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Periodontal Abscess
Huan Xin Meng*
* Beijing Medical University, Beijing, China.

This review focuses on the classification of periodontal abscesses,

which are localized purulent infections of periodontal tissues,
and discusses their etiology and clinical characteristics. Ann
Periodontol 1999;4:79-82.
KEY WORDS
Periapical abscess/classification; periapical abscess/etiology;
periodontal abscess/classification; gingival abscess.

periodontal abscess is a localized

purulent infection of periodontal
tissues and can be a common clinical feature in patients with moderate or
advanced periodontitis.1-8 Although it is
more frequently seen in untreated than in
treated periodontitis patients, a recent retrospective study5 indicated that it may
also occur in patients receiving maintenance treatments. This review focuses on
the classification of periodontal abscesses
and discusses their etiology and clinical
characteristics.
MICROBIOLOGY
Streptococcus viridans is the most common isolate in the exudate of periodontal abscesses when aerobic techniques
are used.9 It has been reported that the
microorganisms that colonize the periodontal abscesses are primarily Gramnegative anaerobic rods.10,11 Although
not found in all cases of periodontal
abscesses, high frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Campylobacter rectus, and Capnocytophaga spp
have been reported.10,12-15 Actinobacillus actinomycetemcomitans is not usually
detected.10 The disappearance of P. gingivalis from abscessed sites after treatment suggests a close association of this
microorganism with abscess formation.12
Spirochetes have been found as the predominant cell type (mean, 40.6%
10.9%) in periodontal abscesses when
assessed by darkfield microscopy.16
Strains of Peptostreptococcus, Streptococcus milleri (S. anginosus and S. inter79

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Periodontal Abscess

medius), Bacteroides capillosus, Veillonella, B. fragilis,

and Eikenella corrodens have also been isolated.11
Overall, studies have noted that the microbiota found
in abscesses are similar to those in deep periodontal
pockets.
FACTORS ASSOCIATED WITH DEVELOPMENT
OF PERIODONTAL ABSCESSES
Periodontal abscesses usually result from pre-existing
cases of chronic periodontitis4-8 and are precipitated
by changes in the subgingival microflora, decreased
host resistance, or both.17 Among the factors that have
been associated with the formation of acute periodontal
abscesses are: 1) occlusion of pocket orifices; 2) furcation involvement; 3) systemic antibiotic treatment;
and 4) diabetes.
Occlusion of the Orifice of a Deep Periodontal
Pocket
Most investigators believe that periodontal abscesses
are induced by occlusion of the periodontal pocket orifice leading to reduced clearance of bacteria and accumulation of host cells.1-3,6,18 As a consequence, the
infection spreads from the pocket into supporting tissues and is then localized. Tissue damage in the
abscessed area is considered to be the result of lysosomal enzymes released from neutrophils participating in the defense of the host.19 Occlusion of pocket orifices caused by local factors such as impaction of food
and foreign bodies20-22 prevents drainage of exudate
formed by inflamed tissues adjacent to the pocket. Periodontal abscesses are rare in children and, if they occur,
are usually caused by the introduction of a foreign body
into previously healthy periodontal tissues.23,24
Periodontal abscess formation may also occur as a
result of incomplete removal of calculus during treatment of a periodontal pocket.1-3,25 In such cases, the
gingival wall shrinks, occluding the pocket orifice, and
the abscess occurs in the sealed-off portion of the
pocket. The fact that patients were undergoing periodontal treatment when abscesses developed could
indicate that instrumentation may force bacteria into
the tissues, provoking a localized purulent exudate.7,26
Furcation Involvement
Abscesses are frequently found in furcations.27 In one
study addressing the incidence of acute periodontal
abscesses, clinical and/or radiologic evidence of furcation involvement was noted in the majority of the
molars.7 In another study, most periodontal abscesses
occurred in molars (37 of 40 cases, 92.5%).28 A study
in a private periodontal practice reported periodontal
abscess was the primary reason for molar extraction.29
Furthermore, when loss of abscessed teeth was compared between furcated and nonfurcated teeth, more
furcated teeth were lost than nonfurcated teeth.3
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Systemic Antibiotic Therapy

