ODONTOGENIC INFECTIONS

Dr Isimeli ULUIBAU

Senior Lecturer

Oral and Maxillofacial Surgery

 Introduction

This section gives an overview and discussions of the process, aetiology,

microbiology, complication, management of odontogenic infection collectively

integrated and correlated with existing knowledge currently known.

It is common for non-odontogenic infection to present with clinical presentation

mimicking odontogenic infections. Examples are infected salivary glands secondary

to blocked salivary duct to sialolith, infected mandibular fractures, loose fixation

devices for osteotomies and fracture fixations are other common sources of infection.

But in this review the focus is on odontogenic infections and deep fascial space

infections [1] particularly abscess or infections having the teeth to be the foci of the

infections.
Odontogenic infection.

Dentoalveolar bacterial infection of the oral cavity may commonly remain localised at

the offending tooth or spread rapidly to surrounding tissue and to distant sites or

deeper tissue spaces.

Spreading of the bacterial infections depends primarily on the balance between the

general factors of patient resistance and the bacterial quantity and virulence. These is

usually as a sequence of tooth pulpal death cause by dental caries or trauma to teeth or

jaw.

Pulpal death from tooth decay is the most common cause of odontogenic infections

spreading to tissue spaces, other are progressive pericoronitis secondary to partially

erupted impacted wisdom teeth, periodontal infections, surgery to the dentoalveolar

process, infected extraction sockets are also commonly encounted causes.

Because of the complexity and diversity of the oral microflora and their adaptation

in different conditions within the oral tissues, and when the balance between host and

oral flora tips favouring the growth of the micro-organism, infections can progress if

not treated.

These if not controlled or adequately treated may cause the infection to spread along

the planes of least resistance to the tissue spaces closes to the infected site or rarely to

distant sites.

Bridgeman et al. in their study found the aetiology of maxillofacial infections

(table X)predominantly odontogenic causes, Seventy five per cent of the infection

were odontogenic arising from the teeth and their supporting structures, with pulpal
necrosis being the predominant cause.

Ariji et al in their study included 46 patients with extended odontogenic infection

treated between July 1996 and November 2000 were reviewed. Out of the 46 patients

with odontogenic infection, 33 patients with extensions of infection into the

submandibular space were enrolled actually in their analysis. 16 patients followed

pericoronitis or extraction of the mandibular third molar, 14 originated in the lower

first or second molar and three from incisor or premolar.[2]

Peter et al reported 128 patients admitted during the period of October 1, 1984 and

March 31, 1995 with maxillofacial infection of dental origin were retrospectively

identified by medical review. Their study was focused on identifying potential risk

factors associated with increasing hospital length of stay(LOS) in patient with

odontogenic maxillofacial infections.

Bross-Soriano et al reported 107 (89%) patients, of the 121 included in their study

the primary source of infections was identified to be odontogenic in origin.[3].

Bross-Soriano et al did a retrospective, open, non-comparative, observational, and

longitudinal descriptive study from January 1, 1983 to December 31, 2000 an 18

years experience in which a total of clinical register of patients with the diagnosis of

Ludwig’s angina included and reviewed. Their ages ranged from 15 to87 years with a

median age of 48 years. A large numbers of patients were older, in the 51 to 60 year

range. Female was most affected 68 (56%) of patients versus 53 (44%) male

patients. Ninety one patients belong to a low socioeconomic level, 26 patients belong

to a medium socioeconomic level, and only 4 patients belong to a high socioeconomic

level.
Juang et al in their study [4]reported 14 cases of Ludwig’s angina, 12 of which (86%)

were of dental in origin.

Huang et al in their analysis of 185 patients found that odontogenic infections was one

of the most common cause of infections with their series of deep neck infections

accounting for about 53.2% of odontogenic in origin.[5]

In Bridgeman et al study few common non odontogenic causes were collectively

accounted for which, less than twenty five per cent of the cases.[6]

This finding in general is not uncommon, sometimes non odontogenic causes may

present with facial swelling mimicking acute presentation of odontogenic causes.

These presentation may make it difficult for the examiner on physical examinations,

to determine a cause especially when patients are unable to fully open their mouth due

to the spasm and pain within the mascles of mastication involved in the infection.

Refer to the next table, taken from Bridgeman et al study.

Table X. Aetiology of maxillofacial Infections.[6]

Odontogenic causes (%)

Pulp necrosis 45.3

Pericoronitis 7.5

Postoperative 18.9

Infected cyst 5.7

Total 76.4

Non –odontogenic causes (%)

Trauma 8.5

Fixation devices 7.5

Osteotomyelitis

Bone grafts 7.6

Sialadenitis

Gun Shot wounds

Total 23.6

The microbiology [7-10]of the odontogenic infection or the orofacial region

a most commonly polymicrobial or mixed infection of strict anaerobes with

facultative anaerobes generally in the secondary stage of progressive infections.

Usually the primary micro-organisms are aerobic in the early stages of the dental

infections, if not treated and controlled the population of the microflora are replaced

mainly by strict anaerobes.

Sakamoto et al with their study on semiquantitative bacteriology of closed

odontogenic abscess where pus samples from 23 dentoalveolar abscess were collected

by needle aspiration and examined by direct inoculation technique using 6 different

aerobic and anaerobic agar plates and from this 23 closed odontogenic abscess

samples, a total of 112 bacterial strains were isolated, 81 strains (72.3%) were strict

anaerobes, and 31 strains (27.7%) were common isolates.

The mean number of bacterial strains per positive samples was 4.86. Oral

streptocococci, Prevotella, Fusobacterium, Peptostreptococcus and Veillonella were

common isolates. The combination of oral streptococci and prevotella was found in

11 patients (47.8%), and that of Prevotella and Peptostreptococcus in 12 patients

(52.2%). [11]

Their conclusion remain consistent with many other findings which were,

odontogenic infections generally are polymicrobial infection infections of both the

aerobes and anaerobes. This also highlights the importance of pus specimen

collection and handling.

