Dahlen 2002 Micro Abscess and Perio Endo

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Periodontology 2000, Vol. 28, 2002, 206239 Copyright C Munksgaard 2002Printed in Denmark All rights reserved

PERIODONTOLOGY 2000ISSN 0906-6713

Microbiology and treatment ofdental abscesses and

periodontal-endodontic lesionsGUNNARDAHLEN

Dental or dentoalveolar abscesses are infections ofdental origin, the majority with an endodontic or aperiodontal pocket origin. Dental abscesses also in-clude pericoronitis and abscesses caused by trauma

and surgical infections. The incidence of seriousodontogenic infections has decreased dramaticallyover the last half century due to preventive dentalcare and the availability of more effective antibiotics.However, dental abscesses still occur, and they maylead to serious consequences by spreading, involvingthe bone or various spatia, which might result in life-threatening conditions. Periapical and periodontalabscesses may advance into combined periodontal-endodontic lesions. Most dental abscesses arecaused by the resident oral microflora that entersnormally sterile tissues. Mechanical removal of ne-crotic infected tissues and surgical drainage are themost important treatment steps. Antibiotics are indi-cated in case of systemic symptoms and to limit thespread of the infection. This chapter reviews presentknowledge of the dental abscess in respect to pathol-ogy, microbiology and treatment.

Definition and clinicalcharacterization of dental abscesses

and periodontal-endodontic lesions

An abscess is a localized collection of pus in a cavityformed by the disintegration of tissues. The forma-tion of pus is termed suppuration. To emphasize thepresence of pus in abscesses, the term purulent ab-scess is often used. Abscesses of odontogenic originare dental abscesses formed in or around the toothand dentoalveolar abscesses that also involve the al-veolar bone, but the two terms are often used syn-onymously. Dentoalveolar abscesses consist of two

206

main types: the endodontic (periapical) abscessformed after necrosis of the dental pulp and sub-sequent infection of the root canal, and the peri-odontal abscess formed after infection of the peri-

odontal tissues by bacteria of the subgingival micro-biota. A special variant of the periodontal abscess ispericoronitis, which may develop as an infection ofthe pericoronal soft tissue overlying the crown of thetooth. Inflamed pockets normally drain continu-ously, but microorganisms and debris may becomeentrapped in the pocket, leading to an acute infec-tion.

Abscess formation is readily identified clinicallydue to concurrent signs and symptoms such as pain,redness and swelling of the abscess area, regionallymph node enlargement, spasm of the muscles andtrismus (57). The expanding lesion can spread con-siderably through soft tissue. An abscess that only in-volves soft tissue is termed cellulitis. The spreadingmay also involve bone (osteitis) or the bone marrow(osteomyelitis), which both constitute serious com-plications (147). Destruction of bony tissue may notoccur immediately, and radiographic signs of bonedestruction are not always detectable. Dental ab-scesses and abscesses in general expand throughtissue providing least resistance by forming a sinustract (fistula). In case of the periodontal abscess,

drainage is most likely to take place through the peri-odontal pocket since this is usually the path of leastresistance. In case of a periapical abscess, the spreadis primarily dictated by the thickness of the overlyingbone and the location of the abscess in relation tomuscle attachments. In the maxilla, periapical ab-scesses drain through the palatal bone into the oralcavityor rarelyinto sinus maxillarisor thenasal cavity.The mandibular periapical abscess drains commonlythrough the buccal bone into the oral cavity. Infectionmay occasionally spread along facial spaces or by the


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Microbiology and treatment of dental abscesses and periodontal-endodontic lesions

Fig. 1. Equation of infection

lymphatics to regional lymph nodes (18). Spread viathe bloodstream is rare; however, in patients under-going surgical incision and drainage of the dentoalve-olar abscess, bacterial spreading by blood is quitecommon (56, 140). The mandibular periapical ab-scess may expand below musculus myohyoideus and

reach facial spaces. If the sublingual and submandib-ular (Ludwigs angina) or pterygomandibular spaceare involved, respiratory obstruction or other life-threatening conditions may occur (20). Mediastinitis,orbital infections and brain involvement are rarecomplications of dental abscesses (58, 132, 190).

In periodontal health, the fistula drains rarelyfrom a periapical abscess along the root surface intothe gingival pocket. On the other hand, in peri-odontally diseased sites, it is plausible that the peri-apical infection drains through the deep periodontalpocket to form a periodontal-endodontic lesion.

Even after drainage of the abscess, the causativebacteria may not be completely eliminated but mayreside in the tissues, such as in the apical part of theroot canal or in the root-cement layer of the tooth.If so, the abscess may transform into a chronic state.

Pathology of dental abscess

Anaerobic infection

The vast majority of dental abscesses are polymicrob-

ial anaerobic infections (54). Anaerobic infections areopportunistic in the sense that they develop undercertain general and/or local predisposing conditions(54). Diabetes mellitus, corticosteroids, neutropenia,hypogammaglobulinemia, malignancy, immunosup-pression and cytotoxic drugs are well-known systemicconditions that favor the bacteria in the delicate bal-ance (microbial homeostasis) between the host andthe parasites (140). Local factors that may disrupt themicrobial homeostasis and facilitate the tissue in-vasion of microorganisms are related to decreased

207

redox potential (216). Obstruction, stasis, necrosis,tissue destruction, vascular insufficiency and foreign-body presence are local factorscommonly involved indental abscess development.

Acute and chronic infection

Infection can be defined as the invasion of the bodyby pathogenic microorganisms and reaction of thetissues to their presence or to the toxins generatedby them (42). The acute infection is characterizedby invading and multiplying bacteria. Host tissuesrespond with vascular dilatation and increasedblood flow, accumulation of liquid (edema) and in-flux of phagocytic leukocytes, in particular polymor-phonuclear leukocytes, possibly resulting in abscessformation. The tissue reaction is a rapid and primar-ily unspecific inflammatory response to foreign ma-terials, bacteria and bacterial products entering the

tissues. If bacteria and their products are acciden-tally forced into the tissue, such as by pocket probingor endodontic instrumentation beyond the apex, thehost response may be efficient enough to phagocyt-ize entering microorganisms with no clinically de-tectable consequences. The critical stage arises whenbacteria survive and start multiplying within thetissues (185). The anaerobic infection is usually poly-microbial and thus different from infections causedby many facultative pathogens. The frequently lowvirulence of single anaerobic species and the needfor cooperation and synergism between bacteria toform pathogenic combinations are characteristics ofanaerobic infections (159). It is also probable thatin a locally or systemically compromised host, thepresence of certain virulent microorganisms or anincreased number of microorganisms or combi-nations of certain microorganisms may invade hostcells or tissue and induce clinical infection (Fig. 1).Evidence for the occurrence of bacterial invasion inoral tissues is given in Table 1. Depending on the

Table 1.Evidence for tissue invasion by oralbacteria

Invasion due to trauma bacteremia

Invasion due to bacterial growth bacteria in dentinetubuli in caries lesions and root surfaces inperiodontitis

Invasion due to bacterial motility spirochetal invasionin acute necrotizing ulcerative gingivitis

Invasion due to cell phagocytosis neutrophilicgranulocytes and pocket epithelial cells


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Dahlen

efficiency of the host defense to combat invadingbacteria or their products and depending on theability of the bacteria to survive and withstand thehost defense, the abscess may cease or continue toexpand. An important outcome of the host defenseis the limitation of the infection, supported by for-mation of a fibrotic capsule. The formation of a sinus

tract to drain the area of pus is also an importantstep in controlling clinical infection.If the host response is insufficient, the bacteria

continue to multiply, with the risk of expanding theinfection. The bacteria may then enter the lymphaticsystem. The lymph nodes react with increased bloodflow, swelling and pain. Systemic symptoms such asgeneral discomfort, fever and dizziness indicate pro-gressive infection. In rare cases spread into the bloodsystem (bacteremia or sepsis) may occur.

Pain and other symptoms of dental infections canbe abundant and lead patients to seek emergency

dental care. Hard tissues may be involved, but theresorption of bone and teeth is not always identifi-able on radiographs, making the infection difficultto localize. Furthermore, dental abscesses may causepain and tenderness over a large area, complicatingidentification of the infected tooth.

Chronic infections occur when microorganismscease to be invasive but for various reasons are re-tained within the tissues. The development of achronic inflammatory lesion is quite common fordental abscesses due to possibility for bacterial re-tention, either endodontically in the root canal (api-cal portion) or periodontally in deep pockets or inthe necrotic root-cement layer. Adhering bacteriashow increased resistance to phagocytosis by neu-trophils (225), favoring bacterial retention. Chronicinflammation is related to the formation of a granu-lation tissue with a variety of cells, especiallylymphocytes that participate in immunological ac-tivities (116). The granuloma forms in response toinflammatory stimuli that activate components ofthe immune system and is characterized more bytissue reorganization than tissue destruction. Granu-

lation tissue aims to confine bacterial presence tothe area of the original infection. However, the for-mation of relatively infection-resistant tissue has itsprice in terms of loss of normal tissue. Similarly toacute infection, chronic infections may also involvebone destruction which, however, is usually detect-able on radiographs. In longstanding chronic peri-apical lesions, the bone surrounding the lesion maybe sclerotic, thereby potentiating the demarcation ofthe infection (35).

