explained here is the some of the gingival infections ANUG , acute herpatic gingivostomatitis and Acute pericoronitis .. Dr Harshavardhan Patwal

1. Dr Harshavardhan Patwal
ACUTE GINGIVAL
INFECTIONS

2. Contents
Introduction
Various Acute Gingival Diseases
Abscess
ANUG
Acute Herpetic gingivostomatitis
Acute Pericoronitis
Other acute gingival infections

3. INTRODUCTION
INFECTION -The lodgment and multiplication of a
parasite in or on the tissue of a host constitute infection. It
does not invariably results in disease. In fact, disease is but a
rare consequences of infection, which is a common natural
event.
Gingival disease are a diverse family of complex & distinct
pathological entities which are the result of variety of
processes.
The inflammatory response initiated in gingival disease
appears to be prerequisite for destruction of connective tissue
attachment apical to CEJ. (Page et al 1997)

4. The identification & treatment of gingival disease is important
step in preventing more serious periodontal ailments.
Acute lesions have a rapid onset & is accompanied by pain.
Acute lesions are by definition, of sudden onset, limited
duration & with well defined features in contrast with
chronic lesions.

5. ABSCESS

6. Definition:
An abscess is a cavity containing pus and surrounded by
inflammed tissue, formed as a result of a localized
infection.
The formation of pus is termed suppuration.

7. Classification: Meng 1999
It has been classified into three diagnostic groups:
Gingival abscess-
Involves the marginal gingival and interdental tissues.
Periodontal abscess-
Is an infection located contiguous to the periodontal pocket and
may result in destruction of the PDL & alveolar bone.
Pericoronal abscess-
Is associated with the crown of incompletely erupted tooth.

8. Gingival Abscess
A localized purulent infection that involves the
marginal gingiva or interdental papilla

9. Gingival Abscess
Etiology
Acute inflammatory response to foreign substances
forced into the gingiva
Clinical Features
Localized swelling of marginal gingiva or papilla
A red, smooth, shiny surface
May be painful and appear pointed
Purulent exudate may be present
No previous periodontal disease

10. Treatment
Treatment of gingival abscess is aimed at
reversal of the acute phase and removal of
the cause.
1. Topical or local anaesthesia by infiltration
is administered.
2. When possible, SRP are completed to
establish drainage and remove microbial
deposits.
3. In acute cases, the fluctuant area is incised
with a #15 scalpel blade and exudate may
be expressed by gentle digital pressure.

11. 4. Any foreign material is removed.
5. The area is irrigated with warm saline water and covered with
moist gauze under light pressure.
6. Once bleeding has stopped, patient is dismissed with
instructions to rinse with warm saline water every 2 hrs.
7. After 24 hrs, the area is reassessed, and if resolution is
sufficient, scaling not previously completed is undertaken.
8. If the lesion is large or poorly accessible, surgical access may
be required.

12. Periodontal Abscess
Definition:
• A periodontal abscess is defined as a localized purulent infection
affecting the tissues surrounding a periodontal pocket that can lead to the
destruction of supporting structures (Meng 1999).
• It is also known as a lateral abscess or parietal abscess.
• It is the third most frequent dental emergency, representing 7–14% of all
dental emergencies, and affecting 6–7‰ of all patients seen in a dental
clinic.
• It is typically found in patients with untreated periodontitis and in
association with moderate to deep periodontal pockets. (Takei HH 2002)

13. Periodontal Abscess

14. Classification
• Depending on the etiology
• Periodontitis- related abscess
• Non periodontitis- related abscess
• Depending on the course of the lesion (Galego-Feal 1995).
• Acute
• Chronic
• Depending on the number (Topoll et al. 1990).
• Single
• Multiple

15. Etiology
• The existence of deep, tortuous pockets, with cul-de-sac, which eventually
become isolated, may favour the formation of abscesses (Carranza 1990).
• The marginal closure of a periodontal pocket, may lead to an extension of the
infection into the surrounding periodontal tissues due to the pressure of the
suppuration inside the closed pocket( DeWitt. 1985).
• Fibrin secretions, leading to the local accumulation of pus may favour the
closure of the gingival margin to the tooth surface (Galego-Feal 1995).
• Changes in the composition of the microflora, bacterial virulence, or in host
defenses (Kareha 1981) could also make the pocket lumen inefficient to drain
the increased suppuration.

16. Clinical Features
Smooth, shiny swelling of the
gingiva
Painful, tender to palpation
Purulent exudate
Increased probing depth
Mobile and/or percussion sensitive
Tooth usually vital

17. Treatment
Administer Anesthesia
Establish drainage
Via sulcus is the preferred method
Surgical access for debridement
Incision and drainage
Extraction

18. Antibiotic options AAP 2004
Antibiotic of choice:
Amoxicillin, 500mg
Loading dose- 1gm
then 500mg tds for 3 days
Reevaluation after 3 days to determine the need for continued or
adjusted antibiotic therapy.
Cephalexin or clindamycin can be used if the infection is not
responding in 24 to 48 hours.

