This document discusses gingival enlargement, including inflammatory and drug-induced forms. Inflammatory enlargement can be acute or chronic and is caused by plaque, trauma, or mouth breathing. Drug-induced gingival overgrowth is caused by medications like phenytoin, calcium channel blockers, and cyclosporine. It occurs through effects on fibroblasts that impair collagen metabolism and degradation. Treatment involves managing local factors through plaque control while the underlying cause, such as a medication, is addressed.

1. GINGIVAL
ENLARGEMENT
Chapter 19

2.  A change in the dimensions of gingival tissue is
always a pathologic event. Gingival enlargement
can be transient and reversible or can be chronic
and irreversible. It is important to identify the
cause and confounding etiologic factors.
 Inflammation of the periodontal tissues results in
three outcomes:
• complete resolution of inflammation and restoration
of tissue integrity
• Destruction of periodontal tissues and loss of
attachment (chronic periodontitis)
• Fibrosis

3.  Fibrosis is a component of the defense mechanism against
progression of periodontal inflammation.
 Fibroblasts generate excessive amounts of collagen and
non-collagenous proteins of the extra-cellular matrix.
Increased matrix deposition is not sufficiently balanced by
the enzymatic degradation of the matrix composition,
resulting in fibrotic changes in soft tissues.
 Fibrosis of gingival tissues is commonly referred to as
gingival hyperplasia.
 In contrast to other tissues with fibrosis, gingival lesions are
usually inflamed due to accumulation of bacteria and
reduced oral care.

4.  Hyperplasia: an increase in the number of cells
 Hypertrophy: increased cell size
 Hyperplastic, hypertrophic, and fibrotic changes are
observed during gingival enlargement and cannot be
accurately differentiated. Therefore, accepted current
terminology for this condition is gingival enlargement and
gingival overgrowth (GO).
 Classification of GO is based on etiologic factors. The most
common form results from systemic use of medications and
is called drug-induced gingival overgrowth (DIGO).
Terminology and Classification

5. CLASSIFICATION
I. Inflammatory enlargement due to gingivitis
A. Chronic
B. Acute
C. Plasma cell gingivitis
II. Drug-induced enlargement (anticonvulsants, calcium
channel blockers and immunosuppressants)
III. Associated with systemic conditions
1. Pregnancy
2. Puberty
3. Nutrition (Vit. C deficiency)

6. CLASSIFICATION
IV. Associated with systemic diseases
1. Leukemia
2. Wegener granulomatosis
3. Sarcoidosis
V. Gingival Fibromatosis
IV. Other forms
A. Neoplastic enlargement (benign & malignant
tumors
B. False enlargement
 Any form that can’t be classified among these forms is known
as idiopathic GO.

7. Using the criteria of location and distribution,
gingival enlargement is designated as follows:
Localized: Limited to the gingiva adjacent to a single
tooth or group of teeth
Generalized: Involving the gingiva throughout the mouth
Marginal: Confined to the marginal gingiva
Papillary: Confined to the interdental papilla
Diffuse: Involving the marginal and attached gingiva
and papillae
Discrete: An isolated sessile or pedunculated tumor-like
enlargement

8. The degree of gingival enlargement can be scored as
follows:
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

9. INFLAMMATORY ENLARGEMENT
A. Chronic Inflammatory Enlargement
In some cases, gingival enlargement is a direct
outcome of gingivitis without any complicating
factors or involvement of systemic conditions.
Initial assessment: visual examination of abnormalities
of gingival contours, texture, and color, accompanied
by a detailed medical history to exclude potential
systemic factors and conditions.

10. CLINICAL FEATURES
 Slight ballooning of the interdental papilla and
the marginal gingiva which can increase in size
until it covers part of the crowns
 Localized or generalized
 Grows slowly and painlessly unless complicated
by acute infection or trauma
 Occasionally as a discrete sessile or pedunculated
mass resembling a tumor
 interproximal or on the marginal or attached
gingiva
 painful ulceration sometimes occurs

11. INFLAMMATORY GINGIVAL ENLARGEMNT

12. ETIOLOGY
Microbial biofilm
 Factors that favor plaque accumulation and
retention include poor oral hygiene as well as
irritation by anatomic abnormalities, misaligned
teeth, open bite, improper restorative and
orthodontic appliances.

