Acute gingival condition *

Dr: Shaimaa Morsy

What is the difference between acute and chronic?
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.
Primary herpetic gingivostomatitis

Necrotizing ulcerative gingivitis (NUG)

Pericoronitis

Abscesses of periodontium
 * ACUTE NECROTISING ULCERATIVE
GINGIVITIS
* Historical terminology
* Vincent’s disease
* Trench mouth
* Acute necrotizing ulcerative gingivitis (ANUG)…this
terminology changed in 2000
- VINCENT’S INFECTION
-TRENCH MOUTH arose during World
War 1 as many soldiers developed the
disease, probably because of the poor
conditions and extreme psychological
stress.
- ACUTE ULCEROMEMBRANEOUS GINGIVITIS
-PHAGEDENIC GINGIVITIS
-FUSOSPIROCHETAL GINGIVITIS
* the most severe inflammatory disorders
caused by plaque bacteria in the context
of an impaired host response.

*Noncontagious
* They are rapidly destructive and debilitating
* Characterized by necrosis and sloughing of
gingival tissues, and it presents with
characteristic signs and symptoms.
•acute inflammatory process of rapid onset.

•Ulceration & necrosis (punched out crater like

depression of IDP)
.
•Psudomembrane upon removal leave red shiny
hemorrhgic G.

•Linear erythema

•Bleeding, either spontaneous or to gentle

manipulation.

•Foul odor, bad metallic taste, increased

salivation
Extraoral and Systemic Signs and
Symptoms
*Regional lymphadenopathy
*Slight elevation of temp.
In Severe case:
* high fever
*Leukocytosis
*GI disturbance
*Tachycardia
*Loss of appetite
*Sever in children
ACCORDING TO HORNING AND COHEN:

*Stage 1 : Necrosis of tip of the interdental papilla (IDP) (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%)

 *Stage of progression

. If untreated, NUG may lead to NUP

with a progressive destruction of the
Tip of IDP then periodontium and denudation of the
extend to roots.
Extend to it does not usually lead to periodontal
marginal
gingiva cause
attached pocket formation because the necrotic
changes involve the marginal gingiva
punched out gingiva causing recession rather than pocket
formation. It is rare in edentulous
papilla mouths,
 (a) Necrosis extending into Noma or cancrum orise
buccal or labial mucosa Necrosis lead to perforation of
(b) Necrotizing stomatitis cheek skin
affecting the mandible It is often lethal and it affects mainly
of an HIV-seropositive malnourished children or otherwise
patient. Two years after compromised patients.
treatment
*
*Complex bacterial organisms but requires underlying
lowered tissue resistance induced by local or
systemic factors
*Bacterial etiology: increased bacterial count in acute
phase of disease ( spirochetes, fusiform bacilli, P.
intermedia, streptococci)
Predisposing Factors
•Local factors:
•Deep periodontal pockets and
pericoronal Flaps because they offer a
favorable environment for the
proliferation of anaerobic fusiform
bacilli and spirochetes.
•Areas of the gingiva traumatized by
opposing teeth in malocclusion, such
as the palatal surface behind the
maxillary incisors
•Smoking (nicotine stimulates
vasoconstriction of peripheral blood
vessels and decrease phagocytic
activity of leukocytes)
•Systemic factors: as altered host response:
•Systemic disease, for example ulcerative colitis,
blood dyscrasias.
•Abnormalities of white blood cell function (as in
AIDS).
•Malnutrition (Poor nutritional habits and
insufficient protein intake)
•Psycologic stress. Increase autonomic nervous
activity, Hypothalamic-pituitary-adrenal axis
activation resulting in cortisol secretion and
decrease in immune response.
*Microbiology
*The smear from the lesion reveals: Spirochetes, Fusiform bacilli,
Vibrios, Fillamentiuos organisms

*Microscopically
*The pseudomembrane contains dead epithelial cells,
inflammatory cells, a fibrin meshwork and various
microorganisms
*Diagnosis
*Based on clinical findings of pain, ulceration and bleeding.
 *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
* 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
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
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
Differential diagnosis
 *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
under topical aneathesia 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)
*Surgical procedures other than emergencies
postponed until pt is symptom free for 4 weeks
*Antibiotic regimen (amoxicillin 250 mg orally
every 6 hrs for 3-5 days) in moderate to severe
cases
*Metronidazole (250 mg 3 times daily)
*Tetracycline 250 mg 4 times daily for 4 days.
*Emergency procedures along with systemic
antibiotics
*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 tooth brushing to removal of surface debris,
ultrasoft brush, bland dentrifice
• Analgesics
• Avoid tobacco, alcohol
• Report back in 1-2 days
• Motivation
 *
*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

Third visit
*2 days after 2nd visit
*Patient should be symptom free
*Repeat scaling and root planing
*Discontinue hydrogen peroxide mouthwash and antibiotic but continue CHX
mouthwash

*Patient instructed in plaque control procedures

*Treat local predisposing factors as overhanging margin
*Treat the residual condition, The patient should be reevaluated at 1 month to
determine the potential need for reconstructive or esthetic surgery.
 *Acute herpetic
gingivostomatitis
•Due to primary infection with
Herpes simplex virus type 1
•Age: < 2years
•Prodrome: sudden with
fever, malais, cervical
lymphadenitis.
•Clinically: the entire gingival becomes intensely red, sore followed by appearance
of Discrete spherical grey vesicles which rupture to give shallow painful ulcers
covered by a grayish membrane and surrounded by red halo, heal without scar.

