seminar on inflammatory gingival enlargement

1. INFLAMMATORY GINGIVAL
ENLARGMENT
DR L.ACHYUTH KUMAR
POST GRADUATE

2. CONTENTS
 Introduction
 Terminologies
 Classification
 Measuring of gingival overgrowth
 Chronic inflammatory gingival enlargements
 Acute inflammatory gingival enlargements
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess
 Difference between gingival and periodontal abscess
 Conclusion
 References

3. Introduction
 One of the common and evident features of periodontal pathology is increase in
size of gingiva.
 This is termed as gingival enlargement /gingival overgrowth.
 Enlargement of the gingiva may occur due to variety of reasons. which may
include inflammation, hypertrophy, hyperplasia (or) other causes.
Gingival enlargement- ‘increase in size of gingiva’

4.  Gingival enlargements may occur due to local causes (or) may be a local
manifestation of a systemic process.
 Plaque is such case that acts as a-
Precipitating (or)
Aggravating (or)
Causative (or)
Coexisting factors.

5. Terminologies:
 Gingival Enlargement: An overgrowth or increase in size of the gingiva.
 Gingival Hyperplasia: An enlargement of the gingiva due to an increase in the
number of cells.
 Gingival Hypertrophy: An enlargement of the gingiva due to an increase in the
size of cells.
(According to the Glossary of Periodontal Terms, 4th Edition, 2001)

6. CLASSIFICATION OF GINGIVAL ENLARGEMENT
i) Inflammatory
enlargement
ii) Drug-induced
enlargement
iii) Enlargements
associated with
systemic diseases
iv) Neoplastic
enlargement
(gingival tumors)
v) False
enlargement
b) Chronic
a) Acute
a) Conditioned
Gingival
Enlargement
b) Systemic
Diseases
Causing GE
Pregnancy,
puberty, Vit C
deficiency
Leukemia
Non-specific
conditioned GE
(pyogenic
granuloma)
Granulomatous
diseases
(Wegener’s
granulomatosis,
Sarcoidosis)
Plasma cell
gingivitis
a) Benign
tumors
b) Malignant
tumors

7. Based on location and distribution
a) Localized
b) Generalized
c) Marginal
d) Papillary
e) Diffuse
f) Discrete
a)
b)
c)
d)
e)
f)

8. 0 = no overgrowth seen
INDICES FOR MEASURING GINGIVAL OVERGROWTH
Harris & Ewart (1942)
1 = early changes detectable, perhaps a more
granular appearance to the papilla tip without
encroachment of the tooth.
2 = moderate changes evident, with increased interdental papillae and slight
encroachment of the gingival tissues onto the tooth surface.
3 = marked changes with obvious encroachment of the gingival tissues onto the tooth
surfaces, possibly interfering with function.

9. 0 = no gingival overgrowth
1 = mild gingival overgrowth (thickening of the marginal gingiva and/or lobular granulation
of the gingival pocket with gingival overgrowth covering upto 1/3 of the crown)
2 = moderate gingival overgrowth (overgrowth extending to the middle of the crown)
3 = severe gingival overgrowth (overgrowth covering 2/3 of the crown of affectation of the
attached gingiva)
GINGIVAL OVERGROWTH INDEX
(Angelopoulos and Goaz, 1972)
 Assesses the vertical dimension and the gingival
changes in the development of gingival overgrowth

10. 0 = no gingival overgrowth or enlargement
1 = mild hyperplasia defined as blunting of the papilla
2 = moderate hyperplasia with tissue covering upto ½ of the crown
3 = marked hyperplasia with tissue on more than ½ the crown
HYPERPLASTIC INDEX
(Conrad et al. 1974)
 Assesses gingival overgrowth in the horizontal dimension only

11. GINGIVAL OVERGROWTH INDEX
(Seymour et al. 1985)
 The upper and lower anterior segments are each divided into 5 gingival units
both buccally and lingually

12. The degree of gingival thickening on both labial and lingual aspects is graded as follows:
0 = normal
1 = thickening from the normal up to 2 mm
2 = thickening from the normal greater than 2 mm

13.  The extent of encroachment of the gingival tissues onto the adjacent crowns was also
graded 0, 1, 2 and 3 on the labial and lingual surfaces as shown-

14.  Where there was discrepancy between encroachments on 2 adjacent tooth surfaces in
the same unit, the higher score is given
 The 2 scores (thickening and gingival encroachments) are added, thus giving a
hyperplasia score for each gingival unit
 The maximum score obtainable using this method is 5

