Curr Oral Health Rep (2017) 4:294–300
DOI 10.1007/s40496-017-0157-8
EPIDEMIOLOGY (M LAINE, SECTION EDITOR)
Periodontal Abscess: a Review and the Role
of Antimicrobial Therapy
Sachiyo Tomita 1 & Atsushi Saito 1,2
Published online: 9 October 2017
# Springer International Publishing AG 2017
Abstract
Purpose of Review The aim was to summarize current
knowledge about periodontal abscesses and describe recent
research on antimicrobial treatment.
Recent Findings For periodontal abscess treatment, antimi-
crobial therapy is implemented as an adjunct modality to
subgingival debridement and/or abscess drainage. Among
available systemic antimicrobial agents, amoxicillin (plus
clavulanate), metronidazole, and azithromycin are often used
with good clinical results. In our studies of patients with acute
periodontal lesions, systemic administration of a new
fluoroquinolone, sitafloxacin, yielded a significant improvement
in clinical parameters, and was effective against
subgingival bacteria, with no significant impact on the
antimicrobial susceptibility of periodontal bacteria.
Summary Plaque control during initial periodontal therapy or
maintenance care is critical for the prevention and treatment of
periodontal abscesses. In the case of acute periodontal
abscesses, drainage is considered first. When drainage is
not possible or insufficient, antimicrobial therapy should
then be considered. Microbiological testing can contribute
to the successful treatment.
Keywords Periodontal abscess . Acute periodontal lesion .
Periodontitis . Periodontal disease . Antimicrobial therapy .
Antimicrobial susceptibility
This article is part of the Topical Collection on Epidemiology
* Atsushi Saito
atsaito@tdc.ac.jp
1
Department of Periodontology, Tokyo Dental College, 2-9-18
Misaki-cho, Chiyoda-ku, Tokyo 101-0061, Japan
2
Oral Health Science Center, Tokyo Dental College, Tokyo, Japan
Introduction
Effectively addressing patients’ symptoms and concerns is of
paramount importance in periodontal practice. In cases of
periodontal abscess, a rapid destruction of periodontal tissue
can occur during a short period of time, with marked clinical
symptoms [1, 2]. Periodontal abscesses are important because
they are a relatively common dental emergency [3••] and can
compromise the fate of the affected tooth [4]. Immediate at-
tention is needed because of acute symptoms, and the bacteria
within the abscess can spread and cause infections beyond
oral lesions.
“Acute periodontal lesions” include acute periodontal ab-
scesses and necrotizing periodontal disease [5]. According to
t h e cl a s s i f i ca t i o n b y t h e A m e r i c an A c a d em y o f
Periodontology [6], a periodontal abscess is defined as “a
localized purulent infection of periodontal tissues and can be
a common clinical feature in patients with moderate or ad-
vanced periodontitis” [7]. It includes gingival, periodontal,
and pericoronal abscesses, depending on the tissues affected.
Other gingival and periodontal lesions may also show an acute
presentation, including infectious conditions not related to
oral bacterial biofilms, mucocutaneous disorders, or traumatic
and allergic lesions [3••].
In this review, we mainly focus on gingival and periodontal
abscesses.
Etiology of Periodontal Abscesses
Pathogenesis and Progression
Periodontal abscesses can occur in sites with periodontal
tissue breakdown or in periodontally healthy sites [3••].
The presence of deep, complex periodontal pockets, furcation
Curr Oral Health Rep (2017) 4:294–300
involvement, or intrabony defects can contribute to the patho-
genesis and progression (Fig. 1). Marginal closure of the peri-
odontal pocket can induce an increased internal pressure, due to
the activities of remaining plaque bacteria, which in turn lead to
spread of the infection into surrounding periodontal tissues
[8–10]. Changes in the composition of subgingival microflora,
with an increase in bacterial virulence or a decrease in the host
immune response, could also result in a compromised ability to
suppress the increased suppuration [3••].
Periodontal abscesses can occur in patients with periodonti-
tis under different situations [3••]:
& Following non-surgical periodontal therapy. After scaling
and root planing or professional tooth cleaning, detached
calculus or plaque fragments are pushed into the tissues
[11]. Even meticulous scaling may allow calculus to re-
main in deep or complex pockets. When marginal closure
occurs as a result of normal healing, this can contribute to
the development of periodontal abscesses [12].
