Med Oral Patol Oral Cir Bucal 2007;12:E154-9.

Management of odontogenic infection

Management of odontogenic infection of pulpal and periodontal origin

Roberto Lpez-Priz 1, Lorenzo Aguilar 2, Maria Jos Gimnez 3

(1) Degree in Medicine and Surgery. Degree in Odontology. Doctoral student

(2) Doctor in Medicine and Surgery
(3) Doctor in Pharmacy. Microbiology Department, Faculty of Medicine, UCM

Correspondence:
Dr. Roberto Lpez-Priz.
C/ General lvarez de Castro, n 5, 1 B.
28010. Madrid.
E-mail: lopezpiriz@telefonica.net
Lpez-Priz R, Aguilar L, Gimnez MJ. Management of odontogenic
infection of pulpal and periodontal origin. Med Oral Patol Oral Cir
Received: 12-11-2006 Bucal 2007;12:E154-9.
Accepted: 25-01-2007 Medicina Oral S. L. C.I.F. B 96689336 - ISSN 1698-6946

Indexed in:
-Index Medicus / MEDLINE / PubMed
-EMBASE, Excerpta Medica
-SCOPUS
-Indice Mdico Espaol
-IBECS

ABSTRACT
The dental biofilm is a complex bacterial ecosystem that undergoes evolution, maturing and development, and thus leads
to odontogenic infection. The infection is normally located in the tissues of the dental organ itself, and follows a chronic
course of evolution. However, bacterial pathogens express virulence factors in the biofilm, and this together with chan-
ges in host immunity, may cause clinical exacerbations and spread of infection to other areas of the body. Odontogenic
infection management should take into consideration the fact that therapeutic success lies in the control of the infectious
aetiologic agent, using mechanical-surgical debridement and/or antimicrobial therapy. Debridement techniques have a
fundamentally quantitative effect (by reducing the size of the inoculum) and therefore if these techniques are used alone to
control infection, despite an initial clinical improvement that is sometimes prematurely considered as therapeutic success,
odontopathogens may persist and the process may recur or become chronic. Microbiological examination may be helpful
in defining therapeutic success in a more reliable way, it could define the prognosis of recurrence more precisely, and
could enable the most appropriate antibiotic to be selected, thus increasing therapeutic efficacy. Antimicrobial therapy
brings about a quantitative and qualitative change in the bacterial composition of the biofilm, in addition to being able
to act on sites that are inaccessible through mechanical debridement. However, incorrect antimicrobial use can lead to
a selection of resistant bacterial species in the biofilm, in addition to side effects and ecological alterations in the host.
In order to minimise this risk, and obtain maximum antimicrobial effect, we need to know in which clinical situations
their use is indicated, and the efficacy of different antibiotics with regard to bacteria isolated in odontogenic infection.

Key words: Odontogenic infection, treatment, odontogenic infection, microbiological diagnosis, dental biofilm, dental abs-
cess.

RESUMEN
La biopelcula dental es un ecosistema bacteriano complejo cuya evolucin, maduracin y desarrollo ocasiona la infec-
cin odontognica. Habitualmente la infeccin se encuentra localizada en los tejidos del propio rgano dentario y sigue
un curso evolutivo crnico, aunque la expresin de factores de virulencia bacterianos en la biopelcula o cambios en
la situacin inmune del husped pueden ocasionar exacerbaciones clnicas y la extensin de la infeccin a otras zonas
del organismo. En el abordaje de la infeccin odontognica debemos tener presente que el xito teraputico radica en
el control del agente etiolgico infeccioso, mediante desbridamiento con tcnicas mecnico-quirrgicas y/o administra-
cin de antimicrobianos. El efecto de las tcnicas de desbridamiento sobre la biopelcula es fundamentalmente de tipo
cuantitativo (disminuye el tamao del inculo) de modo que su empleo como nico medio de control de la infeccin
puede suponer la persistencia de odontopatgenos y la recurrencia o cronificacin del proceso, aunque obtengamos una
mejora clnica inicial que en ocasiones consideramos xito teraputico de modo precipitado. Realizar un estudio micro-

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biolgico podra ayudar a definir el xito teraputico con mayor fiabilidad, dar ms exactitud a nuestros pronsticos de
recurrencia, y seleccionar el antibitico ms apropiado aumentando la eficacia teraputica. El tratamiento antimicrobiano
ocasiona un cambio cuantitativo y cualitativo en la composicin bacteriana de la biopelcula, adems de poder actuar
en lugares no accesibles al desbridamiento mecnico. Sin embargo, un mal uso de los antimicrobianos puede ocasionar
seleccin de especies bacterianas resistentes en la biopelcula adems de efectos secundarios y alteraciones ecolgicas
en el husped. Para minimizar este riesgo y obtener el mximo rendimiento del empleo de antimicrobianos es preciso
conocer las situaciones clnicas que indican su uso y la eficacia de los distintos antibiticos frente a los aislados en la
infeccin odontognica.

