6. According location and distribution:
• 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
9. The degree of gingival enlargement can be
scored as follows :
Grade 0: No signs of gingival enlargement.
Grade I: Enlargement confined to interdental
papilla.
Grade II: Enlargement involves papilla and
marginal gingiva.
Grade III: Enlargement covers three quarters or
more of the crown.
Bokenkamp et al, 1994
10. 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 2mm
Grade 2: >2mm
Miller and Damm (1992)
11. 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.
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:
12. 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
Miranda and Brunet index (2001)
14. Chronic inflammatory enlargement
• Clinical features:
Originates as a slight ballooning
of the
interdental papilla and marginal
gingiva.
Life preserver shaped bulge
around the involved teeth,
which can increase in size until it
covers part of the crowns
As a discrete sessile or
pedunculated mass that
resembles a tumor. It can be
interproximal or located on the
marginal or attached gingiva.
Painful ulceration sometimes
occurs in the fold between the
mass and the adjacent gingiva
14
15. Histopatholog
y
• Lesions that are deep red or bluish
red are soft and friable with a
smooth, shiny surface, and bleed
easily.
• inflammatory cells and fluid, along
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
16. • Etiology
Microbial
biofilm
• lack of proper oral hygiene
• orthodontic appliances
• faulty restoration margins
• misaligned teeth
• oral habits
Factors that favor plaque
accumulation and retention include
• irritation by
anatomic
abnormalities
• Improper restorative
and orthodontic
appliances
17. Management
• Chronic enlargement of the gingiva due to gingivitis is reversible and
can be resolved by removal of the etiologic factors, including the
biofilm, and correction of environmental factors.
• In severe forms of inflammatory enlargement, surgical approaches
may be required
18. Enlargement associated with mouth breathing:
• The gingiva appears red and edematous, with a diffuse
surface shininess of the exposed area.
• The maxillary anterior region is commonly involved. In
many cases, the altered gingiva is clearly demarcated
from the adjacent, unexposed normal gingiva.
• Irritation from surface dehydration is attributed to
mouth breathing.
• (However, comparable changes could not be reproduced by air-
drying the gingiva of experimental animals, suggesting that the
pathogenesis of mouth breathing–associated gingival changes is
far more complex)
19. Acute inflammatory enlargement
• Gingival abscess
Typically limited to the marginal
gingiva or the interdental papilla.
In early stages, it appears as a
red swelling with a smooth, shiny
surface.
In 24 to 48 hours, usually
becomes fluctuant and pointed,
with a surface orifice and a
purulent exudate. Adjacent
teeth may become sensitive to
percussion
The lesion usually ruptures
spontaneously.
19
20. • Etiology
Trauma
Mechanical, chemical, irritation
from
Impacted food items
Traumatic lesions occur when a
substance (e.g.,
bristle) is forcefully
in the gingiva and
by resident
foreign
toothbrush
embedded
complicated
microbes.
21. • Histopathology
The gingival abscess consists of a
purulent exudate of a diffuse
infiltration of polymorphonuclear
leukocytes, edematous tissue, and
vascularization
The surface epithelium has various
degrees of intracellular and
extracellular edema, invasion by
leukocytes, and sometimes
ulceration
22. • The periodontal abscess is an infection located contiguous to the periodontal
pocket and may result in destruction of the periodontal ligament and alveolar
bone.
• Poorly controlled diabetes mellitus has been considered a predisposing factor
for periodontal abscess formation
• Shape and consistency vary from dome-like and firm to pointed and soft. Pus is
usually expressed from the margin on gentle digital pressure
Periodontal abscess
23. Periodontal abscesses are classified according to location as follows:
• 1. Abscess in the supporting periodontal tissues along the lateral aspect of the root.
With this condition, a sinus generally occurs in the bone that extends laterally from
the abscess to the external surface.
• 2. Abscess in the soft-tissue wall of a deep periodontal pocket
• Conditions in which periodontal abscesses are not related to
inflammatory periodontal disease include tooth perforation or fracture
24. Etiology:
1.
• Extension of infection and localization of the suppurative inflammatory process
along the lateral aspect of the root.
2.
• Lateral extension of inflammation from tissue surface of the periodontal pocket
into connective tissue of the pocket wall.
3.
