1.
PRESENTED BY: DR. VEENA VENUGOPAL

2.
• INTRODUCTION
• CLASSIFICATION
• GINGIVAL ENLARGEMENT INDICES
• INFLAMATORY GINGIVAL ENLARGEMENT
• DRUG-INDUCED GINGIVAL ENLARGEMENT
• IDEOPATHIC GINGIVAL ENLARGEMENT
• Enlargements associated with systemic diseases or conditions
• Neoplastic enlargement (gingival tumours)
• FALSE ENLARGEMENT
• TREATMENT OF GINGIVAL ENLARGEMENT
• CONCLUSION
• REFERENCES

3.
• An increase in size of the gingiva is a common feature of
gingival disease. The accepted current terms for this
condition are gingival enlargement and gingival
overgrowth.
• These are strictly clinical descriptive terms, and they
avoid the erroneous pathologic connotations of terms
used in the past, such as hypertrophic gingivitis and
gingival hyperplasia.
• Accroding to Glossary of Periodontal Terms:
• “An overgrowth or increase in size of the gingiva”.

4.
The many types of gingival enlargement can be classified according to
etiologic factors and pathologic changes as follows:
I. Inflammatory enlargement
A. Chronic
B. Acute
II. Drug-induced enlargement
A. Anticonvulsants
B. Immunosuppressants
C. Calcium channel blockers

5.
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 (pyogenic
granuloma)
B. Systemic diseases that cause gingival enlargement
1. Leukemia
2.Granulomatous diseases (e.g., Wegener’s
granulomatosis,
sarcoidosis)
IV. Neoplastic enlargement (gingival tumors)
A. Benign tumors
B. Malignant tumors
V. False enlargement

6.
With the use of 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 a pedunculated, tumor-like
enlargement

7.
Angelopoulos and Goaz (1972) described an index for
measuring the vertical component of gingiva. Three
grades based on the enlargement covering the clinical
crown were described as:
Grade 0: None.
Grade I: Not more than 1/3rd of the clinical crown covered.
Grade II: Any part of the middle third of the crown covered.
Grade III: Greater than 2/3rd of the crown covered.

8.
Miller and Damm (1992) modified the original Angelopoulos and Goaz
index for enhanced assessment of gingival overgrowth.
Vertical component
Horizontal component
The 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.
The horizontal gingival overgrowth index is described as:
Grade 0: < 1mm
Grade 1: 1 to 2 mm
Grade 2: > 2 mm

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

10.
Eva and Ingles (1999) introduced a new index for measuring
gingival overgrowth caused due to drugs. In this index for
standardization, the buccal and lingual papillae were scored separately.
The criteria by which scores were divided are as mentioned below:
Grade 0:
 No overgrowth, firm adaptation of the attached gingiva to the
underlying alveolar bone.
 There is slight stippling; there is no granular appearance.
 A knife-edged papilla is present toward the occlusal surface and no
increase in density or size of the gingiva.


11.
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.

12.
Grade 2:
Moderate overgrowth, manifested by an increase in the
size of the papilla and/ or rolled gingival margins.
The contour of the margin is still concave or straight.
Also the enlargement has a bucco-lingual dimension of
up to 2mm, measured from the tip of the papilla outward.
The probing depth is equal to or less than 6 mm and
the papilla is somewhat retractable.

13.
Grade 3:
Marked overgrowth, represented by encroachment of
the gingiva onto the clinical crown.
Contour of the margin is convex rather than concave.
The enlargement has a bucco-lingual dimension of
approximately 3 mm or more, measured from the tip of
the papilla outward.
The probing depth is greater than 6mm and the papilla
is clearly retractable.

14.
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.

15.
• Inflammatory enlargements are usually a secondary
complication of any of the other types of enlargement,
thereby creating a combined gingival enlargement.
• In these cases, it is important to understand the double
etiology and to treat both causes adequately.
Chronic Inflammatory Enlargement
Etiology
• Prolonged exposure to dental plaque.
• Poor oral hygiene,
• Irritation by anatomic abnormalities,
• Improper restorative and orthodontic appliances.

16.
Clinical Features
 Slight ballooning of the interdental papilla and marginal
gingiva.
 In the early stages, it produces a life-preserver – shaped bulge
around the involved teeth. This bulge can increase in size until
it covers part of the crowns
 Discrete sessile or pedunculated mass that resembles a
tumor.
 It may be interproximal or on the marginal or attached gingiva.
 The lesions are slow-growing masses, and they are usually
painless.

17.
Histopathology
• Chronic inflammatory gingival enlargements show the
exudative and proliferative features of chronic
inflammation.
• 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.

18.
Gingival Changes Associated with Mouth
Breathing.
• The gingiva appears red and edematous, with a diffuse
surface shininess of the exposed area.
• The maxillary anterior region is the common site of such
involvement.
• In many cases, the altered gingiva is clearly demarcated
from the adjacent unexposed normal gingiva.

19.
GINGIVAL ABCESS
Etiology.
• Bacteria carried deep into the tissues when a foreign
substance (e.g., toothbrush bristle, piece of apple core, lobster
shell fragment) is forcefully embedded into the gingiva.
• The lesion is confined to the gingiva and should not be
confused with periodontal or lateral abscesses.
CLINICAL FEATURE:
• A gingival abscess is a localized, painful, rapidly expanding
lesion that usually has a sudden onset.
• It is generally limited to the marginal gingiva or the interdental
papilla.

20.
• In its early stages, it appears as a red swelling with a
smooth, shiny surface. Within 24 to 48 hours, the lesion
usually becomes fluctuant and pointed, with a surface
orifice from which a purulent exudate may be expressed.
• The adjacent teeth are often sensitive to percussion. If
permitted to progress, the lesion generally ruptures
spontaneously.

21.
Histopathology.
• The gingival abscess consists of 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
intracellular and extracellular edema, invasion by
leukocytes, and sometimes ulceration.

22.
Drug-induced gingival overgrowth was first reported in
1939 (Kimball 1939)
Clinically and histologically, gingival overgrowth induced
by different drugs, are virtually indistinguishable (Wysocki
et al, 1983. Tyldesley & Rotter 1984)
However, the prevalence of this unwanted effect does
show differences between the agents, with approximately
50% of patients medicated with phenytoin experiencing
significant gingival changes (Angeiopoulous & Goaz 1972),
whilst the figures for cyclosporin and nifedipine are closer
to 30% and 20% respectively (Seymour et al, 1987, Barclay ct ai,
1992).

