This presentation describes the classification, grading, various types of enlargement in detail and their treatment.

1. GINGIVAL
ENLARGEMENT
DR MANISHA SINHA
II YEAR PG
RAJARAJESWARI DENTAL COLLEGE AND HOSPITAL

2. CONTENTS
 INTRODUCTION
 CLASSIFICATIONS
 GRADING
 INFLAMMATORY GINGIVAL
ENLARGEMENT
 DRUG-INDUCED ENLARGEMENT
 IDIOPATHIC ENLARGEMENT
 ENLARGEMENTS ASS. WITH SYSTEMIC DISEASES
 NEOPLASTIC ENLARGEMENT
 FALSE ENLARGEMENT
 TREATMENT OF GINGIVAL ENLARGEMENT
 CONCLUSION

3. INTRODUCTION
 Gingival enlargement is the proliferation and intensification of the gingiva which is a prevailing
character of the diseased gingival tissues.
 Gingival enlargement and gingival overgrowth are terms used interchangeably with hyperplasia,
hypertrophy, and fibrosis.
 Hyperplasia is an increase in the number of cells in tissues that results in increased tissue volume.
Hypertrophy refers to increased tissue size and volume resulting from increased cell size.
 Fibrosis refers to a pathologic process in which disrupted wound healing is associated with
defective cell proliferation, cell-to-cell interactions, cell-to-matrix interactions, and matrix
deposition and with an impaired immune system response.

4. CLASSIFICATION
I. Inflammatory enlargement
A. Chronic
B. Acute
II. Drug-induced enlargement
III. Enlargements associated with systemic diseases or
conditions
A. Conditioned enlargement
1. Pregnancy
2. Puberty
3. Vitamin C deficiency
4. Plasma cell gingivitis
5. Nonspecific conditioned enlargement (granuloma
pyogenicum)
B. Systemic diseases causing gingival enlargement
1. Leukemia
2. Granulomatous disease (Wegener’s granulomatosis,
sarcoidosis)
IV. Neoplastic enlargement (gingival tumors)
A. Benign tumors
B. Malignant tumors
V. False enlargement

5. Using the criteria of location & distribution, gingival
enlargement is designated as follows:
LOCALISED GENERALISED MARGINAL
PAPILLARY
DIFFUSE DISCRETE

6. The degree of gingival enlargement can be scored as follows:
ANGELOPOULOS
AND GOAZ (1972)
None.
Not more than 1/3rd of the clinical
crown covered.
Any part of the middle
third of the crown covered.
Greater than
2/3rd of the
crown covered.
1
0
2
3

7. 0 = No encroachment of the interdental
papilla onto the tooth surface
1 = Mild encroachment of the interdental
papilla, producing a blunted appearance to
papilla tip
2 = Moderate encroachment, involving lateral
spread of papilla across buccal tooth surface
of less than one quarter of tooth width.
3 = Marked encroachment of papilla, i.e. more
than 1/4th tooth width. Loss of normal
papilla form
Seymour et al 1985

8. Miller and Damm (1992)
Horizontal gingival overgrowth index
is described as:
Grade 0: < 1mm
Grade 1: 1 to 2 mm
Grade 2: >2mm
Vertical gingival overgrowth index
is described as:
Grade 0: Normal gingival, no alteration
Grade 1: Minimal overgrowth, ≤ 2mm, gingiva covering the
cervical third or less of the anatomic crown.
Grade 2: Moderate overgrowth: 2 to 4 mm, gingival
covering the middle third of the anatomic crown.
Grade 3: Severe overgrowth: ≥4mm, nodular
growth, gingival covering more than two thirds
of the dental crown.

9. Bokenkamp A and Bohnhorst B (1994)
 Grade 0: No signs of gingival overgrowth
 Grade I: Gingival hyperplasia confined to interdental papilla .
 Grade II: Hyperplasia of interdental papilla and marginal
gingiva
 Grade III: Gingival hyperplasia covering at least three-quarters
of tooth crowns

10. Eva and Ingles (1999)
Grade 0: No overgrowth,
firm adaptation of the
attached gingiva to the
underlying alveolar bone
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. The probing
depth is equal to or less
than 6mm and the papilla
is somewhat retractable.
Grade 3: Marked
overgrowth, represented
by encroachment of the
gingiva onto the clinical
crown. Contour of the
margin is convex rather
than concave. 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

11. Miranda and Brunet index (2001)
 described an index in which horizontal measurement of the enlargement is possible.
This index is also termed as nodullary papilla index.
 In this index the measurement is carried out with the help of a periodontal probe
from the enamel surface of the interdental contact point to the outer papillary area.
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

12. INFLAMMATORY
ENLARGEMENT
 Gingival enlargement may result from chronic or acute
inflammatory changes; chronic changes are much
more common.
 In addition, inflammatory enlargements usually are a
secondary complication to any of the other types of
enlargement, creating a combined gingival
enlargement.
 In these cases it is important to understand the double
etiology and treat them adequately.

