Treatment of gingival enlargement and cauded

1. Cont…………..

2. Enlargements associated with
systemic diseases
 Wegener granulomatosis,
 sarcoidosis,
 Crohn’s disease,
 Type 1 neurofibromatosis
 ulcerative colitis
 Kaposi sarcoma
 acute leukaemia, lymphoma or aplastic
anaemia
 tuberculosis

3. Wegner’s granulomatosis
 Is a rare disease charachterized by
paravascular granulomas with initial signs
of sinusitis, rhinorrhea, otitis media and
pulmonary findings.
 These clinical symptoms being concurrent
with the development of polyvasculitis
and/or glomerulonephritis.

4.  The gingival lesions noted as one
manifestation of Wegener's granulomatosis
have been described as hyperplastic, ulcerative
or granular surfaces with a red colour
('strawberry gums'), which can either be
restricted to a single dental papilla or
generalized .
 The prevalence of gingival involvement is
somewhat unclear, but Walton summarizing
56 cases, observed that the initial symptoms
were located in the gingiva in cases.

5.  Gingivitis starts in IDP , spreads
throughout the gingivae into the
periodontium shows petechia and a
granular apperance.

6.  The microscopic features of the gingival
biopsies described by Scott and Finch and
Hdwards and Buekerfield were
granulomatous infiltration with
polymorphonuclear leucocytes, eosinophils,
plasma cells and lymphocytes.
 Collagen degeneration was observed at the
periphery of the granulomatous mass, but no
evidence of necrotizing vasculitis was found.
 Cohen and Meltzer have also described
vasculitis in the gingiva,

7. Sarcoidosis
 Oral involvement in sarcoidosis is
uncommon.
 In the soft tissues of the oral cavity ,buccal
mucosa is the commonest site affected
followed by gingiva , lips , floor of the
mouth/sublingual gland , tongue , palate ,
submandibular gland .
 When involving gingiva ,it can cause
gingivitis, gingival hyperplasia and gingival
recession.

8. Von Recklinghausen’ disease
 First described by in 1882 by the German
anatomopathologist Von Recklinghausen.
This disease is a slowly evolving
neurodermic dysplasia.
 This is dominant autosomal hereditary
disease with total penetrance and variable
expression; about 50% of cases, however,
are sporadic,

9.  Absence, impactions and malposition of the
teeth can be found (D’Ambrosio et al. 1988).
 Lesions of the soft tissues of the oral cavity
are present in up to 10% of the cases
 Like other cephalic lesions, they are most
often unilateral (Slama et al. 1987).
 They form tumors on the tongue , gingiva
(Salazar 1976) palate , cheeks, lips, floor of
the mouth, or pharynx.
 These tumors are nearly always nodular, but
cases of diffuse macroglossia have been
reported (Baden et al. 1984, Shapiro et al.
1984).

10.  There is unilateral
generalized expression of
the gingival hyperplasia
which is evocative of a
neurological or vascular
problem.
 The gingival hyperplasia
can induce tooth
displacements, with
multiple diastemas in the
first and fourth quadrants
and a deviation of the
midline to the left.

11. Leukemic Gingival Enlargement
 Malignant haematopoietic and
lymphoreticular diseases may manifest either
as localised dense aggregations of
neoplastic cells and thus as tumor or tumor-
like lesions or they may be characterized by
the circulation of neoplastic cells in the
peripheral blood and the subsequent
infiltration of several tissues and organs.
 They are divided in leukaemias, malignant
lymphomas and immunoproliferative
diseases.

12.  Leukaemias may be acute or chronic,
based mainly on the clinical course of the
disease.
 Acute leukemia are characterized by the
proliferation of immature cells known as
blast cells in the bone marrow and the
rapid progression of the disease, which if
left untreated it becomes fatal in a short
period of time.
 Chronic leukaemias are characterized by
the proliferation of more mature cells and
progress slowly.

13.  All types of leukaemia, especially the
acute leukaemias, may present oral
manifestations.
 Acute monoblastic/monocytic leukaemia
and acute myelomonocytic leukaemia
(according to the WHO classification for
myeloid malignancies), are the most
commonly encountered in the oral cavity.
 While acute lymphocytic leukaemia (ALL)
is rarely associated with oral signs.

