This document discusses various types of gingival pathology including acute and chronic conditions, localized and generalized manifestations, and inflammatory and neoplastic enlargements. It reviews clinical findings such as bleeding, color changes, consistency changes, surface texture changes, position changes and contour changes. Specific acute gingival infections discussed include necrotizing ulcerative gingivitis, primary herpetic gingivostomatitis, and pericoronitis. Chronic conditions and enlargements covered include inflammatory, drug-induced, idiopathic, pregnancy-related, puberty-related, vitamin C deficiency, plasma cell, leukemia-associated, and neoplastic enlargements. Treatment approaches are presented for different conditions.

1. GINGIVAL PATHOLOGY
Presented by
Dr. Shraddha kode

2. 2

3. 3
COURSE AND DURATION
ACUTE
CHRONIC
RECURRENT
LOCALISED
GENERALISED
MARGINAL
DIFFUSE
PAPILLARY

4. 4

5. 1.
CLINICAL FINDINGS

6. 6
BLEEDING ON PROBING
Earliest sign
Objective sign
Widely used since PPD is of limited value
Histopathologic alterations
Cause
Depends on intensity of inflammation
Association with systemic diseases

7. 7
COLOR CHANGES
Factors
‘CORAL PINK’
Metallic pigmentation
Systemic factors
Endogenous Exogenous

8. 8
CHANGES IN CONSISTENCY
‘FIRM AND RESILIENT’
Calcified masses in gingiva
Toothbrushing effects

9. 9

10. 10
CHANGES IN SURFACE TEXTURE
ORANGE PEEL appearance called as STIPPLING
Location
Loss = Early sign of gingivitis
Manifestations

11. 11
CHANGES IN POSITION OF GINGIVA
Definition
Actual and apparent position
Location of gingiva rather than condition
Increase with age
Cumulative effect
Etiology
Predisposing factors

12. 12
CHANGES IN CONTOUR
STILLMAN’S CLEFTS McCALL’S FESTOONS

13. NON-PLAQUE INDUCED TRAUMATIC GINGIVAL LESIONS
13
PHYSICAL INJURIES
CHEMICAL INJURIES
THERMAL INJURIES
03
01 02

14. 2.
GINGIVAL INFLAMMATION

15. 15

16. Let’s review some concepts
Yellow
Is the color of gold, butter and
ripe lemons. In the spectrum of
visible light, yellow is found
between green and orange.
Blue
Is the colour of the clear sky
and the deep sea. It is located
between violet and green on
the optical spectrum.
Red
Is the color of blood, and
because of this it has
historically been associated
with sacrifice, danger and
courage.
16
Yellow
Is the color of gold, butter and
ripe lemons. In the spectrum of
visible light, yellow is found
between green and orange.
Blue
Is the colour of the clear sky
and the deep sea. It is located
between violet and green on
the optical spectrum.
Red
Is the color of blood, and
because of this it has
historically been associated
with sacrifice, danger and
courage.

17. “
17

18. 3.
GINGIVAL ENLARGEMENT

19. 19
Increase in the size of gingiva
Old terms
New terms
Classifications

20. 20
CHRONIC INFLAMMATORY GINGIVAL
ENALARGEMENT
‘Slight ballooning of interdental papilla
and marginal gingiva
Discrete, sessile, pedunculated mass
that resembles a tumor
Site
Slow growing masses – painless
Painful ulceration in between fold and
adjacent gingiva
Etiology: Prolonged exposure to dental
plaque
Histopathology
Exudative
Proliferative

21. 21
ACUTE INFLAMMATORY GINGIVAL
ENALARGEMENT
Localised painful rapidly expanding
lesion that has a sudden onset
Site : Marginal gingiva and interdental
papilla
Early stage : Red swelling with smooth
shiny surface
Within 24 to 48 hours lesion becomes
fluctuant and pointed with a surface
orifice from which purulant exudate is
expressed
Etiology
Histopathology
GINGIVAL ABSCESS

22. 22
ACUTE INFLAMMATORY GINGIVAL
ENALARGEMENT
Involves surrounding periodontal
tissues
Also called lateral or parietal abscess
Etiology : Incomplete removal of
calculus, extension of inflammation from
periodontal pocket into supporting
tissues, drainage into pocket space is
impaired, perforation of lateral wall of
pocket in endodontic therapy
Histopathology
PERIODONTAL ABSCESS

