Transcript GINGIVAL ENLARGEMENT (NXPowerLite)1 - tooth

GINGIVAL ENLARGEMENT
1
CLASSIFICATION BASED ON ETIOLOGY
 INFLAMMATORY
ENLARGEMENT
Acute
Chronic
 FIBROTIC
ENLARGEMENT
 drug
induced enlargement
 Idiopathic enlargement
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enlargement associated with
systemic disease
–Conditioned enlargement
Puberty
Vita C deficiency
Pregnancy
Plasma cell gingivitis
Nonspecific conditioned enlargement(granuloma
pyogenicum)
Systemic diseases causing gingival
enlargement
Leukemia
Granulomatous disease(sarcoidosis,wegener’s
granulomatosis)
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Neoplastic enlargement
 Benign
tumors
 Malignant tumors
 False
enlargement
Underlying osseous lesion
Underlying dental tissues
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Criteria for assessing ge
 Grade
I Grade II Grade III Grade IV-
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CLASSIFICATION BASED ON
LOCATION & DISTRIBUTION
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LOCALISED: 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 & attached gingiva
& papilla
Discrete :an isolated sessile or pedunculated
tumor like enlargement
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PREDISPOSING FACTORS
 AGE-younger
age groups are more
affected
 SEX-males are more affected
 SITE-anterior facial areas especially
the canine region is more prone
 INFLAMMATION-predisposes to
enlargement
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Age
 AGE-younger
age groups are more
affected
 Higher dosage may be administered
 As age advances the metabolic
process in gingival tissue like
glycosaminoglycans synthesis
reduces
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Sex
 SEX-males
are more susceptible
 Progesterone a female sex harmone
decreases glycosaminoglycan
synthesis by human gingival
fibroblasts.
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SITE
Anterior regions are more affected
especially the canine region is more prone
 Buccal side is more affected than lingual.
 Dentulous areas are more prone than
edentulous area
 Related to plaque control & drying of
mucosa .
 Temperature difference.
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INFLAMMATION
 INFLAMMATION-predisposes
to
enlargement.
 Enlargement may predisposes to
plaque accumulation
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Drug induced gingival enlargement
 Calcium
channel blockers
 Immuno suppressants
 Anti-epileptic
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Calcium channel blockers
 Nifedipine
 Amlodipine
 Verapamil
 Dilitiazem
 Oxodipine
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 Drug
discovered-1960
 Therapeutic usage-1980
 Class I-affect the heart(verapemil)
 Class II-affect mainly blood vessels
&vasodilation(dihydropyridines)
 Class III-minimal or slight inotropic
effects(dilitiazem)
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 M.O.A-alter
the Ca++ metabolism
,the influx of Ca++ across the cell
membrane is decreased due to
reduced membrane permeability.
 Contraction of muscle cells occurs
when increased intracellular Ca++
binds to trophonin & in the presence
of ATP causes the myosin bridge to
contract the actin filaments.
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 Although
dosage & duration of
medication were cited as possible
explanations no clear evidence
available.
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Histologic features
 Hyperkeratosis
 Acanthosis
 Elongation
of rete pegs(test tube
shape)
 Fibroblast with prominent RER
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Pathogenesis
 Apoptosis
is characterized by nuclear
& cytoplasmic
condensation,membrane
budding,formation of apoptotic
bodies, on-random fragmentation of
DNA.
 Calcium plays an important signaling
pathway in triggering apoptosis
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 Prolongation
of cell life through
inhibition of keratinocyte apoptosis.
 Ca++ is needed for keratinocyte DNA
fragmentation.
 Low Ca++ expresses Bcl-2 gene
which suppresses apoptosis
 High Ca++ expresses Bax gene which
induces apoptosis
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Indirect action of nifedipine may occur by
stimulating either production of IL-2 by Tcells or metabolites of testosterone by
gingival fibroblasts which in turn
stimulates proliferation or increased
collagen synthesis.
 Responsiveness of the cells appear to be
inversely proportional to the IL-1 β levels.
 Medullasin(a neutrophil elastase-like
proteases) plays a role in development of
inflammation & mechanism is not known.
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A
role of TGFβ,bFGF & heparan
sulphate glycosaminoglycan.
 The site specificity in the
accumulation of collagenous proteins
in the ECM may be due to the
relatively slow synthesis of these
proteins in other tissues or because
of altered deposition/resorption in
susceptible tissues.
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Immuno suppressants
 Cyclosporine
 Tacrolimus
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cyclosporin
 Liphophilic
cyclic endecapeptide
 Used in the prevention of organ
transplant rejection
 Peak plasma conc. reached after 3
hrs.
 Serum half life 17-40hrs.
 mostly bound to erythrocytes &
lipoproteins. only 5% free in plasma.
 Therapeutic conc-135μg
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 The
total amount of drug per weight
in tissue can be upto 20-fold greater
than in plasma & varies between
organs & individuals.
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Pharmacological action
 Cs
suppresses T-helper cell function
leaving T-suppresser cells un
affected.
 Cs selectively suppresses the cellular
immune response by interfering with
IL-2 production.
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MOA
Drug cyclophilin complex binds & inhibits