It is important to appreciate the immune events

208

in chronic infections. Genco & Slots (60) argued thatantibodies and other immune reactions in factstimulate healing and fibrosis of chronic lesions.Similarly, in monkeys preimmunized against bac-terial species that later were introduced into the rootcanal, the host response in periapical lesions showeda more distinct demarcation zone and less inflam-

mation compared with the host response in non-im-munized monkeys (30). Periodontitis cannot be pre-vented by high levels of circulating antibodies in im-munized animals (98), but antibodies may facilitatethe formation of relatively resistant tissue architec-ture and function. Circulating antibodies may alsocombat bacterial species commonly found in experi-mental dental abscesses (33, 44, 62, 104). Immunun-ological reactions of periodontal and periapicallesions are beyond the scope of this chapter and arereviewed elsewhere (41, 98, 116, 187, 199).

A chronic infection shows little or no symptoms,

and patients may not even be aware of the existenceof the lesion. It is also important to recognize that achronic infection may transform into an acute lesiondue to changes in homeostasis between the host andmicroorganisms. This occurs quite often in endo-dontic therapy, by overinstrumentation of the rootcanal file beyond the apex, which creates bleeding orincreased exudation into the canal, which providesstimuli for multiplication of microorganisms. Clin-ically, acute exacerbation is referred to as a flare-up(6). Periodontal probing and scaling may cause asimilar disturbance in the balance (homeostasis) be-tween the host and the subgingival flora, causingcertain bacteria to multiply and invade periodontaltissues. The possibility of an occasional negative ef-fect from periodontal mechanical debridement issparsely recognized in the literature (23, 40).

The pathology of the periapical abscess

The pathological features of the periapical abscessdepend on the microbial activity occurring in the

apical part of the root canal, having little room forexpansion except through the apical foramen. Thenecrotic pulp of the root canal serves as an import-ant source of bacterial nutrition. Proteolytic bacteriapredominate the root canal flora, which changesover time to a more anaerobic microbiota (49, 196).Even when the infection occurs outside the apicalforamen and in the periapical tissues, immediatedrainage is not possible and ongoing tissue destruc-tion and pus formation may result. The abscessusually expands through the bone by a sinus tract


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formation. The dentist may also create drainagethrough the root canal and the pulp chamber.

Actinomycosis

Actinomycosis is a rare disease that mostly is de-scribed in the literature as case reports (161). In its

classical form, actinomycosis is a chronic suppu-rative infection that occurs in three locations: cerv-icofacial, abdominal and pulmonary. The cervico-facial form may develop from a periapical lesionon teeth with infected root canals and exhibits aspecific histological picture ofActinomycescoloniesforming a rosette within an apical granuloma(157). Actinomycotic lesions may also be purulentand drain through multiple fistula. Although Acti-nomyces israelii is the most common etiology, Ar-achnia propionicaand other Actinomycesspp. havealso been isolated from actinomycotic lesions (14,

157). Actinomycesalso occurs in chronic periapicalgranulomas (periapical actinomycosis) in therapy-resistant cases (81, 82). Although Actinomycescellscan be phagocytized in vitrounder experimentalconditions, they collectively evade elimination byphagocytic cells in vivoby forming their character-istic colonies, enabling the organism to surviveduring the acute inflammatory phase (53). Acti-nomycotic osteomyelitis is being increasingly iden-tified and may develop from longstanding peri-apical actinomycosis (7, 99, 141).

The pathology of the periodontal abscess

The periodontal abscess has been defined as a sup-purative lesion associated with periodontal break-down and localized pus in the gingival wall of theperiodontal pocket (90). The prevalence of peri-odontal abscesses is lower than that of periapical ab-scesses (90). Although the pathology of the peri-odontal abscess is not known in detail, it is reason-able to assume that its basic pathogenic mechanismis similar to that of abscesses in general. Multipli-

cation and invasion by one or a group of subgingivalspecies constitute the starting-point of abscess for-mation. The increased bacterial activity may be dueto either (a) a disturbance of the microbial homeo-stasis, (b) a destruction of the epithelial barrier or (c)random events. Reports indicate that treatment withsystemic antibiotics in patients with advanced peri-odontitis may cause abscess formation, probablydue to overgrowth of resistant pathogens (89, 203).Traumatic injury and bleeding may also predisposefor acute exacerbation of untreated periodontitis (23,

209

40). Also if drainage through the pocket is obstructedby gingival occlusion after improved supragingivalhygiene, the result may be increased activity of sub-gingival bacteria and abscess development. Foreignbodies such as calculus and food debris may bepushed into gingival tissue during debridement andcause abscess formation (40). Periodontal abscesses

around barrier membranes in guided tissue re-generation have also been reported (59). In ligature-induced experimental periodontitis in animals (114,115), the foreign body of the ligature placed in theperiodontal pocket apparently drives the balance be-tween bacteria and host in favor of infection, causingrapid periodontal breakdown, although abscess for-mation is usually not reported. UsingStaphylococcusaureusinfected sutures in an experimental model,Elek & Conan (45) showed that 107 cells were neededto cause infection by subcutaneous injection but, ifretained in a suture, less than 100 cells were required

to induce infection.Pericoronitis is a special form of the periodontal

abscess that develops in the pericoronal soft tissuethat partially overlies the crown of the tooth. Ifmicroorganisms and debris become entrapped inthe periodontal pocket and obstruct drainage, thepericoronal infection may spread to form an abscess.Third molar teeth of the mandible are most fre-quently involved.

The pathology of the

periodontal-endodontic lesionThe periodontal-endodontic lesion develops by ex-pansion of either (a) a periodontal destruction apic-ally combining with an existing periapical lesion or(b) an endodontic lesion merging marginally with anexisting periodontal lesion. As long as the pulp is vi-tal, the lesion should be diagnosed as a periodontallesion and treated as such. In case of loss of pulpvitality, it can be difficult to determine whether thelesion is primarily of periodontal or endodontic ori-gin. If there is periodontal breakdown around a non-

vital or root-filled tooth, an endodontic infectionshould always be considered. Diagnostic difficultymay occur if a root canal infection communicateswith the marginal periodontium through lateral ca-nals, perforations or root fractures, which may leadthe dentist to overlook the endodontic inflammation(11). As stated by Bergenholtz et al. (11): Although,clinically, one may be able to bring a probe throughboth lesions, it is important from a therapeutic pointof view to understand that the coronal part is di-rected towards an infection in the marginal peri-


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odontium and the apical part to an infection emerg-ing from the root-canal system. The manifestationof an acute endodontic lesion in the marginal peri-odontium leads to rapid destruction of apical peri-odontal attachment. Drainage may take placethrough two routes: (a) a sinus tract along the peri-odontal ligament or (b) an extraosseous fistulation

(11). Both routes may drain marginally through thegingival pocket.Both clinical and animal experiments have re-

vealed that the vitality of the pulp is not impaired byscaling and root-planing procedures (11). If localizedinflammation occurs in the pulp as a consequenceof root surface instrumentation, it normally healsuneventfully. The prognosis of a tooth with a peri-odontal-endodontic lesion suspected of being pri-marily of endodontic origin is usually good, even incase of nonvital and infected pulp tissue.

Microbiology of dental abscesses

Difficulty in evaluating dental abscessmicrobiology

Dental abscesses contain 37 or even more bacterialspecies with a predominance of anaerobic organ-isms (130). The vast majority of species isolated fromthe dental abscess originate from the resident oralflora. Microbial specificity of dental abscesses is low,and the heterogeneity of the microbial compositionis striking. However, certain organisms are more fre-quently recovered than others and might thereforeplay a determinative role in the infection process.

Earlier studies on the microbiology of acute dentalinfections showed a predominance of streptococciand staphylococci (35, 130), probably mainly due tosample contamination and inadequate anaerobicculture techniques. Moller (153) emphasized the im-portance of proper sampling technique and anaer-obic culture conditions in endodontic microbial ex-aminations. Even though relatively recent studies(130) describe a predominance of facultative cocci,

most studies on dental abscesses over the last 30years have underscored the importance of anaerobicorganisms (Table 2). As listed above, factors of im-portance in the evaluation of dental abscess micro-biota include:

O clinical diagnosisO microbial samplingO microbial transportationO methods for microbiological evaluationO interpretation of microbiological findings.

210

Diagnosis

Many studies do not explicitly describe the preciseorigin (endodontic, periodontal or other) of the den-tal abscesses investigated. However, since the preva-lence of endodontic abscesses is considerably higherthan other types of dentoalveolar abscesses, the re-

ports reviewed in Table 2 may be expected to incor-porate mostly dentoalveolar abscesses of endodonticorigin. Studies on dental abscesses with a designatedorigin as endodontic, periodontal or pericoronitisare reviewed separately (Tables 35).

Microbial sampling

Obtaining samples from dental abscesses withoutcontamination from saliva and the surrounding mu-cosal surface is fraught with difficulties. Studies ofacute dental infections that collected microbial

samples on swabs and cultured samples after poss-ible delay using limited anaerobic culture methodsdescribe an average of 1.01.6 isolates per sampleand a predominance of viridans streptococci andstaphylococci (130). In contrast, studies employingaspiration through a sterilized mucosal surface andpromptly culturing using strict anaerobic techniquesshow a mean number of bacterial isolates persample of 2.57.4 species with a predominance ofstrictly anaerobic organisms.

In samples collected through the periodontalpocket, relevant microorganisms may be over-shadowed by bystanders in the subgingival flora thatdo not necessarily participate in the periodontal ab-scess process. The microbiota responsible specifi-cally for the periodontal abscess process may there-fore be difficult to identify.

Sampling through a fistula is also hampered bycontamination of surface bacteria with little re-lationship to the abscess. In case of a fistula, theproblem might be reduced by antiseptically treatingthe orifice of the fistula and by collecting a separatesample from the orifice and outer part of the fistula

canal to identify the species that might potentiallyconstitute contaminants.