13. HISTOPATHOLOGY
 Exudative: lesions that clinically are deep red or
bluish red are soft and friable with a smooth, shiny
surface, and they bleed easily. They have a
preponderance of inflammatory cells and fluid with
vascular engorgement, new capillary formation,
and associated degenerative changes.
 Proliferative: lesions that are relatively firm,
resilient, and pink have a greater fibrotic
component with an abundance of fibroblasts and
collagen fibers.

14. B. Acute Inflammatory Enlargement
ETIOLOGY
 Mechanical, chemical, or physical irritation, can be resolved by
removal of the irritant. Mouth breathing, impacted food and
poor oral hygiene are usually responsible too.
 Localized to marginal or papillary gingiva.
 The main etiologic factor is trauma. Traumatic lesions occur
when a foreign substance (e.g., toothbrush bristle) is forcefully
embedded in the gingiva and complicated by resident microbes.
 Trauma-induced injuries result in a chronic process
characterized by granulation tissue formation and fibrosis.
Because nerve tissue does not proliferate, pain is uncommon.

15. B. Acute Inflammatory Enlargement
GINGIVAL ABSCESS
 Localized, painful, rapidly expanding lesion
 Limited to the marginal gingiva or interdental
papilla
 In early stages, it appears as a red swelling
with a smooth, shiny surface

16. GINGIVAL ABSCESS UNRELATED TO THE GINGIVAL SULCUS

17.  Within 24 to 48 hours, the lesion usually becomes
fluctuant and pointed with a surface orifice from
which a purulent exudate may be expressed
 Adjacent teeth may become sensitive to percussion
 if permitted to progress, the lesion generally
ruptures spontaneously.
 The lesion is confined to the gingiva, and it should
be distinguished from periodontal abscess.

18. HISTOPATHOLOGY
 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.

19. Gingival Changes Associated with
Mouth Breathing
 Gingivitis and gingival enlargement are often
seen in mouth breathers
 Gingiva appears red and edematous with a
diffuse surface shininess of the exposed area
 Maxillary anterior region commonly involved
 Altered gingiva is clearly demarcated from the
adjacent unexposed normal gingiva
 Harmful effect is generally attributed to
irritation from surface dehydration.

21.  Sometimes manifests as a mild marginal gingival enlargement
that extends to the attached gingiva.
 It is thought to be allergic in origin and possibly a reaction to
components of chewing gum, dentifrices, or various dietary
items. Cessation of exposure to the allergen brings resolution
of the lesion.
 Gingiva appears red, friable, and sometimes granular and
bleeds easily. Usually it does not cause loss of attachment.
 It is located on the oral aspect of the attached gingiva and is
different from plaque-induced gingivitis.
C. Plasma Cell Gingivitis

23. HISTOPATHOLOGY
 Oral epithelium shows spongiosis and infiltration
with inflammatory cells
 There are signs of damage in the lower spinous
layers and the basal layers
 The underlying connective tissue contains a dense
infiltrate of plasma cells that also extends to the oral
epithelium, producing a dissecting type of injury.
 Associated cheilitis and glossitis have been reported.

24. Important Points
 In rare instances, marked inflammatory gingival
enlargements with a predominance of plasma cells can
appear; they are associated with aggressive periodontitis.
 A solitary plasma cell tumor (i.e., plasmocytoma) has been
described in the nasopharynx and rarely in the oral mucosa.
• a slow-growing, pedunculated tumor with a pink and smooth
surface, and is composed of normal plasma cells.
• usually benign, but rarely, it can be an oral manifestation of
multiple myeloma, which is a malignant B-cell tumor of the
bone marrow.