14.  Oral and maxillofacial manifestations of
leukaemias are subdivided into:
 primary manifestations
 secondary manifestation
 tertiary manifestation

15.  Primary manifestations include lesions
caused by the extramedullary neoplastic
infiltration of oral mucosal and
maxillofacial tissues such as
 abrupt generalised or localised gingival
enlargement,
 chloroma,
 alveolar bone destruction,
 bone invasion with pain and tooth
displacement,
 cervical lymphadenopathy,
 tooth ache due the leukaemic infiltration of the
pulp and leukemia

16.  Haematological malignancies can result in a
spectrum of gingival and periodontal
manifestations .
 Gingival enlargement secondary to infiltration
of leukaemic cells is typically associated with
acute myeloid leukaemia (Porter & Scully
1993)
 and has only very rarely been reported in
chronic lymphocytic leukaemia (Wentz et al.
1949, Presant et al. 1973).


17.  Indeed, large study of 1076 adults with leukaemia
showed that only those with myeloid leukaemias
had gingival enlargement (Driezen et al. 1983).
 None of the 231 patients with lymphoblastic or
lymphocytic leukaemias studied had any notable
gingival enlargement.
 It is unclear why gingival infiltration and
enlargement almost exclusively occurs in acute
myeloid leukaemia, but it may reflect the rapid
migration of phagocytes from the peripheral
blood into the gingival tissues (Scully &
Challacombe)

19.  In those affected, the degree of leukaemic
gingival enlargement seems unrelated to levels
of dental bacterial plaque, peripheral blood
white cell count or any tendency for leukaemic
skin infiltration.
 skin infiltration does occur more frequently
with myeloid than lymphoblastic or
lymphocytic leukaemias (Driezen et al. 1983).

20.  Considering gingival enlargement as an
important sign in AL, many reports had
described the pathological changes that
occur due to leukemic infiltration.
 Almost all the available studies agreed
that the M5 and M4 subtypes were the
most common types causing such
enlargement.
 many authors, have denied the possibility
of leukemic infiltration in the alveolar
mucosa in edentulous patients .

23. HEREDITARY GINGIVAL FIBROMATOSIS
(HGF)
 Hereditary gingival fibromatosis (HGF) is a
rare oral disease characterized by a slow and
progressive enlargement of both the maxilla
and mandible gingiva (Bozzo et al. 1994).
 The enlarged gingiva is of normal colour, firm
consistency, non-haemorragic, and
asymptomatic (Bozzo et al. 2000).

24.  HGF occurs as an isolated finding or associated
with other features such as
hypertrichosis,mental retardation, and epilepsy
(Ramon et al. 1967; Horning et al. 1985).
 HGF has an autosomal dominant mode of
inheritance with variable penetrance and
expressivity (Martelli-Junior et al. 2005).
 The most prominent pathologic manifestation of
this disease is an excessive accumulation of
extracellular matrix, predominantly type I
collagen (Araujo et al.2003).

25.  Many studies have shown increased
transcriptional and translational levels of type
I collagen in both tissue and fibroblast
cultures derived from gingiva of HGF patients
(Coletta et al. 1999a; Martelli-Junior et al.
2003).
 HGF fibroblasts produce excessive amounts
ofTGF-b1 (Coletta et al. 1999), which is, in
association with an elevated synthesis of
collagen, an intrinsic characteristic of
myofibroblasts (Desmouliere et al. 2005).

26.  As HGF provides an excellent model for the
study of connective tissue fibrosis, HGF cells
produce abundant extracellular matrix and
high levels ofTGF-b1, and
 Myofibroblasts represent a hallmark of
interstitial fibrosis.
 Pattern of expression of α-SMA (specific
myofibroblast marker smooth muscle
isoform of α-actin), as a marker of
myofibroblast, were eleveted in HGF
compared with normal gingiva (NG).

27.  Myofibroblasts are cells related to fibroblasts and
exhibit a hybrid phenotype between fibroblasts
and smooth muscle cells (Gabbiani 1992).
 When activated, synthesize high levels of
extracellular matrix proteins, particularly collagen
(Desmouliere et al. 2005).
 Several reports have shown the presence of cells
with myofibroblastic features in specialized
normal tissues and in a variety of pathological
situations, such as Dupuytren’s disease,
cyclosporine-induced pancreatic fibrosis, and
pulmonary, renal and hepatic fibrosis ( Ahmed, et
al. 2004).