15. The Hyperplastic Index of Conrad et al. (1974) was modified by King and Fullinfaw to
include an assessment of the vertical component of gingival overgrowth
0 = normal width of free gingival margin
1 = thickening from normal upto 2mm
2 = thickening from the normal greater than 2mm
King & Fullinfaw- MODIFICATION OF HYPERPLASTIC INDEX (1993)

16. 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
 The degree of gingival enlargement can be scored as follows-
-Bokenkamp A et al., 1994

17. INFLAMMATORY
GINGIVAL
ENLARGRMENT
GINGIVAL ABSCESS
PERIODONTAL
ABSCESS
CHRONIC
GINGIVITIS/
PERIODONTITIS/
MOUTHBREATHERS
PERICORONAL
ABSCESS
ACUTE

18. 1) Chronic plaque induced gingivitis and periodontitis
Clinical features-
 Change in colour of gingiva to bluish red.
 Bleeding on slight provocation.
 Slight ballooning of interdental papilla or marginal gingiva and loss of knife
edge contour.
A) CHRONIC INFLAMMATORY GINGIVAL ENLARGEMENT

19.  Consistency - soft and pitting on pressure.
 Loss of surface stippling is seen.
 Pocket formation.
 Base of the pocket is apical to CEJ – true pocket.
 Loss of attachment is seen.
 Bone loss is seen.
 Mobility is seen.
 Disto – labial migration and extrusion of anterior teeth is common
feature of advanced periodontitis.

20.  Food impaction is a common complaint.
 Usually severe pain results from food impacting deep into a periodontal pocket
or from a deep seated periodontal abscess.
 This causes the urge to dig-out.
 Foul breath -halitosis
 Increase in temperature.
 Increase in GCF production.
 Hypersensitivity due to recession.

21.  Increase in inflammation infiltrate.
 Plasma cell are predominant.
 Junctional epithelium decreases up to 10 times.
 Bone loss is evident at the crest of alveolar bone, this increase with increase in
severity of disease.
 Degeneration of sulcular epithelium cells results in ulceration of pocket epithelium.
Histological features:

22.  Gingivitis and gingival enlargement are often seen in mouth breathers
(Lite et al. 1955).
 The gingiva appears red and edematous with a diffuse surface shininess
of the exposed area. The maxillary anterior region is the common site of
such involvement.
2) GINGIVAL CHANGES ASSOCIATED WITH MOUTH BREATHING

23.  In many cases, the altered gingiva is clearly demarcated from the adjacent
unexposed normal gingiva.
 The exact manner in which mouth breathing affects gingival changes has
not been demonstrated. Its harmful effect is generally attributed to irritation
from surface dehydration.
 However, comparable changes could not be produced by air drying the
gingiva of experimental animals by Klingberg et al (1961).

24. B) ACUTE GINGIVAL ENLARGEMENT
1) GINGIVALABSCESS
 Abscess means localized acclamation of pus.
 Sudden start and a short history.
 They involvement is localized.

25. Etiology-
 Bacterial origin
1. when sizable number of bacteria from the surface of gingiva finds entry into deeper
gingival tissues through:
(i) Mastication
(ii) Physical injury by toothpicks and tooth brush.
2. food impaction (popcorn kernel, fish bone, dental floss)
3. after dental treatment.

26. Gingival abscess starts as a swelling in the marginal /interdental gingiva which is
red in colour and has smooth shiny surface.
Pain , tenderness and size increases in 2-3 days
Abscess may become fluctuant and pointed
An orifice eventually develops through which purulent exudate is expelled
With express of pus – pain , tenderness and size of abscess reduce
After drainage –abscess- heals on their own

27. No radiographic changes are seen in gingival abscess

28.  More dense infiltrate of PMNs
 Vessel engorgement
 Leaking intercellular junctions of blood vessels
 Emigration of leukocytes
 Migration of leukocytes
 Edematous tissue [CT+EPI]
 Ulceration on the epithelial surface
Histopathology

29. 2)PERIODONTALABSCESS
 Other names – Lateral abscess / Parietal abscess.
 Definition: it is defined as a localised purulent inflammation in the deeper supporting
periodontal tissues.
 It may or may not involve the gingiva, but it invariably causes a GE.
 3rd most prevalent emergency infection (8%), after acute alveolar (14-25%) and
periodontitis (10-11%).
 More likely to occur in a pre existing periodontal pocket & more in molar site (>50%).