23. 23
Drugs
Pre of inflammation : Painless beadlike
enlargement of interdental papilla
extending to B/L gingiva. Covers crown
surface and interferes with occlusion
Ab of inflammation : Mulberry shaped,
firm, pale pink, resilient with minutely
lobulated surface and no tendency to
bleed. Presence of enlargement makes
plaque control difficult
DRUG-INDUCED GINGIVAL
ENALARGEMENT

24. 24
DRUG-INDUCED GINGIVAL
ENALARGEMENT
Site : More severe in maxillary and mandibular anterior region
Occurs where teeth are present and disappears in areas where teeth
have been extracted
Hassell and colleagues : HYPOTHESIS : Non-inflamed gingiva
fibroblasts are less active and do not respond to these drugs whereas in
the inflamed state fibroblasts are active due to the presence of
inflammatory mediators. Therefore, inflammation is a prerequisite for the
development of enlargement.
Histopathology : Hyperplasia of CT and epithelium. Acanthosis of
epithelium with deep rete pegs. Densely arranged collagen bundles

25. 25
IDIOPATHIC GINGIVAL ENALARGEMENT
Rare condition of undetermined cause
Clinical features : Pink, firm, leathery,
minutely pebbled surface
Site : AG + IP + MG in contrast to
drug induced (GM +IP)

26. 26
IDIOPATHIC GINGIVAL ENALARGEMENT
Etiology : Cause is unknown. Some may have hereditary
basis but the genetic mechanisms involved are not well
understood
Histopathology : Bulbous increase in CT which is
avascular and consists of densely arranged collagen
bundles and fibroblasts. Surface epithelium gets thickened
and acanthotic with elongated rete pegs

27. 27
Vestibulum congue
manifestation of
the systemic
disease
independently of
inflammatory
status of the
gingiva.
magnification
of an existing
inflammation
initiated by
dental plaque
Vestibulum congue
ENLARGEMENT ASSOCIATED WITH
SYSTEMIC DISEASE
HORMONAL
NUTRITIONAL
NOT IDENTIFIED
NEOPLASTIC
CONDITIONED GINGIVAL
ENLARGEMENT
Bacterial plaque is
necessary for the initiation
but not the sole determinant

28. 28
ENLARGEMENT IN PREGNENCY
Increased inflammatory response to
dental plaque. Why??
Marginal : Bright red/magenta, soft
friable, smooth shiny surface. Bleeding
occurs spontaneously
Tumor like : Discrete, mushroom like
flattened spherical mass, dusky red,
deep red pinpoint markings. Usually
appears after 3rd month of pregnancy
Microbiota : Increase in P.intermedia

29. 29
ENLARGEMENT IN PREGNENCY
Histopathology : Also called as
angiogranuloma. Consists of central
mass of CT with engorged capillaries and
moderate fibrous stroma with edema and
chronic inflammatory inflitrate

30. 30
ENLARGEMENT IN PUBERTY
Site : Marginal gingiva with prominent
interproximal papillae
Clinical features similar with chronic
inflammatory gingival disease
How different??? Tendency to recur in
the presence of scant plaque deposits
Microbiota : Capnocytophage, P.
Intermedia and P. nigrescens

31. 31
ENLARGEMENT IN VITAMIN C
DEFICIENCY
Modify the response of gingiva to
plaque
Does not cause inflammation but
hemorrhage, collagen degeneration and
edema. Hence inflammation is
exaggerated and massive GE seen in
scurvy
C/F: Bluish red, soft friable, smooth
shiny, bleeding on slight provocation and
surface necrosis with pseudomembrane
formation

32. 32
PLASMA CELL GINGIVITIS
Allergic in origin to components in
chewing gum, dentrifice, etc
Cessation of exposure to allergen :
Resolution of lesion
Site: Mild marginal gingival
enlargement that extends to
attached gingiva
C/F : Red friable granular gingiva
which bleeds easily

33. 33
NONSPECIFIC CONDITIONED ENLARGEMENT
( PYOGENIC GRANULOMA)
Tumor-like enlargement
Exaggerated conditioned response to
minor trauma
Exact nature not known
Similar in C/F and microbiological
features with GE of pregnancy

