Oral and Maxillofacial infection

Definitions:
Infection: invasion of the body by pathogenic micro-organisms and its
multiplication causing a disease.
Inflammation: is the reaction of the body to noxious stimuli (e.g. thermal,
chemical or microorganism).
This reaction aims to destroy or limit the spread of injurious agents, repair or
replace the damaged tissues and to restore metabolism and function of the host.
These reactions are usually associated with:
A) Local signs and symptoms:
Hotness, redness, pain, swelling and loss of function (5 cardinal signs of
inflammation) and regional lymphadenopathy.
B) General signs and symptoms:
Fever, elevated white blood cell count (Leukocytosis), tachycardia,
tachypnea, dehydration and malaise.
Infection is usually associated with inflammation but not vice versa.

Classifications of oral and maxillofacial infections:

I- Based on the origin:
Oral and maxillofacial infections are commonly caused from the teeth, they are
referred as odontogenic infections.
- Odontogenic (90-95% of cases):
- Periapical abscess (70% of odontogenic cases)
- Pericoronitis
- Periodontitis
- Non-odontogenic e.g. trauma, sinusitis, sialadenitis, postoperative infection

II- Based on causative microorganism:

- Viral
- Bacterial: - specific (e.g. TB, syphilis and actinomycosis) or
- non-specific)
- Fungal

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 III- Based on the onset, duration and severity:
- Acute
- Subacute
- Chronic

Life threatening sequelae:

- Septicemia
- Cavernous sinus thrombosis
- Airway obstruction
- Mediastinitis

Microbiologic considerations in odontogenic infections

- Indigenous bacteria: normal oral flora

- Polymicrobial
- Aerobic – Anaerobic composition
Aerobic bacteria Anerobic bacteria
Gram positive cocci: Gram positive cocci:
Streptocuccus species Peptostreptococcus species
Staphylococci Peptoccous species

Gram negative cocci Gram negative cocci:

Neisseria species Veillonella species
Gram positive bacilli: Gram positive bacilli:
Corynebacterium species Clostridium species
Actinomyces species
Eubacterium species
Lactobacillus species
Gram negative bacilli: Gram negative bacilli:
Haemophilus species Bacteroids species
Fusobacterium species

Diagnosis of odontogenic infections:

I- History:
History of previous toothaches, onset, duration, presence of fever and
previous treatments.
History of trismus, dysphagia, shortness of breath.

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 II- Clinical examination
Systemic findings:
Vital signs
Temperature: systemic involvement if > 38.5° C
Blood pressure: mild elevation
Pulse (heart rate): (> 100)
Increased respiratory rate (Normal respiratory rate is 14-16/minute)
CNS impairment (decreased level of consciousness, sever headache and
vomiting)
Ophthalmologic examination: extraocular muscle function, proptosis,
presence of orbital (preseptal or postseptal) edema.
Head and neck examination:
Inspection, palpation and percussion are integral parts of the examination.
Begin extraorally and then move intraorally.
- Skin of the face, head and neck for swelling
- Indurated, firm, hard
- Fluctuant, fluid-filled
- Erythema, sinus or fistula formation and subcutaneous crepitus
Assess for cervical lymphadenopathy and fascial space involvement
Assess for the presence and magnitude of trismus
Intraoral examination:
- Inspect teeth for presence of caries and large restorations, localized
swellings, fistulas and mobility.
- Floor of mouth is inspected to assess for fascial space involvement.
- Visualize Wharton’s and Stensen’s ducts for quality of fluid (pus or saliva)
III- Diagnostic aids:
1- Radiographic examination:
Imaging studies can further substantiate diagnosis
Plain films, CT, MRI
CTs or MRIs should be obtained when infection has spread into deep
fascial spaces in the orbit or neck.
Panorex or even periapical x-rays are sufficient for diagnosis of localized
infections.

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 2- Blood work:
Elevated white blood cells (Leukocytosis)
(Normal number of WBCs is 4,000-11,000/ml blood)
Elevated ESR (Erythrocyte Sedimentation Rate)
Blood culture for detection of systemic involvement
3- Local tissue culture to detect the causative micro-organism

Fate of infection:
1- Resolution: occurs when the mico-organisms are of low virulence or
attenuated by proper treatment and when the host resistance is high
2- Chronicity: this condition occurs when low virulent MO and low host resistance
or with therapeutic treatment without eradication of the infection. It’s
characterized by gradual onset and mild manifestations or complications. e.g.
Garre’s osteomylitis
3- Spread (Acuteness): occurs with highly virulent MO with increased numbers
and low host resistance without proper treatment. The acute condition is
characterized by sudden onset and severe complications.
Factors governing the severity of odontogenic infections:
These factors depends primarily on the balance between the general factors of
patient resistance and microorganism number and virulence.

These factors are as follows:

1- Microbial factors which depends on:
Number of microorganisms: ↑ number → ↑ severity of infection
Virulence of microorganisms: the degree or intensity of pathogenicity of the
microorganism
2- Host general factors which include:
- Cellular immunity (leukocytes)
- Humoral immunity (antibodies)
- Nutritional status of the patient
In state of homeostasis the integrity of the host factors are existing.

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 When disturbance of these factors happens for e.g. in burned patient, the
general resistance is altered due to fluid loss, allowing the organisms that
previously kept in check to become pathogens and the patient gets infected.
Starvation also affects the systemic immunity due to lack of antibodies
production.
3- Local circulation of the infected tissues (compromised blood supply)
- In cases of irradiated jaw, the local resistance is compromised due to end
artritis oblitrans leading to osteoradionecrosis
- Presence of necrotic tissues or traumatic surgery will compromise local
resistance.
- Presence of edema or hematoma inside the tissues exert pressure on the
blood vessels and thus decrease the blood supply

That is why when we treat a patient with acute infection we should:

1) Decrease the number of microorganism
a) Removal of the cause either by RCT or tooth extraction.
b) Incision and drainage of pus
c) Local irrigation with antiseptic solution
d) Removal of necrotic and dead tissues.
e) Prescription of proper antibiotics.
2) Improve the patient resistance.
a) Hydration
b) High protein and vitamins diet
c) Good analgesics
d) Bed rest
e) Management of any systemic diseases
3) Improve the local circulation
a) Removal of the cause, Incision &Drainage and debridement of necrotic
tissues
b) Increase blood supply by hot fomentations will improve the local
circulation which permit arrival of natural immune elements and
antibiotics to the area
c) Increase Oxygen supply (hyperbaric oxygen) in chronic cases as in
osteoradionecrosis

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Periapical (dentoalveolar) abscess:
Natural history of progression of dento-alveolar abscess:
Dental pulp necrosis (due to caries, trauma or deep pockets)
↓
Periapical osteitis (Periapical periodontitis)
↓
Acute dentoalveolar abscees early stage (Intrabony abscess)
↓
Spread of pus into soft tissues (Cellulitis)
↓
Abscess

- The pulp tissue respond to the bacterial invasion by inflammation, and pulp
death occur because the pulp chamber can not expand to withstand the
swelled pulp tissue, the obstruction of the BV occur leading to liquefaction
and disintegration of the pulp tissue.
- The bacteria and toxic products escape to the periapical region through the
apical foramen causing apical periodontitis.
- This inflammation will stimulate WBC migration from the capillaries to
populate the area and fight the invading microbes
- The end results of this battle is killing of a large number of both microbes
and WBCs which liberate a proteolytic enzymes that causes dissolution and
liquefaction of their own bodies and surrounding tissues.
- The serous exudate from the capillaries, dead polymorph nuclear
leukocytes, living and dead microorganisms, and cell debris form a liquid
called pus and the process called suppuration.
- The body tries to limit these foci of liquefaction and necrosis by
precipitating a fibrin layer from extravasated plasma which is later crowded
with leukocytes, this wall is called pyogenic membrane which prevent the
escape of micro-organisms and their toxic product from involving more
tissues unless this membrane is traumatized Or inteupted by bacterial
toxins
- This condition is called (acute dento-alveolar abscess of the early stage )

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Acute dentoalveolar abscess “ADAA”
Definition:
A suppurative inflammatory infection involving the apex of the involved tooth and
its surrounding periapical structures.

Stages:
Early stage: confined within the bone with no soft tissue involvement
Late stage: perforate bone with soft tissue involvement

Clinical presentation of DAA:

- Subcutaneous abscess origin at inferior from a mandibular tooth
- Fascial abscess (submandibular)

Cellulitis Vs abscess:
Cellulitis is an acute diffuse infection, which spreads into the loose subcutaneous
tissue (spreading phase)
Pus is an effective defense against spreading infection.

Early stage:
Clinical signs and symptoms:
- Severe throbbing pain
- Extrusion of the tooth
- Severe tenderness on percussion
- Cardinal signs of inflammation
- Systemic manifestations of acute inflammation (Fever – Headache –
Malaise – Raised pulse and respiration rate - insomnia)

N.B: The severity of the pain depends on the stage of development of the
inflammation. In the initial phase the pain is dull and continuous and
worsens during percussion of the responsible tooth or when it comes into
contact with antagonist teeth. If the pain is very severe and pulsates, it
means that the accumulation of pus is still within the bone or underneath
the periosteum.
Relief of pain begins as soon as the pus perforates the periosteum and exits
into the soft tissues.

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Radiographic examination: In the early stage of ADAA, x-ray examination is
negative. But, sometimes widening of the periodontal space or
disturbance of the lamina dura around the involved tooth can be seen.

• Also, ill-defined radiolucency at the periapical region can be seen if the

condition is the result of acute excerbation of chronic abscess.

Treatment of acute dentoalveolar abscess early stage:

Prompt evacuation (drainage) of pus is mandatory in this stage to release the
internal pressure which leads to involvement of more spongiosa, particularly if a
virulent micro-organisms are involved. This should be done in the first visit
through either pulp extirpation or extraction of caused tooth.
1) Removal of the cause and pus evacuation by:
a) Pulp extirpation and apical foramen patency to permit evacuation of pus
through the pulp chamber with good irrigation of saline solution & diluted H2O2
and calcium hydroxide paste injected into the apical region to counteract the
acidity of periapical infection.
b) Extraction of unrepairable, priodontally affected teeth, or deciduous teeth.
Proper timing for extraction
In ADAA the proper timing is the immediate extraction as it allows complete
eradication and drainage of pus and toxic product through the alveolus.
Immediate extraction in all situations is the basic line of management except in
the following conditions:
1) Cases that more than simple extraction may be needed.
2) Apprehensive patients.
3) Cases that LA nerve block will not be effective because of infection.
N.B. in the last 2 conditions the GA is another alternative to use for immediate
extraction
The philosophy of never extracting a tooth during an acute
condition of an abscess has long been abandoned

- Antibiotic therapy
- Analgesics
- Warm saline or antiseptic mouth wash to promote drainage
- Raising body resistance by: Multivitamins, fluids, high protein rich diet &bed rest
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Acute Dentoalveolar Abscess Late stage:
Spread of infection from ADAA early stage taking place along the path of least resistance
↓
Formation of subperiosteal abscess
↓
Formation of diffuse, large, non-fluctuant, indurated & tender swelling (cellulitis)
↓
Extraoral or intraoral fistula formation (Chronic abscess)

Perforate bone and soft tissue involvement.

Begins as cellulitis (painful swelling of the soft tissue of the mouth & face or neck
resulting from a diffuse spreading of purulent exudate along the fascial planes
that separate the muscle bundles ( fascial spaces).) then after localization it
becomes true abscess (small localized and pus formation and fluctuation).
Cellulitis hot fomentation + antibiotics True abscess
P.O.C Cellulitis Abscess
Duration 3-5 days 5-7 days
Pain Severe and generalize Localized
Size Large Small
Localization Diffuse Well-circumscribed
Palpation Doughy (firm) Fluctuant
Presence of pus No Yes
Seriousness High Low
Skin quality Thickened Centrally undermined
Loss of function Sever Moderately sever
Tissue fluid Inflammatory exudates Pus
Bacteria Mixed Mainly anerobes

Signs and symptoms:

- Swelling: Intraoral (if within muscle attachment)
Extraoral (if beyond muscle attachment)
- Its presentation depends on the stage of inflammation.
- The swelling may be due to edema move within the tissues and
accumulates at sites least constrained by fascia e.g. lips and eyelids

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 - The swelling may be indurated due to the cellular infiltrate of
inflammation “cellulitis”
- The swelling may be fluctuant due to pus formation “abscess”
- Redness and local hotness of the swelling is due to ↑ blood flow
- Pain (deep): after perforation of the periosteum → deep dull aching pain
- Tenderness
- Trismus: in case of masticatory space infection
- Lymphadenopathy: submandibular and superficial cervical LNs
General signs and symptoms (Headache-fever-malaise)

Radiographic examination:
Widening of PDL membrane as a uniform radiolucent line approximately 1 mm
width around the apex of the tooth due to thickening of periodontal membrane
After 3-4 weeks interruption of lamina dura with ill-defined radiolucency with
hazy margin appear.

