A detailed seminar on etiology, pathogenesis, diagnosis, and treatment planning of various types of gingival enlargement.

1. Gingival
enlargement
Presented by: Shashi kiran
4/6/19
1

2. Contents: Part 1
2

3. Contents: Part 2
3

4. Terminology
Hyperplasia- Increase in number of cells
Hypertrophy- Increase in size of cells
Enlargement
Overgrowth
4

5. Classification
1. Inflammatory enlargement a. Acute
b. chronic
2. Drug induced gingival enlargement a. Anti-convulsants
b. Calcium channel blockers
c. Immunosuppressants
3. Enlargements associated with systemic
diseases or conditions
a. Conditioned enlargement
• Pregnancy
• Puberty
• Vitamin C deficiency
• Plasma cell gingivitis
• Nonspecific conditioned enlargement
b. Enlargement associated with systemic diseases
• Leukemia
• Granulomatous disease
4. Neoplastic enlargements a. Benign
b. Malignant
5. False enlargements
carranza 12th edition 5

6. Classification
carranza 12th edition
LocalizedGeneralized
Marginal
Based on
location and
distribution
Papillary
DiscreteDiffuse
6

7. Indices to measure gingival enlargement
Grade 0 no signs of gingival enlargement
Grade I enlargement confined to interdental
papilla
Grade II enlargement involves papilla and
marginal gingiva
Grade III enlargement covers three-fourths or
more of the crown
Bokenkemp and Bonhorst 1994 7

8. • Angelopoulos and Goaz (1972) described an index for measuring the vertical
component of gingiva. Three grades based on the enlargement covering the
clinical crown were described as:
Grade 0 None.
Grade I Not more than 1/3rd of the clinical crown covered
Grade II Any part of the middle third of the crown covered
Grade III Greater than 2/3rd of the crown covered
8

9. Miranda and Brunet index (2001) described an index in which
horizontal measurement (Bucco-lingual) of the enlargement is possible.
The scores of this index is as mentioned below:
• Score 0: Papilla thickness < 1 mm
• Score 1: Papilla thickness 1- 2 mm
• Score 2: Papilla thickness > 2 mm
9

10. • Eva and Ingles (1999) introduced a new index for measuring gingival overgrowth caused due to
drugs. In this index for standardization, the buccal and lingual papillae were scored separately.
Grade 0 No overgrowth, firm adaptation of the attached gingiva to the underlying
alveolar bone. There is slight stippling; there is no granular appearance. A
knife-edged papilla is present toward the occlusal surface and no increase
in density or size of the gingiva.
Grade 1 Early overgrowth, as evidenced by an increase in density of the gingiva
with marked stippling and granular appearance. The tip of the papilla is
rounded and the probing depth is less than or equal to 3mm
Grade 2 Moderate overgrowth, manifested by an increase in the size of the papilla
and/ or rolled gingival margins. The contour of the margin is still concave or
straight. Also the enlargement has a buccolingual dimension of up to
2mm, measured from the tip of the papilla outward. The probing depth is
equal to or less than 6mm and the papilla is somewhat retractable.
10

11. Grade 3 Marked overgrowth, represented by encroachment of the gingiva onto
the clinical crown. Contour of the margin is convex rather than concave.
The enlargement has a buccolingual dimension of approximately 3 mm
or more, measured from the tip of the papilla outward. The probing depth
is greater than 6mm and the papilla is clearly retractable
Grade 4 Severe overgrowth, characterized by a profound thickening of the gingiva.
A large percentage of the clinical crown is covered. The papilla is
retractable, the probing depth is greater than 6 mm and the buccolingual
dimension is approximately 3 mm
Eva and Ingles 1999 11

12. Inflammatory gingival enlargement
Inflammatory
gingival
enlargement
Acute
Gingival abscess
Periodontal
abscess
Chronic
12

13. Chronic inflammatory enlargement
• Clinical features:
Originates as a slight ballooning
of the
interdental papilla and marginal
gingiva.
Life preserver shaped bulge
around the involved teeth,
which can increase in size until it
covers part of the crowns
As a discrete sessile or
pedunculated mass that
resembles a tumor. It can be
interproximal or located on the
marginal or attached gingiva.
Painful ulceration sometimes
occurs in the fold between the
mass and the adjacent gingiva
13

14. Histopathology
• Lesions that are deep red or bluish
red are soft and friable with a
smooth, shiny surface, and bleed
easily.
• 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
14

15. • Etiology
Microbial
biofilm
• lack of proper oral hygiene
• orthodontic appliances
• faulty restoration margins
• misaligned teeth
• oral habits
Factors that favor plaque
accumulation and retention include
• irritation by anatomic
abnormalities
• Improper restorative and
orthodontic appliances
15

16. Management
• Chronic enlargement of the gingiva due to gingivitis is reversible and
can be resolved by removal of the etiologic factors, including the
biofilm, and correction of environmental factors.
• In severe forms of inflammatory enlargement, surgical approaches
may be required
16

17. Enlargement associated with mouth breathing:
• The gingiva appears red and edematous, with a diffuse
surface shininess of the exposed area.
• The maxillary anterior region is commonly involved. In
many cases, the altered gingiva is clearly demarcated
from the adjacent, unexposed normal gingiva.
• Irritation from surface dehydration is attributed to
mouth breathing.
• (However, comparable changes could not be reproduced by air-
drying the gingiva of experimental animals, suggesting that the
pathogenesis of mouth breathing–associated gingival changes is
far more complex)
17

18. Acute inflammatory enlargement
• Gingival abscess
Typically limited to the marginal
gingiva or the interdental papilla.
In early stages, it appears as a
red swelling with a smooth, shiny
surface.
In 24 to 48 hours, usually
becomes fluctuant and pointed,
with a surface orifice and a
purulent exudate. Adjacent
teeth may become sensitive to
percussion
The lesion usually ruptures
spontaneously.
18