Heimdahl et al in their study[12] found that 174 anaerobic and 22 aerobic stains were

isolated. Anaerobic gram-negative rods were isolated more frequently from the

patients with severe infections than mild infections(p<0.05). Fusobacterium

nucleatum was more frequently associated with severe infections than with mild ones

(P<0.05). Streptococcus milleri was also more often isolated from severe than mild

infections, but the difference was not statistically significant(P>0.05). A total of 58

patients age 21 to 77 years(33males and 25 females) with orofacial odontogenic

infections were treated. All patients requiring surgical drainage and additional

antimicrobial therapy.
Viridans streptococci in dentoalveolar infections in particular is a most common

isolate, also in periodontitis, and pericoronitis others include peptostreptococcus,

porphyromonas, prevotella and Fusobacterium[7, 9, 13, 14].

Huang et al in their experience[5] noted also that one of the most common organism

they found was streptococcus viridans which accounted for 33.9% were identified

through pus cultures.

Kuriyama et al in their work recently demonstrated the microbiology of odontogenic

infection which shown from their bacterial examination of 664 strains which were

isolated from their test cases, In this case hundred and sixty three patients were

included.[10].refer table 1.

As consistent with other reports[8, 15], Viridans streptococci, Peptostreptococcus,

gemella, pigmented and non pigmented prevotella, porphyromonas, and

Fusobacterium were predominant.[10]

Kuriyama et al findings were consistent with the data compiled from a good series of

references which were adapted by Peterson, L.J.[14] in table 2 of his paper which he

outlines the micro-organism associated with odontogenic infections (per cent of

isolates in 404 patients with average of 3.8 isolates per patients.

Table 1. Organisms isolated from orofacial odontogenic infections

Aerobes No. of isolates Anaerobes No. of isolates.

Viridans 139 Peptostreptococus 105

streptococci

Staphylococcus 9 Pigmented 93
prevotella

Corynebacterium 9 Fusobacterium 90

Campylobacter 9 Nonpigmented 56
Prevotella

Neisseria 8 Gemella 36

Actinomyces 7 Porphyromonas 35

Lactobacillus 6 Bacteroids 14

Enterobacter 3 Eubacterium 9

Haemophilus 3 Veillonella 8

Pseudomonas 2 Propionibacterium 2

Micrococcus 1 Unidentified 1
anaerobic gram-
positive coccus.

Enterococcus 1 Unidentified 6
anaerobic gram –
positive rods.

Klebsiella 1 Unidentified 6
anaerobic gram-
negative rods

Branhamella 1

Unidentified 1
aerobic gram-
negative rod.
TOTAL 200 464

The above table adapted from Kuriyama, T. et al. [10]

Regarding to (table 1), we see that viridans streptococci, anaerobic gram

positive cocci, and anaerobic gram-negative rods were isolates frequently encounter

from orofacial odontogenic infections. This are consistent with varies reports in the

literature.

Mixed infection of strict anaerobes with facultative anaerobes, especially viridans

streptococci, was predominant in odontogenic infections regardless of the type of

infection,[10] which is a common finding.

Clinical practice in oral surgery shows that odontogenic infection still represent the

most commonly en-counted infection of the head and neck, odontogenic infection

most commonly arise in fit healthy individuals and can become serious, severe

complication or death can occur to medically compromise patients[5, 16] as seen in

Huang et al study.

A case report by Furst et al whom reported a case of odontogenic infection leading

Ludwig’s angina and mediastinitis, a 74 year old woman who had a medical history of

hypertension, remote thyrotoxicosis and a previous breast biopsy who saw her dentist

for removal of a deep mesio-occlusal- buccal (MOB) caries of tooth 37 and

restoration with amalgam. The procedure was uncomplicated, with no pulp exposure.

And the patient was told that the tooth might require root canal or removal if pulp

dies. Six month later patient return to see her dentist and complains of mild tenderness

on this tooth but generally asymptomatic. Two weeks later patient developed

spontaneous pain in the tooth but elected not to call her dentist, as it was a Friday

afternoon. Seventy two hours after the pain appeared, the patient returned to the

dentist with massive facial swelling that developed over a 24 hour period, a
presentation of Ludwig’s angina and mediastinitis was reported for this lady.[17]

Even though the increase in technology in medicine particularly advances in the

management of bacterial infection, especially in the use of antibiotics, microbiology

and culture techniques and their known management, there are still a few progressive

infection that really presents as a “nightmare” and brings signs of caution in their

proper management.

This especially aggressive infection that bilaterally involves the submandibular,

sublingual and submental regions(Ludwig angina).

Juang et al in their study [4]reported 14 cases of Ludwig’s angina, 12 of of which

(86%) were of dental in origin, but there were no death in his series of cases. Most of

their cases were treated with crystalline penicillin with or without and

aminoglycosides. Only one patients in this group received tracheostomy.

Literature records that this spread of infection were fatal despite

management[18]usually as a consequence of spreading infection encroaching the

upper airway leading to difficulty in breathing, and death as a result of upper airway

obstructions. Death in cases of Ludwig’s angina has decreased dramatically since the

cases reported in the 1940’s

Patterson et al reported 20 cases, and no death in their serious of study.[19]

Huang et al, of their 185 cases of deep infections mean age of 49.5 +- 20years, thirty

patients 16.2%) had major complications during admission among them 18 patients

received tracheotomies. There were 63 patients had associated systemic disease, with

88.9% of those having diabetes mellitus. Three death were recorded in this study,
mortality rate of (1.6%). All this 3 death had underlying systemic disease and were

older than 72 years of age.

These infections as we know are variable in their ways of presentations and

un-predictable in their course, that they may present as local dentoalveolar abscess to

spreading severe life threatening cellulitis and abscess of the head and neck region

that threatens the patients general health as we see from the case reports and

studies presented.

These life threatening complications are upper airway obstruction, septic shock,

descending mediastinitis, pleural empyema, pericarditis, jugular vein thrombosis,

carotid rupture, carotid pseudoaneurysm, cavernous sinus thrombosis[17, 20-28].