Treatment:
Same as early stage + hot moist dressing 15 minutes/hour and hot saline mouth
wash every hour with a full glass of hot saline.
1) It increases the blood supply to the area.
2) Stimulate phagocytosis.
3) Help in localization and pus formation.
With proper management of cellulitis stage accumulation of pus occurs leading to
abscess formation.
- When suppuration does occur and the infection localizes, the condition is
termed as, acute soft tissue abscess
- If cellulitis stage of ADAA is improperly managed, the body local or systemic
immunity is compromised with highly virulent bacteria, more tissue
destruction and more spreading occurs to dangerous areas and patient life
may be threatened.

Chronic dentoalveolar abscess:

It’s a long standing gradual infection of the periapical region with mild
manifestations

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Causes:
1- Acute infection in high body resistance → chronic abscess
2- Chronic from the start due to low grade virulence and high body resistance
The pus invade the bone and open to the surface over the skin or mucous
membrane which leads to fistula formation, the abscess evacuate itself through
an opening calledfistula.
The fistulous tract is lined by granulation tissue and epithelium and should be
excised surgically after abscess treatment.
Intermittent evacuation and healing of this fistula occurs according to the amount
of pus formed
Signs and symptoms of chronic dentoalveolar abscess:
It is generally asymptomatic but the patient may feel:
1) Fullness or uncomfortable of the affected tooth
2) The gum covering appears normal or slightly inflamed
3) Intraoral fistula is usually close to the apex of the involved tooth
4) Extraoral fistula observed near to the affected tooth or at some remote area
5) The skin around the fistula is contracted to the bone forming unsightly dimpling
or scar
6) Enlargement slightly tender of draining lymph nodes
Radiographic examination:
irregular radiolucent area around the tooth apex and this differentiate it from
granuloma or cyst which appears regular and well defined.

Treatment of CDAA:
1- Antibiotics (based on culture and sensitivity test)
2- RCT or extraction of affected tooth
3- Excision of the chronic skin fistula (after it stops draining pus)
In intraoral fistulas, the fistulous tract disappears a few days after
endodontic therapy begins,without requiring intervention
for excision of the opening.
In extraoral fistulas, a) An elliptical incision of the skin and subcutaneous tissue
encircling the scar is carried out.
b) The fistulous tract is dissected down to the bone and removed.
c) The skin is undermined so that the skin edges meet each other without tension,
sutured with 4 or 5 0 black silk and dressed.

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 Pericoronitis
Definition: infection of pericoronal tissues surrounding partially erupted tooth,
commonly seen in the partially erupted lower third molar.
Bacteriology: mainly anerobic as streptococci, staphylococci, fusiform and
bacteroids.
The area under the operculm is an ideal place for bacterial growth:
a- Humidity, warmth, relative deficiency of oxygen
b- Relative immobility of and rigidity of tissues involved
c- Accumulation of food debris, darkness
d- Protection from the washing influence of saliva
e- Continuous traumatization by the opposing maxillary third molar that
weakens the local resistance
Clinical picture: It may be acute or chronic
Acute pericoronitis:
Signs:
- The pericoronal tissues appear shiny, erythematous and edematous
- Lymph node enlargement (Submandibular lymphnodes)
Symptoms:
- Sever pain
- Trismus: as the area lies in close proximity to the insertion of temporalis
and masseter muscles.
- Difficult eating and swallowing
- Foul odor
- Systemic signs of acute inflammation
Spread of infection:
The infection may spread anteriorly to involve the buccal space and posteriorly to
the masseteric, pterygomandibular and lateral pharyngeal spaces.

Treatment of acute pericoronitis:

- Antibiotic and analgesic
- Irrigation beneath the flap with warm saline, also hydrogen peroxide can be
used to render the area aerobic.
- Grinding of the opposing third molar to prevent trauma to the operculum
or extracting it
- If pericoronal abscess develops (Incision and drainage)

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 - Raising body resistance: a- multivitamins b- fluids
c- high protein diet d- bed rest
- After acute phase subsided: tooth extraction or operculectomy (preferably
using laser or electrosurgery)

Factors governing the spread of Odontogenic infections:

1- Virulence of microorganisms Severity and fate of infection

2- Number of invading microorganisms
3- Resistance of the patient

4- Position of the tooth apex in the alveolus

Spread of infection
5- Relation of the root apices to muscle attachment.
6- Organization of fascial spaces.

1- Virulence of microorganisms:
It’s the degree or intensity of pathogenicity (all characteristic of the microbes that
are injurious to the host) of the microorganisms.
It’s determined by 3 characteristics of the pathogen:
a) Invasiveness: ability to spread to adjacent tissues
b) Infectivity: ability to establish focal point of infection
c) Pathogenic potential: degree to which pathogen can cause damage to host
Aspects of pathogenic potential:
Toxiginicity: The ability to produce toxins and enzymes within the tissues
that facilitate the invasion of the microbes within the tissues and neutralizes
host defenses.
Immunopathology: is the ability of microbe to trigger exaggerated immune
response.

Staphylococci produce a localized infection while, streptococci produce a more

spreading infection due to the following:
1- Bacterial enzymes and toxins produced by bacteria:
- Staphylococci produces coagulase enzyme favors the formation of fibrin
barrier at and around the site of infection which enhances localization of
infection.
- Streptococci produces fibrinolysin and hyaluronidase enzymes dissolution
of the fibrin barrier which favors the spreading of infection.

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 - Anerobic bacteroids produces endotoxins which only released after bacterial
cell death and lysis. Thus when using the specific antibiotic (clindamycin or
metronidazole) a rapid release of endotoxins into tissues that enhances
spreading of infection after initial use of antibiotic.
The bacteroids endotoxins include:
- Proteolytic enzymes which hydrolyze the collagen and fibrin leading to
infection spread.
- Heparinase enzyme which encourages the devolpment of thrombophlbitis as
it inactivate the effect of anticoagulant effect of heparin which normally
present in human tissues.
- It should be expected in:
- Tissue necrosis,
- Foul odor and
- Presence of Gram negative rods in culture.
2- The ability of bacteria to attract PNL
Chemotaxis: accelerated movement of leukocytes outside the capillaries
toward a particular object.
First, the leukocytes leave the main stream and become attached to the
endothelial lining of the blood capillaries (margination or
pavementation), then withdraw itself between the endothelial cells
(diapedesis) to go out of the capillaries toward the infected area.

Staphylococci has the greatest chemotactic effect on leukocytes and thus

favors localization of infection
Streptococci has less chemotactic effect and thus favors spreading of
infection
3- The mode of growth
Staphylococci grows in groups or colonies → thus favors localization of
infection, while streptococci grow singly, paired or in chain thus favors
spread of infection.

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2- Number of microorganisms:
While the body defense mechanisms can deal with a few microorganisms, it fails
with large number.
It’s estimated that the number of microorganisms required to produce an invasive
tissue infection is 105/ml of body fluid or gram of tissue.
Body resistance plays the key role in determining the critical number of micro-
organisms that persist and cause dissemination of infection.

3- Body resistance (host defense system)

A- Local barriers:
Skin, mucous membrane, saliva and microbial flora act as local defense system
and provide the first line of defense through mechanical, chemical and biological
barriers.
Mechanical barriers: intact skin and mucous membrane, cleansing by salivary
flow, high epithelial turnover and sloughing, taking with it adherent bacteria.
Chemical barrier: through secretory IgA of saliva, sweat and sebum.
Biological barrier: through variety of micro-flora normally preventing a single
species of microorganisms from flourishing up and causing infection by
competing for nutrients or release of by-products that inhibits each others.

B- Specific immunity:
Immune system: a collection of cells and molecules that protect the body against
infection and malignant cells.
Immune system are 2 branches:
Innate immunity: a general response to anything other than recognized “self cells”
The adaptive immune system: A specific counter-assault against a “known
foreign” invader (previously recognized) i.e. the body is previously exposed to it.
Innate immunity The adaptive immune system
Response is non-specific response Response is specific to specific
pathogen or antigen
Exposure lead to immediate maximal Lag time between exposure and
response maximal response
Cell mediated and humoral components Cell mediated and humoral components
No immunological memory Exposure leads to immunological
memory

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 Cell mediated:
The lymphocytes involved natural killer cells, B cells, T-cells and dendritic cells
which derived from bone marrow and play a key role in processing and
penetration of antigens.
Phagocyte, engulf and kill microbes
Lymphocytes produce lymphokines and immunoglobulins (aids humoral)
Lymphokines stimulate reproduction of other lymphocytes, and kills antigens.

Humoral immune system:

Constitutes a protein component of cell free fluids or serum and it is formed of:
Complement system:
The complement system is a biochemical cascade similar to coagulation cascade
that helps clear the pathogens, it induces more than 20 plasma proteins and protein
fragments circulate in inactive zymogens and activated only by antigen-antibody
reaction.
Unlike antibodies, binding of the complement to the antigen is non-specific
Antibody system:
Formed by B lymphocytes mediated by signals from T cells and bind specifically
to certain anigen.

Medically compromised patients:

Uncontrolled metabolic diseases
Uncontrolled diabetes milletus
Alcoholism
Malnutrition
Suppressing diseases:
Leukemia
Lymphoma
Malignant tumors
Suppressing drugs:
Chemotherapeutic agents
Immunosuppressive
Management: Aggressive doses of bactericidal specific antibiotics
Prompt surgical interference

4- Position of tooth apices in the alveolus:

Pus usually penetrates the thinnest area of the cortical plate of bone (way of least
resistance).
Maxillary teeth: 1 and 3 → labial spread
2 palatal spread
4,5,6,7 and 8: Buccal roots→ buccal spread
Palatal roots → palatal spread

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Mandibular teeth: 1, 2, 3 → labial spread
4 & 5 → buccal spread and occasionally lingual spread
6 & 7 → in the center of the mandible (buccal or lingual spread)
8 → closer to the lingual plate (lingual spread)

5- Relation of the root apices to muscle attachment:

- The attachment of various muscles and fascia to the alveolar process vary
with each individual.
- If the pus in the maxillary teeth breaks through the muscle attachment
related to their apices, the muscle and fascia serve as a superior boundary
of pus and limit it intraorally.
- If pus breaks through above these muscle attachments, the pus will
accumulate extarorally.
- In the mandible, if the pus breaks through above the muscle attachment
related to their apices, the muscle and fascia serve as an inferior boundary
that limit inferior migration of pus and limit it intraorally and vice versa.

Buccal space infection submandibular space submental space

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6- Organization of the deep cervical fasciae (fascial spaces).
Fascial spaces are secondary sites of spread of odontogenic infection, involved when
the pus breaks through beyond muscle attachment, it will be presented in extraorally
and thus fascial spaces involvement occur.
- These are either clefts (potential spaces between fascisal layers) or compartment
containing connective tissue and various anatomic structures.
- They are not voids in the tissues.
- They are not present in healthy tissues but become filled with pus during infections.
- When filled with loose areolar tissues, it is called clefts
Fascia: are continuous layers of dense connective tissues.
The two layers of cervical fascia controlling spread of infection
{superficial cervical fascia + deep cervical fascia).
- The fascia are destroyed and penetrated by infection.

Fascial spaces
- Fascial spaces potentially exist between fascial layers and may become filled
with purulent material from spreading orofacial infections.
- Fascial spaces are anatomic highways for infection to spread.
- Spread of infection can be predicted by anatomic boundaries.
- Fascial spaces are contagious and infection readily spreads from one space to
another (open primary and secondary spaces).
- Antibiotics availability in fascial spaces is limited due to poor vascularity.
- Treatment of fascial space infections depend on incision and drainage.
- Despite incision and drainage, the etiologic tooth must be removed.
- Spaces that become directly involved are termed spaces of primary
involvement. Infections may spread to additional spaces, which are termed
secondary.
Primary spaces: are directly adjacent to the origin of the odontogenic infections.
Infections spread from the origin into these spaces.
Secondary spaces: are those that become involved following spread of infection
from primary spaces.