28. Distribution of α-SMA: an immunofluorescence
microscopy
Normal Gingiva HGF Gingiva

29.  myofibroblasts are the main cellular type
involved in extracellular matrix deposition
during tissue repair.
 Evidences obtained from both human and
animal models show that transforming
growth factor-b1 (TGF-b1) stimulates
myofibroblast transdifferentiation.

30.  Although the underlying mechanisms of the
gingival fibrosis that characterize HGF remain
unclear, it has been proposed that gingival
overgrowth develops through activation or
selection of the resident tissue fibroblasts,
phenotypically characterized by increased
proliferation, low levels of extracellular
matrix-degrading metalloproteinases (MMP-
1 and MMP-2), and abnormally high collagen
production (Coletta et al. 1998, 1999a, b).

31.  Several evidences have demonstrated that HGF
is clinically, genetically, and biologically
heterogeneous.
 Regarding the disease in the families Although
in both families the disease manifests as an
isolated finding affecting all the gingival tissue,
in Family 1 it is more severe and frequently
associated with both aesthetic and functional
problems, including
 diastemas,
 malpositioning of teeth,
 prolongedretention of primary dentition,
 delayed eruption, cross and open bites,
 prominent lips, and open lip posture
(Bozzo et al. 2000)

32.  Moreover, recurrence is more frequent in
patients from Family 1 than in patients from
Family 2.
 While gene penetrance is incomplete and
very low in HGF Family 2, as revealed by an
offspring recurrence risk of 0.078 (7.8%) and a
sibling recurrence risk of 0.085 (8.5%)
 In HGF Family 1 it is complete, with
approximately half of the descendants being
affected by HGF (Martelli-Junior et al. 2005).

33.  unaffected individuals in Family 2 transmit HGF
in an autosomal dominant pattern to their
offspring without themselves being clinically
affected.
 In the study by Bitu CC et al (2006),
demonstrating that myofibroblasts are
associated with HGF Family 2 (5 fibroblast cell
lines) gingival overgrowth tissues, but not with
HGF Family 1 (5 fibroblast cell lines from affected
members with HGF).
 Taken together, these findings suggest that the
HGF phenotype may be caused by distinct
biological mechanisms.

34. TGF-β
myofibroblast
transdifferentiation
fibroblasts
ECM synthesis and accumulation
renal epithelial
cells
CTGF
Zhang et al. 2004

35.  Three forms of HGF have been identified
based on the genes affected
 GINGF1 (2p21-p22)- Zang et al.
 GINGF2 (5q13-q22) -Xiao et al 2001,Hart
et al 2002)
 GINGF3 (2p22.3 – p23.3)- Ye et al.(2005)

36.  For autosomal dominant forms of HGF have
been localized to chromosome 2p21-p22
(HGF1) and chromosome 5q13-q22 (HGF2).
 Sequencing of these genes, in affected and
unaffected HGF1 family members, identified
a mutation in the Son of sevenless-1 (SOS1)
gene in affected individuals.
 Insertion of a cytosine between nucleotides
126,142 and 126,143 in codon 1083 of the
SOS1 gene is responsible for HGF1.

37.  This insertion mutation, which segregates
in a dominant manner over four
generations, introduces a frameshift and
creates a premature stop codon,
abolishing four functionally important
proline-rich SH3 binding domains normally
present in the carboxyl-terminal region of
the SOS1 protein.

38. Histology:
1. bundles of coarse collagenous fibers
2. high degree of differentiation with
young
fibroblasts and scarce blood vessels
3. epithelium is dense, with elongated
papillae and hyperkeratosis
• Small calcified particles, islands of osseous
metaplasia, ulceration of the overlying mucosa,
deposition of amyloid and islands of odontogenic
epithelium have also been reported in previous
cases (Günhan et al. 1995)

39. I-cell disease:(mucolipidosis II)
 I-cell disease (mucolipidosis II) is a rare metabolic
disorder resulting from the deficiency of a
specific lysosomal enzyme, acetylglucosamine-1-
phosphotransferease. which is one of two
enzymes involved in the biosynthesis of
mannose-6-phosphate.
 The disease presents as a mental and motor
developmental delay with oral manifestations
that include severe gingival hyperplasia usually
seen before one year of age.