34. 34
LEUKEMIA ASSOCIATED GINGIVAL
ENLARGEMENT
Bluish red gingiva with a shiny surface
Moderately firm consistency with a
tendency towards friability and
hemorrhage
Often associated with acute leukemia
(seldom with chronic)
Histopathology: Dense mass of
immature and proliferating leukocytes

35. 35
WEGENER’S GRANULOMATOSIS
Immunologically mediated tissue injury
Rare
Acute granulomatous lesions of
respiratory tract
O/E : Oral mucosal ulceration, gingival
enlargement, teeth mobility, exfoliation of
teeth, delayed healing
GRANULOMATOUS DISEASES
STRAWBERRY GINGIVITIS

36. 36
SARCOIDOSIS
Red, smooth, painless gingival
enlargement
Unknown etiology
Involves almost any organ including
gingiva

37. 37
NEOPLASTIC ENLARGEMENT
EPULIS : Discrete tumours or
tumourlike masses (generic term)
FIBROMA : Slow growing spherical
tumours (firm nodular and soft vascular),
usually pedunculated
BENIGN TUMOURS

38. 38
NEOPLASTIC ENLARGEMENT
PGCG : Interdentally or at gingival margin
PAPILLOMA : Benign proliferation of
surface epithelium, wart-like or cauliflower
like protruberance (irregular surface)
CGCG : Giant cell lesion of jaw, creates
deformity of jaw
BENIGN TUMOURS

39. 39
NEOPLASTIC ENLARGEMENT
SQUAMOUS CELL CARCINOMA : Most common
MALIGNANT MELANOMA
MALIGNANT TUMOURS

40. 40
FALSE ENLARGEMENT
Not true enlargement
Appears due to increase in size of underlying osseous/dental
tissues
Tori or exostoses
Pagets disease
Fibrous dysplasia
Cherubism, etc
Labial gingiva may show bulbous
marginal distortion due to superimposition
of bulk of gingiva on enamel in gingival
half of crown – Persists till JE has
migrated from enamel to CEJ
DEVELOPMENTAL ENLARGEMENT

41. TREATMENT
41

42. 42
CHRONIC INFLAMMATORY ENLARGEMENT
SRP
No shrinkage
Fibrous component
present
No access to depositsSURGICAL REMOVAL
GINGIVECTOMY FLAP OPERATION
Soft and friable
gingiva
Firm tissue to adequately
perform incision
Gingivectomy if performed
removes all AG creating
mucogingival problem

43. 43
DRUG INDUCED INFLAMMATORY ENLARGEMENT
SUBSTITUTION OF DRUG
PHENYTOIN : Carbamazepine/
Valproic acid
NIFEDIPINE : Diltiazem/
Verampamil
CYCLOSPORINE : TacrolimusALLOW 6-12 MONTHS HEALING PERIOD
PLAQUE CONTROL
SURGICAL TREATMENT
PERSISTS
GINGIVECTOMY FLAP OPERATION
Small areas (< 6
teeth)
Abundance of
keratinised tissue
Horizontal bone
loss Large areas (> 6
teeth)
Limited keratinised
tissue
Osseous defects

44. 44
LEUKEMIC GINGIVAL ENLARGEMENT
CONSENT FROM HEMATOLOGIST
SRP UNDER TOPICAL LA
SUPERFICIAL SCALINNG + PLAQUE CONTROL
DEEPER SCALINGS AT SUBSEQUENT VISITS
ANTIBIOTICS BEFORE AND 48 HOURS AFTER TREATMENT TO
REDUCE THE RISK OF INFECTION

45. 45
GINGIVAL ENLARGEMENT IN PREGNANCY
ELIMINATE LOCAL IRRITANTS
MARGINAL AND INTERDENTAL
GINGIVA
TUMOUR LIKE GINGIVAL
ENLARGEMENT
SCALING AND CURETTAGE
SURGICAL EXCISION
SRP Interfere with
mastication
Produce esthetic
disfigurement
WHEN TO TREAT???
Prevent gingival disease before it
occurs
Treat gingival disease before it
worsens