In some cases, multiple periodontal abscesses cannot
be explained by local factors alone, and it has been
suggested that systemic administration of antibiotics
may trigger their formation. It has been reported that
periodontal abscesses occurred in patients with
untreated advanced periodontal disease shortly after
receiving antibiotics for non-oral infections.8,30 In one
of these studies, Bacteroides gingivalis, Fusobacterium
nucleatum, and Streptococcus intermedius were the
most prevalent species associated with the multiple
periodontal abscesses8 and in the other, a significant
increase in subgingival Staphylococcus aureus was
found.30 Based on these results it appears that the systemic administration of antibiotics in patients with
untreated periodontitis may lead to superinfection with
opportunistic organisms resulting in development of
periodontal abscesses.
Diabetes
The predisposition of patients with diabetes to purulent infections makes them prone to acute periodontal abscesses. Systemic alterations in diabetics that
may have a significant influence on the formation of
periodontal abscesses include lowered host resistance
such as impaired cellular immunity, decreased leukocyte chemotaxis/phagocytosis and bactericidal activity. Diabetics also have vascular changes and altered
collagen metabolism that may increase susceptibility
to abscess formation.18,31 Enhanced interaction of
advanced glycosylation end products (AGEs) with their
cellular receptor (RAGE) has been suggested as one
of the pathogenic mechanisms of accelerated periodontal disease in diabetes.32 Critical consequences of
hyperglycemia are non-enzymatic glycation and oxidation of proteins and lipids, resulting in the formation
of the AGEs which accumulate in plasma, tissues,33
and gingiva of diabetic patients.34
Other Factors
Other factors associated with periodontal abscess formation include trauma to the tooth such as perforation
of the lateral wall of the root in endodontic therapy1-3,35
and anatomic dental anomalies such as enamel pearls36
in molar furcations and invaginated roots.37
CLINICAL FEATURES
An abscessed area may manifest the following signs
and symptoms: swelling, suppuration, visible redness,
extrusion of the tooth involved, loosening, and tenderness to even slight percussion. A slight temperature elevation is an occasional finding.4,7,19 Types of
abscesses that affect the periodontium include: gingival, periodontal, pericoronal, and periapical. Periapical abscesses are discussed in another paper.38
Previously periodontal abscesses were also referred
to as lateral and parietal abscesses. However, these

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terms may be misleading and therefore their use

should be discontinued.
Gingival Abscess
A gingival abscess is a localized, painful, rapidly
expanding lesion involving the marginal gingiva or interdental papilla sometimes in a previously disease-free
area. It is usually an acute inflammatory response to foreign substances forced into the gingiva and in its early
stages appears as a red swelling with a smooth, shiny
surface. Within 24 to 48 hours, the lesion is usually
fluctuant and pointed, with a surface orifice from which
a purulent exudate may be expressed. If permitted to
progress, the lesion generally ruptures spontaneously.
Symptoms may include pulpal hypersensitivity.1-4
Periodontal Abscesses
A periodontal abscess is a localized accumulation of
pus within the gingival wall of a periodontal pocket
resulting in the destruction of the collagen fiber attachment and the loss of nearby alveolar bone. It is usually associated with more advanced involvement of
periodontal structures, including tortuous periodontal
pockets, furcation involvement, and intrabony defects.
Calculus is often detected on the root surface. The
lesions may be acute or chronic. A localized acute
abscess may progress to a chronic abscess if its purulent contents drain through a fistula into the outer gingival surface or into the periodontal pocket.1-5
An acute periodontal abscess appears as an ovoid
elevation of the gingiva along the lateral aspect of the
root. The gingiva is edematous and red, with a smooth,
shiny surface. In most cases, pus may be expressed
from the gingival margin by gentle digital pressure.
The symptoms of an acute periodontal abscess vary
from slight discomfort to severe pain and swelling. As
an abscess develops, a feeling of pressure in the
gums is common. Inflammation involving the supporting structures may be accompanied by increased
tooth mobility, elevation of the tooth in its socket, and
tenderness to percussion or on mastication. Regional
lymphadenopathy can be detected in some patients.1-8,19
If an acute periodontal abscess is left untreated, it
may become a chronic lesion. A chronic periodontal
abscess may exist for an extended period and have a
history of intermittent exudation for which patients
seek treatment. It usually presents as a fistulous tract
that originates from deep supporting tissues and opens
onto the gingival mucosa along the length of the root.
The orifice of the fistula may appear as a difficult-todetect pinpoint opening and be covered by a small,
pink mass of granulation tissue. A chronic periodontal abscess is usually asymptomatic. However, some
patients may feel dull or gnawing pain, slight elevation
of the tooth, and a desire to bite tightly and grind.
Chronic lesions may become acute abscesses if the orifice of the sinus tract becomes occluded.4