& Following surgical periodontal therapy. This is related to
the presence of foreign bodies, such as barrier membranes
or sutures [13].
& Acute exacerbation of untreated periodontitis sites [11].
& Acute exacerbation during maintenance or supportive
periodontal therapy [14–16].
Gingival or periodontal abscesses can also occur in previ-
ously healthy sites (i.e., non-periodontitis-related periodontal
abscesses) as a result of impaction of foreign bodies or alter-
ation of root surfaces. They can also occur in relation to dental
implant therapy [17].
The development of a periodontal abscess is initiated by
bacterial dissemination into soft tissues surrounding the peri-
odontal pocket [3••]. This triggers an inflammatory process
through cytokines and chemokines released by the interaction
between bacteria and recruited inflammatory cells, which can
lead to the destruction of connective tissues, encapsulation of
bacterial infection, and production of pus. Once the abscess is
formed, the rate of destruction within the abscess is dependent
on the bacterial growth, their virulence, and local pH [10].
Fig. 1 A periodontal abscess buccal to the maxillary right central incisor
is shown
295
Microbiological Profiles
In periodontal abscesses, Gram-negative bacteria have been
reported to be more prevalent than Gram-positive bacteria,
rods predominated over cocci, and larger proportions of strict
anaerobes are observed [8, 18, 19]. Porphyromonas gingivalis
has been reported to form a considerable proportion of micro-
organisms from periodontal abscesses [1, 19–22]. Other prev-
alent anaerobes include Prevotella intermedia, Prevotella
melaninogenica, Fusobacterium nucleatum, Tannerella
forsythia, Treponema spp., Parvimonas micra, Actinomyces
spp., and Bifidobacterium spp. [3••]. Facultative anaerobic
Gram-negative bacteria, Capnocytophaga spp.,
Campylobacter spp., and Aggregatibacter
actinomycetemcomitans have also been identified [1], as well
as Gram-negative enteric rods [21]. It should be kept in mind
that, in some cases, samples from the abscesses have been
unintentionally mixed with the microflora from the periodon-
tal pockets [5, 23]. As for the analysis of subgingival plaque
samples, in our study of acute periodontal lesions in 30 pa-
tients with periodontitis, P. micra, P. intermedia, and
Streptococcus mitis were the most prevalent bacteria identified
by culture technique [24•], while T. forsythia and Treponema
denticola were the most prevalent bacteria identified by PCR-
Invader technique [25].
In a study using dark-field microscopy, the percentage of
spirochetes was reported to be higher in periodontal abscesses
than in periapical abscesses [26]. However, microbiological
findings from abscess exudate or subgingival samples are gen-
erally considered to have limited value in the differential
diagnosis.
Clinical Diagnosis of Periodontal Abscesses
The diagnosis of a periodontal abscess is made based
on comprehensive assessment of the patient, including
systemic, periodontal, microbiological, and radiographic
examinations. A variety of clinical signs and symptoms
(ranging from light discomfort to severe pain, gingival
swelling, edema, redness, tooth mobility, and tenderness
of the tooth to palpation) have been shown to be associated
with an abscess [5, 17, 19].
The most prominent oral sign is the presence of gingival
swelling along the root. Abscesses occurring deep in the
periodontal tissue may be more difficult to identify [3••].
Another common sign is suppuration through a fistula or
the pocket opening. This may be spontaneous or occurs
after applying pressure on a particular site. The abscess is
usually found at a site with a deep periodontal pocket with
signs of periodontitis, including bleeding on probing or
increased tooth mobility [1, 19]. It has been suggested that
a pocket depth of 6 mm is associated with a periodontal
296
abscess for research purposes [20]; however, an abscess
may occur in sites with shallower pockets [5].
Radiographic examination may show a normal appearance,
or some forms of bone loss [3••]. Since a tooth with history of
endodontic therapy or a post-retained restoration may also be
the cause of abscess, radiographic images should be carefully
interpreted and correlated with clinical findings [5].