•It is self limiting (1-2 weeks) and heals spontaneously without scars.
•The virus ascends through the sensory or autonomic nerves and persists in the
neuronal ganglia that innervate the site as a latent HSV
 *Pericoronitits
•Inflammation of the gingival covering
the crown of partially erupted tooth
(mostly mandibular 3rd molar).
•Inflammation is due to accumulation
of food debris and bacterial growth.
•Inflammatory edema increases the
bulk of the gingival leading to more
trauma.
•Pain may radiate to the ear, throat or
floor of the mouth.
•Systemic manifestations may be
associated.
 Interferes with
complete closure Aggrevation of
Inflammatory
Increase in bulk of jaws or can the
fluid and
of the flap be traumatized inflammatory
cellular exudate
by contact with involvement
opposing jaw
 *

Chronic – no clinical signs or symptoms (chronic

inflammation and ulceration on inner surface)
* Acute (Inflammatory involvement +systemic
complications)

* 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
*
* Localized- pericoronal abscess

* Spread- submaxillary, posterior cervical, deep cervical and retropharyngeal

lymph nodes

* cellulitis, Ludwig’s angina

Pericoronal abscess Ludwig’s angina

Treatment
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
* Abscess drainage

* Antibiotics

* Decision to retain or extract the tooth after acute symptoms subside

* Retaining tooth- removal of pericoronal flap using periodontal knives or
electrosurgery
 *
*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 swelling

confined to Marginal gingiva/interdental
papilla
 *
*A localized suppurative inflammation in the
periodontal tissues
 *
*Extension of infection from a
periodontal pocket deeply into the
supporting periodontal tissues and
localization of the suppurative
inflammatory process along the lateral
aspect of the root.
*2. Lateral extension of inflammation
from the inner surface of a periodontal
pocket into the connective tissue of
the pocket wall. Formation of the
abscess results when drainage into the
pocket space is impaired.
*3. Formation in a pocket with a tortuous course around
the root. A periodontal abscess may form in the cul-de-
sac, the deep end of which is shut off from the surface.

*
*Incomplete removal of calculus during treatment of a
periodontal pocket. The gingival wall shrinks, thereby
occluding the pocket orifce, and a periodontal abscess
occurs in the sealed-off portion of the pocket.
*
5. After trauma to the tooth or with perforation of the
lateral wall of the root in endodontic therapy. In these
situations, a periodontal abscess may occur in the
absence of periodontal disease.
*Periodontal abscesses are classifed
according to location as follows:

1. Abscess in the supporting periodontal

tissues along the lateral aspect of the
root. With this condition, a sinus
generally occurs in the bone that
extends laterally from the abscess to the
external surface.

2.Abscess in the soft-tissue wall of a deep

periodontal pocket
 *
* 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
 *
* 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
*
 Periodontal Vs. Periapical Abscess
Periodontal Abscess
•Vital tooth
• No caries
• Pocket, bone loss
• Lateral radiolucency
• Mobility
• Percussion sensitivity variable
• Sinus tract opens via
keratinized gingiva
•Dull localized pain
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
 Aim

* Alleviat pain
Control spread of infection
Established a drain

Drain through pocket flat instrument

carfully introduce throuh the pocket
distending the pocket wall to establish a
drain
* Drain through an external incision
*Abcess palpated to locate the most fluctuant
area and vertical incision is made through the
most fluctuant area extending from mucogingival
fold to the marginal gingiva
* Chlorhexidine mouthwash

* Local antibiotic should be introduced

in to the lesion , the process should be
repeated every 24 hours until acute
condition subsides.

* Warm saline gargles

* Analgesics/antibiotics
* After healing of the abcess, residual
pocket should be surgically treated if
indicated after 4-6 weeks
 *
*Clinical signs and radiological signs Mobility, tooth elevation, pocket

*Ovoid elevation on lateral side of root Bone loss

*Fistula, suppuration Systemic effects

*Pain, tenderness, swelling

*Sensitivitry to percussion
 *
* Periapical abscess

* Lateral periapical cyst

* Vertical root fractures

* Endo-perio abscesses

* Parrish et al (1989)- 3 cases of osteomyelitis

*Chronic Desquamative Gingivitis

Chronic desquamative
gingivitis is characterized
by intense redness and
desquamation of the
surface epithelium of the
attached gingiva.
etiology
Dermatoses
a) Cicatricial pemphigoid
b) Pemphigus
c) Lichen Planus
d) Erythema Multiforme
e) Lupus Erythematosis
f) Linear IgA disease

2) Hormonal influence
a) Estrogen deficiency following oophorectomy & post menopausal women
b) Testosterone imbalance
c) Hypothyroidism

3) Abnormal response to irritation

4) Chronic infection
a) Tuberculosis
b) Chronic candidiasis
c) Histoplasmosis
5) Aging
6) Idiopathic
 Clinical features of
desquamative gingivitis
vary in severity
 Mild form
Moderate
form
Severe form
Mild form:
Erythema
Painless
Females - 17-23
yrs
*Moderate form:
*Patchy distribution of bright red and gray
areas involving marginal and attached
gingiva

*Smooth and shiny.

*Slight pitting with pressure
*Massaging of the gingiva with the finger
results in peeling of the epithelium and
exposure of the bleeding connective
tissue, burning sensation and sensitevity
to thermal change, Occurs in 30 and 40
years of age
* Severe form:
*

shredded
 Clinical history
Onset Acute, subacute

Chief complaint Symptoms

Intraoral
Infections
examination
LocationTopical substances

Clinical presentation
Drug intake
Extraoral
examination
Other mucosae

Skin
Cell –cell attachment,
Histopathology Internal organs
Acantholysis, epithelial
Epithelial changes thickening

Basement membrane alterations BM integrity and staining

Involved tissue DIF
Immunopathology Lamina propria Inflammatory infiltrate
Serum IIF