ODONTOGENIC INFECTION

Dr Mathew Jose, Prof &HOD

Sree Mookambika Institute of
Dental Sciences
 CONTENTS
 Introduction
 Definitions
 Progression of odontogenic infection
 Neck fascia & it’s functions
 Classification of fascial spaces
 Surgical anatomy of each spaces
 Stages of infection
 Factors affecting spread of infection
 Microbiology
 Routes of spread
 Pathway of odontogenic infection
 Sites of localization
 Investigation
 Treatment
 Conclusion
 references
Infection
• Infection is the process or the state wherein an
infectious agent invade and multiple in the
body tissues of the host. It could result to the
manifestation of symptoms and disease when the
immune response of the host is activated
• Infection is defined as "a microbial phenomenon
characterized by an inflammatory response to
the microorganisms or the invasion of normally
sterile tissue by those organisms."
 Fascial Spaces

The fascial spaces in head and neck are the potential

spaces between the various layers of fascia normally
filled with loose connective tissue and bounded by
anatomical barriers, usually of bone, muscle or fascial
layers.
( Moore-1975)
 Shapiro defined fascial spaces as potential spaces
between layer of fascia. Its filled with loose connective
tissues and various anatomical structures

 Fascial planes offer anatomic highways for

infection to spread from superficial to deep
planes
 Functions of the fascia
• Acts as a musculovenous pump-
• Limits outward expansion of muscles as they
contract.
• Contraction of muscles compresses the intramuscular
veins (push the blood towards the heart).
• Determine the direction of spread of infection
•Classification of Fascial Spaces
• Grodinsky and Holyoke in 1938 described

• Space 1: superficial to the platysma as well

as between the latter and the deep fascia.

• Space 2: lies in the anterior triangle between

the superficial layer of deep fascia and the

deep surface of the sternothyroid sheath

• Space 3: between the visceral fascia and the

sternothyroid- thyrohyoid layer anteriorly, the

carotid sheath laterally, and the alar fascia

posteriorly
• Space 3a: Lincoln’s highway
• A viscerovascular space coined by Mosher 1929- is
the carotid sheath from the jugular foramen &
carotid canal at the base of the skull to the middle
mediastinum
Carotid space- Visceral Vascular
space
• Mosher 1929- Liccoln’s Highway( First National
Intercontinental paved highway in US 1913)

• All three Layers of deep cervical fascia contribute

to carotid sheath
• Less areolar tissue
• Space 4: also known as danger
space, lies between alar &
prevertebral fascia.

• Space 4a: posterior triangle

space posterior to carotid sheath
• Space 5: prevertebral
space.

• Space 5a: fascia enclosed by

prevertebral fascia
 Danger space
• Immediately posterior to the
retropharyngeal space and
immediately anterior to the
prevertebral space

• Spread within the danger space

tends to occur rapidly because of the
loose areolar tissue that occupies this
region. This spread can lead to
mediastinitis, empyema, and sepsis
BASED ON MODE OF INVOLVEMENT
1. Direct Involvement. (Primary Spaces)
» Maxillary Spaces – Canine, buccal,infratemporal
» Mandibular Spaces – Submental,
Submandibular, Sublingual, Buccal
2. Indirect involvement (Secondary Spaces)
»Masseteric
»Pterygomandibular
» Superficial and deep temporal
»Lateral and retro pharyngeal
» Prevertebral, parotid, carotid
sheath,peritonsillar and danger spaces.
Based on clinical significance-

Face- Buccal, canine, parotid, masticatory.

Suprahyoid- Sublingual, submental, submandibular,
lateral pharyngeal, peritonsillar.

Infrahyoid- Pretracheal.
Spaces of total neck- Retropharyngeal, space of
carotid sheath.
Surgical anatomy of deep facial spaces
of head and neck
8
Etiology-
Infected mandibular & maxillary premolars & molars.