30.  Kaldahl et al (1996) in a 7-year prospective longitudinal treatment study for
occurrence of periodontal abscess. From the 51 patients included, 27 developed
abscesses were detected.
 16 out of the 27 abscess sites had an initial probing pocket depth greater than 6 mm,
and in about 8 sites the periodontal probing depth was 5-6 mm.
 Gray et al (1994) monitored periodontal patients in an army clinic and found that
periodontal abscess had a prevalence of 27.5%. In this population, 13.5% of patients
undergoing active periodontal treatment had abscess formation and while in untreated
patients it is 59.7%.

32. Classification of Periodontal Abscess
GINGIVALABSCESS
 Localized purulent infection that involves the marginal gingiva and
interdental papilla.
PERIODONTAL ABSCESS
 Localized purulent infection within the tissues adjacent to periodontal
pocket that may lead to destruction of PDL and alveolar bone.
Location (Gillette & Van House 1980/Meng,1990)

33. ACUTE
 short duration,
 lasts for a few days or weeks,
 pain on biting,
 associated lymph node
enlargement.
Course of lesion (Pini prato et al 1988)
CHRONIC
 Spontaneous drainage, associated with nasty taste
and spontaneous bleeding.
 Pus may be present
 Discharge from the gingival crevice or from a sinus
in the mucosa overlying the affected root.
 Pain is usually of low intensity, often associated
with regional lymphadenopathy and
 occasionally slight elevation of body temperature.

34.  Single periodontal abscesses are usually related to local factors which
contribute to the closure of the drainage of a periodontal pocket.
 Multiple periodontal abscesses have been reported in uncontrolled diabetes
mellitus, medically compromised patients, and in patients with untreated
periodontitis after systemic antibiotic therapy for non-oral reasons.
(Helovuo & Paunio 1989, Helovuo et al. 1993, Topoll et al. 1990)
Number (Topoll et al 1990)

35. 1) Gingival abscess: in previously healthy sites and caused by impaction of foreign bodies.
2) Periodontal abscess: either acute or chronic, developing into a periodontal pocket.
3) Peri-coronal abscess: in incompletely erupted teeth.
Based on the periodontal tissues involved
(Meng et al 1999)

36. 1) Periodontitis related abscess: when the acute infection originates from biofilm
present in a deepened periodontal pocket.
2) Non periodontitis related abscess: when the acute infection originates from the
other local sources, such as foreign body impaction or alteration in root integrity.
Depending on cause of acute infection process
(Lindhe)

37. Etiology
 Periodontal abscesses have been either directly associated to periodontitis or
to sites without the prior existence of a periodontal pocket.
 In periodontitis, a periodontal abscess represents a period of active bone
destruction (exacerbation), although such events also occur without abscess
formation.

38. Tortuous periodontal pockets specially associated with furcation involvement which
eventually become isolated and can favor formation of an abscess. Carranza 1990
Closure of margins of periodontal pockets may lead to extension of the infection into the
surrounding tissue. Due to the pressure of the suppuration inside the closed pocket.
DeWitt et al 1985
Fibrin secretions, leading to the local accumulation of pus may favor the closure of gingival
margin to the tooth surface.
Galego Feal et al
1995
Changes in the composition of the microflora, bacterial virulence or in host defenses also
make the pocket lumen inefficient to drain the increased suppuration.
Kareha et al 1981

39. After nonsurgical periodontal therapy-
After scaling or professional prophylaxis, dislodged calculus fragments can be
pushed into the tissues or inadequate scaling may allow calculus to remain in deep
pockets, whilst the coronal part will occlude the normal drainage
After surgical periodontal therapy-
associated with the presence of foreign bodies, such as membranes for regeneration
or sutures (106)
Different subgroups distinguished:

40.  acute exacerbation of an untreated periodontitis and refractory periodontitis.
 acute exacerbation in supportive periodontal therapy.
 systemic antimicrobial intake without subgingival debridement.
 in patients with severe periodontitis this may also cause abscess formation,
probably related to an overgrowth of opportunistic bacteria.

