Gingival enlargement can result from chronic or acute inflammation, drugs, or systemic conditions. Drug-induced enlargement is common with anticonvulsants like phenytoin and presents as a painless, bead-like enlargement of the papillae that progresses to cover tooth crowns. Histologically, there is pronounced hyperplasia of connective tissue and epithelium. While the enlargement is caused by the drug, secondary inflammation from plaque complicates the condition, adding to the size and producing redness. Approximately 50% of patients on phenytoin experience gingival overgrowth.

1. Presented by:
Surbhi Kapoor
MDS 2nd year

2.  Gingival enlargement is the proliferation and intensification of the gingiva
which is a prevailing character of the diseased gingival tissues.
 Thus, increase in size of the gingiva is a common feature of gingival disease.
 Accepted current terminology for this condition is GINGIVAL
ENLARGEMENT OR GINGIVAL OVERGROWTH.
 However “Hypertrophic Gingivitis”, “Gingival Hypertrophy” and “Gingival
Hyperplasia” were the former histopathological loculations which are not
applicable these days considering that it is unable to differentiate clinically in
the increase in the number of cells or in the size of the cells.

3. 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
Classification ( Acc. to etiological factors & pathological
changes)

4. 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 gingivae and papillae
Discrete: An isolated sessile or
pedunculated, tumor like enlargement
Using the criteria of location & distribution, gingival enlargement is
designated as follows:

5. The degree of gingival enlargement can be scored as follows:
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.
Seymour et al 1985
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

6. Miller and Damm (1992)
enlargement was divided into a vertical and a
horizontal component and abbreviated as GOI index.
Vertical component is measured from CEJ to the free
gingival margin and the horizontal component from
the enamel surface at the point of contact to the
external margin of the interdental papilla.
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.
horizontal gingival overgrowth index is described
as:
Grade 0: < 1mm
Grade 1: 1 to 2 mm
Grade 2: >2mm
Bokenkamp A and Bohnhorst
B (1994)
Grade 0: No signs of gingival
overgrowth
Grade I: Gingival hyperplasia
confined to interdental papilla c.
Grade II: Hyperplasia of interdental
papilla and marginal gingiva
Grade III: Gingival hyperplasia
covering at least three-quarters of
tooth crowns

7. 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.
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.

8. 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

9. 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.
A) Chronic Inflammatory Enlargement
Etiology
•Prolonged exposure to dental plaque.
Factors that favor plaque accumulation and retention include -poor oral
hygiene.
-irritation by anatomic abnormalities.
-Improper restorative and orthodontic appliances.
-Mouth breathing
INFLAMMATORY ENLARGEMENT

10. 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.
Chronic inflammatory
gingival enlargement
localized to anterior region

11. Discrete sessile or
pedunculated mass
•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.
Gingival Changes Associated with Mouth
Breathing
• Gingiva appears red and edematous with a diffuse surface
shininess of the exposed area.
•maxillary anterior region -common site
• Harmful effect is attributed to irritation from surface
dehydration.

12. 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.
Demarcation
between exposed
gingiva and
unexposed
gingiva

13. B) Acute Inflammatory Enlargement
GINGIVALABSCESS
•localized, painful, rapidly expanding lesion
•usually of sudden onset.
• Generally limited to marginal gingiva or interdental papilla.
•In its early stages –appears as red swelling with a smooth, shiny surface.
•Within 24 to 48 hours, -fluctuant and pointed with a surface orifice from which a
purulent exudate may be expressed.
Adjacent teeth are sensitive to percussion.
Etiology
Acute inflammatory gingival enlargement results from bacteria carried deep into the
tissues when foreign substances such as a toothbrush bristle, a piece of apple core, or
a lobster shell fragment is forcefully embedded into the gingiva. (Lesion is confined
to gingiva).

14. 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.
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.

