Oral & Maxillofacial Infection

 Definition
- Infection is the “Invasion of the body by pathogenic microorganisms & the
reaction of the body to them”.
- Inflammation  Bodily reaction towards an insult (parasite – burn – insect –
bacteria, ect…..). The reaction is "a defense mechanism that limits, localizes
& destroys the insult".

 Spread of infection
- Infection tends to spread from local areas to remote areas through the following
routes:
1) Local spread 2) Lymphatics 3) Blood stream 4) Tissue continuity
1) Local spread (tissue fluids):
- Infection spreads locally through tissue fluids, depending on;
a) Functional status of capillaries:
Pathogenic microorganisms move with tissue fluids from areas of high
pressure to areas of lower pressure.
b) Pulsation of vessels:
Pulsations push pathogenic microorganisms away from site of infection.
c) Movements of muscles:
Muscle contractions aid in pushing tissue fluids filled by pathogenic
microorganisms away from site of infection.
2) Lymphatics:
- Infection of the head and neck region is drained by regional lymph vessels to
the regional lymph nodes (e.g. Submandibular LND, Sublingual LND,
Submental LND, Preauricular LND, Buccal LND) causing inflammation of
the lymph node (lymphadenitis).
- The inflamed lymph node will become enlarged, palpable, tender, and soft.
3) Blood stream:
- Pathogenic microorganisms invade blood through injured blood vessels and
thus are carried to remote areas of the body causing lung or brain abscesses.
- Pathogenic microorganisms cause inflammation of the walls of veins
(thrombophelebitis) producing thrombi and septic emboli in the systemic
circulation resulting in pyemia, bacteremia, or septicemia.
- Veins of the body are valvular; this allows blood to move only in one
direction towards the heart. On the other hand veins of the head & neck are
valveless; this allows blood to move in both directions but in fact gravity
causes blood to move towards the heart, also pathogenic microorganisms in
veins of the head & neck can move in either direction.
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- Emissary veins:
Def.: “Veins that pass through skull foramina to connect
intracranial veins (dural venous sinuses) with extracranial
veins.”
Function: Equalize intra and extra cranial pressures
Disadv.: Spread of infection (If it spreads intracranially it may cause
cavernous sinus thrombosis)
Number: Nine emissary veins are present (2 from sup sagittal sinus, 3
from sigmoid sinus, 4 from cavernous sinus)
4) Tissue continuity (direct spread):
- Infection may spreads directly from one region to other through fascial spaces

Acute Dento-Alveolar Abscess (ADAA)

- Definition:
It is a circumscribed suppurative type (pus forming) of inflammation involving
primarily the tooth and the investing alveolar bone.
- Types (Stages):
(I) Early stage: Inflammation is confined to the investing bone without
involvement of the overlying soft tissues.
(II) Late stage: Inflammatory exudate perforates the bone and burrow through
the fascial planes to distant parts of the face.
- Etiology:
- The pathogenic microorganisms gain entrance into the periapical tissues
through any of the following routes:
1- Dentinal tubules & pulp of a carious or fractured tooth.
2- Gingival crevice and periodontal membrane of a periodontally affected tooth.
3- Accidental pulp exposure during an operative procedure.
4- Direct extension of infection from adjacent infected tooth.
5- Blood stream in patients suffering from bacteremia or septicemia.
(I) ADAA of Early stage:
a) Signs & Symptoms:
1- Severe throbbing pain.
2- Patient feels elongation of the tooth.
3- Severe tenderness to percussion and touch.
4- Fever & malaise
5- Lymphadenitis.
6- No swelling can be detected in this stage.
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b) Radiographic picture:
- Negative
 No changes can be noticed except for a slight widening of the periodontal
ligament space in the periapical area & interruption of the lamina dura.
- An ill-defined radiolucency is only seen if the condition is the result of acute
exacerbation of a chronic infected tooth.
N.B: Periapical cyst or granuloma  Well defined radiolucency
c) Pathogenesis:
Microbial irritation of the pulp  Pulp hyperemia (Pain on hot & cold that
disappears quickly if stimulus is removed)  Pulpitis (More prolonged pain on
hot & cold)  Pulp necrosis (Loss of sensation of the pulp) Acute periapical
periodontitis (Thickening of lamina dura)  Periapical abscess (Extrusion of
tooth, pain & tenderness, breakdown of alveolar bone)  Alveolitis (Irregular
radiolucent area around apex of tooth, interruption of lamina dura).
d) Treatment:
1- Analgesics for pain.
2- Antibiotics
3- Anaesthesia for operative manipulation (Nerve block anaesthesia is indicated,
but if proper anesthesia is not obtainable by nerve block techniques then
general anaesthesia is indicated. / Avoid Infiltration anaesthesia)
4- Drainage through the pulp by violating the apex during root canal treatment or
through the socket by extraction of the affected tooth.
5- Treatment of the causative tooth (Root canal treatment with or without
apicoectomy OR Extraction)
Extraction is done if root canal filling can’t be performed (e.g. severe
curvature, or apicoectomy is difficult as in molars & lower canines, or tooth is
loose, or tooth is deciduous), or there is insufficient periodontal support, or
there is a vertical root fracture, or the tooth is mutilated & non-restorable.
6- Postoperative care (Gentle irrigation of the socket)
e) Fate:
1- Resolution
2- Progress to ADAA of late stage
3- Chronic dento-alveolar abscess

(II) ADAA of Late stage:

a) Signs & Symptoms:
1- Deep, dull aching pain.
2- Swelling which is at first brawny hard; but as more pus is formed it becomes
fluctuant. (Site of swelling depends on the tooth involved and its relation to
the fascial spaces in the vicinity)
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3- Trismus
4- Skin over entire region of infection is tender to palpation
5- Lymphadenitis
6- Fever, malaise, loss of appetite, and headache.
b) Radiographic picture:
Ill-defined radiolucent area in the periapical region, widening of the periodontal
ligament space and interruption of lamina dura.
c) Pathogenesis:
ADAA of early stage or acute exacerbation of chronic abscess  Breaks through
the alveolar bone  Formation of subperiosteal abscess  Pus ruptures through
the mucous membrane OR Infection burrows through different tissue spaces
causing cellulitis then a chronic skin fistula.

 Factors governing spread of infection

A) Microbial factors B) Host physiological factors C) Host anatomical factors
A) Microbial factors:
Pathogenicity: Is the ability of microorganism to cause a disease, and this depends
on; i) Virulence of microorganism
ii) Number of microorganism
i) Virulence of microorganism:
- Microorganisms are capable of producing disease in susceptible hosts by:
a) Enzymes:
e.g1. Staphylococci  Coagulase enzyme  Favor formation of fibrin at site of
infection  Favor localization of infection
e.g2. Streptococci  Fibrinolysin & Hyalurnidase enzymes  Dissolve fibrin
around infection  Favor spread of infection
b) Chemotaxis:
Microorganisms attract leucocytes (PMNL) outside the blood vessels to areas of
infection by Chemotaxis.
e.g1. Staphylococci  Great chemotactic effect on PMNL  Accumulation of
large number of PMNL around invading microorganism  Favor
localization of infection.
e.g2. Streptococci  Less chemotactic effect on PMNL  Limited number of
PMNL around invading microorganism  Favor spread of infection.
c) Mode of growth:
e.g1. Staphylococci  Grows in groups or colonies  Favor localization of
infection.
e.g2. Streptococci  Grows in chains  Favor spread of infection.

