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2. •Contents:
•Introduction
•Classification
•Scoring of gingival
enlargement
•Inflammatory enlargement
•Drug induced enlargement
•Enlargement associated with
systemic disorder
•Neoplastic enlargement
•False enlargement
•Conclusion
• References
Gingival enlargement

3. Gingival enlargement
 increase in the size of the gingiva
 clinical descriptive term
 Avoid pathological terms used in the past, such as
hypertrophic gingivitis and gingival hyperplasia.
•

4. CLASSIFICATION

5. Gingival enlargement has been classified based on etiologic factors and pathological changes, they are
Inflammatory enlargement
a. Acute
b .Chronic
Drug induced enlargement
•General information
•Anticonvulsants
•Immunosuppressant
•Calcium channel blockers
•Hereditary gingival fibromatosis
Enlargement associated with systemic diseases or conditions:
a. Conditioned enlargement:
•Pregnancy
•Puberty
•Vitamin C
•Plasma Cell Gingivitis
•Nonspecific Conditioned Enlargement (Pyogenic Granuloma)
b. Systemic diseases that cause gingival enlargement:
•Leukemia
•Granulomatous disease (e.g. Wegener’s Granulomatosis)
Neoplastic enlargement (gingival tumors)
•Benign
•False enlargement Malignant

6. BASED ON THE LOCATION AND DISTRIBUTION.
Localized: Limited to the gingiva adjacent to a single tooth or group of tooth.
Generalized: involving the gingiva throughout the mouth.

7. Marginal: confined to the marginal gingiva.
Papillary: confined to the interdental papilla.

8. Discrete: an isolated sessile or pendunculated tumor like
enlargement
Diffuse: involving the marginal and attached gingiva and papilla

9. SCORING OF GINGIVAL ENLARGEMENT:
BUCHNER AND HANSEN 1969
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 quarters or more
of the crown

11. INFLAMMATORY ENLARGEMENT:
CHRONIC INFLAMMATORY ENLARGEMENT:
Hirschfield et al:
Dental plaque-
poor oral hygiene,
Irritation by anatomic
abnormalities,
Improper restorative
and orthodontic
appliances.

12. Clinical features
•appear bluish or deep red.
•ballooning of the interdental papilla and marginal gingiva-It may
be proximal or on the marginal or attached gingiva.
•life preserver shaped bulge around the involved tooth.
•Soft and friable and easy to bleed.
•.

13. Examples

14. Histopathology:
•Exudative and proliferative features.
•Contains inflammatory cells and fluid ,with vascular engorgement, new capillary
formation, and associated degenerative changes.
•Lesions with firm, resilent and pink have fibrotic component with an abundance of
fibroblasts and collagen fibers

15. Management:
•scaling and root planning is the first choice of treatment.
•If fibrotic component does not resolve -surgical removal is the only
treatment of choice.
•The most widely employed surgical approaches for the treatment of
gingival enlargements is
•Gingivectomy- by laser, electrocautery or conventional means
• Flap technique.

16. Examples

17. GINGIVAL ENLARGEMENT IN MOUTH BREATHERS:
Lite,Diamo et al 1955
Etiopathogenesis:
•The exact mechanism of enlargement in mouth breathers is not clear.
•It is thought to be due to alternate wetting and drying of the gingival surface.
•Its harmful effect is generally attributed to irritation from surface dehydration.
•However comparable changes could not be produced by air drying the gingiva
of experimental animals- Maier et al.

18. OCCURENCE
Patients present with mouth breathing habit that may be due to
•short upper lip,
•hyperactive labii superioris,
•proclined incisors,
• rhinitis.

19. Clinical features:
The gingiva appears red and edematous with diffuse
shiny surface.
enlargement in maxillary and mandibular anterior regions
and no involvement of posteriors.
In a typical bimaxillary protrusion case, the enlargement
will be limited to palatal aspect of maxillary anteriors and
labial aspect of mandibular anteriors.

