Periodontal Abscess


A periodontal abscess is defined as suppurative lesion associated with periodontal breakdown and localized accumulation of pus within the gingival wall of a periodontal pocket.
The periodontal abscess has also been defined as a lesion with an expressed periodontal breakdown, occurring during a limited period of time and with easily detectable clinical symptoms, with a localised accumulation of pus, located within the gingival wall of the periodontal pocket.

A. Depending on the location of the lesion:
• Periapical abscess
• Periodontal abscess
 • Pericoronal abscess

B. Depending on the course of lesion:
• Acute abscess
• Chronic abscess
C. Depending on the tissue involved:
• Gingival abscess
• Periodontal abscess

D. Depending on the cause of the acute infectious
process, two types of periodontal abscess may occur:
• Periodontitis-related abscess
• Non-periodontitis-related abscess

E. Depending on the number of abscess
• Single
• Multiple

1. Pain of acute periodontal abscess is throbbing and radiating whereas in chronic periodontal abscess pain is dull and gnawing.
2. The gingiva is edematous and red, with a smooth, shiny, ovoid elevation (Fig1).
3. Suppuration may be spontaneous or occur after putting pressure on the outer surface of the gingiva.
4. Swelling
5. Sensitivity to percussion of the affected tooth
6. Tooth elevation
7. During the periodontal examination, the abscess is usually found at a site with a deep periodontal pocket.
8. Bleeding on probing
9. Pinpoint orifice of sinus may be present. Sinus may be covered by small, pink, bed - like mass of granulation tissue (Fig. 2).

Fig. 1: Periodontal abscess associated with palatal surface of upper right molar

Fig2: Periodontal abscess associated with lower left central incisor

Extra Oral Signs
In some patients the occurrence of a periodontal abscess
may be associated with:
  •  Elevated body temperature
  •  Malaise
  •  Regional lymphadenopathy

Acute periodontal abscess is associated with:
Sensitivity to palpation
Suppuration upon gentle pressure
Chronic abscess is associated with :
Sinus tract
Usually asymptomatic

The microflora related with periodontal abscess is complex, dominated by gram-negative, strict anaerobe rods resembling the microbiota of chronic periodontitis lesions. Gram-negative anaerobic species are nonfermentative and display moderate to strong proteolytic activity mainly Porphyromonas gingivalis, Prevotella intermedia. Strict anaerobic, gram positive bacterial species in periodontal abscesses include Peptostreptococcus micros, Actinomyces spp.

Following are the factors that may provoke the formation of an abscess:
1. Obstruction to the opening of deep pocket, frequently one which is tortuous or associated with furcation defect.
2. Gingival injury with a foreign body, e.g. toothbrush bristle or woodstick, which carries bacteria into the
tissues. Careless subgingival scaling may also carry microorganisms into damaged tissue, as can powerful irrigation of a pocket.
3. Incomplete removal of plaque and subgingival calculus from the depths of a pocket. Frequently after scaling there is a tightening of the gingival cuff which occludes a pocket containing bacteria.
4. Infection of tissues damaged by excessive occlusal stress which may be produced by:
• Bruxism
• Excessive orthodontic forces.
5. As a consequence of pulp disease:
• Where a periapical lesion spreads up to the lateral surface of a tooth
• Where lateral pulp canal links with the periodontal ligament. This is especially common in the furcation.
• Perforation of the lateral wall of a tooth during endodontics.
6. Altered host response as in diabetes.
The formation of periodontal abscess is initiated b the bacterial invasion of the soft tissue wall of the pocket and then multiply therein. An inflammatory infiltrate is formed followed by destruction of the connective tissues, encapsulation of the bacterial mass and pus formation.
The lowered host resistance and the virulence as well as the number of bacteria present determine the course of the infection. Tissue destruction is caused by the extracellular enzymes and inflammatory cells itself. An acidic environment will favor the activity of lysosomal enzymes and promote tissue destruction. Periodontal abscess contains bacteria, bacterial products, inflammatory cells, tissue breakdown products and serum. Neutrophils are found in the central area of the abscess and close to soft tissue debris (Fig. 3). At a later stage, a pyogenic membrane, composed of macrophages and neutrophils, is organized.


