gingival infections

1. ACUTE GINGIVAL
INFECTIONS

2. CONTENTS
 Introduction
 Primary herpetic gingivostomatitis
 Necrotizing ulcerative gingivitis (NUG)
 Pericoronitis
 Abscesses of periodontium

3. INTRODUCTION
 An acute lesion is of sudden onset and short duration
and is painful.
 They are manifested with severe pain along with
systemic manifestations
 Thus these lesions must be treated at the earliest
with a proper treatment protocol.

4. Primary herpetic gingivostomatitis

5.  HSV- type 1
 Infants/ children younger than 6 yrs
 Males=females
 Primary infection asymptomatic
 The virus ascends through the sensory or autonomic
nerves and persists in the neuronal ganglia that innervate
the site as a latent HSV
 Sunlight, fever, trauma, stress , after oral surgical
procedures

6. Secondary manifestations
 Herpes labialis
 Herpetic stomatitis
 Herpes genitalis
 Ocular herpes
 Herpetic encephalitis

7. Early stage
Late stage showing brownish
crusted lesions

8. CLINICAL FEATURES
Intra-oral
 Diffuse, erythematous, shiny
involvement of the gingiva and
adjacent oral mucosa
 Varying degree of edema and
gingival bleeding
 Discrete spherical grey vesicles
Primary herpetic
gingivostomatitis

9.  Rupture of vesicles and formation of ulcers after 24 hrs
 Ulcers– small , painful, red, elevated, halo-like margin
with depressed yellowish/greyish white central portion
 Widely spread/clusters
 7-10 days
 No scarring

10.  Soreness, difficulty in eating and drinking
 Ruptured vesicles sensitive to touch, thermal changes,
foods such as condiments and fruit juices
 Infants show irritability and refusal to take food

11. Extra-oral
 Cervical adenitis
 Fever (101ͦ -105ͦ F)
 Generalized malaise

12. HISTOPATHOLOGY
Virus targets epithelial cells
Ballooning degeneration (acantholysis, nuclear clearing,
nuclear enlargement)
Tzanck cells

13. Fusing of infected cells
Formation of multinucleated cells and intercellular edema
Formation of intraepithelial vesicles
Rupture
Secondary inflammatory response with fibropurulent exudate
Ulcers with central portion of acute inflammation and exudation
surrounded by zone rich in engorged blood vessels

14. DIAGNOSIS
 Early diagnosis important (reducing symptoms and
recurrences)
 History/clinical findings
 Virus culture
 Immunologic tests using monoclonal antibodies or DNA
hybridization techniques

15. DIFFERENTIAL DIAGNOSIS

16. Erythema multiforme:
o More extensive vesicles with pseudomembrane
formation on rupture
o Tongue more involved
o Skin lesions present
o Prolonged involvement may occur for weeks

17.  Stevens-Johnson syndrome: rare form of EM
characterized by hemorrhagic lesions in the oral cavity,
hemorrhagic occular lesions and bullous skin lesions

18. Bullous lichen plannus:
 Rare & painful condition
 Large blisters on tongue & skin- rupture
undergo ulceration
 Skin lesions + oral involvement
 Prolonged indefinite course
 Linear, grey, lacelike lesions of lichen
plannus inter-spread among bullous
eruptions

19. Desquamative gingivitis
 Chronic condition
 Diffuse involvement of gingiva
 Varying degree of peeling of epithelium

20. Recurrent aphthous stomatitis
 Small well defined round shallow
ulcers, yellowish grey central
areas & red halo
 H/o previous mucosal ulcers is
dignostic, unknown etiology
 No diffuse erythematous
involvement of the gingiva, no
acute toxic symptoms

21. COMMUNICABILITY
 Contagious
 Most adults develop immunity due to infection during
childhood – subclinical infection
 Hence seen in infants & children
 Recent studies have demonstrated HSV in periodontal
pockets (Slots J 2000)

22. TREATMENT
Consists of early diagnosis & immediate initiation of antiviral
therapy.
Antivirals :
o Acyclovir suspension 15mg/kg is given 5 times daily for 7
days (Amir et al,1997)
o It reduces days of fever, pain, lesion and virus shedding

23. o Acyclovir does not affect normal cells but inhibits DNA
replication in HSV infected cells
o Newer antivirals like Valacyclovir and Famicyclovir can
also be used
o <3 days– antiviral
o >3 days- (immunocompetent pt) limited value