25. Treatment
 Chronic enlargement of the gingiva due to gingivitis is
reversible and can be resolved by removal of the etiologic
factors, including biofilm and correction of environmental
factors.
 In severe forms of inflammatory enlargement, surgical
approaches may be required.
 In addition to the acute and chronic forms of GO associated
with gingivitis, systemic conditions also cause inflammatory
changes in gingiva.
 The distinction should be made very early in treatment
planning, and the involvement of drugs, systemic conditions,
and neoplastic lesions should be carefully ruled out.

26. DRUG-INDUCED GINGIVAL OVERGROWTH
(DIGO)
 Consequence of the administration of some anticonvulsants
(phenytoin), immunosuppressants (cyclosporine), and
calcium channel blockers (nifedipine).
 Prevalence: 30% to 80%
 Genetic factors, drug dosage, and local factors can affect
the development and severity of DIGO.
 DIGO results in impaired oral hygiene, biofilm accumulation,
gingival inflammation and infection.
 Alternative drugs have also been linked to DIGO

27. CLINICAL FEATURES
 Lesions usually develop fast and become chronic over time.
Because most of these medications are prescribed for an
extended time, the lesions expand and cover the crowns of the
teeth. Severe forms may result in complete coverage
 The first signs can be observed as early as 3 months of drug
use as a localized nodular enlargement of the interdental
papilla.
 Biofilm and bacterial infection lead to inflamed tissues
characterized by edema and bleeding. The degree of fibrosis
and inflammation depend on the dose, duration, and type of
drug; oral hygiene; individual susceptibility, including genetic
factors; and environmental influences.

28. ANTICONVULSANTS
 Phenytoin (diphenylhydantoinate)
 Other anticonvulsants such as phenobarbital and valproic acid
have been associated with GO less often than phenytoin.
 Prevalence of phenytoin-induced GO is about 50%. Clinical
onset occurs as early as 1 month, and increasing severity is
seen in 12 to 18 months.
 Lesions frequently occur on the anterior buccal maxilla and
mandible, and the entire dentition can be covered in severe
cases.
 Enlargement of interdental papillae and increased thickening of
the marginal tissues cause aesthetic and functional problems,
such as malpositioning of teeth, difficulty in speech, and
impaired oral hygiene.

30. CALCIUM CHANNEL BLOCKERS
 Some of these drugs can induce gingival enlargement.
 Benzothiazepine derivatives (diltiazem), phenylalkylamine
derivatives (verapamil), and dyhydropyridines (amlodipine,
felodipine, isradipine, nicardipine, nifedipine, nitrendipine,
oxodipine, nimodipine, nisoldipine)
 Prevalence of nifedipine-induced GO: 6% to 83%
 Clinically, interdental papillae are affected, and overgrowth
is limited to attached and marginal gingiva, which usually is
observed on the anterior segments.
 Nifedipine-induced GO can co-exist with periodontitis and
attachment loss that is different from other forms of DIGO.

31. IMMUNOSUPPRESSANTS
 Cyclosporine A is used to prevent organ transplant
rejection and for treatment of autoimmune diseases
 Prevalence of cyclosporin A-induced GO: 30%, but can
be much higher, especially for pediatric populations
 Lesions are more inflamed and bleed more than other
forms of DIGO, and are limited to buccal surfaces.
 Severity can be similar to those of phenytoin and
nifedipine. They affect the entire dentition and
interfere with occlusion, mastication and speech.

32. HISTOPATHOLOGY
 Phenytoin: a thick, stratified squamous epithelium
with long, thin rete pegs extending deep into the
connective tissue. Fibrosis with minimal inflammatory
cell infiltration is a common finding.
 Calcium channel blockers: similar to phenytoin-
induced lesions, including epithelial thickness, rete
peg formation, and excessive matrix accumulation.
 Cyclosporin A: a thickened epithelium, rete peg
formation, and irregular collagen fibers. Lesions,
however, are characterized with more inflammatory
infiltration and vascularization compared with the
other two.