Differential Diagnosis
The differential diagnosis is critical because periodontal ab-
scesses may be similar to other oral conditions [3••]:
& Other abscesses in the oral cavity such as periapical,
dentoalveolar, or endodontic abscesses, lateral periapical
cysts, root fractures [27, 28], endo-periodontal lesions
[29], and postoperative infection [30]
& Other oral diseases including osteomyelitis in patients
with periodontitis [31], squamous cell carcinomas [32],
metastatic carcinomas [33], and granulomas [34, 35]
& Self-inflicted gingival injuries [36, 37]
As stated earlier, a periodontal abscess is a purulent infec-
tion. Many reactive and neoplastic lesions may share clinical
signs of periodontal tissue swelling. Because these lesions,
with the exception of super-infection, are not purulent, and
often without pain, they should not be misdiagnosed as peri-
odontal abscesses [5].
Systemic and Environmental Conditions
Periodontal abscesses may be associated with elevated body
temperature, malaise, and regional lymphadenopathy [17, 19].
It has been reported that 30% of patients may have elevated
levels of blood leukocytes [19].
Periodontal abscesses can be considered as a possible oral
clinical diagnostic criterion for diabetes mellitus. Careful as-
sessment for systemic conditions must be performed for pa-
tients visiting dental offices. In patients with other systemic
diseases such as acute leukemia, gingival enlargement similar
to a periodontal abscess can be observed [38]. Medical pro-
fessionals are advised to consider oral conditions in the assess-
ment of systemic status [39].
It is of interest to note that a potential relationship between
acute phase of chronic periodontitis and meteorological fac-
tors was reported [40]. In particular, maximum hourly de-
crease in barometric pressure, maximum hourly increase in
temperature, and maximum daily wind speed were signifi-
cantly associated with the occurrence of acute phase of chron-
ic periodontitis without direct-triggered episodes. Further
studies are necessary to elucidate the effect of environmental
factors on the periodontal conditions.
Curr Oral Health Rep (2017) 4:294–300
Treatment
Treatment of periodontal abscess should comprise two phases:
(1) control of the acute condition to relieve symptoms and
arrest tissue destruction and (2) management of a pre-
existing and/or residual lesion, especially in patients with peri-
odontitis [3••].
1. Control of the Acute Condition
For control of the acute condition, the following
treatment options can be considered: (1) drainage and
debridement, (2) antimicrobial therapy, (3) surgery, and (4)
tooth removal.
(1) Drainage and Debridement The fundamental treatment
of a periodontal abscess is drainage (through the pocket
or an external incision) and thorough irrigation with a
sterilized physiological saline solution or antiseptics. In
abscesses presenting with severe inflammation, aggres-
sive mechanical instrumentation should be delayed, and
antimicrobial therapy should be considered first. This
may prevent damage to healthy contiguous periodontal
tissues [41, 42]. If the abscess is caused by foreign-body
impaction, the object must be removed by careful de-
bridement [43]. Occlusal adjustment may be provided
after careful assessment of the occlusion [44].
Recall appointments 24–48 h after drainage and
debridement are recommended to re-evaluate resolution
of the abscess and to determine the duration of an-
timicrobial administration [3••].
(2) Antimicrobial Therapy Systemic or local antimicrobials
may be used as the sole treatment, as initial treatment, or
as an adjunctive treatment to drainage. Generally,
antimicrobial therapy alone without subsequent drainage
and/or subgingival debridement is contraindicated [1].
Such treatment may only be recommended if there is a
need for premedication, if the infection is not localized,
or if adequate drainage cannot be provided [45]. As ad-
junctive treatment, systemic antimicrobials should be
considered if systemic involvement is apparent [45].
Among available systemic antimicrobial agents,
amoxicillin (plus clavulanate) [46], tetracycline [1],
metronidazole, and azithromycin [46] are often used
with good clinical results. After drainage and irrigation,
local drug delivery of minocycline-HCl to the
periodontal pocket may be used [44]. Preferably, micro-
biological testing should be included in the
treatment regimen. Any antimicrobial agent should be
used after careful evaluation of its side effects and con-
traindications. Given the general increase in bacterial
resistance in recent years, one must carefully con-
sider the antimicrobial susceptibilities of target
Curr Oral Health Rep (2017) 4:294–300
bacteria. Our recent findings on the use of a new
generation of fluoroquinolone (sitafloxacin), including
its effect on antimicrobial susceptibility, are described
later in this article. Suggested antimicrobial agents for
the adjunct treatment of periodontal abscesses are shown
in Table 1.