20. Acute Inflammatory Enlargement
GINGIVALABSCESS:
PERIODONTAL ABSCESS:
PERICORONITIS

21. Within 24 to 48 hrs, the lesion usually becomes fluctuant and
pointed with a surface orifice from which purulent exudates
may be expressed
•Due to bacteria carried deep into tissues when a foreign substance e.g. tooth brush, piece of apple core
or lobster shell fragment embedded into the gingiva.
In early stages, it appears as red
swelling with smooth, shiny
surface.
Limited to marginal gingiva or interdental
papilla.

22. PERIODONTALABSCESS:
supporting
tissues.
localized purulent
inflammation.
closely related with
periodontitis and
periodontal pockets,.
the main causes of
tooth extraction and
tooth loss, mainly
in maintenance
patients.
may result in
complications,
due to
bacteremia, that
may cause
infections in
distant locations.

23. Pericoronitis

24. Periapical abscess

25. DRUG INDUCED GINGIVAL ENLARGEMENT
(DIGO or DIGE):
Drugs associated with gingival overgrowth can be categorized broadly into major
groups according to their therapeutic actions, namely
•anticonvulsants,
•immunosuppressant
•calcium channel blocker
•Contraceptives

26. Clinical featureswithin 2-4 month of initiation of drug intake.
there is no pain.
as beadlike enlargement of the interdental papilla and eventually may involve marginal
gingiva.
the enlargement looks like mulberry shape,
firm, pink and resilient with minute lobulations
no bleeding on probing.
prominent in maxillary and mandibular anteriors.
absent in edentulous areas and will disappear in areas where teeth are extracted.
Moritti et al 1999

27. When infected secondarily, there is increase in the size of existing enlargement and
adds characteristic features of inflammatory enlargement.

29. Prevalence
0%
10%
20%
30%
40%
50%
60%
prevalnce
prevalance
Phenytoin -
50%
Cyclosporine
25%
Nifedipine-
15%

30. ANTICONVULSANTS
PHENYTOIN
•Phenytoin (5-diphenylhydantoniate) -seizure disorders in
patients with epilepsy -Merritt & Putnam in 1938.
•its low cost and availability,
•over the last 60 years,

31. Phenytoin induced gingival enlargement
initial enlargement of the
interdental papilla
present a granular or
pebbly surface, with the
enlarged papillae
extending facially and
lingually, obscuring the
adjacent tissue and tooth
surfaces.
resulting in the clinical
presence of pseudoclefts.

32. CYCLOSPORIN-INDUCED GINGIVAL
ENLARGEMENT:
•Cyclosporin A -Switzerland in 1970 as a metabolite of the
fungus species Tolypocludium.
potent immunosuppressive action, cyclosporine A prolongs
survival of allergenic transplants involving skin, heart, kidney,
liver, pancreas, bone marrow, small intestine and lung

33. Clinical Appearance:
Develops in first 6 months
Pebbly or papillary and is mostly restricted to the
keratinized gingiva, but it may grow in size with
time and cover the crowns of teeth causing
difficulties in mastication, speech, and profound
esthetic and psychological problem
more hyperemic and more prone to bleeding on
probing than Phenytoin

34. Calcium channel blockers
Dihydropyridines
•treatment of cardiovascular diseases such as
•hypertension,
•angina pectoris,
•coronary artery spasm and
• arrhythmia by reduced burden on the heart, decreased systemic
vascular resistance, smooth muscle vasodilatation and reduced heart
rate

35. Clinical Changes
Clinical changes appear 1-3 months after administration.
gingival overgrowth as a lobular or nodular enlargement on interdental
papilla located in the anterior interproximal regions.
Associated with local factors
Edentulous areas have not been seen however, it can affect the mucus around
the implant.