24. Palliative measures:
o Removal of food debris, plaque and supra gingival
calculus
o NSAID (FEVER AND PAIN)
o Extensive periodontal therapy to be postponed
o Local /systemic antibiotics to prevent opportunistic
infection especially in immuno-compromised patients

25. o The patient must be informed that the disease is contagious,
thus precautions must be taken (vesicles –highest viral titer)
Supportive measures:
o Copious fluid intake
o Nutritional supplements
o Topical anesthetics while eating

26.  Infection of fingers of health professional treating
infected patients may occur and is known as Herpetic
Whitlows

27. Necrotizing ulcerative gingivitis

28.  Necrotizing Gingivitis, Necrotizing Periodontitis and
Necrotizing Stomatitis are the most severe inflammatory
disorders caused by plaque bacteria
 They are rapidly destructive and debilitating
 A distinction between these diseases has not always been
made in the literature

29.  Microbial diseases affecting gingiva/ periodontium in the
context of an impaired host response
 Characterized by death and sloughing of tissues

30. HISTORY
 Fourth century BC, Xenophon mentioned that Greek soldiers
were affected with “sore mouth” and foul-smelling breath
 In 1778, John Hunter described the clinical findings and
differentiated ANUG from scurvy and chronic destructive
periodontal disease
 ANUG occurred in epidemic form in the French army in the
19th century

31.  In 1886, Hersch, a German pathologist, discussed some of
the features associated with the disease such as enlarged
lymph nodes, fever, malaise and increased salivation
 In 1890s, Plaut and Vincent described the disease and
attributed its origin to fusiform bacilli and spirochetes

32. NOMENCLATURE
 Ulceromembranous gingivitis
 Acute necrotizing ulcerative gingivitis
 Trench mouth
 Vincent’s gingivostomatitis
 Phagedenic gingivitis
 Fusospirallary periodontitis
 Plaut-Vincent stomatitis

33. CLINICAL FEATURES
Classification
 Acute
 Subacute (Repeated remissions and exacerbations)
 Recurrent
 Single tooth, group of teeth
 Entire mouth

34. NUP
(long standing, severe immunosuppression)
NUS
Noma

35. ORAL SIGNS AND SYMPTOMS
 Punched out, craterlike depressions at the crest of the
interdental papilla
 Can extend into the marginal gingiva, attached gingiva and
oral mucosa
 Grey pseudomembranous slough
 Linear erythema
 Removing slough exposes red, hemorrhagic, shiny surface
which bleeds easily

36.  Fetid odor
 Metallic taste
 Increased salivation/pasty saliva
 Can be superimposed on chronic gingivitis/periodontitis
 Recession rather than pocket formation

37.  Constant radiating, gnawing pain that is intensified on
eating spicy and hot foods and on chewing
 Lesions extremely sensitive to touch
 Low socioeconomic groups
 Seasonal variations (Skach et al, 1970)

38. EXTRAORAL AND SYSTEMIC SIGNS AND
SYMPTOMS
 Local lymphadenopathy
 Fever
 Increased pulse rate, leukocytosis, loss of apetite and
general lassitude additionally seen in severe cases
 Insomnia, constipation, GI disorders, headache and
mental depression in children

39. OTHER SEVERE SEQUELAE
1) Fusospirochetal meningitis
2) Peritonitis
3) Pulmonary infection
4) Toxemia
5) Fatal brain abscess
6) Noma

40. CLINICAL COURSE
ACCORDING TO HORNING AND COHEN:
 Stage 1 : Necrosis of tip of the interdental papilla (93%).
 Stage 2 : Necrosis of entire papilla (19%)
 Stage 3 : Necrosis extending to gingival margin (21%)
 Stage 4 : Necrosis extending to attached gingiva (1%)
 Stage 5 : Necrosis extending to buccal / labial mucosa (6%)
 Stage 6 : Necrosis exposing alveolar bone (1%)
 Stage 7 : Necrosis perforating skin and check (0%)

41. ACCORDING TO PINDBORG:
 Stage 1: Erosion of only tip of interdental papilla
 Stage 2: Lesion extending to marginal gingiva and causing
potentially a complete loss of papilla
 Stage 3: Involving attached gingiva
 Stage 4: Exposure of bone