Clinical Features-
Obliteration of nasolabial fold.
Angle of mouth shifted to opposite side.
Swelling in cheek extending to corner of mouth.
Buccal space associated with temporal space – Dumb bell
shaped appearance due to lack of swelling over zygomatic
arch.
TREATMENT:- (I & D)
• Antibiotic prophylaxis.
• Intra oral horizontal vestibular
incision.
• Extra oral (2 stab) incisions
below the lower border of the
mandible with No. 11 blade.
• Drainage – Hemostat is passed
from anterior incision and
taken out from the posterior
incision then the rubber drain
is inserted and secured with
pins and dressing is done.
 Infratemporal Space
Boundaries-
Superiorly: infratemporal surface of
greater wing of sphenoid.
Inferiorly: lateral pterygoid muscle.
Laterally: temporalis tendon &
coronoid process.
Medially: lateral pterygoid plate &
lateral pharyngeal wall.
Posteriorly: condyle & lateral
pterygoid muscles.
Anteriorly: infratemporal surface of
maxilla & posterior surface of
zygomatic bone.
Clinical features:
Extraoral: trismus, bulging of temporalis muscle,
swelling of the face on affected side in front of the
ear, eye is often closed
Intraoral: swelling in the tuberosity area, elevated
temp: upto 104 F
 TREATMENT
Incision & drainage

Incision made of 1.5 to 2 cm below border of mandiblesinus

forceps inserted superior & posteriorly on lingual side of mandib
below mylohyoid – pus- drained & sutured
Etiology-
Infected mandibular 3rdmolars(mesioangular/horizontal)
Pericoronitis.
Infected needles or contaminated LA solution.
Clinical Features-
Absence of extra-oral swelling.
Severe trismus.
Difficulty in swallowing.
Anterior bulging of half of soft palate & tonsillar pillars with
deviation of uvula to unaffected side.
Spread of Infection-
Superiorly to infratemporal space.
Medially to lateral pharyngeal space.
To submandibular space.
 SICHER’S APPROACH

• Sicher suggested approach to all compartments –

incision through pterygomandibular raphae

• Feasible in cadavers - not trismus

• Oral approach-compromise airway
• purulent oozing pus
• Difficult drain - loosening
 I&D

• MASSETRIC + PTERYGOID SPACE-

• Extra-oral – easier technically & prudent
• Sharp dissection - external angle of the mandible
• Allows dependent drainage of both spaces
PAROTID SPACEINFECTION

Clinical features
Severe pain
Swelling at masseter
muscle
Pus escapes from
stenson’s duct
NATURAL HISTORY OF PROGRESSIONOF ODONTOGENICINFECTION

• Once bacteria has reached periapical tissue an

active lesion is established
• Infection will spread equally in all directions, but
preferentially along the lines of least resistance
• Spread through cancellous bone until it encounters a
cortical plate
• If thin cortical plate, infection erodes through bone
and enters soft tissue
• It appears in predictable locations
 Location of infection from a specific tooth is
determinedby

• The thickness of bone overlying the apex of the tooth

• The relationship of the site of perforation of bone to

muscle attachments of the maxilla and mandible
 Stages of infection
Infections generally pass through these 4 stages before they undergo
complete resolution.

• Stage I – Inoculation
Time between exposure of microorganism and the first set of
symptoms .
During 1-3 days, Swelling is soft, mildly tender, doughy in consistency

• Stage II – cellulitis
Chronic stage-fistulous/sinus tract or osteomyelitis
During 3-7 days, centre of lesion begins to soften
Stage III –After day 5 underlying abscess undermines skin or
mucosa making it compressible.

