This presentation including the information about various types of gingival enlargment, it's mechanism and treatment.

1. GINGIVAL ENLARGMENT
AND IT’S TREATMENT
Prepared By: Dr. Riya Shah
2nd year PG in Periodontology

2. CONTENTS
◉ Introduction
◉ Classification
◉ Indices
◉ Inflammatory Enlargement
◉ Drug-induced enlargement
◉ Enlargements associated with systemic diseases
◉ Neoplastic enlargement
◉ Idiopathic gingival enlargement
◉ False enlargement
◉ Conclusion
◉ References
2

3. INTRODUCTION
3
Gingival
enlargement
Gingival
hyperplasia
Gingival
Hypertrophy
Atrophy

4. According To Etiologic Factors And Pathologic Changes As Follows:
Gingival
enlargement
Inflammatory
enlargement
Chronic Acute
Drug-
induced
enlargement
Enlargements
associated with
systemic diseases
A. Conditioned
enlargement
Pregnancy Puberty
Vitamin C
deficiency
Plasma
cell
gingivitis
Nonspecific
conditioned
enlargement
B. Systemic
diseases causing
gingival
enlargement
Leukemia
Granulomat
ous diseases
Neoplastic
enlargement
(gingival tumors)
Benign
tumors
Malignant
tumors
False
enlargement
4

5. According location and distribution,
gingival enlargement is designated as
follows:
Localized Generalized
Papillary
5
Diffuse DiscreteMarginal

6. Babcock and Nelson (1964)
Minimal: No
hyperplasia, or as
little as to be
dubious.
Moderate: Definite
hyperplasia of
gingiva, with
encroachment on the
clinical crown of the
teeth, but with no
interference of
function.
Severe: Gingival
enlargement
interfering with
function.
6
INDICES

7. Degree of gingival hyperplasia according to modified index
by Angelopoulos & Goaz 1972
Grade Hyperplasia Size Tooth
coverage
0 No Normal No
1 Minimal <2 mm Cervical 3rd or
less
2 Moderate 2-4 mm Middle 3rd
3 Severe >4 mm Morethan
2/3rd
7

8. INDICES
Grade 0 - No signs of gingival
enlargement
Grade 1 – Enlargement confined
to IDP
Grade 2 - Enlargement involves
IDP & marginal gingiva
Grade 3 - Enlargement covers
three quarters / more of crown
Bokenkamp &
Bohnhorst 1994
8

9. NEW CLINICAL INDEX FOR DRUG INDUCED GINGIVAL
OVERGROWTH by INGLES IN 1999
9
1 Noovergrowth; firm adaptation of the attached gingiva to the
underlying alveolar bone.
2 There is slight stippling; there is no granular appearance
3 A knife-edged papilla is present toward the occlusalsurface.
4 There is no increase in density or size of thegingiva.
1 Early overgrowth, as evidenced by an increase in density of the
gingiva with marked stippling and granularappearance.
2 The tip of the papilla isrounded.
3 The probing depth is less than or equal to 3mm.
G
R
A
D
E
0
G
R
A
D
E
1

10. 10
G
R
A
D
E
2
G
R
A
D
E
3
1 Moderate overgrowth, manifested by an increase in the size of the papillaand/or
rolled gingival margins.
2 The contour of the gingival margin is still concave or straight.
3 Gingival enlargement has a bucco-lingual dimension of up to 2 mm,measured
from the tip of the papillaoutward.
4 The probing depth is equal to or less than 6mm.
5 The papilla is somewhat retractable.
1 Marked overgrowth, represented by encroachment of the gingiva onto the
clinical crown.
2 The contour of the gingival margin is convex rather than concave.
3 Gingival enlargement has a bucco-lingual dimension of approximately 3 mmor
more, measured from the tip of the papillaoutward.
4 The probing depth is greater than 6 mm.
5 The papilla is clearly retractable.