Sampling from an endodontic abscess may be fa-cilitated by taking the sample through the root canal.The tooth can readily be isolated with a rubber damand thoroughly sterilized with high percentage hy-drogen peroxide and iodine tincture and the sterilityverified by a sample of the field of operation (153).

Another problem in sampling of dental abscessesis the risk of false-negative results. False-negativecultures may occur in sampling pus in the central


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Table2.Microbialfindingsin

studiesofdentoalveolarabscessesofmixedornon-specifiedoriginthatcontainedpusbyaspiration

Total

Totalnumber

ofisolatesandpredominantspecieswi

thineachbacterialgroup

Number

Total

numberof

of

n

umber

anaerobes

Gram-positive

Gram-negative

Gram-po

sitive

Gram-negative

F

acultatively

Study

abscesses

ofisolates

(%)

anaerobiccoc

ci

anaerobiccocci

anaerobicrods

anaerobicrods

a

naerobicisolates

Sabiston&

8

25

17(68)

2

Nodata

3

12

7

Gold(174)

Peptostreptoco

ccus

Actinomy

cesspp.

Bacteroidesspp.4

S

treptococcusspp.6

spp.

Lactobacillusspp.

Fusobacteriumspp.1S

.epidermidis

F.nucleatum7

Ingham

25

185

134(72)

26

19

37

52

5

1

etal.(95)

Veillonellaspp.

B.

melaninogenicus13S

treptococcusspp.21

Fusobacteriumspp.10S

.aureus2

S

.albus13

N

eisseriaspp.6

H

aemophilusspp.6

Chow

31

119

93(78)

28

3

13

49

2

2

etal.(24)

P.micros8

Veillonellaspp.

Actinomy

cesspp.4

B.

melaninogenicus15S

treptococcusspp.14

P.anaerobius6

Lactobacillusspp.3

B.

oralis4

P

seudomonasspp.3

P.intermedius

4

Eubacteriumspp.4

B.

pneumosintes4

C

andidaspp.2

B.

fragilis3

B.

capillosus3

B.

corrodens3

B.

ruminicola3

Fusobacteriumspp.7

Campylobacterspp.2

Bartlett&

20

124

91(73)

25

3

28

25

2

6

OKeefe(8)

Peptostreptoco

ccus

Veillonellaspp.3

Actinomy

cesspp.2

Bacteroidesspp.18

S

treptococcusspp.6

spp.2

A.

naeslundii2

B.

melaninogenicus9h

emolyticstreptococci5

P.intermedius

5

Propionib

acterium

B.

corrodens2

a

lpha-streptococci13

P.anaerobius4

spp.4

E

.corrodens3

P.micros3

Lactobacillusspp.1

P.prevotiispp.4

E.

lentum

8

P.magnus3

E.

limnos

um2

P.asaccharolyticus2

P.morbillorum

2

Kannagara

61

201

118(59)

39

4

2

53

8

2

etal.(101)

P.intermedius

4

V.parvula3

A.

israelii6

B.

fragilis18

S

treptococcusspp.7

P.constellatus

7

Actinomy

cesspp.5

B.

capillosus7

S

.epidermidis27

P.morbillorum

4

Eubacteriumspp.5

B.

furcosus4

S

.aureus6

P.anaerobius3

B.

corrodens4

E

nterococcusspp.5

P.micros3

B.

coagulans4

N

eisseriaspp.4

P.prevotii4

Fusobacteriumspp.6K

lebsiellaspp.4

C

orynebacteriumspp.9

211


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Dahlen

Table2.continued

Total

Totalnumber



Number

Total

numberof

of

n

umber

anaerobes

Gram-positive

Gram-negative

Gram-po

sitive

Gram-negative

F

acultatively

Study

abscesses

ofisolates

(%)

anaerobiccoc

ci

anaerobiccocci

anaerobicrods

anaerobicrods

a

naerobicisolates

vonKonow

57

203

178(88)

30

9

31

92

2

5

etal.(111)

S.constellatus

7

V.parvula9

Actinomy

cesspp.2

B.

intermedius3

S

.milleri9

S.intermedius

22

Propionib

acterium

B.

melaninogenicus3S

treptococcusspp.7

Peptostreptoco

ccus

spp.3

B.

oralis15

S

.faecalis4

spp.2

Lactobacillusspp.6

B.

ureolyticus2

H

aemophilusspp.2

P.micros4

Bifidobac

teriumspp.2

B.

distasonis1

P.asaccharolyticus6

Eubacteriumspp.5

B.

capillosus2

P.magnus7

E.

lentum

5

B.

uniformis1

P.prevotii3

Clostridiu

mspp.2

Bacteroidesspp.27

Fusobacteriumspp.29

F.nucleatum9

vonKonow

55

177

157(89)

35

9

29

85

2

0

&Nord(112)

S.intermedius

11

V.parvula9

Lactobacillusspp.7

Bacteroidesspp.15

S

.milleri15

S.morbillorum

2

Eubacteriumspp.5

B.

melaninogenicus15S

.mitior3

P.micros15

E.

lentum

13

B.

ruminicola14

B.

corrodens6

F.nucleatum20

Labriola

50

162

115(71)

23

5

10

77

4

7

etal.(124)

Peptostreptoco

ccus

V.parvula5

P.acnes2

Bacteroidesspp.10

S

treptococcusspp.45

spp.2

Lactobacillusspp.2

B.

intermedius12

S

.aureus3

P.productus4

Bifidobac

teriumspp.2

B.

melaninogenicus10S

.epidermidis4

P.anaerobius2

Eubacterium4

B.

ruminicola12

E

nterobacterspp.2

P.magnus6

B.

distasonis2

A

cinetobacterspp.2

P.asaccharolyticus4

B.

capillosus2

B.

asaccharolyticus4

F.nucleatum3

Fusobacteriumspp.5

Cumming

10

25

5(20)

1

2

0

3

1

9

etal.(27)

B.

asaccharolyticus2S

.albus4

S

treptococcusspp.8

E

.corrodens3

B

.catarrhalis3

Heimdahl

58

196

174(89)

40

10

28

96

2

2

etal.(88)

Streptococcusspp.8

V.parvula10

Lactobacillusspp.7

B.

asaccharolyticus3S

.milleri18

S.constellatus

2

E.

lentum

11

P.melaninogenica15S

treptococcusspp.4

S.intermedius

10

Eubacteriumspp.7

P.oralis5

S.morbillorum

2

P.ruminicola17

P.micros17

B.

ureolyticus5

B.

capillosus2

F.nucleatum26

212


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Table2.continued

Total

Totalnumber



Number

Total

numberof

of

n

umber

anaerobes

Gram-positive

Gram-negative

Gram-po

sitive

Gram-negative

F

acultatively

Study

abscesses

ofisolates

(%)

anaerobiccoc

ci

anaerobiccocci

anaerobicrods

anaerobicrods

a

naerobicisolates

Lewis

50

166

130(78)

50

3

9

68

3

6

etal.(128)

Peptostreptoco

ccus

Veillonella3

Lactobacillusspp.3

B.

oralis20

S

.milleri25

spp.14

Actinomy

cesspp.3

B.

gingivalis14

S

.mitior3

Peptococcusspp.32

P.melaninogenica12S

.sanguis3

S.intermedius

3

P.ruminicola6

H

.parainfluenzae2

S.constellatus

1

F.nucleatum6

C

.ochracea1

E

.corrodens1

vonKonow

59

284

220(77)

58

9

29

121

6

4

etal.(113)

S.constellatus

6

V.parvula5

Actinomy

cesspp.3

B.

asaccharolyticus4S

.milleri18

S.intermedius

16

Lactobacillusspp.6

B.

corrodens4

S

.mitior18

P.micros27

Eubacteriumspp.19

B.

ruminicola16

S

treptococcusspp.7

B.

ureolyticus5

S

taphylococcusspp.8

Bacteroidesspp.47

H

aemophilusspp.5

F.nucleatum18

Fusobacterium24

Ashimoto

27

Polymerase

Nodata

Nodata

Nodata

Nodata

B.

forsythus22%

E

.corrodens19%

etal.(4)

chain

P.endodontalis59%

reaction

P.gingivalis93%

analysisfor

T.denticola85%

fivespecies

213


9/34


10/34


Table3.continued

Total

Totalnumber



Number

Total

numberof

of

n

umber

anaerobes

Gram-positive

Gram-negative

Gram-po

sitive

Gram-negative

F

acultatively

Study

abscesses

ofisolates

(%)

anaerobiccoc

ci

anaerobiccocci

anaerobicrods

anaerobicrods

a

naerobicisolates

Sklavounos

40

83

28(34)

17

1

4

6

5

5

etal.(182)

P.productus5

Bacteroidesspp.6

S

.epidermidis29

P.anaerobius3

S

.aureus5

P.intermedius

3

S

treptococcusspp.