These are rare complication and most commonly can result from sequelae of

odontogenic infections leading to extremely devastating complications.

Papalia et al in their recent look at Descending necrotizing medistinitis[26] in which

they reported 13 series of cases, between April 1994 and April 2000. Patients were

within mean age of 39.23+-18.47(median 38, range 16-67) years. Six patients (46%)

primarily had odontogenic causes, 5 had peritonsillar abscess and 2 had post traumatic

cervical abscess.

Mihos et al looked 6 patients with descending necrotizing mediastinitis, a lethal form

of mediastinitis, between January 1990 and June 2001, the patients mean age 54.5

years, and range from 19 to 72 years. In this group 1 patient died of multiorgan failure

related to postoperative septic shock.

Mihos et al found odontogenic causes to be the primary aetiology in half of their

patients. Odontogenic infections leading to severe complications is a consistent

findings in most published literatures.

This complications are rare as mentioned but must be remembered as the causes of the

infections could been eliminated very early therefore all the complications arising

from odontogenic infections could have been prevented, as an old adage “ Prevention

is better than cure”.

This just shows the severity of ongoing dental infections and the seriousness of dental

infection complicating patients general health if not treated or un-adequately treated.

Spreading bacterial infection in different areas of the jaw can vary significantly in

their presentation[29]generally anatomic factors, such as orientation of tooth as

oppose to muscle attachment, tissues of least resistance etc usually dictates the spread

of odontogenic infection to deep facial spaces of the neck[30-33].

There are acute odontogenic infection which if does not progress or worsen a treatable

by extractions alone, which may allow for spontaneous drainage via the tooth socket

or minor intraoral drainage can be establish with a course of supplementary antibiotic

therapy.

The key issue here that needs to be remembered, is that antibiotic alone cannot

resolve odontogenic infection satisfactory. Basically quick recovery of patients results

according to proper basic management

But there are group of patients with odontogenic infections when uncontrolled or

severe warrants extensive management, aggressive surgical therapy and medical

intervention, such as multiple incisions intra-orally and extra-orally, removal of

multiple offending and suspicious carious teeth, together with prolonged

intravenous fluid and antibiotic therapy[34, 35].

Postoperative airway care in severe cases may warrant intensive care or high

dependency care as a result of extensive facial infection, which could lead to

increased the length of hospital stay, hospital cost and this issues are a significant

stress to patients and treating team.

With the significant use of antibiotics and the practice of aggressive surgical therapy,

spreading dentoalveolar infections to the head and neck region are rarely fatal, fatality

are generally related to underlying medical conditions such as diabetes, debilitated or

immuno-compromised status[5, 36, 37].

But must be remembered that death with uncontrolled infections can occur in fit and

healthy individuals.

Papalia et al study as discussed previously, in his study out of the 13 patients he

reported, 10 patients recovered well and were discharged without major sequelae, but

3 patients died (mortality rate of 23%) of multi-organ failure related to septic shock.

Green et al reported a case of a fit young male patient who died from spreading

maxillofacial infections, which resulted in massive haemorrhage from the subclavian

vein into the pleural cavity.[25]

But these severe cases of progressive dental infections, the obstruction of the upper

airway remains the most common cause of death to this group of dental patients,

especially when odontogenic infection becomes uncontrolled, spreading to deep

cervical tissue spaces that often encroach the upper airway.

The principles in the surgical treatment of odontogenic infections with associated

facial space involvement are simple to follow and when promptly adhered to

devastating complication can be minimised or prevented.

As emphasizes by Flynn.[13] the primary principle in the treatment of odontogenic

infections is the establishment of dependent drainage and removal of the dental cause.

As now known Antibiotic therapy alone is not sufficient enough to completely resolve

the infection satisfactory.

Basic management principle:

1. Identify the cause.

2. Remove the cause.

3. Establish dependent drainage.

4. Obtain culture.

5. Empiric antibiotic therapy.

Prompt institution of surgical drainage of odontogenic infections, aided by

appropriate antibiotic therapy significantly will help the management of this sought of

infections and generally rapid recovery of the patient.

As commonly observed most clinician often treat odontogenic infections

primarily with antibiotics. Antibiotics should not be prescribed as a substitute for

proper dental treatment.[38]

Therefore surgical drainage of spreading odontogenic infections is should always be

the primary treatment coupled by boaster on the host response with supplementation

of appropriate antibiotics.

A note on surgical drainage, Peleg and Hyman et al examine the value of

ultrasonography as a diagnostic tool in the treatment of superficial acute odontogenic

infections. 50 patients in the study group in whom both radiographic and sonographic

examination, as well as needle aspiration, were performed. And they did reported that

purulent fluid was aspirated in 22 of the 50 patients. Six patients diagnosed as

suffering from cellulitis had a repeated ultrasonography scan, in four, abscess

formation was diagnosed on the third day.

They concluded that ultrasonography is an effective diagnostic tool to confirm

abscess formation in the superficial spaces and is highly predictable in detecting the

stage of infections.[39]

Yusa and Yosida et al in their look at ultrasound guided surgical drainage of the face

and neck abscess in which grey-scale and colour Doppler ultrasonography were

combined, they did found that it provided easy detection and accurate, reliable

penetration of the abscess that were difficult locate by physical examination. And they

concluded that Colour Doppler ultrasonography is particularly useful for

differentiating blood vessel from the static space of abscess.[40]

This avoids the problems of careless surgical drainage, in which the insertion of

instrument in the tissues spaces can result in damage to blood vessel. This technique

is a sound plan for surgical drainage of large facial swelling, making sure that all

spaces are explored and drained. It appears to be a quick and relatively inexpensive,

non-invasive, sensitive, and accessible diagnostic tool for identifying the location and

extend of the head and neck abscess.[40]

Thiruchelvam et al in their study[41] on Intraoperative ultrasound imaging to aid

abscess drainage. They demonstrated in their study that ultrasound provided adequacy

of drainage and helped the surgeon to position the drain in the correct tissue space.