11. 11
1 Severe overgrowth, characterized by a profound thickening of the gingiva
2 Alarge percentage of the clinical crown iscovered.
3 Same as for grade 3: The papilla is retractable, the probing depth isgreater
than 6 mm, and the buccolingually dimension is approximately 3mm.
G
R
A
D
E
4

12. Chronic
enlargement
Acute
enlargement
12
1. INFLAMMATORY ENLARGEMENT
Gingival abscess
Periodontal abscess

13. Acute inflammatory enlargement
Trauma
Mechanical
Chemical
Physical
Irritation
Mouth
Breathing
Impacted
Food
Items
Poor Oral
Hygiene
Foreign
Substance
13

14. Gingival Abscess
14

15. PERIODONTAL ABSCESS
15

16. Etio-pathogenesis
PERIODONTITIS
RELATED
Extension of infection
from PD pocket
Lateral extension of
inflammation
Pocket with a tortuous
course
Incomplete removal of
calculus
NON PERIODONTITIS
RELATED
Impaction of foreign
bodies
Endodontic perforation
Lateral cyst infection
Factors affecting
morphology of root
16

17. TREATMENT
◉ For the treatment of gingival abscess, should include the elimination of
foreign object, through careful debridement( Abrams 1983), drainage
through the sulcus with probe, rinsing with warm saline and follow-up
after 24-48 hrs.
◉ For the treatment of periodontal abscess, a similar protocol is : drainage
through the pocket, scaling, compression and debridement of soft tissue
wall and irrigation with sterile saline. 1 week later, the definitive
treatment should be carried out( Ammons1996).
◉ The combination of incision and drainage with the systemic
administration of penicillin has been considered as “often
successful”(Genco 1991).
17

18. ANTIBIOTIC OPTIONS FOR PERIODONTAL INFECTIONS
• 1 g loading dose, then 500 mg three times a
day for 3 days.
• Reevaluation after 3 days to determine need
for continued or adjusted antibiotic therapy.
AMOXICILLIN,
500 mg
• Clindamycin
• 600 mg loading dose, then 300 mg four times
a day for 3 days.
• Azithromycin
• 1 g loading dose, then 500 mg four times a
day for 3 days.
PENICILLIN
ALLERGY
18

19. Etiology
Plaque
accumulation &
retention
Poor oral
hygiene
Anatomic
abnormalities
Improper
restoration
Orthodontic
appliances
Malocclusion
Chronic inflammatory enlargement
19

20. Clinical Features
20

21. 21
Histopathology
•Lesions that are deep red or bluish red are soft and
friable with a smooth, shiny surface, and they bleed
easily.
•They also have a preponderance of inflammatory
cells and fluid, along with vascular engorgement,
new capillary formation, and associated
degenerative changes.
• Lesions that are relatively firm, resilient, and pink
have a greater fibrotic component, with an
abundance of fibroblasts and collagen fibers

22. TREATMENT
22
Two techniques available for
this purpose are-
Gingivectomy
Flap operation.
Selection of the technique
depends on the
•Clinical features
•Etiology
•size
•character of the tissue
•Extent & severity of enlargement

23. Drug-Induced
Overgrowth of Gingiva
[DIGO]

24. Drugs associated with gingival overgrowth
Anticonvulsants
Phenytoin
Sodium valproate
Phenobarbitone
Vigabatrin
Immunosuppressant
Cyclosporin
Calcium channel
blockers
Dihydro pyridines
Nifedipine
Felopdipine
Amlodipine
Phenyl
alkylamine
Verapamil
Benzothiazepine
Diltiazem
24

25. Prevalence of DIGO
◉ 50 % - phenytoin
( Angelopoulous & Goaz1972)
◉ 30% - Cyclosporine
◉ 10% -Nifedipine
(Seymour 1987 , Barclay 1992)
◉ In India, 57% of epileptic children - aged 8-13 years-
phenytoin therapy
Prasad et al 2002
25

26. ANTICONVULSANTS
27
HYDANTOINS SUCCINIMIDES VALPROIC ACID
Ethotoin (Peganone®)
Mephenytoin (Mesantoin®)
Phenytoin (Dilantin®)
Ethosuximide (Zarontin®)
Methsuximide (Celontin®)
Phensuximide (Milontin®)
Depakene (Depakote®)
Kimball 1939 - First to report gingival enlargement with chronic usage
of Phenytoin.
Children
Adolescents Adults
Anterior region
PosteriorRegion
26

27. 29
Immunosuppressant (Cyclosporin – A)
First isolated in
Switzerland – 1970,
Jean Borel
First case reported by
- Rateitschak
Pluss,1983
Suppress some
humoral immunity (B -
lymphocytes) and to a
much greater extent,
cell-mediated
immunity (T-
lymphocytes)
Inhibits IL-2
synthesis
and release.
27

