Prof.
Elena Firkova, PhD,
DDS
ACUTE GINGIVAL
INFECTIONS
Dept. Periodontology and
Oral Diseases
FDM
Diseases of short duration, recent or rapid
onset, and which present with a certain degree
of discomfort and pain are termed “acute.”
Acute gingival infections are not especially
common and are more often associated with
pain at the time of presentation.
They include:
• necrotizing gingivitis (NG)—formerly called
acute necrotizing ulcerative gingivitis (ANUG)
and necrotizing ulcerative gingivitis (NUG)
• primary herpetic gingivostomatitis
• pericoronitis
PRIMARY HERPETIC GINGIVOSTOMATITIS
Acute herpetic gingivostomatitis usually occurs in infants and children because
most adults have developed immunity to herpes simplex virus from childhood
exposure, often with mild or no symptoms.
Etiology: HSV-1.
History: There is an acute onset of symptoms. As part of the primary infection,
the virus ascends through the sensory and autonomic nerves, where it persists as
latent HSV in the neuronal ganglia that innervate the site.
Clinical signs and symptoms: During its initial stage, it is characterized
• by discrete, spherical, gray vesicles, which can occur on the gingiva, labial
and buccal mucosa, soft palate, pharynx, sublingual mucosa, and tongue.
The ruptured vesicles are the focal sites of pain; they are particularly sensitive
to touch, thermal changes, foods such as condiments and fruit juices, and
the action of coarse foods.
In infants, the disease is marked by irritability and refusal to take food. The
course of the disease is limited to 7–10 days. Cervical lymphadenitis, fever as
high as 38°–40.6°C, and generalized malaise are common.
Histopathology: The virus targets the epithelial cells, which become large,
rounded keratinocytes with an area of acantholysis around them. These are
called Tzanck cells after fusing together to form multinucleated cells. The
intercellular edema leads to the formation of intraepithelial vesicles that rupture
and develop a secondary inflammatory response with a fibropurulent exudate.
Differences between necrotizing gingivitis and primary herpetic gingivostomatitis
Necrotizing Gingivitis Primary Herpetic Gingivostomatitis
Etiology Caused by interaction between host and bacteria, Caused by specific viral infection
most often fusospirochetes (HSV-1)
Characteristic Necrosis Diffuse erythema and vesicular
clinical eruption
feature
Description of Punched-out IDP and gingival margin; Vesicles that rupture and leave
ulcer pseudomembrane that peels off and leaves raw slightly
areas depressed oval or spherical ulcer
Affected Marginal gingiva affected; other oral tissues rarely Diffuse involvement of gingiva; may
mucosa affected include buccal mucosa and lips
Population Uncommon in children Occurs more frequently in children
Duration No definite duration Duration 7–10 days
Disease Contagion not demonstrated Contagious
PERICORONITIS AND PERICORONAL ABSCESS
Pericoronitis – inflammation of the gingiva in relation to the crown of an uncompletely
erupted tooth.
Most often - adjacent to mandibular third molars in young adults, usually caused by
impaction of debris under the soft tissue
When complicated by purulence, it can lead to pericoronal abscess with pus discharge.