23.
Anticonvulsants:
Hydantoins Ethotonin
Mephenytoin
Phenytoin
Succinimide Ethosuximide
Methsuximide
Phensuximide
Valproic acid Valproic acid
Immunosuppressants: Cylcosporine A
Calcium channel blockers:
Dehydropyridine derivatives Amlodipine
Felodipine
Nicardipine
Verapamil
Diltiazem

24.
Clinical Features:
The growth starts as a painless, beadlike enlargement of
the interdental papilla that then extends to the facial and
lingual gingival margins.
As the condition progresses, the marginal and papillary
enlargements unite, and they may develop into a
massive tissue fold that covers a considerable portion of
the crowns; this may interfere with occlusion.
When uncomplicated by inflammation, the lesion is
mulberry shaped, firm, pale pink, and resilient, with a
minutely lobulated surface and no tendency to bleed.

25.
The enlargement characteristically appears to project
from beneath the gingival margin, from which it is
separated by a linear groove.
However, the presence of the enlargement makes plaque
control difficult, often resulting in a secondary
inflammatory process that complicates the gingival
overgrowth caused by the drug.

26.
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 not only add to the size
of the lesion caused by the drug but also produce a red
or bluish-red discoloration, obliterate the lobulated
surface demarcations, and increase bleeding tendency.

27.
• The enlargement is usually generalized throughout the
mouth, but it is more severe in the maxillary and
mandibular anterior regions.
• It occurs in areas in which teeth are present (not in
edentulous spaces), and the enlargement disappears in
areas from which teeth have been extracted.
• Hyperplasia of the mucosa in edentulous mouths has
been reported but is rare.
• Drug-induced enlargement may occur in mouths with little
or no plaque, and it may be absent in mouths with
abundant deposits.

28.
• Hassell and colleagues have hypothesized that, in
noninflammed 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 that are present.
• The enlargement is chronic, and it slowly increases in
size. Even if it is surgically removed, it recurs.
Spontaneous disappearance occurs within a few months
after the discontinuation of the drug.

29.
Histopathological feature:
• Drug-induced gingival enlargement consists of a
pronounced hyperplasia of the connective tissue and
epithelium.
• There is 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 has also
been reported.
• Structural changes in the outer epithelial cell surface
have been reported with cyclosporine-induced

30.
• The enlargement begins as a hyperplasia of the
connective tissue core of the marginal gingiva and
increases by its proliferation and expansion beyond the
crest of the gingival margin. An inflammatory infiltrate
may be found at the bottom of the sulcus or pocket.
• Cyclosporine enlargements usually involve more highly
vascularized connective tissue, with foci of chronic
inflammatory cells (particularly plasma cells).
• The “mature” phenytoin enlargement has a fibroblast-to-
collagen ratio that is equal to that of normal gingiva from
normal individuals, which suggests that, at some point in
the development of the lesion, fibroblastic proliferation
must have been abnormally high.

31.
• The multifactorial nature of drug-induced gingival
overgrowth, with particular reference to the following
factors:
Age;
Genetic predisposition;
Pharmacokinetic variables;
Drug-induced alterations in gingival
Connective tissue homeostasis;
Histopathology, ultrastructural factors & inflammatory
changes;
Drug-induced action on growth factors

32.
• Clinical studies suggest that children and adolescents
appear more susceptible to drug-induced gingival
overgrowth than adults (Esterberg & White 1945, Hefti et al.
1994).
• Fibroblasts obtained from both cyclosporin and
phenytoin-induced gingival overgrowth cases failed to
show an age-dependent decrease in protein synthesis
and collagen production (Sobhani et al. 1989,Johnson et a!.
1990).
• The failure of these cell culture investigations to confirm
the clinical findings may be related to a unique fibroblast
phenotype or the influence of androgen metabolism

33.
• A drug-related increase in gingival fibroblast androgen
metabolism could be a significant factor in the
pathogenesis of drug-induced gingival overgrowth.
• The active androgen metabolites could "target" sub-
populations of gingival fibroblasts and cause either an
increase in collagen synthesis and/or a decrease in
collagenase activity.
• Such changes in androgen metabolism may account for
the increased propensity of this unwanted effect in
children and adolescents.

34.
• It is now widely recognized that gingival fibroblasts
exhibit functional heterogeneity in response to various
stimuli (Hassell et al. 1976).
• From this finding, it was shown subsequently that
phenytoin (and its major metabolite pHPPH) could react
with a phenotypically distinct subpopulation of gingival
fibroblasts and cause an increase in protein synthesis
and cell proliferation rate (Hassell & Gilbert 1983)
• Comparable results have also been shown for
cyclosporin (Hassell et al. 1988) and its major metabolite OL-
17 (Jacobs et al. 1990)

35.
• Cell cultural studies from monozygous and dizygous
twins have confirmed the functional heterogeneity of
gingival fibroblasts (Cockey et al. 1989).
• Paired cultures from dizygotic twins showed significantly
greater (P<0.01) within pair division rates when
compared with paired gingival fibroblast from
monozygotic twins.
• A marked heterogeneity of response of gingival
fibroblasts to cyclosporin or calcium channel blockers,
had also been reported.

36.
• Fibroblast heterogeneity has also been investigated with
respect to the collagenolytic response to cyclosporine
(Tipton et al. 1991).
• Collagenase, and tissue inhibitor of metalloproteinase
(TIMP), activity were determined in each cell population
both at baseline and after challenge with cyclosporine
(0.1-0.75 ug/ml)
• As with phenytoin, the heterogeneity of the collagenolytic
response of different gingival fibroblast strains and their
subpopulations to cyclosporine treatment may partly
explain the variable gingival response noted in patients
taking this drug. It is clear that overgrowth-inducing drugs
are capable of altering the metabolism of human gingival
fibroblasts.