(3) Surgery Surgical procedures are mainly considered for
abscesses associated with deep vertical defects [9] or
abscesses occurring after scaling and root planing in
which residual subgingival calculus remains after
treatment [11]. For abscesses with severe inflammation,
surgical intervention should be delayed in favor of anti-
microbial therapy followed by subgingival debridement
to reduce the extent of inflammation.
(4) Tooth Removal If the prognosis of a tooth is hopeless,
tooth extraction is often the only treatment option [47].
Similar to surgery, pronounced inflammation must be
suppressed before tooth extraction is performed.
2. Management of a Pre-existing and/or Residual Lesion
Comprehensive periodontal examination should be
performed after resolution of the acute phase [3••]. If
the patient has not received treatment previously, then
appropriate periodontal treatment should be implemented.
If the patient is currently receiving active periodontal
therapy, the planned therapy should be provided once
the acute lesion has been controlled. In patients receiving
supportive periodontal therapy or maintenance care, careful
evaluation of the recurrence of the abscess is necessary, as
well as assessment of the tissue damage and how this
affects tooth prognosis.
Use of a New Generation of Fluoroquinolone
for the Treatment of Acute Periodontal Lesions
New quinolones have been shown to be effective against
various anaerobes [49] and A. actinomycetemcomitans
[50], a pathogen associated with aggressive periodontitis.
Table 1 Suggested antimicrobial
agents for the adjunct treatment of Administration Agent
periodontal abscesses
Systemic Amoxicillin plus clavulanate
Tetracycline
Metronidazole
Azithromycin
Sitafloxacin
Local 2% minocycline-HCl
297
However, their antimicrobial activities against other peri-
odontal pathogens such as P. gingivalis, F. nucleatum,
P. intermedia, and T. forsythia were reported to be less than
optimal [51]. Sitafloxacin is an oral fluoroquinolone anti-
microbial agent with broad-spectrum antibacterial activity
against Gram-positive and Gram-negative aerobes and an-
aerobes [52, 53]. Since June 2008, this drug has been used
clinically in Japan and Thailand for a number of conditions
including pneumonia, cystitis, and pyelonephritis [54, 55].
In a clinical study, systemic administration of sitafloxacin
was shown to improve periodontal health of older patients
during supportive periodontal therapy [56, 57]. In the fol-
lowing subsections, we describe our two recent studies on
the use of sitafloxacin as an adjunct treatment modality for
acute periodontal lesions.
Systemic Administration of Sitafloxacin
and Antimicrobial Susceptibilities
In this first study, we assessed the effects of a new
fluoroquinolone, sitafloxacin, on subgingival microbial
profiles of acute periodontal lesions [24•]. Patients with
acute phases of chronic periodontitis were subjected to
clinical examination and microbiological assessment of
their subgingival plaque samples by culture technique.
Patients were excluded from the study if they had a
pronounced periodontal abscess that might require drain-
age through an external incision or tooth extraction. All
patients (n = 30) received systemic administration of
sitafloxacin (100 mg/day for 5 days). A total of 355
clinical isolates (34 different bacterial species) were identified
from sampled sites. Systemic administration of sitafloxacin
yielded a significant improvement in clinical and microbio-
logical parameters. Among antimicrobials tested, sitafloxacin
was the most potent when comparing the susceptibilities of
clinical isolates classified as red, orange, or yellow complex
bacteria [58]. These periodontal bacteria were highly suscep-
tible to sitafloxacin (Table 2).
The results suggested that systemic administration of
sitafloxacin is effective against subgingival bacteria isolated
from acute periodontal lesions.