46. 46
GINGIVAL ENLARGEMENT IN PUBERTY
SRP + PLAQUE CONTROL
SEVERE CASES
SURGICAL REMOVAL

47. 47
PERIODONTAL ABSCESS
DRAINAGE THROUGH POCKET DRAINAGE THROUGH EXTERNAL
INCISION
LA INJECTED AROUND PERIPHERY
INSERT CURETTE TO DISTEND THE
POCKET WALL FOR DRAINAGE
CURETTAGE
VERTICAL INCISION OVER MOST
FLUCTUANT PART OF SWELLING
INSERT CURETTE TO ELEVATE
TISSUE AND CREATE DRAINAGE
PUSH EXTERNAL ASPECT TO DRAIN
PURULENT MATERIAL
APPROXIMATE WOUND EDGES
ANTIBIOTICS &
ANALGESICS

48. 48
GINGIVAL ABSCESS
LA INJECTED AROUND PERIPHERY
Impacted foreign
object
FLUCTUANT AREA INCISED AND
CLEANSE WITH WARM WATER
WIDEN TO PERMIT DRAINAGE
APPROXIMATE WOUND EDGES

49. 4.
ACUTE GINGIVAL INFECTIONS

50. 50
NECROTISING ULCERATIVE
GINGIVITIS
Impaired host response
Term ‘acute’ is a misnomer since no
chronic form
Inadequate rest, poor nutrition, tobacco
use and psychological stress
O/E : Punched out, crater like
depressions at the crest of interdental
papillae that extend to marginal gingiva.
Rarely to attached gingiva
Covered by gray,
pseudomembranous slough
Spontaneous gingival
hemorrhage, fetid odour,
salivation

51. 51
NECROTISING ULCERATIVE
GINGIVITIS
No periodontal pocket
formation because necrotic
changes involve the junctional
epithelium. A viable junctional
epithelium is required for pocket
formation
Rare in edentulous mouth but
isolated spherical lesions are
occasionally seen on soft plate
Oral symptoms : Lesions are
sensitive to touch, constant
radiating, gnawing pain, metallic
foul taste, pasty saliva
Local lymphadenopathy, slight
elevation of temperature, high
fever, increased pulse rate,
leukocytosis, loss of appetite,
malaise

52. 52

53. 53
Histopathology : Surface
epithelium is destroyed and
replaced by a meshwork of fibrin,
necrotic, epithelial cells, PMN’s and
micro-organisms. This zone is the
pseudomembrane
CT is hyperemic. Engorged
capillaries and dense infiltrate of
PMN’s

54. 54
NUG is transmissible not communicable. Transmissible is the
maintenance of an infectious agent in successive passages through
a susceptible animal host. Communicable means the capacity for
maintenance of infection by natural modes of spread (direct contact
through drinking water, food, eating through utensils via airborne
route or means of arthropod vectors.
The occurence of NUG in epidemic outbreaks does not mean it is
contagious. The group may be afflicted due to common predisposing
factors rather than spread from person to person.

55. 55
PRIMARY HERPETIC
GINGIVOSTOMATITIS
HSV-1
Infants and children < 6 years. Seen in
adults also
Primary infection : asymptomatic –
latent HSV in neuronal ganglia
Secondary manifestations due to stimuli
like sunlight, trauma, fever and stress
Secondary manifestations : herpes
labialis, herpes genitalis, herpes
stomatitis, ocular herpes, herpes
stomatitis

56. 56
PRIMARY HERPETIC
GINGIVOSTOMATITIS
C/F : Diffuse erythematous shiny
involvement of gingiva and oral mucosa
Oral symptoms : Generalised soreness
which interferes with eating, drinking and
oral hygiene. Ruptured vesicles are focal
sites of pain.
Systemic : Cervical adenitis, high fever,
general malaise
Histopathology : Virus targets
epithelial cells = ballooning
degeneration = Tzank cells

57. 57
PERICORONITIS
Inflammation of gingiva in relation to
crown of an incompletely erupted tooth
OPERCULUM – Ideal area for bacterial
growth
O/E : Red swollen suppurating lesion
that is tender with radiating pain. Foul
taste and inability to close jaw,
lymphadenitis, trismus & systemic : fever
malaise and leukocytosis