41. Periodontal abscesses can also occur in previously healthy sites
(i.e. non periodontitis periodontal abscesses) owing to impaction
of foreign bodies or to alteration of the root surfaces:

42. Impaction of foreign bodies such as tooth brush bristle ,food (fish
bone) into the gingival tissue.
Kareha 1981
After procedures like scaling where calculus is dislodged and
pushed into the soft tissue. It may also be due to inadequate scaling
which will allow calculus to remain in the deepest pocket area,
while the resolution of the inflammation at the coronal pocket area
will occlude the normal drainage, and entrapment of the
subgingival flora in the deepest part of the pocket then cause
abscess formation.
Dellorusso
1985

43. Treatment with systemic antibiotics without subgingival
debridement in patients with advanced periodontitis leads to a
change in the composition of the subgingival microbiota leading to
super infection and abscess formation.
Helovuo et al
1993
As a consequence of perforation of lateral wall of a tooth by an
endodontic instrument during a root canal therapy.
Carranza 1990

44. External root resorption Carranza 1990
Invaginated tooth. DeWitt et al 1985
Cracked tooth Galego Feal et al 1995
Local factors effecting morphology of roots such as cemental tears Kareha et al 1981
Possible local predisposing factors for periodontal abscess formation:

45. Systemic Antibiotic Therapy
 Multiple periodontal abscesses cannot be explained by local factors
alone, and it has been suggested that systemic administration of
antibiotics may trigger their formation.
 Helovuo H et al 1993 results it appears that the systemic administration
of antibiotics in patients with untreated periodontitis may lead to
superinfection with opportunistic organisms resulting in development of
periodontal abscesses.

46.  Topell et al (1990) reported on the development of multiple abscess (4-10)
in 10 untreated periodontal patients who received systemic antibiotic
therapy. (Penicillin, tetracycline) for non-oral infections.
 Koller-Benz et al (1992) showed that after initiation of nifedipine therapy, 8
abscesses appeared in 5 days. O The nifedipine therapy was discontinued,
and the abscesses resolved. 3 weeks later the treatment was resumed, and
after 2 weeks another abscess was detected.

47.  Helovuo et al. (1993) studied 72 patients with untreated periodontitis, who were
followed for 12 weeks, after intake of systemic antibiotics for non-oral reasons.
 Patients were divided into 3 groups according to the antibiotic used, 10 out of
24 patients (42%) in the penicillin group developed abscesses within the next 4
weeks. The number of abscesses ranged between 1-10.
 No abscesses were detected in the erythromycin or the control groups.

48. Diabetes
 Systemic alterations in diabetics that may have a significant influence on the
formation of periodontal abscesses include-
 lowered host resistance such as impaired cellular immunity,
 decreased leukocyte chemotaxis/phagocytosis and bactericidal activity.
 Enhanced interaction of advanced glycosylation end products (AGEs) with their
cellular receptor (RAGE) has been suggested as one of the pathogenic
mechanisms of accelerated periodontal disease in diabetes.

49. Etiopathogenesis:
 Pus formation – inflammation - in pockets.
 If the drainage is restricted (or) is totally blocked pus collects and an abscess results
(blocked by calculus, food debris or other foreign objects)
Periodontal abscess have been either directly associated to periodontitis or to sites with
out the prior existence of a periodontal pocket.

50. I) Periodontal abscess in periodontitis patients
 In periodontitis, a periodontal abscess represents a period of active bone destruction
(exacerbation).
 The existence of pockets with cul-de-sac, which eventually become isolated, may
favour the formation of abscess.

51.  The marginal closure of a periodontal pocket, may lead to an extension of the
infection into the surrounding periodontal tissues due to the presence of the
suppuration inside the closed pocket.
 The fibrin secretions leading to the local accumulation of pus may favour the
closure of the gingival margin to the tooth surface.

52. Kareha et al (1981):
 Changes in the composition of the microflora, bacterial virulence (or) in host
defence could also make the pocket lumen inefficient to drain the increased
suppuration.
 The development of a periodontal abscess in periodontitis may occur at different
stages during the course of the infection.

53. 1) as an acute exacerbation of an untreated periodontitis- Dello Ruso 1985
2) during periodontal therapy- Dello Russo 1985,Carranza 1990
3) in refractory periodontitis- Fine 1994
4) during periodontal maintenance- Chace and Low 1993, Mc Leo 1997

54. Different mechanisms behind formation are:
A) exacerbation of chronic lesions:
-it occur without any obvious external influences.
B) post therapy periodontal abscess:
-it occurs immediately after scaling (or) routine prophylaxis due to in
adequate scaling which will allow calculus to remain in the deepest pocket area.
-while the resolution of the inflammation at the coronal pocket area will
occlude the normal drainage and then cause the abscess formation.

55. -when the periodontal abscess occurs immediately after scaling or after
a routine prophylaxis it has been related to the dislodging of calculus
fragments which can be pushed in to the tissue.
C) Post – surgery periodontal abscess:
-incomplete removal of sub gingival calculus or the presence of foreign
substance.
-eg. Suture, regenerative device, perio pack.