37.
• The 3 drug groups that are known to induce gingival
overgrowth are each metabolised by members of the
cytochrome P450 enzyme family. The dihydropyridines
and cyclosporine are metabolised by the glucocorticoid
inducible enzyme CYP3A4 (Guengerich et al. 1985, Kronbach et
al. 1988) whereas phenytoin is metabolised mainly by
CYP2C9 (Veronese et al. 1993).
• Further evidence that genetic factors may relate to the
expression of drug-induced gingival overgrowth has
come from investigation of human lymphocyte antigen
(HLA) expression (Pernu et al. 1994).
• The group of patients with moderate or severe
overgrowth had significantly lower frequency of HLA-
DRI+ and higher frequency of HLA-DR2+ expression,
when compared to those with little or no overgrowth.

38.
• Patients who expressed HLA-DR1+ appeared to be
afforded a degree of protection against the development
of this unwanted effect, whilst those exhibiting HLA-DR2
+ showed an increased risk for drug-induced gingival
overgrowth. Whether there is any link between HLA
expression, and gingival fibroblast phenotype, remains to
be elucidated.
• These include gingival fibroblast functional heterogeneity,
collagenolytic activity (as expressed by collagenase and
TIMP production), drug receptor binding, drug
metabolism, collagen synthesis and many more factors.
HLA expression may prove to be a useful genetic marker
for the identification of patients a risk of developing drug-
induced gingival overgrowth.

39.
• A direct relationship between the degree of salivary
phenytoin and gingival overgrowth has been
demonstrated in institutionalised epileptic patients
(Babcock & Nelson 1964).
• Cyclosporine concentration in stimulated saliva and the
extent of the gingival overgrowth (McGaw et al. 1987,
Hefti et al. 1994).
• By contrast, a lack of correlation between unstimulated
salivary cyclosporine levels and gingival overgrowth has
been reported (King et al. 1993).

40.
• The possibility that the dental plaque may act as a
reservoir for cyclosporine, which is released by the
actions of developing stimulated saliva flow, may well
explain the conflicting findings reported (McGaw et al. 1987,
King et al. 1993).
• A role for dental plaque as a reservoir for phenytoin in
drug-induced gingival overgrowth has also been
proposed. (Steinberg 1980)
• It has been reported that the oral mucosal exposure to
cyclosporine was approximately 130 times greater when
the drug was administered as a mixture as opposed to
capsule form. (Modeeret al. 1992)

41.
• It has been shown that both nifedipine and amlodipine
can be detected in GCF and significant sequestration of
the drug occurs in patients exhibiting gingival overgrowth
(Ellis et al. 1992, Seymour et al. 1994)

42.
• Collagen production from gingival fibroblasts is controlled
by the co-ordination of transcripted and post-transplation
collagen regulatory mechanisms, including intracelluiar
degradation. The latter is controlled by synthesis and
release of metalloproteinase and tissue inhibitors of
metalloproteinase (TIMPs).
• Exposure of gingival fibroblasts to phenytoin increases
the level of translatable collagen RNA. (Benveniste & Bitar
1980).
• Overproduction of collagen by gingival Fibroblasts in
phenytoin-induced gingival enlargement involves an
increased steady state level of collagen mRNA and not a
decrease in collagen degradation (Narayanan et al. 1988).
Such fibroblasts may be selected during the development
of overgrowth.

43.
• Gingival fibroblasts from healthy volunteers were
incubated with varying concentrations of nifedipine (100
and 200 ng/ml) and phenytoin (5-10 /ug/ml) (Salo et al.
1990). After 7 days, both drugs reduced total protein and
collagen synthesis in the cultures.
• In addition, the level of mRNA for type I collagen was
also decreased, whereas the level of type 1 collagenase
mRNA was unaffected.
• By contrast, a more recent controlled study investigated
the expression of type IV collagen genes and type IV
collagen distribution in tissue and cell lines obtained from
patients with either nifedipine or phenytoin- induced
gingival overgrowth.

44.
• Immunohistochemistry and Northern blot analysis
showed an increased deposition of type IV collagen and
an enhanced expression of type IV collagen genes.
• Such increase may be important in the expression of
either phenytoin or nifedipine- induced gingival
overgrowth (Shikata et al. 1993).
• The findings from these 2 studies imply that both
phenytoin and nifedipine could alter differentially the
expression of both type I and type IV collagen genes.
Since type IV collagen appears resistant to both bacterial
collagenase and various matrix metalloproteinase. it
would remain in the tissue in the presence of plaque-
induced gingival inflammation (Romanos et al. 1993)

45.
• cyclosporin causes a significant increase in collagen
synthesis in cultured gingival fibroblast. but not DNA
synthesis (Schincaglia et al. 1992).
• In particular, the cyclosporine-induced changes were
related to a rise in the level of type I procollagen. The
effects of the drug on the fibroblasts correlated well with
an increase in type I procollagen mRNA indicating
increased synthesis with increased secretion.

46.
• Non-collagenous matrix comprise 20% of the dry weight
in gingival tissue from phenytoin patients and only 7% in
normal tissue (Ballard & Butler J974).
• Patients on prolonged phenytoin therapy have
significantly raised levels of hexosamine, uronic acid and
total protein per wet weight of tissue when compared with
controls (Goultschin et al. 1983)
• Overgrowth has a significantly higher volume density of
the non-collagenous matrix than of the collagenous
matrix (Dahllof et al. 1984)

47.
• It is uncertain whether the increased amount of
glycosaminoglycans in phenytoin-induced gingival
overgrowth is due to increased synthesis or reduced
degradation.
• The effect of cyclosporin and nifedipine on non-
collagenous matrix has been investigated with respect to
3H glucosamine utilization (Zebrowski et al. 1994).

