIC GINGIVITS:
• CLINICAL CHANGES:
1]soggy puffiness that pits on
pressure.
2]marked softness and friability
on exploration with probe.
3]pinpoint surface areas of
redness and desquamation.
• MICROSCOPIC FEATURES:
1]infiltration by fluid and cells of
inflammatory exudate.
2]degeneration of connective
tissue and epithelium.
3] rete pegs are elongated to
connective tissue.
ACUTE GINGIVITIS:
• CLINICAL CHANGES:
1]diffuse puffiness.
2]vesicle formation.
3]sloughing with grayish flakes of
particle debris adhering to tooth
surface.
• MICROSCOPIC FEATURES:
1]diffuse intercellular and
intracellular edema of inflammatory
origin with degeneration of nucleus
and cytoplasm and rupture of cell
wall.
2]necrosis with formation of
pseudomembrane composed of
bacteria,PMNLs and degenerated
epithelial cells in fibrinous
meshwork.

33. SIZE
Increased in disease.Known as gingival
enlargements.
SHAPE
Lost in disease.Recession,Clefts,crater
etc.

34. CHANGES IN SURFACE TEXTURE OF GINGIVA:
• The surface of normal gingiva exhibits
STIPPLING.
• These are numerous small depressions and
elevations which gives the tissue an orange
peel like appearance.
• Stippling is restricted to attached gingiva and
is predominantly localised to subpapillary area
but extends to variable degree in interdental
papilla.
• Absence of stippling may not indicate disease
as its presence may vary with age and among
individuals.
• In case of chronic inflammation there may be
loss of stippling(to confirm recheck at next
appointment always in natural light or in
reflected light).

35. CHANGES IN POSITION OF GINGIVA:
Normally 1mm above CEJ
• Gingival recession is the gradual apical shift in the position of
the gingiva.
• It is most likely the result of the cumulative effect of minor
pathologic involvement and repeated minor direct trauma.
• Gingival recession occurs due to faulty toothbrushing
technique,tooth malposition,friction from soft
tissues,gingival inflammation,abnormal frenal attachment
and iatrogenic dentistry.
• There is exposure of root surface so its becomes more
susceptible to caries,abrasion or erosion of cementum leaves
underlying dentine exposed leading to sensitivity,increases
plaque accumulation on irregular surface.

37. BLEEDING ON PROBING:
• Bleeding on probing is a valuable diagnosis of the
gingival inflammation as it preceeds even the color
change due to inflammation.
• It indicates an inflammatory lesion both in the
epithelium and connective tissue that exhibits specific
histologic differences compared with healthy gingiva.
• Indicates active tissue destruction.
• Absence of BOP is an excellent negative predictor of
future attachment loss.
• Widely used by clinicians and epidemiologists to
measure disease prevalence and progression,outcomes
of treatment and patient motivation.
• Bleeding indices have been developed.

38. GINGIVAL BLEEDING:
LOCAL FACTORS:
• CHRONIC AND
RECURRENT
BLEEDING:provoked by
mechanical
traumavessels are
damaged and ruptured
and hemostasis is
induceda fibrous clot is
formedbleeding recurs
when the area is again
irritated.
SYTEMIC FACTORS:
• Vitamin C deficiency,
platelet disorders,
coagulation defects
Hypertension.

39. TREATMENT OF GINGIVAL
INFLAMMATION:
PERFORM PATIENT EDUCATION AND MOTIVATION.
PROPER BRUSHING INSTRUCTION TO ELIMINATE
PLAQUE.
ANTIMICROBIAL MOUTH RINSE.
FOLLOW UP SESSIONS.
RECONTOURING OF RESTORATIONS OR PROSTHESIS TO ELIMINATE
PLAQUE RETENTIVE RECESS.