13. A) Acute Inflammatory Enlargement
 Acute inflammatory enlargement of the gingiva usually is caused by a mechanical,
chemical, or physical irritation and can be resolved by removal of the irritant.
 Mouth breathing, impacted food items, and poor oral hygiene are usually responsible for
acute inflammatory reactions in gingival tissues.
 Acute lesions are usually localized to marginal or papillary gingiva.
 Acute inflammatory enlargement can lead to the formation of gingival abscess. Gingival
abscess is a localized, painful, and rapidly expanding lesion.

14. GINGIVAL ABSCESS
 In its early stages, it appears as a red swelling with a smooth, shiny surface.
The lesion usually becomes fluctuant and pointed, with a surface orifice and
a purulent exudate in 24 to 48 hours
 Generally limited to marginal gingiva or interdental papilla.
 Etiology- caused by a mechanical, chemical, or physical irritation and can be
resolved by removal of the irritant. Mouth breathing, impacted food items,
and poor oral hygiene

15. Histopathology:-
A purulent focus in the connective tissue, surrounded by a diffuse infiltration of
polymorphonuclear leukocytes, edematous tissue, and vascular engorgement.
The surface epithelium has varying degrees of intra- and extracellular edema,
invasion by leukocytes, and sometimes ulceration.
The lesion is confined to the gingiva, and it should be distinguished from
periodontal abscess.

16. PERIODONTAL (LATERAL) ABSCESS
 It is a localized purulent inflammation in the periodontal tissues.
 Also known as Lateral or Parietal abscess.
 It involves the supporting periodontal tissues causing enlargement of gingiva.

17.  Periodontal abscess formation may occur in the following ways:
--Infection from
a periodontal
pocket deeply
into the
supporting
periodontal
tissues.
-- localization of
the suppurative
inflammatory
process
Lateral
extension of
inflammation
from the inner
surface of a
periodontal
pocket into the
connective tissue
of the pocket
wall.
pocket --
tortuous course
around the root,
a periodontal
abscess may
form in the cul -
de- sac.
Incomplete
removal of
calculus during
treatment of a
periodontal
pocket.
the absence of
periodontal
disease after
trauma to the
tooth or
perforation of
the lateral wall
of the root in
endodontic
therapy

18. B) CHRONIC INFLAMMATORY ENLARGEMENT
Etiology:--Prolonged exposure to dental plaque.
 Factors that favour plaque accumulation and retention include:-
Poor oral
hygiene.
Irritation by
anatomic
abnormalities
Improper
restorative and
orthodontic
appliances
Mouth
breathing

19. CLINICAL FEATURES
 Originates as Slight ballooning of the interdental papilla and/or the marginal gingiva.
 Produces a life preserver-shaped bulge around the involved teeth in early stages.
 May be localized or generalized and progresses slowly & painlessly, unless it is
complicated by acute infection or trauma.

20.  Occasionally, occurs as a discrete sessile or pedunculated mass resembling a
tumor.
 May be interproximal or on the marginal or attached gingiva.
 Lesions are slow-growing masses and usually painless.
 They may undergo spontaneous reduction in size,
followed by exacerbation and continued enlargement.
 Painful ulceration
sometimes occurs in the fold between the mass and the adjacent
gingiva

21. Gingival Changes Associated with Mouth
Breathing:-
o Gingiva appears red and edematous with a
diffuse surface shininess of the exposed area.
o Maxillary anterior region -common site
o Harmful effect is attributed to irritation from
surface dehydration.
Histopathology
 Show the exudative and proliferative features of chronic inflammation.
 Lesions that are clinically deep red or bluish red are soft and friable with a smooth, shiny surface, and they
bleed easily.
 They also have a preponderance of inflammatory cells and fluid, with vascular engorgement, new capillary
formation, and associated degenerative changes.
 Lesions that are relatively firm, resilient, and pink have a greater fibrotic component with an abundance of
fibroblasts and collagen fibers.

