Space infection

By,
Nr. Melesse
 INTRODUCTION
• Odontogenic infections are the most common of
all infections of head and neck . Although most
of these infections can be managed successfully
with minimal complications, some can produce
serious morbidity and even death.
• The key to successful management is prompt
therapy.
• The use of antibiotics has had a profound
influence on the treatment of the space
infections not only by aiding the body’s
own defenses but also by permitting
earlier surgical intervention .
 MICROBIOLOGY
• The bacteria that cause infection are most
commonly part of the indigenous bacteria .
• Odontogenic infections are no exception ,
since the bacteria that cause odontogenic
infections are the normal oral flora .
• Table 16.3 page 411 Peterson
FACTORS INFLUENCING THE SPREAD
OF INFECTION
• GENERAL FACTORS
A) Microbial factors
B) Host factors
C) Combination of both
D) Environmental factors
• LOCAL FACTORS
Alveolar bone
Periosteum
Fascia
Muscles
MICROBIAL FACTORS HOST FACTORS

Level of virulence General state of health

No of organisms introduced into the Integrity of surface defenses

body

Degree of invasiveness Level of immunity

Impact of medical intervention

 FASCIA
• The term fascia is used to describe the
broad sheaths of dense connective tissue
whose function is to separate the
structures that must pass over each other
during movement ,such as muscles and
glands and serve as path ways for the
course of vascular and neural structures.
 FASCIA
 SUPERFICIAL FASCIA
 DEEP CERVICAL FASCIA
• 1) Anterior layer - Investing fascia
- Parotidomasseteric
- Temporal fascia
• 2) Middle layer -sternohyoid-omohyoid division
-sternothyroid-thyrohyoid division
-visceral division
Buccopharengeal fascia
Pretracheal fascia
Retropharengeal fascia
• 3) Posterior layer -Alar division
-Prevertebral division
 Carotid sheath
Superficial fascia
• Layer of dense connective
tissue that courses deep to
the subcutaneous tissue
throughout the body.
• Lies between the dermis of
the skin and the deep cervical
fascia.
• Contains the platysma ,
cutaneous nerves, blood,
lymphatic vessels
• Also contains a varying
amount of fat &loose areolar
tissue- its distinguishing
characteristic.
 Investing layer of Deep cervical fascia

• It lies under cover of platysma.

• It is the most superficial layer of
deep cervical fascia.
• It surrounds the structures of
neck.
• It is remarkable for the
frequency with which it splits
into two.
• Infection : Invasion and multiplication of
microorganisms in the body tissues,
especially that causing local cellular injury
due to competitive metabolism, toxins ,
intracellular replication or antigen-antibody
reactions.
• The location of infection from a specific tooth is
determined by 2 major factors
1) The thickness of bone overlying the apex of the
tooth.
2) The relationship of the site of perforation of
bone to muscle attachments of the maxilla and
mandible.
• Table 16.4 page 412 peterson
 Stages of infection
• 4 stages of infection.
 Inoculation
 Cellulitis
 Abscess
 Resolution
• Stage of Inoculation:
• Considered as early spread of infection
• Microorganisms enter the adjoining tissue spaces
and multiply with manifesting mild inflammatory
tissue reactions.
• This period may range from several hours to a few
days.
• Stage of Cellulitis:
• During this stage the microorganisms release the
toxins and other metabolic bye products ,which are
responsible for inflammatory reactions.
• The spread of the infection is facilitated by the
release of the toxins like streptokinase,
hyaluronidase & streptodornase .
• This period may range from 3-7 days.
• In this stage the process of the inflammation is
paramount, resulting in deeply reddened , diffuse,
indurated, tender swelling.
• Stage of abscess formation:
• In this stage , necrosis predominates.
• There is central softening of the cellulitic region,
which may become fluctuant.
• this stage manifests mostly after 5 days of onset
of infection.
• Stage of resolution:
• In10-15 days of time the pus and other
infected material may drain out of the tissue
spaces in the natural course or may be
evacuated by surgical means.
• After which the process of resolution sets in.
• This is supported by the immune system
through the antibodies and activated T
lymphocytes .
• Histologically this process is usually
described as round cell infiltration.
• Topaz table9-1
 ETIOLOGY
• The infections that manifest in oro-facial region are
Odontogenic.
• Common cause
Periapical inflammation(acute dentoalveolar abscess)
Periodontal abscess
Non-vital teeth
Pericornitis
Tooth extractions
Periapical granulomas that cannot be treated
Infected cysts
• Rare causes
• Postoperative trauma
• Defects due to fracture
• Salivary gland lesions
• Lymph node lesions
• Infections as a result of local anesthesia
 CLASSIFICATION: Laskin
• Primary maxillary spaces
• Canine space
• Buccal space
• Infra temporal space
• Primary mandibular spaces
• Sublingual space
• Submandibular space
• Submental space
• Buccal space
• Secondary spaces
• Masseteric space
• Pterygomandibular space
• Superficial and deep temporal space
• Lateral pharyngeal space
• Retro pharyngeal space
• Pre vertebral space
 Principles In Treating Facial
Space Infections
• 1) Admission of the patient
• 2) Maintenance of airway
• 3) Determine severity of the infection
(Cellulitis or abscess)
• 4) Evaluate the state of patient host defensive
mechanism
a) Medical conditions that compromise host
defense.
b) Medical support to correct host defense
compromises.
• 5) Empirical antibiotic therapy .
• 6) Early surgical management by I&D.
• 7) Supportive therapy
• 8) Definitive treatment of infection after culture
sensitivity test.
• 9) constant re-evaluation of patient.
 Principles of incision and
drainage
• 1) Incise in healthy mucosa and skin when possible.
• 2)Place the incision in an esthetically acceptable area.
• 3)place the incision in a dependent position to encourage
drainage by gravity.
• 4)Dissect bluntly, with a closed surgical clamp or finger.
• 5) Place a drain and stabilize with sutures
• 6) consider the use of through-and-through drains in
bilateral space infections
• 7) do not leave the drains in place for an overly extended
period of time.
• 8) clean wound margins daily under sterile conditions to
remove clots and debris.
 CANINE SPACE
• It is the region in b/w
anterior surface of the
maxilla and overlying
muscles of the upper
lip.
• Boundaries :
• Superiorly: levator labii
superioris
• Medially : levator labii
superioris alaque nasii
• Laterally :
zygomaticus major
• Superficially: levator
labii superioris
• Deep : Anterior
surface of maxilla ,
levator anguli oris
• Contents:
- Infraorbital
nerve
- Angular artery &
• Clinical Features :
• oedema of the cheek and upper lip
• Obliteration of naso-labial fold
• Swelling of the upper lip produces a drooping of the
angle of the mouth
• Abscess is pointed below the medial canthus of the eye.
• Treatment:
• The incision is made intraorally high in the
maxillary vestibular sulcus.
• A small hemostat is inserted through the
levator anguli oris muscle into the abscess
cavity.
• A rubber drain is placed into the canine space
and sutured to the lower margin of the
incision
 BUCCAL SPACE