19. Penicillin allergy:-
• Clindamycin
Loading dose- 600mg
then 300mg qid for 3 days.
- Drug of choice in case of rapid local spread
• Azithromycin ( or clarithromycin)
Loading dose- 1gm
then 500mg qid for 3 days
• Metronidazole
200 - 400 mg tds 5-7 days

20. Pericoronal Abscess
A localized purulent
infection within the tissue
surrounding the crown of
a partially erupted tooth.
Most common adjacent to
mandibular third molars in
young adults; usually
caused by impaction of
debris under the soft tissue
flap

21. Pericoronal Abscess
Clinical Features
Operculum (soft tissue flap)
Localized red, swollen tissue
Area painful to touch
Tissue trauma from opposing tooth common
Purulent exudate, trismus, lymphadenopathy, fever, and
malaise may be present

22. Pericoronal Abscess
Treatment Options
Debride/irrigate under pericoronal flap
Tissue recontouring (removing tissue flap)
Extraction of involved and/or opposing tooth
Antimicrobials (local and/or systemic as needed)
Culture and sensitivity
Follow-up

23. ACUTE NECROTIZING
ULCERATIVE GINGIVITIS

24. Necrotizing ulcerative gingivitis , necrotizing periodontitis,
necrotizing stomatitis are the most severe inflammatory
periodontal disorders caused by plaque bacteria.
They are rapidly destructive & debilitating & represents
various stages of same disease process (Horing & Cohen
1995).
They are also referred to as ulceromembraneous gingivitis,
necrotizing gingivostomatitis, vincent’s gingivostomatitis,&
trench mouth( Pickard 1973, Johnson & Engle 1986, Horing
& Cohen 1995).
It is characterized by death & sloughing of gingival tissue &
presents with characteristics signs & symptoms.

25. EPIDEMIOLOGY & PREVALENCE
NUG often occurs in groups in an epidemic form.
During world war I & II “ epidemics “ broke out among the allied
troops. Epidemic like outbreaks have also occurred among civilian
populations.
In developing countries, the prevalence of NPD is higher than in the
industrialized countries, & the disease frequently affects the
children.
In India, 54- 64 % of NPD cases occurred in children below 10 yrs
of age.( Migliani& Sharma 1965; Pindborg et al 1996).
NUG occurs at all ages, with the highest incidence reported between
ages 20 & 30 yrs & ages 15 -20 yrs.

26. The disease seems to occur slightly more among HIV infected
individuals. Studies among groups of HIV infected individuals
have revealed prevalence of NPD between 0 & 27.7%.
(Reichart et al 2003).
NP was found in 1% of 200 HIV seropositive individuals
(Riley et al 1992) & the prevalence may not in fact, differ from
much of the general population ( Drinkard et al 1991 );This is
particularly true after introduction of antiretroviral therapy.

27. ETIOLOGY
It includes,
 Role of microorganism
 Role of host response
 Predisposing factors includes
1. Local predisposing factor
2. Systemic predisposing factor

28. ROLE OF BACTERIA
Plaut & Vincent introduced the concept that NUG is caused by
specific bacteria ; fusiform bacillus & spirochetal organism.
Loesche et al described a predominant constant flora & a variable
flora associated with NUG. The constant flora is composed of
prevotella intermedia, treponema sp, selenomonas sp, &
fusobacterium sp. The variable flora consists of heterogeneous
array of bacterial types.
The bacteriologic findings have been supported by immunologic
data from Chung et al. - reported increased antibody titers for
spirochetes & P.intermedia in NUG patients compared with titers in
those with chronic gingivitis & healthy controls.

29. Borrelia, gram positive cocci, b-hemolytic streptococci &
Candida albicans have been isolated from the lesions of HIV
associated NUP.(Reichart & Schiodt 1989).
It has also been proposed that human cytomegalovirus may
play a role in the pathogenesis of NPD. (Sabiston 1986).

30. Pathogenic potential of microorganism
An important aspects in the pathogenesis of periodontitis is the
capacity of the microorganism to invade the host tissues.
Among the bacteria isolated from necrotizing lesions, spirochetes &
fusobacterium can in fact invade the epithelium. (Heylings 1967).
The spirochetes can also invade the vital connective tissue
(Lisgarten 1965).
The pathogenic potential is further substantiated by the fact that both
fusobacterium & spirochetes can liberate endotoxins
(Kristoffersen et al).

31. Gram negative bacteria liberate endotoxins in close contact with
connective tissue. Endotoxins may produce tissue destruction both
by direct toxic effects & indirectly by activating & modifying
tissue responses of the host.(Wilton & Lehner 1980)
Through a direct effect, endotoxins may lead to damage of cells &
vessels. Necrosis is a prominent feature so-called Schwartzman
reaction which is caused by endotoxins.
Indirectly endotoxins contribute to tissue damage in several ways;
They can function as antigens & elicit immune reactions.
They can activate compliment directly through the alternative
pathway & thereby liberate chemotoxins.

32. They can also activate macrophages, T & B lymphocytes &
influence the host immune reactions by interfering with
cytokines produced by these cells.
Studies have shown that endotoxins can stimulate catabolic
processes with degradation of both connective tissue & bone
induced by the released cytokines.
The extent to which such reactions contribute to the host
defense or tissue damage is not yet known.

33. Fusobacterium & Spirochetes are found in moderate numbers of
other oral diseases, as well as in apparently healthy mouths suggests
that predisposing factors are essential to the development of ANUG.
The disease has never been produced experimentally in either human
beings or animals simply by oral inoculation of materials from lesion
in patients with disease. (Schwartz & Grossman).
King also attempted to produce disease in his own mouth by
inoculation of infected material but he was unsuccessful even after
traumatizing gingiva & the organism promptly disappeared.
But he did show characteristic signs of ANUG however after he
became ill with several colds, a short time later.

34. ROLE OF HOST RESPONSE
Regardless of whether specific bacteria are implicated in the
etiology of NUG, the presence of these organism is insufficient
to cause the disease.
The role of an impaired host response in NUG has long been
recognized.
It is particularly evident for HIV-infected patients that the
disease is associated with diminished host resistance; among
other predisposing factors, the basic mechanism may include
altered host immunity.
Changes in leukocyte function & the immune system have been
observed.(Johnson & Engle et al)

35. NUG is not found in well nourished individuals with a fully
functional immune system. All the predisposing factor for NUG
is associated with immunosuppresion.
Cohen et al described a depression in host defense mechanism
particularly in PMN.
Total leukocyte count have been found to be similar for patients
& controls. Patients with NG shows marked depression in
polymorphonuclear leukocyte chemotaxis & phagocytosis as
compared with control individuals.
Reduced proliferation of peripheral blood lymphocytes has also
been found in those patients.
It was also suggested that elevated levels of blood steroids may
account for the reduced chemotactic & phagocytic responses.