28. CALCIUM CHANNEL BLOCKERS
31
Dihydropyridine
derivatives
Benzothiazine derivatives Phenylalkylamine
derivatives
Amlodipine
(Lotrel®, Norvasc ®)
Diltiazem
(Cardizem®, Dilacor®,
Tiazac®)
Verapamil HCL
(Calan®, Isoptin®,
Verelan®)
Felodipine (Plendil®)
Nifedipine
(Adalat®, Procardia ®)
Nimodipine (Nimotop®)
Lederman et al, 1984 - First to report gingival enlargement with
chronic usage of Nifedipine
28

29. CLINICAL FEATURES OF DRUG
INDUCED GINGIVAL
ENLARGEMENT

30. CLINICAL FEATURES OF DRUG INDUCED
GINGIVAL ENLARGEMENT
• Growth starts as:
o Apainless beadlike enlargement of the interdentalpapilla
o Extends to facial &lingual gingival margins.
• On progression:
o Marginal &papillary enlargementsunite
o Develop into massive tissue fold covering large partof crown
o Sometimes it may Interfere with occlusion
• When uncomplicated by inflammation:
o Lesionis mulberry shaped
o Firm and resilient
o Pale pink
o Minutely lobulated surface
o Notendency to bleed 30

31. • Enlargement characteristically appears to:
o Project from beneath the gingival margin
o From which it is separated by a linear groove.
• Enlargement is usually generalized
• More severe in maxillary & mandibular anterior regions.
• Occurs in areas in which teeth are present & not in edentulous spaces.
• Plaque control becomes difficult due to the enlargement
Resulting
Secondary inflammatory process
(Further complicates the gingival overgrowth caused by the drug)
31

32. Resultant enlargement
Increase in size caused by the drug + plaque induced inflammation.
• Drug-induced enlargement may occur in mouths:
o With little or no plaque
o May be absent in mouths with abundant deposits.
• Enlargement is:
o Chronic
o Slowly increases in size.
o When surgically removed, it can be re-occurs.
o Spontaneous disappearance occurswithin a few months
after discontinuation of the drug. 32

33. • Pronounced hyperplasia of the
connective tissue & epithelium.
• Acanthosis of the epithelium.
• Elongated rete pegs extending deep
into the connective tissue.
• Densely arranged collagen bundles.
• Increase in the number of fibroblasts &
new bloodvessels.
33
HISTOPATHOLOGY

34. PATHOGENESIS OF DIGO
Pathogenesis
Increased collagen
synthesis
Decreased collagen
degradation
• Extracellular pathway
• Intracellular pathway
Combination
43
34

35. DRUG METABOLITES (Phenytoin, Nifedipine, Cyclosporin)
• Increased collagen production
• Increased extracellular matrix synthesis
T- lymphocytes
TH2response
IL-13,1,4
Elevated level
of Cytokines
Macrophages
TGF-β
CTGF
FGF-2
PDGF
INCREASED COLLAGEN SYNTHESIS
FIBROBLASTS
Proliferation of highly active fibroblasts
35
elevated levels of collagen synthesis.

36. DECREASED COLLAGEN DEGRADATION
Decreased production of active
collagenase
Decreased uptake of Ca2+ dependant
folic acid byfibroblasts
Decreased influx of Ca2+ into fibroblast
Disturbance in calcium homeostasis
Decreased MMP 1, 2 & 3 mediated
collagen degradation
Increased expression of TIMP
36
Drugs associated with gingival enlargement
(Anticonvulsants, Immunosuppressants, CCB, others)

37. Phenytoin induced
Re
Dec
with Fibroblast
Decreased Endocytosis
is
Increased number of fibroblasts
Extracellular matrix accumulation
Kantarci PA,2007
Phenytoin induced
duced α2β1 Integrin expression on Decreased Fibroblast apoptos
fibroblasts
α 2β1 receptors
Contribute to fibrosis
reased adhesion of Type 1 Collagen
INTRACELLULAR PATHWAY
Decreased collagen phagocytosis
• Phenytoin induced
• reduced α2β1 Integrin expression on fibroblasts
• decreased adhesion of Type 1 Collagen with Fibroblast
• Decreased Endocytosis Decreased phagocytosis of Type
1 collagen
Fibroblast Apoptosis
• Phenytoin induced
• Increased keretinocyte life span
• Decreased or inhibit Fibroblast apoptosis
• Increased number of fibroblasts Extracellular
matrix accumulation

38. Joiceetal:Phenytoin Induced Gingival overgrowth: Areview of the cellular, molecular and inflammatory
Modification of immune
cells by drug metabolites
Imbalance in production ofcytokines
and other mediators
Increased TGFβ1,FGF-2
and others
TGFβ1
Increases synthesis and
deposit of collagen.
Regulation ofTIMP.
Reduction of collagen
phagocytosis.
Myofibroblasts are
associated with
later stages of
tissue turnover.
4838

39. Treatment of DIGO

40. 40
Decision tree for treatment
of drug-induced gingival
enlargements.