• Boundaries :
• Medially: The buccinator muscle and its covering
buccopharyngeal fascia
• Laterally :Skin & subcutaneous tissue
• Anteriorly: The posterior border of
the zygomaticus major muscle
above &
The depressor anguli oris muscle
below
• Posteriorly: The anterior edge of the masseter muscle
• Superiorly: Zygomatic arch
• Inferiorly : Lower border of the mandible
• Contents : Buccal fat pad
Parotid duct
Anterior facial artery and vein
Transverse facial artery and vein
• Communications:
• Buccinator muscle sweeps around the anterior border of
the mandible to join the superior constrictor muscle at
pterygomandibular raphae.
• This creates communication B/W buccal space and sub
massetric space.
• Infection also may pass B/W anterior border of masseter
muscle & the buccinator muscle to enter
pterygomandibular space.
• Infections from buccal space can extend upwards along
the course of the buccal fat pad to invade infra temporal
space & superficial temporal space.
• Infections may also pass around the posterior surface of
the maxilla to enter infra temporal portion of deep
temporal space
• Clinical features:
• It is a ovoid swelling.
• Swelling of cheek extending from the
zygomatic arch above and inferior border of
mandible below and from anterior border
masseter to corner of mouth.
• The skin appears red and shiny, with or
without fluctuation.
• Treatment :
• Intraorally , horizontal incision should be
placed just above the depth of the vestibule.
• This will provide dependent drainage as well
as prevents cutting of the parotid duct.
• Extraorally , two stab incisions are placed
below the lower border of the mandible b/c
this provides dependent drainage and
incisions are hidden under the shadow of the
mandible .
 Sublingual space
• Boundaries :
• Superiorly: oral mucosa
• Inferiorly : mylohyoid muscle
• Laterally & Anteriorly: Lingual aspect of the mandible
• Posteriorly : body of the hyoid bone (at the mid line)
• Medially :geniohyoid ,genioglossus, styloglossus
• Contents :
Sublingual gland
Wharton’s duct
Sublingual artery & nerve
Lingual nerve
• Communications:
• The styloglossus muscle passes B/W superior and middle
constrictor muscle muscles, lateral to the hyoid bone.
• This is known as buccopharyngeal gap.
• sublingual space infections pass through this gap to enter
LPS.
• It also communicates with submandibular space at
the posterior border of the mylohyoid muscle where
the submandibular gland curves around the free edge
or the posterior border of the mylohyoid muscle.
• Clinical features:
• Painful swelling of mucosa on the affected in the anterior
part of floor of the mouth.
• Elevation of tongue
• Swelling is shiny and gelatinous in appearance
• Mandibular lingual sulcus is obliterated
• Pain and discomfort while eating, speech and other
movements of tongue.
• Treatment :
• Incision is placed intraorally at the base of the
alveolar process in the lingual sulcus so that the
sublingual gland, lingual nerve & submandibular duct
are not injured.
 Submandibular space
• Inverted cone shaped
• Laterally :The skin ,superficial fascia, platysma &superficial
layer of deep cervical fascia.
• Medially: the mylohyoid , hyoglossus & styloglossus
• Antero-Inferiorly: anterior bellies of digastric
• Posterio-inferiorly: posterior belly of digastric & stylohyoid
muscle
• Superiorly: the medial aspect of the mandible & the attachment
of the mylohyoid muscle
• Contents:
Submandibular gland
Facial artery
Lymph nodes
• Communications:
• Anteriorly submandibular space infections may pass
around anterior belly of digastric muscle to submental
space.
• Posteriorly infection can spread into LPS through
-the gap B/W the styloglossus & stylohyoid muscles
-around the posterior belly of digastric muscle
-along the lateral surface of pharyngeal constrictors.
• Clinical features:
• Triangular swelling begins at the lower border of the
mandible and extends to the level of the hyoid bone.
• Redness of the overlying skin.
• Pain during swallowing and speech.
• Mild trismus can be noticed.
• Treatment :
• The incision is made app 1cm beneath and parallel to the
inferior border of the mandible.
 Submental space
• Laterally :The anterior bellies of digastric muscle
• Superiorly : the mylohyoid muscle
• Inferiorly :the skin, superficial fascia, platysma
muscle & deep cervical fascia
• Contents:
• Anterior jugular vein
• Lymph nodes
• Clinical features :
• The swelling is confined to the chin and the area just beneath
it.
• It is indurated and painful.
• Later it may become fluctuant and may even spread as far as
hyoid bone.
• Treatment :
• I&D
• Extraction of offending tooth
 Pterygomandibular space
• Laterally :the medial surface of ramus of mandible
• Medially : lateral surface of medial pterygoid muscle
• Superiorly :lateral pterygoid muscle
• Anteriorly :Pterygomandibular raphae
• Posteriorly : parotid gland
• Contents :
Inferior alveolar nerve
&vessels
Lingual nerve
Buccal fat pad
• Communications:
• Infection may spread superiorly into deep temporal space by
passing around the lateral pterygoid muscle.
• Infections may also spread into LPS by passing around anterior
border of medial pterygoid muscle and lateral surface of the
superior constrictor muscle.
• Clinical features :
• Intraorally anterior bulging of half of the soft palate &
the anterior tonsillar pillar
• Deviation of the edematous uvula to the unaffected
side.
• Severe trismus and difficulty in swallowing.
• Extra orally no evidence of swelling
• Treatment :
• I&D
• Extraction of the offending tooth.
• The incision is made through the mucosa in the area between
the medial aspect of the mandible and the Pterygomandibular
raphae.
 Sub Masseteric space
• Laterally : Masseter muscle
• Medially : Lateral surface the ramus of mandible
• Anteriorly : Anterior extension of parotid-masseteric fascia,
mucosa of retro molar area
• Posteriorly : Parotid fascia & Parotid gland
• Superiorly : communicates with superficial temporal space
• Communications:
• Superiorly it directly communicates with superficial temporal
space and infra temporal space.
• It communicates with pterygomandibular space through the
sigmoid notch.
• Infection may pass around the
anterior border of ramus of mandible
and spread into pterygomandibular space.
• Clinical features :
• Deep-seated severe throbbing pain
• Tenderness over mandibular ramus area
• Severe trismus
• Swelling extends from posterior border of ramus of the
mandible as far as anterior border of masseter muscle.
• Intraorally, oedema is present at retromolar area & the anterior
border of ramus .
• Fluctuation cannot be elicited .
• If the infection is severe pus may discharge at the anterior
border of ramus or backwards at the angle of mandible.
• Treatment :
• The established submassetric infection must be
decompressed .
• The incision is made over the lower part of the anterior
border of the ramus and deepened to the bone.
• Forceps is then passed along the lateral surface of
ramus down wards and backwards and loculus of pus is
opened
• When the mouth cannot be opened , skin incision is
made behind the angle of mandible.
Infra -temporal space
• Medially : The lateral pterygoid plate,
The inferior portion of the
lateral pterygoid muscle &
The lateral
pharyngeal wall
• Superiorly :The infratemporal
surface of the greater wing of the
sphenoid bone
• Laterally : The temporal tendon &
coronoid process
• Posterolaterally: Mandibular condyle,
Temporalis &
Lateral pterygoid muscle
• Anteriorly : The infra temporal surface of
the maxilla & The
posterior surface of the zygomatic bone
• Inferiorly : Communicates with
Pterygomandibular space
• Contents:
Pterygoid plexus
Maxillary artery & vein
Mandibular division of trigeminal nerve
• Communications:
• Communicates with cavernous sinus & causes CST.
• Pterygomandibular space
• Submassetric space
• Deep temporal space
• Clinical features:
• Produces extra oral swelling over the region of the sigmoid
notch
• Intraoral swelling in the tuberosity area.
• Severe trismus is present.
• Treatment : I &D
• Intra orally incision is made just medial to the upper extent of
the anterior border of ramus of mandible.
• Hemostat is passed superiorly along the medial aspect of the
coronoid process into the infra temporal region.
• Extra orally a small horizontal incision, parallel to the
zygomatic branch facial nerve, is made posterior to the
junction of the frontal and temporal process of zygoma.
• References
• Contemporary oral and maxillofacial surgery- 2nd edition
Peterson, Ellis, Hupp,Tucker
• Oral and maxillofacial surgery - VOL- 2
Daniel M. Laskin
• Oral and maxillofacial infections- 4th edition
Richard G. Topazian
• Oral and maxillofacial infections- 4th edition
J.R.Moore
• Deep neck space infections
B. Jankowska A. Salami, G. Cordone, S. Ottoboni, R. Mora
Department of Surgery, Anaesthesiology and Organ
Transplants E.N.T. Clinic, University of Genoa, Genoa, Italy
International Congress Series 1240 (2003) 1497– 1500
(source: internet)
THANK YOU
LUDWIG’S ANGINA

Dr VINAY K N
 Definition
It is an overwhelming, acute, inflammatory,
diffused, rapidly spreading, septic,
undulated, gangrenous cellulitis of the
floor of the mouth and neck involving the 3
spaces bilaterally namely submandibular,
sub mental and sub lingual.
• Wilhem Von Ludwig(1837) described
infection must involve each side of the
mylohyoid diaphragm simultaneously to
constitute the condition.
 Harvey’s Criteria

