Gingival
Inflammation
Pathologic changes in gingivitis are associated with
the presence of microorganisms in gingival sulcus
Microorganisms
Collagenase, Hyaluronidase, Protease
Chondroitin sulfatase,Endotoxin
Cause
Damage to epithelial & connective tissue cells & to
Intercellular constituents like Collagen
Results in
Widening of spaces between junctional epithelial cells
Permit
Injurious agents derived from bacteria or
bacteria themselves gain access to the connective tissue
Microbial products activate monocytes and macrophages to
produce vasoactive substances such as
prostaglandin E2
Interferon
Interleukin-I
Sequence of events in the development of
gingivitis is analyzed in 3 different stages
Stage I Gingivitis The Initial Lesion
Stage II Gingivitis The Early Lesion
Stage III Gingivitis The Established Lesion
Stage IV The Advanced Lesion
Initial Lesion
Clinical Manifestations
Clinically initial response of the gingiva to bacterial
plaque is not visible
Initial Lesion
Microscopic changes
 Features of acute inflammation are seen in connective
tissue beneath junctional epithelium.
 Changes in blood vessel morphologic features
(Widening)
 Adherence of neutrophils to vessels (Margination)
 Leukocytes mainly PMN’s leave the capillaries by
migrating through walls (Diapedisis, Emigration)
 Exudation of fluid from the gingival sulcus
Initial Lesion
The character and intensity of the host response
determines whether the initial lesion resolves
rapidly or evolves into a chronic inflammatory
lesion
Initial Lesion
Early Lesion
Clinical Manifestations
 Erythema (proliferation
of capillaries increased,
formation of capillary
loops between retepegs
or ridges)
 Bleeding on probing
Early Lesion
Microscopic Changes
 Leukocyte infiltration (Lymphocyte-75%,
Neutrophils,Macrophages,plasmacells,& Mast cells.)
 All changes seen in initial lesion intensified
 J.E –densely infiltrated with neutrophils and starts to show
development of retepegs
Early Lesion
 Increase in amount of collagen destruction
 Main fiber groups affected –circular & Gingivodental
 PMN’s travel to epithelium and engulf bacteria
 Fibroblasts show cytotoxic alterations with a
decreased capacity for collagen production
Early Lesion
Established Lesion
Clinical Manifestations
 Localized gingival anoxemia
-blood vessels become engorged and congested ,venous
return impaired & blood flow becomes sluggish
-Extravasation of RBC’s into connective tissue and
breakdown of hemoglobin into its component pigments
(impose bluish hue)
 The established lesion can be described clinically as
moderately to severely inflamed gingiva
Established Lesion
Microscopic Changes
 Intense chronic inflammatory reaction is observed
 Increase in plasma cells
 Extra vascular immunoglobulins are present
 J.E develops widened intercellular spaces filled with
granular cellular debris
 J.E develops retepegs that protrude into the connective
tissue and the basal lamina is destroyed in some areas
Established Lesion
Enzyme histometry studies
Chronically inflamed gingiva has elevated levels of Acid phosphatase β-
Glucoronidase
β-Galactosidase esterase
amino peptidase cytochrome oxidase
elastase lactic dehydrogenase
aryul sulfatase
all of which result from bacteria and tissue destruction
Established Lesion
Stage IV – Advanced Lesion
Extension of inflammation into Alveolar bone characterizes a 4th
stage –
advanced lesion or phase of periodontal breakdown.
Advanced Lesion
Normal gingiva
Normal gingiva Gingivitis
Gingivitis
Colour
Colour Pale pink
Pale pink (melanin
(melanin
pigmentation common
pigmentation common
in certain groups)
in certain groups)
Reddish/bluish
Reddish/bluish
red
red
Size
Size Papillary gingiva fills
Papillary gingiva fills
interdental spaces;
interdental spaces;
marginal gingiva
marginal gingiva
forms knife edge with
forms knife edge with
tooth surface; sulcus
tooth surface; sulcus
depth
depth <
< 3 mm
3 mm
Swelling both
Swelling both
coronally and
coronally and
buccolingually;
buccolingually;
false pocket
false pocket
formation
formation
Consistenc
Consistenc
y
y
Firm
Firm Soft; pressure
Soft; pressure
induced pitting
induced pitting
due to edema
due to edema
Normal Gingiva
Normal Gingiva Gingivitis
Gingivitis
Contour
Contour Scalloped
Scalloped
troughs in
troughs in
marginal areas
marginal areas
rise to peaks in
rise to peaks in
interdental
interdental
areas
areas
Edema which
Edema which
blunts the
blunts the
marginal and
marginal and
papillary tissues
papillary tissues
leads to loss of
leads to loss of
knife edge
knife edge
adaptation.
adaptation.
Marginal
Marginal
swelling leads to
swelling leads to
less accentuated
less accentuated
scalloping
scalloping
Normal Gingiva
Normal Gingiva Gingivitis
Gingivitis
Tendency to
Tendency to
bleed
bleed
No bleeding to
No bleeding to
normal probing
normal probing
Bleeding on
Bleeding on
probing
probing


Gingival Inflammation in periodontitis ppt

  • 1.