19. • Etiology
Trauma
 Mechanical, chemical, irritation
from
 Impacted food items
 Traumatic lesions occur when a
foreign substance (e.g.,
toothbrush bristle) is forcefully
embedded in the gingiva and
complicated by resident
microbes.
19

20. • Histopathology
The gingival abscess consists of a
purulent exudate of a diffuse
infiltration of polymorphonuclear
leukocytes, edematous tissue, and
vascularization
The surface epithelium has various
degrees of intracellular and
extracellular edema, invasion by
leukocytes, and sometimes
ulceration
20

21. Periodontal abscess
• The periodontal abscess is an infection located contiguous to the periodontal
pocket and may result in destruction of the periodontal ligament and alveolar
bone.
• Poorly controlled diabetes mellitus has been considered a predisposing factor
for periodontal abscess formation
• Shape and consistency vary from dome-like and firm to pointed and soft. Pus is
usually expressed from the margin on gentle digital pressure
21

22. Periodontal abscesses are classified according to location as follows:
• 1. Abscess in the supporting periodontal tissues along the lateral aspect of the root.
With this condition, a sinus generally occurs in the bone that extends laterally from
the abscess to the external surface.
• 2. Abscess in the soft-tissue wall of a deep periodontal pocket
• Conditions in which periodontal abscesses are not related to
inflammatory periodontal disease include tooth perforation or fracture
22

23. Etiology:
1.
• Extension of infection and localization of the suppurative inflammatory process
along the lateral aspect of the root.
2.
• Lateral extension of inflammation from tissue surface of the periodontal pocket
into connective tissue of the pocket wall.
3.
• In a pocket which describes a tortuous course around the root, periodontal
abscess may form in the cul de sac, the deep end of which is shut from the
surface
4.
• Incomplete removal of calculus during treatment of periodontal pocket, here
the gingival wall shrinks occluding the pocket orifice and an abscess results in
the sealed off portion of the pocket.
23

24. Microflora associated with periodontal abscess
• Streptococcus viridans is the most
common isolate in the exudate of
periodontal abscesses.
Jaramillo et al 2005
24

25. • Signs and symptoms of periodontal abscess:
Acute Abscess
• Mild to severe discomfort
• Localized red, ovoid swelling
• Periodontal pocket
• Mobility
• Tooth elevation in socket
• Tenderness to percussion or
biting
• Exudation
• Elevated temperature
• Regional lymphadenopathy
Chronic Abscess
• No pain or dull pain
• Localized inflammatory lesion
• Slight tooth elevation
• Intermittent exudation
• Fistulous tract often
associated with a deep
pocket
• Usually without systemic
involvement
25

26. Management
Immediate management
The common antibiotics which are used
are:
1. Amoxycillin 250 - 500 mg tds 5-7 days
2. Metronidazole 200 - 400 mg tds 5-7
days
If allergic to penicillin, these antibiotics
are used:
1. Erythromycin 250 –500 mg qid 5-7
days
2. Doxycyline 100 mg bd 7-14 days
3. Clindamycin 150-300 mg qid 5-7 days.
Treatment options
• 1.Drainage through pocket retraction
or incision
• 2. Scaling and root planning
• 3. Periodontal surgery
• 4. Systemic antibiotics
• 5. Tooth removal
26

27. Drug induced gingival overgrowth (DIGO)
27

28. • First reported in 1939 by Kimball associated with
chronic usage of the anti-epileptic drug
Phenytoin(sodium diphenyl hydantoinate (dilantin))
• Clinically and histologically, gingival overgrowth
induced by different drugs, are virtually
indistinguishable.(Wysocki et al. 1983, Tyldesley
& Rotter 1984)
• Children and adolescents >>> Adults
• Anterior >>> Posterior gingival tissues.
• Males 3 times more likely than females
28

29. Drug-induced gingival overgrowth is known as an
adverse effect with three types of drug:
• phenytoin, an antiepileptic;
• cyclosporine A, an immunosuppressant
• calcium channel blockers, such as
dihydropyridines (nifedipine), diltiazem, and
verapamil
• Clinical relevance- - Speech, masticatory, hygiene,
aesthetic problems….
29

30. Prevalence
0
20
40
60
80
100
120
Phenytoin cyclosporine nefedipine
Series 1 Series 2 Series 3
30

31. 31

32. General features
Starts as a painless bead like
enlargement of the interdental papilla
that extends into the facial and lingual
marginal gingiva.
Marginal and interdental
enlargements unite - - massive fold of
tissue…
If no inflammation - - mulberry
shaped, firm , pale pink and resilient
with minutely lobulated surface - - no
tendency to bleed.
32

33. General features
Characteristically project from
beneath the marginal gingiva.
If inflammation - - enlargement
combination of inflammatory and
drug induced… - - bluish red hue and
bleeding tendency….
Generalized - - more severe in
anterior region…
Occurs where teeth are present
33

34. General histopathology
Pronounced hyperplasia of
epithelium
Acanthosis of epithelium, elongated
rete pegs extend deep into
conn.tissue
Conn. tissue shows densely arranged
collagen bundles, numerous
fibroblasts and new blood vessels
34

35. Anti-convulsants
• Anticonvulsants are a diverse group of
pharmacological agents used in the
treatment of epileptic seizures.
• Phenytoin (diphenylhydantoinate) is
the drug of choice - - grand mal,
temporal lobe, and psychomotor
seizures
• it has been linked to GO for more than
70 years.
• Phenytoin is a hydantoin that was first
introduced by Meritt and Putnam in
1938 for the treatment of all forms of
epilepsy except petit mal seizures.
• Gingival enlargement - - in 50% of
patients receiving drugs (3 - 84.5%)
35

36. • Other hydantoins - - ethotoin,
mephenytoin
• Other anti-convulsants - -
ethosuximide, methsuximide and
valporic acid
• Clinical onset occurs as early as 1
month, and increasing severity is seen
in 12 to 18 months.
36