36. LOCAL PREDISPOSING FACTORS
It includes poor oral hygiene, preexisting gingivitis , injury to
gingiva, & smoking
It may also occur in disease free mouth, it most often occurs
superimposed on preexisting chronic gingival disease &
periodontal pockets.
Areas of gingiva traumatized by opposing teeth in malocclusion –
may predispose to NUG.
Pindborg et al – 98% of his patients with NUG were smokers &
that the frequency of disease increases with an increase exposure
to smoke.

37. Systemic predisposing factors
It includes
nutritional deficiency (malnutrition),
debilitating diseases,
fatigue caused by chronic sleep deficiency,
psychological stress,
immunodeficiency,
other health habits like alcohol & drug abuse.

38. MALNUTRITION
Malnutrition results in lowered tissue resistance - most common
public health problem affecting children who are most often
affected by NPD. (Enwonwu 1985, 1994).
In response to periodontal pathogens phagocytes elaborate
destructive oxidants, proteinases & other factors.
Periodontal damage may often occur as a result of the balance
between these two factors, antioxidants & host derived anti
proteinases.

39. Malnutrition is characterized by marked tissue depletion of the
key antioxidant nutrients, & impaired acute phase reactions to
the infections. This is due to impairment in the production &
cellular action of cytokines.
Malnutrition – defective mucosal integrity, hormonal
imbalance.
Malnutrition usually involves concomitant deficiencies of
several essential macro & micronutrients, & therefore has the
potential to adversely influence the prognosis of periodontal
infections. (Enwonwu 1994).
It also accentuates the severity of the pathologic changes when
fusospirocheal complex is injected to the animals.
(Smith DT et al)

40. Debilitating disease
Debilitating systemic disease may predispose the patient to the
development of NUG.
It includes chronic disease ( eg. Syphilis, cancer), severe
gastrointestinal disorders such as ulcerative colitis, blood
dyscracias (anemia , leukemia) & acquired immunodeficiency
syndrome.
Nutritional deficiency resulting from debilitating disease may be
an additional pre disposing factor.
Ulceronecrotic lesions appear in the gingival margins of hamsters
exposed to total body irradiation.(Mayo J et al)

41. PSYCOSOMATIC FACTORS
Psychological factors appear to be important in the etiology of
NUG.
The disease often occur with association with stressful situation
(Induction in to armed forces, examination periods, emotional disorders, patients
feeling inadequate at handling life situations).
Cohen – Cole et al – psychiatric disturbance and the impact of
negative life events may lead to activation of hypothalamic-
pituitary adrenal axis resulting in elevation of cortisol levels.
This may reduce gingival microcirculation & salivary flow &
enhance nutrition to prevotella intermedia, but also depresses
neutrophil & lymphocyte functions which facilitate bacterial
invasion & damage.(Johnson et al)

42. Significant correlation between the disease incidence & two
personality traits – dominance & abasement – suggests the
presence of an ANUG prone personality.(Formicola AJ et al).
The mechanisms whereby psychological factors create or
predispose to gingival damage have not been established, but
alterations in digital & gingival capillary response suggestive
of increased autonomic nervous activity have been
demonstrated in patients with ANUG.

43. Smoking
The relationship between tobacco usage & NPD appears to be
complex.
Smokers in general poorer oral hygiene than the non smokers.
Smoking could lead to increased disease activity by influencing
host response & tissue reactions. As examples, smokers have
depressed numbers of T- helper lymphocytes, & tobacco smoke
can also impair chemotaxis and phagocytosis of oral & peripheral
phagocytes.( Lannan et al 1992, Selby et al 1992)
Nicotine- induced secretion of epinephrine resulting in gingival
vasoconstriction – possible mechanism by which smoking may
influence tissue susceptibility.( Bergstrom & Preber 1986)

44. HIV infection
HIV infection attacks the T- helper cells of the body, causing
drastic change in the T-helper (CD4+)/T-suppressor(CD8+) ratio
with severe impairment of the host resistance to infection.
Depleted T- helper lymphocyte counts correlate closely with the
occurrence of NG as demonstrated in the study of 390 US HIV
seropositive soldiers (Thompson et al 1992).
A complete absence of T cells in gingival tissue of HIV infected
patients with periodontitis. (Steidley et al 1992).
The lack of local immune effectors & regulatory cells in the HIV
seropositive individuals could explain the characteristic &
rapidly progressive nature of periodontitis in these patients.

45. Moreover, a protective effect has been encountered with
antiviral treatment of the HIV infection against NPD (Tappuni
& Flemming et al 2001) as well as against HIV-associated
gingivitis & periodontitis. (Masouredis et al 1992).

46. Clinical features - Oral signs
NG – an inflammatory destructive gingival condition,
characterized by punched out crater like depressions at the crest
of the interdental papillae, subsequently extending to the marginal
gingiva and rarely to the attached gingiva & oral mucosa.
The surface of the craters is covered by a gray pseudomembranous
slough, demarcated from the remainder of the gingival mucosa by
a pronounced linear erythema.
In some cases the lesions are denuded of the surface
pseudomembrane, exposing the gingival margin which is red,
shiny, & hemorrhagic. The characteristic lesion may progressively
destroy the gingiva & underlying periodontal tissues.

47. Initial punched out lesion

48. Spontaneous gingival hemorrhage or pronounced bleeding
after the slight stimulation are characteristic clinical signs.
A characteristic & pronounced foetor ex ore is often associated
with this disease & also there is increased salivation.

49. Oral symptoms
The lesion is extremely sensitive to touch, & the patient may
often complains of a constant radiating, gnawing pain that is
often intensified by eating spicy or hot foods & chewing.
There is metallic foul taste & an excessive amount of pasty
saliva.