41. Management of drug-induced gingival overgrowth include:-
Non-Surgical
Approaches
Scaling & Root
planning
Antiseptic
mouthwashes
Systemic
antibiotics
Change in
medication
Surgical
approaches
Scalpel
Gingivectomy
Electrosurgery
Laser Gingivectomy
Flap Surgery
41

42. 58
Mouth wash
Chlorhexidine Gluconate – 0.2 %
Metronidazole
Usage is controversial
Increases drug
metabolites
of Cyclosporin in blood.
Adverse drug effects
of Cyclosporin Seen
ANTIBIOTICS
Azithromycin
Mechanism of Action:
 High intracellular accumulation(Azithromycin
metabolites):
o Endogenous defensecells
o Tissuesaffected by inflammatory changes
 Increase phagocytosis of collagen fibres
Counter acts
Decreasing accumulation of extracellular matrix
42

43. SUBSTITUTE FOR
NIFEDIPINE
SUBSTITUTE
FOR
CYCLOSPORIN
SUBSTITUTE FOR
PHENYTOIN
Isradipine 20
mg BD
Tacrolimus
(0.15-0.2/kg/d)
Phenobarbital
60 mg TDS
ACE Inhibitors
- Captopril
12.5 - 50 mg BD
- Enalapril (2.5 - 20
mg OD)
Rapamycin Primidone
100 mg TDS
Carbamazepine
200 – 400 mg TDS
Valproic acid
200 – 500 mg TDS
Drug Substitute
43

44. No sufficient data exists to indicate folic acid therapy is
beneficial in Phenytoin induced Gingival enlargement
44
PHENYTOIN INDUCED GINGIVAL
ENLARGEMENT
Therapeutic
benefits
Inove & Harrison, Prasad et al
No therapeutic
benefits
Brown et al, Majota et al
Supplement Folic acid therapy

45. Surgical technique
Gingivectomy
Scalpel
Gingivectomy
Electrosurgery
Laser
Gingivectomy
Chemosurgery
45
Robicsek (1884) pioneered the so
called procedure gingivectomy.
Gingivectomy was later defined by
Grant et al(1979) as being “the
excision of soft tissue wall of a
pathologic periodontal pocket”.

46. 46
The gingivectomy
procedure employed
today was described in
1951 by Goldman.
Scalpel
Gingivectomy

47. GINGIVECTOMY BY ELECTROSURGERY:
Advantages:
◉ Permits adequate contouring of tissue and controls hemorrhage.
Disadvantages:
◉ Electrosurgery cannot be used in patients who have noncompatible or poorly
shielded cardiac pace makers.
◉ The treatment causes an unpleasant odour.
◉ The heat generated can cause tissue damage and loss of periodontal support
when electrode is used close to bone.
47

48. • The removal of gingival enlargements and gingivoplasty is performed with needle
electrode, supplemented by the small ovoid loop or the diamond–shaped electrodes
for festooning.
Technique:
• In all reshaping procedures, the electrode is activated and moved in a concise
shaving motion.
A blended cutting and coagulation (fully rectified) current is used.
• Hemorrhage must be controlled by direct pressure (via compression or hemostat)
first; then the surface is lightly touched by coagulation current.
For heamostasis, ball electrode is used.
• Bleeding areas located interproximally are reached with a thin, bar shaped
electrode.
Electrosurgery is helpful for the controlling of isolated bleeding
points.
48

49. GINGIVECTOMY BY CHEMOSURGERY:
Techniques to remove gingiva using chemicals such as 5%
formaldehyde or potassium hydroxide have been described in the
past but not currently used.
Disadvantages:
◉ The depth of action cannot be controlled, and therefore healthy
connective tissue underlying pocket may be injured.
◉ Gingival remodeling cannot be accomplished effectively.
◉ Epithelialization and re-formation of junctional epithelium and re-
establishment of the alveolar crest fiber system occur more slowly in
chemically treated gingival wounds than in those produced by
scalpel.
49