40.  was first described by Leroy and DeMars (1967)
 The life expectancy of children with this condition is
poor, with death usually occurring around the fifth
year.
 This compound is a common marker enabling
lysosomal enzymes to be transported to the
lysosomal compartment of all cells.Without the
transferase, lysosomal enzymes escape into the
extra-cellular fluid resulting in marked elevation of
lysosomal enzymes in plasma.
 This transferase deficiency, and consequent
lysosomal depletion, results in the accumulation of a
number of macromolecules, mucopolysaccharides
and mucolipids, in the lysosome.

41.  This can be seen as coarse cytoplasmic
granular inclusions in cultured skin fibroblasts
giving rise to the name ‘I-cell’ disease.
 Infants with I-cell disease are typically
underweight at birth, below 10th percentile,
small, with muscle hypotonia, and coarse
facial features
 the full clinical picture of the disorder
presenting at between 6 and 8 months.

42.  Orofacial features associated with I-cell disease.
1. Coarse facial features
2. Normal head circumference relative to body size
3. Puffy eyelids with slight exophthalmia
4. Excessive prominence of the epicanthic folds
5. Depressed nasal bridge
6. Full cheeks exhibiting multiple fine telangectasia
7. Incompetent lips
8. Gingival and alveolar enlargement with buried
teeth
9.Thick tongue

44.  Quite often the teeth appear.
 contributing factor to the non-eruption
 there is accumulation of mucolipid storage
material in the dental follicles
 the gingival enlargement.
 The teeth that do erupt are hypocalcified,
usually the lower incisors, tend to lack lamina
dura and may have a unique ‘screwdriver-
shaped’ crown

45.  Diagnosis :
 marked elevations of lysosomal enzymes in the
plasma is an accurate diagnostic test for this
disorder.
 Also, a diagnosis is often obtained from the
peripheral lymphocytes, which contain large
lysosomal inclusions.
 Because of the severity of the disorder, families
often opt for prenatal diagnosis.
 This is carried out by measuring the levels of
lysosomal enzymes in cell-free amniotic fluid
obtained at 14–17 weeks’ gestation or by
chorionic villus biopsy.

46.  The only therapeutic approach currently
available is bone marrow transplantation to
supply a source of structurally normal
lysosomal enzymes.

47. Tuberculous GingivalEnlargement
 Tuberculosis remains the leading cause of
death worldwide from a single infectious
organism. Approximately 32% of the world’s
population is infected with tuberculosis and
an estimated 2 million people die annually
from this treatable disease
 In the Indian population, the average
prevalence of all forms of tuberculosis has
been reported to be 5.05 per 1,000, the
prevalence of smear-positive cases is 2.27 per
1,000 and the average annual incidence of
smear-positive cases is 84 per million

48.  Tuberculosis is a chronic granulomatous
infectious disease caused by Mycobacterium
tuberculosis,
 it can affect any part of the body including the
oral cavity.
 Extrapulmonary tuberculosis is rare, occurring in
10% to 15% of all cases.
 Since the introduction of effective drug therapy,
tuberculous lesions of the oral cavity have
become so rare that this manifestation of the
disease is often forgotten.

49.  Oral tuberculosis can be primary or secondary.
 Primary oral tuberculous lesions are
extremely rare and generally occur in young
adults with associated caseation of the
dependent lymph nodes; the lesion itself
remains painless in most cases.
 In contrast, secondary oral tuberculosis is
seen in about 0.05% to 1.5% of cases and
usually in older adults.

50.  In oral tuberculosis, the most commonly
affected site is the tongue; other sites include
the lip, cheek, soft palate, uvula, gingiva and
alveolar mucosa.
 The lesions are seen as superficial ulcers,
patches, indurated soft tissue lesions or even
lesions within the jaw in the form of
tuberculous osteomyelitis.

51.  the first case report of primary tuberculous
gingival enlargement as an early presenting
sign of tuberculosis, with no regional lymph
node involvement and no evidence of
systemic tuberculosis. ( Dr.A. R. Pradeep and
Dr. Karthikeyan : J Can Dent Assoc 2006 )

52.  The mechanism of primary inoculation into the
oral mucous membrane is not clearly
understood.
 One reason for the rare occurrence of
tuberculosis of the gingiva may be that the intact
squamous epithelium of the oral cavity resists
direct penetration by bacilli.
(FujibayashiT et al, 1979 )
 This resistance has been attributed to the
thickness of the oral epithelium, the cleansing
action of saliva, local pH and antibodies in saliva.