Stage IV - Finally there is resolution of abscess that may be

spontaneous or after surgical drainage. During resolution phase, the
involved region is firm on palpation due to process of removing
tissue and bacterial debris.
 Differences between cellulitis and abscess
Characteristics Cellulitis Abscess

Duration. Acute phase Chronic phase

Pain Severe and generalised Localised

Size Large. Small

Localization Diffuse borders Well-demarcated

Palpation Doughy / indurated Fluctuant

Presence of pus No Yes

Degree of seriousness Greater Less

Bacteria. Aerobic Anaerobic/mixed

Factors affecting Spread of Infection
General factors-
1. Microbial factors-
Level of virulence.
No. of organisms introduced.
2. Host factors-
General state of health.
Integrity of surface defence.
Level of immunity.
Capacity for inflammatory & immune response.
Impact of medical intervention.
3. Combination of both factors.
 Microbiology –Space infection
Aerobic bacteria (25%)
Gram positive cocci (85%)–
Streptococcus species( 90% ) -
• S.Milleri
• S.sanguis
• S.Salivarius
• S.Mutans
Staphylococcus species (6 %)

Anaerobic bacteria (75%)

Gram positive cocci (30%)–
Peptococcus species 33%
Pepto Streptococcus species 33%
Gram pasitive bacilli (50%) –
Prevotella species, Porphyromonas species (75%)
Fusobacterium -20%

Micro-organisms and Odontogenic infections 2009 ADJ

•Staphylococcus causes – osteomyelitis and abscess
Streptococcus causes - cellulitis

• In an abscess, common causative organisms are

anaerobic (Higher percentage) & Aerobic.

• Fusobacterium + strep. Milleri – cause aggressive

infections. Eg.,.mediastinum.infections.
 Routes of Spread
Direct spread-
a) Spread into superficial soft tissues as-
Abscess- pathological thick walled cavity filled with pus.
Cellulitis- diffuse subcutaneous/submucous inflammation of
soft tissues. Tends to spread along fascial
planes.
b) Spread into adjacent fascial spaces.
c) Into deep medullary spaces of bone- osteomyelitis

Indirect spread-
a) Lymphatic routes to regional nodes.
b) Hematogenous route to other organs such as brain.
Pathway of spread
Sepsis
• In disseminated bacterial infections, the
inflammatory reaction is systemic and causes
widespread pathologic abnormalities. This
reaction has been called sepsis, which is one
form of the systemic inflammatory response
syndrome.
SIRS
• Systemic Effects of Inflammation ■ Fever: cytokines
(TNF, IL-1) stimulate production of prostaglandins in
hypothalamus ■ Production of acute-phase proteins:
C-reactive protein, others; synthesis stimulated by
cytokines (IL-6, others) acting on liver cells ■
Leukocytosis: cytokines (colony-stimulating factors)
stimulate production of leukocytes from precursors
in the bone marrow ■ In some severe infections,
septic shock: fall in blood pressure, disseminated
intravascular coagulation, metabolic abnormalities;
induced by high levels of TNF and other cytokines
CRP-C reactive Protein
• CRP is increased in Inflammation
• Pentamer , Released from liver
• Tillet & Francis-1930- C-carbohydrate antigen of
the capsule of peumococci.
Functions
Recognition and clearence of foreign pathogens
and damaged cells
Activate compliment pathway
• Compared to ESR CRP levels rise and fall rapidly
with onset and removal of inflammatory stimulus
• <.3microgm/dl - normal
• 1-10 microgm/dl- Moderate (RA,SLE)
• >10 ------------------Marked( A/C bacterial viral
systemic infection, Vasculitis)
• >50------------------- Severe (A/c Bacterial
infections)
• Objectively, SIRS is defined by the satisfaction
of any two of the criteria below:
• Body temperature over 38 or under 36 degrees
Celsius.
• Heart rate greater than 90 beats/minute
• Respiratory rate greater than 20 breaths/minute
or partial pressure of CO2 less than 32 mmHg
• Leukocyte count greater than 12000 or less than
4000 /microliters or over 10% immature forms
or bands.
SIRS
• still in use clinically, SIRS as a definition has been
abandoned since 2016