Basic step from 1-5 above on principles of management of odontogenic infection

when followed results in rapid improvement in the progress of patients.

Penicillin remain to be the gold standards of antibiotic regimen in patients presenting

with odontogenic infection with systemic signs and signs of extension of spread of

infections
 -In severe infection try to commence on empiric antibiotic therapy with the

combination with Metronidazole before the culture results is available, in

severe infections. Metronidazole is a bactericidal antibiotic, which is very

effective against anaerobes but has little or no activity against common oral

gram positive aerobes including streptococci. It major adverse effects include

gastrointestinal upset, metallic taste, central nervous system stimulation, and

discoloured urine[42].In combination with a penicillin has good antibiotic

activity if a resistant anaerobe component is suspected as this first line of

antibiotic choice in spreading infection on acute presentation should be started

with this if not hypersensitive(3-5% of the population) to penicillin while

microbiology and culture sensitivity is plan, but one must not wait for

microbiology and sensitivity to arrive, therefore prompt addition of

appropriated antibiotics on suspected microbes with the infections we are

dealing with is important, the combination here works well against most

causative bacteria.[10, 38]Especially penicillin is susceptible to gram positive

aerobes and intraoral anaerobes, commonly expected microbes in odontogenic

infection and on the other hand strict anaerobes susceptible microbes can be

tackled by metronidazole.

Therefore with odontogenic infections it is appropriate to always begin with

empiric antibiotic regimen with correlation with clinical presentation thinking

of most likely suspected microorganisms involved in the infections.

As demonstrated by Kuriyama et al in their study[9, 10] on the antimicrobial

susceptibility to penicillin G confirms still the effectiveness of this antibiotic to

common isolates of odontogenic infections.

I demonstrate here is some of the susceptibility of antimicrobial in relations to

common microbes in odontogenic infections. Especially the common use drugs, an

insights from[10].

Antimicrobial susceptibility to penicillin G.

Pathogen Susceptibility rates %

Viridans streptococci 77%

_____________________________________________________________________
Peptostreptococcus 86%
_____________________________________________________________________
Pigmented Prevotella 72%
_____________________________________________________________________
Nonpigmented Prevotella 82%
_____________________________________________________________________
Porphyromonas 100%
_____________________________________________________________________
Fusobacterium 89%

This table shows that penicillins still possesses powerful antimicrobial activity against

major pathogens in orofacial odontogenic infections.[10]

But with this result doctors must bare in the emergence of resistance now arising in

major hospitals, Kuriyama et al found that past administration of β-lactam antibiotics

and increase in the emergence of β-lactamase producing bacteria in patients with

orofacial odontogenic infections and concluded that β-lactamase stable antibiotics

should be prescribed to patients with unresolved infections who have received β-

lactams.[43]

Cephalosporins are one antibiotic that a commonly used by oral and maxillofacial
surgeons also and this comes different category or generations depending on the

extend activity of antimicrobial coverage.

The first generation cephosporins such as Cehalex and second generation

cephosporins like Cefuroxime(Ceftin) are some of the effective choices for those

patient with odontogenic infections and who do not have immediate Hypersensitive

response to penicillins. Kuriyama et al[10] a look on the antimicrobial susceptibility

of the cephalosporin particularly Cefazolin.

Antimicrobial susceptibility of Cefazolin

_____________________________________________________________________

Pathogen Susceptibility %
_____________________________________________________________________

Viridans streptococci 100%

_____________________________________________________________________

Peptostreptococcus 100%
_____________________________________________________________________

Pigmented Prevotella 100%

PU 73%
___________ _________________________________________________________

Nonpigmented Prevotella 100%

PU 30%
_____________________________________________________________________

Porphyromonas 100%
_____________________________________________________________________

Fusobacterium 100%
_____________________________________________________________________
PU-penicillin G unsusceptible strains.

This table demonstrated that cefazolin worked well with most of the commonly

isolated microorganisms. But had a significantly smaller susceptibility rates[10] to

some strains of the pigmented and non pigmented strains.

But overall has a good effective antimicrobial activity on odontogenic infections

microorganisms. Therefore appear to have excellent activity on most extensive facial

infections of suspected microbes and are use frequently by our unit when surgical

drainage are performed.

Antimicrobial susceptibility to erythromycin

_____________________________________________________________________

Pathogen Susceptibility %
______________________________________________
Viridans streptococci 55%
0%
____________________________________________________________________

Peptostreptococcus 89%
80%
_____________________________________________________________________

Pigmented Prevotella 100%

77%
_____________________________________________________________________

Nonpigmented Prevotella 89%

80%
_____________________________________________________________________

Porhyromonas 94%
_____________________________________________________________________

Fusobacterium 29%
0%
_____________________________________________________________________

This table demonstrated that erythromycin is susceptible only to particular isolates in

the common microbes in this area of odontogenic infections but does not show its

greater activity or encouraging actions on common microbes 0 susceptibility in some

strains.

Erythromycin a bacteriostatic drug which is among the macrolide antibiotics has a

narrow spectrum, and many anaerobes are resistant to this drug, it displays good

efficacy in uncomplicated cases this are simple localised dental infections and

advocated to be used only in penicillin-allergic patients with mild dental infections.

The major adverse effects of erythromycin are gastrointestinal upset[42].

Clarithromycin and azithromycin offer expanded activity against anaerobes with

much less gastrointestinal upset[42]. This has shown to have some positive

antimicrobial action on some common micro-organism in odontogenic infections.

Clindamycin has proven clinically to have its role in the management of odontogenic

infections especially patients hypersensitive to penicillins. It has bacteriostatic activity

with excellent antimicrobial action on anaerobic microbes especially the advanced

clinical stage of odontogenic infections and as well as facultative streptococci[42]. It

should be considered only as the first line of choice if the patients have had an allergic

reaction to penicillin.