Classification of fascial spaces: (By Topazian):

1- Face:
Buccal
Canine (Infraorbital)
Masticatory (Masseteric – Pterygoid – Zygomaticotemporal)
Parotid

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 2- Suprahyoid:
Spaces of the body of the mandible
Submaxillary
Sublingual
Submental
Lateral pharyngeal
Peritonsillar
3- Infrahyoid anterovisceral (pretracheal)
4- Spaces of total neck: retropharyngeal
Danger space
Prevertebral space
Classification of fascial spaces: (By Peterson)
Primary Maxillary spaces
1- Canine (infraorbital)
2- Buccal
3- Infratemporal
Primary mandibular spaces
1- Buccal
2- Submental
3- Submaxillary Submandibular spaces
4- Sublingual
Secondary fascial spaces
1- Submasseteric
2- Pterygomandibular Masticatory spaces
3- Temporal
4- Lateral pharyngeal
5- Retropharyngeal
6- Danger space (space 4)
7- Prevertebral space
8- Carotid sheath
9- Parotid

Potentially infected spaces related to the mandible:

Submandibular spaces lies within and below the body of the mandible and
constitute the following spaces:
1) Submaxillary space which contain the submaxillary salivary gland, LN

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2) Submental, that part of Suprahyoid region extend from anterior limit of
submaxillary space
3) Sublingual, area bounded superiorly by the mucous membrane of the floor of
the mouth and inferiorly by the mylohyoid muscle

- The submaxillary and sublingual spaces are considered as one surgical unit
because of their proximity and frequent dual involvement
- Anteriorly the sublingual space communicates with submental space and with
the sublingual of the other side and this explain the mechanism of Ludwig's
angina existence.
- Posteriorly the sublingual space communicates with the lateral pharyngeal space

I- Submental space infection:

Boundaries:
- Above: Mylohyoid muscle
- Below: platysma muscle, superficial cervical fascia and skin
- Laterally: anterior belly of digastric muscle
Contents: anterior jugular vein and submental LNs
Source of infection: directly from lower anteriors (if infection perforating the
labial cortex below the attachment of mentalis muscle) and
indirectly from sublingual or submandibular space infection
Signs and symptoms: firm circumscribed swelling over or beneath the anterior
mandible.
Surgical treatment: extraoral incision beneath the chin in a horizontal direction
and parallel to the anterior border of the mandible in healthy
area under the most dependent area of the swelling in the
natural skin crease.

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II- Sublingual space infections:
Boundaries:
- Above: mucosa of the floor of the mouth
- Below: mylohyoid muscle
- Anteriorly and laterally: medial surface of mandible
- Medially: by the lingual septum
- Posteriorly: by the hyoid bone
Contents: Submandibular duct (Wharton’s duct)
Sublingual salivary gland and part of submandibular salivary gland
Lingual nerve and terminal branches of lingual artery.
Source of infection: infection of the lower 4, 5 or 6
(towards the lingual side whose apices are above the mylohyoid muscle)
Spread of infection from other spaces e.g. submandibular, submental, lateral
pharyngeal)
Signs and symptoms: - The tongue is raised
- Firm painful swelling in the anterior floor of the mouth
- Pain and discomfort during swallowing
- Enlarged submental and submandibular lymph nodes

Surgical treatment:
- If sublingual space is involved alone intraoral incision in the lingual sulcus
adjacent to the lingual cortex in the mucous membrane to avoid injury to
sublingual gland, lingual nerve, submandibular duct

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 - If the sublingual space is involved secondary to the submaxillary space,
(Extraoral incision) however both spaces are considered as a distinct units,
but should be considered as one surgical unit, when their drainage is
considered due to proximity and frequent dual involvement in odontogenic
infections.
In this case it is drained through submandibular incision and blunt evacuation by
dissection through the submaxillary space and mylohyoid muscle

III- Submaxillary space infection:

Boundaries:
Anteriorly: anterior belly of digastrics muscle
Posteriorly: posterior belly of digastrics muscle
Medially: Hyoglossus + mylohyoid
Laterally: deep fascia, platysma muscle and skin

Content: submandibular salivary gland + submandibular LNs + Submandibular

duct (which provides a route of communication with the sublingual space)
Source of infection: lower 7 & 8
Or result of infection spread from submental and sublingual spaces.
Signs and symptoms: Firm swelling in submandibular area
Trismus
Surgical treatment: Extraoral incision and drainage
Skin incision parallel and 1-2 cm below inferior border of the
mandible (to avoid injury to marginal mandibular branch of facial nerve)
Then an artery forceps is used to reach space bluntly towards lingual side of
mandible and evacuate the pus and drain is inserted and fixed.

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 Ludwig’s angina
Definition: It a firm, acute, toxic cellulitis of submandibular spaces bilaterally
characterized by the following 3 fs: to be feared, Rarely fluctuant, often be fatal.

Etiology:
1. Periapical, periodontal, or pricoronal infection of mandibular molars
2. Traumatic injuries & Infected lesions in the molar region
3. Infective conditions such as osteomyelitis

Pathogenesis:
1) Infection reaches first the submaxillary space.
2) From here the infection spread through the deep part of submandibular
salivary gland above the mylohyoid muscle to reach the sublingual space
3) From one side of the sublingual space it moves across the loose connective
tissue separating the sublingual spaces and reaches the other side, it then
crosses behind the mylohyoid muscle & reach the opposite side submaxillary
space.
4) Submental space get involved either via Lymphatics or spread directly through
fascial spaces from submandibular space.
5) It spreads posteriorly along the course of sublingual artery producing edema in
the laryngeal inlet
6) From submaxillary space it can pass posteriorly to involve Parapharyngeal and
then retropharyngeal spaces

Clinical picture:
Systemic features: Pyrexia , dehydration , dysphagia , dyspnea , horsiness of voice
and stridor (noisy breathing)
Extra-oral features: Hard to firm brawny indurated swelling , the skin over the
swelling appears erythematous, stretched and tender with
local rise in temperature
Intra-oral features : Trismus , floor of the mouth and tongue are raised upwards
and increased salivation
Difficulty in closing the mouth and drooling of saliva
Treatment:
1- Hospitalization (ICU) and aggressive airway care

23
 2- Airway maintenance: intubation is contraindicated as perforation of
infected swelled areas may lead to aspiration of pus, tracheostomy or
cricothyroidotomy is advisable.
3- Surgical decompression:
Decompression improves vascularity, release the pressure around the
respiratory passages.
4- Parentral antibiotic therapy. Empirical antibiotics should be prescribed IV
until culture and sensitivity results
Amoxixillin + Cloxacillin
Metronidazole infusion or clindamycin injection
5- Steroids to reduce edema (used routinely when airway compromise is
suspected) Dexamethasone 10-20 mg IV then 4-6 mg Q6 for 8 doses.
6- Hydration of the patient: it’s necessary to put the patient on IV fluids.
7- Removal of cause: extraction or endodontic treatment of the offending
tooth
8- The patient is extubated after resolution of the edema
9- Continue an oral antibiotics and follow up
Complications of Ludwig’s angina:
1) Death due to airway compromise
2) Septicemia
3) Aspiration of pus
4) Mediastinitis due to retropharyngeal or danger space involvement

VI- Buccal space:

Boundaries:
Medially: buccinators muscle
Posteriorly: Masseter muscle
Laterally: skin and subcutaneous tissue
Anteriorly: posterior border of zygomaticus major muscle above and
depressor anguli oris below
Superiorly: zygomatic arch
Inferiorly: lower border of mandible
Contents: Anterior facial artery and vein
Buccal pad of fat
Parotid duct
24
Source of infection: upper and lower premolars and molars
Connects to: infraorbital space, periorbital tissues, superficial temporal space.
Signs and symptoms: Swelling of the cheek, which extends from the zygomatic
arch as far as the inferior border of the mandible, and from the anterior
border of the ramus to the corner of the mouth.
The skin appears red and taut with or without fluctuation of abscess which, if
neglected, may result in spontaneous drainage.
Surgical treatment:
Intraoral incision: through a horizontal incision at the depth of the buccal
vestibule to provide dependent drainage and to avoid injury to the parotid duct;
this technique is more difficult, with the maintenance of drainage becoming less
predictable.
• Access to the buccal space is usually intraoral for 3 main reasons:
1. Because the abscess fluctuates intraorally in the majority of cases.
2. To avoid injuring the facial nerve.
3. For esthetic reasons
Extraoral submandibular skin incision:
Submandibular incision through the skin and subcutaneous tissues.
Communications:
Posteriorly: communicate with the submasseteric space.
Other communications:
- Pterygomandibular space
- Infratemporal space
- Lateral pharyngeal space (via pterygomandibular raphe)
- Superficial temporal space
- Subcutaneous spaces (superficial to submandibular space)

Potentially infected spaces related to the maxilla:

1- Canine space / infraorbital space infection:
A potential space present on the anterior surface of the maxilla between bone and
canine fossa musculature.
Anatomic location: the canine fossa, which is a small space between the levator
labii superioris and the levator anguli oris muscles

25
Source of infection: Infection from upper canine or 1st premolar (when the apex of
the tooth above the levator anguli oris muscle)
Boundaries:
Superiorly: Levator labii superioris
Inferiorly: Levator anguli oris
Anteriorly: Lateral wall of nose
Posteriorly: communication with buccal space
Contents: infraorbital nerve and angular vessels
“Angular vein is valveless vein that communicates with the cavernous sinus”
Signs and symptoms: painful reddish swelling localized in the infraorbital fossa –
- Obliterate nasolabial fold.
- Superior extension can cause swelling of lower eyelid
- Drooping of angle of mouth
Surgical treatment:
Incision and drainage is performed intraorally high at the mucobuccal fold parallel
to the alveolar bone in the canine region and with blunt evacuation of pus using
small hemostat through levator anguli superioris muscle to evacuate all pus
locules.

drain is inserted and sutured into the lower margin of

vestibular incision.

2- Infratemporal space:
• The infratemporal space is the inferior portion of the deep temporal space.
- It’s the superior extension of the pterygomandibular space
Boundaries:
Laterally: ramus, temporalis muscle
Medially: lateral pterygoid plate, part of lateral pterygoid muscle
and lateral pharyngeal wall
Superiorly: greater wing of sphenoid.
Inferiorly: the pterygomandibular space
Anteriorly: the infratemporal surface of maxilla
Contents:
Pterygoid plexus of veins
Mandibular nerve
Origin of pterygoid muscles

26
Source of infection: 1) Maxillary third molar
2) Osteomyelitis of condyle or coronoid process
3) Infection from pterygomandibular space
Signs and symptoms:
- Sever trismus, bulging of temporalis muscle
This situation is dangerous because of involvement of pterygoid venous plexus and
its communication with cavernous sinus through an emissary veins.
Communications: - The pterygomandibular space inferiorly
- Inferior orbital fissure to the orbit
- Mandibular nerve coming from foramen ovale
- Middle meningeal artery through foramen spinosum
Diagnosed by CT scan
Surgical treatment: Intraoral incision
a) Medial and parallel to the anterior aspect of ascending ramus through the
mucous membrane and submucous tissue only to avoid injury to the lingual
nerve, curved hemostat is advanced upward and then opened in different
directions to facilitate drainage, then a rubber drain is inserted and sutured in
place (drainage through pterygomandibular space).
b) Incision through mucobuccal fold lateral to the upper third molar, a curved
hemostat is inserted behind the tuberosity and directed upward and medially
to evacuate the pus, then rubber drain is inserted
Complication:
Secondary spaces to infratemporal space:
I. Deep temporal space is present between the medial surface of the temporalis
muscle & the periosteum of the temporal bone and communicates with
infratemporal space, usually both temporal and infratemporal spaces are
considered one surgical unit
II. Orbital cellulitis (preseptal or postseptal:Ocular
findings include erythema and swelling of the eyelids, and ophthalmoplegia
(paralysis or weakness of one or more of the muscles that control eye movement).
III. Cavernous sinus thrombosis
a) Can result from hematogenous spread of odontogenic infections.
b) Veins of the face and orbit are valveless so retrograde flow can occur caring
infection to the cavernous sinus.
c) Bacterial routes of spread:
1. Posterior: via pterygoid plexus through emissary veins
2. Anterior: via angular vein through inferior or superior ophthalmic veins to the
cavernous sinus
27
Secondary fascial spaces:
Masticatory space infections: It composed of 3 spaces:
- Submasseteric space
- Pterygomandibular space
- Temporal space

Sources of infection:
Pericoronitis of lower 8
Spread of infection from submandibular or lateral pharyngeal spaces

Singns and symptoms:

- Trismus
- Swelling in the area of mandibular angle and medial side of mandible in
retromolar angle.
- Difficulty in swallowing
- Pain
- Fever

Submasseteric (masseteric) space:

Lies between the masseter muscle and lateral surface of ramus
Boundaries:
Laterally: masseter muscle
Medially: the lateral spect of the mandibular ramus
Posteriorly: parotid gland
Anteriorly: the mucosa of the retromolar area
Source of infection: generally occurs from buccal space primary involvement,
periapical or pericoronal infection of lower third molar
Clinical presentation:
External facial swelling confined to masseter muscle, severe trismus and
tendernes
Infection may spread to the parotid posteriorly or to the buccal space anteriorly.
Treatment:
A. Extraoral approach is indicated when severe trismus and intraoral approach
can not be done

28
1) Horizontal incision 2.5 cm below the lower border of the mandible.
2) Sub-platysmal flap raised and the masseter muscle breached to expose the
abscess

3) Drain out the pus using curved hemostat.