22. DRUG
INDUCED
ENLARGEMENT

23.  Predilection for anterior gingiva
 Higher prevalence in children
 Onset within 3 months
 Change in gingival contour leading to modifi
cation of gingival size
 Enlargement fi rst observed at the interdental
papilla
 Change in gingival color
 Increased gingival exudate
 Bleeding upon provocation
 Found in gingiva with or without bone loss but is not
associated with attachment loss
 Pronounced inflammatory response of gingiva in
relation to the plaque present
 Reductions in dental plaque can limit the severity of
lesion
 Must be using phenytoin, cyclosporine A or certain
calcium channel blockers; the plasma concentrations to
induce the lesion have not been clearly defi ned in
humans
Characteristics of drug-influenced gingival enlargement (Mariotti 1999)

24. Clinical Features
 Growth starts as a painless, bead-like enlargement of the interdental papilla
and extends to the facial and lingual gingival margins.
Case of phenytoin induced gingival enlargement
speech, mastication, tooth eruption,
and aesthetic problems.
ANTICONVULSANTS,
IMMUNOSUPPRESSANTS, AND CALCIUM
CHANNEL BLOCKERS

25.  As the condition progresses, the marginal and papillary enlargements unite
and may develop into a massive tissue fold covering a considerable portion
of the crowns; they may interfere with occlusion.
 Spontaneous disappearance occurs within a few months after
discontinuation of the drug.
 When UNCOMPLICATED BY INFLAMMATION- lesion is
mulberry shaped, firm,
Pale pink, and resilient
minutely lobulated surface
and no tendency to bleed.

26.  The presence of the enlargement makes plaque control difficult resulting in a
secondary inflammatory process that complicates the gingival overgrowth caused
by the drug.
 The resultant enlargement then becomes a combination of the increase in size caused
by the drug and the complicating inflammation caused by bacteria.
 Secondary inflammatory changes add to the size of the lesion caused by the drug
and produce a red or bluish red discoloration, obliterate the lobulated surface
demarcations, and increase bleeding tendency.
 Some investigators believe that inflammation is a prerequisite for development of
the enlargement, which therefore could be prevented by plaque removal and
fastidious oral hygiene (Ciancio and Yaffe J periodontol 1972)

27. Hassell et al (1982) have
hypothesized that in noninflamed
gingiva, fibroblasts are less active
or even quiescent and do not
respond to circulating phenytoin,
whereas fibroblasts within
inflamed tissue are in an active
state as a result of the
inflammatory mediators and the
endogenous growth factors
present.
Barclay S et al
(J Clin Periodontol 1992)
evaluated the incidence and
severity of nifedipine-induced
gingival overgrowth and
concluded that nifedipine therapy
results in significant gingival
changes, an effect which may be
mediated by the drug's action on
calcium transport.
Thomason JM et al
( J Clin Periodontol 1993)
studied the prevalence and
severity of cyclosporin and
nifedipine induced gingival
overgrowth and concluded that
patients taking cyclosporin or
cyclosporin and nifedipine
experience gingival overgrowth
and that the severity of the
overgrowth is greater in
patients taking the combined
therapy.

28. Histopathology
 Pronounced hyperplasia of the
connective tissue and epithelium.
 Acanthosis of the epithelium, and
elongated rete pegs extend deep into
the connective tissue, which exhibits
densely arranged collagen bundles
with an increase in the number of
fibroblasts and new blood vessels.
 An abundance of amorphous ground
substance as well as marked plasma
cell; infiltration has also been
reported (Mariani et al 1993).

29. Cyclosporine
enlargements
-- a more highly
vascularized
connective tissue with
foci of chronic
inflammatory cells,
particularly plasma
cells.
“mature” phenytoin
enlargements
fibroblast/collagen
ratio equal to that of
normal gingiva
from normal
individuals,
suggesting that at
some point in the
development of the
lesion, fibroblastic
proliferation must
have been
abnormally high
Recurring phenytoin
enlargements
appear as granulation
tissue composed of
numerous young
capillaries and fibroblasts
and irregularly arranged
collagen fibrils with
occasional lymphocytes

30. ANTICONVULSANTS
Phenytoin (Dilantin)
Ethotoin (Peganone)
and mephenytoin
(Mesantoin).
Succinimides
(ethosuximide
[Zarontin],
Methsuximide
[Celontin])
Valproic acid
[Depakene]).

31. Prevalence
Gingival overgrowth becomes clinically noticeable within 2 to 3 months after initial
administration of phenytoin and reaches its maximal severity at 12 to 18 months. (Livingston S
1990)
 occurs in 50% of patients receiving the drug, (Taicher S et al1991)
 Range is 3% to 84.5%. (Goaz PW,1972; Glickman 1941)
 It occurs more often in younger patients .
 Its occurrence and severity are not necessarily related to the dosage after a threshold level has
been exceeded.

