 Introduction

 Factors influencing spread of

infection
 Clinical stages of progression of
infection
 Routes of spread
 Cellulitis
 Ludwig’s angina
 Space infections
 Cavernous Sinus Thrombosis
 Focal infection
 Conclusion
Infection: is defined as the pathological state of disease
caused by invasion of pathogenic micro-organisms with
in the body. (The Intensive Care Society 2009)
INFECTION
(INTERACTION OF ) HOST +ORGANISM
+ENVIRONMENT
In healthy state there is a balance if this balance is lost

 DISEASE OCCURS
Odontogenic infections: are the most common infections
of head & neck . Most of these can be managed
successfully with minimum complications, some can
produce death.
General- Type of organisms
- Physical
-state of patient
Quantity of micro-
 Loca organisms Anatomical
l- features
- Thickness of
cortical plates
- Attachment of
muscles
-Relation of tissue
spaces
- Bacterial Virulence: determine by those Qualities of
organism which favor invasiveness and have
deleterious effects on host. These include:
Production of lytic enzymes Potent exotoxins &
endotoxins
E.g. In a healthy individual
In person with low resistance
 Patient’s resistance: depends upon the immune
system of the patient.
it influence pathogenic potential by enhancing their
ability to overcome the protective host factors & by
increasing concentration of toxic products.
Once the balance between host
resistance & microbial
pathogenicity is tipped in
favour of invading organisms
the role of local barriers come
into play.
Alveolar bone: represents the
locally limiting barrier to the
further spread of infection
Once infection progress with in the bone:
it tends to spread

until it extends through one of the cortical

plate
For extension through cortical plates site of perforation
of cortical plates is determined by:

Relation of root apices to alveolar process

 Maxillary teeth
Central incisor Labial
Lateral incisor Labial n palatal
Canine Labial
Premolars Buccal n palatal
Molars Buccal n palatal

12
 Mandibular teeth
Incisors Labial
Canine Labial
Premolars Buccal
First molar Buccal n lingual
Second molar Buccal n lingual

Third molar Lingual

13
Once infection progressed through bone
next local barrier is periosteum.
 Periosteum delay further spread leading

to development of subperiosteal abscess.

In most instances periosteum does not provide
much resistance and infection spread to
surrounding soft tissues.
Once this barrier has overcome then the
anatomical arrangement of adjacent muscles
and fascia determines the next possible site of
localization.
Routes of
spread

15
I. Through tissue
spaces
II. Through
lymphatics
III. Blood

16
Tissue spaces (Shaprio) defined space as a potential
tissue space present between planes of fascia that form
natural pathway along which infection may spread
producing cellulitis.

17
Spaces:
- Primary: Directly related to teeth
- Secondary: Not directly related to
teeth

18
Primary maxillary spaces: Canine
Buccal
Infratempor
al
i. Primary mandibular spaces: Sublingu

ii. Submandibular al
Subment
iii al
. Buccal
19
Parotid space infection
Temporal space
infection
Phyrangeal space
infection

20
Diffuse inflammation of soft tissues
If an abscess is not able to establish drainage through
surface of skin and oral cavity.
It may spread diffusely through facial planes of soft
tissues.
 Causative agents:
strep.pyogens
staph. aures
Infection cause diffuse rapidly spreading infection bcz of
enzymes produced by the organisms.
Enzymes include – hyaluronidase
- fibrinolysins
Which Breakdown Hyaluronic Acid ,Universal
Intercellular Cement Substance And
Fibrin .
Streptococci Are Particularly Potent Producers Of
Hyaluronidase And A Common Causative Organism
In their growth phase consume local oxygen and
metabolize nutrients to produce an acidic environment

Growth of anaerobes that destroys

collagen .
Anaerobes: Prevotella
Porphyromonas
Cellulitis of face & neck is most common..... It
results from dental infections:
-pericoronitis
- apical abscess
-periodontal infection
- following tooth extraction
- following jaw fracture
Patient is moderately ill (Chills n
fever)
Raised temp.
Swelling of involved tissue it’s
-Painful
-firm
-brawny n tender
If superficial tissue spaces are involved:
Skin is inflamed with orange peel appearance Purplish
(some time)
If spread is in deeper planes:
overlying skin is normal