50. Extra oral & systemic signs & symptoms
In mild & moderate stages of disease
Local lymphadenopathy & slight elevation in temperature.
In severe cases
High fever, increased pulse rate, leucocytois, loss of appetite &
general lassitude.
Systemic reactions are more severe in children.
Insomnia, constipation, gastro-intestinal disorders, headache, &
mental depression sometimes accompany the condition.
In very rare cases, severe squeal such as gangrenous stomatitis
& noma have been described.

51. Stages in the progress of NUG BY PINDBORG et al

52. Stages of oral necrotizing disease – by
Horning & Cohen
Stage 1- necrosis of the top of the interdental papilla.
Stage 2- necrosis of entire papilla
Stage 3- necrosis extending to the gingival margin.
Stage 4- necrosis extending to the attached gingiva.
Stage 5– necrosis extending to labial & buccal mucosa.
Stage 6- necrosis exposing alveolar bone.
Stage 7– necrosis perforating skin of cheek.

53. The lesion are seldom associated with deep pocket formation, -
extensive gingival necrosis coincides with rapid loss of crestal
alveolar bone.
The gingival necrosis develops rapidly & within a few days the
involved papillae is often separated into one facial & one lingual
portion with an interposed necrotic depression.
The central necrosis produces considerable tissue destruction &
regular crater is formed.
At this stage of disease, the disease process usually involves the
periodontal ligament & alveolar bone.(NECROTIZING
PERIODONTITIS)

54. Further progression of disease leads to involvement of
underlying bone resulting in sequestrum formation (necrosis
of small or large parts of alveolar bone).
Also the necrotic process progress beyond the mucogingival
junction , the condition is referred to as Necrotizing
Stomatitis.

55. Necrotizing Ulcerative Periodontitis

56. Necrotizing stomatitis
NOMA- Cancrum oris

57. HISTOPATOLOGICAL FEATURE
Histopathologically, NG lesions is characterized by ulceration
with necrosis of epithelium & superficial layers of the connective
tissue & an non specific inflammatory reaction.
The histological findings demonstrate the formation of regular
layers with certain characteristics (Lisgarten 1965) but there may
be variations in regularity.
The surface epithelium is destroyed & replaced by a meshwork of
fibrin, necrotic epithelium, PMNs & various types of
microorganism. This appears clinically as the surface
pseudomembrane.
Below this necrotic pseudomembrane, the epithelium is
edematous, & the individual cells exhibit varying degrees of
hydropic degeneration.

58. The underlying connective
tissue is extremely hyperemic
with numerous engorged
capillaries & dense infiltration
of PMNs. This acutely inflamed
zone appears clinically as the
linear erythema.
Numerous plasma cells may
appear in the periphery of the
infiltrate. This is interpreted as
an area of established chronic
gingivitis on which acute lesion
is superimposed.

59. RELATION OF BACTERIA TO THE
CHARACTERISTIC LESION
The light microscope & the electron microscope have been used
to study the relationship of bacteria to the characteristic lesion
of ANUG.
LISGARTEN described the following four zones which blend
with each other & may not all be present in every case;
Zone1 – bacterial zone
Zone 2 – neutrophil rich zone
Zone 3 – necrotic zone
Zone 4 – zone of spirochetal infiltration

60. Electron micrograph demonstrating phagocytosing (N)neutrophil close
to the surface of a sequestrum, numerous spirochetes and rods.

61. DIAGNOSIS
The diagnosis of NG, NP, NS is based on clinical findings as
described above.
The histopathology of the necrotizing disease is not
pathognomonic of NG & biopsy is not certainly indicated.
Bacterial studies are useful in the differential diagnosis of NUG
& specific infections of oral cavity.

62. Diagnostic essentials for NUG
Lesions are painful.
Lesions are gingival ulcers, punched out crater like of
interdental papilla & may involve marginal gingiva.
Non essential clinical features of NUG the
absence which does not preclude the
diagnosis of NUG
Pseudomembrane of sloughed necrotic debris & bacteria
covering the ulcerated area.
Foetor ex ore.
Fever, malaise & lymphadenopathy

63. Differential diagnosis
Herpetic gingivostomatitis
Desquamative gingivitis
Streptococcal gingivostomatitis
Apthous stomatitis
Candidiasis
Agranulocytosis
Gonococcal gingivostomatitis
Tuberculous gingival lesion

64. Important characteristics for differential
diagnosis between NPD & PHG
NPD PHG
Etiology Bacteria Herpes simplex virus
Age 15-30 Frequently children
Site Interdental papilla. Rarely outside
the gingiva
Gingiva and entire oral mucosa
Symptoms •Ulcerations and necrotic tissue
and a yellowish –white plaque
•Fetor ex ore
•Moderate Fever may occur
•Multiple vesicles which disrupt,
leaving small round fibrin covered
ulcerations
•Fetor ex ore
•Fever
Duration 1-2 days if treated 1-2weeks
Contagious - +
Immunity - Partial
Healing Destruction of periodontal tissue
remains
No permanent destruction

66. TREATMENT
The treatment of necrotizing periodontal disease is divided into
two phases,
1)acute phase treatment
2)maintenance phase treatment
ACUTE PHASE TREATMENT
The aim is to eliminate the disease activity as manifest by ongoing
tissue necrosis developing laterally & apically.
It is also to avoid pain & general discomfort which may severely
compromise food intake.

67. FIRST VISIT
General examination of the patient
The oral cavity is examined for the characteristic feature of
NUG, its distribution,& possible involvement of oropharyngeal
region.
Oral hygiene is evaluated with special attention to the presence
of pericoronal flaps, periodontal pockets & local factors.
Treatment during initial visits includes,
It is mainly confined to the acutely involved areas
After application of topical anesthetics, the pseudomembrane
& non attached surface debris is removed using a moistened
cotton pellet.