• Deep and tender swelling involving

Bilaterally submandibular, sub mental and
sub lingual space.
• Open mouth appearance with elevated
and protruded tongue.
• Swelling i.e. the floor of the mouth.
• It is type of cellulitis with diffuse
inflammatory reaction in which the bacteria
are able to overcome or avoid the host
defenses so that the infection is not
confined to one area. Instead it may
progress through the surrounding tissue
and along fascial planes to areas away
from the original site of infection.
• Cellulitis readily resolves with treatment , if
it persists it can become localized,
forming an abscess.
 Types

• Septic Suppurative: Inflammatory disease

of the above spaces and pus can be
drained –prognosis is more favourable.
• Septic non-Suppurative : Inflammatory
diseases of the spaces and tissues under
tensions and compressed due to oedema
No pus present.
 Etiology

1) 90% ondontogenic infections of lower teeth

• primarily from periapical, deep periodontal infections
from lower molar teeth. Directly extend into lingual side
of mandible.
• Secondary from – infection following extraction of
infected lower teeth.
• Direct extension from pericoronal infection from lower
3rd molar.
• The 2nd and 3rd molar most common teeth, because
roots lie below mylohyoid muscle. First molar rarely
causes.
• contaminated needles – during infiltration on
lingual side.
• Sub-mandibular or sublingual sialadenitis or as a
result of secondary infections from lymph nodes
• Compound # of mandible with osteomyelitis
• Oral soft tissue laceration , penetrating injury to
floor of mouth such as gun shot wound or stab
wound.
• Lymphatic spread.
 BACTERIOLOGY

• Mixed infection gram positive and negative both

aerobic and anerobic type organism.
• Main causative organism is streptococcus
haemolyticus and non-haemolyticus (viridans)
and some strains of staplylococcus aureus,
albus.
• Other organism found are bacteroids,
klebsiella, diphtheroids, pseudomonas
aeruginosa, haemoplius influenza, brauhanulla
catarrhalis, vincents organisms.
 PATHOGENESIS

• Infection from a periapical region in the 2nd

and 3rd molar region (when root apex are below
mylolyoid attachment :- spreads directly to
submandibular space :- then spreads around the
deep part of submandibular gland to the sub
lingual space on same side :- then crosses the
midline and spreads from our sublingual space
to opposite side sublingual space :- then to the
submandibular space on the same side.
• The sub mental space gets infected either by
lymphatic or from submandibular space at the
anterior end.
• The tongue is raised by volume of exudates
in floor. Infection in floor and cleft between the
hyoglossus and genioglosus has direct access
to the laryengeal regions and in the sublingual
space through the pterygoid and lateral
pharyngeal spaces.
• The infection spreads uniformly from the anterior part of
neck to the clavicle, giving the face a swollen
appearance right from the chin to sternum region.
• Infection then spreads to involve the tissue space
between the muscles of larynx.
• The more possible explanation is that infection starts in
the sublingual space (when root apex above mylohyoid
attachment), spreads bilaterally and then extends
posteriorly over the edge of the myloloid muscle and
possible even through the muscle to involve the
submental spaces and submandibular spaces.
 Clinical features

• General signs and symptoms:

• 1) Pt looks very ill
• 2) Toxic
• 3) Dehydrated
• 4) High temperature 105 deg F < chills and
rigors
• 5) Malaise
• 6) increase salivation
• 7) speech and deglutition difficult.
 E/O Examination

• Extensive diffused, non fluctuant, brawny

indurated swelling which is bilateral and extends
down the anterior part of the neck upto the
clavicles. Does not put on pressure.
• Tissues are firm and board like, painful to touch
• Tissues may become gangrenous & a sharp
demarcation is seen between normal and
infected tissues, when cut – peculiar pale &
lifeless appearance.
 I/O Examination

- Partial trismus
– Patient has typical open mouth appearance
– Floor of the mouth is raised
– Tongue is pushed of against palate
– Tongue may protrude through mouth and
stiffness sets in
– Patient has difficulty in swallowing, so drooling
of the saliva from the corner of mouth
– Difficulty in speech
– Difficulty in respiration in massive care due to
backward spread of infection- larynx may become
oedematus – resulting hoarse voice and difficulty in
respiration, accompanied by dysphagia and
suffocation.
– In untreated case- oedema of glottis result into
complete respiratory obstructions.
– Patient may die of asphyxia within 12 to 24 hours.
– If patient spared death from suffocation, he may still
succumb to septicaemia, mediastinitis or aspiration
pneumonia.
 Treatment

• Early detection of disease (prompt diagnosis)

• Maintenance of airway (Emergency treatment) in
case of respiratory stridor – by emergency
tracheostomy.
• Emphiric massive and prolonged antibiotic
therapy.
• Early surgical intervention to relieve tension
• Treat the cause
• Supportive therapy.
• Bed rest.
 Early detection of disease

• In early stage with slight swelling in

fascial space due to any infected tooth,
treat the condition either by RCT or
Extraction.
 Maintenance of airway

• In case of any respiratory distress emergency

tracheostomy done under L.A.
• If difficulty is there to reach trachea due to
massive oedeomatous swelling and
haemorrhage from inflammated tissues aspirate
air from trachea with wide bore needle or do
laryngotomy.
• G.A contraindicated may cause paralysis of
voluntary muscle.
 Massive antibiotic therapy

• Gun shot therapy: drug of choice

• Crystalline penicillin – 10-20 lakhs-6th
hourly-iv
• Gentamycin- 2 to 3 mg/kg – 8th hourly
• Metronidazol-500 mg/8th hourly.
 If allergic to penicillin

• Erythromycin-600mg iv slow -8th hourly.

• Gentamycin – 2-3 mg/kg – 8th hourly
• Later select appropriate antibiotic on the
basis of culture and sensitivity
• Sometimes continue antibiotic at least for
10 -14 days.
• There will be resolution of swelling by
antibiotic therapy.
 SURGICAL INTERVENTION
• Early surgical intervention to relieve tension:
• In case of massive swelling, tissue is under tension,
with respiratory distress. I and D to be done to
decompress the tissues, to release tissue under
tension.
– To release any pus if present
– To reduce the pressure of oedimatous tissue on the airway
and allow prompt drainage should suppuration develop.
– It also provide opportunity to obtain, pus for Culture and
Sensitivity.
– In conscious pt better to avoid G.A.
– Local infiitration of skin and subcutaneous tissue with 2%
lignocaine – safe.
– In tracheotomy cases under G.A better. Two views to be
considered for decompressure.
 1st view
• no longer advocated
• horse shoe shaped incisor beneath lower border
mandible extends from the greater corner of one side to
other side of hyoid bone.
• Dissect tissues in submandibular region in layers. skin –
superficial fascia- platysma – investing layer of deep
fascia – encroach into submandibular space.
• In anterior region – cut the mylohyoid muscle and enter
to sublingual space.
• Expose the tissue spaces for pus pockets
• Insert drainage tube and secure it to skin with sutures.
• Do not suture wound immediately.
 2nd view
• more conservative approach
• 2 small submandibular incisions deep subcanteneous
below lower border,2cm away.
• blunt dissection carried to explore submandibular
spaces on both sides- using lister sinus forceps to break
pus pockets

• After exploration of submandibular spaces,independent

opening by putting vertical midline incision below the
chin is done to explore sub mental space and by cutting
the mylohyoid, sublingual space can be reached or a
separate I/O incision medial to plicalingularis is done to
explore sublingual space.
• After the exploration of these space, to relieve tension,
or to drain the pus – obtain specimen for C&S.
• Place 2 penrose or corrugated rubber drainage passed
from the sub mandibular to sub mental space and
separate for sub lingual space and secure the same skin
and mucous membrane with sutures.
• Maintain the drainage till tissue tension relieved, or
discharge cases, daily irrigation to be done with
antiseptics through the drainage tube.
• Once the discharge is reduced or stops – remove the
tube and suture the wound.
 Treat the cause
• Extraction of causative tooth done, if
cannot be conserved.
 Supportive treatment

• Maintenance of fluid balance.