Palabras clave: Infeccin odontognica/tratamiento, infeccin odontognica, diagnstico microbiolgico, biopelcula dental,
absceso dental.

EPIDEMIOLOGY and their relation with health or disease. Purple (with

Odontogenic infection is the most prevalent disease fundamentally aerobic and immobile flora), yellow and
worldwide and it is the principal reason for seeking dental green complexes are not associated with disease, whilst
care. The commonest emergency odontogenic infections orange (F. nucleatum/periodonticum, P. intermedia, P.
are periapical abscess (25%), pericoronitis (11%) and micros) and red (P. gingivalis, T. forsythia, T. denticola)
periodontal abscess (7%). Its significance in health proble- complexes cause disease in the presence of virulent clones
ms is also reflected by the fact that 12% of antibiotics are with intra- and extrachromosomic genetic information in
prescribed for odontological reasons. (1) a sufficient quantity to overcome the immune resistance of
the host. A. actinomycetemcomitans is also considered as
AETIOLOGY OF ODONTOGENIC INFECTION a periodontal pathogen although it is not included in any
The World Health Organisation accepts that the dental particular group.
biofilm is the aetiological agent of odontogenic infection,
and defines biofilm as a proliferative bacterial, enzyme- PATHOGENICS OF ODONTOGENIC INFEC-
active ecosystem. As soon as a baby is born, a colonisation TION
process commences and this results in the development of The supragingival biofilm is fundamentally gram-positive,
a pioneer community in the mouth with predominance of facultative and saccharolytic, which means that in the
Streptococcus salivarius. At the age of six months (when the presence of sugars, it produces acids that demineralise
first teeth appear) this community has a majority presence enamel, facilitating biofilm infiltration of dentin and pulp.
of S. sanguis and S. mutans, and by the time dentition has With the bacterial invasion of the tooths internal tissue,
been completed, there is a heterogeneous aerobic and anae- the biofilm evolves, and thus root canals are infected with
robic community. It is estimated that up to 700 species may predominantly gram-negative, anaerobic and proteolytic
colonise the mouth, 400 of which colonise the subgingival bacteria. Some of these bacteria have virulence factors that
area. Biofilm evolution is an autogenic succession process enable them to invade periapical tissues through the apical
based on bacterial interactions that occur through physical foramen. (3) More than half of active periapical lesions
contact, metabolic exchange, communication through sig- cannot be detected on X-ray because they measure less than
nalling (quorum sensing) and genetic material exchange. 0.1 mm2. (4) If the host immune response causes an accu-
Coaggregation is based on specific recognition of different mulation of neutrophils, this will cause a periapical abscess,
bacterial species and one of the principle mechanisms of which is a destructive tissue lesion. But if the response is
evolution and maintenance of the biofilm. (2) predominantly mediated by macrophages and T-cells, an
Odontogenic infection is polymicrobial and mixed. It is apical granuloma will develop, characterised more by tissue
the result of biofilm maturing that consists of a change reorganisation than by tissue destruction. Changes in host
in the predominant bacterial species (from predominantly immunity or in bacterial virulence may cause reactivation
gram-positive, facultative and saccharolytic flora to predo- of silent periapical lesions.
minantly gram-negative, anaerobic and proteolytic flora), Odontogenic infection may also originate in periodontal
the association of different bacterial morphotypes and tissues. When the subgingival biofilm evolves and incorpo-
increased bacterial diversity. Fusobacterium nucleatum is rates periodontal pathogens that express virulence factors,
considered as the central structural component of biofilm this triggers an immune response in the host causing damage
because it coaggregates with the biofilm components that tending to chronicity that finally causes periodontal bone
do not cause disease and with periodontal pathogens, thus loss. The periodontal abscess may originate from an exa-
permitting biofilm evolution into odontogenic infection. cerbation of chronic periodontitis, the presence of dental
In 1992, Socransky modified Kochs postulates, laying defects that facilitate bacterial invasion (e.g. development
down criteria for identifying periodontal pathogens. (3) grooves, root fusion, etc.) or it may be of iatrogenic origin,
Biofilm study using DNA hybridisation techniques ena- due to impaction of a calculus in the epithelium of the
bled detection of associations of specific bacterial species periodontal pocket during scaling or incorrect debridement