32. Pathogenesis:-
Direct stimulating
action on gingival
fibroblasts or mast-cells
with secondary
fibroblastic involvement.
(Shafer et al 1960)
Existence of differential
proportions of fibroblast
subsets in each
individual which exhibit
a fibrogenic response to
these medications
(JISP 2013)
Fibroblasts with
abnormal susceptibility
to drug.
fibroblasts from
overgrown gingiva in
phenytoin treated
patients are
characterized by elevated
levels of proteins, esp.
Collagen
(J Periodontol 2004)

33. Genetic predisposition is a suspected factor .
Hassell et al (1994) hypothesized that gingival enlargement may result from the genetically determined
ability or inability of the host to deal effectively with prolonged administration of phenytoin.
Other proposed mechanisms include:
 the production of inactive fibroblastic collagenase causing a decrease in collagen turnover.
Phenytoin may induce a decrease in collagen degradation as a result of the production of an
inactive fibroblastic collagenase. (Hassell 1982)
 phenytoin-induced folic acid deficiency that can cause degenerative changes in the sulcular
epithelium and exacerbate the inflammatory response
 phenytoin-induced increase in the synthesis of testosterone metabolites by gingival fibroblasts
with resultant overgrowth

34. IMMUNOSUPPRESSANTS
potent immunosuppressive
agent used to prevent
organ transplant rejection
and to treat several
diseases of autoimmune
origin.
MOA-not known
selectively and reversibly
inhibit helperT cells,
which play a role in
cellular and humoral
immune responses.
Cyclosporin A
(Sandimmune, Neoral) is
administered
intravenously or by mouth
--dosages greater than 500
mg/day have been reported
to induce gingival
overgrowth.(Daley TD
1986)
Occurrence varies from
25% to 70% (Romito GA
2004)
CYCLOSPORINE

35.  Gingival enlargement is greater in patients who are medicated with both
cyclosporine and calcium channel blockers. (Taylor J 1987)
 The microscopic finding of many plasma cells plus the presence of an abundant
amorphous extracellular substance has suggested that the enlargement is a
hypersensitivity response to the cyclosporine.(Mariani G et al 1993)
 In addition to gingival enlargement, cyclosporine induces other major side effects
such as –nephrotoxicity,hypertension, hypertrichosis
 Another immunosuppressive drug, TACROLIMUS, has been used effectively and is
also nephrotoxic, but it results in much less severe hypertension, hypertrichosis, and
gingival overgrowth.(Bader G 1988)

36. CALCIUM CHANNEL BLOCKERS
They inhibit calcium ion influx across the cell membrane of heart and smooth muscle
cells, blocking intracellular mobilization of calcium. This induces direct dilation of
the coronary arteries and arterioles, improving oxygen supply to the heart muscle; it
also reduces hypertension by dilating the peripheral vasculature.
Drugs developed for the treatment of cardiovascular conditions such as
hypertension, angina pectoris, coronary artery spasms, and cardiac arrythmias.

37. • DIHYDROPYRIDINE
DERIVATIVES
(amlodipine [Lotrel,
Norvasc], felodipine
[Plendil], nicardipine
[Cardene], nifedipine
[Adalat, Procardia])
• BENZOTHIAZINE
DERIVATIVES(diltiazem
[Cardizem, Dilacor XR,
Tiazac])
• PHENYLALKYLAMINE
DERIVATIVES (verapamil
[Calan, Isoptin, Verelan,
Covera HS]).
 Nifedipine, one of the most often used, induces gingival enlargement in 20% of patients.
(Lucas RM 1985)

38.  It has been postulated that the drug may stimulate cell proliferation and
synthesis indirectly by one of three mechanisms:-
1. By giving rise to
the formation of a
more potent
Metabolic
byproduct.
2. By stimulating the
production of either
interleukin 2 by T cells or
metabolites of
testosterone by gingival
fibroblasts that in turn
would promote cellular
proliferation and
synthesis
(Nishikawa S 1991)
3.By causing a calcium
dependent inhibitory
effect on T cells that would
increase gingival
susceptibility to bacterial
infection through
immunosuppression.
(Seymour RA 1991)

40. IDIOPATHIC
GINGIVAL
ENLARGEMENT

41.  Idiopathic gingival enlargement is a rare condition of undetermined cause.
Etiology
 The cause is unknown and thus designated as idiopathic.
 Some cases- Hereditary basis but the genetic mechanisms are not well understood.
 Mode of inheritance is found to be autosomal recessive in some cases and autosomal dominant in
others. (Cocker et al 1974)
 Recently a locus for autosomal dominant HGF has been mapped to a region on chromosome 2 (Hart
et al. 1998, Xiao et al. 2000)
 In some families the gingival enlargement may be linked to impairment of physical development.
(Collan Y et al 1978)
Gingivomatosis,
elephantiasis, idiopathic
fibromatosis, hereditary
gingival hyperplasia, and
congenital familial
fibromatosis.