PERICORONITIS
The space between the crown and the overlying gingival flap (operculum) is
an ideal area for the accumulation of food debris and bacterial growth
Aggravating Potential
factors complications
➢ Traumatic ➢ Pericoronal
occlusion abscess
➢ Foreign body ➢ Peritonsillar
trapped abscess
underneath the ➢ Cellulitis
flap
Clinical symptoms Clinical signs
➢Pain
➢Foul taste
➢Inability to close the mouth Red, swollen, suppurating
➢Trismus lesion in gingival flap
➢Swelling at the region of the (operculum) ovelying crown of
angle of the mandible partially eruptedor impacted
➢Lymphadenopathy, fever tooth
and malaise may be present
(toxic systemic complications)
PERICORONITIS – TREATMENT
1. Non-surgical - management of pain and resolving the infection
➢ Subside acute symptoms
➢Further eruption into a good functional position
➢ Pain-killers (ibuprofen)
➢ Gently flush the area with warm water to remove debris and exudate
➢ Swab with antiseptic after elevating the flap gently from the tooth with a scaler
➢ Remove underlying debris, flush with warm water
➢ If the flap is fluctuant – establish a drainage with anteroposterior incision (blade #15)
➢ Antibiotics in severe cases
2. Surgical treatment
➢Operculectomy
(scalpel, laser)
➢Removal of the tooth
EXTRACTION OF THE TOOTH –
DECISION MAKING
1. Stage of eruption
2. Position of the tooth – if it can function
3. Impacted wisdom
Extraction eliminates any future occurrences of
pericorontitis
Periodontal abscess
Desctructive process;
Localized purulent inflammation in the
periodontal tissues
PREVALENCE
➢3d most prevalent emergency infection
➢More likely to occur in a pre-existing periodontal pocket
➢More in molar sites (>50%) (complex anatomy, deep pockets)
CLASSIFICATION
I. Depending on the location of the abscess
➢ gingival – localized painful swelling affecting only the marginal and
interdental gingiva
• Mainly due to impaction of foreign objects
• May be present on a previously healthy gingiva
➢ periodontal – similar symptoms, usually affects deeper periodontal
structures, including deep pockets, furcations and vertical osseous defects.
Usually located beyond mucogingival junction
➢ pericoronal – in incompletely erupted teeth
CLASSIFICATION
II. Depending on the course of the lesion
➢ acute periodontal abscess – symptoms like pain, tenderness, sensitivity to
palpation and suppuration upon gently pressure
➢ chronic periodontal abscess – normally associated with a sinus tract (fistula);
usually asymptomatic or with mild symptoms
CLASSIFICATION
III. Depending on the number of teeth affected
➢ single periodontal abscess – related to local factors, which contribute to the
closure of the drainage of a pocket
➢ multiple periodontal abscesses – seen in uncontrolled diabetes mellitus or
medically compromised patients; or in patients, with untreated periodontitis
after systemic antibiotic therapy for non-oral lesions
CLASSIFICATION
IV. Depending on the cause of the acute inflammatory process
➢periodontitis-related - originates from the biofilm presented in a deep pocket
➢non-periodontitis-related – the origin is from other local reason, such as
foreign body impaction or alteration in tooth integrity (fracture)
GINGIVAL ABSCESS
Localized in the gingiva
Caused by injury to the outer surface of the
gingiva
Does not involve the supporting structures
Etiology
acute inflammatory response
to foreign substances forced in
the gingiva
GINGIVAL ABSCESS
Clinical features
- localized swelling of marginal gingiva or papilla
- red, smooth, shiny surface
- may be painful and appear pointed
- purulent exudate may be present
- no previous periodontal disease
GINGIVAL ABSCESS
Treatment
➢Elimination of foreign object
➢Drainage through sulcus with probe or light scaling
➢Follow-up after 24-48 hours
PERIODONTAL ABSCESS
Localized purulent infection within the tissues
adjacent to the periodontal pocket that may
lead to the destruction of periodontal ligament
and alveolar bone
ETIOLOGY
Periodontal abscess in periodontitis (periodontitis-related)
➢The existence of tortuous pockets, with cul-de-sac, may favor the formation
of abscess
➢Changes in the composition of the microflora, bacterial virulence or in host
defenses – increased suppuration
Periodontal abscess can occur at different stages during the course of the
infection:
- as an acute exacerbation of an untreated periodontitis
- during periodontal therapy
- during maintenance phase
➢PA is a period of active bone destruction
PERIODONTAL ABSCESS FORMATION
MAY OCCUR IN THE FOLLOWING
WAYS:
1. Extention of infection from a pocket deeply into the supporting
periodontal tissues and localization of the suppurative process along the
lateral aspect of the root
2. Lateral extention of inflammation from the inner surface of a pocket into
the connective tissue of the pocket wall. Drainage of the pocket is
impaired – formation of an abscess
PERIODONTAL ABSCESS FORMATION
MAY OCCUR IN THE FOLLOWING
WAYS:
3. Incomplete removal of calculus during SRP. The gingival wall shrinks, closing
the pocket orifice; the abscess occurs in the sealed off portion of the pocket
4. After trauma/perforation of the lateral root surface during endodontic
treatment
PATHOGENESIS
Occlusion of
Prevent the
periodontal
drainage
pocket
Abscess Extention of the
formation infection from
the pocket
HISTOPATHOLOGY
The main reasons for destruction
of the connective tissue and
pus formation - accumulation of
Leu and formation of an acute
inflammatory infiltrate
MICROBIOLOGY
Microflora – polymicrobial
➢Dominated by non-motile, Gr (-), strict anaerobic, rod-shaped spirochetes
- P. gingivalis – most virulent, found in 50 – 100% of abscesses
➢Other mo, usually found:
- P. intermedia
- P. melaninogenica
- F. nucleatum
- T. forsythia
DIAGNOSIS
Overall evaluation and interpretation of patient’s chief complaints, together
with clinical and radiographic findings
Patient’s chief complaints:
- Pain – light discomfort to severe pain
- Tenderness of the gingiva
- Swelling
- Sensitivity to percussion
- “Tooth is longer”
Most prominent symptom – presence of an ovoid
elevation in the gingival tissues along the lateral
side of the tooth
Other symptoms:
➢BOP
➢Increased tooth mobility
Abscess located deep in the periodontium
may be more difficult to identify – a diffuse
swelling or simply red area
SUPPURATION – FROM FISTULA OR FROM THE POCKET
(APPLY PRESSURE ON THE OUTER SURFACE OF THE GUM)
CHRONIC ABSCESS
➢No pain or dull pain
➢Localized inflammatory lesion
➢Slight tooth elevation
➢Intermittent exudation
➢Fistulous tract often associated with a deep pocket
➢Usually without systemic involvement
X-RAY
➢Either a normal appearance of the interdental bone
➢Or evident bone loss – from just a widening of PDL space to serious bone
loss involving most of the affected root
10mm pocket. This tooth was very loose upon examination, with severe
inflammation and heavy bleeding noted. Symptoms included tender
and painful gums, odor, pus coming out from all areas around the tooth,
and shifting or extruding of the tooth.
13mm pocket with an advanced furcation defect advanced bone loss and mobility of 36
DIFFERENTIAL DIAGNOSIS -
PERIODONTAL VS. PERIAPICAL
ABSCESS
Periodontal abscess Periapical abscess
- vital tooth - non-vital tooth
- no caries - caries
- pocket - no pocket
- lateral radiolucency - apical radiolucency
- mobility - no or minimal mobility
- percussion sensitivity variable - percussion sensitivity
- sinus tract opens via keratinized - sinus tract opens via alveolar
gingiva mucosa
PERIODONTAL ABSCESS – TREATMENT
➢1. Management of the acute lesion
➢2. Appropriate treatment of the original and/or residual lesion, once the
emergency situation is controlled
MANAGEMENT OF THE ACUTE LESION
Alternatives:
1. Incision and drainage
2. SRP
3. Periodontal surgery
4. Use of different systemically administered antibiotics
INCISION AND DRAINAGE
➢ Anesthesia
➢ Establish drainage
- via sulcus is the preferred method
PERIODONTAL ABSCESS
Other treatment considerations:
• Antimicrobials
• Limited occlusal adjustment
A periodontal evaluation following resolution of acute symptoms is essential!!!
PERIODONTAL ABSCESS
Antibiotics (if indicated, due to fever, lymphadenopathy or inability to obtain drainage)
• Amoxicillin – 500 mg/
• 1g loading dose, then 500 mg tid, 3 days
Penicillin – allergy
• Azithromycin – 1 g loading dose, then 500 mg for 3 days
• Clindamycin – 600 mg loading dose, then 300 mg qid, 3 days
• Gingivectomy
• Periodontal flap surgery
PERIODONTAL ABSCESS – TOOTH
FRACTURE
COMPLICATIONS - TOOTH LOSS
Tooth with a history of repeated abscesses has a
questionable prognosis