Meng

Pericoronal Abscess
The pericoronal abscess is a localized accumulation of
pus within the overlying gingival flap surrounding the
crown of an incompletely erupted tooth, usually occurring in the mandibular third molar area. The gingival
flap appears red and swollen. The infection may spread
posteriorly into the oropharyngeal area and medially
to the base of the tongue and involve the regional
lymph nodes. Patients usually have a history of pericoronitis and may experience difficulty in swallowing.
The severity of pericoronitis and development of
abscess formation have been associated with increasing proportions of Gram-negative anaerobic pathogens.39
Some patients may also have systemic symptoms such
as fever, leukocytosis, or malaise.1-3
DIAGNOSIS
Periodontal abscesses are the most common type of
abscesses involving the periodontium. A diagnosis of
periodontal abscess should be made after on overall
evaluation and interpretation of the patients chief complaint, medical/dental history, and clinical and radiographic examinations. A periodontal abscess is usually associated with pre-existing periodontitis. Drainage
of the pus may occur during periodontal probing or
without provocation. Most periodontal abscesses occur
interstitially,7 but they do not always drain on the same
surface of the root on which the pocket is present. For
instance, a pocket on the facial surface may give rise
to a periodontal abscess interproximally.1-3 Radiographs and assessment of pulp status may provide
additional information relative to the etiology of the
swelling.4 The percentage of spirochetes as seen by
darkfield microscopy may be of value.16,40
CONCLUSION
A periodontal abscess is a localized purulent infection
of periodontal tissues and can be a common clinical
finding among patients with moderate to advanced periodontitis. The microorganisms in periodontal abscesses
are primarily Gram-negative anaerobic rods, and are
similar to bacteria detected in deep periodontal pockets. However, no specific microorganism has been found
in periodontal abscesses. Several factors are associated with the formation of the acute abscess, including occlusion of the orifice of a deep periodontal pocket,
systemic antibiotic therapy in the absence of periodontal
treatment, and poorly controlled diabetes. The diagnosis of a periodontal abscess is based on information
from patient history and clinical and radiographic examinations. The periodontal abscess needs to be differentiated from gingival abscess and periapical abscesses.
If the abscess is limited to marginal gingiva or interdental papilla with no previous disease, and a foreign
material or trauma exists, the lesion is likely to be a gingival abscess. If the abscessed tooth is nonvital, the
lesion is most likely a periapical abscess. According to
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Volume 4 Number 1 December 1999

the tissues affected, in this review, 3 types of abscesses

of the periodontium have been described.
REFERENCES
1. Carranza FA Jr. Gingival enlargement. In Carranza FA Jr.,
Newman MG, eds. Glickmans Clinical Periodontology,
8th ed. Philadelphia: WB Saunders Co.; 1996:234-235.
2. Carranza FA Jr. The periodontal pocket. In Carranza FA
Jr., Newman MG, eds. Glickmans Clinical Periodontology,
8th ed. Philadelphia: WB Saunders Co.; 1996:292-295.
3. Carranza FA Jr. Clinical diagnosis. In Carranza FA Jr.,
Newman MG, eds. Glickmans Clinical Periodontology,
8th ed. Philadelphia: WB Saunders Co.; 1996:358-360.
4. Ahl DR, Hilgeman JL, Snyder JD. Periodontal emergencies. Dent Clinics N Am 1986;30:459-472.
5. McLeod DE, Lainson PA, Spivey JD. Tooth loss due to
periodontal abscess: A retrospective study. J Periodontol 1997;68:963-966.
6. Prichard JF. Management of the periodontal abscess. In:
Advanced Periodontal Disease, 2nd ed. Philadelphia: WB
Saunders Co.; 1972:602-637.
7. Smith RG, Davies RM. Acute lateral periodontal
abscesses. Br Dent J 1986;161:176-178.
8. Topoll HH, Lange DE, Mller RF. Multiple periodontal
abscesses after systemic antibiotic therapy. J Clin Periodontol 1990;17:268-272.
9. Epstein S, Scopp IW. Antibiotics and the intraoral
abscess. J Periodontol 1977;48:236-238.
10. Newman MG, Sims TN. The predominant cultivable
microbiota of the periodontal abscess. J Periodontol
1979;50:350-354
11. Chen CM. Bacteriological investigation of anaerobes in
11 cases of periodontal abscess and methods to improve
its detection rate (in Chinese). Chung Hua Kou Chiang
Ko Tsa Chih 1983;18:209-211.
12. Hafstrm CA, Wikstrm MB, Renvert SN, Dahln GG.
Effect of treatment on some periodontopathogens and
their antibody levels in periodontal abscesses. J Periodontol 1994;65:1022-1028.
13. van Winkelhoff AJ, van Steenbergen TJM, de Graaff J.
The role of black-pigmented Bacteroides in human oral
infections. J Clin Periodontol 1988;15:145-155.
14. Aitken S, Birek P, Kulkarni GV, Lee WL, McCulloch CAG.
Serial doxycycline and metronidazole in prevention of
recurrent periodontitis in high-risk patients. J Periodontol 1992;63:87-92.
15. Kulkarni GV, Lee WK, Aitken A, Birek P, McCulloch CA.
A randomized, placebo-controlled trial of doxycycline:
Effect on the microflora of recurrent periodontitis lesions
in high risk patients. J Periodontol 1991;62:197-202.
16. Trope M, Tronstad L, Rosenberg ES, Listgarten M. Darkfield microscopy as a diagnostic aid in differentiating
exudates from endodontic and periodontal abscesses. J
Endod 1988;14:35-38.
17. Kryshtalskyj E. Management of the periodontal abscess.
J Can Dent Assoc 1987;53:519-522.
18. Schluger S, Yuodelis R, Page RC, Johnson RH. Acute
inflammatory periodontal diseases. In: Periodontal Diseases, 2nd ed. Philadelphia: Lea & Febiger 1990:263-265.
19. Ryan GB, Majno G. Acute inflammation. A review. Am
J Pathol 1977;86:185-276.
20. McFall WT. The periodontal abscess. J N Carolina Dent
Soc 1964;47:34-39.
21. Palmer RM. Acute lateral periodontal abscess. Br Dent
J 1984;157:311-312.