37. Dose
multidrug
anticonvulsants,
bacterial plaque,
host genetics
dropped levels of serum
folic acid.
Dosage -50% Girgis et al
found correlation .
Age-younger patient
dose,
bacterial plaque,
age,
Multidrug treatment,
gender
graft.
less in patients over 40 years
due to the growth hormone
and high metabolism of
fibroblast in childhood and
adolescence.
Taylor cyclosporine with
nifedipine caused a 6-fold.
HLA 37
Plaque
Dose
Age
Gender
genetic
polymorphism,
cytochrome P450

38. Drug variable
plaque-induced
inflammatory
changes in the
gingival tissues
genetic factors –
determining the
heterogeneity of
the gingival
Fibroblast
.
Three significant factors
Seymour and Thomas.

40. Debate is ongoing regarding whether
drug-induced gingival overgrowth is
due to hyperplasia of the gingival
epithelium or of submucosal
connective tissue, and/or both/
Genetic?

41. phenytoin first reported in 1939 by Kimball.
1939 Faurbye and in 1959, Strean & Leoni -alkalinity of phenytoin might be the cause of the
gingival side effect.
1948, Brandon hypothesized -direct action on the gingival tissues.
1975, Angelopoulos argued that phenytoin induced degranulation of mast cells which resulted in
the generation of a substance that increased collagen formation.
Larmas, in 1976-proliferating effect primarily on the basal cell layer of the oral epithelium thus
increasing the epithelium-connective tissue interface area, which was confirmed by Hassel et al.
1977, Vogel speculated -end-organ folic acid deficiency, which could lead the gingival tissues
susceptible to inflammation by causing degenerative changes in the gingival sulcular epithelium,
the main physical barrier against local irritants.

42. CsA-induced gingival hyperplasia was first reported by Seymour et al. in
1983.
Despite the cellular and molecular basis of the development of CsA-
induced gingival hyperplasia, the exact mechanism underlying this
condition is still unclear.
A recent study suggested that the imbalance between cell proliferation
and apoptosis may contribute to the pathogenesis of the hypercellularity
observed in CsA-induced gingival hyperplasia.

43. Calcium channel blocker
•Nifedipine-induced gingival enlargement was
first reported by Lederman in 1984 .
•first case of amlodipine-associated
gingival overgrowth was reported by Ellis
in 1993.

45. Mechanism

47. •Platelet derived growth
factor B
•mitogen and chemo attractant for
fibroblast proliferation and
synthesis of glycosoaminoglycans,
fibronectin, and collagen..
Jung et al 2008

48. he best hypothesis so far is that calcium
antagonists inhibit the influx of calcium ions which is
needed for the degradation and synthesis of collagen.
The accumulated collagen and extracellular matrix not
degraded owing to inhibition of calcium influx by calcium
antagonists is suggested to cause gingival hyperplasia.

49. Side effects
.
Nephrotoxicity
Neurotoxicity
Hypertension
Hypertrichosis
Metabolite OL_17
megaloblastic anemia
Accelerate gingival
wound healing and
increase the tensile
strength of abdominal
wounds.
Metabolite: 5 -
parahydroxyphenyl- 5
-phenylhydantoin and
accounts for 50-75%
of the daily dose.
Nifedipine+diabetes
Type II =periodontal
destruction.
tachycardia and facial
redness can be seen in
patients taking these
drugs.

50. Histological characteristics -phenytoin
•thick stratified squamous epithelium with long
thin rete pegs, often acanthotic
•lamina propria is characterized by
proliferation of fibroblasts and increased
collagen formation, accompanied by an
increase in non-collagenous proteins

51. Histopathology- Cyclosporine
•Seen changes in Connective tissue and secularization
as well as focal inflammatory cells particularly plasma
cells.
•Pisantly argued that gingival enlargement is simply
due to the epithelial acanthosis and accumulation of
extracellular matrix and the connective tissue does not
change in size.

52. Histopathological Changes-nifedipine:
•In the study conducted by Barak, the gingival epithelium
proliferation was more responsible for gingival enlargement
than connective tissue proliferation.
•An increase was reported in production of acid
mucopolysaccharides and the number of cytoplasmic secretory
granules.