68. After the area is cleansed with warm water supragingival calculus
is removed using ultrasonic scalers.
Subgingival scaling & curettage is contraindicated at this time.
Procedures such as extractions or periodontal surgery are
postponed until the patient has been symptom free for 4 weeks, to
minimize the likelihood of exacerbating the acute symptoms.
Patients with moderate or severe NUG & local lymphadenopathy
or systemic signs or symptoms are placed on an antibiotic
regimen of amoxicillin, 500mg orally every 6 hrs for 10 days.
Other antibiotics such as erythromycin (500mg every 6 hrs) or
metronidazole (500mg twice daily for 7 days) are used.

69. Metronidazole three times daily has been found effective against
spirochetes & appears to be the first choice treatment of NPD.
(Loesche et al).
The adjunctive use of metronidazole in HIV associated NPD is
reported to be extremely effective in reducing acute pain &
promoting rapid healing.(Scully et al).
Topical application of antibiotics is not indicated in the treatment
of NPD because intralesional bacteria are frequent &topical
application does not results in sufficient intralesional
concentration of antibiotics.

70. Hydrogen peroxide & other oxygen releasing agents also have
a long standing tradition in the treatment of NPD.
Hydrogen peroxide (3%) is used for debridement in necrotic
areas & as a mouth rinse (equal portions 3% H2O2 & warm
water).
Favorable effects of hydrogen peroxide may be due to
mechanical cleaning,& the influence on anaerobic bacterial
flora of the liberated oxygen. (Macphee & Cowley 1981).
Further adjunctive local therapy of NPD showed a more rapid
clinical restitution with less periodontal destruction than in a
group without oxygen therapy. (Gaggl et al 2006)

71. Twice daily rinsing with a 0.2% chlorhexidine solution is a very
effective adjunct to reduce plaque formation, when particularly
tooth brushing is not performed. It also assists self performed oral
hygiene during the first weeks of treatment.
Appropriate treatment alleviates symptoms with in few days.(5
days)
Second visit
Systematic subgingival scaling should be continued with
increasing intensity as the symptoms subside.
Correction of restoration margins & polishing of restorations &
root surfaces should be completed after healing of ulcers.
When ulcerated areas are healed local treatment is supplemented
with oral hygiene & patient motivation.

72. Supportive systemic treatment
In addition to systemic antibiotics, supportive treatment
consists of copious fluid consumption & administration of
analgesics for relief of pain.
Bed rest is necessary for the patients with systemic
complication such as high fever, malaise, anorexia & general
debility.

73. Nutritional supplements
The rationale for the nutritional supplements in the treatment of
ANUG is based on the following;
1) lesions resembling those of the ANUG have been produced
experimentally in animals with nutritional deficiencies.
2) isolated clinical studies report fewer recurrences when local
treatment of ANUG is supplemented with vitamin B & vitamin C.
(Linghorne WJ et al)
And hence nutritional supplements may be indicated along with
local treatment to ward off deficiencies of these vitamins.

74. MAINTENANCE PHASE TREATMENT
On further visits,
When the acute phase treatment has been completed, necrosis &
acute symptoms in NPD have disappeared.
The formerly necrotic areas are healed & the gingival craters are
reduced in size, although some defects usually persists.
Bacterial plaque accumulates & therefore may predispose to
recurrences of NPD or to further destruction because of a
persisting chronic inflammatory process or both.
These sites therefore requires surgical correction.

75. Shallow craters can be removed by simple gingivectomy, while
the elimination of deep defects may require flap surgery.
Treatment of NG is not completed until all gingival defects
have been eliminated & optimal conditions for future plaque
control have been established.
Elimination of predisposing factors is also very important to
prevent recurrences.

76. Gingival changes with healing
The characteristic lesion of NUG undergoes the following changes in
the course of healing in response to treatment,
Removal of pseudomembrane exposes the underlying red
haemorrhagic crater like depression in the gingiva.
In the next stage, the bulk & redness of the crater margins are
reduced.
Followed by the early signs of restoration of normal gingival
contour & colour.
In the final stage the normal gingival consistency, surface texture,
& contour may be restored. Portion of the root exposed by the
acute disease may be covered by healthy gingiva.

77. Persistent or recurrent cases
Adequate local therapy with optimal home care will resolve most
cases of NUG. If it persists despite therapy or recurs , the patient
should be revaluated with the focus on the following factors,
Reassessment of differential diagnosis to rule out the disease that
resembles NUG.
Underlying systemic disease that cause immunosuppresion.
Inadequate local therapy.
Inadequate compliance

79. PRIMARY HERPETIC
GINGIVOSTOMATITIS

80. INTRODUCTION
Herpetic gingivostomatitis is acute infection that can involve the
gingiva, other oral tissues, the lips, & occasionally the face
circumorally.
Primary infection with herpes virus leads to acute herpetic
gingivostomatitis. The primary attack is believed to confer
immunity.
It is caused by herpes simplex virus type-1 (HSV-1). It occurs
most often in the children younger than 6 years of age, but it is
also seen in adolescents & adults.
It occurs with equal frequency in male & female patients. In most
patients, the primary infection is asymptomatic.

81. HERPES SIMPLEX VIRUS
Herpes simplex Virus is a DNA virus & is a member of the human
herpes virus family (HHV) family known as herpetoviridae.
TYPES
 Type 1 – HSV 1 or HHV 2
 Type 2 – HSV 2 or HHV 2
Other members of HHV family includes
 Varicella zoster virus ( HHV 3)
 Epstein barr virus ( HHV 4)
 Cytomegalo virus ( HHV 5)
 Others – HHV 6, HHV 7, HHV 8

82. Humans are the only natural reservoirs and all the HHVs have
the ability to reside for life within the infected host.
After the initial infection variable periods of latency &
reactivation with viral shedding are seen.
The two types of HSV are structurally similar structurally but
different antigenically.
HSV -1 is spread predominantly through infected saliva or
active perioral lesions. HSV-1 - responsible for oral, facial,
and ocular lesions.