Antimicrobial susceptibility to clindamycin

Pathogen Susceptibility %

Viridans streptococci 54%

0%
____________________________________________________________________

Peptostreptococcus 100%
_____________________________________________________________________

Pigmented Prevotella 100%

_____________________________________________________________________

Nonpigmented Prevotella 100%

_____________________________________________________________________
Porhyromonas 100%
_____________________________________________________________________

Fusobacterium 100%
_____________________________________________________________________

This table demonstrated that clindamycin work strongly against all strict anaerobes

tested in Kuriyama et al study.

Gilmore et al did a prospective double-blind evaluation of penicillin versus

clinidamycin in the treatment of odontogenic infections which was compared in

treatment of moderate to severe orofacial infections of odontogenic infections which

pus was obtained on aspiration. Resistance found in this their study showed that

anaerobic isolates were 8.9% with penicillin and 1.9% to clindamycin. They

concluded that penicillin and clindamycin produces similar good results in treating

odontogenic infections.[44]

The most concern in the use of this drug is that it predisposes some patients to the

over growth of Clostridium dificile, a toxigenic microbe harboured by only 5% of

normal healthy adults.[42] to the development of pseudomembranous colitis.

But this drug, clindamycin also have good intraosseous penetration and particulary

with odontogenic infection destroying the jaws this drug clinically indicated for

spreading odontogenic infections on selected cases, clinically this has to be based on

individual patient to patient assessment.

Key issue:

Antibiotic should not be prescribed as a substitute for proper surgical treatment.

Remember when dealing with odontogenic infections, when treated promptly and correctly
resolves quickly but when basic management principles are not followed devastating and life
threatening complication can occur.
1. Clinical Presentations
Acute odontogenic infection or oral and maxillofacial infections usually presents with

signs and symptoms generally of pain, swelling, redness pyrexia, trismus and

difficulty swallowing.

Generally patients may appear systemically ill on presentations.

In this section, the sequela of odontogenic infection and anatomy of the fascial spaces

is revised and clinical presentations of odontogenic infections are integrated with the

knowledge reviewed from the literatures and discussion of the peri-operative issues

on the signs and symptoms of odontogenic infection

.
Process of odontogenic infection leading to signs and symptoms are not a process

that occur overnight it is usually an infection process that can take a long course of

infective process before the patient becomes symptomatic.

The most common and frequently encounted cause of odontogenic infections is dental

caries or tooth decay leading to pulpal death or necrosis and eventually leading to

periapical infections (periapical abscess or acute apical periodontitis).

The other common way for micro-organisms to infect a tooth is via the invasion of the

dental pulp through secondary canals coming from the periodontal ligaments or from

the area of infection when periodontitis is in process.

When periapical pathology or infection occur it tend to spread following the path of

least resistance and most commonly will spread within the vicinity of the tooth where

it may perforates the cortical bone toward the subperiosteal membrane with

subsequent localization of swelling or abscess.

If infection from the teeth once established on the periapical region of a tooth

infection can subsequently spread away from the tooth and beyond the dentoalveolar
process to distant sites or involving deeper facial tissue spaces.

The understanding of the anatomy of fascial spaces[30, 32, 45-47] is essential for the

diagnosis and treatment of odontogenic infections that had spread to fascial spaces,

because the anatomy or fascial planes of the head and neck is such that it is an

effective barrier to the spread of infection and gives a vital key role to the possible

location or clinical localisation of the abscess or the involvement of cellulitis in

fascial spaces and aids in the surgical drainage.

The process of odontogenic infection, which infection spreads from the teeth or the

periapical region of a tooth and away from the tooth and the dento-alveolar process,

and how the muscular attachments fascia of the jaws guides or directs the passage of

spread of the infectious process into the spaces around the mandible and maxilla and

deep to the cervical spaces of the head and neck Laskin[32] to be the current

fundamental knowledge of understanding of anatomy by which most surgeons used in

relations to spread of infections through anatomical pathways.

Grondinsky and Holyoke work in 1938 where they used dyed gelatin injections to

determine the likely pathway of the spread of infections through the fascial planes,

a brilliant work indeed and it is this work that initially formed the modern

understanding[45].

The most likely pathways of infections arising from each tooth are listed in table 3.

Also find below cross references of some of the fascial and space names used here

with synonyms used else where.[33] refer table 2.

Table 2. Synonyms for Deep Fascial Spaces of the
Head and Neck.

Name Synonym

*Space of the body of the mandible Mandibular space

Submandibular space Submaxillary space

Submylohyoid space
Masticator space Masticatory space
Masseteric space
Masseter-mandibular / pterygoid space

Temporal spaces Temporal pouches

Infratemporal space Postzygomatic space

Buccal space Buccinator space

Infraorbital space Canine space

Lateral pharyngeal space Parapharyngeal space

Pharyngomaxillary space

Retropharyngeal space Retroesophageal space

Pretracheal space Perivisceral space

Paravisceral space
Paratracheal space

Carotid shealth Visceral vascular space.

Adapted from Granite.[33]

* The space of the body of the mandible is essentially the subperiosteal space formed
by the splitting of the anterior layer of DCF around the body of the mandible. This
subperiosteal space contiues posteriorly to cover the ramus and condyle of the
mandible as well. It contains the mandible, teeth, and inferior alveolar neurovascular
bundle. Infections spreading beyond the periosteum of the mandible immediately
enter the vestibular, buccal, sublingual, submandibular, or masticator space.[33, 46]
Table 3. Relations of Deep Spaces in Infections.

Space Likely contents Neighboring Approach for

causes spaces I & D*

Buccal Upper Parotid duct Infraorbital . Intraoral(small)

bicuspids. Anterior facial Pterygomandibular. Extraoral(large)
Upper artery and Infratemporal.
molar vein.
Lower Transverse
bicuspid. facial artry and
vein.
Buccal fat pad.

Infraorbital Upper Angularartery Buccal . Intraoral.

cuspid. and vein.
Infraorbital
nerve.