4) A corrugated rubber drain is inserted

B. Intraoral approach: is indicated if the patient can open his Mouth little pit
1) An Incision at the anterolateral border of the mandible
2) Dissection until the anterior attachment of masseter muscle
3) A curved hemostat is inserted between the masseter muscle and lateral
surface of the mandible
4) Irrigation using antiseptic solutions and then insert rubber drain
5) Complete drainage using this approach is questionable

Pterygomandibular space:
It lies between medial surface of ramus and medial pterygoid muscle.
It communicates posteriorly with para-pharyngeal space.
Lateral pterygoid muscle forms its roof
Content: Inferior alveolar nerves and vessels.
Lingual nerve
Loose areolar tissues, communicates with infratemporal space
Source of infection:
1. Infection from lower third molars & acute pericoronitis
2. Secondary infection results from spread from the sublingual and submaxillary
spaces
3. Compound fracture to mandibular angle
4. From infratemporal space infection
Clinical features:
1) Trismus is usually an early sign
2) Intra oral swelling in the medial aspect of the ramus of the mandible deviating
the pharynx
3) Dysphagia
4) Occasionally edematous uvula is displaced to the other side
5) Deep cervical lymph node enlargement
6) Systemic signs of acute infection is usually presented

29
Incision & Drainage
I. Intraoral incision over the anterior border of the ramus of the mandible,
blunt dissection medial to the ramus using curved hemostat in different
pouches of pus accumulations, irrigation with antiseptic solutions, insert
rubber drain, follow up.
II. Extra oral incision below and behind the angle of the mandible. The
medial pterygoid muscle then dissected, and curved hemostat is
introduced between the mandible and the muscle,

Temporal spaces:
Location: posterior and superior to the masseteric and pterygomandibular spaces.
It’s the superior communication of infratemporal space
Boundaries:
bounded laterally by temporalis fascia and medially by temporal bone
The space is divided into:
1- Superficial temporal space: lies superficial to temporalis muscle
2- Deep temporal space: lies deep to temporalis muscle
Etiology: Infection of the temporal space is caused by the spread of infection
from the infratemporal space, with which it communicates.
Clinical presentation:
Swelling confined to the shape of the muscle extending from the lateral orbital
rim, above the zygomatic arch, covering of the lateral aspect of the skull
Communications:
Deep temporal space is freely communicate with infratemporal space and more
inferiorly by pterygomandibular
The superficial temporal space is communicate with masseteric and parotid
spaces as infection goes upward above the zygomatic arch
Surgical treatment:
- The incision and drainage is performed horizontally at the margin of the
scalp hair and approximately 3 cm above the zygomatic arch.
- It then continues carefully between the 2 layers of the temporal fascia as
far as the temporalis muscle.
- A curved hemostat is then used to drain the abscess

30
Parotid space infection:
Boundaries: it’s formed by superficial layer of deep cervical
fascia surrounding parotid gland.
Contents:
1) The parotid gland
2) Stenson’s duct (Parotid gland duct)
3) Facial nerve
4) Posterior facial vein
5) Internal maxillary and superficial temporal arteries (branches of external
carotid artery)
6) Auriculotemporal nerve

Source of infection
a) Lateral border of Masticator space
b) Lateral pharyngeal space
c) Middle ear and mastoid process
Incision & drainage: 1-2 cm incision below and behind the angle of the mandible
through skin, subcutaneous tissue and parotid capsule to avoid injury to the facial
nerve which lies within the gland tissue, blunt evacuation of pus using hemostat,
irrigation with antiseptic solution, then a rubber drain is inserted

Deep Neck infections

Lateral pharyngeal (parapharyngeal) space infection
Inverted cons shape with its base at the skull base and its apex at the hyoid bone.
Boundaries: Superior: base of skull
Inferior: hyoid bone
Medial: pharynx
Lateral: medial pterygoid muscle
Contents:
1) Deep cervical Lymph nodes
31
 2) Facial and ascending pharyngeal arteries
3) Carotid sheath and cervical sympathetic chain
4) Glossopharyngeal, accessory, and hypoglossal nerves

Source of infection
a) Peritonsillar suppuration
b) From pterygomandibular space
c) Parotid space infection
Clinical presentation
1. Lateral swelling of the neck
2. Bulging of the lateral pharyngeal wall
3. Tonsils & lateral pharyngeal wall are pushed to the midline
4. Posterior compartment involvement can result carotid sheath
involvement
Surgical treatment: IO vertical incision placed parallel with pterygomandibular
Raphe followed by blunt dissection directed posteriorly
medial to medial pterygoid muscle.

Retropharyngeal space:
Boundaries: lies between posterior wall of pharynx and prevertebral fascia
It provides a direct route to the mediastinum
1. Posteromedial to the lateral pharyngeal space and anterior to the danger space or
space 4
2. Anterior: superior pharyngeal constrictor muscle
3. Posterior: alar layer of prevertebral fascia
4. Extends from skull base superiorly to C7 to T1 inferiorly
5. Retropharyngeal space infections can spread to mediastinum
6. Other complications as:a)Airway obstruction b)Aspiration of pus in the event of
spontaneous rupture during endotracheal intubation

Prevertebral Space
Anterior border is prevertebral fascia
Posterior border is vertebral bodies and deep neck muscles
Extends along entire length of vertebral column
Its involvement may leads to spinal epidural collections of pusor vertebral
osteomyelitis
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Danger Space ( space 4)
- Potential space between two layers of prevertebral fascia (alar and
prevertebral layers).
- Extends from skull base superiorly to the diaphragm inferiorly
- Mediastinitis is concern with danger space infections similarly to
retropharyngeal space infections
Mediastinum: The area between the lungs. The organs in the mediastinum
include the heart and its large veins and arteries, the trachea,
the esophagus, the bronchi.
- Potential complications a) Laryngeal inflammation
b) Rupture with aspiration
c) Descending necrotizing mediastinitis
d) Pericardial involvement

Treatment of deep neck infection

- ICU hospitalization
- Airway protection
For deep neck spaces involvement the most important part in management is
the airway protection
1. Security of airway compromise is the most important initial step in
managing these infections
2. Airway loss is primary cause of death in these patients
3. Initially intact airway must be continuously reevaluated during treatment
4. Signs of airway compromise as inability to assume a supine position,
drooling, dysphonia, stridor, and restlessness …etc.
5. Surgeon must decide the need, timing and method to establish an
emergency airway
- Proper Antibiotic therapy
- Surgical drainage
- High fluids intake
- High protein and vitamins diet
- Close observation

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 Principles of management of acute odontogenic infections:
1- Determine the severity of infection
2- Evaluate host defense
3- Decide on the setting of care
4- Choose and prescribe antibiotic therapy
5- Administer the antibiotic therapy
6- Treat surgically
7- Support medically
8- Evaluate the patient frequently

1- Determine the severity of infection:

A careful history and thorough physical and radiographic examination to
determine:
1) Anatomic location of infection: potential for airway compromise or
affecting vital organs (the heart and mediastinum or the cranial contents)
2) Rate of progression (rapidly progressive infections)
3) The potential of airway compromise or neurologic involvement
1. Anatomic Location
The anatomic spaces of the head and neck can be graded in severity by the
level to which they threaten the airway or vital structures, such as the heart
and mediastinum or the brain into:
1) Low risk
2) Moderate risk
3) High risk
4) Extreme high risk
The severity score for a given patient is the sum of the severity scores for all of the
spaces involved by cellulitis or abscess, based on clinical and radiographic
examinations.
Severity score Anatomic spaces
1 (Low risk to airway or vital Vestibular
structures) Subperiosteal
Space of the body of the mandible
Infraorbital (canine) soace
Buccal
2 (Moderate risk to airway or Submaxillary
vital structures) Submental
Sublingual
Pterygomandibular
Submasseteric
Superficial and deep temporal spaces
Infratemporal

34
3 (High risk to airway or vital Lateral pharyngeal
structures) Retropharyngeal
Pretracheal
4 (extreme risk to airway or Danger space (space 4)
vital structures) Mediastinum
Intracranial infections

2. Rate of Progression
Rate of progression is defined by:
1) Onset of swelling, pain, trismus
2) Number of days passed before the patient seeks treatment will give an
indication about the rate of progression of infection.
Normally odontogenic infections generally pass through 3 stages before resolving.
1) During the first 1 to 3 days the swelling is soft, mildly tender, and doughy in
consistency.
2) Between days 2 and 5 the swelling becomes hard, red, and severely tender. Its
borders are diffuse and spreading.
3) Between the 5th and 7th days the center of the cellulitis begins to soften and the
abscess undermines the skin or mucosa, making it compressible and shiny.
4) The final stage of odontogenic infection is resolution, which generally occurs
after spontaneous or surgical drainage of an abscess cavity.
5) The swelling then begins to decrease in size, redness, and tenderness.

3. Airway Compromise
- The most frequent cause of death from odontogenic infection is airway
obstruction.
- Evaluate possible airway obstruction in first few moments when evaluating the
patient with a head and neck infection.
- Complete airway obstruction is a surgical emergency, It is diagnosed by
insufficient or absent air movement in spite of inspiratory efforts.
- Airway security by cricothyroidotomy or tracheotomy is very important in
complete airway obstruction.

2- Evaluate host defense:

Factors decreasing the effectiveness of Immune system
A) Patient related pathologic systemic factors:
1) Diabetes has leukocyte migration defect and impairs blood flow to the infected
tissue
2) Malignancy (leukemia, lymphoma, agranulocytosis )
3) Fluid imbalance

35
4) Drugs suppress the immune system as chemotherapy, immunosuppressive,
steroid therapy.
5) Chronic renal disease inhibits activation of TH lymphocytes
6) Malnutrition affects the production of Antibodies
7) Alcoholism affects the NO of leukocytes
8) End –stage AIDS, affect the T lymphocytes function

B) Physiologic causes of compromised immunity: obesity and old age

When you treat a patient with incompetent immune system, treat your patient
aggressively and stick to the principles.

Systemic reserve
- The host response to severe infection can place a sever physiologic load on
the body, fever can increase fluid loss and calories.
- A prolonged fever may cause dehydration , which can decrease
cardiovascular reserve and deplete glycogen stores, and shifting the body
metabolism to a catabolic state.
- Elderly are not able to tolerate high fevers, so elevated temperature in
elderly is not only a sign of a particularly severe infection, but also an
indication of decreased cardiovascular and metabolic reserve.
- The white blood cell count has an important role in determining the severity
of infection as well as in estimating the length of hospital stay.
- Mild or moderate infection may be a significant threat to the patient with
systemic disease because they lack of systemic reserve

3- Decide on the setting of care:

Hospitalize your patient
1) Temperature > 38.5° C, signs of septicemia
2) Dehydration, dry skin and mucous membrane, chipped lips, loss of normal skin
fullness or tension, elevated urine specific gravity (over 1.030) or elevated
blood urea nitrogen.
3) Threat the airway obstruction
4) Need for general anesthesia for I & D
5) Need for inpatient to control of systemic disease especially in
immunocompromised patients

4- Choose and prescribe antibiotic therapy

- Removal of the cause, drainage and supportive care more important than
antibiotic therapy.
- Infections are cured by the patient’s defenses, not antibiotics.