53. Other drugs
Gingival overgrowth has been associated with the use of
erythromycin -Valsecchi et al in 1992: Lombardi et al in 1989

54. CONTRACEPTIVES
Gingival enlargement associated with contraceptives was
first reported in 1967 by Lynn.
Despite case reports, contraceptives are not known as
inducers of gingival enlargement.
After a few months of administration, the cumulative
dose will be 6-15 times greater than the expected and the
effects will disappear by stopping the administration.
Norethindrone Mestranol

55. Treatment

56. Key strategies in gingival
enlargement.
•Plaque control
•medical management
•periodontal surgical procedures
•multidisciplinary dental care

57. Nifedipine with Isradipine ( 20 mg BD).(westbrook in 2001)
ACE Inhibitors like Captopril (12.5 to 50mgBD), Enalapril
(2.5to20 mg OD) to control hypertension
Phenytoin with Phenobarbital(60 mg TDS), Primidone (
100mg TDS) Carbamezepine (200-400mg TDS) Valproic acid
(200-500mg TDS)
Cyclosporin A with Tacrolimus (0.15 to 0.20/kg/d) Rapamycin
Drugs substitute:

58. Gingivectomy
Excision of gingiva. Simple & quick technique
Advantages
Permits an adequate contouring of the tissue Controls hemorrhage
Disadvantages Unpleasant odour Irreparable damage to bone Use
limited to superficial procedures Heat generated can cause tissue damage
& loss of periodontal support.

59. Co2 lasers used for excision of gingiva
Advantages Excellent soft tissue ablation
Haemostatic characteristic
Disadvantages Healing is delayed
Requires precautionary measures
Application to root surface or alveolar bone
causes carbonization & major thermal
damage.
Electrocautery

60. IDIOPATHIC GINGIVAL
ENLARGEMENT:
•Also referred to as congenital familial fibromatosis,
gingivomatosis, idiopathic fibromatosis, elephantiasis and
hereditary gingival hyperplasia.
•It presents as unusual fibrotic gingival enlargement of
localized or generalized extent.
•It may present as a specific entity or as a part of syndrome.
•Autosomal recessive and autosomal dominance.

61. •Diagnosis can be made by a positive family history of gingival
enlargement.
•It usually begins with the eruption of the primary or permanent
dentition.
•A frequent finding could be presence of firm bulky
enlargement of gingiva restricted to maxillary and mandibular
second and third molar areas only.
•The enlarged mass may be pink or reddish and may be firm/
nodular, pebbly on palpation.
•Involve attached gingiva, marginal gingiva and interdental
papilla
•It affects the marginal gingival, attached gingival and
interdental

62. •Alveolar bone is rarely affected, but presence of pseudo-
pockets and difficulty in maintaining oral hygiene may lead
to some periodontal problems.
•Extensive overgrowths can lead to esthetic and functional
concerns to the patient.
•Seen in tuberous sclerosis –inherited disorder characterized
by triad of epilepsy, mental deficiency and cutaneous
Angiofibromas-stirrups et al 1972 :Thomas et al 1992

63. CONDITIONED GINGIVAL ENLARGEMENT
Hormonal:
•Generalized gingival hyperplasia, during pregnancy and puberty,
is influenced by hormonal changes that pretentious the response to
local irritants.
•The interproximal gingiva shows more prominent enlargement
than the facial and/or lingual surfaces .
•The enlarged gingiva usually is soft and friable, bright red or
magenta, with a smooth, shiny surface.

64. •Bleeding may occur extemporaneously or on mild
stimulation.
The enlargement may reduce spontaneously after the delivery,
but complete elimination may require the removal of all local
irritants and additional surgical intervention of any fibrotic
remnants.

65. VITAMIN C DEFICIENCY:
•Deficiency of vitamin C is defined as a serum ascorbic acid level
< 2 μg/mL
•Diabetes, stress and smoking are the commonly labeled factors
leading to mild vitamin C deficiency.
•Causes hemorrhage, collagen degeneration and
edema
•The gingiva, of vitamin C deficiency associated enlargement, is
bluish red, soft and friable with a smooth, shiny surface.
•Involve marginal.
•Bleeding may occur spontaneously or on slight irritation.
•Surface necrosis with pseudomembrane formation is also
frequently seen.