• Replaced with Sequential Organ Failure

Assessment (SOFA).
Assessment In SOFA
• Respiratory system - The ratio of arterial oxygen
tension to fraction of inspired oxygen
(PaO 2/FiO 2)
• Cardiovascular system - Mean arterial pressure
(MAP) and presence of vasopressor
medication(s)
• Hepatic system - Bilirubin level
• Coagulation system - Platelet concentration
• Neurologic system - Glasgow Coma Score
• Renal system - Serum creatinine or urine output
Leukocyte chemotactic response
• Once the leukocytes are activated, their effector
mechanisms do not distinguish between offender
and host.
• During activation and phagocytosis, neutrophils
and macrophages produce microbicidal
substances (ROS(reactive oxygen Species), NO,
and lysosomal enzymes) within the
phagolysosome;
• these substances are also released into the
extracellular space.
• These released substances are capable of
damaging normal cells and vascular
endothelium, and may thus amplify the effects of
the initial injurious agent.
• If unchecked or inappropriately directed against
host tissues, the leukocyte infiltrate itself
becomes the offender,
• leukocyte-dependent tissue injury underlies
many acute and chronic human diseases
Leukocyte Activation and
Removal of Offending Agents ■
• Leukocytes can eliminate microbes and dead
cells by phagocytosis, followed by their
destruction in phagolysosomes. ■ Destruction is
caused by free radicals (ROS(reactive oxygen
Species), NO) generated in activated leukocytes
and lysosomal enzymes. ■ Neutrophils can
extrude their nuclear contents to form
extracellular nets that trap and destroy microbes.
■
• Enzymes and ROS may be released into the
extracellular environment. ■ The mechanisms
that function to eliminate microbes and dead
cells (the physiologic role of inflammation) are
also capable of damaging normal tissues (the
pathologic consequences of inflammation). ■
Antiinflammatory mediators terminate the acute
inflammatory reaction when it is no longer
needed.
 Abscess
• Abscess occur when an area of tissue becomes
infected and the body's immune system tries to
fight and contain it. White blood cells (WBCs)
move through the walls of the blood vessels into
the area of the infection and collect in the
damaged tissue. During this process, pus forms.
•Pus is the buildup of fluid,
living and dead white blood
cells, dead tissue, and bacteria
or other foreign substances.
 Investigations

 Culture sensitivity test – to identify the causative organism

 Routine blood investigations

 PLAIN FILM
OPG
• Extent of pathology of
odontogenic orgin

• AP/LATERAL CERVICAL
• Lesser penetration c-spine
• Pharyngeal/ cervical
airway
 COMPUTED TOMOGRAPHY

• Widely used
• Contrast enchanced - 95% sensitivity
• Assess integrity cortical bone
• Short time –extent , epicentre
• Availability
• Relative low cost
 ULTRASONOGRAPHY

• Superficial
• inability-osseous penetration
• Parotid /submandibular/ neck
• Differentiates solid / cystic
 MAGNETIC RESONANCE IMAGING

• Not uncommon
• Coronal and saggital planes

• T1- anatomic detail

• T2- disease process sensitive

• Intravenous contrast agents- safer

• T1 + gadolinium
T1-weighted neck magnetic resonance imaging with gadolinium injection showed huge ill-defined
inhomogeneous mass in right parapharyngeal and retropharyngeal space with internal, irregular,
geographic abscess formation (a, b: arrow). At the hypopharynx level, there is a displacement and
deformity distortion in the airway (c: asterisk). This mass anteriorly extended into the ipsilateral
carotid space with partial encasement of carotid sheath vessels and related structures (d:
MS (masticatory space) (green)
PPS parapharyngeal space (yellow) and
the SLS sublingual space (medial purple) communicate at the posterior border of
mylohyoid muscle. PS, parotid space (red); PMS, pharyngeal mucosal space (blue); SMS,
submandibular space (lateral purple)
 Management
Goals of management :