Sub Lower Submandibular Sublingual. Extraoral.

mandibular molars. gland. Submental .
Facial artery Lateral pharyngeal.
and vein. Buccal..
Lymph nodes.

Submental Lower Anterior Submandibular Extraoral.

anterior jugular vein. (on either side).
teeth. Lymph nodes.
Fracture of
symphysis.

Sublingual Lower Sublingual Submandibular Intraoral

bicuspids. glands. Lateral pharyngeal Intraoral –
Lower Whartons’s Visceral(trachea Extraoral.
molars. duct. and esophagus).
Direct Lingual nerve.
trauma. Sublingual
artery.
Pterygo Lower Mandibular Buccal. Intraoral.
mandibular third division of Lateral pharyngeal. Intraoral-
molars. trigeminal Submasseteric. extraoral.
nerve. Deep temporal.
Inferior Parotid.
alveolar artery Peritonsillar.
and vein.

Submasseteric Lower Masseteric Buccal. Intraoral.

third artery and Pterygomandibular Intraoral-
molars. vein. Superficial extraoral.
Fracture of temporal.
angle. Parotid.

Lateral Lower Carotid artery. Pterygomandibular Intraoral.

pharyngeal. third Internal Submandibular. Intraoral-
molars. jugular vein. Sublingual. extraoral.
Tonsils Vagus nerve. Peritonsillar.
Infections Retropharyngeal.
in
neighbring
spaces.

*I & D indicates incision and drainage.

Continuation from Table 3.

Adapted from Laskin. [32]
a. Pain.

Bridgeman et al, in their study at the Royal Melbourne Hospital in which they

reviewed records of 107 consecutive patients over a 57 month period.

The clinical presentations of the patients in this study demonstrated that all the 107

patients presented with pain, a prevalence of 100% , these are the most common

reasons for presentation.

In most experiences patients neglect intermittent pain and in some cases where the

history of pain is more than 1 week to a month or worse scenario more and this in

most cases patient do not act by seeing a dentist early rather present to a doctor when

the pain is severe or very late in the process of the infection. And in this case the

process of infections could be to late for simple conservative treatment and may

require extensive surgical and medical treatment in a hospital setting.

Odontogenic infections can become very painful which is rather a common finding,

in almost all patients with acute odontogenic presentation.

This is not just the sensation of mild pain; most are truly in agony when first seen

especially in severe conditions, patients often limit themselves from taking anything

orally or decrease their oral intake, again this varies from patient to patient depending

on individual pain tolerance and severity of the infection.

Patients are obviously and commonly symptomatic in acute conditions, on the other

hand chronic infection with low grade infection and those patients whose had prolong

course of antibiotics and clinically may have a localized swelling and infection,

usually most may complain of the sensation of discomfort rather than pain.

Patients tend to ignore pain alone as a symptom.

b. Swelling.

There were 105 patients in Bridgeman et al study who presented with swelling, and a

prevalence of 98%. Obviously another common finding of spreading odontogenic

infection either locally or deep to the cervical tissue space of the neck.

Swelling may be appear well pronounced or be diffuse , thus swelling may be easily

picked up by clinical examination or may well be hidden deeper in the patients

oro-pharynx or upper airway which often difficult to judge from physical examination

alone.

Especially progressing deeper swelling particularly when the patient cannot open the

mouth fully to allow physical examination.

Facial swelling in particular facial cellulitis were often managed differently in the past

where administration of antibiotics appears to be the first mode of therapy before

surgical intervention is instituted.

As we all know from present understanding the presentation of acute odontogenic

infections could present clinically as :

• Cellulitis stage

or

• Abscess stage.

This presentation of either cellulitis or abscess may depend on the anatomical

location, host immune status, the virulence of the micro-organism, the region may be

isolated from surrounding tissues by the formation of abscess therefore causing the

walling off the infection preventing further spread. But if these process of walling or

abscess formation fails this can lead to diffuse spread of infection causing severe
inflammation or oedema , termed as cellulitis[42]

The idea of waiting and see while one is able to ascertain abscess formation or

fluctuance of the facial swelling could may be prolonged in progressive cellulitis

and may threatens the involvement of other tissue spaces.

The cellulitis stage often are diffusely presented and they are normally taught warm

and painful and may be involving multiple spaces.

These can be serious, if progressive involvement of deep spaces therefore waiting

and see could result in serious clinical deterioration, and that I believe in a way,

waiting for abscess or fluctuance of deep space infections may be difficult for the

examiner to determine clinically even though an abscess is truly present deeper to the

swelling.

And secondly while waiting for the abscess stage in a more superficial tissue space,

the infection may be progressing to the cellulitis stage that may be involving other

deeper tissue spaces within its vicinity.[13]

This way of management is potentially asking for trouble.

These can result in disastrous situation where the airway can close or other vital

structures at risk of disruption as infectious process progresses therefore increasing

the morbidity and mortality of patient with odontogenic infections.

Especially when infection like this can be easily managed and obtaining swift

recovery if basic management principles are followed.

The feeling among oral surgeons in the past are the incision and drainage of fascial
infections when the swelling is fluctuant. This were in line with Kruger’s view in the

pre-antibiotic era.

Kruger who recommends incision and drainage when pus is diagnosed and states that

treatment in the cellulitis stage of infection may disrupt physiologic boundaries and

facilitate diffusion and extension of the infection. [48]This I believe is true in a sense

and may apply to cases with inadequate antibiotic therapy or no antibiotic is given

especially.

Kruger’s point here was the general feeling in the past around the pre-antibiotic era.

Clinically, now the practice of early incisions and drainage is recommended which

basically aid in the decompression of the swelling and prevent the progress of

infection and therefore quickens the recovery of patients.

On the other hand as discussed earlier, Goldberg and Topazian state that incision and

drainage should be performed only when an abscess is fluctuant, prior to spontaneous

rupture and drainage.[49]

These again are issues in which complications that a avoidable, and best achieve if

early incisions and drainage of all facial swelling occurs.