83. Clinically evident infections with HSV -1 exhibit two patterns.
The initial exposure to an individual without antibodies to the
virus is called the primary infection.
Occurs at an young age & often is asymptomatic.
The virus is then taken up by the sensory nerves & transported to
the associated sensory or less frequently, the autonomic ganglia.
With oral HSV 1 infection the trigeminal ganglion is colonized
and the virus remains at this site in a latent state.
The viruses uses the axons of the sensory neurons to travel back &
froth to the peripheral skin or mucosa.

84. SECONDARY , RECURRENT OR RECRUDESENT HSV 1
INFECTION occurs with reactivation of the virus although
many patients may show only asymptomatic viral shedding in
the saliva.
Symptomatic recurrences are fairly common & affect the
epithelium fairly supplied by the sensory ganglion.
Spread to an uninfected host can occur easily during periods of
asymptomatic viral shedding or from symptomatic active
lesions.
Numerous conditions such as old age, ultraviolet light,
emotional stress, pregnancy, allergy, trauma, respiratory
illness, systemic disease or malignancy are associated with
reactivation of virus.

85. Recurrent Oral Herpes

86. HSV does not survive in the external environment & almost all
the primary infections occur from contact with an infected
person who is releasing the virus.
The usual incubation period is 3 to 9 days.
HSV -1 is acquired from contact with contaminated saliva or
active perioral lesions, poor hygiene promote exposure.

87. CLINICAL FEATURES

88. Most cases of acute herpetic gingivostomatitis arise between the
ages of 6 months & 5 years.
The onset is abrupt & accompanied by anterior cervical
lymphadenopathy, fever, anorexia, irritability, and sore mouth
lesions.
Initially the affected mucosa develops numerous pinhead vesicles,
which rapidly collapse to form numerous small red lesions.
These initial lesions enlarge slightly & develop central areas of
ulceration which are covered by yellow fibrin.
Both the movable & attached oral mucosa can be affected,& the
number of lesions is highly variable.
In all the cases the gingiva is enlarged, painful, & extremely
erythematous.

90. In addition the affected gingiva often exhibits distinctive punched
out erosions along the mid facial free gingival margins.
An important diagnostic criteria in this disease is the appearance
of a generalized acute marginal gingivitis. The entire gingiva is
edematous & inflamed. Several small gingival ulcers are also
present.
There is inflammation in the posterior pharynx & the
submandibular & cervical lymph nodes are enlarged & tender.
Satellite vesicles of the perioral skin are fairly common.
Mild cases usually resolve within 5 to 7 days; severe cases may
extend to 2 weeks.

91. Primary HSV in other wise healthy children is a self limiting
disease.
The fever ordinarily disappears within 3 or 4 days & the lesion
begin healing in a week to 10 days, although to continue to be
present in the saliva for up to a 10 month after the onset of
disease.

92. Secondary herpes labialis
A patient who has suffered an attack of HGS carries humoral &
possibly cellular antibodies throughout life.
After infection has taken place some virus survives in a latent stage
in the nerve ganglion & may on provocation produce a recurrence.
(secondary herpes labialis, fever blister, cold sore)
The fever blister is a single vesicle or a group of vesicles on the
vermilion border of the lip before an eruption occurs there is often a
prodromal period of burning & tingling in the area.
The blisters break after a few days & form a crust. The lesion heals
after about 2 weeks.

93. Recurrent herpes labialis & recurrent intraoral herpes

94. Recurrences can also affect the oral mucosa. In the
immunocompetent patient, involvement is almost always
limited to keratinized mucosa, which is bound to bone
(attached gingiva and hard palate).
The lesion begins as 1 to 3 mm vesicles, which rapidly collapse
to form a cluster of erythematous macules.
The damaged epithelium is lost & a central area of ulceration
develops. Healing takes place within 7 to 10 days.

95. TRANSFER OF INFECTIONS
Transfer of the herpes virus may be by direct contact or by
contact with contaminated materials or surfaces.
The dental professional is at risk & an infection occasionally
affects on the hand or finger ( HERPETIC WHITLOW). From
such sites the virus may be transferred to the patients.
Each infected individual serves as a permanent carrier who is
intermittently infectious.

97. HISTOPATHOLOGICAL FEATURE
The virus exerts its main effects on
the epithelial cells. infected epithelial
cells exhibits acantholysis , nuclear
clearing,& nuclear enlargement –
ballooning degeneration.
The acantholytic epithelial cells are
termed as TZANCK CELLS. There is
presence of intranuclear inclusion
bodies – lipschutz bodies.
Nucleolar fragmentation occurs with
the condensation of chromatin around
the periphery of the nucleus. -peri
inclusion halo.

98. Intracellular edema leads
to the development of
intraepithelial vesicles.
The vesicle ruptures & the
mucosal lesion
demonstrate a surface
fibrinopurulent membrane.
There is secondary
infiltration by
inflammatory cells in
subadjacent connective
tissue.

99. DIAGNOSIS
Patients are easily diagnosed - who present with atypical clinical
picture of generalized symptoms followed by an eruption of oral
vesicles, round shallow symmetrical oral ulcers & acute
marginal gingivitis & who do not have a history of recurrent
herpes.
Materials may be obtained from the lesions & submitted to the
laboratory for confirmatory tests, including virus culture and
immunologic tests using monoclonal antibodies or DNA
hybridization techniques.

100. Most commonly used diagnostic procedures - cytological
smear & tissue biopsy
Serological tests for HSV antibodies are positive 4 to 8 days
after initial exposure.
These antibody titers are useful in documenting past exposure
& are used primarily in epidemiologic studies.