1. Airway protection.

2. Surgical drainage.

3. Identification of etiologic bacteria.

4. Selection of appropriate antibiotic therapy.

5. Medical & supportive therapy.

 Who should be hospitalized
??
Signs & symptoms
? of CNS symptoms
toxicity
level of consciousness
• Dyspnoea
• Evidence of meningeal
• Dysphagia
irritation
• Paleness
(severe headache)
• Tachypnoea
• Tachycardia • Eyelid edema & abnormal
eye signs
• Fever
• Lethargy
 Principles of antibiotic therapy
• Identification of the causative organism
• Determination of antibiotic sensitivity
• Use of a specific, narrow spectrum antibiotic
• Use of the least toxic antibiotics
• Patients drug history
• Use of a bactericidal rather than a bacteriostatic drug
• Use of the antibiotic with a proven history of success
• Cost of the antibiotic
• Encorage patient compliance
 Selection of Antibiotic therapy
1. Parenteral penicillin.
2. Metronidazole in combination with penicillin can be
used in severe infections.

3. Clindamycin for penicillin-allergic patients.

4. Cephalosporins (1st & 2ndgeneration cephalosporins).

5. Antibiotics do not substitute for incision and drainage
in cases of significant odontogenic infections.

6. Causes for clinical failure include inadequate drainage

or antibiotic resistance.
 Surgical Management
1. Surgical treatment may range from simply opening
tooth & extirpation of pulp to complex incision &
drainage.
2. Primary goal in surgical management is to remove
cause of infection.
3. Secondary goal is to provide drainage of accumulated pus
& necrotic debris.

Extraction provides both removal of cause of infection and

drainage of pus & debris.
 Incision & Drainage
Incision & drainage helps-

• To get rid of toxic purulent material. To

decompress odematous tissues.
• To allow better perfusion of blood, containing antibiotics &
defensive elements.
• To increase oxygenation of infected area.

Removal of the cause; such as infected tooth, a segment of

necrotic bone, a foreign body should be done at the time of
I & D procedure.
 Incision and Drainage
1. Incise in healthy skin and mucosa when possible. An incision placed at the site of
maximum fluctuance where the tissues are necrotic or beginning to perforate may
result in a puckered, unesthetic scar.

2. Place the incision in an aesthetically acceptable area, such as under the shadow of
the jaw or in a natural skin fold or crease.

3. When possible, place the incision in a dependent position to encourage drainage by

gravity.

4. Dissect bluntly, with a closed surgical clamp or finger, through deeper tissues and
explore all portions of the abscess cavity thoroughly so that compartmentalized
areas of pus are disrupted and excavated. Extend the dissection to the roots of teeth
responsible for the infection.
5. Place a drain (sterile latex or catheter) and stabilize it with
sutures.

6 Consider use of through-and-through drains in bilateral,

submandibular space infections.

7 Do not leave drains in place for an overly extended period;

remove them when drainage becomes minimal. The presence
of the drain itself may produce some exudate and can be a
portal for secondary bacterial invaders.

8. Clean wound margins daily under sterile conditions to remove

clots and debris.
 Hilton’s method of I & D

1. Topical anesthesia achieved with spray or infiltration.

2. Stab incision given through skin & s/c tissue.
3. If pus is not encountered, further deepening of surgical site
done with sinus forceps.
4. Abscess cavity is entered and forceps opened in direction
parallel to vital structures.
5. Explore the entire cavity for additional loculi.
6. Cavity irrigated with saline & antiseptic solutions.
7. Placement of drain.
8. Dressing.
 Drainage of Fascial Spaces
• Canine, Sublingual and Vestibular abscesses are drained
intraorally.

• Masseteric, Pterygomandibular, Buccal and

Lateral Pharyngeal space abscesses can be
drained with combination of intraoral and
extraoral drainage.