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d) Toxins
- Exotoxins are substances produced & excreted by bacteria during
multiplication.
- Endotoxins are substances released by bacteria when they are killed by PMNL
or antibiotics.
e.g. Bacteroids Proteolytic enz.  Destroys fibrin  Spread of infection.
 Heparinase enz.  Inactivates the anticoagulant effect of
heparin causing thrombophelebitis.
ii) Number of microorganism:
- It was estimated that the number of microorganisms required to produce an
invasive tissue infection is 10 million/ml of body fluid.
Virulence × Number of organism (disease process equation)
Resistance of host

B) Host physiological factors:

i) Nutritional status of patient:
- Infection adversely affects the nutritional status of the patient through:
i- Interfere with food intake (dysphagia and trismus)
ii- Loss of salts by excessive sweating due to fever
iii- ↑ Demand for cellular energy (normal caloric requirement is 1.8 kcal/day
& it increases 11-13% for each 10 C increase in body temperature).
The end result is Starvation, as body starts to consume the endogenous fuel
available (Catabolic stress response).
- Infection becomes more severe because of malnutrition, and malnutrition
becomes worse because of the infection.
ii) Immuno-humoral mechanism:
- When antigen enters the body, it will stimulate formation of antibodies
forming Ag-Ab complex which will activate the complement system to
facilitate phagocytosis.
- Factors that reduce the immuno-humoral resistance are:
1) Deficiency of blood supply to the area  ↓ antibodies in the area
2) Presence of necrotic tissue
3) Foreign body and heamatoma
4) Chronic intake of steroids, radiotherapy & organ transplant therapy
5) Disease e.g Diabetes and HIV
C) Host anatomical factors:
- Position of tooth in alveolus
- Relation of tooth apex to muscle attachment
- Organization of deep fascia (fascial spaces)

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i) Position of tooth in alveolus:

- Maxillary teeth: vary in their position in the alveolus. Infection will go through path
of least resistance.
1 , 3 , buccal roots of 4 5 6 7 are covered buccally by a very thin cortical plate of bone
 Therefore infection will be seen buccally in the vestibule.
2 , palatal roots of 4 6 7 are much closer to the palatal cortical plate  Therefore
infection will be seen palatally.

- Mandibular teeth also vary in their relation in the alveolus.

1 2 3 4 5 are located closer to the labial cortical plate of bone  Therefore infection
tend to occur labially in the vestibule.
6 7 are located centrally in the alveolus  Therefore infection may occur buccally or
lingually.

ii) Relation of tooth apex to muscle attachment:

- Maxillary incisors:
1- Apices of maxillary incisors are located below the
attachments of levator labii superioris, nasolabialis,
& depressor septi muscles  So they limit the
superior spread of pus  infection will be seen
intraorally causing labial subperiosteal abscess.
2- However if pus breaks superior to these muscles
 upper lip abscess.
3- Also pus can break palatally  palatal subperiosteal
abscess.
4- Pus can also spread up into the nasal cavity.

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- Maxillary canines:
1- Pus breaking inferior to attachment of caninus ms (levator
anguli oris)  intraoral labial subperiosteal abscess.
2- Pus breaking superior to attachment of the caninus ms
 infraorbital space abscess (canine space abscess).
3- Also pus can break palatally  palatal subperiosteal
abscess.
- Maxillary premolars:
1- Pus can break buccally  buccal subperiosteal abscess.
2- Pus can break palatally  palatal subperiosteal abscess.
3- Infection may also spread to maxillary sinus.
- Maxillary molars:
1- Pus breaking inferior to attachment of the buccinator ms
 intraoral buccal subperiosteal abscess.
2- Pus breaking superior to attachment of the buccinator ms
 buccal space abscess.
3- Pus may also spread to maxillary sinus.
4- Pus can break palatally  palatal subperiosteal abscess.
- Mandibular anterior teeth:
1- Pus breaking labially superior to attachments of incisive
& mentalis muscles  intraoral labial subperiosteal abscess.
2- Pus breaking labially inferior to attachments of incisive &
mentalis muscles  extraoral subcutaneous abscess.
3- Pus breaking lingually superior to attachment of mylohyoid
muscle  sublingual space abscess.
4- Pus breaking lingually inferior to attachment of mylohyoid
muscle  submental space abscess.
- Mandibular premolars:
1- Pus breaking buccally  buccal subperiosteal abscess.
2- Pus breaking lingually superior to attachment of mylohyoid
muscle  sublingual space abscess.
- Mandibular molars:
1- Pus breaking buccally superior to attachment of buccinator ms
 buccal subperiosteal abscess.
2- Pus breaking buccally inferior to attachment of buccinator ms
 buccal space abscess.
3- Pus breaking lingually superior to attachment of mylohyoid
muscle  sublingual space abscess.
4- Pus breaking lingually inferior to attachment of mylohyoid
muscle  submandibular space abscess.
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iii) Organization of cervical fascia (fascial spaces):

- Fasciae are continuous layers of connective tissue consisting of superficial & deep
layers. They envelop all anatomic structures and direct the spread of infection.
- Fascial spaces are potential spaces (not empty spaces) between the layers of fascia.
These spaces communicate with each other and are normally filled with loose
connective tissues and various anatomical structures like veins, arteries, glands and
lymph nodes. (Space is a misnomer as there are no empty spaces in the tissues in actual
reality)
- Organization of the cervical fascia:
The neck is composed of:
1) Anterior (visceral) region;  devoted to aero-digestive function
2) Posterior (somatic) region;  containing muscles & vertebrae
I- Superficial fascia:
Attached to skin and invests the platysma & muscles of facial expression.
II- Deep fascia:
Invests muscles, vessels, nerves & viscera of the neck. It is further divided into:
i) Superficial layer (Investing layer) of deep cervical fascia:
It surrounds the neck like a collar, deep to the skin, superficial fascia and the
platysma. It splits to enclose two muscles, the trapezius (posteriorly) and
sternocleidomastoid (anteriorly).
ii) Middle layer of deep cervical fascia (Pretracheal fascia):
It lies anterior to the visceral compartment of the neck extending from the front
of one carotid sheath to the opposite one and splits in between to enclose the
thyroid gland.
iii) Deep layer of deep cervical fascia (Prevertebral fascia):
It lies infront of the prevertebral muscles and posterior to the visceral
compartment of the neck.
N.B: - Danger space (Space 4 of Grodinsky): is the potential space between alar fascia
& prevertebral fascia extending superiorly from base of skull to mediastinum
where infections can gain rapid access to thoracic cavity.
- Prevertebral space: is the potential space lying posterior to prevertebral fascia.
- The alar fascia lies between the retropharyngeal space & the danger space.
- Retropharyngeal space is bounded anteriorly by buccopharyngeal fascia &
posteriorly by alar fascia
- Carotid Sheath (Lincoln Highway) is found between the anterior & posterior
compartments of deep cervical fascia and it contains the Internal/Common
carotid artery, Internal jugular vein & Vagus nerve.
- 1ry fascial spaces  Spaces where pus passes to them directly from teeth.
(Vestibular, Canine, Buccal, Submental, Sublingual & Submandibular spaces)
- 2ry facial spaces  Spaces where pus passes to them through other infected
spaces.
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(1) Submental space:

a) Location: - One triangular space below the mandible in the anterior region.
b) Boundaries: - Above: Mylohyoid muscle.
- Below: Deep fascia, platysma, superficial fascia, & skin.
- Laterally: Anterior bellies of digastric muscle & mandibular body.
c) Contents: - Submental lymph nodes.
d) Communications: - Posteriorly with submandibular space.
e) Infection reaches space: - Infected submental lymph node.
- Dental infection in lower anterior teeth.
- Direct spread of infection from submandibular space.
- Symphyseal fractures of the mandible.
f) Signs & Symptoms: - Localized firm swelling beneath the chin.
- It does not affect mastication nor mandibular movements
because it’s away from muscles of mastication.
g) Treatment: - Extraoral submental incision & drainage in midline of neck.

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(2) Submandibular space:

a) Location: - It is extension from submental space bilaterally & it is located
below and medial to posterior aspect of mandible.
b) Boundaries: - Above: Mandible & Mylohyoid muscle.
- Below: Hyoid bone.
- Laterally: Skin, subcutaneous tissues, and platysma.
- Medially: Hyoglossus & digastric muscles.
c) Contents: - Submandibular LND, submandibular gland, facial a. & lingual a.
d) Communications: - Posteriorly with pterygomandibular & lat pharyngeal. spaces
- Anteriorly with submental space around the digastric ms.
- Superiorly with sublingual space.
e) Infection reaches space: - Infected submandibular lymph node.
- Dental infection in lower posterior teeth (especially
lower 7 & 8) below attachment of mylohyoid muscle.
- Spread of infection from one of the communicating
spaces.
f) Signs & Symptoms: - Extraoral swelling below the mandible.
- Trismus (rare finding).
- Severe pain during swallowing (Dysphagia).
g) Treatment: - Extraoral Submandibular incision & drainage made 1cm
below & parallel to the lower border of the mandible to obtain
dependent drainage.

(3) Sublingual space:

a) Location: - It is a V-shaped trough lateral to the tongue.
b) Boundaries: - Above: Mucosa of the floor of the mouth.
- Below: Mylohyoid muscle.
- Laterally: Body of the mandible.
- Medially: Medial raphe of the tongue.
c) Contents: - Sublingual gland, submandibular gland (deep part) & duct.
- Genioglossus & Geniohyoid muscles.
- Lingual nerve and hypoglossal nerve
d) Communications: - Sublingual space of the opposite side.
- Submandibular space.
- Lateral pharyngeal & Pterygomandibular spaces.
e) Infection reaches space: - Dental infection in lower posterior teeth (especially
lower 5 & 6) above attachment of mylohyoid muscle.
-Spread of infection from one of communicating spaces

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f) Signs & Symptoms: - Intraoral unilateral or bilateral firm painful swelling of the
anterior part of floor of the mouth. (No anatomic barrier that
separates the sublingual spaces from each other)
- Tongue becomes stiff, elevated & protruded.
- Sialorrhea is common due to inability to clear secretions.
- Pain & discomfort during swallowing (Dysphagia).
- Patient may sit forward with flexion & extension of head &
neck to improve the airway.
- Lymphadenopathy
g) Treatment: - Intraoral incision & drainage in the floor of the mouth lateral
and parallel to sublingual duct. (Lack of dependent drainage)
- If the Submental or Submandibular spaces are also infected
the sublingual space is reached from the Submental or
Submandibular extraoral incisions. (Dependent drainage)
Ludwig’s Angina:
- Definition: Infection involving the submental space, bilateral sublingual spaces,
& bilateral submandibular spaces (All 5 spaces).
- Etiology: Dentoalveolar abscess  Submandibular space  Sublingual space
 Opposite sublingual space  Opposite submandibular space 
Submental space.
- Signs & Symptoms:
1- Rapidly (24hrs) developing brawny “board like” swelling in floor of the mouth.
2- Swelling is firm, painful, diffuse, & shows no evidence of localization.
3- Difficulty in swallowing & breathing.
4- Tongue is stiff, elevated, and protruded having a wooden appearance.
5- High fever, rapid pulse, fast respiration, & moderate leukocytosis.
6- Complete airway obstruction can occur resulting in suffocation then death. (it is
an emergency situation)
- Treatment:
1- Anaesthesia:
- General anaesthesia  it is difficult to insert the endotracheal tube, so
awake intubation is recommended.
- Local anaesthesia  it can be obtained by regional cervical block
analgesia.
2- Tracheostomy:
- It should be ready & kept as a last resort to be used in case of emergency.
3- Surgery: (A secure airway must be established before surgical therapy)
- Incision  incision of all involve spaces

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- Drainage  evacuation of pus from all locules is done using a curved

heamostat, then a pen rose drain or corrugated rubber drain is inserted to
pass through & through from one incision to the other (through & through
drain connecting the involved spaces)
- Dressing of the wound then follows.
4- Antibiotics & Supportive measures:
- Massive doses of antibiotics are given.
- High caloric diet
5- Culture & sensitivity tests:
6- Postoperative care:
- Dressing is changed every 24-48 hrs & daily irrigation is performed
(4) Buccal space:
a) Boundaries: - Above: Zygoma.
- Below: Inferior border of the mandible.
- Antero-medial: Buccinator muscle.
- Postero-medial: Masseter, anterior border of the ramus.
- Lateral: Skin & fascia.
- Posteriorly: Pterygomandibular raphe.
b) Contents: - Buccal pad fat (act as impediment for spread of infection)
- Parotid gland duct
- Buccal lymph node
- Facial vessels & nerve
c) Communications: - Posteriorly  Pterygomandibular space.
- Superiorly  Infratemporal space.
- Inferiorly  Submandibular space
- Anteriorly  Infraorbital space
d) Infection reaches space: - Dental infection in lower posterior teeth (1st molar &
premolars) below attachment of buccinator muscle.
- Dental infection in upper posterior teeth (molars &
premolars) above attachment of buccinator muscle.
- Spread of infection from communicating spaces.
f) Signs & Symptoms: - Extraoral swelling in cheek.
g) Treatment: - Intraoral horizontal incision & drainage in the vestibule
(preferably the mandibular vestibule), through the attachment
of the buccinator muscle into the buccal space.
- Also an extraoral incision (submandibular approach) can be
done to obtain dependent drainage.