• In a pocket which describes a tortuous course around the root, periodontal
abscess may form in the cul de sac, the deep end of which is shut from the
surface
4.
• Incomplete removal of calculus during treatment of periodontal pocket, here
the gingival wall shrinks occluding the pocket orifice and an abscess results in
the sealed off portion of the pocket.
25. Microflora associated with periodontal
abscess
• Streptococcus viridans is the most
common isolate in the exudate of
periodontal abscesses.
Jaramillo et al 2005
26. • Signs and symptoms of periodontal abscess:
Acute Abscess
• Mild to severe discomfort
• Localized red, ovoid swelling
• Periodontal pocket
• Mobility
• Tooth elevation in socket
• Tenderness to percussion or
biting
• Exudation
• Elevated temperature
• Regional lymphadenopathy
Chronic Abscess
• No pain or dull pain
• Localized inflammatory lesion
• Slight tooth elevation
• Intermittent exudation
• Fistulous tract often
associated with a deep
pocket
• Usually without systemic
involvement
27. 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 ofabscess.
-An acute inflammatory reaction surrounds the purulent area & overlying
epithelium exhibits intracellular & extracellular edema and invasion ofleukocytes.
-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 notresolved
28. Management
28
Immediate management
The common antibiotics which are used
are:
1. Amoxycillin 250 - 500 mg tds 5-7 days
2.Metronidazole 200 - 400 mg tds 5-7
days
If allergic to penicillin, these antibiotics
are used:
1.Erythromycin 250 –500 mg qid 5-7
days
2. Doxycyline 100 mg bd 7-14 days
3. Clindamycin 150-300 mg qid 5-7 days.
Treatment options
• 1.Drainage through pocket retraction
or incision
• 2. Scaling and root planning
• 3. Periodontal surgery
• 4. Systemic antibiotics
• 5. Tooth removal
29. DRUG INDUCED
GINGIVAL ENLARGEMENT
Gingival enlargement is a well known consequence of
administration of :
1. Anticonvulsants
2. Immuno suppressants
3. Calcium channel blockers.
4. Phenylalkylamine
5. miscellaneous
31. GENERAL INFORMATION
Clinical features:
starts as painless bead like enlargement of
interdental papilla and extends to facial and
lingual margins
soon , the marginal and papillary
enlargements unite.
May develop into massive tissue folds
covering the crown.
the lesion is mulberry shaped , firm ,pale pink
and resilient with lobulated surface.
32. Drug induced enlargement may occur in mouths with
little or no plaque and may be absent in mouth with
abundant deposits.
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
33. 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.
34. 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
35. 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)
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.
36. 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.
37. Histopathology :
Consist of hyperplasia of the connective
tissue and epithelium
Acanthosis of epithelium.
Elongated rete pegs ,densely arranged
collagen bundles ,
increase in the number of fibroblast and blood
vessels .
38. 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.
39. Anticonvulsants :
Merritt and Putnam in 1938 repoted hyperplasia in
all type of treatment of epilepsy except Petitmal.
Seen commonly with phenytoin.
Other hydantoins known to cause enlargement :
ethotoin , mephenytoin. Other anticonvulsants are
succinimide,methsuxinimide and valproic acid.
Phenytoin stimulates
proliferation of fibroblast
like cells and epithelium
40. 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.
41. Phenytoin may induce a decrease in collagen
degradation as a result the production of an
inactive fibroblast collagenase. Hassell TM
1981.
Systemic administration of phenytoin
accelerates the healing of gingival wounds in
non epileptic humans. Shapiro M 1958.
42. 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 .
43. 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.
44. 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)
45. Calcium channel blockers :
Drugs developed for the treatment of cardiovascular conditions such ashypertension,
angina pectoris, coronary artery spasms, and cardiac arrythmias.
They inhibit calcium ion influx across the cell membrane of heart and smoothmuscle
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 peripheralvasculature.
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)
46. Nifedipine gingival enlargement has been induced
experimentally in rats, where it appears to be dose dependent; in
humans, however, this dose dependency is not clear.
One report indicates that nifedipine increases the risk of
periodontal destruction in patients with diabetes mellitus type 2.
(Wang X et al 2008)
47. oDiltiazem, felodipine,
enlargement.
nitrendipine, and verapamil also induce gingival
(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.