66. PLASMA CELL GINGIVITIS:
•The etiology difficult to establish,
•Appears due to hypersensitivity reaction with affluent
plasma cells seen histologically.
•Usual allergens known to be associated with this lesion
could be, e.g., toothpaste, food product particularly
cinnamon, chewing gum or unknown origin
•Associated with
cheliosis and
Glossitis,
Rapid progressive periodontitis

67. •It might bleed on provocation.
•Patients usually complain about burning
sensation on eating hot and spicy food.
• Appearance is reddish in color, involves almost
complete attached gingiva, slight granular
surface appearance is typical.

68. Pyogenic Granuloma
Kerr et al1951
recurrence rate 15%

69. GINGIVAL ENLARGEMENT ASSOCIATED WITH
SYSTEMIC DISEASE:
LEUKEMIA:
•Generalized gingival enlargement associated with leukemia is due to
the massive infiltration of leukemic cells in the gingival connective
tissue.
•Clinically it may mimic inflammatory origin.
Apart from gingival enlargement
other associated features could be
oral ulceration, spontaneous
gingival bleeding,
petechiae,
mucosal pallor,
herpetic infections and candidiasis.

70. •Rarely, numbness in chin and/or tooth pain.
serious condition associated with gingival enlargement
-acute myeloid leukemia.
It can be associated with signs and symptoms of bone
marrow failure, such as ecchymoses, night sweats,
recent infections and lethargy.
An expeditious diagnosis can be made by a simple full
blood count.

71. CLINICAL FEATURES
•enlargement may be diffuse or marginal
•localized or generalized
•may appear as a diffuse enlargement of the
gingival mucosa
•oversized extension of the marginal gingiva, or
a discrete tumor like interproximal mass

72. WEGENER’S GRANULOMATOSIS:
Rare disease affecting respiratory tract and kidney
•Strawberry gingivitis, formed by reddish-purple
exophytic gingival swelling with petechiae
hemorrhages,
•The oral lesions -help in timely diagnosis of this
potentially fatal condition, because they persist for a
long time before multi-organ involvement occurs.

73. •At least two of the following conditions should be fulfilled to
diagnose the condition as Wegener’s Granulomatosis:
(1) Ulcerative lesions of oral mucosa or nasal bleeding or
inflammation;
(2) Nodules, fixed infiltrates or cavities in chest radiograph;
(3) Abnormal urinary sediment; and
(4) Granulomatous inflammation on biopsy

74. •Seen in renal failure patients.
•use of immunosuppressive drugs has
produced prolonged remissions in more than
90% of cases –Kornblut 1980
etiology

75. CLINICAL FEATURES
•reddish purple and bleeds easily on stimulation
•considered an immunologically mediated tissue injury –Cotran
1989

76. BENIGN TUMORS OF THE GINGIVA
:
EPULIS :
•It is a generic term used clinically to designate all discrete tumors
and tumor like masses of the gingiva.
•Most lesions referred to as epulis are inflammatory rather than
neoplastic.

77. FIBROMA
•arise from the gingival connective tissue or from the
periodontal ligament.
•They are slow-growing, spherical tumors that tend to be firm
and nodular but may be soft and vascular.
•Fibromas are usually pendunculated.
HISTOPATHOLGY
Well formed collagen bundles with scattering of fibrocytes

78. PERIPHERAL GIANT CELL GRANULOMA:
•arise interdentally or from the gingival margin.
•Occur most frequently on the labial surface, and may
he sessile or pendunculated.
•Varies from smooth, regularly outlined masses to
irregularly shaped, multilobulated protuberances with
surface indentations.
•Painless.

79. CENTRAL GIANT CELL GRANULOMA:
• These lesions arise within the jaws and produce central
cavitation.
•They occasionally create a deformity of the jaw that makes
the gingiva appear enlarged.