15. Periodontal abscess formation may occur in the following ways:
1. Extension of infection from a periodontal pocket deeply into the supporting
periodontal tissues and localization of the suppurative inflammatory process along
the lateral aspect of the root.
2. Lateral extension of inflammation from the inner surface of a periodontal pocket into
the connective tissue of the pocket wall. Localization of the abscess results when
drainage into the pocket space is impaired .
3. In a pocket that describes a tortuous course around the root, a periodontal abscess
may form in the cul -de- sac, the deep end of which is shut off from the surface.
4. Incomplete removal of calculus during treatment of a periodontal pocket. In this
instance, the gingival wall shrinks, occluding the pocket orifice, and a periodontal
abscess occurs in the sealed-off portion of the pocket.
5. A periodontal abscess may occur in the absence of periodontal disease after trauma to
the tooth or perforation of the lateral wall of the root in endodontic therapy.

16. Periodontal abscesses are classified acc. to location:
1. Abscess in the supporting periodontal tissues along the lateral aspect of the root.- SINUS
FORMATION occur in the bone that extends laterally from the abscess to external surface.
2. Abscess in the soft tissue wall of a deep periodontal pocket.
Histopathology
-localized accumulation of viable & non viable PMNs within the periodontal pocket
wall.
-The PMNs liberate enzymes that digest the cells & other structures forming the
liquid product known as pus, which constitutes the center of abscess.
-An acute inflammatory reaction surrounds the purulent area & overlying
epithelium exhibits intracellular & extracellular edema and invasion of leukocytes.
-The localized acute abscess becomes a chronic abscess when its purulent content
drains through a fistula into the outer gingival surface or into the periodontal
pocket and the infection causing the abscess is not resolved

17. Gingival enlargement is a well-known consequence of the administration of some
anticonvulsants, immunosuppressants, and calcium channel blockers and may create speech,
mastication, tooth eruption, and aesthetic problems.
Clinical Features
•Growth starts as a painless, bead-like enlargement of the interdental papilla and extends to
the facial and lingual gingival margins.
•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
Case of phenytoin
induced gingival
enlargement
DRUG INDUCED GINGIVAL ENLARGEMENT

18. •usually generalized throughout the mouth but 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 are extracted.
•Hyperplasia of the mucosa in edentulous mouths has been
reported but is rare
•The enlargement is chronic and slowly increases in size
•When surgically removed, it recurs.
•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, with a minutely lobulated surface and no tendency to bleed.

19. •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
•Drug-induced enlargement may occur in mouths with little or no plaque and may be
absent in mouths with abundant deposits.
•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)

20.  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.

21. 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).
•Cyclosporine enlargements usually have a more highly vascularized connective
tissue with foci of chronic inflammatory cells, particularly plasma cells.
• The “mature” phenytoin enlargement has a 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.

22. ANTICONVULSANTS
•The first drug-induced gingival enlargements reported were those produced by
phenytoin (Dilantin).
•Other hydantoins known to induce gingival enlargement are ethotoin (Peganone) and
mephenytoin (Mesantoin).
•Other anticonvulsants that have the same side effect are the succinimides
(ethosuximide [Zarontin], methsuximide [Celontin]), and valproic acid [Depakene]).
(Hallmon et al 1999)
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.

23. Pathogenesis
A direct stimulating action on gingival fibroblasts or mast-cells with secondary
fibroblastic involvement have been suggested.
(Shafer et al 1960)
It has also been proposed that susceptibility or resistance to pharmacologically
induced gingival overgrowth may be governed by the existence of differential
proportions of fibroblast subsets in each individual which exhibit a fibrogenic
response to these medications.
(JISP 2013)
It has been hypothesized that only few subsets of patients on phenytoin develop
enlargement. These individuals have fibroblasts with abnormal susceptibility to drug.
Also fibroblasts from overgrown gingiva in phenytoin treated patients are
characterized by elevated levels of proteins, esp. Collagen.
(J Periodontol 2004)
Tissue culture experiments by Shafer in 1960 indicate that phenytoin stimulates
proliferation of fibroblast-like cells and epithelium.
Two analogues of phenytoin (l-allyl-5-phenylhydantoinate and 5-methyl-5-
phenylhydantoinate) have a similar effect on fibroblast-like cells.

24. Fibroblasts from a phenytoin-induced gingival overgrowth show increased synthesis of
sulfated glycosaminoglycans in vitro. (Hassel TM 1983)
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.
(Butler RT 1987, Brown RS 1991)
Genetic predisposition is a suspected factor in determining whether a person treated with
phenytoin will develop enlargement or not.
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.
In conclusion, the pathogenesis of gingival enlargement induced by phenytoin is not known,
but some evidence links it to a direct effect on specific, genetically predetermined
subpopulations of fibroblasts, inactivation of collagenase, and plaque-induced
inflammation.