50. Laser Gingivectomy:
◉ The dental laser may be another useful alternative treatment to
conventional gingivectomy techniques.
◉ Lasers have remarkable cutting ability and they also generate a coagulated
tissue layer along the wall of the laser incision which promotes healing
(Goharkhay et al. 1999)
◉ Other advantages of the use of laser in correcting DIGO include a relative
bloodless operative and post-operative field, greater accuracy in making
incisions, sterilization of the operating field, minimal swelling and scarring,
vaporization and cutting with much less post-operative pain (Barak &
Kaplan 1988, Roed- Petersen 1993, Mavrogiannis et al.2004).
50

51. •Comparison of laser to scalpel excision in the management of DIGO using a
split-mouth crossover design study demonstrated a significantly lower rate
of recurrence for laser gingivectomy over 6-month follow-up period
(Mavrogiannis et al. 2006).
•The study employed the diode laser at a wavelength of 810 nm. Post-
operative pain scores were similar for the two treatments. The laser
gingivectomy was also preferred by the patients.
51

52. 52

53. After adequate anesthesia, bone
sounding is performed with
periodontal probe to determine the
presence and extent of bone
deformities. Depths of periodontal
pockets.
Incision is given on using a #15
surgical blade. The initial scalloped
internal bevel incision is made at least
3 mm coronal to the mucogingival
junction, which includes the creation
of new surgical interdental papillae in
each interproximal space.
Using blade gingival tissues are
thinned in the bucco lingual direction
to the mucogingival junction. The
blade establishes contact with the
alveolar bone, and a full-thickness or
split-thickness flap is elevated.
A similar scalloped internal bevel
incision is given on the palatal aspect at
a point where postoperative gingival
margin is intended. Thinning of palatal
flap is done till the apical extent of the
flap. The mucoperiosteal flap is then
elevated.
Interdental incision is given with the
help of an Orban knife, the base of
each papilla connected to facial and
lingual incisions is released.
Crevicular incisions are made on
buccal, lingual and palatal areas to
detach the collar of tissue. The collar
of tissue is removed using curettes.
Tissues tags are removed using
tissue scissors. The roots surfaces
are thoroughly debrided.
Flap is replaced on to tooth bone
junction and secured using
interrupted or continuous mattress
suture. Periodontal dressing is
placed.
Sutures and dressing is removed after
1–2 weeks depending on the healing
of the surgical area.
FLAP TECHNIQUE FOR GINGIVAL ENLARGEMENT
53

54. ENLARGEMENTS
ASSOCIATED WITH
SYSTEMIC DISEASES

55. ENLARGEMENTS ASSOCIATEDWITH SYSTEMIC
DISEASES
Magnification
of an existing
inflammation
initiated by
dental plaque
conditioned
enlargement
Manifestation
of the systemic
disease
independently
of the
inflammatory
status of the
gingiva
systemic
disease
causing
enlargement
55

56. 1. Conditioned enlargement
• Systemic condition exaggerates or distorts usualgingival
response to plaque
• Bacterial plaque
Types
1. Hormonal – pregnancy , puberty
2. Nutritional – vitamin C deficiency
3. Allergic
4. Non specific conditioned
56

57. 1. Marginal and generalised enlargement
2. Single or multiple tumor like masses
Hormonal changes
- Progesterone and estrogen
- Vascular permeability – edema ,
- inflammatory response
Subgingival microbiota – P.intermedia
a. Enlargement in pregnancy
57

58. 1. Marginal enlargement
- Generalised , moreprominent
interdentally
- Bright red or magentacolour
- Friable , smooth &shiny surface
- Bleeding – spontaneouslyor on
slight provocation
“ Pregnancy rhinitis”
58

59. “Pregnancy tumor”
- Discrete mushroomlike , flattened
spherical mass
- Dusky red or magenta , smooth glistening
surface
- Does not invade underlying bone
- Semi firm – soft, friable
- sessile or pedunculated
- Painless unless its size and shape foster
accumulation of debris
2. Tumor like gingival enlargement
59

60. Angiogranuloma
Thickened epilthelium
Newly formed, engorged
capillaries
Fibrous stroma Inflammatory
infiltrate
Histopathology
60