81. The peripheral odontogenic fibroma (PODF) is
definedas a relatively rare tumor that occurs exclusively in the
soft tissues covering tooth-bearing areas of the jaws.
It is considered to represent the soft tissue counterpart of the central
odontogenic fibroma that occurs in bone.
Confusion existsregarding this gingival entity because it has been
referred to bya number of different names, has a debatable
histogenesis, andis often mistaken for the relatively common reactive
lesion, the peripheral ossifying fibroma

82. Peripheral cemento ossifying fibroma

83. MALIGNANT TUMORS OF THE GINGIVA:
CARCINOMA:
•Oral cancer accounts for less than 3% of all malignant
tumors in the body but is the sixth most common cancer
in males and the twelfth in females." The gingiva is not a
frequent site of oral malignancy (6% of oral cancer).
•Squamous cell carcinoma is the most common
malignant tumor of the gingiva.
It may be exophytic,
presenting as an irregular
outgrowth, or ulcerative,
which appear as flat, erosive
lesions

84. MALIGNANT MELANOMA:
•rare oral tumor that tends to occur in the hard palate and maxillary
gingiva of older persons.
•
•darkly pigmented and is often preceded by the occurrence of
localized pigmentation .
•flat or nodular and is characterized by rapid growth and early
metastasis

85. SARCOMA:
•Fibrosarcoma, lymphosarcoma, and reticulum cell
sarcoma of the gingiva are rare .
•Kaposi's sarcoma often occurs in the oral cavity of
patients with acquired immunodeficiency syndrome
particularly in the palate and the gingiva.

86. METASTASIS:
•not common
•Such metastasis has been reported with various tumors,
including adenocarcinoma of the colon, lung
carcinoma, primary hepatocellular carcinoma.
•Ulcerations that do not respond
• to therapy in the usual manner,
•as well as all gingival tumors
• and tumor like lesions
•must be biopsied and submitted for microscopic
diagnosis.

87. FALSE ENLARGEMENT:
•not true enlargements of the gingival tissues but may appear
as such as a result of in- creases in size of the underlying
osseous or dental tissues.
• The overlying gingiva presents with no abnormal clinical
features except the massive increase in size of the area.

88. UNDERLYING OSSEOUS LESIONS:
•occurs most commonly in tori and exostosis, but it can also
occur in Paget's disease, fibrous dysplasia, cherubism, central
giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma
.
Gingival tissue can appear normal or may have unrelated
inflammatory changes

90. UNDERLYING DENTAL TISSUES:
•During the various stages of eruption, particularly of the
primary dentition, the labial gingiva may show a bulbous
marginal distortion caused by superimposition of the bulk of
the gingiva on the normal prominence of the enamel in the
gingival half of the crown-developmental enlargement
•Physiologic and ordinarily present no problems.

91. GENETIC DISORDERS ASSOCIATED WITH GINGIVAL
ENLARGEMENT:
They can be divided into 4 primary categories based on their etiology,
clinical features and histology.
•Idiopathic Gingival Enlargement
•Lysosomal Storage Disorders,
•Vascular Disorders
•Dental abnormalities
•syndromes typically associated with gingival enlargements:
Apert’s syndrome, Cross–McKusick–Breen syndrome also
known as "Cross syndrome, Melkersson-Rosenthal Syndrome,
Sturge weber syndrome

92. CONCLUSION:
•Inspite of etiology, gingival enlargements can often be diagnosed
by a careful history (e.g., drug influenced or hormonal influenced
gingival enlargement), by location (e.g., mouth-breathing
enlargement around anterior teeth) or by the clinical presentation
(e.g., strawberry gingivitis).
•Presence of local irritants (plaque= and calculus) could be
primary or associated cause of gingival enlargements. Hence,
plaque control is an essential aspect of management in all the
patients.
•An excisional/incisional biopsy and/or hematologic/histologic
examination may be needed occasionally to correctly diagnose the
uncommon cases of gingival enlargement.
•The clinician should have an open mind and consider all
possibilities before coming to the final diagnosis of condition at
hand.

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