101. DIFFERENTIAL DIAGNOSIS
It includes
Necrotizing ulcerative gingivitis
Erythema multiformae
Stevens – Johnson syndrome
Bullous lichen planus
Desquamative gingivitis
Lesions of recurrent aphthous stomatitis

103. TREATMENT
Treatment of primary HSV infection is usually palliative. Milder
cases can be managed by supportive care only, since primary
HSV in otherwise healthy individuals is a self limiting disease.
It is important to instruct patient to avoid contact with active
lesions to prevent the spread to other sites and people.
Systemic use of systemic antiviral drugs is indicated in severe
cases of primary HSV , recurrent disease & in
immunocompromised patients.

104. ANTIVIRAL THERAPY
Amir et al demonstrated that antiviral therapy with 15mg/kg of an
acyclovir suspension given five times daily for 7 days substantially
changes the course of disease without significant side effects.
Acyclovir has shown to decrease symptoms of primary HSV infection
in children, including days of fever & viral shedding.
Newer antiherpes drugs are available, including valacyclovir &
famciclovir. The newer drugs have increased bioavailability allowing
effective treatment with fewer daily doses.
Recommended doses
Acyclovir – 200mg 5 times daily for 10 days.
Valacyclovir – 100mg 2 times daily for 10 days.

105. Studies comparing topical antiviral medications for treating recurrent
herpes labialis have been published.
Topical pencyclovir reduces the duration & pain of RHL by 1 to 2 days.
Acyclovir as well as N –Docosanol cream also available for topical use.
Topical acyclovir has been reported to decrease duration of RHL lesions
by 12 hrs & found to be more effective than N-docosanol in treating
RHL.
Immunosuppressed patients with HSV infection respond well to acyclovir
administered orally or intravenously.
Foscarnet, another antiviral drug has been effective therapy for these
patients.

106. PERICORONITIS

107. INTRODUCTION
A healthy ,fully erupted tooth is surrounded by a gingival tissue that
typically extends not more than 2 to 3mm coronally.
For a variety of anatomical reasons- partial eruption, malposition,
the immediate proximity of the ramus – the crowns of the third
molars & occasionally other teeth may covered with gingiva &
sometimes mucosa.
The potential space between the crown & the soft tissue is of
considerable depth & volume.
A diverse & extensive microflora colonizes these pockets &
gingival inflammation is almost always present.

108. These sites may acutely infected & may produce symptoms
then they are defined as Pericoronitis.
It was first described by GUNNELL in1844.
It is defined as “ an inflammatory condition of the gingiva &
other supporting tissues that surround the crown of an
incompletely or completely erupted tooth, especially distal
tooth in the arch.( kay 1966)
It is an inflammation of gingiva & contiguous tissues about
crown of an incompletely erupted tooth. (Orban)

109. Common sites of involvement
In decreasing order of frequency
Mandibular third molars
Mandibular second molars
Mandibular first molars
Maxillary third molars.

110. RISK FACTORS
LOCAL FACTORS includes
Impacted third molars, more with vertical & distoagular
impactions (taehan, chikkwa, uesa)
Third molars favoring deep distal or distobuccal pocket
formation.
Opposing teeth impinging on operculum.
Poor oral hygiene
SYSTEMIC FACTORS includes
Upper respiratory tract infections
Tonsillitis
Emotional stress
Smoking
General debilitating disease
Chronic fatigue

111. AETIOPATHOGENESIS
MULTIFACTORIAL .it includes
Incomplete eruption due to anatomical limitation.
Food impaction & poor oral hygiene.
Oral microbiota

112. The occlusal surface of an involved tooth may be partly
covered by a flap of tissue, the operculum, which exists during
the eruption of the tooth & may persist afterward.
The operculum is ideal area for accumulation of food debris
and bacterial growth, since the performance of adequate oral
hygiene in this area is difficult.
It is more vulnerable for irritation & is often directly
traumatized when it is caught between the crown that it covers
& the antagonist tooth during closure.
These factors predisposes to acute infection of the pericoronal
tissue.

113. RISK PREDICTORS OF PREICORONITIS
 Based on the criteria;
- Vertical or distal tipping of third molars
- Follicular space more than 3mm, the incidence of
getting pericoronitis is 44 times more.
(ANDREASON)

114. MICROBIOLOGICAL ETIOLOGY
Organism implicated includes
Streptococcus viridans
Spirochetes & fusobacteria
Staphylococcus
Prevotella sp.
Bacteriodes
capnocytophaga

115. CLINICAL FEATURES
Based on the duration , pericoronitis may be
Acute
Sub- acute
Chronic
Also there is an acute exacerbation in chronically inflamed
pericoronal tissue.

116. Acute pericoronitis
 It is identified by varying degrees of inflammatory involvement
of the pericoronal flap & adjacent structures as well as by
systemic complications.
The inflammatory fluid & cellular exudate increases the bulk of
the flap, which may interferes with complete closure of the jaw &
traumatized by contact with the opposing jaw.
There is red, swollen, suppurating lesion that is tender, with
severe throbbing intermittent pain, exaggerated by chewing &
interfering with sleep.
Pain radiates to ear, throat & floor of mouth.
Foul taste, halitosis, & inability to close the mouth.

117. Swelling of the cheek in the angle of the jaw & lymphadenitis
are common.
Systemic complications includes, fever, malaise, leucocytois ,
increased pulse & respiratory rate.
Submandibular lymph nodes may be enlarged & tender on
palpation.

118. Sub acute stage
Continuous dull ache, radiates infrequently
Stiffness of jaws, intraoral swelling, unpleasant taste.
Causes less systemic upset
Trismus might be present
Chronic stage
Dull pain or mild discomfort lasting for only a day or so,
interspersed with remissions lasting for several months.
Unpleasant taste

119. DIAGNOSIS
Can be made by
Careful history taking
Clinical examination
Radiographic examination.

120. TREATMENT
 Treatment of pericoronitis focuses on infection control.
 It depends on initial assessment of two issues.
1. The severity of infection & the extent to which it has
disseminated from the primary site.
2. The relative importance of the affected tooth & whether the
pericoronal tissue can be returned to & maintained in healthy
state.