37. • PGO seems to be more prevalent in
children and teenagers, but there is
no difference on its incidence in
regard to gender or ethnic groups.
• PGO incidence and severity is greater
in the buccal surface of both upper
and lower anterior teeth
37

38. Calcium channel blockers
• Calcium channel blockers - -
hypertension, angina pectoris,
coronary artery spasm, and cardiac
arrhythmia
• The first case of GO associated with
the calcium channel blocker nifedipine
was reported in 1984
• Occurrence - 6% to 83%
38

39. • Inhibit calcium ion flux across cell
membrane - - dilation of coronary
arteries
• Dose - - daily dose of 5 mg or higher
could be a risk factor for gingival
overgrowth in some patients.
• enlargement could be detected
clinically as early as 1–3 months
following the initial dose of CCB
39

40. Immunosupressants
• The first case of cyclosporin A–
induced GO was reported in 1983
(Rateitschak-Pluss et al).
• Cyclosporine - - used to prevent organ
transplant rejection and to treat
autoimmune diseases.
• Selectively and reversibly inhibit
helper T cells
40

41. • Dose> 500mg/day - - gingival
overgrowth
• Occurrence 25 – 70%
• Clinically, the lesions are more
inflamed and bleed more than other
forms of DIGO, and they commonly
are limited to buccal surfaces
41

42. Histopathology
• Cyclosporine enlargement - - more
vascular than phenytoin enlargement
• Abundant plasma cells and
amorphous extracellular matrix
• Suggested to be a hypersensitivity
response
42

43. Pathogenesis of DIGO
1. Synthesis and degradation of
collagen
2. Role of integrins
3. Role of calcium
4. Role of folic acid
5. Role of MMPs
6. Role of inflammatory cytokines
43

44. SYNTHESIS AND DEGRADATION OF TYPE I COLLAGEN
• Collagen may be degraded - - extracellular pathway involving the secretion of
collagenase) and via an intracellular pathway involving phagocytosis by
fibroblasts
• Metabolism - balanced by collagen synthesis and degradation to maintain
tissue volume.
• decreased collagen degradation= = may contribute to the appearance of
gingival overgrowth
KATAOKA et al 2005
44

45. • McCulloch and Knowles showed decreased collagen phagocytosis of fibroblast isolated from
human phenytoin-induced gingival overgrowth than healthy gingiva, and direct inhibitory effects
of nifedipine and phenytoin were also shown on the collagen phagocytosis of fibroblasts
• Phagocytic activity in gingival fibroblasts with a rat experimental model, and
severe inhibition was observed in cyclosporine A-induced gingival overgrowth.
Interestingly, type I collagen and collagenase mRNA expressions were
significantly suppressed by cyclosporin A and nifedipine administration in these
rat experimental models
• Drug-induced gingival overgrowth is not due to the increased synthesis of type I
collagen but the decreased degradation of type I collagen in gingival connective
tissue through the reduction of collagen phagocytosis of fibroblasts.
KATAOKA et al 2005
45

46. • There are a great many studies reporting increased
connective tissue and proliferation of gingival
fibroblasts secondary to the inducing drugs as the
primary causation of DIGO (Brown et al, 1991a;
Seymour et al, 1996).
• Fibrobalsts from phenytoin patients show increased
synthesis of sulphated glycosaminoglycans (Kantor
et.al 1983)
• Both cyclosporin and nifedipine can cause increase in
tissue levels of non –sulphated glycosaminoglycans
(Zebrowski et.al 1994)
Connective
tissue
Collagen
60%
Matrix-
GAGs 35%
Fibroblasts
46

47. ROLE OF α2 INTEGRIN
• Integrins are a large family of heterodimeric
transmembrane receptors for extracellular
matrix molecules. Each heterodimer consists of
an a and b subunit
• Both a1b1 and α2b1 integrins are cell surface
receptors for collagens, and cells expressing the
a1b1 integrin preferentially adhere to type IV
collagen, whereas cells expressing α2b1
preferentially adhere to type I collagen
KATAOKA et al 2005
47

48. • Lee et al. reported that the initial binding step of collagen phagocytosis relies on adhesive
interaction between fibroblasts and collagen, and that α2 integrin plays a critical role in the
phagocytic regulation of collagen internalization
• Katoaka et al showed significantly decreased collagen phagocytosis in fibroblasts in rat
overgrown gingiva induced by cyclosporin A and α2 integrin expression suppressed in
fibroblasts isolated from overgrown gingiva compared to the control
• Chou et al. showed a reduction in collagen phagocytosis of gingival fibroblasts by TNF-a
treatment through the inhibition of collagen binding to cells by the inactivation of α2b1 integrin
• These findings indicate that one etiological factor of drug-induced gingival
overgrowth may be the inhibition of collagen phagocytosis by reducing α2
integrin expression or decrease of the binding activity in gingival fibroblasts
KATAOKA et al 2005
48

49. ROLE OF CALCIUM
• Calcium channel blockers - - block the
influx of calcium ions into cells and to
reduce oxygen consumption.
• Phenytoin - - calcium channel
antagonist and inhibit calcium ion
flux.
• Cyclosporin A - - inhibit the release of
calcium from intracellular stores,
including endoplasmic reticulum and
mitochondria
• α2b1 integrin-mediated collagen
phagocytosis in gingival fibroblasts is
regulated by intracellular calcium
• Cyclosporin A inhibits the α2b1
integrin-binding activity of collagen
phagocytosis through a calcium-
regulated pathway involving ER and
mitochondrial stores
KATAOKA et al 2005, BROWN et al 2014
49

50. ROLE OF CELLULAR FOLATE UPTAKE
• Vogel (1977) proposed that DIGO may be secondary to a localized FA deficiency
• Opladen et al (2010) reported upon the effect of anti-convulsant drugs upon the
folate receptor 1(FOLR1)-dependent 5-methyltetrahydrofolate (MTHF) transport
• They reported that the metabolic breakdown of anti-convulsants as valproate,
carbamazepine, and Phenytoin generates reactive oxygen species (ROS).
(Folate is present in food in a polyglutamate form, which is then converted into monoglutamates by intestinal
conjugase to be absorbed by the jejunum. Phenytoin acts by inhibiting this enzyme, thereby causing folate
deficiency, and thus megaloblastic anemia)
BROWN et al 2014
50

