Complex Odontogenic Infections

Dr. Mohammed Ibrahim

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Introduction To Fascial Spaces

 Fascial spaces are fascia-lined tissue compartments

filled with loose, areolar connective tissue that can
become inflamed when invaded by microorganisms.

 The resulting process of inflammation passes through

stages that are seen clinically as edema (inoculation),
cellulitis, and abscess.

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 Stages of Deep Fascial Space
Infections
•When the bacteria enter the tissues of a
inoculation particular anatomic space

•When an intense inflammatory response causes

Cellulitis all of the classic signs of inflammation

•When small areas of liquefactive necrosis

Abscess coalesce centrally to form pus within the tissues
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 Path of Spread of Infections

 This is primarily based on the

1. Areas of least resistance and

2. Muscle attachment

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5
Infections Arising From Maxillary Teeth
1. Buccal
2. Infraorbital
3. Infratemporal
4. Maxillary and other paranasal sinuses
5. Cavernous sinus thrombosis
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 1. Buccal Space Infection
 Anatomic Location: Overlying skin of
the face laterally and the buccinator
muscle medially
 Source of Infection: Upper premolars,
Upper molars, and Lower premolars
 Clinical Features: Cheek swelling
(below the zygomatic arch and above
the inferior border of the mandible).
 Approach for Incision & Drainage:
Intraoral (small), Extraoral (large)

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 2. Infraorbital Space Infection (Canine space)

 Anatomic Location: Thin potential space

between the levator anguli oris and the
levator labii superioris muscles.

 Source of Infection: Maxillary canine

tooth or infections from the buccal space

 Clinical Features: Swelling of the anterior

face, obliteration of the nasolabial fold &
edema of lower eyelid

 Approach for I & D: Intraoral

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 3. Infratemporal Space Infection

 Lies posterior to the maxilla

 Source of Infection: Maxillary third molar
 Content: Maxillary artery, Pterygoid
venous plexus
 It is the origin of posterior route by
which the infections may spread into the
cavernous sinus.
 Approach for I & D: Intraoral and/or
Extraoral

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4. Maxillary and other paranasal sinuses

 Periapical or periodontal infections of

posterior maxillary teeth may erode
superiorly through the floor of the
maxillary sinus.
 Approximately 20% of cases of
maxillary sinusitis are odontogenic.
 Odontogenic maxillary sinus infections
may also spread superiorly through the
ethmoid sinus or the orbital floor to
cause secondary periorbital or orbital
infections
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 5. Cavernous Sinus Thrombosis

 Life threatening infections that requires

aggressive medical and surgical care.

 Anterior Route: Infections from the

Infraorbital space and the Sinuses via
the common Ophthalmic vein

 Posterior Route: Infection from the

Infratemporal space via the Pterygoid
venous plexus
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 Clinical Features

- Periorbital edema
- Photophobia
- Proptosis (bulging of
the eyeball)
- Ptosis
- Fever
- Headache

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 Treatment of Cavernous Sinus
Thrombosis

 Treat primary source of infection

 Incision & Drainage
 Antibiotics (high dose IV)
 Anticoagulants (Heparin)
 Analgesics
 Corticosteriods

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 Infections Arising From The
Mandibular Teeth

1. Space of the body of the mandible

2. Submandibular
3. Sublingual
4. Submental
5. Masticator space
a. Submasseteric
b. Pterygomandibular
c. Superficial temporal
d. Deep temporal

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 1. Submandibular Space Infection

 Anatomic Location: Lies between the

mylohyoid muscle and the overlying
superficial layer of the deep cervical
fascia.
 The posterior extent of the
submandibular space communicates
with the deep fascial spaces of the
neck
 Source of Infection: Lower molars
 Clinical Features: Extraoral swelling in
the submandibular region
 Approach for I & D: Extraoral 15
 2. Sublingual Space Infection

 Anatomic Location: lies between the oral mucosa of the floor of

the mouth and the mylohyoid muscle. Posterior border is open
and communicates with the submandibular space.
 Source of Infection: Lower premolars and molars, direct trauma
 Clinical Features: Floor of the mouth swelling, Elevated tongue
 Approach for I & D: Intraoral or Intraoral and Extraoral

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 3. Submental Space Infection

 Anatomic Location: Lies between the

anterior bellies of the right and left
digastric muscles and between the
mylohyoid muscle and the overlying
fascia

 Source of Infection: Lower anterior

teeth, symphyseal fracture

 Clinical Features: Extraoral swelling in

the submental region
 Approach for I & D: Extraoral
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 4. Ludwig’s Angina

 Rapidly spreading cellulitis

involving the 3 perimandibular
spaces (submandibular,
sublingual & submental)
bilaterally.