• Analgesics and anti inflammatory drugs.
• High protein diet, multivitamins
recommended
• No sedatives to be given.
 COMPLICATIONS:

• Asphyxia
pt dies if untreated or late treatment due to
asphyxia – due to laryngeal edema
• Spread of infection to mediastinitis and other
potential spaces.
• Meningitis.
• Possibility of cavernous sinus thrombosis.
• Aspiration pneumonia.
• Septicaemia.
• Oedema of glottis.
THANK YOU
 Cavernous Sinus Thrombosis
• :It is one of the major complications of
abscess of the maxillofacial region,
• caused by the direct extension via the
venous system (septic thrombophlebitis)
or by spread of infected emboli.
• The infection usually involves one side
initially but can easily spread to the
opposite side through the circular sinus.
• Infection from the dangerous zone of the
face may spread along the facial veins in
retrograde direction, against the venous
flow due to the absence of valves in the
angular facial and opthalmic veins.
• Infection spread along the pterygoid
plexuses of veins reaching through
emissary veins into cavernous sinus
 The initial symptoms
• Pain in the eye
• Tenderness to pressure
 General Symptoms
• high fluctuating fever,
• chills,
• rapid pulse and
• sweating.
 Cranial nerves
• Paresis of occulomotor, trochlear,
abducent, ophthalmic division of the
trigeminal and carotid sympathetic plexus,
which results in opthalmoplegia,
diminished/ absent corneal reflex, ptosis
and dilation of pupil.
• Terminal stages- Toxaemia and meningitis
(meningeal irritation)
 Treatment
• Dehydration to be taken care of,
• chloramphenicol, 1gm every 6hrs-1v and
penicillin1v.
• blood-culture and sensitivity to be done.
• Anticoagulants to prevent venous
thrombosis.
• Use of steroid also helps.
 Brain abscess
• Is another complication of odontogenic
infections can occur from a bacteremia
accompanying odontogenic infecting
organisms reaching the brain.
• Inflammation, localized edema and septic
thrombosis,
• Single/ multiple abscesses may develop.
Signs and Symptoms:
• Headache,
• nausea
• vomiting.
• Patient is afebrile.
• Hemiplegia, papilloedema, aphasia, convulsions,
hemisensory deficit, hemionopsia and abducens palsy.
• Palsy of the various nerves are the kind of symptoms
produced if the abscess is located in the mid brain of
hind brain.
• Abscess of frontal lobe may cause stupor confusion and
subtle changes in personality.
Diagnosis by clinical findings
• CT and MRI helps in diagnosis
radionucliside scanning.
Organisms:
• streptococcus viridans
• streptococcus pyogenus,
• staphylococcus aureus.
Treatment:
• Massive antibiotics cover-
• iv chloramphenicol initially later sensitivity
to be done.
• Corticosteroids and mannitol to reduce
cerebral edema surgery to provide
drainage. Pt to be refered to neruosurgen
when diagnosed.
 Meningitis
• May also be a sequela to an odontogenic
infection with bacteria reaching the
leptomeninges in septic emboli through
the venous/ arterial system.
• Septic thrombophlebitis in the emissary
veins can lead directly to this
phenomenon/ indirectly by way of a
cavernous sinus thrombosis
 Signs and symptoms
• Headache,
• Fever,
• Stiffness of the neck
• And vomiting.
• Pt may often be confused and may become
comatose.
• Convulsions may occur following which pt may
go into coma
• Increased intracranial tension
 Kernigs sign
• Strong passive resistance when an
attempt is made to extend the knee from
the flexed thigh position
 BrudzinSkins signs
• Abrupt neck flexion in the supine,
• Pt resulting in involuntary flexion of the
knees.
 Diagnosis
• CSF-collected with lumbar puncture and
examination of C.S.F (usually opalascent/
cloudy, contains numerous
polymorphonuclear cells, proteins
increases, glucose decreases .
• Organism: staphylococcus aureus
 Treatment
• Massive antibiotic for long duration. Combination of
chloramphericol and penicillin.G.
• The report of culture and sensitivity, then appropriate
antibiotic-ampicillin.
• -Water and electrolyte balance maintained by iv fluids.
• -Control of cerebral edema and avoidance of vascular
collapse and shock
• Massive doses of steroids & mannitol.
• -Antibiotics to be continued a week after the symptoms
subsides and C.S.F returns to normal.
• -Pt going for septicemic shock may need fresh blood
transfusion.
• -Refer pt to neurosurgeon-immediately.
• -Once acute symptoms subsides remove causative
factors.
THANK YOU
OSTEOMYELITIS OF JAW BONES
dr vinay kn
 INTRODUCTION
• OSTEOMYELITIS of the jaws is a challenging disease
for clinicians and patients despite many advances in
diagnosis and treatment.
• In past ,osteomyelitis was frequent & considered
dreaded disease because
-Prolonged course
-Uncertainty of outcome
-Disfigurement
• Today jaw osteomyelitis is less common because
- Improved nutrition & dental care
- Earlier diagnosis & intervention
- New imaging techniques
- Availability of antibiotic therapy
 DEFINITION -OSTEOMYELITIS

• BOYD 1958 - A boil in the bone

• Literally “inflammation of the bone marrow”
• THOMA: Is an inflammation of the soft tissue of
the bone marrow spaces (of the spongiosa),
haversian system of the cortex and the
periosteum.
• KILLEY & KEY (1975): Inflammatory condition of
the bone which can involve the medullary cavity
and the haversian system of the adjacent cortex.
• TOPAZIAN: An acute, sub-
acute or chronic inflammation
of bone and bone marrow that
may develop as a result of
odontogenic or other infection
 BONE
• Bone is a connective tissue containing deposits of calcium
salts in the ground substance.
• It acts as reservoir of calcium phosphate to mobilize calcium
in case of need.
HISTOLOGY OF BONE

• Periosteum
• Cortex
• Endosteum
• Cancellous /spongy bone
COMPACT BONE - CROSS
SECTION
• The blood supply of the bone is derived from the
following sources
1) Nutrient artery which enters the bone and runs
along the long axis
2) Periosteal vessels run from periosteum to cortex
and supply the superficial part of the cortex.
- They are large and abundant in childhood but
diminishes/scarce in old age.
3) From the muscle attachments
 SURGICAL ANATOMY
• The maxilla and mandible are composed of
-inner cancellous or spongiosa,
-outer cortex with periosteum.
• The cortex of maxilla is thin
• In premolar and molar regions spongiosa is limited to
alveolar process
• In the anterior part of maxilla & the tuberosity ,the
spongiosa is well developed
• Because of this, osteomyelitis in anterior part of maxilla &
the tuberosity is more common than premolar and molar
area.
• The mandible resembles long bones, as
-Extensive medullary cavity,
-Surrounded by dense cortical plates &
-well defined periosteum .
• Osteomyelitis of mandible is more
common than maxilla because
-Maxillary blood supply is more
extensive.
-Thin and porous cortical plates &
-Relative paucity of medullary
tissues in maxilla .
• Regions in the mandible affected by osteomyelitis
decreasing order
-Body
-Symphysis
-Angle
-Ramus
-Condyle
-Coronoid process
 ETIOLOGY
• Odontogenic infections -MOST COMMON CAUSE
-Periapical infections
-Periodontal infections
-Pericoronal infections
-Infected odontogenic cysts or tumors
• Trauma -2nd leading cause
-Traumatic extractions
-compound fractures
• Direct extension from
-Middle ear infections
-Boil or furuncles
• Lymphatic spread
• Hematogenous spread
PREDISPOSING FACTORS
• Virulence of the micro organisms
- Most apical abscess have a pyogenic
membrane, if the virulence of the micro
organisms is high, it can penetrate this
wall & predispose the condition to
osteomyelitis.
• Integrity and effectiveness of host defenses

-Diabetes mellitus
-Autoimmune diseases
-Agranulocytosis
-Leukemia
-Severe anemia
-Malnutrition , tobacco & alcohol usage
-Syphilis, tuberculosis
-Cancer chemotherapy
-Steroid drug usage
-AIDS
• Decrease vascularity of jaw bones
-Radiation
-Osteoporosis
-Osteopetrosis
-Paget’s disease
-Fibrous dysplasia
-Bone malignancy
-Bone necrosis caused by mercury ,arsenic & bismuth
 MICROBIOLOGY

• Staphylococcus aureus
• Staphylococcus epidermidis Most
common

• Streptococci – alfa-hemolyticus
-pyogens
-pneumococcus
• Anaerobic & Gr-ve –peptostreptococci
-klebsiella
-pseudomonas
Occasionally
-proteus
 -Fusobacterium & bacteriods.
-Typhoid bacilli
- Escherichia coli.