53.  Even if the onset of infection is by
hematogenous spread, injured or inflamed
tissue tends to localize bloodborne bacteria.
 However, the mode of entry of the organism
may be through a break in the mucous
membrane caused by local trauma. Where
the infection involves bone, the mode of
entry is thought to be through an extraction
socket. However, there is general consensus
that secondary tuberculosis spreads by a
hematogenous route.

54.  Diagnosis of oral tuberculosis is difficult as
the clinical presentation may take various
forms and the typical constitutional features
are absent in most cases.
 A tuberculin (Montoux) test
 Culture of sputum
 Special staining of formalin-fixed, paraffin-
embedded tissue specimens for
mycobacteria, i.e., Ziehl-Neelsen and
Auramine-Rhodamine stain
 incisional biopsy with Histopathologic
examination

56.  An immunologic test to detect antibodies against
Mycobacterium : ELISA
Polymerase chain reaction (PCR)
Low-magnification micrograph
showing numerous non-caseating
granulomas
Higher-magnification micrograph
of granulomatous process with
Langhan’s giant cells and
epithelioid cells.

57.  Tuberculosis infection of the gingivae is
relatively rare; oral lesions would most
commonly be secondary to pulmonary
tuberculosis. Hence, to characterize oral
lesions as primary tuberculosis, a thorough
examination to rule out other primary sites
should be attempted. With the recent
increase in the incidence of tuberculosis,
clinicians need to be aware of this possibility,
consider tuberculosis in the differential
diagnosis of gingival enlargement and, thus,
play a role in the early detection of this
disease.

58.  consultation with a physician.

 antitubercular therapy initiate
Isoniazid (10 mg/kg body weight), rifampicin
(10–20 mg/kg), pyrazinamide (20–35 mg/kg) and
ethambutol (25 mg/kg) for 2 months
followed by isoniazid (10 mg/kg) and rifampicin
(10–20 mg/kg) for 4 months.
 During this period, the patient instructed not to
undergo any surgical procedure within the oral
cavity and warned about the chance of
transmitting the disease to others via salivary
contamination.

59.  Further, basic periodontal therapy, which
included scaling and root planing, and oral
hygiene instituted.This results in significant
regression of the enlarged gingivae .
 After completion of the 6-month regimen,
perform gingivoplasty to shape and contour
the residual enlargement under universal
aseptic conditions.

60. Conditioned enlargement
 It occurs when the systemic condition of the
patient exaggerates or distort the usual
gingival response to dental plaque.
 Bacterial plaque is necessary for this type of
enlargement.

61.  Conditioned enlargement occurs due to
 pregnancy
 puberty
 vitamin - C gingivitis
 plasma cell gingivitis
 non specific conditioned enlargement

62. Enlargement in pregnancy
 May be marginal and generalized
 may occur as single or multiple tumor like
masses.

63.  During pregnancy there is increased levels of
both progesterone and estrogen , by the end
of third trimester.
 This altered hormonal level of, pregnancy
may have a special role in the physioiogy of
gingiva (Pindborg 1983)

64.  inflammation does not increase progesterone
metabolism in the gingiva of pregnant women
as it does in non-pregnant women.
 Low metabolism maintains the levels of the
active hormone in the tissue.
 This may be responsible for the increased
permeability of gingival vessels noted during
pregnancy (Lindhe & Branemark 1967,
Lundgren & Lindhe 1970)

65.  It is also known that progesterone
concentrations in the maternal circulation are
sufficient to cause immunosuppression.
 Senelar & Bureau (1979) have shown that
pregnancy inhibits the migration of
inflammatory cells and fibroblasts.
 It seems that pregnancy regulates both the
metabolism of progesterone and also
influences the migration of inflammatory cells
in the tissue.

66.  The level of progesterone available in the
active form and the "dysfunction” of
inflammatory cells may have a role in the
development of pregnancy gingivitis and
granuloma formation.
 The co-existance of these two factors prevents
the rapid acute-type of tissue reaction (which
would keep the tissues clinically healthy) to
plaque, but allows an increased chronic
reaction resulting clinically in an exaggerated
appearance of inflammation.