P.parvulus3

(groupA)8

P.constellatus

2

E

.coli9

Brook

39

78

55(70)

18

2

3

32

2

3

etal.(18)

Peptostreptoco

ccus

V.parvula2

Eubacteriumspp.2

B.

oralis4

S

treptococcusspp.14

spp.6

B.

gingivalis7

S

.milleri3

P.anaerobius3

B.

melaninogenicus3S

.faecalis3

P.micros6

B.

intermedius2

H

aemophilusspp.2

P.prevotii2

Bacteroidesspp.7

F.nucleatum5

Fusobacteriumspp.4

Klecki

13

70

42(60)

12

0

6

24

2

8

etal.(118)

Peptostreptoco

ccus

P.intermedia9

S

treptococcusspp.10

spp.12

P.buccae3

S

.epidermidis4

P.ureolytica2

S

.aureus2

Prevotellaspp.4

N

eisseriaspp.4

F.nucleatum5

C

orynebacteriumspp.4

E

.corrodens3

Sakamoto

23

112

81(72)

17

7

3

54

3

1

etal.(176)

Peptostreptoco

ccus

Veillonella7

P.oris9

S

treptococcusspp.8

spp.12

P.intermedia4

S

.constellatus8

P.micros3

P.oralis3

S

.intermedius8

G.

morbillorum2

P.buccae3

S

.epidermidis3

P.melaninogenica3

Prevotellaspp.8

P.gingivalis4

B.

gracilis3

F.nucleatum3

Fusobacteriumspp.10

215


11/34

Dahlen


studiesofperiodontalabscesses

Frequency(%)ofisolatedb

acteria(mean%oftotalviablecount)

Number

N

umberof

Gram-positive

Gram-ne

gative

Gram-positiveanaerobic

Gram-negative

Facultatively

Study

ofcases

anaerobes

anaerobiccocci

anaerobicrods

rods

anaerobicisolatesrods

anaerob

icisolates

Newman&

9

100(63.1)

44(9.1)

11(2.7)

20(6.6)

100(49.0)

100(36.9)

Sims(160)

B.a

saccharolyticus(10.4)

Facultativecocci(17.7)

B.i

ntermedius(4.4)

Fusobacteriumspp.(5.9)

Campylobacterspp.(11.5)

Topoll

20

100(59.5)

Nodata

Nodata

70(13.0)

100(39.0)

45(8.9)

etal.(203)

Actinomycesspp.(6.9)

B.g

ingivalis(19.5)

S.interm

edius(5.6)

Propionibacteriumspp.(3.1)

B.i

ntermedius(4.8)

Lactobacillusspp.(1.7)

F.varium(5.1)

F.nucleatum(6.6)

Hafstrm

20

N

odata

Nodata

Nodata

Nodata

100(37.4)

44(3.8)

etal.(77)

P.gingivalis(22)

Capnocytophagaspp.(3.8)

P.intermedia(7.3)

F.nucleatum(1.8)

C.

rectus(6.3)

Herrera

24

N

odata

Nodata

Nodata

Nodata

Nodata

Nodata

etal.(91)

P.micros

P.gingivalis50(13.6)

A.a

ctinomycetemcomitans0(0)

70.6(9.3)

P.intermedia62.5(8.5)

P.melaninogenica16.7(15.6)

B.f

orsythus47.1(3.6)

F.nucleatum70.8(2.6)

Campylobacterspp.4.2(0.7)

216


12/34



studiesofpericoronitisinfection

s

Frequencyo

fdetection(mean%ofpositivesamples)

Number

Numberof

of

N

umber

anaerobes

Gram-positi

ve

Gram-negative

Gram-po

sitive

Gram-negative

F

acultatively

Study

cases

ofisolates

(%)

anaerobiccocci

anaerobiccocci

anaerobicrods

anaerobicrods

a

naerobicisolates

Nitzan

82

M

ixed

Nodata

Nodata

Nodata

Nodata

Fusobacteriumspp.(80)N

odata

etal.(162)

m

icrobial

Spirochetes(75)

population

(Giemsastain)

Mombelli

6

N

odata

Nodata

6.4

5(5.3)

6(11.3)

6(40)

6

(9.0)

etal.(151)

(GroupC)

Veillonellaspp.4

A.

odonto

lyticus2

B.

gingivalis0

C

apnocytophagaspp.3

A.

naeslundii6

B.

intermedius5

A

.actinomycetem-

A.

viscosu

s6

B.

melaninogenicus1

comitans1

Selenomonasspp.1

Fusobacteriumspp.2

Wadeetal.(208)20

361

302(84)

62

33

60

147

5

9

P.micros43

Veillonellaspp.29

A.

naeslundii12

P.gingivalis0

S

.mitis19

P.anaerobius12

Eubacteriumspp.25

P.intermedia45

S

.sanguis1

A.

viscosu

s6

P.melaninogenica22S

treptococcusspp.19

Bifidobac

teriumspp.5

B.

gracilis11

C

orynebacteriumspp.2

P.oralis6

C

apnocytophagaspp.6

P.oris11

P.buccalis5

F.nucleatum20

Campylobacterspp.6

Selenomonasspp.8

Leung

5

74

54(73)

5

3

16

30

2

0

etal.(126)

(GroupB)

P.micros4

Veillonellaspp.3

Actinomy

cesspp.10

B.

gracilis4

S

treptococcusspp.6

Propionib

acterium

P.gingivalis5

S

.anginosus4

spp.2

Prevotellaspp.9

S

taphylococcus2

Eubacteriumspp.3

Fusobacteriumspp.3N

eisseria1

Campylobacterspp.3H

aemophilus1

C

apnocytophaga6

Rajasuo

11

210

148(70)

16

6

43

83

6

2

etal.(168)

P.micros8

Veillonellaspp.6

A.

odonto

lyticus10

P.intermedia/

S

treptococcus10

P.anaerobius6

Eubacteriumspp.6

nigrescens11

N

eisseriaspp.5

Lactobacillusspp.7

P.melaninogenica8

H

aemophilusspp.5

A.

israelii5

F.nucleatum10

S

.milleri8

B.

gracilis8

S

.mutans5

F.necrophorum4

C

orynebacteriumspp.6

C.

rectus5

C

apnocytophagaspp.10

P.buccae6

P.denticola6

P.gingivalis1

217


13/34


14/34


strictly anaerobic genera, Peptostreptococcus spp.predominate. Commonly isolated species are Pep-tostreptococcus anaerobius, Peptostreptococcusmicrosand Peptostreptococcus prevotii. Peptococcusspecies are less frequently reported, although Pep-tococcus magnus and Peptococcus asaccharolyticushave been identified in several studies. The micro-

aerophilic streptococcal species are frequently re-covered, but some streptococci are true anaerobes(Streptococcus intermedius and Streptococcus con-stellatus), whereas other strains of the Streptococ-cus milleri group (such as Streptococcus ang-inosus) are commonly placed among facultativespecies. Gemella (formerlyStreptococcus) morbillo-rum, belonging to this microaerophilic group, hasalso been reported in dental abscesses.

Gram-negative anaerobic cocci

Gram-negative anaerobic cocci, often represented byVeillonella parvula, are reported in most studies al-though in a limited number of cases (Table 2).

Gram-postive anaerobic rods

Gram-positive anaerobic rods are commonly recov-ered from dental abscesses. Since several species areaero-tolerant and other species are strictly anaer-obic, the classification of the isolates into anaerobesor facultative anaerobes can sometimes give rise toconfusion. Actinomycesisolates are often not speci-ated. However, A. israelii, Actinomyces meyeri, Acti-nomyces odontolyticus,Actinomyces viscosusand Ac-tinomyces naeslundii are among the species re-ported.Actinomycesspp. are important due to theirability to cause actinomycosis, attributed mostly toA. israelii, even if other species may also participate.Actinomycesspecies have been reported to persist inthe periapical granuloma, especially in treatment-re-sistant cases (82, 181).

Lactobacillus is often isolated from dental ab-scesses but, similarly to Actinomyces, it is seldom

speciated.Lactobacillusspp. have been regarded ashaving low virulence (48), even if they are frequentlypresent in endodontic lesions and dental abscesses.The frequent isolation in endodontic failures indi-cates a need for reconsidering the pathogenicity oforal lactobacilli (150). Lactobacillus plantarum,Lactobacillus casei, Lactobacillus acidophilus andLactobacillus fermentumhave been identified in oralinfections. Oral Bifidobacterium isolates belongmainly to the Bifidobacterium brevisspecies. In theEubacteriumgenus, isolates of Eubacterium alacto-

219

lyticus, Eubacterium lentum and Eubacterium yuriare most commonly recovered from the oral cavity(38). Propionibacterium acnes and Propionibacteri-um propionica(formerlyA. propionica) are also re-ported by several studies of oral abscesses (Table 2).Clostridiumspecies are very rare isolates from dentalabscesses.