35. Pathogenesis of DIGO
 The main mechanism: defective function of gingival fibroblasts.
DIGO-associated medications affect the extracellular matrix
metabolism by decreasing collagenase activity and increasing
the production of matrix proteins.
 Fibroblasts in phenytoin: elevated levels of collagen synthesis.
 Nifedipine: defective collagen production due to decreased
collagenase activity, which results in collagen deposition.
 Calcium channel blockers: decrease calcium levels in gingival
fibroblasts and T-cells through interference with calcium
metabolism, hereby affecting T-cell proliferation or activation
and collagen biosynthesis.
 Cyclosporin A: directly impairs collagen synthesis by gingival
fibroblasts, with a concomitant rise in the levels of type I
collagen. It also decreases expression of MMP-1 AND MMP-3.

36.  In addition to collagen, which is the major extracellular matrix
component of gingival tissues, non-collagenous matrix is
affected by the medications that result in DIGO.
 Glycosaminoglycan metabolism is impaired in patients with
phenytoin-induced GO and in response to cyclosporin A
treatment of gingival fibroblasts.
 In addition to fibroblast metabolism and function,
inflammatory regulation of tissue turnover is a major factor in
DIGO pathogenesis.
 Fibroblast functions such as proliferation, differentiation, and
production of extracellular matrix are affected by levels of
cytokines and growth factors.

37.  GO lesions are characterized by increased levels of IL-6, IL-1β,
PDGFB, FGF2, TGF-β, and CTGF. Macrophages are the main
source of these cytokines.
 The TGFβ - CTGF axis is an essential mechanism leading to
DIGO. TGF-β1 regulates cell proliferation and differentiation
and can activate gene expression for the synthesis of
extracellular matrix components, including collagen in
cyclosporin A–induced GO.
 TGF-β1 induces CTGF mRNA and protein expression in gingival
fibroblasts; the TGFβ - CTGF pathway directly regulates
fibrosis, gingival fibroblast lysyl oxidase, and collagen
generation.

38.  CTGF expression is increased in all forms of DIGO, with the
highest levels occurring in phenytoin-induced GO, which also
has the highest levels of fibrosis.
 CTGF expression is not limited to the connective tissue. It also
is demonstrated in the gingival epithelium, predominantly in
the basal epithelial cells close to the connective tissue border,
illustrating a possible mechanism of fibrosis in gingiva, which
may be related to crosstalk between epithelial and connective
tissue cells.
 A key event in the pathogenetic mechanism of DIGO is
epithelial-mesenchymal transition induced by medications.
Highly fibrotic tissues are characterized by increased epithelial-
mesenchymal transition, through which epithelial cells in the
gingiva acquire fibroblast function, and the process is
regulated by CTGF.

39. TREATMENT
 DIGO cannot be prevented by conventional approaches, but
it can be ameliorated by elimination of local factors, plaque
control, and regular periodontal maintenance.
 The most effective treatment is withdrawal or substitution of
medications. Resolution of gingival lesions occurs in 1 to 8
weeks after discontinuing the medication. However, most
alternatives have also been linked to DIGO in recent years.
 Nifedipine Isradipine
 Cyclosporin A Tacrolimus

40. Treatment
 In addition, nonsurgical treatment (SRP) can eliminate the
inflammatory component of DIGO, which can account for
40% of tissue enlargement.
 Because the anterior labial gingiva is frequently affected,
surgery is commonly performed to solve aesthetic problems.
Surgical elimination of lesions involves gingivectomy and
gingivoplasty. However, the recurrence rate is high; the rate
for GO among patients taking cyclosporin A or nifedipine was
approximately 40%, 18 months after the surgery.
 Patients should be given oral hygiene instructions, and
periodontal prophylaxis and removal of calculus should be
done as needed during recall visits.

41. GO Associated With Systemic Conditions
Manifest with amplification of existing inflammation. These
gingival pathologies are referred as “conditioned enlargements”
and include lesions associated with hormonal and nutritional
etiologic factors.
Causes for hormonal changes: Pregnancy and puberty. Nutritional
factors are rare such as vitamin C deficiency. Likewise, allergic
reactions may be linked to GO.
Gingival inflammation due to microbial factors is a prerequisite
that hormonal and nutritional changes modify, and some
researchers classify these lesions as gingivitis-associated
pathologies.