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(5) Pterygomandibular space:

a) Boundaries: - Above: Lateral pterygoid muscle.
- Below: Pterygomasseteric sling
- Anteriorly: Pterygomandibular raphe
- Posteriorly: Parotid gland
- Laterally: Medial surface of ramus.
- Medially: Medial pterygoid muscle.
b) Contents: - Lingual & Inferior alveolar nerves
c) Communications: - Posteriorly  Lateral pharyngeal space.
- Anteriorly  Buccal space
- Laterally  Submasseteric space
- Superiorly  Infratemporal space
d) Infection reaches space:
- Contaminated needles during inferior alveolar nerve block injections.
- Dental infection from lower 3rd molars (e.g Pericoronitis)
- Spread of infection from one of the communicating spaces.
- Angle fracture of the mandible.
f) Signs & Symptoms:
- Dysphagia & numbness of the lower lip & tongue maybe observed.
- Tenderness on palpation of the medial aspect of the mandible
- Severe Trismus due to involvement of medial & lateral pterygoid ms.
g) Treatment:
- Intraoral I & D just medial to anterior border of the ramus & lateral to the
pterygomandibular raphe
(6) Infratemporal space:
a) Location: - It is considered the upper part of Pterygomandibular space
- It is at the intersection of the deep temporal space superiorly & the
pterygomandibular space inferiorly.
b) Boundaries: - Laterally: Masseter, zygomatic arch, ramus, & temporalis.
- Medially: Lateral & medial pterygoid muscles.
c) Contents: - Maxillary artery & n. - Pterygoid venous plexus (Dangerous)
- Mandibular nerve & its branches
d) Communications: - Pterygomandibular space
e) Infection reaches space:
- Dental infection in upper molar teeth specially 8.
- Spread of infection from one of the communicating spaces
- Contaminated needles during posterior superior alveolar nerve block injections.
f) Signs & Symptoms: - Marked limitation of mouth opening (Trismus).
- Swelling over the temporal region.
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g) Treatment: - Intraoral I & D buccal to upper 3rd molar.

- Extraoral I & D in the temporal region within the hairline.
N.B: One of the potential spaces for displacement of maxillary 3rd molars
(7) Lateral pharyngeal space:
a) Location: - It is a cone-shaped space lateral to the pharynx
b) Boundaries: - Laterally: Medial pterygoid ms, Angle of the mandible.
- Medially: Superior & middle constrictor ms of the pharynx.
c) Contents: - Carotid sheath
d) Communications: - Pterygomandibular space - Retropharyngeal space
- Submandibular space - Sublingual space
e) Infection reaches space: - Dental infection from lower 3rd molar.
-Spread of infection from one of communicating spaces
f) Signs & Symptoms: - Limitation of mouth opening & severe pain on deglutition.
- Hearing disturbances due to blockage of eustachian tube
- Dysphonia (due to pressure on recurrent laryngeal n.)
g) Treatment: - Intraoral I & D medial to anterior border of the ramus if
patient mouth can be opened.
- Extraoral I & D one cm behind the angle of the mandible.
(8) Retropharyngeal space:
a) Location: - It lies behind the pharynx
b) Boundaries: - Anteriorly: Post. pharyngeal wall. (Buccopharyngeal fascia)
- Posteriorly: Alar fascia.
- Laterally: Carotid sheath & lateral pharyngeal space
- Superiorly: Base of skull
- Inferiorly: Mediastinum
c) Contents: - Retropharyngeal LND (That’s why it always occur children < 6 yr)
d) Communications: - Laterally  Lateral pharyngeal space
- Inferiorly  Superior mediastinum (very dangerous)
e) Infection reaches space: - Spread of infection from lateral pharyngeal space.
f) Signs & Symptoms: - Severe pain on deglutition (odynophagia & dysphagia),
airway obstruction (dyspnea) & hot potatoe voice (dysphonea)
g) Treatment: - Intraoral incision & drainage
(9) Submasseteric space:
a) Location: - It is a space found lateral to the ramus of the mandible
b) Boundaries: - Laterally: Masseter muscle
- Medially: Ramus of the mandible.
- Superiorly: Zygomatic arch
- Inferiorly: Inferior border of the mandible
- Posteriorly: Parotid gland
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c) Contents: - Masseteric a. & v.

d) Communications: - Pterygomandibular space medially
- Buccal space anterior
- Superficial temporal space superiorly
e) Infection reaches space:
- Dental infection from lower 3rd molar (e.g. Pericoronitis).
- Spread of infection from one of the communicating spaces.
- Angle fracture of the mandible
f) Signs & Symptoms: - Severe limitation of mouth opening (Trismus).
- Moderate facial swelling confined to lower area of ramus
g) Treatment: - Intraoral I & D lateral to anterior border of the ramus if
patient mouth can be opened.
- Extraoral I & D behind the angle of the mandible
(Dependent drainage).
(10) Infraorbital space (Canine space):
a) Boundaries: - Laterally: Buccal space & zygomaticus major muscle
- Medially: Nasal bone
- Superiorly: Orbital septum
- Inferiorly: Orbicularis oris muscle
- Posteriorly: Maxilla
- Anteriorly: Skin
b) Contents: - Angular artery
- Angular vein which communicates directly with cavernous sinus
through the superior & inferior Ophthalmic veins (Dangerous zone)
- Infraorbital foramen and nerve.
c) Communications: - Buccal space
d) Infection reaches space:
- Dental infection from upper canine (3)
- Spread of infection from one of the communicating spaces (i.e Buccal space).
e) Signs & Symptoms: - Facial swelling extending from the nose to anterior boundary
of the buccal space, & from the upper lip to the lower eyelid
g) Treatment: - Intraoral I & D parallel to & in the depth of the maxillary
vestibule.
N.B: Incase of infraorbital space infection it is contraindicated to give labial infiltration
anesthesia nor infraorbital nerve blocks. Extract the tooth under general anesthesia.

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(11) Temporal space:

a) Location: - It is a space that is divided by the Temporalis muscle into:
Superficial temporal space lodged between the temporalis fascia
& temporalis muscle.
 Deep temporal space lodged between the temporal bone and the
temporalis muscle
b) Signs & Symptoms: - Marked limitation of mouth opening (Trismus).
- Swelling over the temporal region.
c) Treatment: - Extraoral I & D in the temporal region within the hairline.
N.B:
# Submandibular spaces  Submandibular , Sublingual & Submental spaces
# Masticator spaces  Pterygomandibular, Submasseteric & Temporal spaces
# Parapharyngeal spaces  Lateral pharyngeal & Retropharyngeal spaces
# Temporal space  Superficial & Deep temporal spaces
# Single spaces  Submental & Retropharyngeal spaces
# Difficulty of breathing is observed in  Retropharyngeal, Lateral pharyngeal &
Submandibular space infections.
# Dysphagia is observed in  Retropharyngeal, Lateral pharyngeal,
Pterygomandibular, Sublingual &
Submandibular space infections.
# Trismus is observed in  Pterygomandibular, Submasseteric, Infratemporal,
Temporal & Lateral pharyngeal space infections.