 Life threatening

 Can obstruct the airway and

commonly spreads posteriorly to
the deep fascial spaces of the
neck.
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Clinical Features of Ludwig’s Angina
 Severe swelling
 Raised floor of the mouth and tongue
 Tense, hard, bilateral induration of submandibular
region
 Trismus
 Drooling of saliva
 Difficulty with swallowing
 Difficulty with breathing
 Severe anxiety
 Upper respiratory tract obstruction which may lead to
death
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Management of Ludwig’s Angina
 Secure the airway

 Early and aggressive I & D

 Treat source of infection

 Supportive medical care

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 5. Masticator Space
 4 compartments or spaces make up
the masticator space:
1. The Submasseteric space
2. The Pterygomandibular space
3. The Superficial temporal space
4. The Deep temporal space
 Clinical feature: All the spaces can get
infected simultaneously or only one at
a time. Limitation in mouth opening is
a common clinical feature.

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 Submasseteric Space Infection
 Anatomic Location: Lies between the
masseter muscle & the lateral surface of
the ascending ramus

 Source of Infection: Buccal space,

mandibular 3rd molars, infected angle
fracture

 Clinical features: Mild swelling over the

angle & ramus, Moderate to severe trismus

 Approach for I & D: Intraoral or Intra oral –

Extra oral
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 Pterygomandibular Space Infection
 Anatomic Location: Lies between the medial
pterygoid muscle & medial surface of
ascending ramus

 Source of Infection: Mandibular 3rd molar

 Clinical features: -
 Little or no facial swelling
 significant trismus
 swelling and erythema of the anterior tonsillar
pillar on the affected side
 deviation of the uvula to the opposite side
 Approach for I & D: Intraoral
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 Superficial & Deep Temporal Space
Infections
 Anatomic Location:
 Superficial temporal space – between
temporalis fascia & temporalis muscle
 Deep temporal space – between
temporalis muscle & the skull
 Source of Infection: Upper molars

 Clinical Features: Swelling over the

temporal region, limitation in mouth
opening

 Approach for I & D: Intraoral or extraoral

or both
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 Deep Cervical Fascial Space
Infections
Infection of the deep fascial spaces of the neck can be life
threatening. They arise from primary spaces.

1. Lateral Pharyngeal
2. Retropharyngeal
3. Prevertebral
4. Danger Space
5. Mediastinum

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Lateral Pharyngeal Space Infection

Source of Infection
 Lower 3rd molars
 Tonsils
 Neighboring spaces e.g. Submandibular, sublingual,
pterygomandibular and retropharyngeal spaces

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 Lateral Pharyngeal Space Infection
Clinical Features
 Trismus,
 Lateral neck swelling,
 Difficulty swallowing,
 High fever
Potential complications:
 Thrombosis of Internal Jugular Vein,
 Erosion of carotid artery & interference with cranial nerves IX,
X, and XII.
 Extension of infection into the retropharyngeal space.

Approach for I & D

 Intraoral & extraoral
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 Retropharyngeal Space Infections
Anatomic Location:
 Begins at the base of the skull and ends
inferiorly around the cervical (C6) and
thoracic (T4) vertebrae

Source of Infection
 Lateral pharyngeal space and other
neighboring spaces

Clinical features
 Difficulty swallowing (Dyshpagia), Difficulty
breathing (Dyspnea), Swelling in posterior
oropharyngeal wall & Spread of infection into
the danger space
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 The Danger Space

 Anatomic Location: Btw alar fascia anteriorly

and the prevertebral fascia posteriorly.
Extends from the base of the skull to the
diaphragm, and it is continuous with the
posterior mediastinum

 Source of Infection: Retropharyngeal space

 Clinical Features: Difficulty breathing,

difficulty swallowing, extension of infection
into the mediastinum 30
 Management of Fascial Space
Infections
 5 goals of management are:

1. Protection of the airway and general medical support

2. Surgical removal of the source of infection as early as possible
3. Surgical drainage of the infection, with proper placement of
drains
4. Administration of correct antibiotics in appropriate doses
5. Frequent reevaluation of the patient's progress toward
resolution

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 Osteomyelitis
 The term osteomyelitis literally means inflammation of the bone
marrow. Clinically, osteomyelitis implies an infection of bone.