67.  Jensen et al. 1981, shown that the ratio of
anaerobic to aerobic bacteria increases the
gingival sulcus during pregnancy.
 According to Kornman & Loesche (1982)
Prevotella Intermedius is able to use
progesterone instead of vitamin K as an
essential growth factor.
 Altered tissue metabolism of progesterone
during pregnancy may thus favor the
colonization of the gingival sulcus by
anaerobic bacteria.

68.  Slight to moderate inflammation occurs in
about half of all pregnant women.
 Pregnancy may also give rise to pregnancy
granulomas (epulis gravidarum).
 The prevalence of granulomas increases to
about 5% during pregnancy (Tiilila 1962).

69. Marginal enlargement:
 Results from aggravation of previous
inflammation
 incidence is -10-70%
 does not occur in absence of plaque
 enlargement is more prominent
interproximally than on facial and lingual
surface.
 Gingiva is bright red, soft and has a smooth
surface.
 Bleeding occurs spontaneously

70. Tumor like gingival
enlargement(angiogranuloma)
 Usually occurs after third month of
pregnancy.
 Incidence- 1.8%- 5%.
 Inflammatory response to plaque modified by
patient’s condition.

71. Clinical features
 Appears as discrete , mushroom ,flattened
spherical mass.
 Tends to expand laterally, pressure from the
tongue and cheek perpetuates flattened
appearance.
 Attached by sessile or pedunculated mass.
 Smooth glistening surface, with numerous
deep red pin point markings.
 Superficial lesion.
 Usually painless lesion.

72. Histopathology:
 Presents with central mass of connective
tissue with numerous diffusely arranged ,
newly formed and engorged capillaries lined
by cuboid epithelial cells and a moderately
fibrous stroma.
 Stratified squamous epithelium is thickened
with prominent rete pegs and some degree of
intercellular and extracellular edema.

73. Enlargement in puberty
 The % of children affected with gingivitis has
been found to increase significantly with age,
and a relationship between puberty and
gingivitis has been postulated in several
clinical studies (Massler et al. 1950,
Muhlemann & Mazor 1958, Sutcliffe 1972).

74.  Hormonal changes are thought to have a direct
effect upon periodontal tissue metabolism by
increasing the permeability of the vascular
system (Hugoson 1970).
 The microbiota of dental plaque may also
react specifically to increased availability of
hormones in the oral fluids.
 Shifts in the composition as well as in
metabolic expressions and in the pathogenic
potential of the plaque micro organisms may
result from altered hormonal levels.

75.  Bacteorides have been identified the subjects
of the prior to the onset of puberty (Van
Oosten et al. 1988),
 it may be anticipated that the hormonal
changes promoted a shift in the composition
of the subgingival plaque towards a more
pathogenic microbiota.

 Steroid hormons in the gingival fluid may
substitute for growth factors for Prevotella
intermedius such as menadione (Gibbons &
Me Donald 1960) and hence, promote the
growth of this organism in vivo (Kornman &
Loesche 1982).

76.  Occurs both in males and females.
 Characterized by prominent bulbous
interproximal papillae.
 Often the facial gingiva is enlarged and the
lingual surfaces are relatively
unaltered;because the mechanical action of
the tongue and excursion of food prevents
the accumulation of local irritants on lingual
surface.

77. Clinical features
 Occurs both in males and females.
 Characterized by prominent bulbous
interproximal papillae.
 Often the facial gingiva is enlarged and the
lingual surfaces are relatively
unaltered;because the mechanical action of
the tongue and excursion of food prevents
the accumulation of local irritants on lingual
surface.

78.  It is the degree of enlargement and tendency
to develop massive recurrences in the
presence of relatively scant plaque deposits
that distinguish pubertal enlargement from
uncomplicated gingival enlargement.
 After puberty , enlargements undergo
spontaneous reduction but disappear until
plaque and calculus are removed.

79. Plasma cell gingivitis (PCG)
 Plasma cell gingivitis (PCG) is a rare condition
characterized by diffuse and massive
infiltration of plasma cells into the sub-
epithelial gingival tissue.

80. Etiology
 The etiology of PCG is not clear, but due to
the obvious presence of plasma cells many
authors are of the opinion that it is an
immunological reaction to allergens;
 these latter may occur in toothpaste,
chewing gum, mint pastels and certain
foods.
 It has been suggested that strong spices
and some herbs such as chilli, pepper and
cardamom may be important factors.