 Signs & Symptoms of acute infection of different spaces:

- General Signs & Symptoms (Cardinal signs)
1- Swelling 2- Pain 3- Hotness 4- Redness 5- Loss of function
- Specific Signs & Symptoms
1- Site of swelling 2- Limitation of mouth opening 3- Dysphagia 4- Others
Space Swelling Limitation Dysphagia
Submental -Extraoral swelling below chin. -No limitation of mouth -Moderate
-No intraoral swelling. opening.
Submandibular -Extraoral swelling below mand. -Moderate limitation. -Moderate
-No intraoral swelling.
Sublingual -Intraoral swelling under tongue. -No limitation. -Moderate
-No extraoral swelling.
Buccal -Extraoral swelling over cheek. -Moderate limitation. -No
-Intraoral swelling over medial -Severe limitation. -Severe
aspect of the ramus.
Pterygomandibular
-Slight extraoral swelling below
angle of the mandible.

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 Oral & Maxillofacial Infection

 Treatment Principles of maxillofacial infection

1) Determine the severity of infection
Anatomical location
Rate of progression
Potential for airway compromise
2) Evaluate the host defenses
3) Decide on the setting of care
4) Treat surgically (Incision and drainage)
5) Support medically
6) Choose & prescribe antibiotic therapy
7) Administer the antibiotic properly
8) Evaluate the patient frequently
1- Determining the severity of infection:
A) Anatomic location:
- The anatomic spaces of the head & 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 cranial contents.
- A severity score (SS) was made to assign a numerical value of 1 to 4 for
involvement of each of the following anatomic spaces.
SS 1  Low risk to airway or vital structures (e.g. Vestibular,
Buccal, Infraorbital spaces)
SS 2  Moderate risk to airway or vital structures (e.g.
Submandibular, Sublingual, Submental,
Pterygomandibular, Submasseteric, Superficial, Deep
& Infratemporal spaces)
SS 3  High risk to airway or vital structures (e.g. Lateral,
Retropharyngeal spaces)
SS 4  Extremely high risk to airway or vital structures (e.g.
Danger space, Mediastinum, Intracranial infections,
Cavernous sinus thrombosis)
- 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 &
radiographic examination.
B) Rate of progression:
- Odontogenic infections pass through 3 stages before they resolve, these
stages are:
1) Inoculation: (The first 0-3 days)
- The swelling is soft and mildly tender

17
 Oral & Maxillofacial Infection

2) Cellulitis: (3 to 5 days)
- The swelling becomes hard, red, diffuse and tender between the 2nd
& 5th day with no evidence of pus formation yet.
3) Abscess: (After 5 days)
- The center of cellulitis begin to soften & become fluctuant & shiny
- The yellow color of the underlying pus may be seen through the
thin epithelium.
- Tenderness becomes more localized
- Finally resolution occurs after spontaneous or surgical drainage of the
abscess cavity.
C) Airway compromise:
- The most frequent cause of death in reported cases of odontogenic
infection is airway obstruction. Therefore rapid intervention is a must,
which is achieved by either of:
i) Endotracheal intubation:
It maybe difficult to be done incases of severe infection.
ii) Surgical airway:
- Cricothyroidotomy; incision at cricothyroid membrane
- Tracheostomy; incision at the 2nd or 3rd tracheal ring
- Clinical signs & symptoms of difficult intubation:
i) Trismus less than 20mm
ii) Decreased thyromental distance (Less than 5 cm)
iii) Deviation of airway laterally on a chest xray or anteriorly on a
lateral view
- Clinical signs & symptoms of partial airway obstruction:
i) Abnormal breath sounds such as stridor and wheezing
ii) Special posture that straighten the airway such as "sniffing
position" in which the head is inclined forward and the chin is
elevated, as if one is sniffing a rose.
iii) An oxygen saturation below 94% on the pulse oximeter indicates
insufficient oxygenation of the tissues.(Normal O2 saturation > 99%)
2- Evaluate the host defenses:
- The following medical conditions (diabetes, steroid therapy, organ transplant,
chemotherapy, chronic renal disease, malnutrition, malignancy, alcoholism,
leukemia, agranulocytosis, Aids) can interfere with proper function of the
immune system which is essential to maintain host defenses against infection.
- Fever increase fluid losses & caloric requirements (normal caloric
requirement is 1.8kcal/day & it increases 11-13% for each 1 degree centigrade
increase in body temperature).
- Infection & prolonged fever depletes the body energy stores & shift the body
metabolism into a catabolic state
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 Oral & Maxillofacial Infection

- Elderly individuals are not able to mount high fevers as children therefore
management of fever in these patients should be respected.
- The physiologic stress of a serious infection can disrupt well established
control of systemic diseases such as diabetes, hypertension & renal disease.
Therefore the surgeon should be careful to evaluate & manage concurrent
systemic diseases in conjunction with direct management of the infection.
3- Decide on the setting of care:
- Indications of hospital admission: (It is safer to go on side of hospital admission)
2) Fever greater than 38.3oC
3) Dehydration
4) Spaces with severity scores 2 & above
5) Need for general anaesthesia (Uncooperative patients as young children,
failure to achieve adequate local anaesthesia, need to secure the airway)
6) Need for inpatient control of systemic disease
4- Treat surgically:
- When to go to the operating room (general anaesthesia) ?
1) To establish airway security
2) Severity score more than 2
3) Involvement of multiple spaces
4) Rapidly progressing infection
5) Need for General anaesthesia
I) Airway security:
- An infrequently used technique that may aid in protecting the airway during
intubation is "needle decompression". In this technique, under local anaesthesia
an abscess of the pterygomandibular or lateral pharyngeal spaces is aspirated
with a large-bore needle inorder to decompress the surrounding tissues.
This maneuver will decrease the risk of abscess rupture during instrumentation of
the airway, redirects the drainage of pus into the oral cavity where it can easily be
removed, & obtain an excellent specimen for culture & sensitivity testing.
II) Surgical incision & drainage (I & D):
- Incision & Drainage (I & D) means surgical evacuation of pus.
# How to judge pus formation?
1) Pus is usually formed after the 5th day
2) Fluctuation on palpation
3) Red pointing appearance
4) Pitting edema (sign of accumulation of pus deep in tissue)
5) Recurrent sudden pyrexia (sign of pus formation)
6) No improvement with adequate antibiotic
7) Ultrasound
8) Needle aspiration
9) CT
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 Oral & Maxillofacial Infection