25. IMMUNOSUPPRESSANTS
•Cyclosporine is a potent immunosuppressive agent used to prevent organ transplant rejection
and to treat several diseases of autoimmune origin.
•Mechanism of action- not well known, but it appears to selectively and reversibly inhibit helper
T cells, which play a role in cellular and humoral immune responses.
•Cyclosporin A (Sandimmune, Neoral) is administered intravenously or by mouth, and dosages
greater than 500 mg/day have been reported to induce gingival overgrowth.(Daley TD 1986)
•Cyclosporine-induced gingival enlargement is more vascularized than phenytoin enlargement .
• Occurrence varies from 25% to 70% (Romito GA 2004)
•Affects children more frequently, and its magnitude appears to be related more to the plasma
concentration than to the patient’s periodontal status.

26. •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)

27. CALCIUM CHANNEL BLOCKERS
•Drugs developed for the treatment of cardiovascular conditions such as hypertension,
angina pectoris, coronary artery spasms, and cardiac arrythmias.
•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.
•These drugs are:
-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)

28. It has been postulated that the drug may stimulate cell proliferation and synthesis indirectly by
one of three mechanisms:
oNifedipine is also used with cyclosporine in kidney transplant recipients, and the combined
use of both drugs induces larger overgrowths.
(Bokenkamp A 1994)
oNifedipine gingival enlargement has been induced experimentally in rats, where it appears to
be dose dependent; in humans, however, this dose dependency is not clear.
oOne report indicates that nifedipine increases the risk of periodontal destruction in patients
with diabetes mellitus type 2.
(Wang X et al 2008)
(3)by causing a calcium-
dependent inhibitory
effect on T cells that
would increase
gingival susceptibility
to bacterial infection
through
immunosuppression.
(Seymour RA 1991)
(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)
(1) by giving rise to
the formation of a
more potent
metabolic
byproduct.

29. oDiltiazem, felodipine, nitrendipine, and verapamil also induce gingival
enlargement.
(Brown RS 1990)
oThe dihydropyridine derivative, isradipine, can replace nifedipine in some cases and
does not induce gingival overgrowth.
(Carlson M et al 1997)
oLars Heijl et al (J Periodontol, 1988) assessed the development of gingival
overgrowth in dogs given nitrendipine, a new antihypertensive dihydropyridine.
The results demonstrated that nitrendipine administered to Beagle dogs during a 20-
week period causes marked overgrowth of gingival tissue of apparently normal
composition.
oLucas R M et al (1984) compared the nifedipine- and phenytoin-induced gingival
hyperplasia at the light microscopic level and concluded that the nifedipine induced
gingival hyperplasia is not only similar to phenytoin-induced gingival hyperplasia in
its histopathologic morphology, but also in its response to treatment.

30. oIdiopathic gingival enlargement is a rare condition of undetermined cause.
oIt has been designated by terms like Gingivomatosis, elephantiasis, idiopathic
fibromatosis, hereditary gingival hyperplasia, and congenital familial fibromatosis.
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)
•The enlargement usually begins with the eruption of the primary or secondary dentition and may
regress after extraction, suggesting that the teeth (or the plaque attached to them) may be
initiating factors. The presence of bacterial plaque is a complicating factor.
IDIOPATHIC GINGIVAL ENLARGEMENT

31. Described in tuberous sclerosis, which is an inherited condition characterized by a
triad of epilepsy, mental deficiency, and cutaneous angiofibromas .
(Thomas D, 1992)
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 favor the accumulation of extracellular
matrix
(Coletta et al. 1999).

32. Clinical Features
•Affects the attached gingiva, as well as the gingival margin and interdental papillae
•The facial and lingual surfaces of the mandible and maxilla are generally affected, but
the involvement may be limited to either jaw.
•Enlarged gingiva is pink, firm, and almost leathery in consistency and has a
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.