• Temporal, Submandibular, Submental, Retropharyngeal and

Parotid space abscesses may mandate extraoral incision and
drainage.
LIFE THREATENING COMPLICATIONS
 Complications of spaceinfection

• Osteomyelitis
• Mediastenitis
• Meningitis
• Brain abscess
• Cavernous sinus thrombosis
• Ludwig’s angina
Ludwigs Angina
Lamierre’s Syndrome
• Septic thromboplebitis of IJV
• Fusobacterium Necrophorum from blood culture
• Tretment- Vancomycin-Metronidazol-
Ceftriaxone
• Enoxaparin
Necrotizing fascitis
Endothelium-Platelet inhibitory
effects
• . An obvious effect of intact endothelium is to
serve as a barrier that shields platelets from
subendothelial vWF and collagen.
• Prostacyclin (PGI2),
• Nitric oxide(NO), and
• Adenosine diphosphatase- degrades ADP, potent
activator of plateletaggregation.
• endothelial cells bind and alter the activity of
thrombin, which is one of the most potent
activators of platelets.
Anticoagulant effects.

• Normal endothelium shields coagulation

• factors from tissue factor in vessel walls and

Thrombomodulin,
• Endothelial protein C receptor,
• Heparin-like molecules, and Tissue factor
pathway inhibitor.
• Thrombomodulin and endothelial protein C
receptor bind thrombin and protein C,respectively,
in a complex on the endothelial cell surface.

• When bound in this complex, thrombin loses its

ability to activate coagulation factors and
platelets,
Thrombus formation

Hyper coagulability

Virchows Triad
Venous Inflammation
stasis
Thromboplibitis
• Inflammation and pus formation both in the
vessel wall and sourrounding the vessel
• Throbotic obstruction of larger veins
• Venous hypertension
• Infarction
 BRAIN ABSCESS
Etiology
Arises from bacteremia – odontogenic
infections Produces- inflammation, edema
and septic thrombosis
Clinical features
• Headache
• Hemiplegia
• Papilloedema
• Aphasia
• Convulsions
• Abducens palsy
Treatment

1) IV chloramphenicol
2) Vancomycin-Metronidazol-ceftriaxone
3) Surgery to provide drainage
 CAVERNOUS SINUS THROMBOSIS

• Orgin- ascending rom maxillary teeth, upper teeth,

nose or orbit
• Through valveless anterior and posterior fascial veins
• Extremely high mortality rate
 INITIAL SIGNS

• Proptosis
• Fever
• Obtunded state of consciousness
• Ophthalmoplegia
• Paresis of –
• occulomotor
• trochlear + abducens nerve
Treatment

Antibiotic therapy
Neurosurgical consultation
Anticoagulants
Surgical drainage
 MEDIASTINITIS

• Extension of infection from deep neck spaces into the

mediastinum

• C/F –

• Chestpain, fever
• Severe dyspnea
• Mediastinal widening
• IV drug abusers- greater risk
• Late complication
• Progressive septicemia-mediastinal
abscess-pleural effusion-empyema-
pericarditis
• Necrotizing mediastinitis-
aerobic+anaerobic
• Treatment- extensive long term antibiotic
therapy and surgical drainage of
mediastinum
• Emergency neurosurgical intervention
 CONCLUSION

We being Oral & maxillofacial surgeons must understand

anatomy of fascial spaces, spread of infection and proper
management for the prevention of further complications and
betterment of health of the patient.
 References
• Textbook of oral & maxillofacial surgery : Neelima Malik.
• Oral & maxillofacial Infections : Topazian
• Textbook of oral & maxillofacial surgery : Laskin
• Manuel Grodixsky And Edward A. Holyoke:The fascia and fascial spaces of
the head, neck and adjacent regions
• Nash et al2005. Does the Investing Layer of the Deep Cervical Fascia Exist?
Journal of American society of anesthetist
• Vincent L Biron et al. Surgical vs ultrasound-guided drainage of deep neck
space abscesses: a randomized controlled trial: surgical vs ultrasound
drainage.Journal of Otolaryngology - Head and Neck Surgery 2013
• Newman, Takei, Klokkevold & Carranza: Carranza’s Clinical
Periodontology: 11th Edition
THANK YOU!!!!