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that only solves gingival distension at a coronal level, pre- fractures that are perpendicular or oblique to the X-ray
venting drainage of apical zone of the pocket. (5) may not be detected.
Some abscesses form a fistula and become chronic. They In addition, pulp vitality tests help to identify target tooth
are generally asymptomatic or paucisymptomatic. A spe- and also the likely origin of bacterial invasion: infection
cial form of recurrent periodontal abscess is pericoronitis, may be of pulpar origin if the test is negative or if there is an
caused by bacterial invasion of the coronal pouch during exaggerated response to stimulus; it may be of periodontal
molar eruption. origin if positive test without discrepancies with that of
It is sometimes unclear as to whether the infection has a other teeth.
periodontal or pulpar origin, and therefore the term endo- However, there is some controversy regarding the utility and
periodontal lesions are used. (4) There is some controversy indication of microbiology diagnostic tests in odontogenic
as to whether a pulpar lesion can cause periodontal damage infections. Clearly there is no need to perform a microbio-
and vice versa, which raises several questions at a clinical le- logy examination in order to diagnose periodontitis, but a
vel: should we perform prophylactic canal treatment of teeth microbiological analysis of the infection may be useful if
with moderate or advanced periodontitis? Should a tooth results enable us to improve our therapeutic strategies and
with pulpar necrosis be replaced by an implant in order to ensure successful treatment, and in any case it serves to
prevent periodontal bone loss? The pulp can be invaded provide epidemiological data. (6)
from the periodontium through dentin tubules, lateral canals Microbiological analysis can help to identify the origin of
and the apical foramen, but it is very rare to find a tooth infection. Although all odontogenic infections are result of
without pulp vitality and free of caries, restoration work or biofilm evolution, and there are therefore marked similari-
trauma to justify it, and therefore periodontal disease and ties in the bacterial composition of odontogenic infections,
periodontal mechanical debridement do not appear to have regardless of their tissue of origin (Table 1), some bacterial
a significant influence on pulp vitality. Teeth without pulp species are specific to abscesses with pulpar origin (e.g. Por-
vitality and with active periapical lesions present greater phiromonas endodontalis); while others will rule out this
marginal bone loss / year than teeth with pulp vitality, but origin (e.g. A. actinomycetemcomitans). (7,8)
these differences are not significant enough in periodontal However, odontological microbiological studies are complex
prognosis to justify preventive tooth extraction. Pulpar to perform. Sampling is a difficult task since samples often
infection can form a fistula in the periodontium, causing a become contaminated, thus altering results. Samples must
deep and narrow periodontal lesion. In general, the presence be transported in appropriate media for mixed flora.
of pulp vitality indicates that the bacterial invasion has oc-
curred from or through the periodontium, and the absence
of pulp vitality suggests an endodontic origin of infection.
If an in-depth clinical examination is carried out, few lesions Table 1. Type of odontogenic infections and organims responsible.
will actually be classified as endoperiodontal lesions.
Infectious process Predominant odontopathogens

DIAGNOSIS OF ODONTOGENIC INFECTION Porphiromonas gingivalis.

Tannerella forsythensis
Diagnosing the origin of odontogenic infection is funda- Actinomyces actinomycetemcomitans
mental in order to manage treatment appropriately. The Periodontitis
Prevotella intermedia
problem tooth needs to be identified, as well as the tissue Fusobacterium nucleatum
Veionella parvula
where the biofilm bacteria have commenced their invasion. Treponema dentcola
Clearly, a thorough physical examination is required, along Streptococcus spp.
with X-rays and pulp vitality tests. Fusobacterium nucleatum
Clinical manifestations may be useful when they are referred Prevotella intermedia
to a specific tooth (e.g. periodontal abscess), but manifesta- Pulpitis with
Peptostretococcus micros
tions are often diffuse or even refer to areas that are adjacent Capnociytophaga ochracea
periapical abscess
Selenomonas sputigena
to the origin of the infection (e.g. pulpitis). Odontogenic Porphiromonas endodontalis
infection may also occur without symptoms (e.g. chronic Streptococcus spp.
periodontitis) or with very few symptoms (e.g. periapical Prevotella intermedia
abscess that has formed a fistula), and this could only be Veionella parvulaPrevotella melaninogenica
manifested on clinical examination. A clinical examination Pericoronitis Fusobacterium nucleatum
Actinomyces israelii/odontolyticus
consisting in inspection and percussion of teeth is essential Streptococcus spp.
to identify the origin of infection.
Fusobacterium nucleatum
X-rays provide essential information but certain limitatio- Prevotella intermedia
ns should be considered: 1. Some periapical cysts may be Periimplantitis Pseudomona aeruginosa
larger than a periapical X-ray film, and therefore only the Staphilococcus spp
contents will be observed; 2. During early stages of infec- Actinomyces actinomycetemcomitans
tion changes in bone density may not be noticeable; 3. Only
bidimensional information can be gained, and therefore