Regional lymphadenitis is present

H/F: diffuse exudates of PMN cells occasional
lymphocytes
Considerable serous fluid and fibrin causing
seperation of connective tissue or muscle
fibers .
Removal of etiology
Administration of antibiotics
Advise: not to massage infected area
Although condition is very serious
resolution occur with adequate treatment
German physician described the seriousness
of disease in 1836.
Term given by: Camerer in 1837.
Wilhelm friedrich von ludwig : Name of
physician
Angina: means to strangle
(because in ludwig’s angina feeling of strangling
is there)
It described as 3F
Feared
Fluctuant
Fatal
Its also k/a Strangulatorious because of choking
effect which patient experience
Definition: it is an acute toxic rapidly
spreading cellulitis of floor of mouth
beginning usually in submandibular
space, secondarily involving sublingual &
submental spaces bilaterally with
elevation of tongue potentially
obstructing airway.( european archives of oto-
rhino laryngology vol-260, no-7 p 401-03)
its not considered to be true unless all submandibular
spaces are involved.
Its most commonly a disease of dental origin.
Lower molar teeth(70%)
SM gland sialadenitis
Oral soft tissue lacerations
Penetrating injury of floor of mouth
Oral Mucosa in compressed. Jaw
fracture
Periphyrangeal abscess
Prevalence is increased in patients who are
immunocompromised secondary to disorders such as:
DM
Organ transplantation
AIDS
Aplastic anemia
It’s a type of spreading infection occur in presence of
the organisms that produce significant amount of
hyaluronidase & fibrinolysins which act to break down
the hyaluronic acid & fibrin.

Streptococci being potent producer always associated

with ludwigs angina.
Swelling of floor of mouth
Swelling- firm, painful, diffuse
Elevation of tongue (Woody Tongue)
Difficulty in eating, swallowing &
breathing
High fever
Rapid pulse
Fast respiration
Swelling involve neck
Edema of glottis
Risk of death due to
suffocation
 Submandibular
space submental
space

sublingual
lat. phyrangeal space

retrophyrangeal

space

Mediastinum
Involvement of sublingual
space:
- Post. Enlargement
- Elevation n protusion of
tongue
- Compromised airway
Involvement of submandibular space:
- Enlargment n tenderness of neck (BULL
NECK)
- Initially unilateral ,later bilateral
- Pain in neck
- Restricted neck movement
- Dysphagia (difficulty in swallowing )
- Dysphonia(difficulty in speaking )
- Dysarthria(unclear articulation of
speech )
- Drooling
- Sore throat
Laryangeal edema
Respiratory Obstruction
Tachypnea(rapid breathing )
Stridor (high pitched wheezing /disrupted air
flow )
Restlessness
Patient need to maintain erect position
Maintain airway
Extraction of offending
tooth
Antibiotics
Surgical drainage
Intracranial complication of dental infection.
It’s a serious condition consisting in the formation of a
thrombus in cavernous sinus or its communicating
branches.(IB anatomy third volume head neck)

44
 45
External route
 Pterygoid venous
plexus

inferior ophthalmic
vein

CAVERNOUS SINUS

Internal route
46
Infection spread by external route is
more dangerous because its very
rapid with short fulminating course
because of the large open system of
veins leading directly to cavernous
sinus.

47
Causative agents: staph.
aures
Streptoccoci
Gram negative rods
Mucormycosis

48
Patient is extremely ill (Chills n
fever)
Periorbital edema
Headache, nausea, vomiting
Photophobia
Ptosis (drooping of upper
eyelid )
Chemosis (swelling of conjuctiva
)
Infection spread to
contralateral side in 24-48 49
Involvement of other venous
sinuses
Septic embolization

50
Ptosis, chemosis, cranial nerve palsy beginning
in one eye progressing to another establish
diagnosis.
LAB TESTS:
Blood cultures
Cerebral angiography
Orbital venography

chemosi
s,
51
Treat primary source of
infection
Broad spectrum i.v
antibiotics
Surgical drainage
Anticoagulants
Manitol