But now the general feeling of most oral and maxillofacial surgeons that is now

practiced in most industrialize countries and particularly in this institution are the

early admission, removal of the cause and incision and drainage of all acute

odontogenic infection with associated tissue space involvement and the administration

of the appropriate antibiotic and fluid therapy.

Flynn in his paper[13] referred to Conover and Donoff, study in which they reviewed
175 hospital admissions for facial infection, proposed a policy of early admission and

incision and drainage for febrile patients with “significant clinical signs.”[50]These is

important that it helps decrease the morbidities involved.

The “wait and see” management, is not recommended by most surgeons, an old wise

adage “never let the sun set on an undrained abscess (PUS)”. This is as true

today as it ever was.

The statement above means if facial infection is diagnosed with associated swelling

either cellulitis or abscess of tissues spaces, early removal of the cause and wide

drainage must be established, this gives good results.

Literatures has revealed that the most common cause of death in odontogenic

infection is airway obstructions due to swelling in the upper airway.

Potter et al compared the costs and outcomes for patients with deep neck infections

who were treated with either tracheotomy or endotracheal intubation, this were 85

patients were retrospectively studied.

In this study 2 patients died, one patient died as a result of unplanned extubation and

the other died following a planned extubation.

This patient demonstrated sufficient air leak around the endotracheal tube and was

extubated without immediate complications. Approximately 30 minutes after

extubation the patient developed progressive respiratory obstruction, and attempts to

reintubate the trachea were unsuccessful due to obstruction and this was confirm

following the post-mortem examination[51].

This case scenario clearly demonstrates that the severity of swelling

preoperatively persist postoperatively and both the surgeon and the anaesthetist

must work together planning the timely fashion to keep the patients with severe

odontogenic infection that has spread to the neck remain intubated

postoperatively and followed up on the decision on the right time to extubate.

Though clinical signs such as air leak around the cuff must be carefully

evaluated and enough time given for more air leak which would demonstrate

significant decrease of the airway swelling as we can see from Potter el. Study that

the second patient died 30 minutes later after extubation despite air leak.

c. Pyrexia.

Generally patients with acute bacterial infections may presents with fever, an

elevation of body temperature above normal (about 37 degrees celsius). It is common

to see patient also not to have fever or pyrexic even though there is an obvious

swelling caused by bacterial infection. Fifty-four patients in Bridgeman et al. had

pyrexia, a prevalence of 50%.

This in general are caused by pyrogens which bring about the fever and this pyrogens

may be exogenous( e.g. endotoxins of gram-negative bacteria) or endogenous(e.g.

cytokines released from host cells in response to the infection).

The microbiology[7, 10, 12, 13] of orofacial infection as demonstrated in this

literature are the most common reasons for fever in a proportion of our patients with

acute odontogenic infections, basically the pyrogens produced as a result of this

bacterial infection act by causing elevation of the set point of the hypothalamic

thermoregulatory centre, which in turn results in vasoconstriction, decreased

peripheral heat loss and fever.

Fever associated with bacterial infection of the head and neck generally resolved

within 24hrs postoperatively if the patients was carefully examined preoperatively and

medical status are stable and treatment proceeded successfully as intended.

Odontogenic infections that has spread to distant sites or to deep cervical tissues of

the neck and that continue to show signs of fever must be carefully examined and

microbiology, culture and sensitivity followed up and the cause identified and

rectified.

Postoperatively the temperature should be monitored as patient spiking temperature

postoperatively as this may be signs of inadequate drainage of abscess, cause of the

infection is not removed, re-infection of surgical wound, inappropriate antibiotic used,

inappropriate antibiotic dose, inadequate frequency of antibiotic administration, septic

or rather infected i.v sites or urinary tract infection.

These are some of the factors that a worth reminded or to be considered when

ongoing fever comes up.

d. Trismus

Finally, trismus are also a common sign of odontogenic Infection, trismus is an

inability to open the mouth fully, that could result especially if bacterial infection

spreads or involve the masticatory tissue spaces or muscles.

Forty nine patients in Bridgeman et al. study had trismus and a prevalence of forty

six per cent. This is a significant number of patients, patients with trismus always
presents difficulty to both the surgeon and especially to the anaesthetist in the

method of intubation and timing for extubation..

This raises the issue whether to extubate the patient early or keep patient intubated

postoperatively, especially when concern for upper airway or uncertainty arises, or the

risk is raised if the patient is extubated and not able to re-intubate the patient again

because of trismus if airway becomes a problem.

And it becomes significantly a problem if an inexperienced anaesthetist intubates the

patient as firstly the airway can be lost, secondly if the are not careful about their

technique for intubation this can cause rupture of the abscess orally and could lead to

aspiration, if one is not aware which in turn could lead to aspiration pneumonia as the

trauma of intubation resulting in rupture of pointing oro pharyngeal swelling or

abscess or result to laryngeal trauma, laryngeal stenosis etc.

Uram and Hauser reported a case of traumatic intubation resulted in a severe, wide

spread neck infection.[52] Though the intubation in Uram and Hauser case was an

emergent intubation at home because of respiratory depression and not odontogenic

related, but the complication of traumatic intubation with odontogenic infection

related patients certainly in this case high light an issue that is worthwhile thinking

about, both the surgeon and anaesthetist especially the anaesthetist.

The trauma to the oro-pharynx resulting to postoperative upper airway oedema

or laryngeal trauma resulting in laryngeal stenosis these can always in turns cause

obstruction of the upper airway and as we have seen in the literatures a significant

number of death from odontogenic infection is obstruction of the airway.

The anaesthetist and the surgeon must always remember that the difficulty of
intubating a patient with trismus at surgery remains after surgical treatment and this

can persist within 24 hrs and 48 thereafter postoperatively.

Therefore keeping the patient intubated in a controlled environment, given

adequate time for the infection to resolve and sufficient time be given before

extubation together with satisfactory clinical signs.

And together both the anaesthetist and the surgeon must agree on the timely

fashion for extubation and also experience anaesthetist and senior surgeon must

be present for extubation in severe infections compromising the airway.