33. ENLARGEMENTS ASSOCIATED WITH SYSTEMIC DISEASES
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).

34. Conditioned Enlargements
•Conditioned enlargement occurs when the systemic condition of the patient
exaggerates or distorts the usual gingival response to dental plaque.
• The specific manner in which the clinical picture of conditioned gingival
enlargement differs from that of chronic gingivitis depends on the nature of the
modifying systemic influence.
•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.

35. A) Enlargement in Pregnancy
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.
(Kornman KS 1980)
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)

36. 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.

37. •Generally dusky red or magenta, it has a smooth, glistening surface that often exhibits
numerous deep-red, pinpoint markings.
•Superficial lesion and usually does not invade the underlying bone.
•Consistency varies; the mass is usually semifirm, but it may have various degrees of softness
and friability.
•Usually painless unless its size and shape foster accumulation of debris under its margin or
interfere with occlusion, in which case, painful ulceration may occur.
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

38. B) Enlargement in Puberty
Enlargement of the gingiva is sometimes seen during puberty and occurs in both male and
female adolescents and appears in areas of plaque accumulation.
The size of the gingival enlargement greatly exceeds that usually seen in association with
comparable local factors.
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;
the mechanical action of the tongue and the excursion of food prevent a heavy accumulation of
local irritants on the lingual surface.

39. Gingival enlargement during puberty has all the clinical features generally associated
with chronic inflammatory gingival disease.
 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.
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

40. C) Enlargement in Vitamin C Deficiency
 Enlargement of the gingiva is generally included in classic descriptions of scurvy.
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.
Gingival enlargement in vitamin C deficiency is marginal; the gingiva is bluish red, soft,
and friable and has a smooth, shiny surface.
 Hemorrhage, occurring either spontaneously or on slight provocation, and surface necrosis
with pseudomembrane formation are common features.

41. D) Plasma Cell Gingivitis
 Consists of a mild marginal gingival enlargement that extends to the attached
gingiva.
Gingiva appears red, friable, and sometimes granular and bleeds easily; usually it
does not induce a loss of attachment.
Lesion is located in the oral aspect of the attached gingiva and therefore differs
from plaque-induced 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.

42. E) Nonspecific Conditioned Enlargement (Pyogenic Granuloma):
tumorlike gingival enlargement that may be conceived as an exaggerated reaction to minor
trauma without it having been possible to demonstrate a definite infectious organism.
more correctly called telangiectatic granuloma, since the lesion
is highly vascular and usually is not purulent as the term
pyogenic suggests.
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.

43. A) Leukemia
malignant neoplasms of WBC precursors characterized by:
(1) Diffuse replacement of the bone marrow with proliferating leukemic cells;
(2) Abnormal numbers and forms of immature WBCs in the circulating blood;
(3) Widespread infiltrates in the liver, spleen, lymph nodes, and other sites throughout
the body.
According to the type of WBC involved, leukemias are classified as:
 lymphocytic
 myelocytic /myelogenous
According to their evolution, leukemias can be
acute, which is rapidly fatal
 subacute
chronic
SYSTEMIC DISEASES CAUSING GINGIVAL ENLARGEMENT

44. Leukemic Infiltration of the Periodontium
Leukemic cells can infiltrate the gingiva and, less frequently, the alveolar bone.
Gingival infiltration often results in leukemic gingival enlargement
Leukemic gingival enlargement consists of a basic infiltration of the gingival corium
by leukemic cells that creates gingival pockets where bacterial plaque accumulates,
initiating a secondary inflammatory lesion that contributes also to the enlargement of
the gingiva.
 It may be localized to the interdental papilla area or expand to include the mar-
ginal gingiva and partially cover the crowns of the teeth
Oral and periodontal manifestations of leukemia may include:
 leukemic infiltration
Bleeding
 oral ulcerations and infections.
The expression of these signs is more common in acute and subacute forms of leukemia than in
chronic forms.

45. Clinically, the gingiva appears bluish red and cyanotic, with a rounding and
tenseness of the gingival margin and has a shiny surface.
Leukemic infiltration causing
localized gingival swelling of the
interdental papillae between the
maxillary CI and LI
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.