52
 It refers to circumscribed area of
tissue, which is infected with exogenous
pathogenic microorganisms and which
is usually located near a mucous or
cutaneous surface.
 It refers to metastasis from
the focus of infection, of
organisms or their products
that are capable of injuring
tissue.
 It may spread by hematogenous or
lymphogenous route. They get localized
in tissues.
 Certain organisms have a predilection for
isolating themselves in specific sites of the
body.
 Toxins or Toxin Products: It may spread
by blood stream or lymphatic channels,
from focus to a distant site, where they
may initiate hypersensitive reaction in
the tissues.
 One example is scarlet fever, which is due
to erythrocyte toxin liberated by the
infective streptococci .
 Infected Periapical Lesion: Particularly
those of chronic nature an area usually
surrounded by the fibrous capsule, which
effectively walls off or separates the area
of infection from the adjacent tissues but
do not prevent the absorption of bacteria
or toxins.
 Periapical granuloma has been described
as a manifestation of vigorous body
defense and repair reaction, while cysts
merely a progressive form of granuloma.
Abscess occurs when the reparative and
defensive phase is minimum
There are reports that the oral foci of infection either
cause, or aggravate many systemic disorders. Most
common are as follows:
Mainly rheumatoid and rheumatic fever type.
Arthritis of rheumatoid type is of unknown etiology.
These patients have high antibody titer to group of
hemolytic streptococci. It is tissue
hypersensitive reaction.
 There are some points in favor of septic foci theory:
 Streptococcal infection of throat, tonsils or nasal
sinus may precede the initial or recurrent attack.
 Dramatic improvement occurs sometimes after the
removal of septic foci.
 Temporary bacteremia may occur immediately after
tonsillectomy, tooth extraction or after vigorous massage
of gums.
 Against the theory, there are some points:
 Often no infective focus can be found.
 Usually when focus is extirpated, no dramatic result
is found.
 There is close similarity, in most instances, between the
etiologic agent of the disease and microorganisms in
the oral cavity, dental pulp and in periapical lesions.
 Symptoms of subacute bacterial endocarditis have been
observed in some instances shortly after extraction of
teeth.
 Transient bacteremia frequently follows tooth extraction.
 Streptococci of viridian type cause majority of sub acute
bacterial endocarditis.
 After tooth extraction, there is streptococcal bacteremia, so
there is occurrence of subacute bacterial endocarditis after
dental operations, dental extractions.
 Premedication of the patient should be done before extraction.
Some workers state that constant swallowing
of microorganisms might lead to variety of
gastrointestinal diseases.
Gastric and duodenal ulcers are produced
by injection of streptococci.
 Factor supporting the hypothesis of Woods the role of
foci of infection in ocular diseases.
 Many ocular diseases occur in which no systemic
cause, other than presence of remote foci of infection
can be demonstrated.
 Numerous instances of prompt and dramatic healing
of ocular diseases are reported following the
removal of these foci.
 Occasionally, sudden transient exacerbation is
observed, after the removal of teeth and
tonsils.
 Presence of blood stream infection in early stages
of ocular disease, are evident.
 Iritis may be produced by intravenous injection of
microorganisms, e.g. streptococci.
There is some objection to these points
Many healthy people have focal infections, but do
no have ocular diseases.
Spontaneous care may occur if nothing is done.
Positive blood cultures are rare in acute iritis
Some forms of eczema and possibly urticaria,
can be related to oral foci of infection.
If the relationship does not exist, the mechanism
is probably sensitization, rather than
metastatic spread of the microorganisms.
Initial inflammation spread of inflammation low-
grade inflammation
Microorganism most commonly involved in urinary
infection is E. coli, staphylococci and streptococci.
Streptococci hemolyticus seems to be the most
common.
Objections to this
Streptococci are uncommon inhabitants of dental
root canals or periapical and gingival areas.
Since the microorganisms commonly involved in renal
infection so it appears that there is little relationship
between oral foci of infection and renal disease.