42.  HGF may be an isolated disease entity or part of a syndrome associated with other
clinical manifestations, such as hypertrichosis, mental retardation ,epilepsy, hearing
loss , growth retardation and abnormalities of extremities.
 Studies have suggested that an important pathogenic mechanism may be enhanced
production of transforming growth factor (TGF-beta 1) reducing the proteolytic
activities of HGF fibroblasts, which again favour the accumulation of extracellular
matrix (Coletta et al. 1999).

43. Clinical Features
Affects the attached gingiva, as well as the
gingival margin and interdental papillae
Enlarged gingiva is pink, firm, and almost
leathery in consistency
characteristic minutely pebbled surface
 Severe cases- teeth are almost completely covered & enlargement
projects into the oral vestibule.
 The jaws appear distorted because of the bulbous enlargement of the
gingiva.

44. ENLARGEMENTS
ASSOCIATED WITH
SYSTEMIC DISEASES

45.  Many systemic diseases can develop oral manifestations that may include gingival
enlargement.
 These diseases and conditions can affect the periodontium by two different
mechanisms, as follows:-
1. Magnification of an existing
inflammation initiated by
dental plaque.
This group of diseases
(Conditioned Enlargements)
includes:
 hormonal conditions (e.g.,
pregnancy and puberty)
 nutritional diseases such as
vitamin C deficiency
 some cases in which the
systemic influence is not
identified (nonspecific
conditioned enlargement).
2.Manifestation of the
systemic disease
independently of the
inflammatory
status of the gingiva.
This group involves Systemic
Diseases Causing Gingival
Enlargement and
Neoplastic Enlargement
(Gingival Tumors)

46. Bacterial plaque is necessary for the initiation of this type of enlargement. However, plaque
is not the sole determinant of the nature of the clinical features.
The three types of conditioned gingival enlargement are:
 Hormonal (pregnancy, puberty),
 Nutritional (associated with vitamin C deficiency),
 Allergic.
Gingival Overgrowth Associated With
Systemic Conditions

47.  Pregnancy gingival enlargement may be marginal and generalized or may occur as single or
multiple tumor-like masses .
 During pregnancy, there is an increase in levels of both progesterone and estrogen, which by
the end of the third trimester reach levels 10 and 30 times the levels during the menstrual
cycle, respectively. (Amar S 1994)
 These hormonal changes induce changes in vascular permeability leading to gingival edema
and an increased inflammatory response to dental plaque.
 The subgingival microbiota may also undergo changes, including an increase in Prevotella
intermedia, Prevotella melaninogenica, and Porphyromonas gingivalis (Kornman KS 1980)
1.Enlargement in Pregnancy
A 55 fold increase in the proportion of P intermedia has been demonstrated in pregnant females as
compared to non pregnant controls, implying a role for gestational hormones in causing a change in
microbial ecology in the gingival pocket. (Jensen et al 1981)

48. MARGINAL GINGIVAL ENLARGEMENT
 Marginal gingival enlargement during
pregnancy results from the aggravation of
previous inflammation,
 Incidence reported as 10%and 70%.
 The enlargement is usually generalized
and tends to be more prominent
interproximally than on the facial and
lingual surfaces.
 The enlarged gingiva is bright red or
magenta, soft, and friable and has a
smooth, shiny surface.
 Bleeding occurs spontaneously or on slight
provocation.
TUMORLIKE GINGIVAL ENLARGEMENT.
 The so-called pregnancy tumor is not a
neoplasm; it is an inflammatory response
to bacterial plaque and is modified by the
patient’s condition.
 Usually appears after the third month of
pregnancy but may occur earlier.
 The reported incidence is 1.8%to 5%.
 Appears as a discrete, mushroomlike,
flattened spherical mass that protrudes
from the gingival margin or more often
from the interproximal space and is
attached by a sessile or pedunculated base.

49. Histopathology
 A central mass of connective tissue, with numerous diffusely arranged, newly formed, and
engorged capillaries lined by cuboid endothelial cells and a moderately fibrous stroma.
 The stratified squamous epithelium is thickened, with prominent rete pegs and some degree of
intracellular and extracellular edema.