42. HISTOPATHOLOGY
 Microscopically the lesion is acute necrotizing inflammation of
the gingiva, involving both the stratified squamous epithelium
and the underlying connective tissue
 Epithelium destroyed and replaced by meshwork of fibrin,
necrotic epithelial cells and PMN’s and various types of
microorganisms (surface pseudomembrane)
 Border: Epithelium edematous and individual cells exhibit
varying degree of hydropic degeneration along with infilteration
of PMN’s in the intercellular spaces

43.  Underlying connective tissue: hyperemic with numerous
engorged capillaries and dense infiltration by PMN’s (linear
erythema)
 Plasma cells at the periphery(underlying chronic condition)
 Epithelium and CT alterations decrease with increase in distance
from the necrotic area and gradually blends with the uninvolved
area

44. Listgarten – described four zones that blend with each other
 ZONE I - BACTERIAL ZONE- The Most superficial
zone
Consists of varied bacteria, including a few spirochetes
of small, medium and large type.
 ZONE II – NEUTROPHIL RICH ZONE - Contains
numerous leukocytes, predominantly neutrophils, with
bacteria, including many spirochetes of various types,
between the leukocytes

45.  ZONE III – NECROTIC ZONE- Consists of disintegrated
tissue cells, fibrillar material, remnants of collagen fibers and
numerous spirochetes of the medium and large types, with
few other organisms
 ZONE IV – SPIROCHETAL INFILTRATION ZONE-
Consists of well preserved tissue infiltrated with medium and
large spirochetes without other organisms.
Spirochetes have been found as deep as 300 microns from the
surface

46. ETIOLOGY
Role of bacteria
o Plaut and Vincent in 1894 and 1896, respectively
introduced the concept NUG is caused by specific
bacteria – namely a fusiform bacillus and a spirochetal
organism.
o Fusiform bacilli and a spirochetal organism are always
found in the disease.

47.  Rosebury and coworkers described a fusospirochetal
complex consisting of T. marcodentium, intermediate
spirochetes, vibrios, fusiform bacilli and filamentous
organisms in addition to several Borrelia species

48.  More recently Loesche and colleagues described a constant
flora and a variable flora
Constant flora :- Fusospirochetal organisms, P.
intermedia, A. odontolyticus and
various spirilla like Selenomonas
species.
Variable flora :- Heterogenous array of bacterial
types

49.  Bacteriologic findings have been supported by
immunological data presented by Chung et al who
reported increased IgG and IgM antibodies to
intermediate spirochetes, P. intermedia in NUG patients
as compared to those with chronic gingivitis and healthy
controls
 Metronidazole effective

50. Role of host response
 Presence of organisms insufficient to cause disease
 NUG is not produced experimentally in humans and
animals by inoculation of bacterial exudates from the
lesion
 Characteristic lesions occurs in animals when they are
under immunosupression
 Not found in well nourished individuals with fully
functional immune system

51.  Immunosupression essential- NUG patients displayed
depression in leukocyte chemotaxis and phagocytosis
(Cogen et al, 1983)
 Nutritional deficiency, fatigue caused by chronic sleep
deprivation, alcohol/drug abuse, psychological factors,
systemic disease
 It is hence concluded that -
The specific cause of NUG has not been established & it is
produced by a complex of bacterial organisms but requires
underlying tissue changes to facilitate the pathogenic activity
of the bacteria.
 HIV

52. LOCAL PREDISPOSING FACTORS
 Pre-existing gingivitis
 Injury to the gingiva (eg: malocclusion)
 Smoking
 98% pts with NUG were smokers & frequency of the disease
increases with increasing exposure to tobacco smoke
(Pindborg et al, 1951)
 Preexisting chronic periodontitis, pericoronal flaps (favourable
environment for anaerobic fusiform bacilli and spirochetes)

53. SYSTEMIC PREDISPOSING FACTORS
Nutritional deficiency
 Produced in animals by giving them nutritionally deficient
diet
 Nutritional deficiencies diminishes immune responses and
alteres the periodontal structures, making them more
susceptible

54. Debilitating disease
 Chronic diseases( syphilis, cancer)
 Severe gastrointestinal disorders (ulcerative colitis)
 Blood dyscrasias( anemia, leukemia)
 AIDS

55. Psychosomatic factors
 Disease often occurs in association with stressful situations
(induction into the armed forces, school examinations)
 Hypothalamic-pituitary-adrenal axis activation resulting in
cortisol secretion and decrease in immune response