Gram-negative anaerobic rods

Gram-negative anaerobic rods are the most frequentisolates in dentoalveolar abscesses. Heimdahl et al.noted that, the more severe the abscesses, the moregram-negative anaerobes and S. milleriwere recov-ered (88). However, the taxonomy is confusing, andliterature older than 10 years refers to isolates aseither Bacteroides or Fusobacterium species. Themost commonly reported group according to mod-ern taxonomy isPrevotellaspp.Prevotella intermedia

may best represent this group of organisms. Currentdifferentiation into P. intermediaand Prevotella nig-rescensshould be considered. It is interesting to notethat, whereas P. intermediatended to be associatedwith severe periodontal infections,Prevotella nigres-censwas more frequently isolated from endodonticinfections (5). Prevotella melaninogenicais also fre-quently reported in dentoalveolar abscesses and, to-gether with P. intermediaand Porphyromonas spe-cies, have placed the black-pigmented gram-nega-tive rods (Bacteroides) in focus as major pathogensin dentoalveolar abscesses (217, 218). The import-ance of black-pigmented species has been furtherstressed by several authors relating these organismsto the presence of symptoms in acute infections.Sundqvist (192) suggested a relationship betweenblack-pigmented Bacteroides and pain and sinustract formation in acute endodontic infections, latersupported by Griffee et al. (71) and Baumgartner etal. (10). These studies also revealed a higher fre-quency of saccharolytic species (Prevotella) than as-accharolytic species (Porphyromonas) in acute endo-dontic infections. On the other hand, Haapasalo et

al. (73) stressed the presence ofPorphyromonasspe-cies in symptomatic cases and isolated bothP. gingi-valis and Porphyromonas endodontalis from acuteendodontic infections. It seems that P. endodontalisfor some reason is selected for in root canal infec-tions and, together with P. intermedia, is present insymptomatic teeth (217, 219). Other studies havealso described a relationship between black-pig-mented gram-negative species and symptoms butalso underscored the importance of other bacterialspecies in acute infections. Non-pigmentedPrevotel-


15/34

Dahlen

la,Peptostreptococcus,Peptococcus,EubacteriumandFusobacterium species have been significantly as-sociated with endodontic symptoms (65, 83, 98, 223).In dentoalveolar abscesses, non-pigmentedPrevotel-laspecies (such as Prevotella oralis,Prevotella rumi-nicola, Prevotella buccae, Prevotella oris, Prevotellabiviusand Prevotella oulorum) are almost as com-

mon as the black-pigmented species (75). However,some reports on species occurrence are difficult tointerpret due to changed taxonomy. Bacteroides ru-minicolashould probably have been classified as P.buccae, P. oris or Prevotella heparinolytica (98).Bacteroides ureolyticusmay sometimes have been re-ferred to as Bacteroides corrodens, whereas the re-lated Bacteroides gracilis (nowCampylobacter gra-cilis) is rarely reported, probably due to misidenti-fication. Species sparsely reported are Dialister(Bacteroides) pneumosintesand Prevotella(Mitsuok-ella) dentalis(24, 74).

In the Fusobacteriumgenus, isolates ofFusobac-terium nucleatum and its subspecies predominate.In fact,F. nucleatumis one of the most frequent iso-lates and is reported in virtually all studies on dentalabscesses (Table 1). Fusobacterium variumand Fu-sobacterium periodonticumas well asFusobacteriumnecrophorumhave also been described in dental ab-scesses, but only sparsely.

Motile bacterial species such as Wolinella andCampylobacter, including Campylobacter rectusandC. gracilis(formerlyB. gracilis) or Selenomonasspp.are sparsely reported in dentoalveolar abscesses.These motile species are present in both endodonticand periodontal infections (including periodontalabscesses) but may have been overlooked in manystudies.

Underestimation is very likely for Treponemaspe-cies, which are not usually recovered in culturestudies. However, if the microbiological analysis iscompleted with microscopic (including immuno-fluorescence) or nucleic acid analysis, Treponemaiscommonly found (205). Dahle et al. (28) suggestedthat Treponemaspecies constitutes 10% of the flora

in endodontic abscesses. The taxonomic classifi-cation ofTreponemais uncertain, and small as wellas large spirochetes have been identified in endo-dontic infections (28, 29).

Gram-positive facultative cocci

Older literature reports on predominance ofStrepto-coccusspecies in dentoalveolar abscesses, and thesespecies may still be overestimated due to the diffi-culty in avoiding contamination from the surface

220

flora and saliva. The microaerophilic streptococcalspecies are the organisms most frequently reported;the polysaccharide-producing species of the virid-ans group are seldom involved in dentoalveolar ab-scesses, and species such as Streptococcus mutans,Streptococcus sanguis,Streptococcus oralisand Strep-tococcus salivariuscan often be suspected of con-

stituting contaminants.The predominant abscess-producing strepto-coccal organisms belong to the S. milleri group,which has been considered synonymously to viri-dans until recently (178), but differs from other al-pha-hemolytic streptococci by being microaero-philic. Some streptococcal species are hemolytic andare grouped in Lancefield group F. b-Hemolytic S.milleristrains were detected in 22% of oral abscesses(178). Hemolytic streptococci of group A have notbeen identified in dental abscesses. Other hemolyticisolates may have been classified as enterococci

(Lancefield group D).The occurrence ofEnterococcusspecies in endo-

dontic infections can create a serious problem dueto its resistance to antimicrobial agents. Enterococciare therefore often selected for by the endodontictreatment procedures. The presence of enterococciin dental abscesses and flare-ups is, however, low,and this species is seldom involved in acute infec-tions. Enterococci occur in high frequency in endo-dontic samples from teeth with therapy-resistant en-dodontic infection or root-filled teeth with periapicaldestruction (149, 197). Molander et al. (149) exam-ined re-treated root-filled teeth and found enteroc-occi in 50% of culture-positive samples. Other fre-quent isolates in that study were streptococci andlactobacilli (149). Streptococci and enterococci arenot very prevalent in dental abscess material, whichmay explain why flare-ups at root-filled teeth withapical periodontitis are rather uncommon despitethe very high prevalence of these organisms in theoral cavity.

Staphylococcusspp. are seldom reported in mod-ern studies, which is in contrast to the literature

from the pre-anaerobic era. The low prevalence ofstaphylococci does not mean that these organismsare irrelevant in dentoalveolar infections. Especiallythe presence of Staphylococcus aureus should beconsidered of potential pathoetiological importance.S. aureusis the most common cause of osteomyelitisin bones of other parts of the body; it may also occurin clinical infections of the jaws. Osteomyelitis oc-curs rarely in the maxilla due to the spongeous bonetexture, which does not predispose for this con-dition, while mandibular osteomyelitis is a quite fre-


16/34


quent complication of oral infections. S. aureusmaysporadically occur in endodontic lesions as well asin jaw fractures, especially in cases with extraoralcommunication, and might be a cause of mandibu-lar osteomyelitis (209). Chow et al. (24) investigated13 cases of suppurative osteomyelitis and foundBacteroides, Fusobacterium, Peptostreptococcus and

Peptococcusspecies but no S. aureus.

Gram-negative facultative cocci

Gram-negative facultative cocci represented byNeis-seria spp. are not usually reported in dental ab-scesses, and if occurring, contamination from thesurface should be suspected (35).

Gram-positive facultative rods

Finding of gram-positive facultative rods other than

those referred to asActinomycesspp. orLactobacillusspp. should be interpreted with caution. Corynebac-terium spp. has been reported sparsely. Contami-nation at the time of sampling or in the laboratoryshould always be suspected ifBacillusspp. occur indental abscess material (35).

Gram-negative facultative rods

Enteric rods including Escherichia coli, Enterobacterspp., Klebsiellaspp. and Pseudomonasspp. are oc-casionally isolated from dentoalveolar abscesses (8,51, 124) and may occur as monoinfections (169). Theorganisms are often resistant to mechanical endo-dontic treatment and may persist in root canal infec-tions that do not respond to conventional therapy (72,180).

Haemophilus, Eikenellaand Capnocytophagaspp.are infrequently found in dental abscesses (67, 68,95, 111, 113, 128).

Yeasts

Yeasts have been isolated in 7% of culture-positivesamples from infected root canals (210). Yeasts areusually isolated in mixed cultures, and the mostcommon species is Candida albicans. The role ofyeasts in endodontic infection is not clear. It is poss-ible that local medicaments allow for the prolifer-ation of yeasts, when other microorganisms are sup-pressed (211). Candidaspp. are rarely isolated fromsamples of dental abscesses and are presented incase reports (142, 146).

Approximately 20% of adult periodontitis patients

221

also harbor subgingival yeasts (36, 183). C. albicansis the most common species isolated (80). Its role inperiodontitis progression is unclear; the organismhas not been reported from periodontal abscesses orpericoronitis infections.

Specific microbiology of the periapical

abscess (Table 3)

The most frequently detected bacterial species inperiapical abscesses are microaerophilic strepto-cocci of the S. milleri group (S. anginosus, S. con-stellatusand S. intermedius), anaerobic streptococci(P. anaerobiusand P. micros), gram-positive anaer-obic rods (Eubacteriumspp., Actinomycesspp. andPropionibacterium spp.) and gram-negative anaer-obic rods (Porphyromonas spp., Prevotella spp.,Bacteroidesspp.,Campylobacterspp.,Fusobacteriumspp. andTreponemaspp.). Although there is striking

microbiological similarity between dental abscessesof various origins, some features are characteristicfor endodontic abscesses. The rare isolation ofP. en-dodontalisin oral infections other than those of en-dodontic origin is one important exception (217,218). Furthermore, Actinobacillus actinomycetem-comitansis very rare in root canal infections and hasnot been reported in periapical abscesses (38). B.forsythusis not usually recovered from infected rootcanals unless specific anarobic methods are em-ployed (66); however, the organism may have beenoverlooked in most abscess studies. The nonoralBacteroides fragilisspecies has been reported in sev-eral studies, but there is reason to believe that theseisolates were misclassified. B. fragilis rarely causesinfections above the mediastinum (54).