121. Well localized mild to moderate pericoronitis affecting a tooth that is
to be retained is managed conservatively.
Consists of debridement & drainage of the pocket by gentle
curettage & external pressure.
During & after curettage the pocket should be irrigated with sterile
saline solution. Irrigation can also be done with antimicrobial
solution such as 10%providone iodine.
In case of fluctuant abscess drainage should be accomplished by
incision.
The patient should be instructed to rinse the area with warm water or
saline solution at frequent intervals until symptoms subside.
Post treatment monitoring is necessary to ensure the resolution of the
acute phase.

122. When signs & symptoms have regressed the need for
corrective surgery should be considered.
Resection of some or all pericoronal tissue (operculectomy)
depending on tooth position in the jaw & soft tissue
relationships, reduces the chances of recurrent infection.
Operculectomy – surgical removal of operculum. It can be
done using hand instruments, or electrosurgery or LASER.

123. Operculectomy – using hand instruments

124. Operculectomy using electrosurgical
scalpel or radiosurgical loop.

125. If an opposing third molar is hyper erupted or will require
removal in the near future & is in contact with the inflamed
tissue over the third molar, it can be removed to help decrease
pain & hasten recovery from pericoronitis.
If the affected tooth is non functional or considered
unsalvageable because of malposition or other reasons
extraction is usually appropriate.
If pericoronitis is localized with no evidence of abscess,
extraction may be proceeded or delayed until the acute
inflammation is subsided.

126. If pus is present , the drainage should be accomplished &
resolution of acute phase before elective extraction.
If immediate extraction is necessary, perioperative and
systemic antimicrobial therapy is used.
Most severe pericoronitis with evidence of regional
dissemination should be treated as described previously. In
addition, antimicrobial chemotherapy should be started
immediately.
Close monitoring of the outcomes is necessary. Extraction
should be postponed until the infection shows definite signs of
localization or has completely resolved.

127. ANTIMICROBIALS- IN TREATMENT OF
PERICORONITIS
Commonly used antibiotics includes,
Amoxicillin 250-500mg
Metronidazole 200-400mg
Alternative drugs includes,
Ampicillin 250-500mg
Erythromycin 250-500mg
Tetracycline 250-500mg
Doxycyline 200mg once daily for the first day followed by
100mg twice daily

128. SEQULAE
The involvement may be localized in the form of a pericoronal
abscess.
It may spread posteriorly into oropharngeal area & medially to
the base of the tongue, making it difficult for the patient to
swallow.
Depending on the severity & extent of the infection there is
involvement of submaxillary, posterior cervical, & the
retropharyngeal lymph nodes.
Untreated pericoronitis may develop into ANUG. Since
pericoronal flaps are one of the primary incubation zones.

129. COMPLICATIONS
LOCALIZED
Cyst formation (craig)
Sinus & fistula formation
Root resorption of second molar (kielley & kay)
LOCAL
Migratory abscess of buccal sulcus
Buccal space infection
Peritonsillar abscess
Retropharyngeal & submandibular space infection.

130. SERIOUS LIFE- THREATENING COMPLICATION
Ludwig’s angina
Acute meningitis
Cavernous sinus thrombosis
These complications are infrequent but potent squeal of acute
pericoronitis.

131. Other acute infections of bacterial
origin- in gingiva
It includes,
Infection with Neisseria gonorrhea (Scully et al 1995)
Treponema pallidum ( Ramirez –Amador et al 1996)
Streptococci, mycobacterium chelonae (Pedersson et
al 1989) or other micro organism.

132. CLINICAL FEATURES
STREPTOCOCCAL GINGIVOSTOMATITIS
It is a rare condition characterized by a diffuse erythema of the
posterior areas of the oral mucosa, sometimes including the gingiva.
Necrosis of the gingival margin is not seen & also there is no
notably fetid odor.

133. GONOCOCCAL STOMATITIS
The oral mucosa is covered with a grayish membrane that
sloughs off in areas to expose an underlying bleeding area.
It is most common in newborns & is caused by transmission of
infection from the maternal passages & in adults it results from
direct contact.

134. Biopsy supplemented by microbiologic examination reveals
the background of the lesions.
Once diagnosed, it is then treated with appropriate
antimicrobials & by conventional means.

135. REFERENCES
 CARRANZA’S CLINICAL PERIODONTOLOGTY
 CLINICALPERIODONTOLOGY & IMPLANT DENTISTRY –JAN LINDHE
 PERIODONTAL & GINGIVAL HEALTH & DISEASE
 DECISION MAKING IN PERIODONTOLOGY - WALTER B. HALL
 PERIODONTICS – GRANT
 PERIODONTICS- ROSE & MALLEY
 ORAL & MAXILLOFACIAL PATHOLOGY – ALLEN
 TEXT BOOK OF ORAL PATHOLOGY - SHAFER
 BURKET’S ORAL MEDICINE
 ORAL & MAXILLOFACIAL INFECTIONS – TOPAZIAN.
 ORAL & MAXILLOFACIAL SURGERY – HARRY ARCHER

136.  OUTLINE OF PERIODONTICS – MANSON & ELLEY
 PERIODONTOLOGY 2OOO – 2002 VOL 30.
 THE DENTAL CLINICS OF NORTH AMERICA – 2005 – 49, 15-29.
 THE PERIODONTAL ABSCESS: A REVIEW HERRERA D, ROLDA´N S, SANZ
M: JOURNAL OF CLINICAL PERIODONTOLOGY2000
 PERIODONTAL ABSCESS: HUAN XIN MENG : ANNALS OF
PERIODONTOLOGY 1999
 DIAGNOSIS OF ACUTE PERIODONTAL LESIONS ESMONDE F CORBETT
2004 PERIODONTOLGY 2000

137. Thank YOU