56.  Increase in the levels of cortisol and catecholamines
leads to reduced gingival microcirculation and salivary
flow which enhances nutrition to P.intermedia
 Depression in neutrophil and lymphocyte function leads
to bacterial invasion and tissue damage.
(Johnson and Engel 1986)

57. DIAGNOSIS
 Clinical findings (gingival pain,ulceration and bleeding)
 Bacterial smear not definitive
 Microscopic examination of biopsy specimen (TB,
neoplastic disease)

58. DIAGNOSTIC CRITERIA
By Genco, Goldman and Cohen:
 Interproximal necrosis and ulceration (punched-out papillae)
 Painful gingiva
 Bleeding (spontaneous or on slight provocation)
 Pseudomembrane (fibrin, debris)
 Fever, malaise, lymphadenopathy
 “Fetor Oris”

59.  Herpetic Gingivostomatitis
 Chronic Periodontitis
 Desquamative Gingivitis
 Streptococcal Gingivostomatitis
 Apthous Stomatitis
 Diptheric And Syphilitic Lesions
 Tuberculous Gingival Lesion
 Candidiasis
 Agranulocytosis
 Dermatoses (Pemphigus, Erythema Multiforme ,Lichen
Planus)

60.  Treatment differs
 Herpes/NUG

63. STREPTOCOCCAL GINGIVOSTOMATITIS
 Characterized by diffuse erythema of the gingiva and other
areas of the oral mucosa
 Necrosis of the gingival margin – not a feature of this
disease.
 No fetid odor
 Bacterial smears– streptococcal forms
 Streptococcus viridans , groupA ß-hemolytic streptococcus

64. GONOCOCCAL STOMATITIS
 Caused by Neisseria gonorrhoeae
 Mucosa is covered with a grayish membrane that sloughs
off in areas to expose an underlying raw bleeding surface
 Most common in new born due to transmission through
maternal passages

65. AGRANULOCYTOSIS
 Characterized by marked decrease in number of circulating
PMN’s
 Lesions similar to NUG
 No marked inflammation due to diminished defense mechanism
 Blood studies can be used to differentiate between NUG and
agranulocytosis

66. VINCENT’S ANGINA
 Fusospirochetal infection of oropharynx and throat,
distinguished from NUG, which affects marginal gingiva.
May extend to the larynx and the middle ear

67. NUG in Leukemia
 Not produced by leukemia per se , but due to reduced
host defense mechanism
 NUG may superimpose on gingival tissue alteration
caused by leukemia

68. NUG IN HIV PATIENTS
 Same clinical features
 Extremely destructive course leading to NUP
 Presenting symptom for HIV

69. COMMUNICABILITY
 Not contageous
 Study by King
 Kitchen facilities (controlled conditions, anaerobic
environment, do not survive on utensils)
 Occurrence in epidemic like outbreaks– due to common
predisposing factors
 Immunosupression+bacteria

70. NUP
 Extension of NUG or different disease entity
 No evidence
 Clinical similarities
 Until distinction can be proved/disproved, classified together
 Classification first adopted in world workshop in clinical
periodontics in 1989

71.  Deep interdental osseous craters
 Recession
 HIV positive patients
 Strongly associated
 Marker of immune supression and diagnosis of AIDS
 HIV-P
 Aggressive form of chronic periodontitis

72. TREATMENT
 Alleviation of the acute symptoms by reducing microbial load
and removal of necrotic tissue
 Treatment of chronic disease either underlying the acute
involvement or elsewhere in the oral cavity

73.  Alleviation of the generalized symptoms such as fever
and malaise
 Correction of the systemic conditions that contribute to
the initiation or progression of gingival changes.

74. SEQUENCE OF TREATMENT
FIRST VISIT
 Complete evaluation
 Comprehensive medical history with special attention to recent
illness, living conditions, dietary backgrounds, type of
employment, hours of rest, cigarette smoking, stress levels, HIV
 Examination should include general appearance, presence of
halitosis, skin lesions, vital signs, lymph nodes

75. o Characteristic lesions
o Oral hygiene (Pericoronal flap Pockets Local irritants)
o Only acutely involved areas
o Isolated with cotton rolls and dried
o Topical anesthetic