• When sinus formation develops –mixed infection

• Mycobacterium tuberculosis
• Treponema pallidum Causes
specific forms of
osteomyelitis
• Actinomyces spp
 PATHOPHYSIOLOGY
• The jaw bones are generally resistant to infection.
• The inflammatory exudates induces resorption of the
overlying cortex and penetrates the periosteum.
• The inflammation of bone results as a result of an element
of ischemia along with bacterial infection.
• The pathological resorption of bone is mediated by
1) Prostaglandins
2) Osteoclast activating factor
3) Monocyte factors
PATHOPHYSIOLOGY

ACUTE INFLAMMATION

INCREASED INTRAMEDULLARY PRESSURE

VASCULAR COLLAPSE
BACTERIA

AVASCULAR BONE
PUS,ORGANISM EXTENSION

HAVERSIAN SYSTEM /NUTRIENT

CANAL INVOLVEMENT

ELEVATION OF PERIOSTEUM

DISRUPTED BLOOD SUPPY

AVASCULAR INFECTED BONE

• Generally odontogenic infections are walled off and
therefore do not spread in the bone.
• The disorganization of the protecting pyogenic membrane
is the exciting cause of osteomyelitis.
• Factors causing disorganization of pyogenic membrane
are
-Injudicial curettage of suppurative lesions
-Operative trauma by which the highly pyogenic
organisms are introduced into normal tissue
-Failure to extract the offending tooth
• Though the protecting pyogenic membrane, wall
off the infection or but if the organisms are more
virulent it break this barrier and lead to acute
inflammatory changes like
-Hyperemia,
-Increased capillary permeability and
-Infiltration of granulocytes,
• Tissue necrosis with liberation of proteolytic
enzymes and as destruction of bacteria and
vascular thrombosis results in pus collection and
intra-medullary pressure increases, resulting in
vascular collapse, venous stasis and Ischemia
and bone necrosis.
• There is spread of infection through an extensive
area of cancellous bone and pus travels along the
Volkmann's canal and haversian system and
accumulate beneath the periosteum by stripping it
and elevating it from the cortex such that it reduces
the periosteal blood supply to cortical plate and
produces more dead bone.
• The compression on neurovascular bundle
accelerates thrombosis and Ischemia results in
osteomyelitis and nerve anesthesia or
Paraesthesia.
• The pus under tension might re-enter other
vascular channels through nutrient foraminae
further along mandible and force bacteria into
unaffected cancellous spaces or may drain to
mucosa or soft tissues by perforating periosteum
and drain outside through fistula.
• Due to effectiveness of host defenses or antibiotic
abuse osteomyelitis may become chronic.
• Inflammation regresses, granulation forms and
the new blood vessels causes lysis of bone, thus
separating the fragments of necrotic bone
(Sequestra) from healthy bone.
• The sequestra is irregular, rough, light in weight,
porous, yellowish grey in colour and freely mobile
• Fate of sequestra : May be
-Re-vascularised
-Remain quiescent
-Resorb
-Infected chronically and required surgical removal before
infection subsides completely
• Smaller sequestra : may get exfoliated through
the sinus or dissolved by the proteolytic action of
the enzymes of purulent fluid.
• Bigger one’s – surgical removal is mandatory
• Spongy bone – 2 to 3 weeks to get sequestrated
• Cortical bone – 2 to 30 months.
• Sequestra are avascular and not penetrated by
antibiotics.
• Larger sections of bone may be isolated by the
bed of granulation tissue which encloses a sheath
of immature new bone (Involucrum).
• This is less densely mineralized than
sequestra.
• Occasionally when sequestrum is large with
collection of pus, the involucrum is perforated by
channels or (Cloacae), through which pus
discharges from sequestrum to an epithelial
surface.
• These opening some time quiescent when no
discharge and some time discharges pus.
• If this prolongs the eventual healing also
prolongs.
• Rarely do sterile abscess (Brodie’s Abscess)
common to long bones occur in the jaws also.
 PERIOSTITIS
• It is an inflammatory reaction of the periosteum which
leads to the formation of a mass of immature bone which
lies along side of the bone.
• Mainly occurs in young children and adolescents.
• It may be bacterial, traumatic or chemical in origin.
• Mandibular- molar area is the common site.
• 2 types-Acute
-chronic
• Acute periostitis:
• Occurs following sub-periosteal abscess ,if the virulence
of the organism is high or resistance of the host is low
and patient is not responding to antibiotic therapy.
• Fulminating infection results in osteomyelitis.
• Localized sub-periosteal abscess, exudates, separates
the periosteum and surface of the bone becomes widely
involved.
– Localized – involves the periosteum over the infected
tooth.
– Suppurative type – severe swelling of the face,
excruciating pain, tenderness of bone, loosening of
tooth.
– Muscle trismus, pus discharging sinus tracts may
form.
– Chills, fever 40 degree Celsius.
• Treatment :
• Antibiotics
• Removal of offending tooth.
• Application of hot moist pack.
• When suppuration develops, I and D.
 CHRONIC PERIOSTITIS

• May follows acute phase or primarily due to low grade

infection.
• In young individuals osteogenic activity may be
stimulated and new bone may be deposited.
• This is known as Ossifying Periostitis
• Radiology
• It shows marked enlargement & increase in radio-
opacity of the periosteum.
• Bone deposition may be seen at periphery of the
bone.
• Treatment
• Antibiotic therapy
• Removal of causative tooth
• Hot moist packs, later I and D
• If sequestra present, sequestrectomy done.
 CLASSIFICATION
TOPAZIAN’S………
NON-SUPPURATIVE
SUPPURATIVE OSTEOMYELITIS
OSTEOMYELITIS

• Acute suppurative • Diffuse sclerosing

osteomyelitis osteomyelitis
• Chronic suppurative • Focal sclerosing
osteomyelitis osteomyelitis
primary-no acute phase (condensing osteitis)
preceding • Proliferative periostitis
secondary-follows acute (garre’s osteomyelitis)
phase • osteoradionecrosis
• Infantile osteomyelitis
 Specific type
-Tuberculous osteomyelitis
-Syphilitic osteomyelitis
-Actinomycotic osteomyelitis
Radiation induced osteomyelitis
Idiopathic osteomyelitis
 PRIMARY ACUTE
CHRONIC
SUPPURATI SUPPUR
VE CLINICAL ATIVE
FINDINGS
4 TYPES