calcineurin a calcium & calmodulin
dependent serine threonine phosphatase.
 This inactivation prevents
dephosphorylation of nuclear factor of
activated T-cells(NF-AT) the nuclear
import of NF-AT complex & the formation
of a transcriptionally active NF-AT
complex. the net consequence is inhibition
of IL-2.
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Pathogenesis
During plaque induced inflammation the
humoral response replaces the cell
mediated response.
 Several cytokines that play important role
in humoral response are known to
influence connective tissue homeostasis.
 IL-1β & IL-6 are cytokines known to play
regulatory function in periodontal tissue
turnover with IL-1β inducing & IL-6
reducing tissue break down.
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 IL-6
is a multifactorial cytokine found
to induce final maturation of B-cells
into immunoglobulin producing
plasma cells.
 The increase in plasma cell number
may promote Cs induced alteration
of the cytokine profile within gingival
tissue, resulting in disruption of
normal connective tissue turn over
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 The
immunosuppresed pts had
markedly lower no of NK cells which
could enhance the ability of Cs to
induce proliferative activity not
directly, but by disrupting the
complex conn tissue-homeostasis
mechanism.
 Cs stimulates TGF-β1,PDGF which
promote fibroblast growth & matrix
production.
 Cs reduces the level of MMP-1 &
MMP-2 & increases the level of TIMP.
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 Cs
reduces gingival
prostacyclin(PGI2)synthesis.
 PGI2 has an antiproliferative effect
via increasing cAMP thus gingival
overgrowth may result.
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 Perlecan
a type of proteoglycans is
increased.
 It has high affinity for growth factors
has been attributed to this
proteoglycans ,which ia able to retain
these factors inside the basement
membrane.
 Perlecan acts as a major reservoir of
FGF-2.
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 Cs
could mimic endogenous signals
for wound repair or remodelling,but
at the usual therapeutic dosage
levels& in the absence of any specific
inflammatory process, its effect is
sub threshold.
 However when specific inflammatory
processes take place within localized
& specific areas the effects of Cs
could act synergistically with
endogenous signals stimulating
excessive repair or growth.
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Side effects of Cs
 Hypertension
 Dihydropyridines
are Ca ++ channel
blockers used to treat hypertension
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Rx
 Conversion
to other drugs in the
same group-tacrolimus
 Reduction or withdraval of the drug
under medical suoervision if
indicated
 gingivectomy
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Anti-epileptic
 Phenytoin
 Sodium
valproate
 Phenobarbital
 Vigabatrin
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Phenytoin
 Macrophages
differ in respect to
location, morphology & function &
they have been recognized to be
major mediator of connective tissue
turnover,maintenence & repair.
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Macrophage 27E10-asociated with
production of pro inflammatory cytokinesIL-1,IL-6 & TNF-α
 A reparative/proliferative Macrophage phenotype
RM3/1 associated with production of PDGFβ,TGF- β1,bFGF.
 Expression of 25F9 antigen is connected with
maturation of macrophage & relative decrease in
25F9 indicates that maturation of tissue
macrophages have been altered.
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 decreases
the level of EGF receptors
in gingival fibroblast resulting in
increased cellular responsiveness to
EGF,which can stimulate cellular DNA
synthesis.
 Phenytoin can stimulate testosterone
metabolism & increases the level of
5α-dihydrotestosterone a stimulator of
fibroblast growth.
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 Phenytoin
interferes with folic acid
metabolism & hence causes folic acid
deficiency
 Folic acid is necessary for DNA
synthesis, thus tissues with a high
turn over could be adversely affected
 PHT can cause immuno suppresion in
long term use like decreased salivary
IgA which could favor inflammation.
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 PHT
& its metabolite P-HPPA induces
the release of factors from
monocytes which activate quiescence
gingival fibroblast to synthesize DNA.
 Decreases ACTH which leads to
increased somatotrophic harm one
which increases fibroblast
proliferation.
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 PHT
leads to production of
collagenase which is inactive.
 Increased PGE2 leading to increased
hyaluronic acid .
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Rx
 Conversion
to other drugs in the
same group
 Reduction or withdraval of the drug
under medical suoervision if
indicated
 gingivectomy
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Others
 Erythromycin
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Acute inflammatory
enlargement
 Gingival
abscess
 Localised,painful expanding lesion
that is usually of sudden onset.
 Generally limited to marginal gingiva
or interdental papilla.
 Red, swelling with a smooth shiny
surface.
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 Within
24-48hrs the lesion usually
becomes fluctuant & pointed with a
surface orifice from which a purulent
exudates may be expressed.
 The adjacent teeth are often
sensitive to percussion.
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Etiology
 Bacteria
carried deep into tissues
when a foreign substance such as
toothbristle,small traumatic injury.
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Histopathology
 Polymorphonuclear
leucocytes.
 Edematous
tissue
 Vascular engorgement
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Rx