# Purposes (Importance) of surgical I & D: “Don’t let sunset on non drained pus”
1- Evacuation of toxic purulent material & gases.
2- Decompress the tissues & hence release the tissue tension.
3- Promote healing by ↑ oxygenation of the infected area
4- Prevent further spread of infection.
5- Relief of pain
6- Increase the efficiency of antibiotic
7- Prevent spontaneous drainage which leads to extraoral skin fistula & sinus.
# Principles of I & D:
1- Incision is placed in healthy skin or mucosa & not over most fluctuant area.
2- Incision is placed in esthetically acceptable areas e.g skin creases, tension lines
3- Incision is placed in dependent positions to encourage drainage by gravity.
4- Blunt dissection is used to avoid damage to nerves and vessels in the area, this
is done by advancing a closed hemostat (Artery forceps) into the incision and
opening it inside. All pus locules should be drained.
5- Drain is placed and secured with sutures to prevent its dislodgement.
# Drains:
- A drain facilitates the passage of pus or blood from the depth of a wound to
the surface.
- Types of drains:

Passive drains Active drains

1- Gauze drains 1- Vacuum drains

- It absorbs pus & blood that cause it’s - Used extraorally only.
plugging. - It is a perforated polyethylene tube
- Used both intra & extraorally. connected to a portable suction apparatus
- Replaced every 24-48 hrs. pinned to the patients gown.

2- Fenestrated rubber dam strips drains

- It does not absorb pus or blood.
- Used both intra & extraorally.
- Replaced every 24-48 hrs.

3- Corrugated rubber drains

- Used extraorally only.
- Does not need replacement, but each day
after irrigation it is shortened by scissors.

4- Penrose drains
- Used extraorally only.
- It is a thin perforated rubber tube.

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 Oral & Maxillofacial Infection

- Drain is inserted loosely into the depth of the wound or abscess cavity.
- A sufficient length should protrude beyond the external surface of the wound
to allow its removal easily.
- Drain all involved spaces
- Dependent drainage
- Through & through drains offer better drainage & irrigation
- Drain should be changed every 24-48 hrs.
- Drain is withdrawn when pus production has stopped on removal of the last
drain.
- Drains are also used after major surgical procedures to remove heamatoma,
serum, and inflammatory exudates formed.

III) Timing of incision & drainage (I & D):

- Optimum time for I & D has no hard rule to follow, but the presence of
fluctuation is the most important single feature that indicates that the abscess
is ready for drainage.
- However it is difficult to decide whether pus is present or not, so aspiration
maybe very helpful.
- Recently; immediate I & D after establishing a secured airway is done even if
there is no pus i.e in the cellulitis stage, because distended tissues will be
relieved, pain will be decreased, and spread of infection into other fascial
planes will be prevented.
- If an abscess is neglected; infection will either spread into other fascial planes
or discharge spontaneously and produce an external scar.
- Others give parenteral antibiotics & do I & D when drainable pus is formed.

IV) Removal of the cause:

1- Root canal treatment with or without apicoectomy
2- Extraction

V) Culture & Sensitivity:

- Culture: is done to know what type of bacteria is causing the infection, where
a culture swab is used to collect a sample of fluid or tissue & then
placing the sample on a special culture medium.
- Sensitivity: is done to know which type of antibiotic will work best to treat the
infection.
- Serious infections should be cultured first then gram stained to know the causative
organism & the sensitivity of the organism to different antibiotics, inorder to choose
the most appropriate antibiotic.
- Specimens for culture are taken by swabbing the infected site or the draining
fistula, or by aspiration.

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 Oral & Maxillofacial Infection

- Indications of culture & sensitivity:

i) Compromised host defence
ii) No improvement after 3 days (Persistent or hospital infection)
iii) Postoperative wound infection
iv) Recurrent infection
v) Osteomyelitis
5- Support medically:
- Medical supportive care for a patient with severe maxillofacial infection is
composed of:
1) Hydration:
- Fluid needs of body increases with each degree rise in body temp.
- If the patient is unable to take fluids by mouth, then intravenous
fluid therapy should be instituted to correct the water loss. This
water and electrolyte loss is either due to lack of water intake or
increased water excretion through sweating.
2) Nutrition:
- Rich protein diets are required to increase antibody production.
- Vitamins deficiency interferes with the immune response therefore
adequate amounts of vitamins should be supplied.
3) Control of fever:
- Adequate hydration is the best method to control fever.
- The next approach to control fever is acetaminophens & aspirin.
- Also cool sponges maybe used.
4) Reestablishment of electrolyte balance:
- Water & electrolyte disturbance is corrected by giving Ringer
lactate and dextrose intravenously by the drip method.
5) Control of systemic disease:
6) Control of pain:
- By prescription of analgesics.
6- Choose & prescribe the appropriate antibiotic:
7- Administer the antibiotic properly:
- READ APPLIED THERAPEUTICS PAGES 4-11 (3RD YEAR)
- Spreading type of infection with moderate to severe constitutional symptoms
need antibiotic therapy inorder to localize the infection & to abort the
inflammatory process completely if pus has not been formed yet.
- If pus is formed, the antibiotics tend to limit the spread of infection, relief
pain, decrease swelling, lowers pyrexia, and lead to immediate clinical
improvement but pus will never disappear unless incision and drainage is
done.
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 Oral & Maxillofacial Infection

- Prolonged intensive antibiotic therapy without incision & drainage will lead to
complete elimination of the pyogenic infection causing pus to become sterile,
and so called a “sterile abscess” or “antibiotic abscess”.
- Penicillin is the antibiotic of choice as it is effective against most gram +ve
cocci (staph. & strept.) and anaerobes.
- Augmentin (Amoxicillin/Clavulanate) has become an alternative to penicillin
due to the developing resistance of bacteria to penicillins.

8- Evaluate patient frequently:

- Signs of improvement: (2-3days)
1) Reduced swelling
2) Cessation of wound drainage
3) Declined leucocytosis
4) Decreased malaise
5) Improved airway

9- Treatment of complications of infection:

Extraoral skin fistula:
- An extraoral skin fistula results when an abscess burst spontaneously due to
its neglection.
- When the source of infection is removed, the sinus will usually heal
spontaneously leaving a residual fistulous tract & an extraoral ugly dimple or
scar.
- The dimple or scar is surgically excised by doing two elliptical incisions
through the skin, and then the skin is undermined and closed.
- The fibrous tract should be excised.