  • 2.
    Pathologic changes ingingivitis are associated with the presence of microorganisms in gingival sulcus
  • 3.
    Microorganisms Collagenase, Hyaluronidase, Protease Chondroitinsulfatase,Endotoxin Cause Damage to epithelial & connective tissue cells & to Intercellular constituents like Collagen Results in Widening of spaces between junctional epithelial cells Permit Injurious agents derived from bacteria or bacteria themselves gain access to the connective tissue
  • 4.
    Microbial products activatemonocytes and macrophages to produce vasoactive substances such as prostaglandin E2 Interferon Interleukin-I
  • 5.
    Sequence of eventsin the development of gingivitis is analyzed in 3 different stages Stage I Gingivitis The Initial Lesion Stage II Gingivitis The Early Lesion Stage III Gingivitis The Established Lesion Stage IV The Advanced Lesion
  • 6.
    Initial Lesion Clinical Manifestations Clinicallyinitial response of the gingiva to bacterial plaque is not visible
  • 7.
    Initial Lesion Microscopic changes Features of acute inflammation are seen in connective tissue beneath junctional epithelium.  Changes in blood vessel morphologic features (Widening)  Adherence of neutrophils to vessels (Margination)  Leukocytes mainly PMN’s leave the capillaries by migrating through walls (Diapedisis, Emigration)  Exudation of fluid from the gingival sulcus
  • 8.
    Initial Lesion The characterand intensity of the host response determines whether the initial lesion resolves rapidly or evolves into a chronic inflammatory lesion
  • 9.
  • 10.
    Early Lesion Clinical Manifestations Erythema (proliferation of capillaries increased, formation of capillary loops between retepegs or ridges)  Bleeding on probing
  • 11.
    Early Lesion Microscopic Changes Leukocyte infiltration (Lymphocyte-75%, Neutrophils,Macrophages,plasmacells,& Mast cells.)  All changes seen in initial lesion intensified  J.E –densely infiltrated with neutrophils and starts to show development of retepegs
  • 12.
    Early Lesion  Increasein amount of collagen destruction  Main fiber groups affected –circular & Gingivodental  PMN’s travel to epithelium and engulf bacteria  Fibroblasts show cytotoxic alterations with a decreased capacity for collagen production
  • 13.
  • 14.
    Established Lesion Clinical Manifestations Localized gingival anoxemia -blood vessels become engorged and congested ,venous return impaired & blood flow becomes sluggish -Extravasation of RBC’s into connective tissue and breakdown of hemoglobin into its component pigments (impose bluish hue)  The established lesion can be described clinically as moderately to severely inflamed gingiva
  • 15.
    Established Lesion Microscopic Changes Intense chronic inflammatory reaction is observed  Increase in plasma cells  Extra vascular immunoglobulins are present  J.E develops widened intercellular spaces filled with granular cellular debris  J.E develops retepegs that protrude into the connective tissue and the basal lamina is destroyed in some areas
  • 16.
    Established Lesion Enzyme histometrystudies Chronically inflamed gingiva has elevated levels of Acid phosphatase β- Glucoronidase β-Galactosidase esterase amino peptidase cytochrome oxidase elastase lactic dehydrogenase aryul sulfatase all of which result from bacteria and tissue destruction
  • 17.
  • 19.
    Stage IV –Advanced Lesion Extension of inflammation into Alveolar bone characterizes a 4th stage – advanced lesion or phase of periodontal breakdown.
  • 20.
  • 21.
    Normal gingiva Normal gingivaGingivitis Gingivitis Colour Colour Pale pink Pale pink (melanin (melanin pigmentation common pigmentation common in certain groups) in certain groups) Reddish/bluish Reddish/bluish red red Size Size Papillary gingiva fills Papillary gingiva fills interdental spaces; interdental spaces; marginal gingiva marginal gingiva forms knife edge with forms knife edge with tooth surface; sulcus tooth surface; sulcus depth depth < < 3 mm 3 mm Swelling both Swelling both coronally and coronally and buccolingually; buccolingually; false pocket false pocket formation formation Consistenc Consistenc y y Firm Firm Soft; pressure Soft; pressure induced pitting induced pitting due to edema due to edema
  • 22.
    Normal Gingiva Normal GingivaGingivitis Gingivitis Contour Contour Scalloped Scalloped troughs in troughs in marginal areas marginal areas rise to peaks in rise to peaks in interdental interdental areas areas Edema which Edema which blunts the blunts the marginal and marginal and papillary tissues papillary tissues leads to loss of leads to loss of knife edge knife edge adaptation. adaptation. Marginal Marginal swelling leads to swelling leads to less accentuated less accentuated scalloping scalloping
  • 23.
    Normal Gingiva Normal GingivaGingivitis Gingivitis Tendency to Tendency to bleed bleed No bleeding to No bleeding to normal probing normal probing Bleeding on Bleeding on probing probing
  • 24.