Dosage Reference
500 + 125 mg, 3 times daily for 8 days [46]
1000 mg/day for 14 days [1]
200 mg, 3 times daily for 5 days [47]
500 mg/day for 3 days [46]
100 mg/day for 5 days [24•, 48•]
Once a week for 4 weeks [44]
298 Curr Oral Health Rep (2017) 4:294–300

Table 2 Minimum inhibitory

concentrations (μg/mL) of Isolates Before STFX administration After STFX administration
sitafloxacin, levofloxacin, and
azithromycin for isolated red, Acute sites Control sites Acute sites Control sites
orange, and yellow complex
periodontal bacteria before and STFX Red complex
after systemic administration of P. gingivalis ND ≤ 0.004–0.015 0.5
sitafloxacin [24•] (reproduced
Orange complex
with permission from Elsevier)
P. intermedia 0.015–0.03 0.015–0.03
P. micra 0.008–0.03 0.015–0.06 0.12 0.015
S. constellatus 0.03–0.06 0.06 0.25 0.12
Yellow complex
S. oralis 0.015–1 0.03–1 0.06–2 0.06–1
S. mitis 0.015–0.5 0.008–0.12 0.03–1 0.03–1
LVFX Red complex
P. gingivalis ND 0.06–0.5 32
Orange complex
P. intermedia 0.25–1 0.25–1
P. micra 0.12–2 0.25–1 4 0.25
S. constellatus 1–2 1 4 2
Yellow complex
S. oralis 0.5–32 1–32 1–64 2–32
S. mitis 0.5–16 0.25–2 1–32 1–64
AZM Red complex
P. gingivalis ND 4–8 1
Orange complex
P. intermedia 0.12–32 0.12–32
P. micra 1–> 64 2–> 64 4 2
S. constellatus 0.5–> 64 1 1 1
Yellow complex
S. oralis 0.06–> 128 0.06–16 0.06–> 128 0.06–32
S. mitis 0.03–> 128 0.03–> 128 0.06–> 128 0.06–> 128

STFX, sitafloxacin; LVFX, levofloxacin; AZM, azithromycin; ND, not determined

Changes in Antimicrobial Susceptibility Profile
and Prevalence of Quinolone Low-sensitive Strains After
Systemic Administration of Sitafloxacin
In a follow-up study, we investigated the changes in
antimicrobial susceptibilities of subgingival bacteria in acute
periodontal lesions following systemic administration of
sitafloxacin and monitored the occurrence and fate of
quinolone low-sensitive strains [48•]. Patients with acute phase
of chronic periodontitis were subjected to microbiological
assessment of their subgingival plaque samples at baseline
(A1). Sitafloxacin was then systemically administered as
described in our previous study [24•]. At 1 week following
administration (A2), microbiological examinations were
repeated and antimicrobial susceptibilities of clinical isolates
were evaluated. At A2, subgingival bacteria with low suscep-
tibility to levofloxacin were found in four patients. These pa-
tients received follow-up microbiological examination
(A3). Depending on their conditions, patients also received
initial and supportive periodontal therapy from A2 to A3.
Some Streptococcus strains isolated at A2 were resistant to
levofloxacin, azithromycin, or clarithromycin. At A3, isolated
streptococci were highly susceptible to levofloxacin.
However, strains resistant to azithromycin or clarithromycin
were still isolated.
These results suggested that the presence of quinolone
low-sensitive strains in initially acute lesions after sitafloxacin
administration was transient, and these bacteria may not be
able to persist in the subgingival area during periodontal
therapy.
These two studies collectively suggest that sitafloxacin
may be an alternative to conventional antimicrobial agents in
adjunctive treatment of periodontal abscesses, especially in
patients who harbor periodontal bacteria with low susceptibility
to conventional antimicrobial agents. Further research is
needed to better understand longitudinal changes in the
prevalence of resistant bacteria in the periodontal milieu
following antimicrobial therapy. Such understanding is
Curr Oral Health Rep (2017) 4:294–300
essential to ensure responsible and optimal antimicrobial
therapy in periodontal treatment.
Conclusions
In the treatment of periodontal abscesses, especially in acute
conditions, drainage must be considered first. When drainage
is not possible or insufficient, antimicrobial therapy should
then be considered. In periodontal treatment, it is sometimes
difficult to incorporate microbiological assessments including
antimicrobial susceptibility testing, mainly due to time and
cost constraints. However, these assessments can significantly
contribute to successful treatment.