81.  Hedin et al. reached the conclusion, based on a
material comprising 14 patients, that -PCG is the
result of an allergic reaction to bacterial plaque,
even though this had been eliminated by means
of conventional periodontal treatment.
 Some authors sub-divide PCG into three
types:
1) caused by an allergen,
2) neoplastic,
3) unknown cause.

82. Clinical features
 Clinically, the illness presents as a diffuse
reddening together with oedematous
swelling of the gingiva, with sharp
demarcation along the muco-gingival border.
 Many authors have found that the condition
occurs in the anterior gingiva, most
frequently in the maxilla.
 Ulceration is rare in the pathologically
changed gingiva
 appears red , friable, and bleeds easily
 usually does not induce loss of attachment.

83. Histological examination
 The histological examination shows
surface epithelium with psoriasiform
hyperplasia, exocytosis and spongiosis.
 Small collections of neutrophils (micro-
abscesses) identified in the parakeratin
layer.
 marked dilatation and an intense
inflammatory infiltrate in the connective
tissue dominated by plasma cells

84.  A localised lesion , referred to as plasma cell
granuloma has also been described
 In one of the case it presented as an exophytic
mass of gingiva, clinically resembling traumatic
fibroma. Histopathologic findings revealed
dense sheets of plasma cells infiltrate.
 Immunohistochemistry for kappa and lambda
light chains showed polyclonal (benign) staining
pattern confirming the diagnosis of plasma cell
granuloma .( Pradeep AR , Karthikeyan BV.Indian J
Dent Res 2004 jul-sept; 15(3):114-6)

85. Vitamin -C gingivitis
 The oral effects ofVitamin C deficiency in
humans occur chiefly in the gingival and
periodontal tissues.
 Vitamin C is necessary for a number of
metabolic processes ,including hydrogen ion
transfers and maintenance of intra cellular
oxidation reduction potentials.
 Also acts as an antioxidant ,facilitates iron
uptake in intestinal tract , and is involved in
formation of folinic acid.

86.  It is critical in hydroxylation reactions which
require reduced iron and copper.
 In general the action of vitamin C appears to
be further the normal development of
intercellular ground substances in bone,
dentin and other connective tissues , since all
signs of deficiency of ascorbic acid are
associated with disturbances in these tissues.

87.  Acute vitamin C deficiency does not cause
gingival inflammation , but it does cause
hemorrhage , collagen degeneration and
edema of the gingival connective tissue.
 These changes modify response of gingiva to
plaque to extent that normal defensive
delimiting reactions inhibited , and the extent
of inflammation is exaggerated.

88. Clinical features
 Interdental and marginal gingiva is bright red
with a swollen , smooth , shiny surface.
 In fully developed scurvy the gingiva becomes
boggy , ulcerates and bleeds .
 Color changes to violaceous red.
 In the severe chronic cases of scurvy ,
hemorrhages into and swelling of periodontal
membranes occur,followed by loss of bone and
exfoliation of teeth ,which eventually exfoliate.

89. Non conditioned gingival
enlargement(pyogenic granuloma)
 Pyogenic granuloma is a local, benign
vascular lesion that often occurs in
response to a chronic, low-grade, local
irritant.
 It is a reactive fibrovascular proliferation of
the connective tissue.
 The lesion does not contain pus and is not
strictly speaking a granuloma.

90.  Because of the absence of pyogenic infection the
term ‘lobular capillary haemangioma’ has been
often used for this condition, which has been
classified as a type of capillary haemangioma.
 Clinically, the pyogenic granuloma is an
exophytic lesion manifested as small, red
erythematous papules on a sessile or
pedunculated base.
 Its clinical development is slow,
asymptomatic and painless.
 The size varies in diameter from a few
millimetres to several centimetres

91.  Minor trauma to the lesion may cause
considerable bleeding, due to its pronounced
vascularity.
 The lesion may also become infected and
ulcerated .
 Depending on its duration, the lesion will vary in
texture from soft to firm, and can be suggestive of
fibroma.
 Pyogenic granuloma occurs predominantly in
females, in the second decade of life.
 Frequent location is in the maxillary anterior
labial gingiva.