There are few reports on the specific bacteriologyof dental abscesses with sinus tract formation, per-haps because these infections are of lower clinicalpriority, because they have passed the acute phaseof infection or because of difficulty in obtaining mi-crobial samples without contaminating bacteria. Themicrobial composition of the sinus tract from a

dentoalveolar abscess that drains through the peri-odontal pocket is impossible to distinguish from thatof the subgingival microbiota. Haapasalo et al. (76)showed in a sinus tract infection sampled by aspir-ation that, although the acute phase of the infectionhad passed after antibiotic treatment, the periapicalregion still harbored metronidazole-resistant bac-teria (microaerophilic streptococci, Propionibacteri-um acnes) and some other anaerobic species (P. in-termedia and Peptostreptococcusspp.). Supposedly,the infection persisted within the periapical tissues


17/34

Dahlen

(the root canal filled with calcium hydroxide interap-pointment paste). Apical surgery was necessary toeliminate the infection. Moller (153) found thatgranulomas did not contain bacteria, but Tronstadet al. (204) showed the presence of bacteria in caseswith sinus tracts, indicating that, in acute forms ofthe periapical lesion, bacteria can persist in the

tissues outside the root canal. In an ultrastructuralstudy, Nair (156) investigated 31 periapical lesions,of which five were symptomatic and contained bac-teria. Weiger et al. (212) performed microbiologicalsampling through the sinus tract of 12 cases andwere able to isolate 6.3 strains per sample. Althoughin that study, the percentage of anaerobes was some-what higher in the root canal than in the sinus tract,most species that were isolated from the canal werealso recovered from the extraradicular sample, in-cluding Peptostreptococcus, Prevotella, Fusobacteri-um, Lactobacillus and microaerophilic streptococci

(S. intermediusand G. morbillorum).

Specific microbiology of the periodontalabscess (Table 4)

In dental abscesses of periodontal origin, P. gingi-valis, B. forsythus, T. denticolaand P. microsare themost prevalent species and are more commonly iso-lated from periodontal than from endodontic ab-scesses (90, 91). Especially P. gingivalisconstitutessignificant proportions, ranging from 1022% of thecultivable flora in periodontal abscesses (77, 91, 160,203). Sims & Newman (160), who performed a pre-dominant culture study of periodontal abscesses andcollected samples with a barbed broach from theapical part of the periodontal abscess, might haveobtained more representative samples than otherstudies that used paper point sampling. All studieson periodontal abscesses, however, suffer from theapparent problem of mixing the abscess flora withthat of the periodontal pocket. It is thus difficult todetermine whether the reported similarity betweenthe flora in periodontal abscesses (Table 4) and that

associated with advanced periodontitis is a relevantfinding or mostly a consequence of the samplingmethod used.

Specific microbiology of pericoronitis(Table 5)

The microbiology of pericoronitis generally showsthe same microbiological profile as other types ofdental abscesses. It also shares the problem withother periodontal lesions in obtaining a representa-

222

tive sample from the infected area and delineatingthe species involved in the disease process. However,it might be possible to use the noninfected contra-lateral site to exclude the microflora normally pres-ent at the site. Leung et al. (126) found no significantdifference between the abscess flora and the flora ofhealthy third molar sites of control patients. An-

aerobic species predominate and gram-negative an-aerobic rods constitute the most frequent organismsof the pericoronitis microbiota (Table 5). While P. in-termedia,P. melaninogenica, C. gracilisand F. nucle-atumwere common isolates in most studies,P. gingi-valisand B. forsythuswere sparsely found or not re-ported in pericoronitis abscess cases (13, 150, 168,208). However, Leung et al. (126) isolated P. gingivalisandP. endodontalisfrom all five pericoronitis lesionswith symptoms but in none from asymptomaticlesions.P. intermediawas recovered in five of six per-icoronitis cases with acute pain and suppuration

from the pericoronal pouch and constituted 29% ofthe cultivable flora (150).

Microbiology of theperiodontal-endodontic lesion

The microbiology of the combined periodontal-en-dodontic lesions reflects the microbiota of the separ-ate endodontic (125) and periodontal lesions. Ac-cordingly, it might be impossible to obtain a samplethat is representative of either the periodontal or theendodontic lesion. The literature contains no de-scription of the periodontal-endodontic lesionmicrobiology. Due to great similarity between themicrobiota of periodontal and endodontic lesions,the periodontal-endodontic lesion might show nounique microbiological profile.

Experimental abscess formation

Experimental infections withoral bacteria

A number of animal models have been developedto study odontogenic diseases. Most studies of oralbacteria aimed to illustrate the virulence of singlebacterial species as well as of various bacterial com-binations. It soon became clear that dental infec-tions involving anaerobic bacteria were usually poly-microbial and originated from the oral resident flora.Dental abscesses thus comprise endogenous oppor-tunistic infections (140).

In the experimental abscess model in animals, itseems clear that abscess formation by anaerobic


18/34


Table6.Experimentalabsces

sformationbyoralmicroorganisms

Observatio

n

Frequencyofpus

Sizeofinoculum

periodfor

orabscess

Experimental

(colony-forming

abscess

formation

Study

Microbialcom

bination

animal

Modelsy

stem

units/ml)

formation

%ofinoculates

Animaldeath

Otherobservations

Takazoe&

B.

melaninogenicus

Guineapigs

Subcutan

eous

107108

3days

100%

Nodata

Heat-killed0%

Nakamura

(B.

oralis)

Single0%

(200)

Corynebacteriumspp.

Diluted1/100%

Anaerobic

Hamster

Cheekpouch

106107

2days

91%

Nodata

Diluted1/100%

Mice

Subcutan

eous

105106

3days

75%

Nodata

Sundqvist

7bacterialcombinations

Guineapigs

Transmis

sible

108

5days

59%

Nodata

Noinfectionsif

etal.(193)

fromdentalrootcanals

subcutan

eous

Bacteroidesspp.was

infection

s

excluded

Mayrand&

B.

asaccharolyticus(oral)

Guineapigs

Subcutan

eous

109

110days

100%with

Yes

Succinateproduced

McBride

K.

pneumoniae

stimulatedgrowth

(143)

withE.

coliwith

Heminsupports

A.v

iscosus

infectivity

Kastelein

B.

asaccharolyticus

Guineapigs

Subcutan

eous

Proportionalto

1day

Severeabscess

Yes

OtherBacteroides

etal.(102)

(strainW83)

bodyweight

Bacteriaisolated

strainsthatW83

Mice

fromthecardiac

werelessvirulent

blood

Lesssevere

Rats

abscessesseenin

rats

vanSteenbergen

26strainsof

Mice

Subcutan

eous

5109

3days

OnlyB.g

ingivalis

60%forW83,W

50

etal.(188)

black-pigmen

ted

strainsproduced

50%for381,382

Bacteroides

abscesses

StrainsW83,W50

and376produced

phlegmonous;the

otherstrainscaused

gravityabscesses

Sundqvist

B.

intermedius

Guineapig

Subcutan

eous

AB13af109

17days

100%

No

W83produceda

etal.(194)

AB13af,PIIa

k

Teflonwound

PIIak109

17days

100%

No

fluidwithhigh

B.

gingivalis

chamber

s

W83109

17days

100%

Yes

proteolyticactivity,

W83,381

W83109

17days

100%

No

degradingvarious

B.

endodontalis

381109

17days

0%

No

typesofserum

BNIIaf

BNIIaf109

17days

0%

No

proteins

Brook

22strainsofa

erobicand

Mice

Groininjection

LD50

7days

100%whentwo

Yes,ifanaerobes

Virulent

etal.(16)

anaerobicstrains

measurement

anaerobeswere

werecombined

combinationswith

combined

withfacultatives

twoanaerobesif

onewas

B.a

saccharolyticus

F.varium

F.nucleatum

B.f

ragilis

223


19/34

Dahlen

Table6.continued

Observatio

n

Frequencyofpus

Sizeofinoculum

periodfor

orabscess

Experimental

(colony-forming

abscess

formation

Study

Microbialcom

bination

animal

Modelsy

stem

units/ml)

formation

%ofinoculates

Animaldeath

Otherobservations

Brook(17)

42combinationsincluding

Mice

Subcutan

eous

107108

13days

100%

Nodata

Bacteroidesspp.

B.

asaccharolyticus

enhancedgrowth

B.

intermedius

rateoffacultatives

B.

melaninogenica

suchasgroupA

B.

fragilis

streptococci

B.

vulgatus

E.

coli

B.

ovatus

S.aureus

K.p

neumoniae

McKee

B.

gingivalis

Mice

Subcutan

eous

51010

214days

Spreading

0100%

Heminenhanced

etal.(144)

W50

infections

themortalityrate

withnecrosis

upto100%

Grenier&

B.

gingivalis

Guineapig

Subcutan

eous

41081011

Nodata

6strainshighly

Nodata

Infectivitycorrelated

Mayrand(70)

infective

withcollagenolytic

activity

Dahlen

8-straincollectionfrom

Rabbit

Subcutan

eous

107

35days

100%

0

Combinationswith

etal.(32)

arootcanalinfection

steelnet

104

abscessde-

30%

0

S.faecalis,

B.o

ralis,

B.

oralis

woundchamber

tectedafter

A.b

ovisgaveabscess

F.nucleatum

3days

in30%

F.necrophorum

5days

S.milleri,

P.anaerobius

P.anaerobius,

P.acnes

B.o

ralis,

A.b

ovis

F.necrophorum,

S.milleri

B.o

ralis,

S.faecalis

F.nucleatumgave

abscessin60%

Dahlen&

B.

gingivalis

Rabbit

Subcutan

eous

1081010

14days

B.

gingivalis381

Immunization

Slots(33)

B.

intermedius

steelnet

100%

No

reducedinfectivity

B.

fragilis

woundchamber

W83100%

Yes100%

ofB.

gingivalis381

A.a

ctinomyce

temcomitans

B.

fragilis100%

No

andW83singleorin

Singleorincombination

A.a

ctinomycetem-

combination

comitans(3strains)

0%

No

B.

gingivalis

A.a

ctinomycetem-

comitans100%

No

B.

intermedius

A.a

ctinomycetem-

comitans100%

No

McKee

B.

gingivalis

Mice

Subcutan

eous

1421days

Spreadinginfections

Bothmutantswere

etal.(145)

W50

7108

withnecrosis

100%

lessvurulentthan

W50/BR1

109

20%

parentstrain

W50/BE1

6109

0%

Neiders

B.