51. • Exposure to PHT could lead to higher
MTHF uptake; however, exposure to
superoxide and hydrogen peroxide
radicals significantly decreased
cellular MTHF uptake
• Therefore, it appears that the FOLR1-
dependent 5-MTHF transport could
also be involved with regard to
inhibited folate transport and
decreased folate uptake in gingival
fibroblasts.
BROWN et al 2014 51

52. Role of matrix metalloproteinases
1
• Collagen synthesis and degradation is controlled by MMPs and the
TIMPs
2
• Collagen fibers are degraded via an extracellular pathway by
secretion of collagenases and via an intracellular pathway via
phagocytosis by fibroblasts
3
• Drugs affect calcium metabolism by reducing the Cα2+ cell influx,
leading to a reduction in the uptake of folic acid, thus limiting the
production of active collagenase. (Livada et al. 2014)
4
• As a result of the reduction in collagen degradation, increased
collagen accumulation occurs.
• E cadherin
• Smad
(TGFb)
• AP 1
• TIMP 1
• MMP 1
BROWN et al 2014 52

53. Brown et al 2014
53

54. Role of inflammatory cytokines
1
• Pro-inflammatory cytokines, such as interleukin-1b and interleukin6 seem to have a
synergistic effect in the enhancement of collagen synthesis by human gingival
fibroblasts.
2
• Interleukin-6 has been shown to target connective tissue cells, such as fibroblasts,
both by enhancing their proliferation and by increasing collagen production and
glycosaminoglycan synthesis
3
• This highlights the role of the bacterial biofilm in inducing gingival inflammation,
production of cytokines and gingival enlargement
54

55. Pathogenesis
Brown et al 2014
56

56. Risk factors for DIGO
• Age
• Gender
• Concomitant medication
• Periodontal variables
• Genetic factors
• Drug factors
57

57. Age
• Clinical studies suggest that children and adolescents are more susceptible to
DIGO (Hefti et al 1994 )
• Although animal studies have confirmed these findings (Kitamura et al. 1990,
Mori-saki et al. 1993), they are not supported by in-vitro investigations.
58

58. Phenytoin Fibroblasts
5-α-DHT
testosterone
↓Collagenase
Activity
↑Collagen
Production
(Sooriyamoorthy et al
1988,archives of oral biology)
Interaction between circulating
androgens and gingival fibroblasts.
Such cells can readily metabolise
testosterone to the active metabolise
5 a-dihydrotestosterone. Phenytoin
enhances this
metabolism(Sooriyamoorthy et al
1988)
Circulating androgen levels will be
higher in adolescents and
teenagers.
59

59. Gender
• Studies showed that males were at greater risk from developing this unwanted
effect than females and that the severity of the changes would be greater in men.
(Thomason et al. 1995, Thomason et al. 1996b)
• Similarly males were shown to be 3 times more likely than females to develop
clinically significant gingival changes when medicated with calcium channel
blockers
• Evidence from animal studies also supports this finding, with male rats being
more prone to drug-induced gingival overgrowth than females (Ishida et al.
1995).
60

60. Concomitant medication
• There is now a considerable body of evidence that the combination of nifedipine
and cyclosporin in organ transplant patients produces more gingival overgrowth
than if either drug was used singularly (Bokenkamp et al. 1994, Margiotta et al. 1996, O’Valle
et al. 1995, Thomason et al. 1995, Thomason et al. 1996, Thomason et al. 1993, Wilson et al. 1998,
Wondimu et al. 1996)
• In adult organ transplant patients, dosages of both prednisolone and azathioprine
appeared to afford the patients some degree of ‘‘protection’’ against the
development of gingival overgrowth
61

61. • Phenytoin is metabolised (hydrolysed) in the liver by P450 enzymes to 5-(4-
hydroxyphenyl)- 5-phenylhydantoin (4-HPPH). This metabolite has been shown to
induce gingival overgrowth in cats (Hassell & Page 1978).
• Anticonvulsants such as phenobarbitone, primidone and carbamazepine have
been shown to induce hepatic P450 isoenzyme and if given in conjunction with
phenytoin will increase serum concentrations of 4- HPPH.
• This may explain the increased prevalence of gingival overgrowth in patients
receiving multiple anticonvulsant therapy
62

62. Periodontal variables
• Plaque scores and gingival inflammation appear to exacerbate the expression of
drug-induced gingival overgrowth, irrespective of the initiating drug (Seymour
(1991), Seymour & Heasman (1988), Seymour & Jacobs (1992)
• Both the oral hygiene and the control group developed significant gingival
changes over the 6-month post-transplant investigation period, although the
magnitude of the changes in the oral hygiene group was less marked. (Seymour &
Smith 1991)
63

63. • In a group of renal transplant patients, the presence of gingival bleeding
increased significantly the risk of developing gingival overgrowth (Pernu et al.
1992).
• It would be reasonable to suggest that proper oral hygiene might be expected to
minimise the severity of drug-induced gingival overgrowth, possibly by
eliminating the inflammatory component of the lesion. Improved oral hygiene in
itself would not appear to prevent overgrowth
64

64. Genetic Factor
• All three drugs are metabolised by the hepatic cytochrome P450 enzymes.
Cytochrome P450 genes exhibit considerable polymorphism which results in
inter-individual variation in enzyme activity
• The one genetic marker that has been investigated in relation to drug-induced
gingival overgrowth is the human lymphocyte antigen expression (HLA).
• HLA-DR1 (Cebeci et al. 1996)
• HLA-DR2 (Thomason et al. 1996)
• HLA-B37 (Margiotta et al. 1996)
65