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Differences in bacterial identification methods are also these techniques do not modify the composition of the bio-
the cause of discrepancy in conclusions drawn by different film and the persistence of odontopathogens that could lead
studies that have analysed the bacterial composition of to recurrence or a chronic state. A. actinomycetemcomitans
odontogenic infections. Bacterial culture is the traditional and P. gingivalis cannot be eliminated in the majority of
method of identification, but some bacteria require special deep periodontal lesions with root debridement alone. (7)
culture methods (e.g. T. forsythia) and others can only be The persistence of S. faecalis in root canals is related to the
identified using immunofluorescent techniques or DNA need to repeat endodontic treatment, and the percentage
hybridisation. (6) of failed root canal treatment according to X-ray results is
Keyes used differential darkfield microscopy to determine estimated at about 50%. (4,8) Furthermore, some bacteria
the level of spirochetes and motile rods, thus ending treat- (Actinomyces israelii; Propionibacterium propionicum)
ment when there was a reduced number found on the biofilm are capable of reaching the dental periapex and remain
examined. (6) It is now known that some bacteria behave as there, requiring an apicectomy in an attempt to eliminate
exogeneous pathogens and some bacterial associations rela- persistent infection.
ted to a low treatment response or high rate of recurrence. (3) Additional techniques to complement mechanical treat-
For example, the presence of A. actinomycetemcomitans; P. ment include chemical debridement by means of topical
gingivalis; or P. intermedia is associated with recurrence in application of antiseptics and antimicrobial agents. It is
periodontal disease activity. Thus, since the microbiological recommended to use antiseptic irrigation concomitantly
examination can identify odontopathogens and determine during mechanical debridement, but the use of topical
their numbers in the biofilm, then it can help to make deci- substances is not indicated during the acute phase because
sions on a specific therapeutic strategy and to monitor resul- they hinder drainage. (5) Root canals can be filled with
ts of clinical studies. In short, microbiology helps to define antiseptic substances for a long period of time, but such
therapeutic success and the risk of relapse more precisely, substances have little or no action at a periapical level. The
thus avoiding a prognosis based exclusively on clinical data topical use of antimicrobials should be restricted because
(i.e. initial improvement following debridement). this favours the development of resistance and their clinical
Microbiological cultures also allow the study of suscepti- effect is limited to the application surface since they do not
bility of odontopathogenic isolates to different antibiotics. act on invasive bacteria. (4,5,7)
They can determine which antimicrobial agents are the The relevance of antimicrobials in the management of
most effective in odontogenic infections, by determining odontogenic infection lies in their clinical utility when
minimum inhibitory concentrations. These data are the administered systemically. Systemic antibiotic therapy pre-
basis of studies relating odontopathogenic susceptibility vents the infection from spreading and it acts in places that
and antimicrobial pharmacokinetics/pharmacodynamics, in mechanical treatment cannot reach. It therefore act more
order to establish the most effective therapeutic regimen. specifically on odontopathogens than debridement does.
(10) It is indicated for therapeutic purposes in fast-progre-
TREATMENT OF ODONTOGENIC INFECTION ssing and recurrent periodontitis, and in all odontogenic
The objective of antibacterial treatment is to control (re- infections with rapidly evolving signs and symptoms (24-48
duce or eliminate) the infective bacterial load. To achieve hours), trismus, oedema, and/or systemic manifestations
this, in the case of odontogenic infection, therapeutic action such as malaise, fever, tachypnoea, dyspnoea, cellulites,
combines mechanical debridement, and/or surgery, and/or lymphadenopathy and hypotension. (11) Systemic antibiotic
systemic antibiotic therapy, where appropriate. therapy is also indicated in the prophylaxis of systemic or
The first step in the case of dental abscess is to drain and distant infection and as a preventive treatment of infection
debride the abscess using mechanical-surgical techniques. in immunodepressed patients or in patients with severe
Drainage is performed by making an incision in the area systemic disease undergoing an invasive or long time dental
of greatest fluctuation. If the abscess is of an endodontic procedure. (10,12,13)
origin, drainage can be performed through the root canals. It has been demonstrated that periodontal abscesses have
Tooth extraction provides a drainage route and eliminates resolved solely by means of systemic antibiotic therapy.
the entrance route for the infection, but it is only indicated in (5,14,15) However, debridement should be the first step
the acute phase after having balanced these benefits against in therapy because draining the infection and eliminating
the risk of spreading bacterial inoculum during surgery. necrotic waste will facilitate antimicrobial action. Treatment
Tooth extractions that require flap surgery or ostectomy with antimicrobials alone is indicated when the severity of
should be delayed until a second stage when infection has the infection advises delaying surgical techniques due to the
been controlled. Mechanical debridement eliminates necro- risk of spreading the infection during debridement itself.
tic tissue and bacterial residues, and consists in debridement (11) Antibiotic prophylaxis achieves better results if the an-
of the root surface in the case of periodontal involvement, timicrobial agent is administered pre-operatively. (10,13)
or of the bone canal in the case of pulpar infection. Paradoxically, treatment of chronic asymptomatic infection
Mechanical-surgical techniques have a quantitative effect can cause an acute exacerbation of the infectious process.
on bacterial load giving the host the opportunity to recover Periodontal scaling and endodontic over-instrumenta-
homeostasis through immune system action. (9) However, tion can cause bleeding and exudates in periodontal and