92.  Another special pyogenic granuloma is the
epulis granulomatosa (epulis
haemangiomatosa), a hemorrhagic gingival
mass of granulation tissue protruding from
the poorly healing bony socket of a recently
extracted tooth.
 A third unique presentation is a draining
granulation tissue mass, or parulis,
surrounding and often hiding the end of a
fistulous tract from an underlying
intraosseous dental infection

93. Histopathology
 Appears as mass of
granulation tissue with
chronic cellular infiltration.
 Endolthelial proliferation
 surface epithelium is
atrophic and hyperplastic in
other areas.
 Surface ulceration and
exudation are common
features.

94. Benign tumors of gingiva

95.  Fibroma
 arises from gingival connective tissue or from
the periodontal ligament.
 Slow growing,spherical tumors that tend be
firm and nodular but may be soft and
vascular..
 Usually pedunculated

96. microscopy
 composed of bundles of
well formed collagen
fibers with scattering of
fibrocytes and a variable
vascularity.
 giant cell fibroma
contains multinucleated
fibroblasts.
 In another variant
mineralized tissue may be
found, this type of
fibroma is called
peripheral ossifying
fibroma,

97. Papilloma
 Benign proliferation of surface epithelium
associated with human papilloma virus.
 Viral subtypes HPV-6 and HPV-11 have been
found
 appear as solitary , wartlike or cauliflower like
protubeances.
 H/P- lesion consist of finger like projections of
stratified squamous epithelium , with
fibrovascular connective tissue.

98. Peripheral giant cell granuloma
 Lesions are essentially response to local
injury and not neoplasms.
 Arise interdentally or from gingival margin,
 occur most frequently on the labial surface
and sessile or pedunculated
 painless ,vary in size and cover several teeth.
 Color vary from pink to deep red .
 can be differentiated from other
enlargements by microscopic examinations.

99.  Numerous foci of
multinucleated giant cells
and hemosiderin particles
in connective tissue
stroma.
 Overlying epithelium is
usually hyperplastic.
 Bone formation occurs
occasionally within the
lesion.

100. Central giant cell granuloma
 Lesions arise within the jaws and produce
central cavitation .
 Occasionally create a deformity of jaw that
,makes gingiva appear enlarged.

101. Gingival cyst
 Gingival cysts of microscopic proportions are
common , but they seldom reach a clinically
significant size.
 Develop from odontogenic epithelium or
from sulcular epithelium traumatically
implanted in the area.
 Appear as localized enlargements that may
involve marginal or attached gingiva.
 Occur in mandibular canine and premolar
areas mostly on lingual surface.
 Painless, but with expansion , cause erosion
of the surface of alveolar bone.

102.  Other benign tumours have also been
descibed
 myoblastoma
 hemangioma
 neurofibroma
 neurilemoma
 ameloblastoma

103. Malignant tumors of gingiva

104.  Gingiva constitutes only 8 % of oral cancers.
 Most commonly -squamous cell carcinoma.
 May be exophytic or ulcerative.
 Usually asymptomatic until complicated by
inflammation.
 Locally invasive involving underlying bone
and periodontal ligament of adjoining teeth.

105. Malignant melanoma
 Rare oral tumor that tends to occur in hard
palate and maxillary gingiva of older persons.
 Arises from melanoblasts in the gingiva ,
cheek or palate.
 Dark pigmented and preceded by occurrence
of localized pigmentation.
 May be flat or nodular and characterized by
rapid growth and early metastasis.

106. Sarcoma
 Fibrosarcoma , lymphosarcoma and
reticulum cell sarcoma of gingiva are rare
 only isolated cases have been described in
literature.

107. False enlargement
 Appear as enlargement of gingiva as a result
of increase in size of underlying osseous or
dental tissues.
 Usually presents with no other abnormal
clinical features.
 They may be due to
 underlying osseous lesions
 underlying dental tissues

108. Underlying osseous lesions
 Enlargement most commonly occurs due
to tori and exostoses .
 Can also occur due to Paget’s disease,
fibrous dysplasia, ameloblastoma,
osteoma etc.

109. Underlying dental tissues
 During various stages of eruption , labial
gingiva may show marginal distortion caused
by superimposition of the bulk of gingiva on
the normal prominence of the enamel in
gingival half of the crown.
 Also called development enlargements.
 Persists until J.E has migrated from enamel to
CEJ.
 Doesn’t present problem unless complicated
by marginal inflammation.