 Fatal complications of maxillofacial infection

(1) Orbital infections (Orbital cellulitis):
I) Route of spread:
- Paranasal sinuses
- Pterygoid venous plexus through a branch from the inferior ophthalmic vein
- Anterior maxilla through the angular vein to the ophthalmic veins
- Posterior maxilla through the infratemporal space
II) Signs & Symptoms:
- Edema & inflammation of eyelid
- Proptosis
- Painful eye movement
- Chemosis (edema of conjunctiva)
- Loss of visual acuity
- Opthalmoplagia
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 Oral & Maxillofacial Infection

III) Treatment:
- Hospitalization
- Broad spectrum antibiotic
- Culture & sensitivity
- Removal of the cause
- Incision & drainage if pus is identified in CT
(2) Cavernous sinus thrombosis:
I) Anatomy:
a) Position:
Cavernous sinus is a paired sinus (2cm long, 1cm wide) located on both
sides of sella turcica extending from superior orbital fissure anteriorly to
apex of petrous part of temporal bone posteriorly.
b) Relations: - Medially: Sella turcica with pituitary gld, Sphenoid air sinus
- Laterally: Temporal lobe of brain, Trigeminal ganglion
- Superiorly: Internal carotid artery
- Inferiorly: Body of sphenoid, Sphenoid air sinus
c) Structures inside the sinus:
- Internal carotid artery
- Abducent n. (VI) – Occulomotor n. (III) –Trochlear n. (IV) – Opthalmic
n. (V D1) – Maxillary n. (V D2)
(So signs & symptoms will be related to affection of these nerves)

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 Oral & Maxillofacial Infection

d) Tributaries: 1. Sup. Ophthalmic v.

2. Inf. Ophthalmic v.
3. Central vein of retina
4. Superficial middle cerebral v.
5. Sup. & Inf. petrosal sinuses
6. Emissary veins from pterygoid venous plexus
7. Spheno-parietal sinus
e) Communications: 1. Opposite cavernous sinus by intercavernous sinuses
2. Pterygoid venous plexus by three emissary veins
3. Facial v. (angular v.) by sup. & inf. ophthalmic veins
4. Pterygomandibular or infratemporal spaces
III) Source of infection:
1. Extension through pterygoid venous plexus & anterior facial vein.
2. Ear infection (Otitis media)
3. Antral infection (Ethmoid & sphenoid air sinuses)
4. Parotid infection
IV) Clinically:
1) Meningitis & Meningeal irritation:
Manifested by severe headache & stiffness of the neck, pyrexia, chills,
rapid pulse, sweating, vomiting, delirium, leukocytosis.
2) Orbital signs:
Due to venous obstruction, which is manifested by chemosis (edema of
conjunctiva), retinal & eyelid edema, ptosis, proptosis, pulsating
exophthalmus and raccoon eyes.
3) Occulomotor, Trochlear, Abducent nerves involvement:
Manifested by limitation of extraoccular movements, diplopia, fixed
dilated pupils, and ophthalmoplagia.
4) Ophthalmic & Maxillary n. involvement:
Pain & parasthesia over areas innervated by these nerves.
V) Imaging:
- MRI & angiography
VI) Treatment:
1) Hospitalization
2) Early massive antibiotics
3) Heparinization (to ↓ clotting mechanisms)
4) Cavernous sinus exploration & drainage (very rare)

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 Oral & Maxillofacial Infection

(3) Brain abscess (Intracranial extension):

I) Routes of spread:
- Ear infection
- Paranasal sinuses (Sphenoid & frontal air sinus)
- Orbital infection
- Odontogenic infection
II) Signs & symptoms:
- Headache (↑ intracranial pressure)
- Low grade fever
- Nuchal rigidity
- Mental state change
- Meningitis (high fever & seizures)
III) Diagnosis:
- By clinical findings
- Lumbar puncture
- CT scan
- MRI
IV) Treatment:
- Hospitalization
- Massive antibiotics (having the ability to cross the BBB)
- Culture & sensitivity
- Steroids (to ↓ intracranial edema that may damage the brain)
- Remove the cause
- Incision & drainage (I & D) by trephination

(4) Mediastinitis:
I) Contents:
- Heart, aortic sheath, trachea, pulmonary artery, oesophagus & carotid a.
II) Routes of spread:
- Anterior neck  Carotid sheath
- Posterior neck  Retropharyngeal & Prevertebral spaces
III) Signs & symptoms:
- Fever
- Tachycardia
- Dyspnea
- Chest pain
- Leukocytosis
IV) Imaging:
Mediastinal widening more than 10cm in chest x-ray

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 Oral & Maxillofacial Infection

V) Treatment:
- Hospitalization
- Massive antibiotics
- Supportive measures
- Remove the cause
- Incision & drainage (I & D)

(5) Necrotizing fasciitis:

I) Definition:
"It is a rapidly spreading infection along the superficial fascia causing
subcutaneous necrosis due to thrombosis of vessels & compromised blood
supply."
II) Predisposing factors:
Immunocompromised patients
III) Clinically:
- Dusky purple discoloration of the skin
- Vesicles
- Purulent discharge
- Necrosis of skin
- Bad odour
IV) Causes of death:
- Necrotizing mediastinitis
- Disseminated Intravascular Coagulation (DIC)
- Fluid & electrolyte disturbance
- Acidosis & shock
V) Treatment:
- Hospitalization
- Massive antibiotics
- Supportive measures
- Debridement
- Incision & drainage (I & D)
- Antiseptic dressing
- Hyperbaric oxygen

(6) Ludwig’s angina:

SEE PAGE 11

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 Oral & Maxillofacial Infection

Osteomyelitis
- Definition:
It is an inflammation of bone & bone marrow with tendency for progression.
- Classification:
(A) Suppurative (Pyogenic) Osteomyelitis:
1. Acute suppurative osteomyelitis
2. Chronic suppurative osteomyelitis
(B) Non Suppurative Osteomyelitis:
1. Chronic sclerosing osteomyelitis
- Diffuse
- Focal
2. Chronic sclerosing osteomyelitis with proliferative periostitis (Garre’s
Osteomyelitis)
(C) Osteomyelitis accompanying systemic disease:
1. Syphilitic osteomyelitis
2. Tuberculous osteomyelitis
3. Actinomycosis
(D) Radiation Osteomyelitis (Osteoradionecrosis)
(E) Chemical Osteomyelitis
- Predisposing factors:
- Decreased blood supply
- Compromised host defences
- Bacterial factors (Virulence) e.g. Streptococci, anaerobes
- Etiology:
1. Odontogenic infection e.g. periapical abscess, periodontal abscess
2. Trauma e.g. compound fractures, gun shot injuries
3. Radiation e.g. osteoradionecrosis
4. Chemical e.g. arsenics used in endodontic treatment
5. Heat e.g. lack of coolant during cutting of bone with surgical burs
6. Heamatogenous spread which occurs in malnourished children
- Incidence:
Mandible > Maxilla due to: ↓ blood supply & ↑ bone density
- Pathogensis:
Bacterial inoculation  Inflammation  Pus formation  ↑ intramedullary
pressure  ↓ blood supply  Spread of infection  Cortex perforation & ↓
periosteal blood supply  Fistula formation draining pus.