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22. OLeary TJ, Standish SM, Bloomer RS. Severe periodontal destruction following impression procedures. J
Periodontol 1973;44:43-48.
23. Fleming P, Strawbridge J. Lateral periodontal abscess in
a child. J Pedod 1989;13:280-283.
24. Fuss Z, Bender IB, Rickoff BD. An unusual periodontal
abscess: J Endod 1986;12:116-118.
25. Dello Russo NM. The post-prophylaxis periodontal
abscess. Etiology and treatment. Int J Periodontal
Restorative Dent 1985;5(1):29-37.
26. Kareha MJ, Rosenberg ES, DeHaven H. Therapeutic
considerations in the management of a periodontal
abscess with an intrabony defect. J Clin Periodontol
1981;8:375-386.
27. Goldman HM, Cohen DW. Characteristics of periodontal diseases. In: Goldman HM, Cohen DW, eds. Periodontal Therapy, 5th ed. St Louis: C.V. Mosby; 1973:74.
28. Yang BQ. Analysis of bacterial cultures from 40 cases
of periodontal abscess and their drug sensitivity (in Chinese). Chung Hua Kou Chiang Hsueh Tsa Chih 1987;22:
327-328, 369.
29. Chace R, Low SB. Survival characteristics of periodontally-involved teeth: A 40-year study. J Periodontol 1993;
64:701-705.
30. Helovuo H, Hakkarainen K, Paunio K. Changes in the
prevalence of subgingival enteric rods, staphylococci
and yeasts after treatment with penicillin and erythromycin. Oral Microbiol Immunol 1993;8:75-79.
31. Ueta E Osaki T, Yoneda K, Yamamoto T. The prevalence of diabetes mellitus in odontogenic infections and
oral candidiasis: an analysis of neutrophil suppression.
J Oral Pathol Med 1993;22:168-174
32. Lalla E, Lamster IB, Schmidt AM. Enhanced interaction
of advanced glycation end products with their cellular
receptor RAGE: Implications for the pathogenesis of
accelerated periodontal disease in diabetes. Ann Periodontol 1998;3:13-19.
33. Brownlee M. Glycation products and the pathogenesis of
diabetic complications. Diabetes Care 1992;15:1835-1843.
34. Schmidt AM, Weidman E, Lalla E, et al. Advanced glycation endproducts (AGEs) induce oxidant stress in the
gingiva: A potential mechanism underlying accelerated
periodontal disease associated with diabetes. J Periodont
Res 1996;31:508-515.
35. Abrams H, Cunningham CJ, Lee SB. Periodontal
changes following coronal/root perforation and formocresol pulpotomy. J Endod 1992;18:399-402
36. Croft LK. Periodontal abscess from enamel pearl. Oral
Surg Oral Med Oral Pathol 1971;32:154.
37. Chen R-J, Yang J-F, Chao T-C. Invaginated tooth associated with periodontal abscess. Oral Surg Oral Med Oral
Pathol 1990;69:659.
38. Meng H-X. Periodontic-endodontic lesions. Ann Peridontol 1999;4:84-89.
39. Mombelli A, Buser D, Lang NP, Berthold H. Suspected
periodontopathogens in erupting third molar sites of periodontally healthy individuals. J Clin Periodontol 1990;17:
48-54.
40. el-Sayed JM, Zahran FM. A bacteriologic aid in the differential diagnosis of periapical and periodontal abscesses.
Egypt Dent J 1995;41:1007-1012.
Send reprint requests to: Dr. Huan Xin Meng, Beijing Medical University, School of Stomatology, Weigongcun, Haidian
District, Beijing 100081 China. Fax: 86-10-6217-3402; email: hxmeng@public.east.cn.net