48.
• Phenytoin-induced gingival overgrowth may be more
related to a lack of collagen breakdown as opposed to an
increase in collagen production (goultchin & shoskan 1980).
• This finding was further supported by evidence that
fibroblasts from patients with phenytoin- induced gingival
overgrowth produce an inactive collagenase thus
favoring collagen deposition.
• Collagenase activity, as measured by the degradation of
c14-collagen, was increased by nifedipine. Decreased by
phenytoin and unaffected by cyclosporine.
• A drug-induced increase in the synthesis of TIMP was
perhaps more significant than a decrease in collagenase
activity,

49.
• Gingival fibroblasts in cyclosporine-induced overgrowth
show characteristics of active protein synthesis and
secretion, with reduced cytotoxic or degenerative
changes.
• An increased proportion of cells containing microfilament
bands with semi periodic dense nodes, nuclear
indentations, and basal lamina associated cell to stromal
junctions has also been found (Yamasaki et al. 1987).
• Cyclosporin induced gingival overgrowth is a
consequence of individual hypersensitivity to the drug
(Deliliers et al. 1986, Mariani et al, 1993)

50.
• It can be argued that plaque-induced inflammatory
changes within the gingival tissues enhance the
interaction between the drug and gingival fibroblasts.
• Cyclosporin has generated renewed interest in this area
because of its selective immunosuppressive properties,
and ability to inhibit production of interieukins. The latter
cytokines are potent stimulators of collagenase
production from fibroblasts (Postlethwaite et al. 1983)
• A patient's susceptibility to cyclosporin-induced gingival
overgrowth may be related to genetically determined
populations of both lymphocytes and fibrobiasts which
are sensitive to the drug.

51.
• The selective infiltration of T-lymphocytes would support
a T-cell mediated immunological mechanism which may
play a role in the pathogenesis of gingival overgrowth.
• The number of Langerhans cells also increase in gingival
epithelium in patients with phenytoin-induced gingival
overgrowth (Kinane et al. 1990).
• The relationship between such an increase in
Langerhans cell and gingival overgrowth remains
speculative, it has been shown that an increase in
interleukin-I is related to an increase m Langerhans ceils
in chronically inflamed gingiva (Walsh et al, 1988)

52.
• Interieukin-1 can stimulate fibroblast proliferation in the
presence of primary growth factors, thus phenytoin-
induced gingival overgrowth and the increase in
Langerhans cells may be mediated via interleukin-1/
growth factor interaction.
• Immunohistochemical analysis of the gingival tissues
showed significantly higher numbers of
monocyte/macrophage (CD68) subsets, plasmacytoid
ceils, and total T-lymphocytes (CD3) in the cyclosporin
treated patients than in gingival tissues obtained from
healthy controls.
• Differences were also found in the helper/inducer T-
lymphocytes tCD4) and cytotoxic/ suppressor T-
lymphocytes (CDS). Similarly, the CD4/CD8 ratio was
higher in the cyclosporin treated patients than in control.

53.
• The degree of gingival overgrowth appeared to be related
to an in increase in CD4+ and CD68+ leucocyte subsets,
together with an increase in CD45+, the common
leucocyte antigen.
• These findings suggest that local populations of
leucocyte subsets may play a pathogenic role in the
development of gingival overgrowth.
• The immune response appears to be suppressed in the
epithelial layer of the gingiva the gingiva through a
decrease in Leu- 6+epithelial dendritic cells, HLADR+
epithelial dendritic cells and T-cell infiltration due to
cyclosporin in plaque.

54.
• Tissue from cyclosporine and phenytoin-induced gingival
overgrowth tissues exhibited less DNA polymerase a in
the basal keratinocytes than control tissues.
• These findings suggest that the epithelial acanthosis
seen in both cyclosporine and phenytoin-induced gingival
overgrowth may be due to an enhanced keratinocyte life
span, rather than an increase of keratinocyte proliferation
(Niimi et al. 1990).
• Phenytoin therapy results in an up regulation of
prostaglandin formation in gingival fibroblasts. Such an
up regulation could cause an increase in
glycosaminoglycan synthesis which would affect the
extracellular gingival matrix (Karlinsky & Goldstein 1989)

55.
• The direct effect of bacterial lipopolysaccharide on tissue
culture models has been investigated,
Lipopolysaccharide is an important component of the
bacterial ceil wall which is known to be cytotoxic for
fibroblast cell lines (Horiba et al, 1989),
• Cyclosporine, in the presence of lipopolysaccharide at a
concentration that would normally inhibit fibroblast
proliferation, has been shown to negate the inhibitory
effect of the lipopolysaccharide and maintain the ability of
the drug to stimulate fibroblast proliferation (Bartold 1989),

56.
• Studies to date have focused on the drug phenytoin and
its interaction with epidermal growth factor (EGF) and
platelet derived growth factor (PDGF)
• Fibroblasts from the 2 patients showed no difference in
the affinity of the receptor for EGF, However, the
responder patients showed an increase in both
internalization of EGF receptor-ligand and steady state
level of EGF receptor mRNA after phenytoin therapy,
whereas in the non-responder a decrease was observed
in both factors.
• These findings suggest that phenytoin causes a down
regulation of EGF receptor metabolism in responder
patients, whilst in non-responders there is an up
regulation.

57.
• Thus phenytoin can cause an increase in the number of
cell surface EGF-receptors. which in turn may cause an
alteration in gingival connective tissue homeostasis. This
effect may be mediated by the action of the drug on
intracellular Ca+2 accumulation (Brunius & Modeer 1989)
• Phenytoin induced increased in PDGF secretion from
macrophages could be an important factor in the
expression of gingival overgrowth. Macrophages play a
fundamental role in orchestrating the plaque induced
inflammatory changes in the gingival tissues. There is
considerable evidence that such inflammatory changes
exacerbate phenytoin-induced gingival overgrowth (Hassell
et al. 1983)

58.
• Brown et al (1991a) further enlarged upon this
mechanism discussion regarding a biochemical
pathway hypothesis which included the following:
• The research evidence regarding an anabolic
hypothesis for causation for DIGO was consistently
contradictory and at best confusing, and without any
unifying conceptual basis (Brown et al (1991a) and McCulloch
and Bordin (1991)
• All of the inducing drugs are known to effect cation (Na+ and
Ca++)channels (Antman et al (1980), DeLorenzo (1980), Colombani et
al (1985), Jones and Wimbish (1985), Messing et al (1985), Dretchen et
al (1986) and Fugii and Kobayashi (1990)

59.
• DIGO appears to be the result of a defect in catabolism
due to increased amounts sulfated glycosaminoglycan
(GAGs/connective tissue) within DIGO gingival tissues.
(Hassell (1982), Kantor and Hassell (1983), Dahllof et al (1986), Deliliers
et al (1986) and Bowman et al (1988)
• Topical folate demonstrated clinical efficacy in the
treatment of DIGO (and systemic folate was not as
efficacious) (Drew et al (1987), Backman et al (1989), Brown et al
(1991b) and Poppell et al (1991)
• Folate cellular uptake is due to both a cation regulated
channel, and by passive diffusion (Ariel et al (1978, 1982), Rose
et al (1978), Eilam et al (1981), Rosenberg et al (1985), Zimmerman et al
(1986) and Zimmerman (1990)