42. A. Pregnancy-Associated GO
Clinical Manifestations
 Single or multiple tumor-like masses at the
gingival margin.
 Results from the aggravation of previous
inflammation
 Incidence: 10% to 70%
 Sometimes, the lesions can be observed as
single enlargements, which are referred to as
pregnancy tumors.

44.  So-called pregnancy tumor is not a neoplasm
 Represent an inflammatory response to
microbial plaque modified by the patient's
condition
 usually appears after the third month of
pregnancy but it may occur earlier.
 Incidence: 1.8% to 5%

45.  Pregnancy-associated GO manifests with a highly
varied clinical picture.
 Enlargement is usually generalized but tends to be
more prominent inter-proximally than buccal/lingual
surfaces
 Gingiva is bright red or magenta, soft, and friable and
has a smooth, shiny surface.
 Spontaneous or on slight provocation bleeding

46.  Lesion appears as a discrete, mushroom-like, flattened
spherical mass protruding from the gingival margin or
more often from the interproximal space and is
attached by a sessile or pedunculated base
 Tends to expand laterally and pressure from the
tongue and the cheek perpetuates its flattened
appearance.
 Dusky red or magenta
 Surface is smooth and glistening and exhibits
numerous deep red, pinpoint markings

47.  Lesion does not invade the underlying bone. The mass is
usually firm, but may have various degrees of softness and
friability. It is usually painless unless its size and shape foster
the accumulation of debris under its margin or interfere with
occlusion, in which case painful ulceration may occur.
 Pyogenic granuloma is similar in clinical and microscopic
appearance to the GO seen during pregnancy. It manifests as a
tumor-like enlargement that is considered to be an exaggerated
response to minor trauma. The exact nature of the systemic
conditioning factor has not been identified.
 The differential diagnosis is based on the patient’s history.

49.  Progesterone and estrogen levels increase 10 to 30
times by the end of the third trimester.
 These hormonal changes induce an increased vascular
permeability, which leads to gingival edema, increased
inflammatory response to dental plaque, and can lead
to modification of the subgingival microbiota.
 Increased presence of Prevotella intermedia,
Prevotella melaninogenica, and Porphyromonas
gingivalis has been linked to pregnancy-associated GO
Etiology

50. HISTOPATHOLOGY
 Gingival enlargement in pregnancy is called angiogranuloma,
referring to its strong clinical presentation with vascular
changes and fibrotic process.
 Central mass of connective tissue with numerous diffusely
arranged, newly formed, and engorged capillaries lined by
cuboid endothelial cells and of a moderately fibrous stroma
with varying 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.

52. TREATMENT
 Lesions can be prevented by good oral hygiene and patients
should be treated by removal of plaque and calculus.
 Severe cases may require removal during the second
trimester; however, removal without establishment of an
optimal oral hygiene ensures recurrence. Although
spontaneous reduction in the size of gingival enlargement
typically follows the termination of pregnancy, complete
elimination of the residual inflammation and GO requires
removal of all plaque deposits and factors that favor its
accumulation, and in some fibrotic cases, surgical intervention.
 Treatment of pyogenic granuloma consists of the removal of
the lesions and the elimination of irritating local factors. The
recurrence rate is about 15%.

53. B. Puberty-Associated GO
Clinical Manifestations
 Occurs in both male and female adolescents.
 Has a strong association with plaque accumulation.
 Lesions are marginal and interdental and is characterized by
prominent bulbous inter-proximal papillae.
 Often only the facial gingivae are enlarged and the lingual
surfaces are relatively unaltered. The mechanical action of
the tongue and the excursion of food prevent a heavy
accumulation of local irritants on the lingual surface.

55. Etiology
 GO during puberty has all of the clinical features that are
associated with chronic inflammatory gingival disease.
 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.

56. Etiology
 Studies implicated that Capnocytophaga species
have a role in the initiation of pubertal gingivitis.
 Hormonal changes coincide with an increase in the
proportion of Prevotella intermedia and Prevotella
nigrescens.