 Osteomyelitis usually begins in the medullary cavity, involving

cancellous bone; then it extends and spreads to cortical bone
and eventually to the periosteum.

 Mandible more commonly involved than maxilla.

 Predisposing factors – Odontogenic infections, fractures.

 Rarely occurs if the host defenses are reasonably intact

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 Acute suppurative osteomyelitis shows little or no
radiographic change because at least 10 to 12 days are
required for lost bone to be detectable radiographically.

 Chronic osteomyelitis usually demonstrates bony

destruction (radiolucency) in the area of infection. Areas of
radiopacity (Sequestra) also may occur within radiolucency.

 Osteomyelitis is treated medically as well as surgically

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 Article 1

Severe odontogenic infection:

An emergency. Case report

J Clin Exp Dent. 2017;9(2):e319-24.

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 Introduction
 Odontogenic infections (OI) are quite frequent, and
usually can be resolved by local medical-surgical means -
though in some cases they may become complicated and
result in morbidity/mortality.

 The spread of an infection depends on the balance

between the patient condition and microbial factors. The
virulence of germs, along with the local and systemic
conditions of the patient, determine host resistance.

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 Ludwig’s angina is a head and neck infection characterized
by rapid progression, with edema and necrosis of the soft
tissues of the neck and floor of the mouth, and is associated
to a high mortality rate .

 The disease involves simultaneous alteration of the

sublingual, submandibular and submental spaces, with
elevation and subsequent displacement of the tongue, which
can eventually obstruct and collapse the respiratory tract .

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Flyn et al. classification of the severity of OI

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 Case report
 A 42-year-old male consulted due to sudden,

progressive and painful tumefaction in the left

submandibular region during the last 48 hours.

 The disease history revealed type 2 diabetes treated

with glibenclamide (50 mg/day), and arterial

hypertension. Both conditions had not been followed-

up on over the last 12 months.

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 He had been initially diagnosed and treated by his dentist for
symptoms of pericoronitis affecting tooth 38, with the
prescription of oral antibiotics (amoxicillin 500 mg +
clavulanic acid 125 mg 3 times a day) and oral nonsteroidal
antiinflammatory drugs (ibuprofen 400 mg 3 times a day).

 Following limited response to the initial medical treatment,

the patient decided to consult the maxillofacial surgery unit.
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 At consultation, the patient was found to be conscious,
with dehydration, fever (38.5ºC), dysphagia, severe
trismus and submaxillary adenopathies.
 Tachycardia and tachypnea (23 rpm), inspiratory
stridor, and oxygen saturation of 93%.
 Marked facial asymmetry, with a painful indurated
tumefaction in the left submandibular region, without
clear boundaries.
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 Ludwig’s angina was diagnosed, secondary to acute
suppurative pericoronitis of tooth 38.

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 Due to the severity of the symptoms, the patient was hospitalized.
 Empirical intravenous antibiotic therapy
• clindamycin 600 mg every 8 hours, and
• ceftriaxone 2 g every 24 hours
 Upon admission the patient presented
• Leukocytosis (20,000 cells/mm3),
• C-reactive protein concentration of 300 mg/l,
• Blood glucose 325 mg/dl, and
• Glycosylated hemoglobin (HbA1c) 17.6%.
 Treatment with insulin was prescribed.
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 Within a few hours the clinical
condition worsened, with a large
edema developing in the floor of the
mouth and breathing difficulties.

 An emergency tracheotomy was

performed due to the impossibility of
intubation and ventilation.

 Patient developed acute renal failure

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 On day four of admission, the causal tooth 38 was
extracted, and an extended cervicotomy was performed to
debride and remove necrotic debris. Drains were placed.

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 Cultures proved positive for Acinetobacter baumannii (AB)
and methicillin-resistant Staphylococcus aureus (MRSA)

 Treatment with tetracycline was prescribed (50 mg every

12 hours i.v. during 14 days).

 The patient evolved favorably, with a decrease in

inflammatory parameters and recovery of renal function.

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 Extubation was carried out after two weeks.

 Twenty days after surgery no obvious signs of infection

are noted. Marked improvement of the patient condition,
with stabilization and compensation of diabetes

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 Discussion

 The underlying infectious process may be of

odontogenic or non-odontogenic origin

 Odontogenic infections are the most common cause.

 Periapical infections of the second and third mandibular

molars as being the most frequent origin (70-80%)

 The most frequent cause of death in patients is

respiratory tract obstruction.