76.  Area swabbed to remove pseudo membrane with moistened
cotton pellet after 2-3 min
 Cleanse area with warm water
 Superficial calculus removed (ultrasonic scalers)
 Subgingival scaling and curettage – contraindicated
(bacteremia, extend infection to deeper tissues)

77.  Surgical procedures other than emergencies postponed
until pt is symptom free for 4 weeks
 Antibiotic regimen (amoxicillin 500 mg orally every 6 hrs
for 10 days) in moderate to severe cases
 Metronidazole (500mg BID 7 days)
 Emergency procedures along with systemic antibiotics

78. PATIENT INSTRUCTIONS
 Patient told to rinse every two hours – glass full of equal
mixture of warm water and 3 % Hydrogen peroxide and /
or twice daily with 0.12%chlorhexidine
 Adequate rest
 Confine toothbrushing to removal of surface debris,
ultrasoft brush, bland dentrifice

79.  Analgesics
 Avoid tobacco, alcohol, condiments
 Report back in 1-2 days
 Motivation

80. SECOND VISIT
 Patient condition – usually improved. Pain is diminished
or no longer present.
 Areas still erythematous but without pseudomembrane
 Shrinkage of gingiva – expose calculus which is then
gently removed.
 Instruction same as previous visit

81. THIRD VISIT
 5 days after 2nd visit
 Patient should be symptom free
 Repeat scaling and root planing
 Discontinue hydrogen peroxide mouthwash but continue CHX
mouthwash
 Patient instructed in plaque control procedures
 Councelling on nutrition, habits

82. SUBSEQUENT VISITS
 Tooth surfaces in the involved areas are scaled.
 Plaque control is checked and corrected if required.
 Patient should now be scheduled for treatment of chronic
disease.

83. GINGIVAL CHANGES WITH HEALING
 Removal of pseudo membrane – exposes red crater like
hemorrhagic depression.(loss of normal barrier function
of epithelium)
 Next day: Bulk and redness of crater margins reduced –
but surface shiny.(reduction in inflammation and
reepithelization)

84.  Early signs of restoration of normal gingival contour and
color. (further reduction in inflammation, reestablishment of
normal barrier function including keratinization)
 Final stage- Normal gingival contour, colour, consistency are
restored. Portions of roots exposed are covered by healthy
gingiva

85. ADDITIONAL TREATMENT CONSIDERATIONS
Countouring of gingiva as adjunctive procedure
 Shelf like margin
 Unesthetic, favours plaque retention
Systemic antibiotics/topical antimicrobials
 Only in pts with systemic complications and local adenopathy
 Drug therapy—adjunctive to local debridement

86. Supportive systemic treatment
 Copious fluid consumption
 Administration of analgesics
 Bed rest

87. Nutritional supplements
RATIONALE
 Lesions similar to NUG have been produced in animals –
with certain nutritional deficiencies
 Difficulty in chewing raw fruits and vegetables may lead
to selection of diet deficient in Vit B and C.
 Fewer recurrences – local treatment of NUG is
supplemented by Vit B or C.
 Supplements may be discontinued after two months

88. PERSISTANT OR RECURRENT CASES
 Reassessment of differential diagnosis to rule out
diseases that resemble NUG
 Underlying systemic disease causing immunosupression
(HIV)
 Inadequate local therapy (mandibular anterior area due to
pericoronal infection)
 Inadequate compliance

89.  Pericoronitis
 Abscesses of the periodontium

92. ACUTE GINGIVAL INFECTIONS-ӀӀ

93. CONTENTS
 Introduction
 Primary herpetic gingivostomatitis
 Necrotizing ulcerative gingivitis/ periodontitis (NUG)
 Pericoronitis
 Abscesses of periodontium
 Conclusion
 References

94. Pericoronitis

95.  Inflammation of the gingiva in relation to the crown of
an incompletely erupted tooth
 Mandibular third molar area

96. Acute
Subacute
Chronic

97. PATHOGENESIS
 Space- ideal area for
accumulation of food debris and
bacterial growth

98. Inflammatory
fluid and
cellular
exudate
Increase in
bulk of the
flap
Interferes with
complete
closure of
jaws or can be
traumatized by
contact with
opposing jaw
Aggrevation
of the
inflammatory
involvement

99. CLINICAL FEATURES
Chronic – no clinical signs or symptoms (chronic
inflammation and ulceration on inner surface)
Acute (trauma, occlusion, foreign body impaction)
Inflammatory involvement +systemic complications