36
- Risk of allergy, toxicity, side effects, resistance and superinfection causing
serious or potentially fatal consequences must be considered.
- Antibiotics should be prescribed whenever possible on the bases of culture and
sensitivity test.
Specific antibiotics: based on culture and sensitivity
Empirical antibiotics: not based on culture and sensitivity

Initial empirical antibiotic therapy is instituted especially in severe infection

depending on the following data:
1) Site and features of the infection.
2) Circumstances leading to infection.
3) Organisms that most commonly cause such infections.
4) Broad spectrum antibiotic could be used
When prescribe empirical antibiotics remember
- Odontogenic infection is caused by polymicrobial from endogenous bacteria.
- Aerobic bacteria alone rarely the causative agents, it just represent about 5%
of all odontogenic infections
- 50 -60% of odontogenic infections are strict anaerobic in nature.
- Mixed infections posses 35-45% are due to mixed flora.

On the basis of culture and sensitivity, the following principles should be applied
1- Use of narrow spectrum antibiotic: Antibiotic with narrowest antibacterial
spectrum should be chosen, e.g. if the organism is sensitive to penicillin,
cephalosporin, and tetracycline; penicillin should be used since it has the narrowest
spectrum, the other two (cephalosporin and tetracycline) have broad-antibacterial
activity against variety of Gm -ve organisms, their use will lead to development of
resistant organisms and superinfection.
2- Least toxic antibiotic: Antibiotics are utilized to kill living bacteria, but some
antibiotics also kill or injure human cells, thus they can be highly toxic.
e.g. If the bacteria that cause the infections are sensitive to penicillin,
streptomycin and chloramphenicol, however chloramphenicol, is very toxic
causing severe bone marrows depression and streptomycin is nephrotoxic
and toxic to 8th cranial nerve. So penicillin is preferable because of its lower
toxicity.
3- Drug history for:
1) Previous allergic reactions.
2) Previous toxic reactions.
- Penicillin allergy must be checked from a reliable source.
- About 10-12% of patient who are allergic to penicillin also exhibit an allergic
reaction to Cephalosporin.

37
- Drug-drug interactions should be reviewed e.g. concomitant administration of
some antibiotics may decrease the effectiveness of birth control pills e.g.
erythromycin.
4. State of the host defense:
- Host defense mechanisms are the most important factors in the final outcome of
bacterial insult.
- If the host defenses are impaired, infection may result from minor bacterial
exposure.
- When dealing with established infection in immunocompromised patient:
An aggressive dose of bactericidal antibiotic therapy must be considered
5. Use of bactericidal rather than bacteriostatic.
Bactericidal antibiotics are more advantageous over bacteriostatic ones, owing to:
1) Antibiotics itself kill the bacteria and not relay on the patient immune
system.
2) Works faster than bacteriostatic drug
6- Use of antibiotic with proven history of success:
• The best evaluation of efficacy of drug is the clinical observation over a
prolonged period of time.
Penicillin and its derivatives are very effective in oral infections, than others.
7- Cost

Note:
- It is important to maintain the peak blood level of AB for an adequate period
of time to obtain maximum tissue penetration and effective bacterial killing (
5 to 7 days) Or
- It should be continued 3 days after the signs and symptoms of infection is
disappeared

5- Administer the antibiotic properly:

Use proper dose:
- The goal of drug therapy is to achieve the desired therapeutic level, but not
enough to cause injury to the host.
- The Minimum Inhibitory Concentrations (MIC) of usual antibiotics for most
common bacteria has been established.
- The therapeutic concentration of antibiotic at the site of infection should be
3-4 times of MIC.
- In severe infection a loading dose at the beginning is recommended
Proper route of administration:
Oral route: should be taken in fasting state 1 hr before meal or 2 hrs after
meal not to affect drug absorption
Disadvantages: GIT upset and unpleasant taste (for some antibiotics)

38
 Parentral route: Indications: sever infection
malabsorption syndrome
when drug is destroyed by gastric secretion
When drug is available only in injectable forms e.g. penicillin G
Proper time interval:
1) Just as there is usual recommended dose of each antibiotic there is usual recommended
dosage interval.
2) Each antibiotic has an established plasma half life during which one half of the
absorbed dose is excreted.

Combination antibiotic therapy

The usual result of combination therapy is a broad spectrum exposure that leads to
depression of the normal host flora and increased resistant bacteria to emerge.
Indications of combination therapy
a) When synergistic effect is desired for treatment of severe infection.
b) When nature of infection is not known (or multiple, mixed organisms are
involved)
c) When development of resistance is a problem, like with TB
Bacteriostatic + bacteriostatic → additive effect
Bactericidal + bactericidal → synergistic effect
Bactericidal + bacteriostatic → antagonistic effect

6- Treat surgically (airway security and drainage of pus)

“The most important therapeutic action in the management of orofacial
infections is the drainage of pus, and antibiotics are merely an adjunct”

Drainage of pus can be:

- Through root canal
- Through socket (by extraction)
- Through incision and drainage
Optimum time for incision and drainage: (How to judge pus localization?)
- Erythematous area or yellow color
- Positive fluctuation test: (Bi-digital palpation)
(Press by index finger of one hand over abscess at one side → fluid wave felt by
index finger of the other hand)
- Pitting on pressure: slight depression on pressure that returns slowly.
- Needle aspiration → pus
- CT or MRI (in deep areas)

N.B: in some situations e.g. Ludwig’s angina, we do immediate I & D without

waiting for localization

39
1. Anesthesia is achieved by General anaesthesia, conscious sedation with regional
blocking
2. The incision is made through skin, superficial fascia, parallel to the main nerves
& vessels in close proximity to that area. The incision should be:
a) In healthy area to avoid aesthetic scar.
b) In esthetic area under the shadow of the jaw or at skin crease
c) In dependent position to encourage complete drainage
3) A curved hemostat is inserted through the incision towards the deep areas of pus
collection.
4) The forceps is entered closed into the tissuesand gently opened inside in a
direction parallel to the important structures . The hemostat should never be
blindly close inside the wound to avoid crashing of the vital structures
5) After the pus is evacuated the cavity should be checked for any necrotic tissue
6) Flushing of the cavity with sterile saline, suitable antiseptic like 10% iodine, 1%
chlorhexidine or diluted hydrogen peroxide especially if anaerobic infection is
expected
7) A rubber drain is inserted and secured to the skin edge.
8) The drain should be applied loosely in the abscess cavity and inserted deep
enough to reach all locules. A loose dressing is placed on the wound
8) Drains should be discontinued when the drainage ceases. They may be withdrew
gradually or removed all at once and no evidence in favor of either techniques
- Pus usually stops flowing from surgically drained abscesses in 24 to 72 hours,
however it may take somewhat longer when opened cellulitis stage.
- It should be kept in mind that latex Penrose drainscan be antigenic, and after
several days they may cause exudation due to foreign body reaction, that is why
it is recommended to change it every 48 hrs.

7- Support medically:
1) Hydration, proper nutrition and control of pain.
2) Maintenance or reestablishment of electrolyte balance and the control of
systemic diseases may also be a crucial part of the necessary supportive medical
care for some cases
3) Fever control because it can become destructive by increasing the basal
metabolic rate and cardiovascular demands beyond physiologic reserve capacity
leading to depleted energy stores and the loss of fluid is significantly increased.
Fever can be controlled by:
a) Adequate hydration is perhaps the best method for controlling fever to substitute
the daily sensible fluid loss, consisting primarily of urine and insensible through
the sweat and evaporation through lung is also increased.
b) Antipyretic analgesic administration e.g. paracetamol or Acetaminophen
c) Cold water or alcohol sponge baths.

40
8- Evaluate the patient frequently
In outpatient infections that have been treated by tooth extraction and intraoral
incision and drainage, the most appropriate initial follow-up appointment is usually
at 2 days postoperatively for:
1. Usually the drainage has ceased and the drain can be discontinued at this time.
2. There is usually an improvement in signs and symptoms allowing the next
treatment decisions to be made.

For odontogenic deep fascial space infections that are serious enough for
hospitalization, the following should be considered:
1. Daily clinical evaluation and wound care are required for 2 to 3 postoperative
days, the clinical signs of improvement should be apparent, such as:
a) Decreasing swelling
b) Cessation of wound drainage
c) Declining white blood cell count
d) Decreased systemic signs and symptoms
e) Decrease in airway swelling
2. If these signs of clinical improvement are not apparent, then it may be necessary
to begin investigations for possible treatment failure.
One of the best methods for reevaluation is the postoperative CT which can:
1) Identify continued airway swelling that may preclude extubation
2) Evaluate further spread of the infection into previously ubdrained anatomic
spaces, or confirm adequate surgical drainage of all the involved anatomic
spaces by the visualization of radiopaque drains in all of the involved fascial
spaces.

Reasons for treatment failure:

Inadequate drainage
Depressed host responses
Foreign body
Antibiotic problems:
- Patient noncompliance
- Drug not reaching the site of infection
- Drug dose too low
- Wrong antibiotic

41
Dry Socket (painful socket, necrotic socket, localized osteomyelitis, alveolar ostitis)

Definition: A postoperative complication following tooth removal, most often in

the area of the mandibular molars
- The blood clot is lost before healing takes place, leaving raw, exposed nerve
endings, with the production of foul odor, without pus formation.
Etiological factors:
1) Pre-existing infection as periapical or periodontal infections
2) Excessive trauma during extraction
3) Contamination of the socket either by saliva loaded with microorganisms
or using contaminated instruments.
4) Increased fibrinolytic activity in or around the dental socket
Other contributing factors
1) Local factors:
a) Injection of local anesthetic solution containing strong vasoconstrictor such as
adrenalin at the site of extraction
b) Excessive curettage or irrigation of the socket after extraction
c) Heavy sucking or spitting after extraction which lead to detachment of the blood
clot from the socket
d) Presence of sclerotic bone or radiotherapy in which blood supply is limited.
e) Presence of remaining root or bone fragment or foreign body in the socket.
f) Smoking.
2) Systemic predisposing factors
a) Uncontrolled diabetes
b) Liver diseases
c) Anemia
d) Hemorrhagic diseases
e) Nutritional deficiency

Pathogenesis of dry socket Destruction of the blood clot either by:

1) Proyeolytic enzymes produced by bacteria leads to inflammation of marrow
spaces which causes liberation of tissue activators (direct activators)
2) Indirect activators as kinase, cortisone and oral contraceptives
These activators converts plasminogen to plasmin that dissolve the fibrin of the
clot.
Activators
Plasminogen plasmin
The violent agonizing pain experienced in dry socket is caused by the release of
kinin in the socket as it acts by stimulating unmyelinated terminal nerve fibers.
Prekininogenase plasmin kininogenase
Kininogen kininogenase Kinin

42
Clinical features:
- Pain usually starts few days after extraction that may continue for a week or
even longer.
- Deep seated, severe aching or throbbing in character.
- Mucous membrane around the socket is red and tender.
- No clot in the socket (Dry).
- When debris is washed away, whitish, dead bone may be seen or felt as
rough area with a probe
Prevention:
1. Minimal trauma.
2. Squeezed the socket edge firmly after extraction.
3. In case of dis-impaction of 3rd molars dry socket can prevented by:
- Meticulous surgical technique.
- Minimum damage to the bone.
- Use prophylactic antibiotic locally in the socket.
4. In osteosclerotic disease: Little damage to bone (surgical extraction)
Prophylactic antibiotic.
5. Stop smoking for 2 days post extraction.

Treatment
A. The aim of the treatment is to keep the open socket clean and to protect the
exposed bone
B. Irrigate the socket by antiseptic solution.
C. Loose obtudant dressing containing some non irritant antiseptic in the
socket. A great variety of dry socket dressing has been formulated:
1) Iodoform-containing preparation.
2) Alveogyl: which is easy to manipulate.
3) Zinc oxide and eugenol pack: in many cases, irrigation of the socket and
replacement of the dressing has to be repeated every other day.
D. Frequent use of mouth wash

Alveogyl rapidly alleviates pain and provides a soothing effect throughout the
healing period.
- Its fibrous consistency allows for easy application in the socket and good
adherence during the entire healing process.
- It includes eugenol for analgesic action, butamben for anesthetic action, and
iodoform for anti-microbial action.