57. HISTOPATHOLOGY
 The microscopic picture is that of chronic inflammation
with prominent edema. It cannot be distinguished
from other forms of gingivitis-associated GO lesions.
TREATMENT
 After puberty, enlargement undergoes spontaneous
reduction, but it does not disappear completely until
the plaque and calculus are removed.

58. C. Nutrition-Associated GO
GO has been observed in cases of chronic vitamin C deficiency
in patients with scurvy. These lesions are no longer common,
but GO is still considered a part of the classic description of
scurvy.
Clinical Manifestations
 Lesions are marginal. Gingiva is bluish red, soft, and friable,
and it has a smooth, shiny surface. Hemorrhage that occurs
spontaneously or on slight provocation and surface necrosis
with pseudo-membrane formations are common features.

60.  Acute vitamin C deficiency does not cause gingival
inflammation, but it does cause hemorrhage,
collagen degeneration and edema of the gingival
connective tissue.
 These changes modify the response of the gingiva
to plaque to the extent that the normal defensive
reaction is inhibited and the extent of the
inflammation is exaggerated, thereby resulting in
the massive gingival enlargement seen in patients
with scurvy.
Etiology

61. HISTOPATHOLOGY
 Chronic inflammatory cellular infiltration with a superficial
acute response.
 Scattered areas of hemorrhage, with engorged capillaries.
 Marked diffuse edema, collagen degeneration and a scarcity
of collagen fibrils or fibroblasts are striking findings.
TREATMENT
 Changes in nutrition accompanied by non-surgical treatment
and good hygiene usually result in complete resolution of the
pathology. In rare cases, surgical removal may be indicated.

62. GO Associated With Systemic Diseases
A. Leukemia-Associated GO
Clinical Manifestations
 May be diffuse or marginal, localized or generalized or a
discrete tumorlike inter-proximal mass.
 Gingiva is bluish red and has a shiny surface.
 consistency is moderately firm, but there is a tendency
toward friability and hemorrhage that occur spontaneously or
with slight irritation.

63.  Acute painful necrotizing ulcerative inflammatory
involvement can occur in the crevice formed at the junction
of the enlarged gingiva and the contiguous tooth surfaces.
 Patients with leukemia may also have a simple chronic
inflammation without the involvement of leukemic cells, and
they can have the same clinical and microscopic features
seen in patients without the systemic disease. But, most
cases have features of simple chronic inflammation and
leukemic infiltrate.
 True leukemic enlargement often occurs with acute
leukemia, but it may also be seen with subacute leukemia.
It seldom occurs with chronic leukemia.

65. HISTOPATHOLOGY
 Various degrees of chronic inflammation.
 Mature leukocytes are seen along with areas of connective
tissue infiltrated with a dense mass of immature and
proliferating leukocytes.
 Engorged capillaries, edematous and degenerated
connective tissue and epithelium with various degrees of
leukocytic infiltration are found.
 Isolated surface areas of acute necrotizing inflammation with
a pseudomembranous meshwork of fibrin, necrotic epithelial
cells, PMN leukocytes, and bacteria are often seen.

66. B. Wegener Granulomatosis
Clinical Manifestations
 Is a rare disease characterized by acute granulomatous
necrotizing lesions of the respiratory tract, including nasal
and oral defects. Renal lesions develop, and acute necrotizing
vasculitis affects the blood vessels.
 Initial manifestations may involve the orofacial region and
include oral mucosal ulceration, gingival enlargement,
abnormal tooth mobility, exfoliation of teeth, and delayed
healing response.
 Gingiva is reddish purple and bleeds easily on stimulation

68. Etiology
 Cause is unknown
 Considered an immunologically mediated tissue injury
 The usual outcome was death from kidney failure
within a few months, but the use of
immunosuppressive drugs has produced prolonged
remissions in more than 90% of cases.