50.  It is marginal and interdental
 characterized by prominent bulbous interproximal papillae
 Often, only the facial gingivae are enlarged, and the lingual surfaces are relatively
unaltered.
 It is the degree of enlargement and its tendency to recur in the presence of relatively
scant plaque deposits that distinguish pubertal gingival enlargement from
uncomplicated chronic inflammatory gingival enlargement.
 After puberty the enlargement undergoes spontaneous reduction but does not
disappear completely until plaque and calculus are removed.
2.Enlargement in Puberty

51.  A longitudinal study of subgingival microbiota of children between ages 11 and 14
and their association with clinical parameters has implicated Capnocytophaga
species in the initiation of pubertal gingivitis.
(Mombelli A, Lang NP ,1990)
 Other studies have reported that hormonal changes coincide with an increase in the
proportion of Prevotella intermedia and Prevotella nigrescens.
(Fujii H, 1994)
The microscopic appearance of gingival enlargement in puberty is chronic inflammation with
prominent edema and associated degenerative changes

52.  Acute vitamin C deficiency itself 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 delimiting reaction is inhibited, and the extent of the
inflammation is exaggerated, resulting in the massive gingival enlargement seen
in scurvy.
3.Enlargement in Vitamin C Deficiency
marginal; the gingiva is bluish red, soft, and friable and has a
smooth, shiny surface.
Hemorrhage, occurring either spontaneously or on slight
provocation
surface necrosis with pseudomembrane formation

53.  Mild marginal gingival enlargement
 Gingiva appears red, friable, and sometimes granular
 Lesion is located in the oral aspect of the attached gingiva
and therefore differs from plaque-induced gingivitis.
4. Plasma Cell Gingivitis
 An associated cheilitis and glossitis have been reported.
 Plasma cell gingivitis is thought to be allergic in origin, possibly related to components of chewing
gum, dentifrices, or various diet components.
 Rare instances-marked inflammatory gingival enlargements with a predominance of plasma cells can
appear; these are associated with rapidly progressive periodontitis.

54.  more correctly called telangiectatic granuloma…
 frequently ulcerated and the appearance of the fibrin-coated ulcer may
resemble purulence.
 may occur in all areas of the oral mucosa, but is most frequently found
on the marginal gingiva (Makek & Sailer 1985).
 may develop rapidly and the size varies considerably.
 reddish or bluish, sometimes lobulated, and may be sessile or
pedunculated.
 Bleeding from the ulcerated lesion is common, but typically it is not
painful.
 Teeth may become separated due to interdental growth of the lesion.
5.Nonspecific Conditioned Enlargement (Pyogenic
Granuloma):

55. Gingival
Overgrowth
Associated With
Systemic Diseases

56. Leukemic Infiltration of the Periodontium
 Leukemic gingival enlargement can be diffuse or marginal and localized or generalized.
 It can appear as a diffuse enlargement of the gingival mucosa, an oversized extension of
the marginal gingiva or a discrete tumor-like interproximal mass.
 In patients with leukemic enlargement, the gingiva is bluish red, and it has a shiny surface.
The consistency is moderately firm, but there is a tendency toward friability and
hemorrhage that occur spontaneously or with slight irritation.
 True leukemic enlargement often occurs with acute leukemia, but it may also be seen with
subacute leukemia. It seldom occurs with chronic leukemia.

57.  Clinically, the gingiva appears bluish red and cyanotic, with a rounding and
tenseness of the gingival margin and has a shiny surface.
 The consistency is moderately firm, but there is a tendency towards friability and
hemorrhage, occurring either spontaneously or on slight irritation.
Enlargement may be diffuse or marginal, localized or generalized.

58.  Appear as a diffuse enlargement of the gingival mucosa, an oversized extension of
the marginal gingiva, or a discrete tumor like inter-proximal mass.
 Acute painful necrotizing ulcerative inflammatory involvement may occur in the
crevice formed at the junction of the enlarged gingiva and the contiguous tooth
surfaces.
Histopathology
 Areas of connective tissue infiltrated with a dense mass of immature and
proliferating leukocytes
 Engorged capillaries, oedematous and degenerated connective tissue, and
epithelium with various degrees of leukocytic infiltration and edema are found.
 Isolated surface areas of acute necrotizing inflammation with a pseudomembranous
meshwork of fibrin, necrotic epithelial cells, polymorphonuclear neutrophils
(PMNs), and bacteria are often seen.

59. 2.Granulomatous Diseases
WEGENER'S GRANULOMATOSIS:
 Rare disease characterized by acute granulomatous necrotizing lesions of the respiratory tract,
including nasal and oral defects.
 immunologically mediated tissue injury. (Cotran RS 1989)
 The initial manifestations of Wegener’s granulomatosis may involve the orofacial region and
include:
oral mucosal ulceration
gingival enlargement
abnormal tooth mobility
exfoliation of teeth
delayed healing response

60.  The granulomatous papillary enlargement is reddish purple and bleeds easily on
stimulation.
Histopathology
Chronic inflammation occurs with scattered giant cells and foci of acute inflammation and
microabscesses covered by a thin acanthotic epithelium.