61. Treatment
• Maintain good oral hygiene
• Meticulous care
• treated by removal of plaque and calculus.
• Severe cases may require removal during the second
trimester
• Tumor like gingival enlargement - surgical excision
• Recurrence
• Spontaneous reduction – termination of pregnancy
61

62. • The lesions are not specific to gender; they occur
in male and female adolescents.
• Plaque accumulation.
• Seen in Marginal and interdental areas
• they are characterized by prominent bulbous
interproximal papillae.
• The degree of enlargement and its tendency to
recur in the setting of relatively scant plaque
deposits ,and profound impact by the hormonal
changes.
• The incidence of puberty associated go lesions
decline with age, further supporting the role of
hormonal changes during puberty.
b. Enlargement in puberty
62

63. • Studies of the subgingival microbiota of children between the ages of
11 and 14 years and their association with clinical parameters
implicated capnocytophaga species in the initiation of pubertal
gingivitis.
• Other studies have reported that hormonal changes coincide with an
increase in the proportion of p. Intermedia and P. Nigrescens.
• The etiologic role of the changes in microbiota, however, is not clear. It
is not known whether changes in inflammatory conditions predispose
to a shift in microbial species.
• After puberty, enlargement undergoes spontaneous reduction, but it
does not disappear completely until the plaque and calculus are
removed.
63

64. c. Enlargement in vitamin C deficiency
• Classic description of scurvy
• Acute deficiency – hemorrhage , collagen
degeneration ,edema
• modify response to plaque
Clinical features
- Bluish red , soft , friable, boggy
- smooth & shiny surface
- Haemorrhage
- Surface necrosis with
pseudomembrane formation
Correction of the deficiency and
treatment of local factors
regresses the enlargement.
64

65. d. Plasma cell gingivitis
• Atypical gingivitis / plasma cellgingivostomatitis
• Plasma cell granuloma – localised form- mild marginal
enlargement extending upto the attached gingiva.
• Allergic in origin
• Non plaque induced
Treatment include
•Cessation of exposure to the
allergen brings resolution of
the lesion
•Professional oral hygiene
measures.
65

66. e. Nonspecific conditioned enlargement
◉ Pyogenic granuloma
Clinical features
◉ Discrete spherical, pedunculated,
tumor like mass ,
◉ smooth surface
◉ Bright red or purple,
◉ friable or firm
◉ Painless
◉ Hemorrhage
66

67. 2.Systemic Disease That Cause Gingival
Enlargement
Leukemia
•malignant neoplasia of WBC precursors
•diffuse replacement of bone marrow
•proliferating leukemic cells
•abnormal number and forms of immature WBCs
•widespread infiltrates
Acute myeloid leukemia
67

68. Clinical features
• Diffuse / marginal
• Localised / generalised
• Overextension ofmarginal
gingiva
• Discrete tumorlike
interproximal mass
• Bluish red , shiny surface
• Firm
• Hemorrhage
68

69. Leukemic infiltration
Secondary inflammatory lesion
Plaque accumulation
Gingival pockets
Gingival thickness
Leukemic cell infiltration of gingival corium
69

70. Histopathology
- Connective tissue – dense mass of immature and
proliferating leukocytes , engorged capillaries ,edema
- Epithelium – degree of leukocytic infiltration andedema
70

71. 71
◉ The rationale is to remove the local irritating factors to control the
inflammatory component of the enlargement.
◉ During acute phases of leukemia, patients should receive only
emergency periodontal care.Any source of potential infection must be
eliminated to prevent systemic dissemination. [Fischman S 1983]
◉ After acute symptoms subside attention is directed to correction of
gingival enlargement.
◉ Administer antibiotic coverage before any periodontal treatment
because infection is a major concern.

72. 2. Granulomatous disease
a.Wegenersgranulomatosis
- Acute granulomatous necrotising lesions of respiratory tract , nasal and
oral defects
- Acute necrotising vasculitis
Clinical features
•oral mucosal ulcerations
•delayed healing
•Papillary enlargement
•reddish purple ,
•bleeds easily
-Strawberry gingiva
72

73. b. Sarcoidosis
- Unknown etiology
- Involve any organ
Clinical features
red, smooth, painless
enlargement may
appear.
73

74. Neoplastic conditions

75. Treatment of a neoplastic
conditions :
Benign tumors
of gingiva:
Fibroma Papilloma
Peripheral
giant cell
granuloma
Gingival
cyst
Malignant
tumors
Squamous
cell
Carcinoma
Malignant
melanoma
Sarcoma
75