60.
• Folate is necessary for protein synthesis and the
conversion of DNA base-pairs necessary for DNA
synthesis (Burka and Marks (1967) and Taheri et al (1982)
• Plaque control decreases the incidence, recurrence, and
severity of DIGO (Nuki and Cooper (1972), Russell and Bay (1978),
Staple et al (1978), O’Neil and Figures (1982), Daley and Wysocki
(1984), Dahllof et al (1986), Dahllof and Modeer (1986), Modeer et al
(1986), Modeer and Dahllof (1987), Fitchie et al (1989) and Francetti et al
(1991)

61.
• Collagenase is necessary for the tissue degradation of
gingival connective tissue and is an inactive enzyme
which requires activation with a matrix
Metalloproteinases (Murphy et al (1982, 1986, 1987), Moy et al
(1985) and Meikle et al (1989)
• Gingival sulcular epithelium has a relatively high turnover
rate which requires protein synthesis (Beagrie and Skougaard
(1962) and Engler et al (1965)

62.
• This hypothesis purports that the biochemical pathway for
DIGO is influenced by bacterial plaque which causes gingival
inflammation which increases the buildup of gingival
connective tissue (glycosaminoglycans—GAGs). The inducing
drugs (anti-convulsants, CCBAs, and calcineurin
inhibitor/immunosuppressive drugs) decrease folate cellular
uptake in gingival fibroblast cells. The secondary effect of
decreased cellular folate is that the synthesis and/or activation
of a particular MMP (or MMPs) is/are decreased and as that
(a) particular MMP(s) is/are necessary to convert inactive
collagenase to active collagenase within the gingiva; therefore,
there is an insufficient amount of active collagenase necessary
to breakdown excess gingival connective tissues (built up
secondary to inflammation) resulting in the side effect of DIGO
(Brown et al, 1991a).

63.
• Chronic Inflammatory Enlargement:
• Of the inflammatory type of gingival enlargement,
treatment consists of the establishment of excellent
oral hygiene, the elimination of all local predisposing
factors and proper home care by the patient.
• In patients with extensive gingival enlargement, the
affected tissues must be removed surgically and the
remaining tissues properly contoured.
• All local irritative factors such as calculus, the margins
of cervical cavities, or areas of food impaction should
be corrected.

64.
• The purpose of treatment of an acute abscess is to
alleviate pain, control the spread of infection and
establish drainage.
• After the cause is diagnosed, the patients general
systemic response should be evaluated and his or her
temperature taken.
• Drainage can be established through the pocket or by
means of an incision from the outer surface; the former is
preferable,
• After application of a topical anesthetic, a flat instrument
or a probe is introduced into the pocket in an attempt to

65.
• With a Bard-Parker no. 11 blade, a vertical incision is
made through the most fluctuant part of the lesion,
extending from the mucogingival fold to the gingival
margin. If the swelling is on the lingual surface, the
incision is started just apical to the swelling and extended
through the gingival margin.
• After the initial extravasation of pus, irrigate the area with
warm water and gently spread the incision to facilitate
drainage..
• If the tooth is extruded, it should be ground slightly to
avoid contact with its agonists.
• In addition to the rinses, penicillin or other antibiotics can
be prescribed patients.
• If the residual size of the lesion is too great (chronic

66.
• After topical anesthesia is applied, the fluctuant area of
the lesion is incised with a Bard-Parker blade, and the
incision is gently widened to permit drainage. The area is
cleansed with warm water and covered with a gauze pad.

67.
• The treatment should be particularly concerned
with cases where there is evidence of gingival
enlargement of patients taking one or more of
these drugs because :
• Poses a plaque control problem
• It may affect mastication
• It may alter tooth eruption
• It may interfere with speech
• It may cause aesthetic concerns.

68.
• The clinician should also emphasize plaque control as
the first step in the treatment of drug induced gingival
enlargement.
• Although the exact role played by bacterial plaque in drug
induced gingival enlargement is unclear, there is
evidence that good oral hygiene and frequent
professional removal of plaque decreases the degree of
the gingival enlargement present and improves overall
gingival health.

69.
• It has been suggested that folic acid is taken up primarily in a
Na++ coupled, Na-- dependent active transport mechanism and
secondarily through passive diffusion.
• The sulcular gingival epithelium has one of the highest cellular
turnover rate increases the need for intracellular folate.
• The favorable results of topical application and the negative
results of systemic administration of folic acid in the treatment
of human support of the concept of an end organ deficiency.
• The topical administration of folic acid would be more likely
than systemic administration to produce an increased
extracellular concentration of folic acid necessary to override
the decreased active transport uptake with increased passive
diffusion.

70.
• It is well established that phenytoin interferes with folic
acid metabolism (Klipstein 1964, Flexner and Hartmann
1363, Jensen and Olsen 1963:).
• The incidence of folic acid deficiency in patients treated
by anticonvulsants has been reported in various studies
as ranging from 37%. to 90%. (Klipstein 1964. Malpas et al 1966,
reynolds et al 1966, Jensen and 0lsen;1969) .

71.
• The mechanism of this deficiency is still not well
understood.
• It has been postulated that phenytoin acts as a weak folic
acid antagonist, thus interfering with its metabolism in
tissues.
• This may be explained by the close structural
resemblance of phenytoin to folic acid. Since phenytoin
inhibits the utilization of folic acid at the cellular level,
• Folic acid deficiency has been associated with increased
gingival inflammation

72.
• The results of several clinical studies have indicated that
supplementation with folic acid, either systemically or by
topical application, is associated with a decrease in the
plaque-induced inflammatory response.
• A controlled clinical trial of topical folate rinse (1mg/ml)
vs. systemic folate (4mg daily) in patients treated with
phenytoin for a minimum of 3 months, also demonstrated
some reduction in overgrowth and mean periodontal
probing depth without any reduction in plaque or gingival
indices (Drew HJ et al 1987).