65. Risk factors
66

66. Management
Non surgical
• Scaling and root planning
• Antiseptic mouthwashes
• Systemic antibiotics
• Drug substitution
Surgical
• Scalpel gingivectomy
• Electrosurgery
• Laser gingivectomy
• Flap surgery
67

67. Management
• Drug substitution
• 6-12 month period
Drug Substitute
Nefidipine • Isradipine
• ACE inhibitors - - Captopril, Enalapril
Phenytoin • Phenobarbitol
• Primidol
• Valporic acid
Cyclosporin • Tacrolimus
• Rapamycin
Samudrala et al 2016
68

68. Samudrala et al 2016
Wahlstrom et al
1994,
Strachan et al
2003
69

69. Samudrala et al 2016
70

70. Contents: Part 2
71

71. Enlargement associated with systemic
conditions and diseases
• Condition- A medical condition is a broad term that includes all
diseases, lesions, disorders, or non-pathologic condition that normally
receives medical treatment, such as pregnancy or childbirth
• Disease- A disease is a particular abnormal condition that negatively
affects the structure or function of part or all of an organism, and that
is not due to any external injury.
• All diseases are conditions, but not all conditions are diseases.
72

72. Two mechanisms:
1. Magnification of pre-existing gingival inflammation initiated by dental plaque
• Conditioned enlargements
• Non-specific conditioned enlargements- pyogenic granuloma
2. Manifestation of systemic disease independently of the inflammatory status
of gingival status.
• Neoplastic enlargements
• Leukemia
• Granulomatous diseases
73
Enlargement associated with systemic
conditions and diseases

73. Conditioned enlargements
Systemic conditions of a patient exaggerates or distorts the usual gingival response
to plaque.
Bacterial plaque is necessary for the initiation of this type of enlargement
• Hormonal conditions- pregnancy, puberty
• Nutritional conditions- vitamin C deficiency
• Allergic reactions
• Non-specific conditioned enlargements- Pyogenic granuloma
74

74. Conditioned enlargements: Pregnancy
• Common- incidence has been
reported as 10% to 70%
• In 1818, Pitcarin described gingival
hyperplasia in pregnancy
• Clinically, it manifests as a single mass
or multiple tumor-like masses at the
gingival margin.
• Pregnancy tumors are not neoplasms;
they represent an inflammatory
response to microbial plaque modified
by the patient's condition. (1.8-5%)
• The prevalence increases toward the
end of pregnancy (when levels of
circulating estrogens are highest), and
they tend to shrink after delivery
• Two presentations- Marginal and
Tumor-like
75

75. Clinical features: Marginal
• Generalized, more prominent interproximally
than on the facial and lingual surfaces.
• The enlarged gingiva is bright red or magenta,
soft, and friable, and it has a smooth, shiny
surface
• Bleeding occurs spontaneously or on slight
provocation
76

76. Clinical features: Pregnancy Tumors
• Discrete, mushroom-like, flattened spherical
mass that protrudes from the gingival margin or,
more often, from the interproximal space, and it
is attached by a sessile or pedunculated base
• Dusky red or magenta; it has a smooth, glistening
surface that often exhibits numerous deep red,
pinpoint markings
• Usually firm, but it may have various degrees of
softness and friability. Usually painless.
77

77. Histopathology
• Angiogranuloma
• Central mass of connective tissue, with numerous
diffusely arranged, newly formed, and engorged
capillaries lined by cuboid endothelial cells
• A moderately fibrous stroma with various degrees
of edema and chronic inflammatory infiltrate.
• The stratified squamous epithelium is thickened,
with prominent rete pegs and some degree of
intracellular and extracellular edema, prominent
intercellular bridges, and leukocytic infiltration.
78

78. Etiology
Subgingival Plaque Composition
• Increase in anaerobic/aerobic ratio
• Higher concentrations of Prevotella
intermedia (i.e., substitutes sex
hormone for vitamin K growth factor)
Kornman and Loeshe (1980)
79
Estrogen and Progesterone
• Increases vascular dilation and
increases permeability, resulting in
edema and accumulation of
inflammatory cells
• Increases proliferation of newly
formed capillaries in gingival tissues
(i.e., increased bleeding tendency)
• Alters rate and pattern of collagen
production

79. Management
• Prevented by good oral hygiene
• SRP and adequate oral hygiene
measures may reduce the size of the
enlargement.
• Severe cases may require removal
during the second trimester;
• Treatment consists of the removal of
the lesions and the elimination of
irritating local factors.
• Removal of the GO lesions without
establishment of an optimal oral
hygiene regimen ensures recurrence
of gingival enlargement (15%)
• Spontaneous reduction in the size of
gingival enlargement typically follows
the termination of pregnancy
• Lesions should be removed surgically
during pregnancy only if they
interfere with mastication or produce
an aesthetic disfigurement.
80

80. Rationale for treatment during 2nd trimester
• Other than good plaque control, it is prudent to avoid elective dental care if
possible during the first trimester and the last half of the third trimester.
• The first trimester is the period of organogenesis, when the fetus is highly
susceptible to environmental influences.
• In the last half of the third trimester, a hazard of premature delivery exists
because the uterus is very sensitive to external stimuli
• Early in the second trimester is the safest period for providing routine dental
care.
81
Carranza’s clinical periodontology, 13th edition

81. Precautions for pregnant patients
Supine hypotensive syndrome
• In a semireclining or supine position, the great vessels, particularly the inferior vena
cava, are compressed by the uterus. By interfering with venous return, this compression
causes maternal hypotension, decreased cardiac output, and eventual loss of
consciousness.
• Supine hypotensive syndrome can usually be reversed by turning the patient on her left
side, which removes pressure on the vena cava and allows blood to return from the
lower extremities and pelvic area.
• A preventive 6-inch soft wedge (i.e., rolled towel) should be placed on the patient’s right
side when she is reclined for clinical treatment.
82
Carranza’s clinical periodontology, 13th edition