100.  Red swollen suppurating lesion
 Tender
 Radiating pain to ear, throat, floor of mouth
 Foul taste
 Inability to close jaws
 Swelling of cheek, lymphadenitis, trismus
 Fever, leukocytosis, malaise

101. COMPLICATIONS
 Localized- pericoronal abscess
 Spread- submaxillary, posterior cervical, deep cervical
and retropharyngeal lymph nodes
 Peritonsillar abscess, cellulitis, Ludwig’s angina
Pericoronal abscess Peri-tonsillar abscess Ludwig’s angina

102. TREATMENT
Severity of inflammation
Systemic
complications
Retaining/extracting
involved tooth

103. Chronic pericoronitis
 Removal as a preventive measure
Acute pericoronitis
 Flushing area with warm water to remove debris and
exudate
 Swabbing with antiseptic after elevating the flap gently
 Occlusal adjustment

104.  Abscess drainage
 Antibiotics
 Decision to retain or extract the tooth after acute
symptoms subside

105.  Decision governed by likelihood of further eruption into
good functional position, bone loss distal to second
molars
 Extraction- Early extraction before root formation is
completed

106.  Retaining tooth- removal of pericoronal flap using
periodontal knives or electrosurgery

107. incorrect
correct
healed site
Surgical procedure to remove operculum

108. Abscesses of the
periodontium

109. DEFINITION
Periodontal abscess is defined as a lesion with expressed
periodontal breakdown occuring during a limited period
of time and with easily detectable clinical symptoms, and
localized accumulation of pus within the gingival wall of
the periodontal pocket (Hafstrom et al, 1994)

110.  Independent disease entity (AAP world workshop, 1999)
 Represents period of active tissue breakdown due to
extension of infection into intact periodontal tissues

111. CLASSIFICATION
According to location (Meng et al, 1999)
 Gingival abscess
 Periodontal abscess
 Pericoronal abscess
According to clinical signs and symptoms
 Acute abscess
 Chronic abscess

112. According to number
 Single
 Multiple (diabetes, immunosupression)
Localized periodontal abscess in pt with
poorly controlled type 2 diabetes mellitus

113. According to aetiology
A) Periodontitis related abscess
1) Exacerbation of chronic lesion
2) Post therapy periodontal abscess
a) Post scaling periodontal abscess (Dello Russo, 1985)—
calculus impaction or obstruction
b) Post surgery periodontal abscess (Garrett et al, 1997)–
foreign body reaction, incomplete removal of calculus
c) Post antibiotic periodontal abscess (no mechanical therapy,
superinfection)
Post scaling abscess

114. B) Non periodontitis related abscess
1) Impaction of foreign body in gingival sulcus
2) Root morphology alterations– invaginated root, fissured
root, external root resorption, root tears, iatrogenic
endodontic perforations

115. GINGIVAL ABSCESS
 Localized acute inflammatory lesion
that may arise from a variety of
sources such as microbial plaque
infection, trauma and foreign body
impaction
 Red, smooth, fluctuant, painful
 Marginal gingiva/interdental papilla

116. PERICORONAL ABSCESS
o Associated with
operculum of partially
erupted tooth
o Mandibular 3rd molars
most frequently affected

117. PERIODONTAL ABSCESS
 A localized purulent infection within the tissues adjacent to
the periodontal pocket that may lead to the destruction of
periodontal ligament and alveolar bone
 In patients with untreated periodontitis
 Moderate to deep pockets

118.  Acute exacerbation of chronic condition
 Incomplete calculus removal, antibiotic therapy,
periodontal surgery
 Occlusion due to deep tortuous pocket, tooth
morphology, debris, closely adapted pocket epithelium

119. ACUTE ABSCESS
 Exacerbation of chronic condition due to increase in number or
virulence of bacteria combined with lowered tissue resistance
and lack of spontaneous drainage
 Exudation
 Sensitivity to percussion
 Pain, Mobility
 Tooth elevation in socket
 Systemic involvement

120. CHRONIC ABSCESS
 Forms when spreading infection has been controlled by
spontaneous drainage, host response or therapy
 No/dull pain
 Fewer/no symptoms
 Fistulous tract
 No systemic involvement