46. 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.
Patients with leukemia may also have a simple chronic inflammation without the
involvement of leukemic cells and may present with the same clinical and
microscopic features seen in patients without the systemic disease.
Most cases reveal features of both simple chronic inflammation and leukemic
infiltrate.

47. Histopathology
•Areas of connective tissue infiltrated with a dense mass of immature and
proliferating leukocytes
•Engorged capillaries, edematous and degenerated connective tissue, and epithelium
with various degrees of leukocytic infiltration 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.

48. B) Granulomatous Diseases
1) WEGENER'S GRANULOMATOSIS:
•Rare disease characterized by acute granulomatous necrotizing lesions of the
respiratory tract, including nasal and oral defects.
•Cause is unknown but it is considered as an immunologically mediated tissue injury.
(Cotran RS 1989)
• Renal lesions develop, and acute necrotizing vasculitis affects the blood vessels.
•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.
• The granulomatous papillary enlargement is reddish purple and bleeds easily on
stimulation

49. Histopathology
Chronic inflammation occurs with scattered giant cells and foci of acute
inflammation and microabscesses covered by a thin acanthotic epithelium.
2) SARCOIDOSIS:
granulomatous disease
unknown etiology.
It starts in individuals in their twenties or thirties, predominantly affects blacks
 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.

50. A) Benign Tumors of the Gingiva
 Epulis is a generic term used clinically to designate all discrete tumors and tumorlike masses
of the gingiva.
It serves to locate the tumor but not to describe it.
Neoplasms account for a comparatively small proportion of gingival enlargements and make up
a small percentage of the total number of oral neoplasms.
In a survey of 257 oral tumors, approximately 8 % occurred on the gingiva.
(Mc Arthy 1941)
 In another study of 868 growths of the gingiva and palate, of which 57% were neoplastic and
the remainder inflammatory, the following incidence of tumors was noted:
carcinoma, 11.0%; fibroma, 9.3%; giant cell tumor, 8.4%; papilloma, 7.3%; leukoplakia, 4.9%;
mixed tumor (salivary gland type), 2.5%; angioma, 1.5%; osteofibroma, 1.3%; sarcoma, 0.5%;
melanoma, 0.5%; myxoma, 0.45%; fibropapilloma, 0.4%; adenoma, 0.4%; and lipoma, 0.3%.
(Bernick S 1948)
NEOPLASTIC ENLARGEMENT (GINGIVAL TUMORS)

51. 1) 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 may
be soft and vascular.
•Fibromas are usually pedunculated.
•Hard fibromas of the gingiva are rare; most of the
lesions diagnosed clinically as “fibromas”
are inflammatory enlargements.
•Also called giant cell fibroma contains multinucleated fibroblasts.
•In another variant of fibroma, mineralised tissue (bone, cementum like material,
dystrophic calcification) may be found and is called peripheral ossifying fibroma.
Histopathology
Bundles of Well-formed collagen fibers with scattering of fibrocytes and a variable
vascularity.

52. 2) Papilloma
•Benign proliferations of surface epithelium associated with the human papilloma
virus (HPV).
•Viral subtypes HPV-6 and HPV-11 have been found in most cases of oral papillomas.
•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.

53. 3) Peripheral Giant Cell Granuloma
•Giant cell lesions of the gingiva arise interdentally or from the gingival margin, occur most
frequently on the labial surface, and may be sessile or pedunculated.
•They vary in appearance from smooth, regularly outlined masses to irregularly shaped,
multilobulated protuberances with surface indentations .
•Ulceration of the margin is occasionally seen.
•The lesions are painless, vary in size, and may cover several teeth.
•They may be firm or spongy, and the color varies from 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

54. Histopathology
Numerous foci of multinuclear giant cells and hemosiderin
particles in CT stroma.
Areas of chronic inflammation are scattered throughout the
lesion, with acute involvement occurring at the surface.
Overlying epithelium is usually hyperplastic, with ulceration at
the base.
Bone formation occasionally occurs within the lesion

55. 4)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 cannot be diagnosed as any other disease.
The cause of leukoplakia remains obscure, although it is associated with the use of tobacco
(smoke or smokeless).
Other probable factors are Candida albicans, HPV-16 and HPV-18, and trauma.
Leukoplakia of the gingiva varies in appearance from a grayish white, flattened, scaly lesion to
a thick, irregularly shaped, keratinous plaque.
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.