43
 Osteomyelitis
Definition: inflammation of bone and bone marrow along with surrounding
periosteum.
A wide variety of organisms cause this illness and its progression is highly
distressing and disfiguring to the patient.
Etiology of osteomyelitis:
1) Odontogenic infections are the most frequent cause of suppurative
osteomyelitis
a- Improper management of acute periapical abscess
b- Curettage of extraction socket of the involved tooth in acute periapical
abscess
c- Infection around buried roots which act as an irritant
2) Excessive heat production in association with the use of rotary burs may
cause bone death
3) Infected teeth in the line of mandibular fractures especially if the tooth is
nonvital or broken
4) Infected intrabony cyst, odontomes and tumors
5) Compound fractures of the mandible
6) Hematogenous dissemination of infection present else in the body

Predisposing factors:
General conditions affecting the host resistance:
1- Diabetes milletus
2- Tuberculosis
3- Sever anemia, leucopenia
4- Leukemia
5- Bisphosphonate chemotherapy
6- Immunosuppressive drugs
7- Malnutrition
8- Chronic alcoholism
9- Acute infection diseases such as scarlet fever, measles and typhoid

44
Local conditions affecting jaw vascularity:
1- Radiation
2- Osteoporosis
3- Ostepetrosis
4- Fibrous dysplasia
5- Peripheral vascular disease

Incidence: (mandible > maxilla)

The incidence of osteomyelitis is much higher in the mandible (particularly the
molar area) due to:
- The dense poorly vascularized cortical plates primarily from the inferior
alveolar artery and most of the bone in that area is dense cortical in nature.
- Less common in the anterior mandibular teeth and in deciduous teeth
It is much less common in the maxilla due to:
- The excellent blood supply from multiple nutrient feeder vessels.
- The maxillary bone is much less dense than the mandible.

Pathogenesis:
1- Virulent organism get entry into medullar ycavity via many routes
(odontogenic, hematogenous, traumatic infections).
2- Localization of infection by inflammatory reactions (Most infections are
localized by a pyogenic membrane)
3) Disorganization of pyogenic membrane by microorganisms enzymes and toxins
or mechanically by continuous movement of improper fixed fracture of Jaw
leading to more infection spreading
4) Accumulation of Pus and edema will increase pressure (causing hypertension)
in Medullary cavity that destroy the pyogenic membrane and compromising
blood supply
5) Pus travel through haversian & Volkmann's canals & accumulate beneath the
periosteum & elevating it from cortex, that reducing the blood supply.
6) Reduced blood supply causes more necrosis of bone.
7) Then pus penetrate the periosteum leading to mucosal & cutaneous fistulae &
thereby discharging pus.
8) Thrombi can cause systemic spread of infection leading to bacteremia and
septicemia)

45
9) Small section of necrotic bone may get completely lysed while large section
separated from the shell of new bone by bed of granulation tissue. The dead
bone (Sequestra) is surrounded by the new viable bone called involucre.
10) Involucre contain one or more holes on the surface and pus find its way from
these orifices (cloacae)

Types of osteomyelitis:
I- Nonspecific osteomyelitis
more than one micro-organism speech of micro-organisms are involved and
usually of mixed type
I. Suppurative osteomyelitis:
a) Acute suppurative osteomyelitis
b) Subacute suppurative osteomyelitis
c) Chronic suppurative (when it persists ˃ 1 month)
* Primary (no acute phase)
* Secondary (acute phase preceding the condition)
II. Non suppurative osteomyelitis:
a) Chronic sclerosing
* Diffuse
* Focal
b) Chronic with proliferative priostitis (Garre’s chronic nonsuppurative
osteomyelitis)
II-Specific osteomyelitis: caused by specific type of microorganism
1) T.B osteomyelitis
2) Syphilitic osteomyelitis
3) Actinomycosis osteomyelitis

Clinical presentation:
Acute suppurative osteomyelitis:
is a destructive lesion of the trabecular bone & bone marrow of an acute
inflammatory origin.
Note: the process of acute osteomyelitis is rapid if the involved microorganisms
are particularly virulent or the host resistance is reduced.
Clinically:
1- Sever pain specially during eating and parathesia

46
 2- Local and systemic signs of acute inflammation

Subacute suppuarative osteomyelitis:

If the disease is not controlled within 10-14 days subacute suppurative
osteomyelitis is established.
- Pus extends through the haversian canals and accumulate under the
periosteum and penetrate into the soft tissues
- The teeth begin to loosen and become sensitive to percussion and the pus
exudes from the gingival sulcus and mucus and skin fistulae.

Chronic suppurative osteomyelitis:

- Fistula
- Induration of soft tissues (wooden characters of the affected area)
- Pain and tenderness on palpation.
- Positive in radiographs

Pain in osteomyelitis: terminal nerve stimulation because of inflammatory

mediators which is a consequence of hypertension in the marrow cavity
(increased pressure), intraosseous pressure in acute osteomyelitis reaches
300-500 mm water (normal value in healthy individual, 60-100 mm water) so
the severity of pain depends on acuteness of the osteomyelitis.

Chronic Sclerosing osteomyelitis:

is a chronic inflammatory process involving bone trabeculae and bone marrow,
occurs in response to a low-grade process rather than a destructive inflammation
caused by virulent bacteria.
Clinically:
- Little or no pain
- Hard swelling because the irritant may be so mild and results in dense
trabeculae & even lay down additional bone
Radiographically appear mottled & more radiopaque than normal
(osteosclerosis)

Types: i) Focal scelorising osteomyelitis

ii) Diffuse Sclerosing osteomyelitis

47
Chronic with proliferative priostitis (Garre’s osteomyelitis)
Clinically:
- Non suppurative.
- Children, young adults
- Mandibular molar teeth involved.
- Subperiosteal bone deposition
- The lesion is usually asymptomatic
X-ray condensation of cortical bone (onion peel appearance).
Pathogenesis:
The inflammatory process extends through the bone from periapical or
periodontal infection to the outer surface, stimulating the periosteum which react
by thickening & lay down excess layers of new bone.
Treatment:
1) Root canal treatment
2) Extraction of affected tooth.
3) Periodontal treatment

Diagnosis:
Investigations:
Laboratory Investigations
CBC with differential leukocytes count shows:
1) Elevated WBC count
2) Left shift: Polymorphonucleocytosis
3) Blood cultures
4) ESR (Normal: < 20 mm/ hr.) Usually elevated > 35mm
5) C-Reactive Protein (Normal: < 8 -10mg/L) Elevated > 10mg/L

Radiographic examination:
1) Conventional Radiography (Plain radiography)
Till at least 30-60% destruction of mineralized portion of bone takes place,
it does not visible on radiographs.
Acute osteomyelitis not visible on radiographs because the exudates firstly
progress through the marrow.
Chronic osteomyelitis: The lesion appear as diffuse radiolucency with mottled
& indistinct margins of the bone due to involvement of the
trabeculae (moth eaten appearance).

48
 Radiopaque islands may be seen (sequestrum) may be appear later on

2) Scintigraphy/ Bone scanning: measures physiological or functional changes in

bone
Technitium 99 bone scanning
A 99 mTc administered intravenously and distributed on the entire skeleton and
Technitium concentrated in areas of increased blood flow and osteoplastic
activity.
A gamma camera is used for imaging after 1-2 hours to detect the isotopes
containing areas denoting the areas of increased activity due to osteomyelitis.
Bone scans are usually positive 24 hours after an acute infection.

3) Computed Tomography (CT) is of value for delineating the extent of medullary

and soft-tissue involvement; and also cavities, sequestra, or cloacae in
osteomyelitis.
- CT scans show soft-tissue edema or bone destruction not seen on plain images,
particularly in case of acute osteomyelitis. Sclerosis, demineralization, and
periosteal reactions present in chronic osteomyelitis.
- CT scanning also helps in evaluating the need for surgery, and it provides vital
information about the extent of disease.

4) MRI (magnetic resonance imaging)

MRI has sensitivity and specificity higher than those of plain radiography and CT
as:
a) Marrow signal abnormality is more sensitive than lytic changes on plain and CT
images
b) Intramedullary bone pathology can be directly visualized with MRI, precede
bone changes in conventional radiology.

Advantages
- No ionizing radiation
- Safer contrast agent
- Better soft tissue detail
- Imaging in multiple planes
- No artifact by dental restorations
Disadvantages
- Increased cost
- Increased examination time

49
 - Dependent on patient cooperation
- Availability

5) Ultrasonography
High-resolution ultrasonography is a good instrumental in establishing a
diagnosis of chronic osteomyelitis.

Treatment:
Successful treatment is based on the followings:
- Early diagnosis and ruling out any bone tumors
- Evaluation and correction of host defines
- Bacterial culture and sensitivity testing followed by Adequate, appropriate
and prompt antibiotic therapy.
- Possible placement of irrigation drain/ polymethylmethacrylate antibiotic
beads.
- Proper surgical intervention to remove loose teeth, sequestra,
debridement, decortication, resection and reconstruction.

[A] Conservative management

1. Complete bed rest
2. Supportive therapy
Nutritional support - High protein diet
- High caloric diet
- Adequate multivitamins
3. Rehydration
- Hydration orally
- Administration of I.V. fluids
4. Control of Pain: analgesic and sedation
5. Proper Antibiotic therapy based on culture and antibiotic testing
a) Systemic antibiotic
b) Local antibiotics
(i) Closed wound irrigation –suction
Large dose of antibiotic will produce unwanted side effects.
To overcome this problem, local application of the antibiotic may be
effective.
(ii) Antibiotic impregnated beads:
PMMA (Poly methyl methacrylate) beads impregnated with
antibiotics may be placed into the diseased bone.
50
 6. Hyperbaric oxygen:
A mode of medical treatment in which the patient is entirely enclosed in a
pressure chamber and breathes 100% Oxygen at a Pressure Greater than 1
atmosphere.
Administration
1) Mono-place chamber: A single patient is placed in a chamber which is then
pressurized with 100% Oxygen. Used to treat stable patients with chronic
medical conditions.
2) Multi-place chamber: When treating critically ill patient requires a medical
attendant within the chamber and anxiety or claustrophobic patient
These chambers are pressurized with compressed air while the patient
breathes100% Oxygen through special masks or Oxygen Hoods.
Hyperbaric oxygen is effective in treatment of osteomyelitis because:
1) The oxygen free radicals are toxic to anaerobic pathogensand inactivate the
exotoxins released by the pathogens.
2) The elevated tissue oxygen level enhances the tissue healing by Increasing
fibroblast proliferation.
3) It helps in neoangiogenesis by encouraging endothelial proliferation. Increased
vascularity

B) Surgical Management:
1. Extraction of offending teeth
2. Incision and drainage and cortical perforations may be needed
3. Sequestrectomy
4. Saucerisation (Removal of bony hollow cavity/ dead space)
- After removal of sequestrum, the margins of the bone which lodge the
sequestra are trimmed down this create a saucer shaped defect instead of
a deep hollow cavity.
This saucer shaped defect can’t accumulate a large clot that will get infected
5. Decortication (decorticetomy)
- Surgical procedure in which the lateral and inferior cortical bone is removed
(then underlying cancellous bone can be mechanically irrigated under pressure
with antibiotic and debrided effectively)
- Necrotic cancellous bone is removed till the uninvolved area which can be
differentiated by the presence of bleeding points in vital bone compared to the
necrotic bone which shows no bleeding when it is cut.