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Important findings to look out for:
• Trismus
• Dysphagia
• Stridor, wheezing ( indicates partial airway
obstruction)
• Oxygen saturation ( below 94 % indicates insufficient
oxygenation of tissues)
• Initial leucocyte count ( >12,000/ mm3 at time of
admission indicates SIRS –systemic inflammatory
response syndrome)
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 Surgical management is based on two principles:
a. elimination of the causal focal point of infection, and
b. surgical voiding of the compromised anatomical spaces together
with adequate drainage.
 Surgical management of the compromised anatomical spaces
must be made aggressively and promptly.
 This approach is based on the concept that prompt emptying and
surgical drainage nullifies the propagation of infection towards
deeper and more severe spaces, even if the infection is in a
Ludwig’s stage.

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 Article 2

Rapidly Progressing Osteomyelitis of

the Mandible

Case Reports in Dentistry

Volume 2013, Article ID 249615, 4 pages

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 Introduction
 Acute osteomyelitis usually exhibits systemic symptoms such as
fever or malaise and local redness or swelling.

 The present paper describes a case of acute osteomyelitis of the

mandible that was rapidly progressing without typical symptoms.

 The patient had liver cirrhosis, which should be one of the

systemic factors that affect immune surveillance and metabolism.

 Actinomycotic druses and filaments were detected from the

sequestrum. These were considered to play a role in the rapid
progression of osteomyelitis without typical symptoms.
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 Case report

 A 77-year-old man was referred to our hospital for

post extraction hemorrhage and spontaneous pain in
the socket of the left mandibular first molar.

 The patient had a 1-month history of spontaneous

pain of the left mandibular first molar.

 At a nearby dental clinic, restorative treatment was

performed. However, as the pain continued, the
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tooth was finally extracted.
 Presentation at first visit

 No swelling in his cheek

 No paresthesia in his lower lip.
 Post- extraction hemorrhage of the
mandibular first molar had already
arrested.
 Clot was absent and the socket
bone was exposed
 There was no redness or swelling in
the regional gum
 No mobility and percussion pain of
the adjacent teeth.

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Panoramic radiograph showed neither abnormal
consolidation nor ill-defined trabecular bone structure
around the socket.

Diagnosis – Dry socket

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 Clarithromycin (CAM) was administered for a week,
but his spontaneous pain did not diminish.
 Mobility of the adjacent teeth and necrosis of the
gum around the socket was present at 10 days after
the first visit.
 Biopsy of the socket and extraction of the left
mandibular second premolar were performed.
 Biopsy results - revealed no malignancy.
 Clarithromycin was administered for 10 more days.
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 CT scans at 14 days after the initial visit showing
remarkable absorption of the cortical bone in the left
mandibular molar region.

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 29 days after the first visit, the sequestrectomy and
corticectomy of the left mandibular molar region and the
extraction of the left mandibular first premolar and second
molar were performed under general anesthesia.
 The surgical site was filled with gauze with pasta of dimethyl
isopropyl azulene and clindamycin.
 Next day hyperbaric oxygen (HBO) utilization (2 atmosphere
absolute, 90 minutes per day) begun for a total of 20 times.

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 The patient was treated with intravenous penicillin for a week.

 After the sequestrectomy, spontaneous pain became bearable,

and there was little clinical evidence of inflammation such as
gum swelling or drainage.

 42 days after the surgery, he had swelling in his cheek. The

patient was treated with intravenous piperacillin and
clindamycin.

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 45 days after the surgery, the mandible was fractured
at the surgical site, and CT scans showed the bone
resorption at the mandibular anterior teeth.
 Actinomycotic druses and filaments were detected
from the sequestrum of the fracture site.
 Segmental resection and reconstruction were
performed at 49 days after the first surgery.

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 Discussion

 Osteomyelitis of the jaws is caused in association with

hematogenous germ spread, drug- or radiation-
related, or local odontogenic or nonodontogenic
processes.

 Schafer states that dental infection is the most

frequent cause of osteomyelitis of the jaws.
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 In the present case, panoramic radiograph at the time of
pre - extraction of the left mandibular first molar showed
neither abnormal consolidation nor ill defined trabecular
bone structure around the tooth, and the running of the
inferior alveolar artery was clear.
 Osteomyelitis was esteemed to occur after the extraction,
but the reason of the spontaneous pain which was the
cause of the extraction was unclear.

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 Impaired immunity and the systemic compromise played a
role in the asymptomatic and rapid progression of
osteomyelitis.

 Correction of the underlying predisposing factors, early

diagnosis and evaluating the therapeutic response of a
multimodality treatment approach as needed would offer
the best course of the disease.
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