73.
• Alternative meditations to phenytoin include
carbamazepine and valproic acid and both of which have
been reported to have a lesser impact in inducing
gingival enlargement.
• For patienls on nifedipine, with prevalence of gingival
enlargement has up to 44%, other calcium channel
blockers such as diltiazem and verapamil may be viable
alternatives, since the prevalence is 20% and 4%,
respectively.
• Also, consideration may be given to the use of another
class of antihypertensive medications

74.
• Drug substitution options for cyclosporin are more limited
due to the fact that few of these options exist.
• Recently, it has been shown that cyclosporin induced
gingival enlargement can spontaneously resolve if the
drug is substituted by tracolimus.
• There is also preliminary evidence that the antibiotic
azithromycin may aid in decreasing the severity of
cyclosporin induced gingival enlargement.
• If any drug substitution is attempted, it is important to
allow for 6-12 months to elapse between discontinuation
of the offending drug and the possible resolution of
gingival enlargement before a decision to implement

75.
• Gingival enlargement may persist, despite drug
substitution attempts and good plaque control.
• These cases need to be treated by periodontal surgery,
either gingivectomy or the periodontal flap.
• Gingivectomy presents with the advantages of technique
simplicity and quickness but, unlike the periodontal flap,
will not allow for osseous recontouring and may sacrifice
keratinized tissue.

76.
• Also, gingivectomy results in healing by secondary
intention, which causes discomfort and an increased
chance of post operative bleeding.
• Small areas (up to six teeth) presenting with drug
induced gingival enlargement where there is no evidence
of attachment loss can be effectively treated with the
gingivectomy technique

77.
• An important aspect is the amount of keratinized tissue
present.
• It is recommended that at least 3 mm of keratinized
tissue in the apicocoronal direction remain after the
surgical procedure is concluded.
• Therefore, if the initial gingivectomy incision needs to be
placed in close proximity to or at the mucogingival
junction, this technique is contraindicated.

78.
The gingivectomy technique used in the treatment of drug-
induced gingival enlargement is as follows.
• Following administration of local anesthesia, the deepest point
in each pocket is marked on the external gingival wall using a
pocket marker or a probe. The series of bleeding points
obtained with pocket marking works as a guideline for the
initial scalloped external bevel incision.
• This incision is accomplished with the Kirkland knife or a # 15
blade if angulation permits.
• A sulcular incision follows the initial external bevel incision and
the release of the interproximal tissue can be achieved with an
Orban knife following excision of most of the enlarged tissue
with curettes.

79.
• Gingivoplasty is performed. The goal of gingivoplasty is to
restore the physiological contour observed in healthy gingiva
and the recreation of gingival festooning.
• Gingivoplasty is performed with surgical scissor, tissue nippers
and high-speed diamonds of various shapes and sizes under
adequate refrigeration.
• Meticulous scaling and root planning should be performed
before application of periodontal dressing to the surgical area.
• Gingivectomy or gingivoplasty can also be performed by
electrosurgery or by a laser device

80.
• Advantages: Electrosurgery permits adequate contouring of
the tissue and controls hemorrhage.
• Disadvantages: Electrosurgery cannot be used in patients
who have a noncompatible or a poorly shielded cardiac
pacemaker. The treatment causes an unpleasant odor.
• The heat generated by injudicious use can cause tissue
damage and loss of periodontal support when the electrode is
used close to bone.
• When the electrode touches the roots, areas of cementum
burn are produced.
• Therefore, the use of electrosurgery should be limited to
superficial procedures such as removal of gingival

81.
• It should not be used for procedures that involve
proximity to the bone, such as flap operations or
mucogingival surgery.
• Technique:
• The removal of gingival enlargements and gingivoplasty
is performed with the needle electrode, supplemented by
the small ovoid loop or the diamond- shaped electrodes
for festooning.
• A blended cutting and coagulating (fully rectified) current
is used. In all reshaping procedures "shaving" motion.

82.
• Larger areas of gingival enlargement (more than six
teeth) or areas where attachment loss combined with
osseous defects is present should be treated with the
periodontal flap.
• Also, any situation in which the gingivectomy technique
may result in the elimination of all keratinized tissue and
consequent creation of mucogingival problems should be
treated with the periodontal flap.

83.
• The initial scalloped internal bevel incision is made with a # 15 blade
at least 3 mm coronal to the mucogingival junction, including the
creation of new interdental papillae.
• It is then used to thin the gingival tissues in the buccolingual
direction; this thinning process should be carried out in the
mucogingival junction.
• At the mucogingival junction level, a full or split thickness flap is
elevated.
• The gingival tissue collar, which attached to the bone and teeth, is
removed with the use of large and small curettes.
• Following debridement and osseous recontouring when necessary;
flap are positioned right on top of the alveolar crest and sutures are
placed

84.
• Another situation in which the periodontal flap is used in the
treatment of DIGO is in assisting tooth eruption in younger
patients.
• The result of the process may be the soft tissue impaction of
the tooth apical to or as its normal occluding position.
• If the gingivectomy technique were to be applied in that
situation, it would result in the complete elimination of all
keratinized tissue and the creation of a mucogingival problem.
• The flap technique follows for the complete exposure of the
impacted tooth or teeth by apically positioning the thinned flap
without, compromising the mucogingival status of the area.

85.
• Idiopathic gingival enlargement is a rare condition of
undetermined cause. It has been designated by such
terms as gingivostomatosis, elephantiasis, idiopathic
fibromatosis, hereditary gingival hyperplasia, and
congenital familial fibromatosis.
• Syndrome associated with IGF:
• Zimmerman – Laband syndrome
• Murray-Puretic Drescher syndrome
• Rutherford syndrome
• Cowden syndrome
• Cross syndrome

86.
Classification
• Isolated HGF
• isolated IGF
• GF with hypertrichosis
• GF with hypertrichosis and mental retardation or
epilepsy.
• GF with mental retardation or epilepsy.
• GF associated with other disease as part of a
syndrome.

87.
Clinical Features
• The enlargement affects the attached gingiva as well as
the gingival margin and the interdental papillae.
• The facial and lingual surfaces of the mandible and
maxilla are generally affected, but the involvement may
be limited to either jaw.

88.
• The enlarged gingiva is pink, firm, and almost a leathery
in consistency, and it 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 as a result of the
bulbous enlargement of the gingiva.
• Secondary inflammatory changes are common at the
gingival margin.