Compliance with Ethical Standards
Conflict of Interest The two studies on antimicrobial susceptibility
(Tomita et al. 2014, 2015) were supported in part by Daiichi Sankyo,
Co., Ltd., Tokyo, Japan. Sachiyo Tomita and Atsushi Saito declare that
they have no other conflicts of interest to report.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
References
Papers of particular interest, published recently, have been
highlighted as:
• Of importance
•• Of major importance
1. Hafström CA, Wikström MB, Renvert SN, Dahlén GG. Effect of
treatment on some periodontopathogens and their antibody levels in
periodontal abscesses. J Periodontol. 1994;65(11):1022–8.
2. Umeda M, Tominaga Y, He T, Yano K, Watanabe H, Ishikawa I.
Microbial flora in the acute phase of periodontitis and the effect of
local administration of minocycline. J Periodontol. 1996;67(4):
422–7.
3.•• Herrera D, Alonso B, de Arriba L, Santa Cruz I, Serrano C, Sanz M.
Acute periodontal lesions. Periodontol. 2014;65(1):149–77. This
paper provides an extensive review on acute periodontal lesions
including periodontal abscess.
4. Albandar JM. Aggressive and acute periodontal diseases.
Periodontol. 2014;65(1):7–12.
5. Corbet EF. Diagnosis of acute periodontal lesions. Periodontol.
2004;34(1):204–16.
6. Armitage GC. Development of a classification system for periodon-
tal diseases and conditions. Ann Periodontol. 1999;4(1):1–6.
7. Meng HX. Periodontal abscess. Ann Periodontol. 1999;4(1):79–82.
8. Newman MG, Sims TN. The predominant cultivable microbiota of
the periodontal abscess. J Periodontol. 1979;50(7):350–4.
9. Kareha MJ, Rosenberg ES, DeHaven H. Therapeutic consider-
ations in the management of a periodontal abscess with an
intrabony defect. J Clin Periodontol. 1981;8(5):375–86.
299
10. DeWitt GV, Cobb CM, Killoy WJ. The acute periodontal abscess:
microbial penetration of the soft tissue wall. Int J Periodontics
Restorative Dent. 1985;5(1):38–51.
11. Dello Russo NM. The post-prophylaxis periodontal abscess: etiol-
ogy and treatment. Int J Periodontics Restorative Dent. 1985;5(1):
28–37.
12. Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK. Long-
term evaluation of periodontal therapy: I. Response to 4 therapeutic
modalities. J Periodontol. 1996;67(2):93–102.
13. Garrett S, Polson AM, Stoller NH, Drisko CL, Caton JG, Harrold
CQ, et al. Comparison of a bioabsorbable GTR barrier to a non-
absorbable barrier in treating human class II furcation defects. A
multi-center parallel design randomized single-blind trial. J
Periodontol. 1997;68(7):667–75.
14. Chace R Sr, Low SB. Survival characteristics of periodontally-
involved teeth: a 40-year study. J Periodontol. 1993;64(8):701–5.
15. McLeod DE, Lainson PA, Spivey JD. Tooth loss due to periodontal
abscess: a retrospective study. J Periodontol. 1997;68(10):963–6.
16. Silva GL, Soares RV, Zenobio EG. Periodontal abscess during sup-
portive periodontal therapy: a review of the literature. J Contemp
Dent Pract. 2008;9(6):82–91.
17. Ibbott CG, Kovach RJ, Carlson-Mann LD. Acute periodontal ab-
scess associated with an immediate implant site in the maintenance
phase: a case report. Int J Oral Maxillofac Implants. 1993;8(6):699–
702.
18. Topoll HH, Lange DE, Müller RF. Multiple periodontal abscesses
after systemic antibiotic therapy. J Clin Periodontol. 1990;17(4):
268–72.
19. Herrera D, Roldán S, González I, Sanz M. The periodontal abscess
(I). Clinical and microbiological findings. J Clin Periodontol.
2000;27(6):387–94.
20. van Winkelhoff AJ, Carlee AW, de Graaff J. Bacteroides
endodontalis and other black-pigmented Bacteroides species in
odontogenic abscesses. Infect Immun. 1985;49(3):494–7.
21. Jaramillo A, Arce RM, Herrera D, Betancourth M, Botero JE,
Contreras A. Clinical and microbiological characterization of peri-
odontal abscesses. J Clin Periodontol. 2005;32(12):1213–8.