58. TREATMENT
58

59. 59
NECROTISING ULCERATIVE GINGIVITIS
GENERAL STATUS ABOUT DIET,
STRESS, RECENT ILLNESS, PALPATION
OF LYMPH NODES
UNDER LA SWAB WITH COTTON PELLET
TO REMOVE PSEUDOMEMBRANE AND
NONATTACHED DEBRIS
REMOVE SUPERFICIAL CALCULUS WITH
ULTRASONICS
SUBGINGIVAL SCALING
CONTRAINDICATED

60. 60
EXTENSIVE PROCEDURES POSTPONED
UNTIL PATIENT IS SYMPTOMFREE FOR 4
WEEKS (to reduce exacerbation of acute
symptoms)
RINSE MOUTH EVERY 2 HOURS WITH
GLASSFUL OF EQUAL MIXTURE OF
WARM WATER AND 3%H2O2.
SYSYTEMIC SYMPTOMS : ANTIBIOTICS
SUBSEQUENT VISITS : SRP + PLAQUE
CONTROL till patient is symptomfree and
acute symptoms subside

61. 61
ACUTE HERPETIC GINGIVOSTOMATITIS
SYSTEMIC ACYCLOVIR
EXTENSIVE PERIODONTAL THERAPY
SHOULD BE POSTPONED UNTIL
SYMPTOMS SUBSIDE
REDUCE GINGIVAL
INFLAMMATION
SRP
PREVENT/ LESSEN
SEVERITY
COPIOUS FLUID INTAKE
SYSTEMIC ANTIBIOTCS
FOR SYSTEMIC
COMPLICATIONS
Clinician may
get infected :
Herpetic whitlow

62. 62
ACUTE PERICORONITIS
FLUSH THEAREA WITH WARM WATER
TO REMOVE DEBRIS AND EXUDATE
ELEVATE FLAP GENTLY WITH A SCALER
TO REMOVE UNDERLYING DEBRIS
IF GINGIVAL FLAP IS SWOLLEN
INCISION AND REMOVE TISSUE DISTAL
TO TOOTH AND FLAP ON OCCLUSAL
SURFACE TO PREVENT POCKET ON
DISTAL ASPECT
Antibiotics
After acute
symptoms
subside, decide
to retain or
extract the tooth

63. 5.
Desquamative gingivitis

64. 64
LICHEN PLANUS
Immunologically mediated
mucocutaneous disorder in which T
lymphocytes play an important role
Types : Reticular, patch, atrophic,
bullous, erosive
C/F : Reticular – Interlacing white lines
with erythematous background. Erosive
is associated with pain. Atrophic –
Erythematous patchy distribution

65. 65
Histopathology : 3 main features : Hyperkeratosis or parakeratosis,
hydropic degeneration of basal layer, dense bandlike infiltrate of T
lymphocytes in lamina propria
Treatment :
Keratotic lesions are asymptomatic. Require evaluation every 6-12
months to monitor for suspicious clinical changes
Erosive or erythematous lesions are treated with high potent topical
corticosteroids (0.05% triamcinoline acetonide). Severe cases
intralesional injection of triamcinoline acetonide (10 to 20mg) / 40mg
Prednisone daily for 5 days followed by 10mg to 20mg daily for 2
weeks
Since candidiasis is associated with symptomatic lichen planus and
topical steroid therapy promotes fungal growth, include antifungals

66. 66
PEMPHIGOID
BULLOUS PEMPHIGOID CICATRICAL PEMPHIGOID
NON-SCARRING DISEASE
AFFECTS SKIN
SCARRING DISEASE
AFFECTS MUCOUS
MEMBRANE

67. 67
BULLOUS PEMPHIGOID
Chronic, autoimmune, subepidermal bullous
disease with tense cutaneous bullae that rupture
and become flaccid
Oral involvement is common
Histopathology : Subepithelial (not intraepithelial)
vesicles. Epithelium separates from CT at BM zone
Oral lesions occur in 40% cases
Treatment : Moderate dose of systemic
Prednisone. High potency topical steroids or
tetracycline when high doses of steroids are
required or steroid alone fails to control the disease