82. • When radiographs are needed for diagnosis (only when necessary and
appropriate to aid in diagnosis and treatment) the most important aid for the
patient is the protective lead apron
• Ideally, no drug should be administered during pregnancy, especially the first
trimester. Fortunately, most common drugs in dental practice can be given during
pregnancy with relative safety, although there are a few important exceptions
83

83. Conditioned enlargements: Puberty
• They occur both in male and female
adolescents.
• The lesions are usually marginal and
interdental, and they are
characterized by prominent bulbous
interproximal papillae.
• Often, only the facial gingivae are
enlarged, and the lingual surfaces are
relatively unaltered.
84

84. • The degree of enlargement and its
tendency to recur in the setting of
relatively scant plaque deposits
distinguish puberty-associated GO
from purely gingivitis-associated
lesions, suggesting a 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.
• The inflamed tissues become
erythematous, lobulated, and
retractable
• The microscopic appearance of
gingival enlargement during puberty is
one of chronic inflammation with
prominent edema.
• Management: After puberty,
enlargement undergoes spontaneous
reduction, but it does not disappear
completely until the plaque and
calculus are removed.
85

85. Conditioned enlargements: Vitamin C deficiency
• These lesions are no longer common,
but GO is still considered a part of the
classic description of scurvy
• Deficiency of vitamin C is defined as a
serum ascorbic acid level < 2 μg/mL.
• A Scottish surgeon in the Royal
Navy, James Lind, is generally credited
with proving that scurvy can be
successfully treated with citrus fruit in
1753
86

86. Clinical Manifestations
• Gingival enlargement with vitamin C
deficiency is marginal. The gingiva is
bluish red, soft, and friable, and it
has a smooth, shiny surface.
• Swollen, tender, spongy, bleeding
putrid gingiva.
• Haemorrhage occurs spontaneously
or on slight provocation and surface
necrosis with pseudo membrane
formations are common features.
87

87. Etiology
• Acute vitamin C deficiency alone does
not cause gingival inflammation, but it
does cause haemorrhage, collagen
degeneration, and edema of the
gingival connective tissue.
• These changes modify the response
of the gingiva to plaque and the
extent of the inflammation is
exaggerated
Histopathology
• In patients with vitamin C deficiency,
the gingiva has a chronic
inflammatory cellular infiltration with
a superficial acute response.
• There are scattered areas of
hemorrhage with engorged
capillaries. Marked diffuse edema,
collagen degeneration, and a scarcity
of collagen fibrils and fibroblasts are
striking findings.
88

88. Plasma cell gingivitis
• Plasma cell gingivitis manifests as a
mild marginal gingival enlargement
that extends to the attached gingiva
• The gingiva appears red, friable, and
sometimes granular, and it bleeds
easily;
• The lesion is located on the oral
aspect of the attached gingiva and is
different from plaque-induced
gingivitis
89

89. Histopathology
• Oral epithelium shows spongiosis and
infiltration with inflammatory cells
• Underlying connective tissue contains
dense infiltration of plasma cells
extending into the epithelium.
• Thought to be an allergic reaction to
an antigen (dentrifices, chewing gums,
cinnamon, mint etc). Removal of
antigen causes resolution.
90

90. Pyogenic granuloma
• Tumor-like enlargement
• Exaggerated response to minor trauma
or local factors
• Presents in adults as smooth surfaced
mass, often ulcerated and grows from
beneath the gingival margin
• These reddish/bluish color mass are
highly vascular, compressible and could
bleed readily
• The mass may penetrate interdentally
and present as bilobular (buccal and
lingual) mass connected through the col
area
• Histologically, the stratified squamous
epithelium is thickened, with prominent
rete pegs and some degree of
intracellular and extracellular edema,
numerous engorged capillaries and
leukocytic infiltration.
91

91. Enlargements associated with systemic
diseases
• Leukemia
• Granulomatous diseases
92

92. Leukemia
• The leukemias are malignant neoplasias of WBC precursors that are
characterized by the following:
93
(1) diffuse replacement of the
bone marrow with proliferating
leukemic cells;
(2) abnormal numbers and
forms of immature WBCs in the
circulating blood;
(3) widespread infiltrates in the
liver, spleen, lymph nodes, and
other body sites.
All leukemias tend to displace normal
components of the bone marrow elements
with leukemic cells, thereby resulting in the
reduced production of normal RBCs, WBCs,
and platelets
ANEMIA
THROMBOCYTOPENIA
LEUKOPENIA

93. • The gingiva is a peculiar bluish red, it is spongelike
and friable, and it bleeds persistently on the
slightest provocation or even spontaneously
• This greatly altered and degenerated tissue is
extremely susceptible to bacterial infection, which
can be so severe as to cause acute gingival necrosis
with pseudomembrane formation or bone exposure
94

94. Leukemic Infiltration
• Leukemic gingival enlargement consists of a basic
infiltration of the gingival corium by leukemic cells
that increases the gingival thickness and
• creates gingival pockets in which bacterial plaque
accumulates,
• thereby initiating a secondary inflammatory lesion
that contributes to the enlargement of the gingiva.
• It may be localized to the interdental papilla area or it
may expand to include the marginal gingiva and
partially cover the crowns of the teeth.
95

95. Histology
• Microscopically, the gingiva exhibits a dense,
diffuse infiltration of predominantly immature
leukocytes in the attached and marginal gingiva.
The normal connective tissue components of the
gingiva are displaced by the leukemic cells
• The blood vessels are distended and contain
predominantly leukemic cells, and the RBCs are
reduced in number. The epithelium shows a
variety of changes, and it may be thinned or
hyperplastic.
96

96. • Scattered foci of plasma cells and lymphocytes with edema
and degeneration are common findings. The inner aspect of the
marginal gingiva is usually ulcerated, and marginal necrosis
with pseudomembrane formation may also be seen
97

97. Management
• The patient's bleeding and clotting times and platelet count should be checked
before treatment, and the hematologist should be consulted before periodontal
treatment is instituted
• The rationale is to remove the local irritating factors to control the inflammatory
component of the enlargement, and this is achieved by scaling and root planning
• The initial treatment steps consist of gently removing all loose debris with cotton
pellets, performing superficial scaling, and instructing the patient in oral hygiene
for biofilm control. This hygiene should include daily use of chlorhexidine
mouthrinses.