22. Eguchi T, Koshy G, Umeda M, Iwanami T, Suga J, Nomura Y, et al.
Microbial changes in patients with acute periodontal abscess after
treatment detected by PadoTest. Oral Dis. 2008;14(2):180–4.
23. Dahlén G. Microbiology and treatment of dental abscesses and
periodontal-endodontic lesions. Periodontol. 2002;28(1):206–39.
24.• Tomita S, Kasai S, Ihara Y, Imamura K, Kita D, Ota K, et al. Effects
of systemic administration of sitafloxacin on subgingival microflora
and antimicrobial susceptibility profile in acute periodontal lesions.
Microb Pathog. 2014;71–72:1–7. A study investigated the effects
of a new fluoroquinolone, sitafloxacin, on subgingival microbial
profiles of acute periodontal lesions
25. Kasai S, Tomita S, Fukaya C, Ihara Y, Saito A, Nakagawa T.
Clinical and microbiological effects of systemic sitafloxacin admin-
istration in the treatment of acute periodontal lesions. J Jpn Soc
Periodontol. 2014;56(1):39–48 (in Japanese with English abstract).
https://doi.org/10.2329/perio.56.39.
26. Trope M, Tronstad L, Rosenberg ES, Listgarten M. Darkfield mi-
croscopy as a diagnostic aid in differentiating exudates from end-
odontic and periodontal abscesses. J Endod. 1988;14(1):35–8.
27. Hiatt WH. Incomplete crown-root fracture in pulpal-periodontal
disease. J Periodontol. 1973;44(6):369–79.
28. Walton RE. Vertical root fracture: factors related to identification. J
Am Dent Assoc. 2017;148(2):100–5.
29. Schmidt JC, Walter C, Amato M, Weiger R. Treatment of
periodontal-endodontic lesions—a systematic review. J Clin
Periodontol. 2014;41(8):779–90.
30. Ahl DR, Hilgeman JL, Snyder JD. Periodontal emergencies. Dent
Clin N Am. 1986;30(3):459–72.
300
31. Parrish LC, Kretzschmar DP, Swan RH. Osteomyelitis associated
with chronic periodontitis: a report of three cases. J Periodontol.
1989;60(12):716–22.
32. Kim OS, Uhm SW, Kim SC, Lee BA, Kim OJ, Kim YJ, et al. A
case of squamous cell carcinoma presenting as localized severe
periodontitis in the maxillary gingiva. J Periodontol. 2012;83(6):
753–6.
33. Elkhoury J, Cacchillo DA, Tatakis DN, Kalmar JR, Allen CM,
Sedghizadeh PP. Undifferentiated malignant neoplasm involving
the interdental gingiva: a case report. J Periodontol. 2004;75(9):
1295–9.
34. Girdler NM. Eosinophilic granuloma presenting as a chronic lateral
periodontal abscess: a lesson in diagnosis? Br Dent J. 1991;170(7):
250.
35. Panseriya BJ, Hungund S. Pyogenic granuloma associated with
periodontal abscess and bone loss—a rare case report. Contemp
Clin Dent. 2011;2(3):240–4.
36. Beckett H, Buxey-Softley G, Gilmour AG. Self-inflicted gingival
injury. Br Dent J. 1995;178(7):246.
37. Sousa D, Pinto D, Araujo R, Rego RO, Moreira-Neto J. Gingival
abscess due to an unusual nail-biting habit: a case report. J Contemp
Dent Pract. 2010;11(2):85–91.
38. Lim HC, Kim CS. Oral signs of acute leukemia for early detection. J
Periodontal Implant Sci. 2014;44(6):293–9.
39. Alagl AS. Periodontal abscess as a possible oral clinical sign in the
diagnosis of undiagnosed diabetes mellitus of elderly in a dental
clinic set up—a 7-year cross-sectional study. J Investig Clin Dent.
2016; https://doi.org/10.1111/jicd.12217.
40. Takeuchi N, Ekuni D, Tomofuji T, Morita M. Relationship between
acute phase of chronic periodontitis and meteorological factors in
the maintenance phase of periodontal treatment: a pilot study. Int J
Environ Res Public Health. 2015;12(8):9119–30.
