gingival diseases in acute conditions Acute necrotizing ulcerative

1. ACUTE GINGIVAL CONDITIONS
Dr / Alzahraa A. Alghriany

2. ACUTE GINGIVAL INFECTIONS
1. Necrotizing Gingivitis.
2. Primary Herpetic Gingivostomatitis .
3. Pericoronitis.
4. Abscess.
5. Thermal, electrical and chemical
Gingivostomatitis.

3. Necrotizing Periodontal Diseases in the new
classifiation (2017)
a. Necrotizing Gingivitis
b. Necrotizing Periodontitis
c. Necrotizing Stomatitis.
-Term ‘Necrotizing Stomatitis’ has been introduced.
(It is caused by extension of necrosis beyond the
mucogingival junction).
- Term ulceration has been retracted from
classification as it is considered secondary to
necrosis.

4. 1.NECROTIZING GINGIVITIS:
Def:
-Necrotizing gingivitis (NG) previously referred to
as necrotizing ulcerative gingivitis (NUG) is a
microbial disease of the gingiva in the context of
an impaired host response.
-Necrotizing gingivitis (NG) results from an
impaired host response to a potentially pathogenic
microbe.
-It is characterized by the necrosis and sloughing
of gingival tissue, and it presents with
characteristic signs and symptoms.

5. Necrotizing gingivitis has been called many
names:
- Trench mouth
- Vincent’s Stomatitis
- Vincent’s Infection
- Fusospirochetal Gingivitis
- Acute Ulcerative Gingivitis
- Necrotizing Gingiviti

6. ETIOLOGY
It includes,
- Role of microorganism
- Role of host response
- Predisposing factors includes:
1. Local predisposing factor
2. Systemic predisposing factor

7. 1. ROLE OF BACTERIA.
-Plaut in 1894 and Vincent in 1896 postulated that NUG was
caused by specific bacteria: fusiform bacillus and a
spirochetal organism.
-In the etiology of NUG, the presence of these organisms
insufficient to cause the disease, this because.
1. The fusiform–spirochete flora is frequently found in
patients who do not have NUG.
2. NUG was associated with physical and emotional stress .
3. NUG is not found in well-nourished individuals with a fully
functional immune system. All of the predisposing factors for
NUG are associated with immunosuppression particularly in
PMN chemotaxis and phagocytosis.

8. 2. ROLE OF THE HOST RESPONSE.
• Immunodeficiency may be related to
1. Nutritional deficiency,
2. Fatigue caused by chronic sleep deprivation,
3. Health habits (e.g., alcohol or drug abuse),
4. Psychosocial factors, or systemic disease.
5. NG may be the presenting symptom for
patients with immunosuppression related to
HIV infection.

9. 3. LOCAL PREDISPOSING FACTORS.
• Preexisting gingivitis, injury to the gingiva, and
smoking are important predisposing factors.
• Deep periodontal pockets and pericoronal flaps are
particularly vulnerable areas, because they offer a
favorable environment for the proliferation of anaerobic
fusiform bacilli and spirochetes.
• Areas of the gingiva that are traumatized by opposing
teeth in malocclusion (e.g., the palatal surface behind
the maxillary incisors, the labial gingival surface of the
mandibular incisors) may predispose an individual to
the development of NUG.

10. 4.SYSTEMIC PREDISPOSING FACTORS
It includes:
-nutritional deficiency (malnutrition):
 A poor diet has been cited as a predisposing factor for NUG and its
sequelae in developing African countries, although the effects appear
primarily to diminish the effectiveness of the immune response.
 Nutritional deficiencies (e.g., vitamin C, vitamin B2) accentuate the
severity of the pathologic changes
-debilitating diseases:
Such systemic disturbances include,
 1. Chronic diseases (e.g., syphilis, cancer),
 2. Gastrointestinal disorders (e.g., ulcerative colitis),
 3. Blood diseases (e.g., leukemia, anemia),
 4. Acquired immunodeficiency syndrome.