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periapical tissues, providing bacteria with nutrients, and Some studies have analysed the susceptibility of bacterial
thus stimulating proliferation, which may overcome the species in the biofilm to antibiotics in Spain. (16)
hosts immune resistance. This factor should be given special These studies show a high rate of resistance to certain
consideration in immunodepressed patients and in patients antimicrobial agents and beta-lactamase production by
whose microbiological studies reveal odontopathogens Prevotella spp, Fusobacterium spp.; Capnocytophaga spp.
or bacterial associations that are particularly resistant to and some strains of Veionella spp.(17-19). From results
therapy. In these cases, it is essential to use an effective obtained (Table 2), there is consensus regarding the treat-
antimicrobial agent. (10,13) ment and prophylaxis of odontogenic infection in which
Only physicians or dentists should select which antimicro- amoxicillin associated with clavulanic acid is indicated as
bial agent to use, because it is a complex clinical process that the first choice antibiotic, and clindamycin as an alternative
is based on empirical evidence and clinical, microbiological in the event of penicillin allergy. (12,13,20)
and pharmacokinetic knowledge. (10) Antimicrobial pharmacodynamics determine the most effec-
The use of an antibiotic with an inappropriate spectrum tive dosage regimen to attain bacterial eradication without
that does not act on certain resistant bacterial species will encouraging the development of resistance. The most common-
lead to excess proliferation of the latter by eliminating other ly used antibiotics in odontology are time-dependent, which
sensitive species. This may trigger acute exacerbations or means that to be effective, their physiological levels must exceed
persistent infection. Wide spectrum antibiotics must be used the minimum inhibitory concentration for at least 40% of the
in view of the polymicrobial, mixed nature of odontogenic time between doses. (16) Taking into account the susceptibility
infections, and such antibiotics must be especially active of isolated bacteria, resistance mechanisms and antibiotic
against the commonest odontopathogens. When selecting pharmacodynamics, high doses of amoxicillin / clavulanic
an antibiotic, consideration should be made for natural acid (875/125 mg three times daily or 2000/125 mg twice
resistance (e.g. Strepococcus sp.; Actinomyces sp. and A. daily) are the most appropriate treatment of caries-associated
acinomycetemcomitans against metronidazole) and the odontogenic infections (pulpitis, abscesses), and of periodontal
possible presence of acquired resistance, which are those infections when so required, and clindamycin provides an al-
that take advantage of incorrect antibiotic use. ternative choice, at a dose of 600 mg three times daily.

Table 2. Activity of different antimicrobial agents against odontopathogens.

A. actino- Peptostrep- Prevotella Porphiro- Fusobac- Strepto-

mycetem- tococcus spp monas terium coccus
comitans spp spp spp oralis

Penicillin G +/- + +/- +/- +/- +/-

Amoxicillin + + +/- +/- +/- +

Amoxicillin /
+ + + + + +
Clavulanic acid

Doxycycline + +/- +/- +/- + +/-

Clindamycin 0 + + + + +

Metronidazole 0 + + + + 0

Macrolides +/- +/- +/- +/- +/- +/-

+ More than 80% sensitive strains. // +/- 30 - 80% sensitive strains. // 0 Less than 30% sensitive
strains.

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