56. 5) Gingival Cyst
•appear as localized enlargements that
may involve the marginal & attached
gingiva.
•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.
•Gingival cysts develop from odontogenic
epithelium or from surface or sulcular
epithelium traumatically implanted in the
area.
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, keratin-
ized stratified squamous epithelium, and
parakeratinized epithelium with
palisading basal cells

57. Other benign tumors or masses have also been described as
rare or infrequent findings in the gingiva.
These include:
Nevus
Myoblastoma
Ameloblastoma
Hemangioma
Neurilemoma
Neurofibroma
Mucoceles

58. B) Malignant Tumors of the Gingiva
Carcinoma
Oral cancer accounts for less than 3% of all malignant
tumors in the body.
The gingiva is not a frequent site of oral malignancy (6%
of oral cancers). (Krolls SO,1976)
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, often going unnoticed until
complicated by inflammatory changes that may mask the
neoplasm but cause pain; sometimes it becomes evident
after tooth extraction.
They are locally invasive, involving the underlying bone
and periodontal ligament of adjoining teeth and the adjacent
mucosa.
mulberry-like tissue between
2nd PM and 1st M

59. Malignant Melanoma
• 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.
Sarcoma
• Fibrosarcoma,
lymphosarcoma, and
reticulum cell sarcoma
of the gingiva are rare
• Kaposi’s sarcoma often
occurs in the oral
cavity of patients with
acquired
immunodeficiency
syndrome (AIDS),
particularly in the
palate and the gingiva
Metastasis
• 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.

60.  False enlargements are not true enlargements of the gingival tissues but may
appear as such as a result of increases in size of the underlying osseous or dental
tissues.
 The gingiva usually presents with no abnormal clinical features except the massive
increase in size of the area.
 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
FALSE ENLARGEMENT
Florid type fibrous dysplasia that
induced osseous enlargement in
mandibular molar areas appearing as
gingival enlargement.

61. 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 persists
until the junctional epithelium has migrated from the enamel to the cementoenamel
junction.
Developmental gingival enlargements are
physiologic and usually present no problems.
However, when such enlargement is
complicated by marginal inflammation, the
composite picture gives the impression of
extensive gingival enlargement
Treatment to alleviate the marginal
inflammation, rather than resection of the
enlargement, is sufficient in these patients.

62. MANAGEMENT OF GINGIVAL ENLARGEMENTS
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.
FLAP OPERATION.
Used when the enlarged gingiva remains
soft and friable even after scaling and
root planing
GINGIVECTOMY
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

63. Gingivectomy procedure

64. 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.

65. DRUG SUBSTITUTES
 Alternative medications to the anticonvulsant PHENYTOIN include
CARBAMAZEPINE AND VALPROIC ACID, both of which have been reported to
have a lesser effect in inducing gingival enlargement.
 For patients taking NIFEDIPINE, which has a reported prevalence of gingival
enlargement of up to 44%, other CALCIUM CHANNEL BLOCKERS, SUCH AS
DILTIAZEM OR VERAPAMIL, may be viable alternatives. Their reported
prevalence of inducing gingival enlargement is 20% and 4%, respectively.
 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.
 For cyclosporine, TACROLIMUS is another immunosuppressant. The incidence of
gingival enlargement in patients under tacrolimus therapy is approximately 65%
lower than in those taking cyclosporine.
 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

66. Treatment of drug induced enlargement

67. 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.
 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.

68. Treatment of gingival enlargement in pregnancy
Treatment requires elimination of all local irritants responsible for precipitating the
gingival changes in pregnancy.
Elimination of local irritants early in pregnancy is a preventive measure against
gingival disease. This is preferable to treatment of gingival enlargement after it occurs.
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.

69. 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 root-
planing 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.
In pregnancy, the emphasis should be on preventing gingival disease
before it occurs and treating existing gingival disease before it worsens.
 All patients should be seen as early as possible in pregnancy.

70. 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.
Those without gingival disease should be checked for potential sources of local
irritation and should be instructed in plaque control procedures.
Those with gingival disease should be treated promptly, before the effects of
pregnancy on the gingiva become apparent.