61. SARCOIDOSIS:
 granulomatous disease
 unknown etiology.
 can involve almost any organ, including the gingiva, in which a red, smooth,
painless enlargement may appear.
Histopathology
 Sarcoid granulomas consist of discrete, noncaseating whorls of epithelioid cells and
multinucleated, foreign body–type giant cells with peripheral mononuclear cells.

62. NEOPLASTIC
ENLARGEMENT
(GINGIVAL TUMORS)

63. arise from the
gingival
connective tissue
or from the
periodontal
ligament
slow-growing,
spherical tumors
that tend to be
firm and nodular
but may be soft
and vascular.
usually
pedunculated
--giant cell
fibroma
--peripheral
ossifying
fibroma
FIBROMA
Histopathology
Bundles of Well-formed collagen fibers with scattering
of fibrocytes and a variable vascularity.
A) Benign Tumors of the Gingiva

64.  Appear as Solitary, wartlike or "cauliflower"-like protuberances and may be small
and discrete or broad, hard elevations with minutely irregular surfaces.
Histopathology
 Finger like projections of stratified squamous epithelium often hyperkeratotic, with
a central core of fibrovascular tissue
PAPILLOMA

65.  Arise interdentally or from the gingival margin
 sessile or pedunculated
 smooth, regularly outlined masses to irregularly
shaped, multilobulated protuberances
 painless, vary in size
 firm or spongy,
 pink to deep red or purplish blue.
 Local irritation or trauma appears to be important
for these lesions to occur.
 It has growth potential and may cause separation of
teeth due to pressure exerted by the growth
PERIPHERAL GIANT CELL
GRANULOMA
Histopathology
Numerous foci of multinuclear giant cells and
hemosiderin particles in CT stroma.
Overlying epithelium is usually hyperplastic, with
ulceration at the base.
Bone formation occasionally occurs within the
lesion

66.  Leukoplakia of the gingiva varies in appearance from a grayish white,
flattened, scaly lesion to a thick, irregularly shaped, keratinous plaque.
LEUKOPLAKIA
Histopathology
•Leukoplakia exhibits hyperkeratosis and acanthosis.
•Premalignant and malignant cases have a variable
degree of atypical epithelial changes that may be mild,
moderate, or severe, depending on the extent of
involvement of the epithelial layers.
•Inflammatory involvement of the underlying connective
tissue is a common associated finding.

67.  involves the marginal & attached gingiva.
 occur in the mandibular canine and premolar areas.
 painless, but with expansion.
GINGIVAL CYST
Histopathology:-
 A gingival 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.

68. B) Malignant Tumors of the Gingiva
Carcinoma:-
 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.
 It is often symptom free,
 locally invasive.

69. Malignant Melanoma
Sarcoma Metastasis
Rare oral tumor that tends to
occur in the hard palate and
maxillary gingiva of older
persons.
• Usually darkly pigmented
and is often preceded by
localized pigmentation.
• May be 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
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 (AIDS),
particularly in the
palate and the gingiva
Tumor metastasis to the
gingiva occurs
infrequently.
• Such metastasis has
been reported with
various tumors,
including
adenocarcinoma of the
colon, lung carcinoma,
melanoma, renal cell
carcinoma,
hypernephroma,
chondrosarcoma, and
testicular tumor.

70. FALSE
ENLARGEMENT

71. Underlying osseous lesions
Enlargement of bone subjacent to the gingival area occurs most often in tori and
exostoses but it can also occur in Paget’s disease, fibrous dysplasia, cherubism,central
giant cell granuloma, ameloblastoma, osteoma, and osteosarcoma.
The gingival tissue can appear normal or may have unrelated inflammatory changes.
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.
This enlargement has been termed developmental enlargement
and often persist until the junctional epithelium has migrated from
the enamel to the cementoenamel

72. MANAGEMENT OF GINGIVAL
ENLARGEMENTS

73. Treatment of chronic inflammatory enlargement
Treated by SCALING AND ROOT PLANING, (provided the size of the enlargement
does not interfere with complete removal of deposits from the involved tooth surfaces).
When chronic inflammatory gingival enlargements include a significant fibrotic
component that does not undergo shrinkage after scaling and root planing or are of such
size that they obscure deposits on the tooth surfaces and interfere with access to them.
SURGICAL REMOVAL is the treatment of choice
GINGIVECTOMY FLAP OPERATION.
Used when the enlarged gingiva
remains soft and friable even after
scaling and root planing
Indicated if the gingivectomy incision removes all of the
attached, keratinized gingiva, which will create a
mucogingival problem
Tumorlike inflammatory enlargements are treated by gingivectomy.