Incision and
drainage.
Abscess.swf
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Chronic inflammatory enlargement
 Slight
ballooning of the interdental
papilla &/or the marginal gingiva.
 Early stages it produces a life
preserver –like bulge around the
teeth.
 Progresses slowly & painless.
 Enlargement is generally papillary or
marginal.
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 Occasionally
it may occur as a
discrete sessile or pedunculated
mass resembling a tumor.
 Painful ulceration sometimes may
occur
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 Prolonged
Etiology
exposure to dental plaque.
 Factors that favor plaque accumulation
 Poor oral hygiene
 Abnormal relationship of adjacent
teeth
 Overhanging margin
 Food impaction
 Orthodontic appliance
 RPD
 Nasal obstruction
 Improperly contoured restoration &
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Histopathology
 Exudative
& proliferative features of
chronic inflammation is seen.
 Edematous tissue
Inflammatory cells
Vascular engorgement
 Fibrotic
tissue
Abuntance of fibroblasts & collagen fibers
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Treatment
 Removal
of plaque
 Control of inflammation
 Scaling & root planning
 Fibrotic enlargement –gingivectomy.
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Enlargement associated with
mouth breathing
 Gingiva
appears red & edematous
 Diffuse surface shininess of the
exposed area
 Common site-maxillary anterior
region.
 Attributed to irritation from surface
dehydration
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Idiopathic gingival enlargement
 Gingivostomatosis
 Elephantiasis
 Diffuse
fibroma
 Familial elephantiasis
 Idiopathic fibromatosis
 Hereditary gingival hyperplasia
 Congenital familial fibromatosis
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Clinical features
 It
affects the attached gingiva as
well as the marginal gingiva &
interdental gingiva.
 Pink, firm & almost leathery in
consistency & has a characteristic
minutely pebbled surface.
 In severe cases the teeth are almost
covered & projects into the vestibule.
 Jaws appears distorted because of
bulbous enlargement.
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Combined enlargement
Gingival hyperplasia is complicated by
secondary inflammatory changes because
it produces conditions favorable for
accumulation of plaque by accentuating
the depth of gingival sulcus.
 It consist of 2 portions.
 A primary or basic hyperplasia of the
connective tissue & epithelium.
 A secondary complicating inflammatory
component
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Enlargement associated with
systemic disease
 Conditioned
enlargement
 The condition itself does not cause
the condition, the altered tissue
metabolism accentuates the
response to local irritants.
 Magnification of an existing
inflammation initiated by dental
plaque.
Puberty
Pregnancy(harmonal)
Vita C deficiency (nutritional disturbances)
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Enlargement in pregnancy
Pregnancy does not cause the condition,
the altered tissue metabolism in
pregnancy accentuates the response to
local irritants.
 Gingival enlargement in pregnancy is
called ANGIOGRANULOMA.
 Enlargement may be marginal, mostly
generalized & more prominent in
interdental papilla.
 Sometimes it occur as a discrete,
mushroom like flattened spherical mass
attached by a sessile pedunculated base.

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Puberty
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Vita C
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Non specific conditioned
enlargement
 Granuloma
pyogenicum – is a
tumour like enlargement that is
considered an exaggerated response
to minor trauma.
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Systemic diseases causing gingival
enlargement
Leukemia
Granulomatous disease
Sarcoidosis
wegener’s granulomatosis
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Neoplastic enlargement
 Benign
tumors
 Epulis – is a generic term used
clinically to designate all discrete
tumors & tumor like masses of the
gingiva.
 Most epulis are inflammatory rather
than neolastic.
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Benign tumors
 Fibroma
 Papilloma
 Peripheral
giant cell granuloma
 Central giant cell carcinoma
 Gingival cyst
 Leukoplakia
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Malignant tumors
Squamous cell carcinoma
 Malignant melanoma
 Metastasis

–
–
–
–
–
–
–
Adenocarcinoma of colon
Lung carcinoma
Primary hepatocellular carcinoma
Renal cell carcinoma
Hypernephroma
Chondrosarcoma
Testicular tumor
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Apoptosis
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Rx

gingivectomy
Scaling.swf
gingivoplasty.swf
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