56. Garretl et al 1997:
Conducted a clinical study on guided tissue regeneration & reported that 10 out of 80
controls (non-resorbable barrier) and 4 out of 80 tests (bio-absorbable barrier) showed
abscess formation or suppuration at the treated sites.
Post antibiotic periodontal abscess:
 Treatment with systemic antibiotics without subgingival debridement in patients
with advanced periodontitis may also cause abscess formation.
 It is attributed to a likely change in the composition of subgingival microbiota
leading to a super infection and inflammation.

57. II) Periodontal abscess in the absence of periodontitis:
 Impaction of foreign bodies.
 Periodontal abscess caused by foreign bodies related with oral hygiene aids so it has
been named as “oral hygiene abscess”.
 Carranza 1990- perforation of the tooth wall by an endodontic instrumentation.
 Kareha et al 1981- infection of lateral cyst local factors affecting the morphology of
the root may predispose to periodontal abscess formation.

58. Clinical features
Acute form:
 Overlying and surrounding gingiva-enlarge and edematous
 Tender and painful
 Surface is smooth and shiny
 Adjoining teeth –tender, painful, increase in mobility.
 Pus may be expressed spontaneously or on applying digital pressure
through the abscess sinus or from the underlying periodontal pocket.

59. Chronic form:
 The pus formed within the diseased periodontal tissue can easily drain out, i.e., there is
no collection of pus within the periodontal pocket.
 An acute abscess converts to a chronic one, which results in relief from the pain,
tenderness and swelling.
 The other associated clinical features also shows regression and become milder.
 A chronic periodontal abscess may aggravate to become acute if the channel through
which the pus drains gets blocked.
 In some cases, a periodontal abscess may occur in association with a periapical abscess.

61.  No changes in very recent origin or acute condition.
1. radiolucent area- lateral sides of root
2. size of area increases with time.
3. size of area decreases with treatment.
4. some time may not visible due to:
A) located on buccal/lingual gingiva of the teeth (superimposition by roots).
B) lingual/buccal cortical plate(superimposition by bony plate).
C) concavity of curved root.
Radiographic features

62. 5. periodontal abscess occurring along with and communicating with periapical abscess.
 No clear cut distribution can be made radiographically between the boundaries of the two.
 The same periodontal abscess may present different radiological images depending on-
A) its location.
B) stage of development and on going pathological change.
C) angle at which the radiograph is taken.

63.  The intact neutrophils are found surrounding a central area of soft tissue debris and
destroyed leukocytes.
 At a later stage, a pyogenic membrane composed of macrophages and neutrophils is
organized.
 The rate of destruction in the abscess will depend on the growth of bacteria and its
virulence, as well as the local pH (since an acidic environment will favour the action
of lysozymal enzyme).
Histopathological features:

64. De witt et al 1985:
 Studied biopsy punches taken from 12 abscess. They observe from the outside to
the inside.
A) a normal oral epithelium and lamina propria.
B) an acute inflammatory infiltrate.
C) an intense foci of inflammation (neutrophils-lymphocytes with the surrounding
connective tissue destroyed and necrotic).
D) a destroyed and ulcerated pocket epithelium.
E) a central region as a mass of granules acidophilic and amorphs debris.

66. MICROBIOLOGY
 The most frequent type of bacteria were gram-negative anaerobic rods and gram-
positive facultative cocci.
 In general, gram-negatives predominated over gram positives and rods over cocci.
 The periodontal abscess microbiota is usually indistinguishable from the microflora
found in the subgingival plaque in adult periodontitis.

67.  The microflora from abscesses and deep pockets was similar and harbored higher
proportions of pathogens when compared to the microflora of shallow pockets.
 Bacterial species with capacity of producing proteinases, such as P. intermedia, are
important, since they may increase the availability of nutrients, and thereby, increasing
the number of bacteria inside the abscess (Jansen & Van der Hoeven 1997).

68. Culture studies of periodontal abscesses have revealed high prevalences of:
 Porphyromonas gingivalis (55-100%),
 Prevotella intermedia (25-100%), and
 Fusobacterium nucleatum (44-65%)
Other pathogens which have been reported are-
 Actinobacillus actinomycetemcomitans (25%)
 Campylobacter Rectus (80%)

69. Radiographs
• Intra oral radiographs, include peri apical and vertical bitewing views, are used to
assess marginal bone loss and peri apical condition of the tooth involved.
• Gutta percha point placed through sinus might locate the source of abscess.
• Dental radiographs (peri apical, bitewing and OPG) could be used for a general
survey for a marginal bone loss of the whole dentition.
Pulp vitality test
• Thermal or electric test could be used to assess the vitality of the tooth.
Microbial test
• Sample of pus from the sinus, abscess or expressed from gingival sulcus could be
sent for culture and sensitivity test.