41. Sanz M, Herrera D, van Winkelhoff AJ: The periodontal abscess.
In: Lindhe J, editor. Clinical Periodontology. Copenhagen:
Munksgaard; 2000.
42. Melnick PR, Takei HH. Treatment of periodontal abscess. In:
Newman MG, Takei HH, Carranza FA, editors. Carranza’s clinical
periodontology. 12th ed. Philadelphia: Elsevier Saunders; 2015.
43. Abrams H, Kopczyk RA. Gingival sequela from a retained piece of
dental floss. J Am Dent Assoc. 1983;106(1):57–8.
44. Japanese Society of Periodontology. JSP clinical practice guideline
for the periodontal treatment, 2015. Tokyo: Ishiyaku Publishers;
2016.
45. Lewis MA, McGowan DA, MacFarlane TW. Short-course high-
dosage amoxycillin in the treatment of acute dentoalveolar abscess.
Br Dent J. 1986;161(8):299–302.
46. Herrera D, Roldán S, O’Connor A, Sanz M. The periodontal ab-
scess (II). Short-term clinical and microbiological efficacy of 2
systemic antibiotic regimes. J Clin Periodontol. 2000;27:395–404.
Curr Oral Health Rep (2017) 4:294–300
47. Smith RG, Davies RM. Acute lateral periodontal abscesses. Br
Dent J. 1986;161(5):176–8.
48.• Tomita S, Kasai S, Imamura K, Ihara Y, Kita D, Ota K, et al.
Changes in antimicrobial susceptibility profile and prevalence of
quinolone low-sensitive strains in subgingival plaque from acute
periodontal lesions after systemic administration of sitafloxacin.
Microb Pathog. 2015;79:41–6. This study assessed the changes
in antimicrobial susceptibilities of subgingival bacteria in acute
periodontal lesions following systemic administration of
sitafloxacin, and monitored the occurrence and fate of quino-
lone low-sensitive strains
49. Wexler HM, Molitoris E, Finegold SM. In vitro activities of three of
the newer quinolones against anaerobic bacteria. Antimicrob
Agents Chemother. 1992;36(1):239–43.
50. Pavicić MJ, van Winkelhoff AJ, de Graaff J. In vitro susceptibilities
of Actinobacillus actinomycetemcomitans to a number of antimi-
crobial combinations. Antimicrob Agents Chemother. 1992;36(12):
2634–8.
51. Maeda R, Ishihara K, Hosaka Y, Nakagawa T. Antibacterial activity
of antibiotics against periodontopathic bacteria. J Jpn Soc
Periodontol. 2005;47(3):146–152 (in Japanese with English ab-
stract). https://doi.org/10.2329/perio.47.146.
52. Sato K, Hoshino K, Tanaka M, Hayakawa I, Osada Y.
Antimicrobial activity of DU-6859, a new potent fluoroquinolone,
against clinical isolates. Antimicrob Agents Chemother.
1992;36(7):1491–8.
53. Keating GM. Sitafloxacin: in bacterial infections. Drugs.
2011;71(6):731–44.
54. Kohno S, Niki Y, Kadota J, Yanagihara K, Kaku M, Watanabe A,
et al. Clinical dose findings of sitafloxacin treatment:
pharmacokinetic-pharmacodynamic analysis of two clinical trial
results for community-acquired respiratory tract infections. J
Infect Chemother. 2013;19(3):486–94.
55. Manosuthi W, Wiboonchutikul S. Treatment outcomes of oral
sitafloxacin in acute complicated urinary tract infection and pyelo-
nephritis. Spring. 2016;5(1):410.
56. Nakajima T, Okui T, Miyauchi S, Honda T, Shimada Y, Ito H, et al.
Effects of systemic sitafloxacin on periodontal infection control in
elderly patients. Gerodontology. 2012;29(2):e1024–32.
57. Nakajima T, Okui T, Ito H, Nakajima M, Honda T, Shimada Y, et al.
Microbiological and clinical effects of sitafloxacin and
azithromycin in periodontitis patients receiving supportive peri-
odontal therapy. Antimicrob Agents Chemother. 2016;60(3):
1779–87.
58. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr.
Microbial complexes in subgingival plaque. J Clin Periodontol.
1998;25(2):134–44.