98. • Definitive scaling and root planing are carried out at subsequent visits using
local anesthesia.
• Treatment sessions are confined to a small area of the mouth if hemostasis
poses a challenge.
• Antibiotics are administered systemically the evening before and for a week
after each treatment to reduce the risk of infection.
99

99. Wegener’s granulomatosis
• Wegener granulomatosis is a rare disease
of unknown origin that is characterized
by acute granulomatous necrotizing
lesions of the respiratory tract, including
nasal and oral defects and vasculitis of
small and medium vessels
• The initial manifestations of Wegener
granulomatosis can involve the orofacial
region and include oral mucosal
ulceration, gingival enlargement,
abnormal tooth mobility, exfoliation of
teeth, and a delayed healing response.
• Oral cavity: ‘Strawberry gingivitis’,
underlying bone destruction with
loosening of teeth, non-specific
ulcerations
100

100. • Histopathology- scattered giant cells,
foci of acute inflammation, and
micro-abscesses covered by an
acanthotic epithelium
• The cause of Wegener granulomatosis
is unknown, but the condition is
considered an immunologically
mediated tissue injury
101

101. Hereditary gingival fibromatosis
• Gingival fibromatosis can be
hereditary or idiopathic. These
lesions are rare and occur as highly
fibrotic forms of GO
• The enlargement affects the attached
gingiva, the gingival margin, and the
interdental papillae. The facial and
lingual surfaces of the mandible and
maxilla usually are affected
• The enlarged gingiva is pink, firm, and
almost leathery in consistency, and it
has a characteristic minutely pebbled
surface
102

102. • In severe cases, the teeth are almost
completely covered, and the
enlargement projects into the oral
vestibule.
• The jaws appear distorted because of
the bulbous enlargement of the
gingiva.
• Secondary inflammatory changes are
common at the gingival margin.
103

103. • Histopathology- lesions are highly
fibrotic, with a bulbous increase in
connective tissue that is relatively
avascular and consists of densely
arranged collagen bundles and
numerous fibroblasts.
• The surface epithelium is thickened
and acanthotic, with elongated rete
pegs. Histopathology is similar to
phenytoin-induced GO with low levels
of inflammatory infiltration
104

104. Pathogenesis
105
Coletta et al
2006

105. 106

106. 107

107. Neoplasia
• Benign
• Fibroma
• Papilloma
• Peripheral giant cell
granuloma
• Gingival cyst
• Malignant
• Carcinoma
• Malignant melanoma
108

108. Fibroma
• Slow growing spherical tumor that
tend to be firm and nodular or soft
and vascular.
• Usually pedunculated.
• Composed of bundles of well formed
collagen fibres with scattered
fibrocytes and variable vascularity.
• Other variant- bone, cementum like
material or dystrophic calcifications
may be found- Peripheral ossifying
fibroma.
109

109. • The peripheral ossifying or
cementifying fibroma is found
exclusively on the gingiva
• Clinically, it varies from pale pink to
cherry red and is typically located in
the interdental papilla region
• This reactive proliferation is named
because of the histologic evidence of
calcifications that are seen in the
context of a hypercellular fibroblastic
stroma.
110

110. Papilloma
• Benign proliferations of surface
epithelium most often associated with
HPV (6, 11)
• Solitary wart-like or cauliflower like
protuberances
• Small and discrete or broad hard
elevations with minutely irregular
surface
• Finger like projections of
hyperkeratotic stratified squamous
epithelium with central core of
fibrovascular connective tissue.
111

111. Peripheral giant cell granuloma
• Arise interdentally or from gingival
margin
• Sessile or pedunculated
• Smooth regularly outlined masses or
irregularly shaped multilobulated
protuberances with surface
indentations
• Painless, firm or spongy, pink – deep
red – purplish blue.
• Numerous foci of multinucleated
giant cells and hemosiderin particles
in conn. Tissue.
112

112. Gingival cyst
• Gingival cysts of microscopic
proportions (incidence-0.5%)
• may involve the marginal and
attached gingiva.
• They are painless, but with expansion
they can cause erosion of the surface
of the alveolar bone
• The cyst is lined by thin epithelium
and shows a lumen usually filled with
desquamated keratin, occasionally
containing inflammatory cells
113

113. Squamous cell carcinoma
• It may be Exophytic, manifesting as an
irregular cauliflower like outgrowth, or
Ulcerative, appearing as a flat, erosive
lesion (Non-healing ulcer).
• These masses are locally invasive, and
they involve the underlying bone
(moth eaten appearance) and
periodontal ligament of adjoining
teeth and the adjacent mucosa
• It is often symptom free, going
unnoticed until complicated by
inflammatory changes
• Dysplastic features
114

114. Malignant melanoma
• Malignant melanoma is a rare oral
tumor that tends to occur in the hard
palate and maxillary gingiva
• It is usually darkly pigmented
• It can be flat or nodular, and it is
characterized by rapid growth and
early metastasis
• Infiltration into the underlying bone
and metastasis to cervical and axillary
lymph nodes
115

115. False enlargements
• Not true enlargements of gingiva - -
due to increase in size of underlying
osseous tissue
• Underlying osseous lesions - - tori,
exostoses, ameloblastoma, fibrous
dysplasia, Paget’s disease,
cherubism, CGCG, osteoma,
osteosarcoma
• Developmental enlargement
116