121. Periodontal Vs. Periapical Abscess
Periapical Abscess
•Non-vital tooth
• Caries, restoration
• No pocket
• Apical radiolucency
• No or minimal mobility
• Percussion sensitivity
• Sinus tract opens via
alveolar mucosa
•Severe, diffuse pain
Periodontal Abscess
•Vital tooth
• No caries
• Pocket, bone loss
• Lateral radiolucency
• Mobility
• Percussion sensitivity variable
• Sinus tract opens via
keratinized gingiva
•Dull localized pain

122. PREVALENCE
 8-14% among all dental conditions
needing emergency treatment (Ahl et
al, 1986)
 Positively correlated with pocket depth
 High prevalence in molars- 50%
(Smith and Davies, 1986)
 3rd most frequent dental emergency

123. PATHOGENESIS AND HISTOPATHOLOGY
 Contains bacteria, bacterial products, inflammatory cells,
tissue breakdown products and serum
 Occlusion of pocket lumen, extension of infection into
soft tissues
 Entry of bacteria into soft tissue pocket wall

124.  Accumulation of leukocytes,
connective tissue destruction,
bacterial encapsulation,
formation of pus
 Central area
 Rate of tissue destruction
depends on– growth and
virulence of bacteria, Ph

125. MICROBIOLOGY
 Polymicrobial, mainly caused by endogenous bacteria
(Tabaqhali, 1988)
 Similar to flora of chronic periodontitis
 Domination by gram negative, non-motile, strict
anaerobic, rod-shaped species
 Pg

126.  Pi, Tf, Fn, spirochetes (anaerobic species)
 Bifidobacterium spp, Actinomyces spp (gram positive,
strict anaerobic)
 Aa, Capnocytophaga spp, Campylobacter spp (gram
negative, facultative anaerobic)

127. DIAGNOSIS
 Clinical signs and radiological signs
 Ovoid elevation on lateral side of root
 Fistula, suppuration
 Pain, tenderness, swelling
 Sensitivitry to percussion

128.  Mobility, tooth elevation, pocket
 Bone loss
 Systemic effects
 Use of dark field microscopy ( Trope et al, 1988)
 PET (Liu, 1996)

129. DIFFERENTIAL DIAGNOSIS
 Periapical abscess
 Lateral periapical cyst
 Vertical root fractures
 Endo-perio abscesses
 Parrish et al (1989)- 3 cases of osteomyelitis

130. TREATMENT
1) Resolving acute lesion
2) Management of the resulting chronic condition

131. ACUTE ABSCESS
 Drainage through pocket retraction or incision
 Scaling/ root planing
 Periodontal surgery
 Short term high dose adjunctive systemic antibiotics
 Tooth removal
 Avoid aggressive mechanical instrumentation in initial stage

132.  Reduce exertion
 Fluid intake
 Chlorhexidine mouthwash
 Warm saline gargles
 Analgesics/antibiotics

133. Chronic abscess
 SPT, surgery/ antibiotics
Gingival abscess
 Scaling/ root planing
 Drainage
 Removal of cause
 Warm saline gargles

134. Pericoronal abscess
 Drainage
 Irrigation to remove debris
 Warm saline gargles, antibiotics
 Analgesics
 Operculectomy/ extraction

136. COMPLICATIONS
A) Tooth loss
B) Dissemination of infection
1) Dissemination of bacteria inside the tissues during
therapy
2) Bacterial dissemination through blood stream due to
bacteriema from an untreated abscess

137.  Pulmonary actinomycosis
 Brain abscess
 Cellulitis
 Cervical necrotizing fasciitis
 Necrotizing cavernositis

138. CONCLUSION
 Acute gingival infections lead to severe discomfort and
may lead to life-threatening complications, and therefore
they need to be treated promptly
 Adequate patient education and motivation is necessary
as patients do not complete the treatment once the acute
phase has subsided

139. REFERENCES
o Newman, Takei, Klokkevold, Carranza: Carrazanza’s Clinical
Periodontology, Saunders, 10th edition.
o Acute necrotizing ulcerative gingivitis: risk factors involving
host defense mechanisms.-- Yoji, Hidemi, Atsushi:
Periodontology 2000, Vol. 6, 1994, 116-124.
o Burkitt – Textbook of oral medicine
o Shafer –Textbook of oral pathology

140. o Lindhe, Lang, Karring: Clinical Periodontology and Implant
Dentistry. Blackwell Munksgaard, 5th edition.
o The Periodontal abscess– A Review: Herrera et al, JCP 2000;
27: 377-386