Fig.3: Diagrammatic representation of histopathology of periodontal abscess

The diagnosis of a periodontal abscess is made by the overall evaluation, interpretation of the patient’s chief complaint and the clinical and radiographic findings. The suspected area is probed carefully along the gingival margin in relation to each tooth surface to detect a tract from the marginal area to deeper periodontal tissues. The radiographic examination may either reveal a normal appearance of the interdental bone, or some bone loss, ranging from a widening of the periodontal ligament space to bone loss involving most of the affected tooth. Radiographs taken in the earliest stage of periodontal abscess provide little useful information, but once the lesion is established its position can be identified. Radiolucent area along the lateral surface of the rootsuggests the presence of periodontal abscess. A radiograph taken with gutta percha point inserted gently into the suspected pocket can help to define the origin of the abscess.
The differential diagnosis of periodontal abscess can bemade with other abscesses that occur in the oral cavity. Gingival abscess, periapical abscess, endo-periodontal abscess (Fig..4), lateral periapical cysts and vertical root fractures may have a similar appearance. Gingival abscess is a localized painful, rapidly expanding lesion usually of sudden onset. It is generally limited to the marginal gingiva or interdental papilla. Signs such as lack of pulp vitality, the presence of deep caries lesions, the presence of a sinus tract and findings made in the radiographic examination, will aid in the distinction between abscesses of different etiologies.

Fig. 4: Various abscesses that occur in oral cavity

Fig. 23.5: Radiographic appearance of periapical abscess

Treatment depends upon the stage of abscess development, amount of bone loss and whether pulp pathology is also involved or not.

Gingival Abscess
After topical anesthesia is applied, the fluctuant area of the lesion is incised with a Bard – Parker handle and surgical blade, and the incision is gently widened to permit drainage. The area is cleansed with warm water and covered with a gauze pad. After bleeding stops, the patient is dismissed for 24 hours and instructed to rinse every 2 hours with a glassful of warm water.

Acute Periodontal Abscess (Incision and drainage)
Drainage through the pocket: After application of a topical anesthesia flat instrument or a probe is carefully introduced into the pocket in an attempt to distend the pocket wall. A small curette or a Morse scaler can then
be gently used to penetrate the tissue and establish drainage. Drainage through an external incision: After LA is given, with a Bard – Parker handle and blade no. 11, a vertical incision is made through the most fluctuant part of the lesion, extending from the mucogingival fold to the gingival margin (Fig. 6). If swelling is on the lingual surface, the incision is started just apical to the swelling extending through the gingival margin. The blade should penetrate to firm tissue to be sure of reaching deep, purulent areas. After initial extravasation of blood and pus, irrigate the area with warm water and gently spread the incision to facilitate drainage. Postoperative instructions are given to rinse hourly with a solution of a teaspoon of salt in a glass of warm water. Antibiotic Penicillin and Metronidazole

Chronic Periodontal Abscess
Treatment by Flap operation: All deposits are scaled fro the teeth, and the root surfaces are planed with the hoe scalers and smoothened with curettes. Systemic antibiotics Amoxicillin and Metronidazole are prescribed. To locate the abscess area, probing is done around the gingival margin, following tortuous pockets to their termination. If a sinus is present, the abscess may be probed through it.
Anesthesize: The area is anesthetized with localm infiltration.
Incision: Two vertical incisions are made from the gingival margin to the mucobuccal fold, outlining the field of operation. If the lingual approach is used; the incisions are made from the gingival margin to the level of the root apices. After the vertical incisions are made, a mesiodistal incision is made across the interdental papilla with a knife to facilitate the detachment of the flap (Fig. 7).
Reflect the flap: A full thickness flap is raised with aperiosteal elevator and held in position with a retractor.
Remove granulation tissue: The granulation tissue is removed with curettes to provide a clear view of the root. If a sinus is present, it is explored and curetted.
Control bleeding: The facial and lingual surfaces are covered with a piece of gauze shaped into a U, which is held in position until the bleeding stops.
Suture: The gauze is then removed, and the flap is sutured and covered with a periodontal pack. Sorrin’s operation—A type of flap approach in the treatment of a periodontal abscess; especially suitable when the marginal gingiva appears well adapted and gives no access to the abscess area. A semilunar incision is made below the involved area in the attached gingiva, leaving gingival margin undisturbed. A flap is raised, allowing access to the abscessed area for curettage.