89.
Histopathology
• Idiopathic gingival enlargement shows a bulbous
increase in the amount of connective tissue that is
relatively avascular and that consists of densely arranged
collagen bundles and numerous fibroblasts.
• The surface epithelium is thickened and acanthotic,
with elongated rete pegs.

90.
• The magnification of an existing inflammation initiated by
dental plaque. This group of diseases, which are
discussed in the Conditioned Enlargements section,
includes some hormonal conditions (e.g., pregnancy,
puberty), some nutritional diseases (e.g., vitamin C
deficiency), and some cases in which the systemic
influence is not identified (i.e., nonspecific conditioned
enlargement).
• The manifestation of the systemic disease independently
of the inflammatory status of the gingiva. These
mechanisms are described in the Systemic Diseases that
Cause Gingival Enlargement section and the Neoplastic
Enlargement (Gingival Tumors) section.

91.
Conditioned Enlargements
• Conditioned enlargements occur when the systemic
condition of the patient exaggerates or distorts the usual
gingival response to dental plaque.
• Bacterial plaque is necessary for the initiation of this
type of enlargement.
• The three types of conditioned gingival enlargement :
• Hormonal (pregnancy, puberty),
• Nutritional (associated with vitamin c deficiency),
• Allergic.

92.
• These hormonal changes induce changes in vascular
permeability, which leads to gingival edema and an
increased inflammatory response to dental plaque.
• The sub gingival microbiota may also undergo changes,
including an increase in Prevotella intermedia.
Marginal Enlargement.
• The enlargement is usually generalized, and it tends to
be more prominent interproximal than on the facial and
lingual surfaces.
• The enlarged gingiva is bright red or magenta, soft, and
friable, and it has a smooth, shiny surface. Bleeding
occurs spontaneously or on slight provocation.

93.
Tumor like Gingival Enlargement.
• The so-called pregnancy tumor is not a neoplasm; it is an
inflammatory response to bacterial plaque, and it is
modified by the patient’s condition.
• It usually appears after the third month of pregnancy.
• The lesion appears as a discrete, mushroom like,
flattened spherical mass that protrudes from the gingival
margin or more often from the interproximal space, and it
is attached by a sessile or pedunculated base.

94.
• It tends to expand laterally, and pressure from the tongue
and the cheek perpetuates its flattened appearance.
• It is generally dusky red or magenta in color; it has a
smooth, glistening surface that often exhibits numerous
deep-red, pinpoint markings.
• It is a superficial lesion that usually does not invade the
underlying bone.
• It is usually painless.

95.
Histopathology.
• Gingival enlargement in pregnancy is called
angiogranuloma.
• Both marginal and tumor like enlargements consist of a
central mass of connective tissue, with numerous
diffusely arranged, newly formed, and engorged
capillaries lined by cuboid endothelial cells as well as 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.

96.
TREATMENT
• Treatment requires the elimination of all local irritants that
may be responsible for precipitating the gingival changes
that occur during pregnancy.
• The elimination of local irritants early in pregnancy is
preventive measure against gingival disease, which is
preferable to the treatment of gingival enlargement after it
occurs.
• Marginal and interdental gingival inflammation and
enlargement are treated by scaling and curettage.

97.
• The treatment of tumor like gingival enlargements
consists of surgical excision as well as the scaling and
planing of the tooth surface.
• The enlargement recurs unless all irritants are removed.
Food impaction is frequently an inciting factor.
Timing of Treatment and Indications
• Gingival lesions during pregnancy should be treated as
soon as they are detected, although not necessarily by
surgical means.
• Scaling and root planing procedures and adequate oral
hygiene measures may reduce the size of the
enlargement.

98.
• Gingival enlargements do shrink after pregnancy, but
they usually do not disappear.
• Lesions should be removed surgically during pregnancy
only if they interfere with mastication or produce an
aesthetic disfigurement that the patient wants removed.

99.
• It is marginal and interdental, and it is characterized by
prominent bulbous interproximal 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.
• After puberty, the enlargement undergoes spontaneous
reduction, but does not disappear completely until the
plaque and calculus are removed.

100.
• A longitudinal study of the subgingival microbiota of
children between the ages of 11 and 14 years and their
association with clinical parameters implicated
Capnocytophaga species in the initiation of pubertal
gingivitis.
• Other studies have reported that hormonal changes
coincide with an increase in the proportion of Prevotella
intermedia and Prevotella nigrescens.

101.
TREATMENT
• Gingival enlargement during puberty is treated by
performing scaling and curettage, removing all sources of
irritation, and controlling plaque.
• Surgical removal may be required in severe cases.
• The main problem in these patients is recurrence, which
is caused by poor oral hygiene.

102.
• Acute vitamin C deficiency itself does not cause gingival
inflammation, but it does cause haemorrhage, collagen
degeneration, and edema of the gingival connective
tissue.
• These changes modify the response of the gingiva to
plaque to the extent that the normal defensive delimiting
reaction is inhibited and the extent of the inflammation is
exaggerated, thereby resulting in the massive gingival
enlargement seen in patients with scurvy.

103.
• Gingival enlargement with vitamin C deficiency is
marginal; the gingiva is bluish red, soft, and friable, and it
has a smooth, shiny surface.
• Hemorrhage that occurs either spontaneously or on slight
provocation as well as surface necrosis with pseudo
membrane formation are common features.

104.
• Plasma cell gingivitis consists of a mild marginal gingival
enlargement that extends to the attached gingiva.
• The gingiva appears red, friable, and sometimes
granular, and it bleeds easily; usually it does not induce a
loss of attachment.
• This lesion is located in the oral aspect of the attached
gingiva and therefore differs from plaque-induced
gingivitis.

105.
• Pyogenic granuloma is a tumor like gingival enlargement
that is considered an exaggerated conditioned response
to minor trauma.
• Pyogenic granuloma is similar in clinical and microscopic
appearance to the conditioned gingival enlargement seen
during pregnancy. The differential diagnosis is based on
the patient’s history.

106.
Leukemia.
• Leukemic gingival enlargement may be diffuse or
marginal and localized or generalized.
• It may appear as a diffuse enlargement of the gingival
mucosa, an oversized extension of the marginal gingiva,
or a discrete tumor like interproximal mass.