Control of the airway is paramount in the controlled of the airway

postoperatively with intubated patients and tracheotomized patients and must

always be in the mind of both the teams involved, especially the presence of

senior team member.

Issues around the pre – referral of patients with
odontogenic infections to a specialist.

Nothing replaces a good oral and maxillofacial diagnosis and treatment planning

when a clinician first come in contact with this group of patients and this is formed

from the collated information collectively derived from a comprehensive history and

thorough clinical examination.

This early contact with the patient the must remember the signs and symptoms of

severe infection that could lead to airway compromise, distant spread and septic state.

These are all vital information that lead to a successful management of patients, that

is the idea of a comprehensive examination. And as always emphasized in clinical

practice from general practice point of view, anything beyond a clinician or

practitioners scope of care must be referred to the appropriate specialist.

As Bridgeman et al discussed …“that the ability to diagnose and surgically

managed initial maxillofacial infections and to recognise those cases which

should be referred immediately to a specialist oral and maxillofacial surgeon are

essential general practice skills”…[6]

Refer appropriately is the fundamental knowledge of clinical practice when cases

beyond our care could be managed properly by a specialist.

Particularly general dental practitioners and general medical practitioners

as indicated in Bridgeman et al. results, many patients had sought treatment from

dentists, and that a large proportion of patients had received sub-optimal management

prior to referral.
Forty seven per cent of patients had actually received initial treatments, the common

features of their pre-referral management included delays in diagnosis, failure to

establish and maintain drainage of infections, and a reliance upon antimicrobials

as a primary mode of management, frequency using an antimicrobial of

inappropriate spectrum, dosage, route or duration.[6]

These pre-referral features are consistent with experience in this state oral and

maxillofacial unit.

Most issues that can be deduced from the literature review in relation to patients with

infections especially odontogenic infections spreading to involve other sites or alleged

inadequate management etc brings the issues on the medico legal aspects[53] of

infections though rarely we have this patiens taking legal actions on the treating team,

but these are important issues that needs to be pointed out to treating and referring

teams involve in their management.

Find next are some of the clinical key presentations of patients with odontogenic

infections presenting to medical practitioners to identify and refer cases that can be

managed by Dentists and those that require direct referral to the specialist Oral and

Maxillofacial Surgoens especially an OMFS unit in the closes Hospital.

Fig b. Schematic diagram for referrals of odontogenic
infections for medical practitioners.

Medical
Practitioners

Refer to OMFS* unit in

Refer to a Dentist if :
the closes Hospital if :

• Large Facial Swelling. • Small

• Involving facial spaces Localized
of the head & Neck. swelling to
• Difficulty opening the jaw.
mouth. • No difficulty
• Febrile in mouth
• Medically opening.
compromised. • Afebrile
• Difficulty swallowing. • Requires
• Swelling floor of simple tooth
mouth, decrease removal
tongue mobility.
(ask patient to move the
tonque, push tongue
forward and side to side.)

NEVER LET THE SUN SET ON PUS

Do not Delay any Referral. Odontogenic infections are unpredictable in

their course and they can easily progress to severe life threatening
conditions.

*OMFS – Oral and Maxillofacial Surgery.

For Dentist refer to decision-making flow diagram next.

 Patient presents to general dentist

• History (including antimicrobials taken

recently).
• Clinical features.
• Special tests ( radiographs, pulp vitality
testing).

Diagnosis

• Undertake management in dental practice?.

NO YES

Localized collection of pus amenable to

• Swelling/tenderness in floor of mouth intraoral drainage.
• Raised/swollen tongue
• Dysphagia/odynophagia Identifiable cause of infection.
• Shortness of breath
• Medically compromised Local anaesthetic achievable.
• Facial space spread
• Failure of local anaesthesia Patient compliant and available for review
• Severe trismus
• Requires extra-oral diagnosis
Immediate surgery
• Multiple infection sites
Remove cause establish
• Late presentation(>3days) drainage.
• Antimicrobial course failed
• Febrile “toxic” patienc

Immediate referral to oral

and maxillofacial surgeon
Fig. c. Decision – Making Flow diagram.
Note : If in doubt and if you feel its beyond your capabilities refer to the oral & maxillofacial surgeon.
Do not put the patients at risk of developing serious complication from your inadequate care.
Outcome of neglected tooth ache.

Slight modification of decision making flow diagram as adapted from Brigeman et al.
 Toothache

Dentist
If Not treated
Restoration
of the tooth

Root filling

Removal of
the tooth.

If not resolve can lead to :

Localised dental abscess

Spreading extending odontogenic

infection of the head and neck.

Requires
surgery. If severe can die or can suffer major
life threatening complication.
Cut to the
neck +- Airway obstruction

Removal of Septic shock – multiorgan

all failure
suspicious
teeth Cavernous sinus thrombosis

Descending mediastinistis

Pleural empyema
Intensive Care can be prolong, & Pericarditis
stressful to patient & relatives.
This is a very expensive journey.
Jugular vein thrombosis
Carotid rupture
Carotid pseudoaneurysm.

This flow diagram on the outcome of untreated toothache can result in severe

odontogenic infections if not treated early by a dentist or if the cause of the infections
is quick as known that process of odontogenic infections can be very unpredictable

from slow progressing swelling to rapid growth of the swelling and this situation the

referral to an oral and maxillofacial surgery unit in a hospital requires urgent

attention, the identification of the problem and referral directly to the unit for

management.

Never delay referral.

Because simple dental infections if not treated adequately or neglected can result in

devastating complication and worse death can occur

Simple dental problem if not managed properly can result in death of a

patient whom if treated correctly would have recovered completely and this
is the penalty that treating doctors both general medical practitioners general
dental practitioners still take in putting patients life at risk by optimising the
treatment offered.

Really needs the care of the oral and maxillofacial surgeons, therefore
prompt referral and treatment is the essence.

ODONTOGENIC INFECTIONS IS A SERIOUS INFECTION.

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