48. Pathogenesis of
DIGO
1. Synthesis and degradation of
collagen
2. Role of integrins
3. Role of calcium
4. Role of folic acid
5. Role of MMPs
6. Role of inflammatory cytokines
49. SYNTHESIS AND DEGRADATION OF TYPE I
COLLAGEN
• Collagen may be degraded - - extracellular pathway involving the secretion of
collagenase) and via an intracellular pathway involving phagocytosis by
fibroblasts
• Metabolism - balanced by collagen synthesis and degradation to maintain
tissue volume.
• decreased collagen degradation= = may contribute to the appearance of
gingival overgrowth
50. • McCulloch and Knowles showed decreased collagen phagocytosis of fibroblast isolated from
human phenytoin-induced gingival overgrowth than healthy gingiva, and direct inhibitory effects
of nifedipine and phenytoin were also shown on the collagen phagocytosis of fibroblasts
• Phagocytic activity in gingival fibroblasts with a rat experimental model, and
severe inhibition was observed in cyclosporine A-induced gingival overgrowth.
Interestingly, type I collagen and collagenase mRNA expressions were
significantly suppressed by cyclosporin A and nifedipine administration in these
rat experimental models
• Drug-induced gingival overgrowth is not due to the increased synthesis of type I
collagen but the decreased degradation of type I collagen in gingival connective
tissue through the reduction of collagen phagocytosis of fibroblasts.
51. • There are a great many studies reporting increased
connective tissue and proliferation of gingival
fibroblasts secondary to the inducing drugs as the
primary causation of DIGO (Brown et al, 1991a;
Seymour et al, 1996).
• Fibrobalsts from phenytoin patients show increased
synthesis of sulphated glycosaminoglycans (Kantor
et.al 1983)
• Both cyclosporin and nifedipine can cause increase in
tissue levels of non –sulphated glycosaminoglycans
(Zebrowski et.al 1994)
Connective
tissue
Collagen
60%
Matrix-
GAGs 35%
Fibroblasts
52. ROLE OF α2 INTEGRIN
• Integrins are a large family of heterodimeric
transmembrane receptors for extracellular
matrix molecules. Each heterodimer consists of
an a and b subunit
• Both a1b1 and α2b1 integrins are cell surface
receptors for collagens, and cells expressing the
a1b1 integrin preferentially adhere to type IV
collagen, whereas cells expressing α2b1
preferentially adhere to type I collagen
53. • Lee et al. reported that the initial binding step of collagen phagocytosis relies on adhesive
interaction between fibroblasts and collagen, and that α2 integrin plays a critical role in the
phagocytic regulation of collagen internalization
• Katoaka et al showed significantly decreased collagen phagocytosis in fibroblasts in rat
overgrown gingiva induced by cyclosporin A and α2 integrin expression suppressed in
fibroblasts isolated from overgrown gingiva compared to the control
• Chou et al. showed a reduction in collagen phagocytosis of gingival fibroblasts by TNF-a
treatment through the inhibition of collagen binding to cells by the inactivation of α2b1 integrin
• These findings indicate that one etiological factor of drug-induced gingival
overgrowth may be the inhibition of collagen phagocytosis by reducing α2
integrin expression or decrease of the binding activity in gingival fibroblasts
54. ROLE OF CALCIUM
54
• Calcium channel blockers - - block the
influx of calcium ions into cells and to
reduce oxygen consumption.
• Phenytoin - - calcium channel
antagonist and inhibit calcium ion
flux.
• Cyclosporin A - - inhibit the release of
calcium from intracellular stores,
including endoplasmic reticulum and
mitochondria
• α2b1 integrin-mediated collagen
phagocytosis in gingival fibroblasts is
regulated by intracellular calcium
• Cyclosporin A inhibits the α2b1
integrin-binding activity of collagen
phagocytosis through a calcium-
regulated pathway involving ER and
mitochondrial stores
55. ROLE OF CELLULAR FOLATE UPTAKE
• Vogel (1977) proposed that DIGO may be secondary to a localized FA deficiency
• Opladen et al (2010) reported upon the effect of anti-convulsant drugs upon the
folate receptor 1(FOLR1)-dependent 5-methyltetrahydrofolate (MTHF) transport
• They reported that the metabolic breakdown of anti-convulsants as valproate,
carbamazepine, and Phenytoin generates reactive oxygen species (ROS).