NONSUP SECONDAR
Y CHRONIC
PURATIV SUPPURATI
E VE
 ACUTE SUPPURATIVE

• Deep intensive neuralgic type of pain

• Rigors followed by high grade fever- 1050F
• Rapid pulse, respiratory rate
• Nausea, vomiting, dehydration and acidosis may
accompany, toxemia, Malaise.
• Paraesthesia or anaesthesia of mental nerve (helps in
differentiating this condition from alveolar abscess)
• INITIAL PHASE :
• Teeth may not be tender or loose
• Edema of the overlying tissue which is tender.
• Moderate indurated swelling of the face or soft tissue
over the area.
• Fistula not present
(At this juncture it is a true intra-medullary disease. can
be cured by antibiotic therapy.)
• Lymphadenopathy, trismus
• Referred pain to ear and head ache.
• Leucocytosis, Hb% and RBC decrease
• Increase in polymorphonuclear leucocytes.
• ESTABLISHED CASES:
• Deep pain – intermittent.
• Swelling lasting for 4 or 5 days with intermittent
exacerbation
• Malaise, increase fever and anorexia
• Within 10 – 14 days after onset discharge of pus through
gingival sulcus or cutaneous fistula on face
• Teeth sensitive to percussion, begin to loose
• Fetid odour.
• When suppuration takes place, the adjoining mucosa gets
inflamed and swollen with localized abscess with warmth –
associated cellulitis of the face.
• Erythema, tenderness on palpation.
• Paraesthesia of lower lip.
Due to thrombosis of the inferior dental vessel exert its
pressure over inferior dental canal. This rise in pressure
within the canal affects nerve and vessel result in loss
of conduction.
• Trismus may or may not be present.
• Temperature 1010F to 1020F, dehydration, ESR increase
• Firm swelling over the part of jaw.
• Regional lymphadenopathy, tender
• Osteomyelitis of maxilla shows ocular symptoms like
epiphora, proptosis.
 CHRONIC PRIMARY
SUPPURATIVE
• Not preceded by an episode of acute symptoms
• When host resistance is good or if virulence of
causative organism is low.
• Low grade infection, insidious in onset.
• Slight pain, slow increase in jaw size
• Gradual development of sequestra often without
fistula
(should be left until it shell out off itself,
limited surgery is wiser to avoid defect and also
sclerosed bone doesn’t yield).
 CHRONIC SECONDARY SUPPURATIVE
(antibiotic abuse with out any surgery)
• Recurrent flare up of acute or sub acute inflammation
• Regional lymphadenopathy – constant finding in
incompletely treated osteomyelitis.
• Focus of infection in the form of Sequestrum or non vital
tooth.
• Sinus present, pus discharges through multiple sinuses in
the alveolar process up the periodontal membrane of
adjacent teeth and also externally.
• At times there is no discharge of pus but a sclerosis of bone
occurs.
-Localized sclerosis near apex of the tooth- younger age
group
-Diffuse sclerosis - older edentulous cases.
• When probe passed through the sinus, rough bone felt,
-if sequestrum is small gets exfoliated
- Larger sequestrum takes longer duration of months.
• Thickened or wooden character of bone with pain and
tenderness on palpation – in sub-periosteal type.
• Induration of soft tissue on face & Facial asymmetry
• Pathologic # may occur when bone is extensively
weakened.
• Non toxic, WBC normal, increase during acute
exacerbation
 PRINCIPLES OF TREATMENT OF
OSTEOMYELITIS
• Evaluation and correction of host defense
mechanisms
• Gram staining, culture and sensitivity
• Imaging to rule out bone tumors
• Administration of stain-guided empirical
antibiotics
• Removal of loose teeth and sequestra.
• Administration of culture-guided
antibiotics :repeated cultures
• Possible placement of irrigating drains/
polymethymethacrylate beads
 IMAGING

• Proper imaging helps in

-Extent and degree of the disease
-The location of sequestra
-In the planning and extent of surgery
-To determine when the treatment may be stopped.
-It assists in distinguishing osteomyelitis from other bone
tumors
• 30%-60% of the mineralized portion of bone must be
destroyed before significant radiographic changes can
be distinguished .
• It requires a minimum of 4 and up to 14 days after
onset of acute osteomyelitis.
• The full extent of bone dissolution cannot be
determined radiographycally until 3 weeks after the
initiation of osteomyelitis process.
• In early stages of the disease- History & Clinical
features form basis of diagnosis.
• Radiographic changes clearly lag behind the actual
clinical situation in early and late stages of the disease
process.
• INITIALLY: “SPOTTY OR MOTTLED ” appearance.
-Approximately for first 10 days
-It is due to widening of medullary spaces and
enlargement of the volkaman’s canals secondary to
lysis and replacement with granulation tissue.
• PROGRESSES TO:“IRREGULAR RAREFACTIONS”
-It is due to destruction of trabeculae of the spongiosa
and further enlargement of cancellous space.
• LATER: “ ISLANDS OF RADIO-OPACITY”
-Due to bone destruction of varied extent “islands of radio
opacity” can be noticed. ie SEQUESTRA
-As the condition progresses the attempts to isolate the
sequestrum by the formation of the granulation tissue
around the sequestrum can be seen
-the sequestrum appears radio-opaque in an x-ray and
separated by a zone of irregular radiolucency gives
“MOTH EATEN APPEARENCE”
• The sequestrum appears whiter than the surrounding bone
because of its high calcium content (No
mobilization of ca+).
• “STIPPLED OR GRANULAR” densification of bone
caused by sub-periosteal deposition of new bone
obscuring the intrinsic bone structures or deposition of
new bone on surfaces of existing trabeculae at the
expenses of marrow space
• According to (Indian journal of radio imaging) IJRI
2005 15:4:447-451, CT patterns of is
osteomyelitis classified into 4 types
 Lytic
 Sclerotic
 Mixed
 Sequestrum
 TYPES OF IMAGING

• Plain radiography – opg, pa view, pns view, etc..

• Radionuclide imaging
• CT scan
• MRI
 LOCAL ANTIBIOTIC
THERAPY
• CLOSED WOUND IRRIGATION –SUCTION:
• It done after intra oral debridement, saucerization or
decortication.
• Small pediatric naso-gastric feeding tubes, french
catheters of 3-4 mm in diameter, 6-10 inches length are
used.
• The tubes are placed into the bone bed through separate
skin incisions.
• 2 tubes can also be used.
• Water tight closure of the wound is achieved.
• Various irrigation solutions used are
-Normal saline
-Neospirin .G.U irrigant
(Bacitracin zinc-neomycin Sulpfate-polymyxin B sulfate)
-1%Neomycin with 0.1% Polymyxin B.
• These can be instilled in 12hr cycle, drug is left there for
3hrs,then suctioning can be done.
• The wound should not be over filled.
• It should be followed by repeated culturing.
• Systemic antibiotics should be continued for at least 2
months after cessation of clinical evidence of the disease.
• ANTIBIOTIC IMPREGNATED BEADS:
• AIM:
-To deliver high concentrations of antibiotics into the wound
bed &
-In the immediate proximity to the infected bone.
• The antibiotic is leached from the beads, producing high
local concentrations thus reducing systemic toxicity.
• Acrylic beads containing
-Clindamycin
-Tobramycin
-Gentamycin
• Indications :
• Chronically infected bone with #’s
• Chronic sclerosing osteomyelitis refractory to systemic
antibiotics
• After the decortication the chain of beads is placed against
the bleeding surface, a drain is inserted and wound is
closed.
• They are left in place for 10 -14 days.
• Systemic antibiotic are administered simultaneously.
ANTIBIOTIC
THERAPY
• HYPERBARIC OXYGEN:
• HBO therapy consists of breathing 100% oxygen
through face mask or hood in a monoplace or large
chamber.
• Indications :
-Refractive chronic suppurative osteomyelitis
-Chronic diffuse sclerosing osteomyelitis
-Osteoradionecrosis
 SEQUESTRECTOMY

• In osteomyelitis of the maxilla intraoral incisions

are satisfactory.
• In mandibular osteomyelitis
 Alveolar process –intraoral approach
 Inferior border & body of the mandible-extra oral
approach
 Inferior and posterior parts of ramus & angle-
Risdon’s incision
 Condyle –pre-auricular approach
 Coronoid process-incision along the anterior
border of ramus of the mandible
 sigmoid notch- retro mandibular approach
• Generally , the sequestrum lies on the surface of
the bone and sometimes it is exposed.
• So it can be removed with little effort after
periosteum has been incised and reflected.
• If sequestrum is encased by involucrum, a window is
made in the involucrum, to allow it to be taken out.
• The best place to make window is at the cloacae.
• The cavity that is exposed almost always contains
granulation tissue in which sequestrum lies.
• The contents are carefully removed by the use of blunt
curette until the bony walls are exposed.
• In case of extra/intra oral approach, decision regarding
method of closure must be made.
1) The wound may be closed • This method is chosen
completely using sutures. only if one is certain that
(primary closure) all diseased tissue has
been removed and that
drain is not necessary.
• In such case antibiotics is
continued for at least
2weeks to control residual
2) The wound may be partly infection.
closed with sutures and
rubber drain may be • It is useful when there is
placed.
suppuration.
3) Primary closure may
• This method is
be combined with
continuous irrigation recommended………
with isotonic saline  if jaw is involved
with indwelling extensively/
catheter in addition  if active suppuration is
to the systemic present/
administration of  if remaining bone has
antibiotics poor circulation and is
sclerotic.
CASE REPORT-1
CASE REPORT-2
 SAUCERIZATION
• Saucerization is the “unroofing” of the bone to expose
the medullary cavity for through debridement.
1) A buccal mucoperiosteal flap is reflected to expose
the infected bone. Extensive tissue reflection is
avoided to preserve blood supply.
Sinus tracts if present should be included, otherwise
they can be excised later
2) The bony walls over hanging in the cavity resulting
from the removal of sequestra and necrotic bone are
cut away with rongeurs or sharp osteotomes.
3) The lateral cortex of the mandible is reduced until bleeding
bone is encountered at all the margins approximately to the
level of unattached mucosa, thus producing a saucer like
defect.
4) If complete primary closure is not practical because the
infected bone cannot be completely removed or acute
suppuration, the wound may be packed loosely with a piece
of iodoform gauze , which is periodically changed to permit
healing from the depth of the bone out ward.
 DECORTICATION

• Removal of chronically infected cortex of the bone.