76. Papilloma:
Benign proliferations of surface epithelium associated with the Human
Papilloma Virus.
Appear as solitary wart-like or cauliflower like protuberances.
May be small and discrete or broad, hard elevations with minutely irregular
surfaces.
Treatment:
Consists of surgical excision including the base of this mucosa into which the
pedicle or stalk inserts.
Removal should never be accomplished through the pedicle.
If the tumor is properly excised recurrence is rare.
76

77. Fibroma:
Arise from the gingival connective tissue or from PDL.
Slow growing spherical tumors .
Tend to be firm or nodular and usually pedunculated.
Treatment:
Conservative surgical excision .
77

78. This uncommon lesion occurs as a reparative response of the
connective tissue to gingival irritants. The biologic origin of the lesion is
thought to be periodontal ligament or the periosteum( Regezi 2003).
Poor oral hygiene is thought to be a predisposing factor(Bhat
1999).
The lesion appears as a broad based blue/red mass.
The most common location is the gingival tissue between the first
molar and the incisors( Regezi 2003).
Surgical excision along with the elimination of irritating agent is the
treatment of choice(Flaitz 2000).
PERIPHERAL GAINT CELL GRANULOMA:
78

79. Gingival cyst:
Appear as localized enlargements that may involve the marginal and
the attached gingiva.
Treatment:
Local surgical excision is recommended .
Removal is followed by uneventful recovery .
Lesions do not tend to recur.
79

80. Squamous cell Carcinoma:
Most common malignant tumor of the gingiva.
It may be exophytic, presents as a irregular outgrowth or ulcerative
which appears as a flat erosive lesion.
It is often symptom free, sometimes it becomes evident after tooth
extraction.
They are locally invasive involving the underlying bone and PDL of
adjoining teeth and adjacent mucosa.
Treatment:
Radiation and surgical removal is done.
But the disadvantages being radiation hazards
and the location of this lesion is a surgical problem.
Prognosis is very poor.
80

81. Sarcoma:
Fibrosarcoma, lymphosarcoma, reticulum cell carcinoma of the gingiva
are rare.
Kaposi sarcoma often occurs in patients with AIDS- particularly
affecting the palate and gingiva.
Treatment:
Antiretroviral agents.
Laser excision.
Radiation therapy or Intralesional injection with
vinblastine(0.1mg).
81

82. Idiopathic gingival enlargement
• Gingivomatosis , Elephantiasis,Idiopathic fibromatosis,
Hereditary gingival hyperplasia , Congenital familial
fibromatosis , Hereditary gingival fibromatosis
• rare oral disease
• autosomal dominant
• hypertrichosis, mental retardation and epilepsy
82

83. • Nodular form
• Symmetric form- most common type
• During eruption of permanentteeth
• most common effects
• diastemas,
• Malpositioning of teeth
• prolonged retention of primaryteeth
• cover the dental crowns
• the alveolar bone is not affected
(Bittencourt et al.2000).
83

84. False enlargement
•Underlying osseous lesions
•Commonly
•Tori
•Exostosis
•Also seen in Paget’s disease, Fibrous dysplasia, Cherubism, Central
giant cell granuloma,Ameloblastoma, Osteoma and Osteosarcoma
84

85. •Underlying dental lesions
•Various stages of eruption of primary dentition
•labial gingiva
•Developmental enlargement
85

86. RECURRENCE OF
GINGIVAL
ENLARGEMENT:

87. ◉ Recurrence is the most common problem after treatment in the
management of gingival enlargement.
◉ Residual local irritation and systemic or hereditary conditions
causing non-inflammatory gingival hyperplasia are the responsible
factors.
◉ If the recurrence of chronic inflammatory enlargement occurs
immediately after treatment indicates that all irritants have not
been removed.
◉ Food impaction and overhanging margins of restorations are the
local conditions, which are commonly overlooked.
◉ If the recurrence occurs after the healing is completed and normal
contour is attained, that indicates inadequate plaque control by the
patient.
87

88. • If the recurrence occurs during the healing period as red, bead like,
granulomatous masses that bleed on slight provocation indicates the
proliferative vascular inflammatory response to local irritation, usually
fragment of calculus on the root.
The condition is corrected by removal of granulation tissue, scaling and
root planning.
88

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