(Folate is present in food in a polyglutamate form, which is then converted into monoglutamates by intestinal
conjugase to be absorbed by the jejunum. Phenytoin acts by inhibiting this enzyme, thereby causing folate
deficiency, and thus megaloblastic anemia)
56. • Exposure to PHT could lead to higher
MTHF uptake; however, exposure to
superoxide and hydrogen peroxide
radicals significantly decreased
cellular MTHF uptake
• Therefore, it appears that the FOLR1-
dependent 5-MTHF transport could
also be involved with regard to
inhibited folate transport and
decreased folate uptake in gingival
fibroblasts.
57. Role of matrix metalloproteinases
1
• Collagen synthesis and degradation is controlled by MMPs and the
TIMPs
2
• Collagen fibers are degraded via an extracellular pathway by
secretion of collagenases and via an intracellular pathway via
phagocytosis by fibroblasts
3
• Drugs affect calcium metabolism by reducing the Cα2+ cell influx,
leading to a reduction in the uptake of folic acid, thus limiting the
production of active collagenase. (Livada et al. 2014)
4
• As a result of the reduction in collagen degradation, increased
collagen accumulation occurs.
• E cadherin
• Smad
(TGFb)
• AP 1
• TIMP 1
• MMP 1
59. Role of inflammatory cytokines
1
• Pro-inflammatory cytokines, such as interleukin-1b and interleukin6 seem to have a
synergistic effect in the enhancement of collagen synthesis by human gingival
fibroblasts.
2
• Interleukin-6 has been shown to target connective tissue cells, such as fibroblasts,
both by enhancing their proliferation and by increasing collagen production and
glycosaminoglycan synthesis
3
• This highlights the role of the bacterial biofilm in inducing gingival inflammation,
production of cytokines and gingival enlargement
61. 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)
62. 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.
63. Fibroblasts froma 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 metabolite
gingival fibroblasts with resultant overgrowth.
(Butler RT 1987, Brown RS
1991)
64. 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.
65. Risk factors for
DIGO
• Age
• Gender
• Concomitant medication
• Periodontal variables
• Genetic factors
• Drug factors
66. Age
• Clinical studies suggest that children and adolescents are more susceptible to
DIGO (Hefti et al 1994 )
• Although animal studies have confirmed these findings (Kitamura et al. 1990,
Mori-saki et al. 1993), they are not supported by in-vitro investigations.
67. 5-α-DHT
testosterone
↓Collagenase
Activity
↑Collagen
Production
(Sooriyamoorthy et al
1988,archives of oral biology)
Phenytoin Fibroblasts
Interaction between circulating
androgens and gingival fibroblasts.
Such cells can readily metabolise
testosterone to the active metabolise
5 a-dihydrotestosterone. Phenytoin
enhances this
metabolism(Sooriyamoorthy et al
1988)
Circulating androgen levels will be
higher in adolescents and
teenagers.
68. Gender
• Studies showed that males were at greater risk from developing this unwanted
effect than females and that the severity of the changes would be greater in men.
(Thomason et al. 1995, Thomason et al. 1996b)
• Similarly males were shown to be 3 times more likely than females to develop
clinically significant gingival changes when medicated with calcium channel
blockers
• Evidence from animal studies also supports this finding, with male rats being
more prone to drug-induced gingival overgrowth than females (Ishida et al.
1995).
69. Concomitant
medication
• There is now a considerable body of evidence that the combination of nifedipine
and cyclosporin in organ transplant patients produces more gingival overgrowth
than if either drug was used singularly (Bokenkamp et al. 1994, Margiotta et al. 1996, O’Valle
et al. 1995, Thomason et al. 1995, Thomason et al. 1996, Thomason et al. 1993, Wilson et al. 1998,
Wondimu et al. 1996)
• In adult organ transplant patients, dosages of both prednisolone and azathioprine
appeared to afford the patients some degree of ‘‘protection’’ against the
development of gingival overgrowth
70. • Phenytoin is metabolised (hydrolysed) in the liver by P450 enzymes to 5-(4-
hydroxyphenyl)- 5-phenylhydantoin (4-HPPH). This metabolite has been shown to
induce gingival overgrowth in cats (Hassell & Page 1978).