gingivalis

Mice

Subcutan

eous

1010

314days

10strainsinvasive

6strainscause

d

etal.(158)

5strainsgavelocaldepth25100%

abscess

224


20/34


Table6.continued

Observatio

n

Frequencyofpus

Sizeofinoculum

periodfor

orabscess

Experimental

(colony-forming

abscess

formation

Study

Microbialcom

bination

animal

Modelsy

stem

units/ml)

formation

%ofinoculates

Animaldeath

Otherobservations

Genco

P.gingivalis

Mice

Subcutan

eous

1081010

26days

A7436100%

Yes80%

Allstrainsreduced

etal.(61)

strainsW83,W

50

steelnet

W8360%

Yes40%

systemicIgG

A7436,W50/B

EI

woundchambers

W5060%

Yes40%

response

HG405,ATCC

33277

W50/BEI75%

No

ATCC3327783%

No

HG405100%

No

Kesavalu

W.r

ecta

Mice

Subcutan

eous

1081011

13days

ATCC332380%

Yes,when

Dexamethasone,

etal.(108)

576100%

sensitizedwith

hydrazinesulfate,

234100%

glucosamine

dextranbeads

enhancedvirulence

immunization

decreasedlesion

size

Baumgartner

P.intermedia

Mice

Subcutan

eous

107108

21days

P.gingivalis

Yes

P.anaerobius,

etal.(9)

P.gingivalis

P.intermedia

P.intermedia

V.parvula,

P.endodontalis

P.asaccharolyticus

F.nucleatum

F.nucleatumwere

P.asaccharolyticus

whencombined

isolatedfrom

pathogenicinpure

P.anaerobius

withF.nucleatum

cardiacblood

culture;

P.micros

P.gingivalisand

V.parvula

P.intermedia

enhanced

F.nucleatum

pathogenicity

Genco

P.gingivalis

Mice

Subcutan

eous

109

128days

A743647%

90%

Immunizationwith

etal.(62)

A7436,W83

woundchambers

W83100%

90%

A7436orW83and

ATCC33277,H

G405

abscessinabdomen

otherP.gingivalis

and381

causedmilder

lesionsandnodeath

Kesavalu

P.gingivalis

Mice

Subcutan

eous

10101011

13days

W5051010

100%

100%

Immunizationwith

etal.(104)

W50

W5021010

80%

100%

formalinkilledcells

ATCC33277

W5011010

60%

100%

oroutermembrane

A7A128

fractionreduced

lesionsizeand

mortalityrate

Kesavalu

P.gingivalis

Mice

Subcutan

eous

1011

15days

W50,3079.03100%

40%

W50treatedwith

etal.(105)

W50

proteaseinhibitor,

3079.03

orinhibitor

NG4B19

deficientmutants

BEI,SW5

causedsmalllesions

andnodeath

225


21/34

Dahlen

Table6.continued

Observatio

n

Frequencyofpus

Sizeofinoculum

periodfor

orabscess

Experimental

(colony-forming

abscess

formation

Study

Microbialcom

bination

animal

Modelsy

stem

units/ml)

formation

%ofinoculates

Animaldeath

Otherobservations

Feuille

P.gingivalis

Mice

Subcutan

eous

1091010

3days

Combinationgave

Nodata

Infectionwith

etal.(52)

T22,NG4B19,3079.03

enhancedspreading

F.nucleatum4hours

F.nucleatum

oflesions

prioror1hourafter

P.gingivalis

enhancedabscess

development

Hafstrm&

P.intermedia(2)

Rabbit

Subcutan

eous

105108

14days

33100%

0

Nodifferencein

Dahlen(78)

P.nigrescens(6)

Teflon

abscessformation

P.gingivalis

woundchambers

betweenP.

S.mitis

intermediaand

A.a

ctinomyce

temcomitans

P.nigrescensisolates

Takemoto

B.

forsythus

Rabbit

Subcutan

eous

109

14days

B.

forsythus,

67%

etal.(201)

P.gingivalis

Teflon

P.gingivalis100%

P.gingivalisand

F.nucleatum

woundchambers

orB.

forsythusand

B.

forsythus

F.nucleatum

isolatedfrom

1675%

cardiacblood

Kesavalu

T.denticola

Mice

Subcutan

eous

1091011

7days

100%

0

Norelationbetween

etal.(106)

T.socranskii

proteaseproduction

T.pectivorum

andvirulence

T.vincentii

Ebersole

P.gingivalis

Mice

Subcutan

eous

1071011

15days

100%dependentonYes

Lesionscouldbe

etal.(44)

W50

challengeanddose

minimizedwith

F.nucleatum

oftwobacterial

developmentof

speciesin

immunity

combination

Kesavalu

T.denticola

Mice

Subcutan

eous

1010

15days

P.gingivalis

Nodata

Proteaseactivity

etal.(107)

P.gingivalis

P.gingivalis

enhancedvirulence

T.denticolagave

greaterlesionsthan

T.denticolaalone

Nagashima

S.constellatus

Mice

Subcutan

eous

Nodata

5days

100%

0

Strongestsynergistic

etal.(155)

S.anginosus

S.milleristrains

effectina

S.intermedius

lessseverethan

combinationof

F.nucleatum

F.nucleatumor

S.constellatusand

combinations

F.nucleatum

Kuriyama

S.constellatus

Mice

Submandible

AF50

abscess

Nodata

AF50108.5

LD501010.6

etal.(120)

P.micros

formation

AF50

1010.2

1011

F.nucleatum

orLD50

lethal

AF50

107

107

P.oralis

dose

AF50

106

108.3

P.gingivalis

Necroticlesions

108.9

P.intermedia

Necroticlesions

109.4

LD50lethaldosefor50%oftheanimals.

AF50abscessformationdosein50%oftheanimals.

226


22/34


bacteria depends on synergism, often in combi-nation with facultative bacteria (94, 165, 166, 214).

Table 6 summarizes studies on the experimentalabscess model using oral bacteria. Pioneering workby Rosebury & Macdonald (135, 136, 172) and Soc-ransky & Gibbons (186) confirmed that oral indigen-ous bacteria were pathogenic and caused clinical in-

fection in polymicrobial mixtures.Takazoe & Nakamura (200) found little differencein infectivity among guinea pigs, hamsters and miceinoculated subcutaneously with oral bacteria. Rats,however seem to develop less severe inflammatoryreactions (102). Sundqvist et al. (193) showed in ex-perimental infections using microbial combinationsfrom endodontic lesions that a species ofBacteroides(later identified as P. endodontalis) was essential todeveloping transferable abscesses.

Similarly to nonoral anaerobic combinations, thesynergistic interaction between oral anaerobic and

facultative species may cause mortality among ex-perimental animals (143). A series of experiments(102, 188) showed that certain strains ofP. gingivaliswere more virulent than others and produced phleg-monous abscesses and mortality among the experi-mental animals. Inoculates of 107 or more cells havebeen commonly used to obtain experimental ab-scesses. However, a mixture of eight different strainsin inoculates of 104 cells was able to induce abscessformation (32, 37). Using virulent strains ofP. gingi-valis, Kesavalu and co-workers (44, 52, 103107)showed in subcutaneous experiments in mice thatdexamethasone, hydrazine, galactosamine, proteaseinhibitors, protease activity and antibodies were im-portant determinants of abscess development. P. in-termedia, P. nigrescens, B. forsythus, Treponemaspp.and C. rectuscan also participate in abscess forma-tion that may lead to the death of the experimentalanimal (77, 103, 106, 107, 201). In several studies, thebacterial strains used to induce abscess formationcould be isolated from cardiac blood, emphasizingthe capacity of oral bacteria to invade and spreadthroughout tissues. Recently, Kuriyama et al. (119

123) used a murine model to determine the viru-lence of anaerobes other than Porphyromonas, Pre-votellaand Bacteroidesspp.S. constellatus,P. microsandF. nucleatumwere lethal to mice when injectedsubcutaneously in various combinations.

Experimental endodontic infections

The dental root canal and the pulp chamber can beused as an experimental model of infection to deter-mine the patho-etiology of endodontic lesions and

227

abscesses in or close to bony tissues (Table 7). Themodel can also be used for endodontic treatmentstudies (137). However, the abscess formation in theroot canal model seems to be relatively mild, andchronic apical periodontitis usually occurs only afterexperiments at durations of months or years (48).The difference in pathological characteristics be-

tween endodontic infections and subcutaneous in-jection or wound chamber experimental infectionsmay be due to the need for relatively few inoculatingcells (infection dose) or due to the minute contactarea in the apical region of the tooth between theroot canal infection and the surrounding periapicaltissues. Rodents have been used, however, for a ran-dom exposure of dental pulps to the oral flora toevaluate the capacity of the oral flora to cause patho-genic changes, including abscess formation in theperiapical tissues (100, 117, 202). Fabricius and co-workers (49, 154) exposed traumatized dental pulps

of monkeys to the oral flora. Their studies showedthat a complex microflora was associated withradiographic and/or histological pathogenic lesionsin almost all cases and clinical abscesses or sinustract formation in 23% of the study teeth (154). Theirstudies also demonstrated the pathogenic import-ance of anaerobes in endodontic infections.