11. -fatigue caused by chronic sleep deficiency,
-psychological stress,
 The disease often occurs in association with stressful situations (e.g., induction
into the armed forces, school examinations).
 Psychologic disturbances as well as increased adrenocortical secretion are also
common in patients with the disease.
 activation of hypothalamicpituitary adrenal axis resulting in elevation of cortisol
levels.
 This may reduce gingival microcirculation & salivary flow &enhance nutrition to
the bacteria, but also depresses neutrophil & lymphocyte functions which
facilitate bacterial invasion & damage.
-immunodeficiency,
 The lack of local immune effectors T cells & regulatory cells in the HIV
seropositive individuals could explain the characteristic & rapidly progressive
nature of periodontitis in these patients.
-other health habits like alcohol & drug abuse.

12. CLINICAL FEATURES
-The lesion appears as a non-specific acute inflammatory process of rapid
onset.
- Pain, ulceration and necrosis of the interdental papillae (punched out
crater like ulcer) covered by a slough or pseudomembrane.
- Bleeding, either spontaneous or to gentle manipulation.
- Foul metallic odor, bad metallic taste, increased salivation and regional
lymphadenopathy.
- The lesion starts at the tip of interdental papilla, extends to the marginal
gingival leading to punched out papilla.
- Later the attached gingival is affected and bone is exposed.
-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.

13. 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.

14. -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)

15. -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.

16. 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.
(NOMA- Cancrum oris)

17. MICROSCOPICALLY
- Ulceration of the gingival epithelium with
necrosis of C.T
-The pseudomembrane contains:
- dead epithelial cells,
- inflammatory cells,
- a fibrin meshwork
- various microorganisms.

18. -The light microscope & the electron microscope
have been used to study the relationship of
bacteria to the characteristic lesion of NG.
-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

19. DIAGNOSIS
-Diagnosis is based on.
1. Clinical findings of gingival pain, ulceration,
and bleeding.
2. Past medical history.
3. A bacterial smear is not necessary or
definitive But are useful for the differential
diagnosis of NUG and specific infections of the
oral cavity (e.g., diphtheria, thrush,
actinomycosis, streptococcal stomatitis).

20. DIFFERENTIAL DIAGNOSIS
- Acute herpetic gingivostomatitis
- Streptococcal gingivitis
- Agranulocytosis
- Diphtheria

21. 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.

22. 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.

23. -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.

24. -Other antibiotics such as erythromycin (500mg every 6 hrs) or
metronidazole (500mg twice daily for 7 days) are used.
-Metronidazole three times daily has been found effective
against spirochetes & appears to be the first choice treatment
of NPD.
-Hydrogen peroxide (3%) is used for debridement in necrotic
areas & as a mouth rinse (equal portions 3% H2O2 & warm
water).
-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.

25. SECOND VISIT
-1 to 2 days later, the patient’s condition is usually improved;
pain diminished or no longer present.
-The gingival margins of the involved areas are erythematous,
but without a superficial pseudomembrane.
-Scaling is performed if necessary and sensitivity permits.
Shrinkage of the gingiva may expose previously covered
calculus, which is gently removed.
-The instructions to the patient are the same as those given
previously.

26. THIRD VISIT:
• 2 to 4 days after the second visit, patient should be
essentially symptom free.
• Scaling and root planing repeated.
• Instructed in plaque control procedures.
• H2O2 rinses discontinued; chlorhexidene rinses maintained
for 2-3 weeks.

27. 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.
-Elimination of predisposing factors is also very important to prevent
recurrences.
-Nutritional supplements may be indicated along with local treatment
to ward off deficiencies of these vitamins.