116. Diagnosis and Treatment
117

117. 118
Diagnosis
Critical
decisions in
periodontology-
Hall

118. Diagnosis
119
Agarwal
2015

119. Sl.no Type of enlargement Characteristic clinical feature
1 Drug induced enlargement Fibrotic, increased stippling, no bleeding
Only marginal and interdental papilla involved
2 Chronic Inflammatory
enlargement
Inflamed and edematous, loss of stippling, bleeding
Marginal, interdental, and attached gingiva involved
3 Hereditary gingival
fibromatosis
Fibrotic
Marginal, interdental and attached gingiva are involved
4 Wegener’s granulomatosis Strawberry gingivitis
5 Plasma cell gingivitis Marginal, interdental and attached gingiva involved
Granular surface
6 Neoplasia Neither inflamed nor fibrotic
7 Pyogenic granuloma Discrete, sessile or pedunculated
Bleeds readily with slightest provocation
Often ulcerated
8 Fibroma Localised and discrete
Fibrotic
9 Papilloma Cauliflower or wart like outgrowth
Localised 120

120. Treatment of Gingival Enlargement
121
Critical
decisions in
periodontology-
Hall

121. Gingivectomy
122
INDICATIONS
• Gingival enlargement or overgrowth.
• Elimination of suprabony pockets, regardless of
their depth, if pocket wall is fibrous and firm.
• Elimination of suprabony periodontal abscesses.
• Crown lengthening in patients with adequate
attached gingiva ( eg. Gummy smile ).
• Idiopathic fibrosis.
CONTRAINDICATIONS
• Need for osseous surgery.
• Infrabony pockets.
• Esthetic considerations, particularly in anterior
maxilla.
ADVANTAGES
• Simplicity
• Predictability
• Ease of pocket elimination
DISADVANTAGES
• Healing by secondary intention
• Post operative bleeding
• Loss of keratinized tissue
• Inability to treat underlying
osseous deformities.

122. • Step 1: The periodontal pocket is
mapped out on the external gingival
surface by inserting a probe to the
bottom of the pocket and puncturing the
external surface of the gingiva at the
depth of probe penetration
• Step 2: Periodontal knives (e.g., Kirkland)
are used for incisions on the facial and
lingual surfaces. Orban periodontal
knives are used for interdental incisions.
Bard– Parker blades (#12 and #15), and
scissors are used as auxiliary
instruments.
• Step 3: Remove the excised pocket wall,
irrigate the area, and examine the root
surface.
• Step 4: Scale and root plane.
• Step 5: Cover the area with a surgical
dressing
123

123. WOUND HEALING AFTER SURGICAL GINGIVECTOMY
• Initial Response- formation of a protective surface clot; the underlying tissue being
acutely inflammed. The clot is then replaced by granulation tissue.
• By 24 hrs- there is an increase in number of connective tissue cells ( angioblasts)
beneath the surface layer of inflammation.
• By 3rd Day- fibroblasts appear in the area. The vascular granulation tissue grows
coronally, creating a new free gingival margin & sulcus.
• After 5 to 14 Days- surface epithelialization is generally complete. Complete
epithelial repair takes about 1 month
• 7 weeks- Complete repair of the connective tissue takes place.
• GCF in humans is initially increased after gingivectomy & decreases as healing
progresses.

124. Flap Operation
Indications
1. For larger areas of gingival enlargement (i.e., more than six teeth), and where
attachment loss and osseous defects are present, flap surgery is
recommended.
2. Situations where gingvectomy technique may result in elimination of all
keratinized tissue and consequent creation of mucogingival problems.
125

125. Procedure
• After anesthetizing the area, sounding of the underlying alveolar bone is performed
with a periodontal probe to determine the presence and extent of the osseous defects.
• On the buccal and lingual aspects, with 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
• The same blade is used to thin the gingival tissues in the buccolingual direction to the
mucogingival junction. At this point, the blade establishes contact with the alveolar bone,
and a full-thickness is elevated.
126

126. • Intrasulcular incisions are made on buccal, lingual, and
palatal areas that are being treated to release the tissue
collar
• The marginal and interdental tissues are removed with
curettes.
• After all tissue tags are removed, the roots are
thoroughly scaled and planed, and the bone is
recontoured as needed.
• The flap is replaced or apically displaced and, if
necessary, retrimmed to reach the bone–tooth junction
exactly (palatal flaps). The flaps are then sutured with an
interrupted or a continuous mattress technique, and the
area is protected with periodontal dressing.
127

127. Conclusion
• Gingival enlargement can be caused by a wide variety of etiologies. The
clinician can often diagnose the cause by a careful history, location or by
the clinical presentation.
• Plaque-induced inflammation can be the sole cause of gingival
enlargement or can be a secondary cause, so in all patients, therapy to
control gingival inflammation is essential.
• Thus correct diagnosis & treatment planning form the most essential part
of the treatment of gingival enlargement to achieve proper functional and
esthetic harmony.

128. References
• carranza 12th edition
• Burket’s oral medicine 11th edition
• Brown RS, Arany PR. Mechanism of drug‐induced gingival overgrowth revisited: a unifying hypothesis.
Oral diseases. 2015 Jan;21(1):e51-61.
• Kataoka M, Kido JI, Shinohara Y, Nagata T. Drug-induced gingival overgrowth—a review. Biological and
Pharmaceutical Bulletin. 2005;28(10):1817-21.
• Seymour RA, Ellis JS, Thomason JM. Risk factors for drug‐induced gingival overgrowth. Journal of
Clinical Periodontology: Review article. 2000 Apr;27(4):217-23.
• Corrêa JD, Queiroz-Junior CM, Costa JE, Teixeira AL, Silva TA. Phenytoin-induced gingival overgrowth: a
review of the molecular, immune, and inflammatory features. ISRN dentistry. 2011 Jul 25;2011.
• Samudrala P, Chava VK, Chandana TS, Suresh R. Drug-induced gingival overgrowth: A critical insight into
case reports from over two decades. Journal of Indian Society of Periodontology. 2016 Sep;20(5):496.
• Hall’s critical decisions in periodontology
129

129. Thank you….
130