• The lateral and inferior border cortex is removed 1 to 2 cm
beyond the affected area thus providing access to medullary
cavity.
• It is based on the premise that the affected cortical bone is
avascular and harbors microorganisms.
• Indications:
 Extensive lesions
 Primary and secondary chronic osteomyelitis
 When initial conservative regimens have failed.
• Procedure :
1) Buccal mucoperiosteal flap is created with a crestal
incision extending along the necks of the teeth.
2) Removal of the teeth in the involved area.
3) Removal of the lateral cortical plate and inferior border
with bur or osteotomes in sections.
• Bone must be cut back to uninvolved areas as demonstrated by
bleeding points along the bone margins.
4) The flap is closed primarily and the dead space is eliminated by
the use of pressure bandage for 24-48 hrs/
Drains/irrigation tubes may be placed through separate stab
incisions and closed irrigation suctions may be used/
Antibiotics Impregnated acrylic beads can be placed for 10-14
days.
5) Repeated aerobic and anaerobic culture and sensitivity testing
& antibiotic therapy should be continued.
 RESECTION

• Excision of apart of a mandible is seldom

necessary.
• Indications of resection:
• If patient has been treated for many months or
years , has constant recurrences and is suffering
because of disability and pain.
 RECONSTRUCTION OF
OSTEOMYELITIS MANDIBLE WITH
PATHOLOGICAL FRACTURE
• Weakening of mandible in osteomyelitis is due to
Rapid bone destruction
Sequestrum formation Which leads to pathological fractures
• Etiology :
Insignificant accident
Rolling in bed
During sequestrectomy and saucerization
 INFANTILE OSTEOMYELITIS
• osteomyelitis of jaws in infants is uncommon disease
• It receives special attention because of risks involved like
-Involvement of eye
-Extension into dural sinuses
-Potential for facial deformities
-Loss of teeth resulting from inappropriate or delayed
treatment
• Occurs most often few weeks after birth
• Usually affects MAXILLA than mandible
• Before antibiotic era, mortality rate was 30%
• Etiology :
-Hematogenous route
-Perinatal trauma of the oral mucosa

-from obstetrician’s finger nails ,

-From the mucus suction bulb used to
clear the air way immediately after
birth
 -Maxillary sinus infection
-Contaminated human or artificial nipples
• Clinical features :
-Initially irritability , malaise precede frank cellulitis.
-Facial cellulitis centered about the orbit
-Hyperpyrexia , anorexia ,severe dehydration
-Convulsions & vomiting may occur.
-Pus is often present in the nostril of the affected side.
 - Inner and outer canthal swelling, palpebral edema, closure
of the eye, conjunctivitis and proptosis may result.
- A purulent discharge may be associated with nose or with
inner canthal sinus.
• Intraorally
- Maxilla on the affected side is swollen buccally and
palatally, especially in molar region.
- Fistulas may exist in alveolar mucosa .
• Investigations :
 Obvious decrease in leukocyte count
 Staphylococcus aureus – more common
 Occasionally streptococci
 During early acute phase little radiographic changes
noted .
• Treatment :
• Intravenous antibiotics
• Drainage of all the abscess should be done
• Repeated culture sensitivity testing should be done.
• Supportive therapy : antipyretics, fluids & proper diet.
• Conservative approach to sequestrectomy is
advisable.
• Complications :
• Permanent Optic damage
• Neurological complications
• Loss of tooth buds
• If the teeth are erupted , they are discolored
• Scarring beneath the eyelid causing ectropion.
 CHRONIC NON SUPPURATIVE
OSTEOMYELITIS
• DRY OSTEOMYELITIS
 2 types
1)Chronic focal sclerosing osteomyelitis/Condensing
osteomyelitis
2)Chronic diffuse sclerosing osteomyelitis
 1) CHRONIC FOCAL SCLEROSING
OSTEOMYELITIS
( CONDENSING OSTEOMYELITIS )
• This condition develops as a result of chronic
inflammation in the bone where resistance of the tissue
against infection is very high or where the virulence of
the infective organisms is low.
• Etiology :
• Chronic pulpitis
• Traumatic occlusion
• Clinical features :
• Usually occurs in young adults at the age of 20 yrs
• Mandibular first molars are commonly involved
• Mostly asymptomatic, discovered in routine examination.
• Radiology :
• Well circumscribed radiopaque mass surrounding and
extending below the apex of the teeth can be seen.
• Entire root outline is identified in radiopaque lesion.
• The radiodensity of the lesion is much higher as compared
to the surrounding normal bone.
• Treatment :
• RCT/Extraction of the offending teeth.

Root outline
 2) CHRONIC DIFFUSE SCLEROSING
OSTEOMYELITIS

• Typically involves major portion of jaws.

• Proliferative reaction of the jaw bone to a low grade
infection or inflammation (not by caries but by periodontal
disease).
• Clinical features:
• mandible is commonly affected , especially in edentulous
area
• Common in older age groups
• More common among blacks , females .
• Vague pain, spontaneous formation of intra oral sinus,
sometime with drainage of pus.
• The sclerotic bone is frequently granite hard and is
surrounded by granulation tissue
• Radiology:
• Appears as areas of diffuse or nodular sclerosis of the bone-
diffuse radio-opaque lesion
• Cotton wool appearance as in paget’s disease
• Some times lytic areas can be seen.
• May show mosaic pattern
 TREATMENT

• Its true nature of is obscure, so the treatment

must be based on empirical findings
• Conservative treatment with antibiotics
• Teeth extracted and periodontal treatment to be
rendered
• Less extensive lesion to be carefully removed
• Because of the hard granite like bone, care
must be taken not to fracture the jaw during
removal of the diseased tissue
• Decortication
• Hyperbaric oxygen
• Cortisone therapy
• Differential diagnosis :
-Fibrous dysplasia
-Sclerosing cemental masses of the jaw
-Paget’s disease of the bone
-Garre’s osteomyelitis
 GARRE’S OSTEOMYELITIS

• CHRONIC OSTEOMYELITIS WITH PROLIFERATIVE

PERIOSTITIS
• It is a non suppurative process in which there is
peripheral sub-periosteal bone deposition caused by mild
irritation and infection
• First described by Carle Garre in 1893
• First described in mandible by Pell et al in 1955
• Pathogenesis :
• It is usually believed that a sustained low grade infection of
the jaw bones, which is occurring in a young person with a
high degree of body resistance and excellent tissue
reactivity may often precipitate Garre’s Osteomyelitis.
• The increase in the mass of bone is probably due to several
factors
-Mild toxic stimulation of periosteal osteoblasts by the
attenuated infection.
-The compensatory thickening of the bone as a mechanical
adaptation to reinforce the area weakened
• Clinical features :
• Involves children and young adults
• Mandible is more commonly involved
• The involved jaw bone often presents a carious, non-vital
tooth (mostly lower 1st molar)
• Localized, hard, non tender swelling over the mandible
• The overlying skin and mucosa appears normal
• No signs of lymphadenopathy, hyperpyrexia,
leukocytosis.
• Differential diagnosis:
• Fracture callus
• Ossifying fibroma
• Ewing’s sarcoma
• Osteoblastic osteosarcoma
• Osteoma
• Metastatic tumor of jaw bone
 Radiology