28. 2-PRIMARY HERPETIC
GINGIVOSTOMATITIS
Def.
• Primary herpetic gingivostomatitis is an infection of the
oral cavity caused by herpes simplex virus (HSV) type 1.
• It occurs most often among infants and children who are
less than 6 years old, but it is also seen in adolescents
and adults.
• It transmitted by droplet infection
• The incubation period is 5-10 days
• It is self limiting (1-2 weeks) and heals spontaneously
without scars.

30. Clinial features:
1- The prodromal symptoms consisted of fever, pyrexia,
headaches, general malaise, mild dysphagia and regional
lymphadenopathy. (persist for days).
2- Followed by the onset of an aggressive marginal gingivitis.
3- Vesicles formation on the gingiva, tongue, palate and buccal
mucosa.
4- The vesicles rupture after a few hours to leave painful ulcer
with red inflamed margins.

31. Treatment
1- Mainly palliative including: bed rest, soft diet and
maintain fluid in take.
2- Paracetamol suspension is given for pyrexia.
3- In severe cases acyclovir suspension is given five
times daily for five days (200mg).

32. 3. PERICORONITIS
-Inflammation of the gingiva in relation to the crown of
an incompletely erupted tooth. It occurs most often in
the mandibular third molar area.
-Pericoronitis may be acute, subacute, or chronic.

33. Clinical Features:
-The partially erupted or impacted mandibular third molar is
the most common site of pericoronitis. The space between
the crown of the tooth and the overlying gingiva (operculum)
is an ideal area for the accumulation of food debris and
bacterial growth.
- Acute inflammatory involvement is a constant possibility︎ it
may be exacerbated by trauma, occlusion, or a foreign body
trapped underneath the
tissue .
- The inflammation and cellular exudate increase the bulk of
the gingiva, which then may interfere with complete closure
of the jaws and which can be traumatized by contact with the
opposing jaw, thereby aggravating the inflammatory
involvement.

34. -The resultant clinical picture is a red, swollen, suppurating
lesion that is tender, with radiating pains to the ear, the throat,
and the floor of the mouth.
- The patient is extremely uncomfortable as a result of pain, a
foul taste, and an inability to close the jaws. Swelling of the
cheek in the region of the angle of the jaw and lymphadenitis
are common findings.
- Trismus may also be a presenting complaint.
- In addition, the patient may have systemic complications such
as fever, leukocytosis, and malaise.

35. Treatment
-Procedure for relieving the pain is surgical removal of the
operculum, inject local anesthetic directly into the overlying
tissue and then cut it away using the outline of the tooth as a
guide for the incision. Sutures are not required .
- Irrigate with a weak (2%) hydrogen peroxide solution.
- Prescribe oral analgesics for comfort as well as penicillin
over the next 10 days (penicillin VK 500mg ).

36. 4-ABSCESS
GINGIVAL ABSCESS
-Localized, painful, rapidly expanding lesion with sudden
onset, limited to marginal gingival or interdental papilla.
-Purulent exudates with sensitivity of the tooth to percussion. It
ruptures spontaneously.

37. 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

38. 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.

39. 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.

40. 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.
Etiology
-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.

41. 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

42. -Treatment:
-Administer Anesthesia
-Establish drainage
Via sulcus is the preferred method
Surgical access for debridement
Incision and drainage
Extraction
-Antibiotic of choice:
Amoxicillin, 500mg Loading dose- 1gm then 500mg tds
for 3 days
Cephalexin or clindamycin can be used if the infection is
not responding in 24 to 48 hours.

43. 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.

44. Periodontal abscesses in new classification 2017:
-Term gingival abscess, pericoronal abscess are not
used as separate terms in recent classification
- Thus only︎ ‘Periodontal abscess’ term has been used.

45. 5-THERMAL, ELECTRICAL AND
CHEMICAL GINGIVOSTOMATITIS
- Eg; topical application of asprin or phenol
- Clinically: gingival inflammation with surface desquamation.
-Diagnosis is based on history of the insult.
- Treatment: palliative.