74. Treatment Of Drug induced gingival enlargement
First, consideration should be given to the possibility of DISCONTINUING THE DRUG
OR CHANGING THE MEDICATION. These possibilities should be examined with the
patient’s physician. Simple discontinuation of the offending drug is usually not practical,
but its SUBSTITUTION WITH ANOTHER MEDICATION might be an option.
Second, the clinician should EMPHASIZE PLAQUE CONTROL as the first step in the
treatment of drug-induced gingival enlargement
Third, in some patients, gingival enlargement persists after careful consideration of the
previous approaches. These patients may require SURGERY, either PERIODONTAL
FLAP OR GINGIVECTOMY.

75. DRUG SUBSTITUTES
PHENYTOIN
CARBAMAZEPINE AND
VALPROIC ACID,
NIFEDIPINE
DILTIAZEM OR
VERAPAMIL
CYCLOSPORINE
TACROLIMUS
 Also, consideration may be given to the use of another class of ANTIHYPERTENSIVE
medications rather than calcium channel blockers, none of which is known to induce gingival
enlargement.
 Clinical trials have also shown that the substitution of cyclosporine by tacrolimus results in a
significant decrease in the severity of gingival enlargement when compared to patients who are
kept on cyclosporine therapy.

80. Treatment of Leukemic gingival enlargement
The patient’s bleeding and clotting times and platelet count should be
checked, and the hematologist should be consulted before periodontal
treatment is instituted.
After acute symptoms subside, attention is directed to correction of the
gingival enlargement.
The rationale for therapy is to remove the local irritating factors to
control the inflammatory component of the enlargement.
The lesion is treated by scaling and root planing performed in stages
with topical and local anesthesia and instructing the patient in oral
hygiene for plaque control.

81. This portion of the therapy may include, at least initially, the
daily use of chlorhexidine mouthwashes. Oral hygiene
procedures are extremely important in these patients and
should be performed by the nurse if necessary.
Progressively deeper scaling is carried out at subsequent
visits. Treatments are confined to a small area of the mouth to
facilitate the control of bleeding.
ANTIBIOTICS are administered systemically the evening
before and for 48 hours after each treatment to reduce the risk
of infection.

82. Treatment of gingival enlargement in pregnancy
 Treatment requires elimination of all local irritants responsible for precipitating the gingival
changes in pregnancy.
 Marginal and interdental gingival inflammation and enlargement are treated by scaling and
root planing.
 Treatment of tumorlike gingival enlargements consists of surgical excision and scaling and
planing of the tooth surface. The enlargement will recur unless all of the irritants are removed

83. Timing of Treatment and Indications:-
 Gingival lesions in pregnancy should be treated as soon as they are detected, although not
necessarily by surgical means. Scaling and rootplaning procedures and adequate oral hygiene
measures may reduce the size of the enlargement.
 Gingival enlargements will shrink after pregnancy but may not completely disappear. After
pregnancy, the entire mouth should be reevaluated, a full set of radiographs taken, and the
necessary treatment undertaken.
 Lesions should be removed surgically during pregnancy only if they interfere with
mastication or produce an esthetic disfigurement that the patient wants removed.

84. Treatment of gingival enlargement in puberty
 Gingival enlargement in puberty is treated by performing scaling and curettage, removing all
sources of irritation, and controlling plaque.
 Surgical removal may be required in severe cases.

85. CONCLUSION
Inspite of a myriad of etiology, gingival enlargements can often be diagnosed
by a careful history, by location or by the clinical presentation. 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.

86. REFERENCES:-
 Newman MG , Takei HH , Klokkevold PR , Carranza FA . Carranza’s Clinical Periodontology, 10th edition
 Newman MG , Takei HH , Klokkevold PR , Carranza FA . Carranza’s Clinical Periodontology, 13th edition
 Atlas of cosmetic and reconstructive periodontal surgery, Cohen
 Marshall R , Bartold M A clinical review of drug induced gingival overgrowth Australian dental journal 1999 ;44:4
219- 232
 Seymour RA, Ellis JS, Thomason JM: Risk factors for druginduced gingival overgrowth.J Clin Periodontol 2000; 27:
217-223.
 Seymour RA , Thomasan JM Pathogenesis of Drug Induced Gingival Overgrowth- J Clin Periodontol 1996;23:165-
175
 Strawberry –like gingival tumor as first sign of Wegener’s Granulomatosis. J Periodontol 2008; 79: 1297-1303
 Seymour RA and Heasman PA: Drugs and the periodoniium. J Clin Periodontol 1988: 15: 1-16