a. Tooth loss: Periodontal abscesses have been suggested as the main cause for tooth extraction during the phase of supportive periodontal therapy.
b. Dissemination of the infection-Cellulitis, subcutaneous infection, phlegmone and mediastinitis can result from odontogenic infections but are very uncommon with periodontal abscess. Mechanical treatment of a periodontal abscess may result in bacteremia which, in patients with, for example endoprosthesis or in immunocompromised states, can result in nonoral infections. Occassional dissemination of periodontal bacteria can result in brain abscess.

DeWitt G, Cobb C, Killoy W. The acute periodontal abscess: microbial penetration of the tissue wall.
International Journal of Periodontics and Restorative Dentistry 1985;1:39-51.
In this study 12 biopsies punches were taken just apical to the area of major fluctuance and processed forhistological examination. Following were the observation from the outside to the inside: (a) a normal oral epithelium and lamina propria; (b) an acute inflammatory infiltrate; (c) an intense foci of inflammation (neutrophil-lymphocyte) with the surrounding connective tissue destroyed and necrotic; (d) a destroyed and ulcerated pocket epithelium; (e) a central region, as a mass of granular, acidophilic, and amorphous debris. In 7 out of 9 specimens evaluated by electron-microscopy, gram-negative bacteria were seen invading the pocket epithelium and altered connective tissue. Bacteria inside the abscess were immersed in tissue exudate and surrounded by necrotic tissues. The presence of fungi inside the abscess was also present.

Multiple periodontal abscesses are seen in diabetes mellitus.
Periodontitis related abscess occurs when the acute infection originates from a biofilm present in a deepened periodontal pocket.
Post-scaling periodontal abscess: This type of abscess formation occur when small fragments of calculus have been forced into the deep, previously noninflamed portion of the periodontal tissues.
Post-surgery periodontal abscess: It is often the result of an incomplete removal of subgingival calculus or to the presence of foreign bodies in the periodontal tissues, such as sutures, regenerative devices or periodontal pack.
Post-antibiotic periodontal abscess: Treatment with systemic antibiotics without subgingival debridement in patients with advanced periodontitis may cause abscess formation.

1. DeWitt G, Cobb C, Killoy W. The acute periodontal abscess:
microbial penetration of the tissue wall. Int J Periodontics and
Restorative Dent 1985;1:39-51.
2. Herrera D, Roldan S, Sanz M. The periodontal abscess: a review.
J Clin Periodontol 2000;27:377-86.
3. Meng HX. Periodontal abscess. Ann Periodontol 1999;4:79-82.
4. Sanz M, Herrera D, Winkelhoff AJ. The Periodontal Abscess. In, Lindhe J, Karring T, Lang NP. Clinical Periodontology and Implant dentistry. 4th ed Blackwell Munksgaard 2003;260-68.
5. Takei HH. Treatment of the periodontal abscess. In, Newman, Takei, Carranza. Clinical Periodontology 9th ed WB Saunders 2003;629-30.
6. The Periodontal Abscess. In, Eley BM, Manson JD. Periodontics 5th ed Wright 2004;328-31.

1. Most abundant cells in the inflammatory exudates of an acute periodontal abscess are:
A. Lymphocytes
B. Neutrophils
C. Monocytes
D. Basophil
2. A young adult shows non – fluctuant, tender and red
swelling in the marginal gingiva:
A. Periapical abscess
B. Periodontal abscess
C. Periapical sinus
D. Gingival abscess
. 1B                      2. D

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