107.
Clinical Features.
• In patients with leukemic enlargement, the gingiva is
generally bluish red, and it has a shiny surface. The
consistency is moderately firm, but there is a tendency
toward friability and hemorrhage that occur either
spontaneously or with slight irritation.
• Acute painful necrotizing ulcerative inflammatory
involvement may occur in the crevice formed at the
junction of the enlarged gingiva and the contiguous tooth
surfaces.

108.
TREATMENT
• After acute symptoms subside, attention is directed to the
correction of the gingival enlargement.
• The enlargement is treated by scaling and root planing,
which are carried out in stages after the patient has
received topical anesthesia.
• The initial treatment consists of gently removing all loose
accumulations with cotton pellets, performing superficial
scaling, and instructing the patient in oral hygiene for
plaque control; this hygiene should include, at least
initially, the daily use of chlorhexidine mouthwashes.

109.
Granulomatous Diseases.
Wegener’s Granulomatosis.
• The initial manifestations of Wegener’s granulomatosis
may involve the oro-facial region and include oral
mucosal ulceration, gingival enlargement, abnormal tooth
mobility, exfoliation of teeth, and delayed healing
response.
• The granulomatous papillary enlargement is reddish
purple and bleeds easily on stimulation.

110.
Sarcoidosis.
• Sarcoidosis is a granulomatous disease of unknown
etiology. It starts in individuals during their twenties or
thirties, it predominantly affects blacks, and it can involve
almost any organ, including the gingiva, in which a red,
smooth, painless enlargement may appear.
Neoplastic Enlargement (Gingival Tumors)
Benign Tumors of the Gingiva
• Epulis is a generic term that is used clinically to
designate all discrete tumors and tumorlike masses of
the gingiva.
•

111.
Fibroma.
• Fibromas of the gingiva 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 that may be soft and vascular. Fibromas
are usually pedunculated.
• Hard fibromas of the gingiva are rare; most of the lesions
that are diagnosed clinically as “fibromas” are
inflammatory enlargements.

112.
Papilloma.
• Papilloma are benign proliferations of surface epithelium
that are, in many (but not all) cases, associated with the
human papillomavirus (HPV).
• Gingival papilloma appear as solitary wartlike or
cauliflower-like protuberances.
• They may be small and discrete, or they may be broad,
hard elevations with minutely irregular surfaces.

113.
Peripheral Giant Cell Granuloma.
• Giant cell lesions of the gingiva arise interdentally or from
the gingival margin; they occur most frequently on the
labial surface, and they may be sessile or pedunculated.
• They vary in appearance from smooth, regularly outlined
masses to irregularly shaped, multilobulated.
protuberances with surface indentations.

114.
• The ulceration of the margin is occasionally seen. The
lesions are painless, they vary in size, and they may
cover several teeth.
• They may be firm or spongy, and their color varies from
pink to deep red or purplish blue.

115.
Central Giant Cell Granuloma.
• Giant cell lesions arise within the jaws and produce
central cavitation. They occasionally create a deformity of
the jaw that makes the gingiva appear enlarged.
Leukoplakia.
• Leukoplakia is a strictly clinical term defined by the World
Health Organization as a white patch or plaque that does
not rub off and that cannot be diagnosed as any other
disease.
• Leukoplakia of the gingiva varies in appearance from a
greyish white, flattened, scaly lesion to a thick, irregularly
shaped, keratinous plaque.

116.
Gingival Cyst.
• Localized enlargements that may involve the marginal and
attached gingiva.
• The cysts occur in the mandibular canine and premolar areas,
most often on the lingual surface.
• They are painless, but, with expansion, they may cause
erosion of the surface of the alveolar bone.
• The gingival cyst should be differentiated from the lateral
periodontal cyst.
• Gingival cysts develop from odontogenic epithelium or from
surface or sulcular epithelium traumatically implanted in the
area.
•

117.
Carcinoma
• Squamous cell carcinoma is the most common malignant
tumour of the gingiva. It may be exophytic, presenting as
an irregular outgrowth, or ulcerative, appearing as flat,
erosive lesions.
• It is often symptom free, going unnoticed until
complicated by inflammatory changes that may mask the
neoplasm but cause pain; sometimes it becomes evident
after tooth extraction.

118.
Malignant Melanoma.
• Malignant melanoma is a rare oral tumour that tends to
occur in the hard palate and maxillary gingiva of older
persons.
• It is usually darkly pigmented, and it is often preceded by
localized pigmentation. It may be flat or nodular, and it is
characterized by rapid growth and early metastasis.

119.
• False enlargements are not true enlargements of the
gingival tissues, but they may appear as such as a result
of increases in the size of the underlying osseous or
dental tissues.
• The gingiva usually presents with no abnormal clinical
features except the massive increase in the size of the
area.
Underlying Osseous Lesions
• Enlargement of the bone subjacent to the gingival area
occurs most often with tori and exostoses, but it can also
occur with Paget’s disease, fibrous dysplasia, cherubism,
central giant cell granuloma, ameloblastoma, osteoma,
and osteosarcoma.

120.
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 the 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 called developmental
enlargement, and often persists until the junctional
epithelium has migrated from the enamel to the
cementoenamel junction.

121.
• Gingival enlargement can be caused by a wide variety of
etiologies
• The clinician can often diagnose the cause by a careful history
(e.g., drug-induced or pregnancy-induced enlargement), by
location (e.g., mouth-breathing enlargement), or by the clinical
presentation (e.g., generalized enlargement with gingival
hematoma formation seen in leukemia).
• Plaque-induced inflammation can be the sole cause of
gingival enlargement or can be a secondary cause, so in all
patients, therapy to control gingival inflammation is essential.
• Thus Correct diagnosis & treatment planning form the most
essential part of the treatment of gingival enlargement to achieve
proper functional and esthetic harmony.

122.
• Newman, Takei, Klollevold, Carranza. Carranza’s clinical
periodontology. 11th edition.
• Eva Ingles. New clinical index for drug-induced gingivai
Overgrowth. Quintessence Int 1999;30:467-73
• RS Brown, PR Arany. Mechanism of drug-induced
gingival overgrowth revisited: a unifying hypothesis. Oral
Diseases 2014
• Seymour RA, ThomasonJM, Ellis JS: The palhogenesis
of drug-induced gingival overgrowth. J Clin Periodontol
1996: 23: 165-75.