71. Gingival abscess
 Confined to marginal and /or
interdental gingiva.
 Occurs in previously disease free
areas.
 Acute inflammatory response of
foreign material into the gingiva.
 No Bone loss.
Periodontal abscess
 Involves supporting
periodontal structure.
 Often occurs in the course of
chronic destructive
periodontitis.
 X-ray-bone loss present.
 Pocket present.

72.  Pain –diffuse
 Many times affect the entire side of the face
 Affected by thermal changes
 Pain –dull
 Localized
 Not affected by thermal changes

73. Periodontal abscess
 Associated with pre-existing periodontal
pockets, caries or both.
 Pulp test –vital.
 Swelling generalized and located around the
involved tooth and gingival margin seldom
with fistulation tract.
 Pain –dull constant less severe ,localized
and patients usually can located the
offending tooth.
Periapical abscess
 Associated with deep restoration
caries or tooth wear.
 Non-vital.
 Swelling localized often with fistulous
tract opening in the apical area.
 Pain –severe ,throbbing last for long
deep the offending tooth.

74.  Pain associated with the movement or
percussion is not as severe as with a
pulpal disease.
 Angular bone defects , furcation
involvement.
 Responds dramatically well to sub
gingival debridement.
 Severe than periodontal abscess.
 Apical radiolucency.
 Endodontically filling or endodontic or
post restorations.
 Responds poorly or not all to periodontal
therapeutic intervention.

75. Radiographic findings
 Ordinarily a radiolucent area
along the lateral surface of the
root suggests the presence of
periodontal abscess.
 A radiolucent area at the apex
of the root suggests periapical
abscess.
Clinical findings such as the presence of extensive caries, pocket formation, lack of
tooth vitality, and the existence of continuity between gingival margin and the abscess
area often prove to be of greater diagnostic value than radiographic appearance.

77. 3) Pericoronal abscess:
 Pericoronitis –it is a inflammatory condition of the gingiva covering and
surrounding the crown of an in completely erupted tooth.
 When suppuration occurs under the peri-coronal flap and the discharge of the pus
is restricted due to any reason causing localization of pus a pericoronal abscess.

78. It can be either-
 acute
 sub - acute or
 chronic
Pain is usually the predominant symptom in acute stages, whereas chronic forms of the
disease may display very few symptoms and present exudate.
Pericoronitis is common in more than 60% of partially impacted third molars.

80. Most commonly seen in mandibular third molars.
Partially erupted /impacted teeth usually covered by completely/partially loose
operculum of gingival tissue.
The space between the occlusal surface and the overlying operculum /flap allows
accumulation of bacterial plaque and food debris.
Etiopathogenesis:

81. As a result of this inflammation occurs in gingival operculum.
Usually –resulting –inflammation is mild does not cause overt clinical features but if
it worsens and localized of pus occurs results in abscess formation.
May worsen by –mechanical transmission from the opposing tooth.

82. Clinical features:
 Tooth is partially erupted and may or may not be impacted.
 The crown of the tooth is completely or partially covered by a flap gingival tissue
[operculum].
 The operculum shows varying degree of inflammatory involvement.
 Inner surface of the operculum is often ulcerated and inflamed even if the top surface
appears normal.

83.  Inflammation– increases bulk of the operculum. In future causes interference with jaw
closure and also results in traumatized of the operculum by teeth of opposing arch.
 The area produces odour that may become very bothersome.
 Muscle trismus of varying degree may set in.
 Swelling of the face on the same side may be seen.
 Draining lymph nodes may become palpable.

85. Conclusion
 Diagnosis of gingival enlargement is very important for a dentist to treat it.
 By knowing the etiology, pathogenesis, clinical features, radiological features
and histological features one can easily can distinguish between the type of
gingival enlargement and thus can treat it properly.

86. References
 Clinical Periodontology : Carranza, Newman 9th Edition O
 Clinical Periodontology and implant dentistry – Lindhe 4th edition
 Textbook of Periodontology (A Conceptual Approch), D.S.KALSI.
 Periodontal abscess: a review. JCDR-2011
 Periodontal Abscess review, JCP-2000, 27:377-386.
 Perio 2000 volume 34, 2004.