69. HISTOPATHOLOGY
 Chronic inflammation involves scattered giant cells,
foci of acute inflammation, and micro-abscesses
covered by a thin, acanthotic epithelium.
 Vascular changes have not been described with
gingival enlargement in patients with Wegener
granulomatosis, probably because of the small size of
the gingival blood vessels.

70.  Granulomatous disease of unknown etiology
 Individuals in their twenties or thirties, affects predominantly
blacks.
 Can involve almost any organ, including the gingiva, where a
red, smooth, painless enlargement may appear.
HISTOPATHOLOGY
 Consist of discrete, epitheliold cells and multinucleated
foreign-body-type giant cells with peripheral mononuclear
cells
B. Sarcoidosis
Clinical Manifestations

71. Gingival Fibromatosis
Clinical Manifestations
 Can be hereditary or idiopathic. These lesions are
rare and occur in highly fibrotic forms of GO.
 Hereditary gingival fibromatosis is the most common
form, and has been linked to several genetic loci.
 Idiopathic gingival enlargement is a rare condition of
undetermined cause.

72.  Affects the attached gingiva, gingival margin and inter-dental
papillae.
 Facial and lingual surfaces of the mandible and maxilla are
usually affected but may be limited to either jaw.
 The enlarged gingiva is pink, firm, and almost leathery in
consistency and has a characteristic minutely pebbled surface.
 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.

74. ETIOLOGY
 Cause is unknown. Some cases have a hereditary basis.
 In some families, gingival enlargement is linked to the
impairment of physical development.
 Idiopathic forms have not been linked to specific genes.
 Enlargement usually begins with the eruption of the primary
or secondary dentition and may regress after extraction,
which suggests that the teeth or the plaque attached to them
may be initiating factors.
 The presence of bacterial plaque is a complicating factor.
 GO has been described in tuberous sclerosis, which is an
inherited condition characterized by the triad of epilepsy,
mental deficiency, and cutaneous angiofibromas.

75. HISTOPATHOLOGY
 Lesions are highly fibrotic with a bulbous increase in
connective tissue that is relatively avascular.
 Consists of densely arranged collagen bundles and numerous
fibroblasts.
 Thickened and acanthotic surface epithelium with elongated
rete pegs.
 Histopathology is similar to phenytoin-induced GO with low
levels of inflammatory infiltration. However, collagen bundle
formation, dominance and orientation are distinctive in areas
where cellular structures are reduced.

76. TREATMENT
 Treatment requires gingivectomy and gingivoplasty.
 Clinical management is difficult because of the high
recurrence rate, and the severity of lesions usually
results in extreme crowding and misalignment of
teeth.
 After removal of the fibromatosis lesions, patients may
require orthodontic treatment.

77. Other Forms of Gingival Enlargement
 The gingiva can be enlarged due to increases in the size of
the underlying osseous and dental tissues. These “false
enlargements” usually have no abnormal clinical features
except for the massive increase in the size of the area.
 Occurs most commonly in tori and exostoses, 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.

78. UNDERLYING DENTAL TISSUES
 DEVELOPMENTAL ENLARGEMENT:
During eruption, particularly of the primary dentition, the labial
gingiva may show a bulbous marginal distortion caused by
superimposition of the bulk of gingiva on the normal prominence
of the enamel in the gingival half of the crown. It often persists
until the junctional epithelium has migrated from the enamel to
the CEJ.
 Physiologic and ordinarily present no problems, However, when
the enlargement is complicated by marginal inflammation, the
composite picture gives the impression of extensive gingival
enlargement.

80. NEOPLASTIC ENLARGEMENT
Benign Tumors of the Gingiva
EPULIS
 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.

81. Fibroma
 Arise from the gingival connective tissue or PDL.
 Slow-growing, spherical tumors that tend to be firm and
nodular but may be soft and vascular. Usually pedunculated.
 Hard fibromas are rare; most of the lesions that are diagnosed
clinically as fibromas are inflammatory enlargements.
HISTOPATHOLGY
 Bundles of Well-formed collagen fibers with scattered
fibrocytes and various degrees of vascularity. Giant cell fibroma
contains multinucleated fibroblasts. In another variant called
peripheral ossifying fibroma, mineralized tissue (bone,
cementum-like material, and dystrophic calcifications) can be
found.