51
6. Resection and reconstruction:
- If all of the above procedures are not effective completely eliminating the
infective process. It may be necessary to resect the infected part of jaw.
- Once the part of the jaw is resected, it may be reconstructed using
reconstruction plates, External pin fixation with or without delayed autologous
bone graft.
7. Postoperative care:
- Continued use of antibiotics
- Warm saline mouthrinses
- Adequate hydration
- Complete bed rest

Osteoradionecrosis
Definition: Pathologic process that develops following irradiation of osseous
tissue (>5000cGy).
- It is characterized by a chronic mucosal ulceration and exposure of the jaw
bone for more than 3 months.
- This complication can occur after dental surgery or extraction of teeth

Pathogenesis:
• Radiation cause inflammation of the BV endothelium, causing vascular
obstruction due to the condition called endarteritis obliterans.
• Results in 3 Hs:
- Hypovascularity
- Hypocellularity
- Hypoxia
Signs and symptoms:
- Exposed necrotic bone and fistulae
- Pathologic fracture
- Radiographic changes in bone trabeculation and radiolucency.
- Chronic pain
- Occurs more in mandible than maxilla
- Late sequestration of bone followed by sever pain
- Permanent deformity of bone and soft tissues

52
Prophylaxis against osteoradionecrosis:
- Dental procedures, such as the pulling of teeth or insertion of dental
implants, performed before starting cancer treatment.
- Regular dental hygiene is more important in cancer Patients because
radiations can affect the teeth and gums.
- Start a course of antibiotics, and regular scrubbing technique prior to
extraction.
- Hyperbaric Oxygen 20 dives before and 10 dives after extraction
- Post-op check up (every 4-8 weeks for the first 6 months post-operatively
and annual recall check up.

Management of osteoradionecrosis:
1. Antibiotic treatments: specific drugs should be selected based upon the culture
and antibiotic sensitivity testing.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs) are often prescribed to reduce
pain.
3. People with clotting disorders may be given blood thinners to reduce clots that
block the blood supply to the bone.
4. Electrical stimulation as soft laser has been used to stimulate bone
regeneration.
5- Hyperbaric oxygen: 30 dives
Marx protocol for HBO:
Pressure 2.4 Atmosphere
Duration 90 minutes
Prophylaxis 20 dives preoperative
10 dives postoperative
Active osteoradionecrosis 30 dives preoperative
10 dives postoperative

Surgical treatment:
1. Core decompression removes the inner cylinder of bone, which reduces
pressure within the bone, increases blood flow, allows more blood vessels to
form and reduces pain
2. This procedure is most effective for patients with early-stage of osteonecrosis
and those with a small area of affected bone.
3. If this procedure is not successful resection and bone grafting by
transplantation of vascularized autogenous graft.

53
 Specific granulomatous osteomyelitis
Actinomycosis
A Cervicofacial Actinomycosis is a chronic granulomatous disease characterized
by abscess formation, draining sinus tracts, fistulae, and tissue fibrosis caused by
Actimomyces Israeli, (a Gram positive branching bacillus).
The organism is found as a normal commensals in the mouth (particularly with
bad teeth) and intestines.
The lesions are in the form of multiple abscesses, each containing one or more
colonies of the organisms, separated by fibrous septa infiltrated by macrophages,
lymphocytes, plasma cells and occasional foreign body giant cells. The bacterial
colonies can sometimes be seen in the pus discharged from the lesions as small,
yellow or brown granules called “sulfur granules”.

Risk factors includes,

- immune suppression,
- oral malignancies or
- radiation

Clinical picture of cervicofacial actinomycosis:

- Posses about 50% of all cases of Actinomyces
- Presents as slow growing, non-tender indurated mass
- Progresses to multiple abscess and fistulae formation with pain, trismus,
and yellow purulent discharge (sulfur granules)
- Usually involves the mandible, but can infect any structure including cheek,
chin, maxillary sinus.

Investigations
- Culture from the exudate and biopsy
- Microscopy: branching filaments
- X-ray: radiolucent areas
- Elevated ESR

54
Treatment
Mild infections: treated with oral Penicillin V 2-4g/day divided q6hrs for 2-6
months
Serious infections: Penicillin G IV 2-4g/day divided q6hrs x 4-6 weeks, followed by
oral penicillin V
Tetracycline and Erythromycin are employed in patients allergic to penicillin
Surgical excision required for complicated abscesses and fistulae

Tuberculous osteomyelitis
Caused by Mycobacterium tuberculosis.
Pathogenesis
1) Through direct inoculation of the mycobacterial T B bacilli into a wound from
infected milk.
2) Direct spread from infected sputum into an extraction socket from TB of the
lung.

Diagnosis:
Clinical features
- Mandible more involved.
- Painless swelling of the jaw.
- Patient complains of chronic discharging sinus.
- Loosening of teeth & sequestration of bone.
- Palpable matted lymph nodes.
Radiographs:
- PA chest radiograph essential.
- Scintigraphy, CT , MRI ,and conventional Radiology

Diagnosis laboratory investigations

1) Culture of pus & sputum identification of acid-fast bacilli in specimen
2) Biopsy of lesion
3) Tuberculin testing (Monteux test)

Treatment of TB
24 months of at least 2 drugs at a time from the following list:
1) Isoniazid, 300 mg
55
2) Rifampicin 450 mg
3) Ethambutol 800 mg
4) Pyrazinamide 1500 mg
Surgical –radical surgical resection and reconstruction

Fatal complications of odontogenic infections:

1) Airway obstruction due to edematous septic involvement of epiglottis and
larynx as in Ludwig's angina posterior compression of airway in deep neck
spaces involvement (retropharyngeal, danger spaces).

2) Mediastinitis
- Mortality of 40%
- Increasing dyspnea, chest pain
- Widened mediastinum
Treatment
•Early recognition and intervention with CT
•Airway security
•Aggressive IV antibiotic therapy
•Surgical drainage

3) Pulmonary abscess due to:

1) Aspiration of infected particulates, usually leads to single pymeic abscess which
appear in radiograph
2) Thrombophlebitis from the infected area through the internal or external
jugular veins and appear in radiograph as a multiple areas

4) Orbital abscess from infratemporal space through inferior orbital fissure, also it
may occur through hematogenous rout from buccal or canine space through the
anterior facial vein, then superior ophthalmic veins and before reaching the
cavernous sinus leading to retrobulbar cellulitis.
It involves CN III, IV, VI and VII (frontal branch) and parasympathetic supply to the
orbit thus there will be:
a) Ptosis (dropping of the upper eyelid)
b) Proptosis
c) Fixed eye
d) Dilated pupil
e) Numbness of the area above and medial to the orbit

56
5) Intracranial suppuration (cavernous sinus thrombosis and brain abscess)
Mode of spread of odontogenic infection into the cranium:
A) Direct spread through:
1. Erosion of the base of the skull from infratemporal fossa, deep temporal,
paranasal sinuses
2. Skull base foramina as foramen oval
3. Infraorbital fissure to retrobulbar, then to the brain
B) Hematogenous spread:
thrombophlebitis can reach through the valveless veins to cause cavernous sinus
thrombosis or brain abscess

Cavernous Sinus Thrombosis

• Serious condition consisting of formation of thrombus in the cavernous sinus or
its communicating branches
• Infection of the head, face and intraoral structures above the maxilla,
particularly lead to this disease
• The veins of the head and neck are valveless veins so the blood flow can pass
into the opposite direction toward cavernous sinus
•There are two routes:
External (anterior) route Infection from the face and lip is carried by facial and
angular veins and nasofrontal veins (danger areas of the face) to the superior
ophthalmic vein.
The internal (posterior) route, the dental infection is carried by the way of the
pterygoid plexus from the inferior orbital fissure into the terminal part of the
inferior ophthalmic vein and then through the superior orbital fissure to the
cavernous sinus.
From pterygoid plexus through emissary vein through foramen oval or lacerum

Clinical Features:
1) Venous congestion symptoms of the orbit
2) Nerve symptoms
a) Cranial nerve involvement ; III, IV, V (ophthalmic), VI
b) Ptosis
c) Dilatation of the eye pupil
d) Restriction of eye movement

57
3) Sepsis symptoms
A) Thrombophlebitis
b) Pain in the eye and tenderness
c) Fever
d) Rapid pulse
e) Vomiting and coma

Management
- ICU
- Aggressive parenteral antibiotic therapy
- Heparinization to prevent extension of thrombosis: Heparin 20,000 units in
1500 ml of 5% Dextrose
- Neurosurgical consultation
- Surgical drainage of primary odontogenic abscess
- Pyogenic emboli may spread most commonly to Brain, lungs, orbit and
kidneys

Symptoms of Life threatening Infections

Respiratory impairment
Difficulty in swallowing
Impairment vision or eye movement or both
Change in voice quality
Lethargy
Agitation, restlessness due to hypoxia

58
 Quiz
1- In addition to sequestrectomy, the following might be added in treating
chronic osteomyelitis:
a- Saucerization
b- Intermaxillary fixation
c- Incisions and drainage
d- All of the above
e- None of the above
2- The following is not a routine treatment for a “Dry Socket”:
a- Frequent irrigations plus a loosely packed Zinc oxide and eugenol dressing
b- Frequent irrigations plus “Alveogyl medicament”
c- Establishment of fresh blood clot by curettage plus antibiotics and
analgesics
d- Analgesics, antibiotics, irrigations and dressings. All together
3- Infections from submental space might pass to the submandibular space
around:
a- The mylohyoid muscle
b- The anterior belly of digastrics
c- The posterior belly of digastrics
d- None of the above
4- Pericoronitis of lower third molar may cause spread of infection to:
a- Parapharyngeal space
b- Submaxillary space
c- Buccal space
d- All of the above
5- Garre’s osteomyelitis is:
a- Chronic sclerosis and nonsuppurative osteomyelitis
b- Chronic focal sclerosis and suppurative osteomyelitis
c- Suppuration and acute pain
d- Chronic diffuse sclerosing osteomyelitis
6- The roof of the pterygomandibular space is formed of:
a- Temporalis b- Medial pterygoid
c- Cranial base d- Lateral pterygoid

59
7- The distinguishing feature of masticatory space infection is:
a- Pain
b- Dysphagia
c- Trismus
d- Swelling
8- A mandibular dental infection which exits the buccal cortical plate above
muscle attachment will cause abscess of:
a- Buccal space
b- Submasseteric space
c- Vestibular sulcus
d- Masticatory space
9- Fascial spaces are filled with:
a- Loose connective tissue
b- Elastic fibers
c- Loose adipose tissue
d- Dead space
10- The infections of masticator space do not enter into neck because:
a- The fascia is tenaciously adherent to mylohyoid line
b- The fascia is firmly adherent to periosteum of lower border of mandible.
c- Before it reaches the neck it follows path of least resistance to open
extraorally or intraorally
d- Masticator spaces is not continous with spaces in the neck
11- Indications for hospital admission in odontogenic infections:
a- Systemic diseases
b- Fever (more than 39°)
c- Threat to the airway
d- All of the above
12- An incision to excise “chronic skin fistula” should be:
a- Elliptical
b- Stab
c- Straight
d- Hockey stick

60
13- Abscess is a localized collection of bacteria which have infected the host
tissue and multiplied:
a- True
b- False
14- Fascial space that is rarely infected is:
a- Canine
b- Buccal
c- Sublingual
d- Infratemporal
e- Pterygomandibular
15- With regard to dental abscess, an abscess treated with administration of
antibiotics alone the infection will resolve
a- True
b- False
16- The most logical explanation for swelling beneath the eye caused by an
abscessed maxillary canine is that:
a- Lymphatics drain superiorly in the region
b- Bone is less porous superior to the root apex
c- Infection has passed into the angular vein which has no valves
d- The root apex lies superior to the attachment of the caninus and levator
labii superioris
17- Ludwig’s angina may cause death by:
a- Heart failure
b- Airway obstruction
c- Convulsion
d- Paralysis of muscles of respiration
e- Pyemia
18- Signs and symptoms of ADAA at early stage include all of the following
except:
a- Feeling of tooth elongation
b- Sever throbbing pain provoked by heat
c- Moderate mobility of the involved tooth
d- Facial cellulitis
e- Regional lymphadenopathy

61
19- Treatment of ADAA at early stage includes:
a- Antibiotics therapy
b- Drainage procedure
c- Warm saline mouthwash
d- All of the above
20- Signs and symptoms that commonly suggest cavernous sinus thrombosis:
a- High fever, seizures and inability to move the eye
b- Trismus and slight extraoral edema beneath the angle of the mandible
c- Pus exudates around gingival sulcus and through fistula
d- Histories of intermittent pain and swelling of the mandible.
21- An acute periapical abscess originating from a mandibular third molar
generally points and drains in the:
a- Submandibular space
b- Pterygomandibular space
c- Buccal vestibule
d- Buccal space
e- All of the above
22- Which fascial space can be involved directly from infection involving teeth
from either maxilla or mandible?
a- Submandibular
b- Sublingual
c- Canine
d- Buccal
e- None of the above
23- Which of the following conditions are susceptible to osteomyelitis:
a- Paget's disease
b- Fibrous dysplasia
c- Radiation
d- All of the above
24. Osteomyelitis is more common in:
A. Maxilla
B. Mandible
C. Zygoma
D. Nasal complex