• Focal ,well-calcified bone proliferation may be seen as

well defined ,smooth, radio-opaque area and often has a
laminated or “onion skin” appearance
• Treatment :
• Removal of the infected tooth and curettage of
the socket
• RCT
• Surgical recontour if necessary.
• Surgery –if there is obvious facial asymmetry
after atleast 6 months waiting period.
 ACTINOMYCOTIC OSTEOMYELITIS
( LUMPY JAW )

• Uncommon condition
• Chronic infection manifesting both granulomatous and
both suppurative features usually involve soft tissues &
occasionally bone.
• 2/3 of the cases are cervico-facial in nature which involve
the mandible & overlying soft tissue, parotid gland, tongue
and maxillary sinus.
• Caused by ACTINOMYCES ISRAELLI
• 1877 J.Israel isolated the organism Actinomyces..
• It presents as a commensal in oral cavity , show low
virulence.
• This is not fungi but rather gram positive anaerobic,micro-
aerophilic, non spore forming ,non acid fast bacteria which
share characteristics of both bacteria & fungi.(sulphur
granules i.e clumps of filamentous masses.)
• Organism gain access to the soft tissue directly or by
extension from bone through periapical or periodontal
lesions, fracture or extraction sites.
• Infection spreads & appears on Cutaneous rather than
mucosal surface.
• CLINICAL FEATURES:
• Firm soft tissue masses on the skin, lobular pseudo tumor like
appearance, purplish, dark red ,only areas with occasional
small zones of fluctuant ,multiple sinus tracts,
• spontaneous drainage of serous fluid containing sulphur
granules (micro colonies of organisms of 1-2 mm which delay
in healing socket)
• Radiology:
• Radiolucency of various size -marked bone sclerosis,
occasional sequestration.
Differential diagnosis:
• Parotitis
• Pyogenic osteomyelitis
• Parotid tumor
• Cervical Tuberculosis
Diagnosis:
• Based on culture or biopsy of the lesion.
Treatment:
• Hospitalization.
• High and long period of antibiotic.
• Drug of choice –penicillin
CHRONIC OSTEOMYELITIS ASSOCIATED WITH SYSTEMIC
DISEASES
• TUBERCULOID OSTEOMYELITIS:
• Common in young children
• Myocobacterium tuberculae gain access to the bone by
following routes
 Direct extension from gingival lesion
 Direct extension from infected sputum through extraction
socket
 Through an open pulp
 Through an hematogenous route with a primary focus in lungs
• Traumatic wounds of jaws provide a portal entry to tubercle
bacilli in patients with pulmonary tuberculosis.
• The trauma of wiring may permit the infection.
• CLINICAL FEATURES:
• Insidious onset, painless swelling of jaw, tender on
palpation, sub-periosteal cold abscess develops &
discharges externally.
• Local swelling softens with sinus formation. Once sinuses
are formed secondary infection occurs.
• The teeth becomes loose ,sequestration is common.
• Increased ESR ,loss of weight ,evening raise of
temperature, general weakness, lymphadenopathy shows
cessation of the disease.
X-Ray:
• Central area of bone rarefaction characterized by multiple
small radiolucent bands.
Treatment:
• Anti-tubercular therapy.
• Surgical:
• Radical, should include electro-cauterization , resection of
jaw in extensive cases.
SYPHILITIC OSTEOMYELITIS:
• Rare now a days.
• Caused by Treponema pallidum.
• Prenatal and acquired form.
• Bone lesion observed in tertiary stage.
Clinical features:
• Common in maxilla as Gumma in hard palate .
• Hard painless lump of rubbery consistency in
subcutaneously.
• when mucosa break down punched out ulcer forms.
• Granulomatous destruction of bone in palate, perforates
palate.
• Diffuse syphilitic osteomyelitis of mandible is similar to
pyogenic osteomyelitis.
• Pain ,swelling ,suppuration.

• TREATMENT:
• Similar to pyogenic osteomyelitis
• Treatment for syphilis
 SALMONELLA OSTEOMYELITIS

• Late complication of typhoid and paratyphoid fever & other

salmonella diseases.
• Treatment for specific disease.
 ACTINOMYCOTIC OSTEOMYELITIS
( LUMPY JAW )

• Uncommon condition
• Chronic infection manifesting both granulomatous and
both suppurative features usually involve soft tissues &
occasionally bone.
• 2/3 of the cases are cervico-facial in nature which involve
the mandible & overlying soft tissue, parotid gland, tongue
and maxillary sinus.
• Caused by ACTINOMYCES ISRAELLI
• 1877 J.Israel isolated the organism Actinomyces..
• It presents as a commensal in oral cavity , show low
virulence.
• This is not fungi but rather gram positive anaerobic,micro-
aerophilic, non spore forming ,non acid fast bacteria which
share characteristics of both bacteria & fungi.(sulphur
granules i.e clumps of filamentous masses.)
• Organism gain access to the soft tissue directly or by
extension from bone through periapical or periodontal
lesions, fracture or extraction sites.
• Infection spreads & appears on Cutaneous rather than
mucosal surface.
• CLINICAL FEATURES:
• Firm soft tissue masses on the skin, lobular pseudo tumor like
appearance, purplish, dark red ,only areas with occasional
small zones of fluctuant ,multiple sinus tracts,
• spontaneous drainage of serous fluid containing sulphur
granules (micro colonies of organisms of 1-2 mm which delay
in healing socket)
• Radiology:
• Radiolucency of various size -marked bone sclerosis,
occasional sequestration.
Differential diagnosis:
• Parotitis
• Pyogenic osteomyelitis
• Parotid tumor
• Cervical Tuberculosis
Diagnosis:
• Based on culture or biopsy of the lesion.
Treatment:
• Hospitalization.
• High and long period of antibiotic.
• Drug of choice –penicillin
 ASEPTIC NECROSIS OF THE JAWS

• Necrosis of the jaw caused by chemical agents is rare today.

• Common causes of chemical necrosis is
-Phosphorus
-Arsenic
-Mercury
CASE REPORT-3
 REFERENCES

• Oral and Maxillofacial infections-Topazian 4th edition

• Oral and Maxillofacial surgery-Laskin vol-2
• Out line of oral surgery-Killey Kay-Part-1
• CT evaluation of mandibular osteomyelitis Indian journal of
radio imaging 2005 15:4 447-451
THANK YOU
 OSTEORADIONECROSIS
• Aka radiation osteomyelitis
• 6500-7000uGy increased incidence of
ORN
• 0.55uGy/hour > increased incidence of
ORN
 Definition
• ORN is an exposure of non viable, non
healing, non septic lesion in the irradiated
bone, which fails to heal without
intervention.
 Etiopathology
• Marx (1983)
– Hypocellularity
– Hypovascularity
– Hypoxia
 Clincal features
• Deep boring pain
• Swelling of face when infected with draing sinuses
• Exposed bone
• Mucositis
• Atrophic mucosa
• Xerostomia
• Radiation caries
• Secondary candidasis
• Fetid odour
• Pyrexia
• Pathologic fracture
 Treatment
• Antibiotics and good oral hygiene
• Topical antiseptics
• Removal sequestra
• Curreting
• Local debridement / burring until normal
bleeding occurs
• Irrigation of wound
 Post radiation care
• Good oral hygiene practice
• Fluoride therapy
• Saliva substitutes
• Restorations
• Avoid dentures
• Extraction
 HBO
• Inhalation of 100% humidified O2 onder
pressure greater than 1 Atm pr
• Each dive is 120mins, 5 days per week for
30 or 60 days , 2ATA
• Marx protocol
 MOA
• Enhances lysosomal degradation potential
of WBC
• Free radicals of O2 are toxic to bacteria
• Exotoxins neutralised
• Tissue hypoxia reversed
• neoangiogenesis
 Contraindication
• Pneumothorax
• COPD
• Optic neuritis
• Acute viral infection
• Uncontrolled epilpsy and high fever
• Psychiatic problems
• h/o ear surgery
• Malignant disease
The End