82. Papilloma
 Benign proliferations of surface epithelium associated with
human papillomavirus (HPV)
 Solitary wartlike or cauliflower-like protuberances and may
be small and discrete or broad, hard elevations with minutely
irregular surfaces.
HISTOPATHOLGY
 Consists of finger-like projections of stratified squamous
epithelium, often hyperkeratotic with central cores of
fibrovascular connective tissue.

84. Peripheral Giant Cell Granuloma
 Arise interdentally or from the gingival margin. Occur most
frequently on the labial surface and may be sessile or
pedunculated.
 Varies from smooth, regularly outlined masses to irregularly
shaped, multilobulated protuberances with surface indentations
 Ulceration of the margin is occasionally seen. Lesions are
painless, vary in size and can cover several teeth.
 May be firm or spongy, and the color varies from pink to deep
red or purplish blue.
 Cannot be easily differentiated from other forms of GO
clinically. Microscopic examination is required for definitive
diagnosis.

86. In some cases, the giant cell granuloma of the gingiva is locally
invasive and causes destruction of the underlying bone.
Complete removal leads to uneventful recovery.
HISTOPATHOLOGY
 Has numerous foci of multinuclear giant cells and
hemosiderin particles in a connective tissue stroma.
 Areas of chronic inflammation are scattered throughout the
lesion, with acute involvement occurring at the surface.
 Overlying epithelium is usually hyperplastic, with ulceration
at the base. Bone destruction occasionally occurs within the
lesion.

87. Gingival Cysts
 Cysts of microscopic proportions are common, but they
seldom reach a clinically significant size that appear as
localized enlargements that may involve the marginal
and attached gingiva.
 Occur in the mandibular canine and premolar areas,
most often on the lingual surface. They are painless, but
with expansion they can cause erosion of the surface of
the alveolar bone.
 Removal is followed by uneventful recovery.

88.  It should be differentiated from the lateral periodontal cyst,
which arises within the alveolar bone adjacent to the root
and is developmental in origin.
 Gingival cysts develop from odontogenic epithelium or from
surface or sulcular epithelium traumatically implanted in the
area.
HISTOPATHOLOGY
 Cyst cavity is lined by a thin, flattened epithelium with or
without localized areas of thickening. Less frequently, the
following types of epithelium can be found: unkeratinized
stratified squamous epithelium, keratinized stratified
squamous epithelium, and parakeratinized epithelium with
palisading basal cells.

89. 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).

90. Squamous cell carcinoma (SCC)
 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.
 Often symptom free, going unnoticed until complicated by
inflammatory changes that can mask the neoplasm but cause
pain. It sometimes becomes evident after tooth extraction.
 Locally invasive, and involves the underlying bone and PDL of
adjoining teeth and the adjacent mucosa.
 Metastasis is usually confined to the region above the clavicle;
however, involvement that is more extensive can include the
lung, liver, or bone.

92. 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.
 Arises from melanoblasts in the gingiva, cheek, or palate.
Infiltration into the underlying bone and metastasis to
cervical and axillary lymph nodes are common.

93. SARCOMA
 Fibrosarcoma, lymphosarcoma, and reticulum
cell sarcoma of the gingiva are rare.
 Kaposi sarcoma often occurs in the oral cavity
of patients with AIDS particularly in the palate
and the gingiva.
 Tumor metastasis to the gingiva occurs
infrequently.

94. Important Points
 The low incidence of oral malignancy should not mislead
the clinician. Ulcerations that do not respond to therapy in
the usual manner and all gingival tumors and tumor-like
lesions must be biopsied.
 In most clinical cases of GO, the clinical appearance is
complicated by inflammation, bleeding, and swelling,
which further creates difficulty in identifying the cause and
pathologic process.
 A thorough knowledge of GO and the patient’s systemic
and oral medical histories are critical for designing the
treatment and maintaining outcomes.