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25- While giving an inferior alveolar nerve block, infection is transposed to:
A. Pterygopalatine fossa
B. Pterygomandibular space
C. Submandibular space
D. Masticator space
26- In osteomyelitis how much bone should have been destroyed before it
manifests radiologically:
A. 10-12%
B. 15%
C. 30-60%
D. 80%
27- A 40-year old patient presented with multiple extraoral sinuses with
yellowish discharge and with history of intermittent remission after antibiotics
treatment two months ago. The disease started after extraction of 2nd
mandibular premolar. It is suggestive of:
A. Tubercular osteomyelitis
B. Actinomycosis
C. Subperiosteal Garres osteomyelitis
D. Dissecting subperiorteal abscess
28- A mandibular dental infection which exits the buccal cortical plate above the
muscle attachment will cause abscess of:
A- Buccal space
B- Masseter space
C- Vestibular sulcus
D- Masticatory space
29- Which of the following is not a primary mandibular space?
A Buccal
b. subilngual
C Submandibular
D. Pterygomandibular
30- Odontogenic infections are mostly caused by:
A. Mixed bacteria
B. Anaerobic bacteria
C. Aerobic bacteria
D. Viruses
31- Involucrum is:
A. Dead bone B. New live bone
C Previous live bone D. Sclerotic bone

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32- Hilton's method deals with:
A- Decompression of cyst
B- Drainage of an abscess
C- Biopsy removal
D- Pre-anaesthetic check-up
33- Which of the following features is not associated with acute osteomyelitis of
mandible:
A- Severe pain
B- Purulent exudates
C- Paresthesia of lower lip
D- Radiographic evidence of bone destruction
34- The incision for drainage in ludwig's angina extends:
A. Up to the neck
B. To the angle of mandible
C. Floor of mouth
D. All of the above
35. A patient has a localized infection with pus formation. Treatment of choice is
to:
A. Wait for drainage
B. Establish drainage
C. Administer antibiotics
D. Apply cold to the area
36. After extraction of upper central incisor, patient develops ophthalmoplegia,
meningitis and lateral rectus paralysis. The diagnosis is:
A. Cavernous sinus thrombosis
B. Not related
C. Cellulites
D. Ludwig's angina
37- Incision and drainage in an area of acute infection should be perfonned
when:
A- Induration has occurred
B. Localization has occurred
C. Acute pain is present
D. Fever above 102 degree fahrenheit
38- Ludwig’s angina involves…………spaces.
A. Submandibular
B. Submental
C. Sublingual
D. All of the above

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39- Life threatening sequel of odontogenic infection include:
a. Lateral pharyngeal space infection
b. Frontal sinusitis
c. Cavernous sinus thrombosis
d. All of the above
40- Submandibular space involvement means spread of infection:
a. From mandibular molars below the attachment of the buccinators muscle
b. From mandibular premolars below the attachment of the mylohyoid muscle
c. From mandibular molars below the attachment of the mylohyoid muscle
d. From mandibular premolars above the attachment of the mylohyoid muscle
41- Intraoral lingual localization of an abscess in the vestibule means spread of
pus:
a. Below the mylohyoid muscle
b. Spread to sublingual space
c. Spread to the submandibular space
d. None of the above
42- Direct spread of infection from lower 8 could be towards:
a- Buccal side below the buccinator muscle
b- Lingual side above the mylohyoid muscle
c- Pterygomandibular space
d- None of the above
43- Major clinical presentation of the acute dentoalveolar abscess late stage
would be:
a- Swelling
b- Sever pain
c- Sever pain provoked by heat
d- None of the above
44- The most important therapeutic action in the management of orofacial
infections is:
a- Giving antibiotics
b- Release of trismus
c- Drainage of pus
d- Giving analgesics
45- In patient with acute dentoalveolar abscess early stage:
a- There is mild pain
b- The abscess is still confined to the periapical bone
c- It takes the form of subperiosteal abscess
d- None of the above

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46- Canine space infection:
a- Drained from the most dependent area extraorally
b- Significant space as it communicates with the emissary veins
c- Invaded through the infected root canals of canine and premolars
d- None of the above
47- Relief of pain in dentoalveolar abscess begins as soon as the pus:
a- Moves buccally or lingually according to the line of least resistance
b- Perforates the periosteum and exits into the soft tissues
c- Moves away from neural elements
d- None of the above
48- From the lower third molar tooth, direct spread of infection is commonly:
a- Below the buccinator muscle, so it appears extraorally
b- Above the mylohyoid muscle, so it appears in the sublingual space
c- Below the mylohyoid muscle, so it appears in the submental space
d- All of the above
49- From the principles of surgical drainage, the incision is performed deep
enough to explore all portions of the abscess:
a- True
b- False
50- In Garre’s osteomyelitis, the patient improves:
a- Immediately after evacuation of pus
b- Immediately after removal of the cause
c- Immediately after giving selected antibiotics
d- None of the above
51- Never do incision and drainage in unfluctuating area:
a- True
b- False
52- In patient with acute dentoalveolar abscess in early stage there is:
a- Sever throbbing pain provoked by cold
b- Feeling of tooth elongation
c- Negative regional lymphadenopathy
d- All of the above

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A 22-year-old woman developed spontaneous pain in the carious left lower 2nd
molar. 72 hours after the pain appeared, the patient noted massive facial
swelling that developed over a 24-hour period. Her mouth opening was 8 mm
and she had a raised floor of mouth.
53- What anatomical spaces may be involved:
a- Buccal, submasseteric and submandibular
b- Submasseteric and submandibular spaces
c- Submandibular, sublingual and pterygomandibular
d- Buccal and lateral pharyngeal spaces
54- What investigations should be performed?
a- Palpation
b- Excisional biopsy
c- Fine needle aspiration biopsy
d- Periapical radiography
A 49-year-old man experienced severe pain related to right upper 1st molar for
one week after which he had a high grade fever, difficulty of opening his mouth,
dysphagia, pain and swelling of the right buccal and temporal areas. Two days
later, he developed periorbital swelling, marked right-sided visual loss,
proptosis and progressive total opthalmoplegia in both eyes
55- What is the diagnosis?
a- Brain abscess following the buccal and temporal space infection
b- Cavernous sinus thrombosis following the masticator and parapharyngeal
space infection
c- Buccal and parapharyngeal space infection
d- None of the above
56- The infection spread upward to the:
a- Buccal space, the infratemporal space, finally to the orbit and from here,
bilaterally to the cavernous sinuses
b- Buccal space, pterygomandibular space infection leading to the
parapharyngeal space involvement
c- All of the above
57- How can a dentist manage this case
a- Diagnosis and treatment with intravenous broad spectrum antibiotics and
surgical intervention
b- Refer to oral and maxillofacial surgeon
c- Refer to a hospital
d- All of the above

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A patient presented complaining of painful diffuse swelling anterior to the right
ear which extend up to the zygomatic arch 24 hours after complicated maxillary
right third molar extraction. History revealed that symptoms of swollen right
eyelids, chills, fever and trismus had started five days after extraction.
58- What anatomical space may be involved in view of trismus?
a- Parotid space
b- Buccal space
c- Sublingual space
d- Infratemporal space
59- Right eyelid were swollen due to:
a- Pus formation
b- Edema
c- Orbital cellulitis
d- None of the above
60- The usual lack of fluctuation in this case is due to:
a- Pus formation deep under muscle that mask this sign
b- Lack of localization
c- Trismus
d- None of the above
61- What should be done to detect the presence of pus in this case:
a- Palpation
b- Inspection
c- Aspiration
d- All of the above
_____________________________________________________________
62- A 60 year old male patient suffering from masseteric space infection with
trismus, the best place of incision at:
a- Anterior border of the mandible
b- Posterior border of the mandible
c- Submandibular incision
d- None of the above
63- Periapical infection of mandibular second molar most commonly spreads
into:
a- Sublingual space
b- Submandibular space
c- Buccal space
d- Oral vestibule

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64- A 50 years diabetic female patient presented to you suffering from sever
swelling at submandibular region bilaterally with difficulty in breathing and
swallowing, the first step in his treatment is:
a- Through and through incision and drainage
b- Airway security
c- High protein diet
d- Proper antibiotic and analgesic prescription
65- An 18-year-old female patient suffering from inflammation of pericoronal
flap over mandibular third molar with severe pain and trismus, the
treatment should start with:
a- Antibiotic for anaerobic microorganisms
b- Antiseptic mouth wash
c- Irrigation under the flap with H2O2 and grinding of impinging cusp
d- Surgical removal of pericoronal flap
A 6.5-year-old male child presented with right facial swelling extending from the
lower border of the right zygomatic arch to the submandibular region. Initially,
it was a small swelling which started 3 weeks ago in the area of the right angle
of the mandible. It was firm and tender to touch and no fluctuation was elicited
on palpation. It was associated with mild pain and low-grade fever. The patient
had history of lower toothache. The interincisal opening was about 1.25 cm.
66- The swelling is:
a- Congenital
b- Neoplastic
c- Cystic
d- Inflammatory
e- None of the above
67- The involved space is:
a- Infratemporal space
b- Buccal space
c- Temporal space
d- Submasseteric space

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Time passing for untreated odontogenic infection:
68- The microorganisms became of mixed type more than either aerobic and
anerobic types.
a- True
b- False
69- Time favors decrease the number of anerobic bacteria by increase
oxygenation:
a- True
b- False
70- The virulence of microorganisms increases
a- True
b- False
71- Antibiotics giving with I & D:
a- No need for antibiotics in medically non-compromised patients
b- You can take culture and sensitivity from the I & D site
c- You can take culture and sensitivity if the patient is taking antibiotics
d- None of the above

72- The difference in the way of progression from a low-grade self-limiting

odontogenic infection to a life threateningfascial space invasion is primarily
related to:
a- The immunity of the patient
b- The use of antibiotics
c- Anatomical factors
d- All of the above
73- In patient with periodontal abscess:
a- The pain is not as severe as those observed in the acute dentoalveolar
abscess
b- The swelling is located more apically than in dentoalveolar abscess
c- The tooth is non-vital
d- All of the above
74- One clinical presentation of the acute dentoalveolar abscess in late stage
would be:
a- Sever pain
b- Swelling
c- Fistula formation
d- All of the above

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75- Radiographic examination of acute dentoalveolar abscess in early stage
could be:
a- Disruption of the lamina dura of the involved root
b- Seen only if it is acute exacerbation of chronic abscess
c- Negative
d- All of the above
76- Pathway of direct spread of dentoalveolar abscess in an early stage could
be:
a- Line of least resistance
b- Virulence and number of the microorganisms and the resistance of the
patient
c- Anatomic location of the root’s apices and the muscle attachments relative
to them
d- All of the above

Essay questions:
- Discuss clinical features and treatment of Ludwig’s angina
- Identify purposes of incision and drainage
- Summarize clinical findings of suppurative osteomyelitis
- Explain Ludwig’s angina and lateral pharyngeal space are potentially lethal
infections
- On the bases of culture and antibiotic sensitivity testing; discuss the
principles applied for choosing the proper antibiotic
- What are the direct spread possibilities of acute periapical abscess related
to mandibular first molar

Answers
1- D 2- C 3- B 4-C
5- A 6-D 7- C 8- C
9- A 10- B 11- D 12- A
13- B 14- D 15- B 16-D
17- B 18-D 19-D 20-A
21-A 22-D 23-D 24-B
25- B
26-C 27-B 28-C 29-D 30-A 31- B
32- B 33-D 34-C 35-B 36-A 37-B 38- D

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39-D 40- C
41- B 42- C 43-a 44-c
45-b 46-b 47-b 48-a
49-b 50-d 51-b 52-b
53-c 54-a 55-b 56-c
57-c 58-d 59-c 60-a
61-d 62-a 63-a 64-b
65-c 66-d 67-d 68-B
69-B 70-A 71-B

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