The rodent model cannot be used for endodonticinfections with selected strains inoculated into thepulp chamber because of difficulty in avoiding con-tamination due to the small tooth size; dog and mon-key models do not experience similar contaminationproblems. However, dogs are less relevant due to aquite different and complex anatomical architecturein the apical part of the root canal causing very littlecontact between the main canal and the periapicaltissues and thus a low frequency of periapical reac-tions (Dahlen, unpublished observations). Monkeysconstitute excellent models due to anatomical andhistological similarities with humans. Inoculatingmicroorganisms into root canals of animals can beused to determine virulence and pathogenicity in thisvery specific endodontic model; however, the rel-

evance of the findings should be interpreted with cau-tion (2, 173). By using monkeys, Fabricius and co-workers (30, 31, 50) evaluated the pathogenicity ofvarious types of bacterial combinations and foundthat abscessesonly developedin the presenceof com-plex microflora. Fabricius et al. (49) also noticed thatabscesses with sinus tract were frequent after 90 daysof inoculation but less frequent after longer periods,indicating that if abscesses drain through a sinustract, they transform into a chronic phase with forma-tion of granulation tissue.


23/34

Dahlen

Table7.Experimentalinfecti

onsinanimalsusingthedentalrootcanalasamodel

Microbial

Radiographic

Histological

Study

combination

Animal

Observationtime

Clinicalobservation

observation

observation

Comments

andconclusions

Kakehashietal.

Oralflora

Rat

142days

Pulpswerenecrotic

Nodata

Abscessformed

(106)

Rosengrenetal.

S.mutans

Rat

31days

Nodata

80%

Abscessesin70%

S.mutansrecoveredfromblood

(173)

Tagger&Massler

Oralflora

Rat

2days1year

Nodata

Periapicaldestru

ction

Abscessformed

(198)

after1month

Allardetal.(2)

S.aureus

Dog

50100days

Nodata

Radiolucency

Chronic

Anachoreticeffectobserved

S.sanguis

observedinmost

inflammation

P.aeruginosa

roots

B.

fragilis

Mlleretal.

Oralflora

Monkey

67months

23%

90%

100%

Predominantspecies:

(154)

Streptococcusspp.

Eubacterium

spp.

Bacteroides

spp.

Fusobacteriumspp.

Fabriciusetal.

Oralflora

Monkey

90days

7abscesses

100%

Nodata

20%ofto

talviablecountfor

(49)

190days

4abscesses

peptostreptococciin2/16

1060days

1abscesses

gram-positiveanaerobicrods7/16

black-pigm

entedanaerobic

rods7/16

Fabriciusetal.

8-straincollection

Monkey

6months

Noabscessfound

92%

Nodata

Allstrainsw

erereisolated;90%of

(50)

formaninfec

ted

theflorawereanaerobes

rootcanal

Dahlenetal.

S.faecalis

Monkey

69months

Noabscessfound

93%(immunized)

69%

Chronicinflammationbutno

(30)

A.b

ovis

87%(nonimmunized)

25%

abscessdet

ected

B.

oralis

Dahlenetal.

S.faecalis

Monkey

69months

Noabscessfound

86%

70%

Noabscess

detected

(31)

A.b

ovis

B.

oralis

F.necrophorum

Tani-Ishgiietal.

Oralflora

Rat

715days

Periapicallesions

Nodata

Nodata

Anaerobes24%

(202)

100%atday15

S.oralis

B.

pneumosintes

B.

ureolyticus

228


24/34


Experimental periodontal abscess model

Experimental animal studies have been widely em-ployed to support the etiological role of microorgan-isms in periodontal disease. Two main models havebeen used: (a) germ-free or specifically infected ro-dents or (b) ligature-induced periodontal breakdown

in dogs or monkeys. Certain microorganisms iso-lated from human periodontal pockets can initiateperiodontal destruction in rodents (96, 97, 133, 222)or even invade gingival rat tissue (3). Placement of aligature in subgingival sites of beagle dogs or mon-keys results in plaque accumulation, gingival in-flammation, pocket formation and loss of peri-odontal attachment. The periodontitis-associatedmicrobiota in animals shows a predominance ofgram-negative anaerobes (114, 115, 224).

Treatment

The strategy in treatment of dentoalveolar abscessesincludes a combination of mechanical treatment,surgery and systemic antibiotics. The purpose ofmechanical treatment and surgical incision is todrain to reduce the infectious load; the purpose ofsystemic antibiotics is to prevent spreading andcomplications from the infection.

Mechanical treatment and surgery

The most important and immediate step in treatinga dentoalveolar abscess, whether it is of endodontic,periodontal or other origin, is to mechanically incisethe abscess and create drainage. Mechanical treat-ment of the root canal or periodontal pocket has asimilar purpose: to debride and clean the root canalwall or the root surface of tissue or debris and tofacilitate drainage. Irrigation with antiseptic solu-tions aims to remove debrided material and kill re-sidual microorganisms.

After the site of an acute infection is identified,

surgical incision of the dental abscess should be per-formed and proper drainage established (63). In anendodontic infection, drainage can be establishedthrough the root canal. With the risk of bacteremiain mind, extraction of the affected tooth is an effec-tive but intrusive means of creating drainage (139).After abscess resolution, endodontic or periodontalinfections should continue to be treated by removingnecrotic infected pulpal tissues or by subgingivalscaling and root planing, especially in anatomicallycomplicated situations such as furcation involve-

229

ment or bony pockets. Removal of necrotic pulpaltissue and drainage are performed by mechanicaldebridement of the root canal wall to the apical for-amen. Apical surgery may sometimes be necessaryto reach the apical part of the root for debridement.Especially in longstanding periapical lesions, theapical part of the cementum may become necrotic

and have to be removed by apical surgery to obtaincomplete healing.Pericoronitis is treated by incision of the lesion

and/or irrigation of the pericoronitis pouch withantiseptics.

Local antiseptics and antibiotics

Periodontal and endodontic lesions can be treatedlocally with antimicrobial agents used in concen-trations that will ensure strong microbicidal activity(22, 153, 171). Root canal treatment has an apparent

advantage, because antimicrobial agents can be ap-plied in the canal for prolonged periods of time (22).On the other hand, antimicrobial agents in the rootcanal exert little or no effect periapically. In the acutephase, placement in a vehicle of local antimicrobialagents is not recommended because of potential in-terference with drainage. Periodontal abscesses canbe successfully treated by a combination of drainageand systemic antibiotics (77). Herrera et al. (92),found a similar response using either azithromycinor amoxicillin and clavulanic acid. In the peri-odontal-endodontic lesions, the value of local anti-microbial agents has not been studied. However, itis recommended that the acute periodontal-endo-dontic lesion be drained and irrigated.

Systemic antibiotics

Systemic antibiotic treatment of dental abscessesaims at preventing bacterial spreading and seriouscomplications. The concentration of antibiotics inthe abscess is considerably lower than that in blood,and because of poor blood supply the concentration

peaks later in the abscess than in blood. In additionto antibiotics, a dental abscess should always receivesurgical and mechanical therapy (177, 179).

Antimicrobial treatment is of secondary import-ance to surgical incision and drainage of abscesses(87). Antimicrobial agents are indicated when thepatient shows signs of fever and general discomfort,indicating that the infectious process is at risk ofspreading. Antimicrobial treatment in immunocom-promised patients is especially important andshould be considered for all dentoalveolar abscesses


25/34

Dahlen

Table8.Thesusceptibilityra

te(%)forgram-negativeanaerobicspeciesisolatedfromorofacialinfectionsaccordingtofourstudie

s(46,119,123,163)

Black-pigmen

tedPrevotella

Non-pigmentedPrevotella

Porphyromonasspp.

Fusobacterium

spp.

Veillonellaspp.

(46)

(11

9)

(123)

(46)

(119)

(123)

(46)

(119)

(123

)

(46)

(119)

(123)

(163)

(46)

Antibiotic

n32

n93

n59

n6

n56

n47

n6

n35

n1

8

n13

n57

n90

n

40

n28

Penicillin

66

72

63

82

83

100

61

71

Ampicillin

1095

081

83

82.5

89

Tetracycline

97

81

94

8197

8

100*

7397*

100

100*

100*

92

98.5*

100*

89

Metronidazole

100

100

100

100

100

100

100

100

100

100

100

100

100

Erythromycin

77

100

8187

8187

2753

94

94

88

029

Clindamycin

100

100

100

93

100

9397

100

100

100

100

98.2

100

100

100

Doxycycline.

*Minocycline.

230

(87). The choice of antibiotics should be based onsound pharmacological and microbiological prin-ciples and include the following three situations:

O The emergency case. Penicillin is still considered tobe the primary choice of antibiotics (63, 64, 69, 79,122, 148). Since resistance to penicillin is increas-

ing, metronidazole or amoxicillin/clavulanic acidmayserve as alternative antibiotics. In case of peni-cillin allergy, metronidazole is the drug of choice.

O The failing case in which a microbiological diag-nosis has been made. Change of drug regimenshould be based on the clinical situation, themicrobiological profile and antibiotic susceptibil-ity testing.

O The failing case in which no microbiological diag-nosis has been made. Change of antibiotic to onewith a broader spectrum is recommended. Amoxi-cillin/clavulanic acid or clindamycin are alterna-

tive antibiotics. Clindamycin is recommended inpenicillin allergy cases.

The duration of antibiotic therapy has becomesteadily shorter over the years. Seven to 10 days ofantibiotics is no longer recommended. Most dentistsprescribe 5 days of penicillin or 3 days of metronida-zole for acute orofacial infections (129). Martin et al.(139) concluded that the duration of anaerobic in-fections in most patients with dentoalveolar infec-tions can be as low as 23 days provided that drain-age has been established.

The susceptibility of oral bacteria to antibioticsmay be significantly different from one country toanother (221). The higher freq

Documents

Dahlen 2002 Micro Abscess and Perio Endo