68. 68
CICATRICAL (MUCOUS
MEMBRANE) PEMPHIGOID
Chronic autoimmune disorder
Involves oral cavity, conjunctiva,
mucous membrane of nose, eosophagus,
etc
Ocular lesions: Adhesions of eyelid to
eyeball(symblepharon), adhesions of the
edges of eyelids(ankylodepharon) results
in narrowing of palpebral fissure
Small vesicular lesions may develop in
conjunctiva producing scarring, corneal
damage and blindness

69. 69
CICATRICAL (MUCOUS
MEMBRANE) PEMPHIGOID
Oral lesions: Erythema, desquamation,
ulceration and vesiculation of attached
gingiva. Bullae have thick roof and rupture
within 2-3 days leaving irregular areas of
ulceration
Histopathology : Subepithelial vesiculation,
separation of epithelium and CT at BM zone,
inflammatory infiltrate in CT
Treatment: Localised cases: Topical steroids
(0.05% Fluocinonide and 0.05% Clobetasol
propionate) Severe & ocular cases: Systemic
steroids

70. 70
PEMPHIGUS VULGARIS
Autoimmune disorder that produces
cutaneous and mucous membrane blisters
Cell-cell adhesion damaged by circulating
autoantibodies
In 60% of patients – oral lesions are the
first sign of the disease
Diff from bullous and cicatrical
pemphigoid??? Acantholysis
Oral lesions: small vesicles to
large bullae, when bullae rupture they leave
large areas of ulceration

71. 71
PEMPHIGUS VULGARIS
Histopathology : Intraepithelial
separation (acantholysis) results in the
formation of a bulla, superficial cell layers
of epithelium are lost leaving only the
basal cells attached to the lamina propria
= tombstone appearance, inflammatory
cell infiltrate in CT
Treatment : Systemic corticosteroids
with or without the addition of other
immunosuppressive agents

72. 72
ERYTHEMA MULTIFORME
Acute bullous and macular inflammatory
mucocutaneous disease that affects mainly
young adults
Cause: herpes simplex infection and drug
reactions
Immune complex vasculitis - complement
fixation that leads to the leukocytoclastic
destruction of vascular walls and small
vessel occlusion - ischemic necrosis of the
epithelium and underlying connective tissue
-Target or “iris” lesions with central clearing

73. 73
ERYTHEMA MULTIFORME
Mild condition (erythema multiforme minor) or a severe and possibly
life-threatening condition (erythema multiforme major or Stevens–
Johnson syndrome)
Oral lesions : multiple large, shallow, painful ulcers with an
erythematous border – Impaired chewing and swallowing
Treatment – No specific symptom. Mild cases - systemic and local
antihistamines together with topical anesthetics and the debridement of
lesions. Severe - corticosteroids are considered the drug of choice

74. 74
LUPUS ERYTHEMATOSUS
SYSTEMIC
Affects vital organs like kidneys and heart
and skin and mucosa
Classic cutaneous lesions characterized
by the presence of a rash on the
malar area with a butterfly distribution
Oral lesions: Ulcerative and similar to
lichen planus
CHRONIC
No systemic signs. Lesions limited to skin
and mucosal surfaces.
Also called discoid lupus erythematosus
SYSTEMIC
CHRONIC CUTANEOUS
SUBACUTE CUTANEOUS

75. 75
LUPUS ERYTHEMATOSUS
Oral lesions: Lichen planus like plaques
on the buccal mucosa, palate and gingiva
Histopathology: Hyperkeratosis,
alternating acanthosis and atrophy, and
hydropic degeneration of the basal layer of
the epithelium. The lamina propria exhibits
a chronic inflammatory cell infiltrate
SUBACUTE
Similar to DLE but lack development of
scarring and atrophy
Treatment : Topical steroids
to nonsteroidal
anti-inflammatory drugs , for
severe systemic involvement,
moderate to high doses of
prednisone along with
immunosuppressive drugs

76. CONCLUSION!
76
Gingival disease can have multiple origins and can be a manifestation of a wide
variety of systemic disease. Gingival tissue inflammation is the most common
lesion encountered in the clinical setting and may be the first symptom in many
types of disease. Gingivitis has important diagnostic relevance and it is important
for clinicians to find out possible causes for correct diagnosis and treatment.

77. thank you