• Anticonvulsants such as phenobarbitone, primidone and carbamazepine have
been shown to induce hepatic P450 isoenzyme and if given in conjunction with
phenytoin will increase serum concentrations of 4- HPPH.
• This may explain the increased prevalence of gingival overgrowth in patients
receiving multiple anticonvulsant therapy
71. Periodontal
variables• Plaque scores and gingival inflammation appear to exacerbate the expression of
drug-induced gingival overgrowth, irrespective of the initiating drug (Seymour
(1991), Seymour & Heasman (1988), Seymour & Jacobs (1992)
• Both the oral hygiene and the control group developed significant gingival
changes over the 6-month post-transplant investigation period, although the
magnitude of the changes in the oral hygiene group was less marked. (Seymour &
Smith 1991)
72. • In a group of renal transplant patients, the presence of gingival bleeding
increased significantly the risk of developing gingival overgrowth (Pernu et al.
1992).
• It would be reasonable to suggest that proper oral hygiene might be expected to
minimise the severity of drug-induced gingival overgrowth, possibly by
eliminating the inflammatory component of the lesion. Improved oral hygiene in
itself would not appear to prevent overgrowth
73. Genetic Factor
• All three drugs are metabolised by the hepatic cytochrome P450 enzymes.
Cytochrome P450 genes exhibit considerable polymorphism which results in
inter-individual variation in enzyme activity
• The one genetic marker that has been investigated in relation to drug-induced
gingival overgrowth is the human lymphocyte antigen expression (HLA).
• HLA-DR1 (Cebeci et al. 1996)
• HLA-DR2 (Thomason et al. 1996)
• HLA-B37 (Margiotta et al. 1996)
80. Gingivectomy
122
INDICATIONS
• Gingival enlargement or overgrowth.
• Elimination of suprabony pockets, regardless
of their depth, if pocket wall is fibrous and
firm.
• Elimination of suprabony periodontal
abscesses.
• Crown lengthening in patients with
adequate attached gingiva ( eg. Gummy
smile ).
• Idiopathic fibrosis.
CONTRAINDICATIO
NS
• Need for osseous surgery.
• Infrabony pockets.
• Esthetic considerations, particularly in anterior
maxilla.
ADVANTAGES
• Simplicity
• Predictability
• Ease of pocket elimination
DISADVANTAGES
• Healing by secondary
intention
• Post operative bleeding
• Loss of keratinized tissue
• Inability to treat
underlying osseous
deformities.
81. • Step 1: The periodontal pocket is
mapped out on the external gingival
surface by inserting a probe to the
bottom of the pocket and puncturing the
external surface of the gingiva at the
depth of probe penetration
• Step 2: Periodontal knives (e.g., Kirkland)
are used for incisions on the facial and
lingual surfaces. Orban periodontal
knives are used for interdental incisions.
Bard– Parker blades (#12 and #15), and
scissors are used as auxiliary
instruments.
• Step 3: Remove the excised pocket wall,
irrigate the area, and examine the root
surface.
• Step 4: Scale and root plane.
• Step 5: Cover the area with a surgical
dressing
123
82. Gingivectomy procedure
A. Enlarged gingival tissue and
pseudopocket.
B. Initial external bevel incision
with krickland knife.
C. Interproximal tissue release
by orbans knife.
D. Gingivoplasty
E. do by tissue nipper or high
speed round bur.
F. Aspect of the surgical
wound at conclusion of the
surgical procedure.
G. Placement of non eugenol
periodontal dressing.
H. Surgical area after 3 month.
83. WOUND HEALING AFTER SURGICAL GINGIVECTOMY
• Initial Response- formation of a protective surface clot; the underlying tissue being
acutely inflammed. The clot is then replaced by granulation tissue.
• By 24 hrs- there is an increase in number of connective tissue cells ( angioblasts)
beneath the surface layer of inflammation.
• By 3rd Day- fibroblasts appear in the area. The vascular granulation tissue grows
coronally, creating a new free gingival margin & sulcus.
• After 5 to 14 Days- surface epithelialization is generally complete. Complete
epithelial repair takes about 1 month
• 7 weeks- Complete repair of the connective tissue takes place.
• GCF in humans is initially increased after gingivectomy & decreases as healing
progresses.