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 Oral & Maxillofacial Infection

- S&S, Radiographic picture & Treatment of Suppurative Osteomyelitis:

Acute Suppurative Osteomyelitis Chronic Suppurative
Osteomyelitis
S&S - Deeply seated severe pain - In addition to signs & symptoms
- Teeth involved are loose & tender of the acute stage:
- Swelling of bone & overlying soft - Pain is less severe
tissues - Sequestration: a dead necrosed
- Bad odor (mimics malignancy) bare bone that become separated
- Trismus, parasthesia of lip (inf. from the living bone
alveolar n.) & pain radiating to the - Sinus tract discharging pus
ear are seen if mandible is affected. - Finally pathologic fracture of the
- Regional lymphadenopathy, fever mandible may occur
- Leukocytosis, ↑ ESR.
X-ray - Negative - Moth eaten appearance (Punched
(Panorama out appearance  Irregular
CT) radiolucencies [granulation tissue]
on areas of sclerotic radioopacities
[sequestrum].
- Sequestrum (dead bone) is more
radioopaque then living bone
because it attracts calcium salts
- Sequestrum is separated from
living bone by a radiolucent line
- Subperiosteal bone formation
(involacrum) can be seen, as an
attempt to strengthen the weakened
bone.
- Sclerosing Osteomyelitis is seen
as Onion peal appearance due to
subperiosteal bone formation.
(MRI - Early detection by MRI & Bone
Bone scan) scan (Tc 99 & Gallium 67)
Treatment 1. General supportive measures: 1. General supportive measures:
- Bed rest - Bed rest
- High caloric diet - High caloric diet
- Fluids - Fluids
- Analgesics for pain - Analgesics for pain
- Multivitamins - Multivitamins
- Heat therapy - Heat therapy
2. Culture & Sensitivity test for 2. Culture & Sensitivity test for
choosing specific antibiotic. choosing specific antibiotic.

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 Oral & Maxillofacial Infection

3. Empirical antibiotics till Culture 3. Sequestrectomy: is the surgical

& sensitivity removal of the loose sequestrum
4. Surgical drainage as early as (dead bone).
possible. 4. Saucerization: is the trimming of
the sharp bony margins that appear
after sequestrectomy.
5. Trephination: drains pus
6. Decortication: is done in
resistant cases by surgical removal
of the buccal cortical plate of bone
& insertion of a catheter to irrigate
the affected area with saline &
antibiotics.
7. Hyperbaric oxygen therapy: is
the inhalation of 100% oxygen
under 2.4 atmospheric pressure for
90 minute (dive), which:
- Reverse hypoxia (↑oxygen blood
supply to the ischemic areas)
- Enhance osteogenesis
- Enhance collagen formation
- Enhance Angiogenesis (↑blood
supply)
- Has a bactericidal action.
- Neutralizes toxins
- Enhance leukocytic function
- Accelerates sequestration
Its use is contraindicated in patients
with Glaucoma & pulmonary
obstructive disease
8. Stabilize the fractured bone by
external pin fixation.
9. Antibiotic impregnated beads
10. Wound irrigation systems
11. Resection of the affected area
when all other treatment measures
have failed.

Osteoradionecrosis (Radiation Induced Osteomyelitis)

- Radiation effects: (Life time effect)
1) Hypoxia 2) Hypocellularity 3) Hypovascularity

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 Oral & Maxillofacial Infection

- Etiology:
- Trauma to radiated bone
- Spontaneous
- Mandible > Maxilla
- Radiation doses > 5000-6000 Rads
- Clinically & radiographically:
As Osteomyelitis
- Treatment:
1) Hospitalization
2) Supportive measures
3) Antibiotics
4) Culture & sensitivity
5) Hyperbaric oxygen (20-30 dives)
6) Debridement
7) Post debridement hyperbaric oxygen (10 dives)
8) Reconstruction by microvascular grafts
- Prevention:
# Pre radiation
1) Extract hopeless non restorable teeth
2) Restore remaining teeth
3) Scaling & gum treatment
4) Flouride application

# Post radiation
1) Do not wear denture for 1 year
2) Use salivary substitutes
3) Root canal treatment is better than extraction (antibiotic prophylaxis &
avoid over instrumentation)
4) If extraction is necessary then:
- It should be atraumatic
- Use local anaesthesia with no vasoconstrictor
- No extensive flaps
- Prophylactic antibiotic
- Hyperbaric oxygen (20 dives pre & 10 dives post extraction)

N.B: Patients with osteoporosis take medications containing Bisphosphonates that

inhibit bone resorption inorder to increase the bone density (on expense of bone
marrow spaces).
Care should be taken during treatment of these patients as any trauma can cause
Bisphosphonate related Osteonecrosis of the jaws in these patients.

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 Oral & Maxillofacial Infection

Dry Socket (Localized Osteomyelitis)

Alveolar Osteitits
- Definition:
It is a complication of dental extraction in which the blood clot disintegrates
exposing the bony walls of the socket, and it is associated with severe pain and
foul odor.
- Etiology:
I) Bacterial component: Disintegration of blood clot due to contamination of the
socket by bacteria.
II) Traumatic component: as traumatic extraction
III) Other factors:
1. Pre existing infection
2. Use of L.A with vasoconstrictor, especially with infiltration technique.
3. Use of non sterile instruments
4. Spitting following extraction
5. Excessive post extraction irrigation or curettage of the socket
6. Patients with systemic disease which affects the reparative power of the body
e.g. diabetes
7. Smoking
- Signs & Symptoms:
1. Severe pain
2. Socket with bare bone or containing necrotic clot
3. Foul odor and taste
- Treatment:
Goal of treatment is to relieve pain which is achieved by:
1. Daily irrigation with warm saline or antiseptic mouth wash
2. Placement of a suitable dressing loosely inside the socket e.g. ZnO &
eugenol which is changed on daily base
3. Analgesics & Antibiotics

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 Oral & Maxillofacial Infection

Pericoronitis
- Definition:
Inflammation of the soft tissues surrounding the crown of a partially erupted
tooth.
- Etiology:
1. Bacterial growth under soft tissue flap.
2. Traumatic irritation of the inflamed soft tissue flap by the cusps of the
opposing tooth.
- Incidence:
Age: 20-25 years
- Signs & Symptoms:
Acute Pericoronitis Subacute & Chronic Pericoronitis
1. Severe pain 1. Dull pain
2. Trismus 2. Stiffness
3. Dysphagia 3. Pus under flap
4. Bad odour 4. Bad taste
5. Lymphadenitis 5. Lymphadenitis
- Treatment:
A) Conservative treatment:
(If the operculum covers less than 1/3 of the occlusal surface of the tooth)
1. Selective grinding of opposite tooth.
2. Irrigation under flap.
3. Rinse with warm saline & hydrogen peroxide mouth wash.
4. Antibiotics & Analgesics.
B) Surgical treatment:
1. Operculectomy (Removal of the soft tissue flap covering the occlusal surface
of the tooth) by electrocautery or by a scalpel.
OR
2. Removal of the offending tooth (If the operculum covers more than 1/3 of the
occlusal surface of the tooth)

33