84. Flap Surgery
125
Indications
1. For larger areas of gingival enlargement (i.e., more than six teeth), and where
attachment loss and osseous defects are present, flap surgery is
recommended.
2. Situations where gingvectomy technique may result in elimination of all
keratinized tissue and consequent creation of mucogingival problems.
85. Procedure
126
• After anesthetizing the area, sounding of the underlying alveolar bone is
performed with a periodontal probe to determine the presence and extent of the
osseous defects.
• On the buccal and lingual aspects, with a #15 surgical blade, the initial scalloped
internal bevel incision is made at least 3 mm coronal to the mucogingival
junction, which includes the creation of new surgical interdental papillae in each
interproximal space
• The same blade is used to thin the gingival tissues in the buccolingual direction
to the mucogingival junction. At this point, the blade establishes contact with the
alveolar bone, and a full-thickness is elevated.
86. • Intrasulcular incisions are made on buccal, lingual, and
palatal areas that are being treated to release the tissue
collar
• The marginal and interdental tissues are removed with
curettes.
• After all tissue tags are removed, the roots are
thoroughly scaled and planed, and the bone is
recontoured as needed.
• The flap is replaced or apically displaced and, if
necessary, retrimmed to reach the bone–tooth junction
exactly (palatal flaps). The flaps are then sutured with an
interrupted or a continuous mattress technique, and the
area is protected with periodontal dressing.
127
87. oIdiopathic gingival enlargement is a rare condition of undeterminedcause.
oIt has been designated by terms like Gingivomatosis, elephantiasis, idiopathic
fibromatosis, hereditary gingival hyperplasia, and congenital familialfibromatosis.
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
88. 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).
89. 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 thegingiva.
90. 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).
91. Conditioned Enlargements
•Conditioned enlargement occurs when the systemic condition of the patient
exaggerates or distorts the usual gingival response to dentalplaque.
•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 clinicalfeatures.
•The three types of conditioned gingival enlargementare:
Hormonal (pregnancy, puberty),
Nutritional (associated with vitamin C deficiency),
Allergic.
92. 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)
93. Marginal gingival enlargement
•Marginal gingival enlargement during
pregnancy results from the aggravation of
previous inflammation,
•Incidence reported as 10% and 70%.
usually
more
on the
generalized
prominent
facial and
•The enlargement is
and tends to be
interproximally than
lingual surfaces.
red or
has a
•The enlarged gingiva is bright
magenta, soft, and friable and
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.
94. •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
95. 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.
96. Gingival enlargement during puberty has all the clinical features generallyassociated
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 enlargementfrom
uncomplicated chronic inflammatory gingival enlargement.
After puberty the enlargement undergoes spontaneous reduction but doesnot
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 inthe
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
97. 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.
98. 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.
99. 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.
100. 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 classifiedas:
lymphocytic
myelocytic /myelogenous
According to their evolution, leukemias can be
acute, which is rapidly fatal
subacute
chronic
SYSTEMIC DISEASES CAUSING GINGIVAL ENLARGEMENT
101. 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.
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 theteeth
102. 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.
103. 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.
104. Histopathology
infiltrated with a dense mass of immature and•Areas of connective tissue
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.
105. 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 bloodvessels.
•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
106. Histopatholog
y
of acuteChronic inflammation occurs with scattered giant cells and foci
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 affectsblacks
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.
107. 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 (GINGIVALTUMORS)
108. 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.
109. 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 irregularsurfaces.
Histopathology
Finger like projections of stratified squamous
epithelium often hyperkeratotic, with a central
core of fibrovascular tissue.
110. 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 pressureexerted
by thegrowth
111. 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
112. 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.
113. 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
114. 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
115. 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
116. 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.
117. 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 areasappearing as
gingival enlargement.
118. 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.
by marginal inflammation,
However,
complicated
composite picture gives the impression
when such enlargement is
the
of
extensive gingival enlargement
marginalTreatment to alleviate
inflammation, rather than
the
resection of the
enlargement, is sufficient in these patients.
119. SUMMARY
Gingival enlargement is a common feature of
gingival disease.
It can be of many types :
Depending on etiology it can be inflammatory
,drug induced, associated with systemic
disease or condition,neoplastic, false
enlargement or idiopathic.
Depending on locatoin it can be localized,
generalized, marginal papillary, diffuse ,
discrete.
