Spread of infection

FACTORS RELATING TO THE HOST

If the host or the patient has a high degree of
body resistance, the distant spread of infection
from the oral cavity is less likely to occur and
vice versa.
FACTORS RELATING TO THE SITE OF
INFECTION
The site of initial involvement of the odontogenic
infection also determines whether it will remain
localized or will make a distant spread.
The thinner cortical plates of bone or loose
tissue spaces around the wound may offer little
resistance to the spread of infection, therefore,
infections from such areas may often spread
diffusely.
FACTORS RELATING TO ORGANISMS
Some organisms producing odontogenic infections
are more virulent than others, moreover, a
few organisms, e.g. Streptococcus aureus can
produce enzymes like hyaluronidase and
fibrinolysins, etc. which help in the spread of
infection into distant areas by breaking tissue
barriers.

CELLULITIS
DEFINITION
Cellulitis is an acute edematous, purulent
inflammatory process, which spreads diffusely
through different tissue spaces or fascial planes.
PATHOGENESIS
• Acute cellulitis is mostly caused by some
unusually virulent bacteria, which often
produce hyaluronidase and fibrinolysins, etc.
• Hyaluronidase and fibrinolysins cause lysis
of the hyaluronic acid (universal intercellular
cement substance) and fibrin respectively, and
cause breakdown of the tissue barriers. The
enzymes, therefore, help the infective process
to spread diffusely into tissue spaces.
• Microorganisms such as Streptococcus pyogenes
and anaerobes, particularly bacteroides most
commonly produce facial cellulitis.
• In acute cellulitis, infection from the lower
anterior teeth perforates the lingual cortical
plate of bone and moves into the superficial
sublingual space, and from there tracks
backwards.
• Infection from lower molar teeth, after
penetrating the lingual cortical plate reaches
the junction of fascial spaces at posterior border
of mylohyoid muscle.
• From there the infection may spread forward
to reach the sublingual and submandibular
space and backwards into the parapharyngeal
spaces.
CLINICAL FEATURES
Cellulitis clinically presents the following features:
• Development of a large, diffuse, painful
swelling over the face or neck with facial
asymmetry
• The soft tissue swelling is usually firm and
brawny.
• When cellulitis involves the superficial tissue
spaces, the overlying skin often appears
purplish.
• However, when the infection spreads along the
deeper tissue spaces, the skin appears normal
• Fever, chill, leukocytosis, etc. are often present,
which make the patient slightly ill.
• Regional lymphadenopathy frequently
develops and in untreated cases cellulitis may
spread over a wide area and sometimes involve
the entire face.
• Trismus, dyspnea and dysphagia are the
common complications.
• in some cases pus discharging intraoral or extraoral
sinuses may develop.
HISTOPATHOLOGIC FEATURES
• Collection of a large amount of fibrin and serum
fluid in the tissue.
• Separation of periosteum and muscles from the
bony surface due to accumulation of fluid.
• Acute inflammatory cell infiltration by PMN
and occasionally lymphocytes.
• Pus may develop in the later stages of the disease.
• Formation of sinus tracts over skin or mucosal
surfaces.
TREATMENT
• Bacteriological examination of the exudate or
pus, etc
• Drainage
• Antibiotic therapy
• Elimination of the primary source of infection
LUDWIG’S ANGINA
DEFINITION
Ludwig’s angina is an overwhelming diffuse,
suppurative cellulitis, which simultaneously
involves the submandibular, sublingual and
submental spaces.
CAUSATIVE MICROORGANISMS
• Hemolytic streptococci are the most frequently
encountered organisms to cause Ludwig’s
angina. However, staphylococci, bacteroides
and fusiform bacilli may also be involved
PATHOGENESIS OF LUDWIG’S ANGINA
• In Ludwig’s angina, all the three important
spaces in the submandibular region, i.e. the
submandibular space, sublingual space and
the submental space, are involved simultaneously.
• Although involvement of these spaces occurs
one after the another, the spread of infection is
so rapid as if it is involving all the spaces
together
• Infection from mandibular second and third
molar teeth often perforates the lingual cortical
plate of bone (buccal cortical plate is usually
not perforated in the molar region as it is much
harder and thicker as compared to the lingual
plate) below the level of attachment of the
mylohyoid muscle and spreads to the
submandibular space.
• Submental space is usually involved by
extension of infection from the neighboring
spaces.
.
CLINICAL FEATURES
• Ludwig’s angina produces a rapidly
spreading, large, diffuse and board-like
aggressive swelling; which involves the upper
part of neck and floor of the mouth bilaterally
with brawny induration.
• The swelling causes elevation of the tongue;
which may be pushed up against the palate
and the patient often has a typical open
mouthed appearance.
• The enlarged tongue may protrude outside the
mouth and the condition is called woody
tongue.
• The swollen area of the neck is firm, painful,
nonfluctuant and does not pit upon pressure.
• The condition is always bilateral and the
patient is often unable to open the mouth, speak
or swallow properly.
• As the condition deteriorates further there
may be development of edema glottis; which
is a serious condition and can result in death
due to asphyxia.
• Other serious consequences of Ludwig’s
angina include the development of cavernous
sinus thrombosis, meningitis, brain abscess
and suppurative encephalitis, etc.
DIAGNOSIS
Diagnosis is usually established by the following
methods:
• Clinical features of the disease are often very
specific.
• Leukocytosis
• Bacterial culture with identification of specific
microorganisms.
TREATMENT
• High dose of antibiotics.
• Drainage by incision at the anterior part of the
Neck.
• Emergency tracheostomy may be required in
cases of airway obstructions
CAVERNOUS SINUS THROMBOSIS
(THROMBOPHLEBITIS)
DEFINITION
Cavernous sinus thrombosis is a serious lifethreatening
condition characterized by formation
of septic thrombi within the cavernous sinus and
its numerous communicating branches
ROUTES OF SPREAD OF INFECTIONS
External Route
• The veins of the maxillary regions of face
anatomically drain into the cavernous sinus
and because of this, infections from upper lip,
face, eye and nares, etc. often reach cavernous
sinus directly through facial and angular
veins.
• Since facial and angular veins are quite longer
vessels and, moreover, they have no valve
in them, infections from the outer face
spread rapidly to the cavernous sinus via this
route.
Internal Route
• Infections from internal structures (especially
upper and lower third molar teeth) reach
cavernous sinus via the pterygoid plexus.
• Spread of infection occurs at a much slower, since
the infection has to pass through many small
and twisted venous passages of the pterygoid
plexus.
CLINICAL FEATURES
• Headache, fever, vomiting, nausea and chill,
etc. are present in the initial stages.
• Patients may also develop tachycardia,
tachypnea, stiffness of the neck and irregular
breathing, etc. with alarming severity.
• Occlusion of the ophthalmic veins causes
photophobia, increased lacrimation, proptosis,
chemosis, dialatation of pupil and
edema of the eyelids, etc.
• Paralysis of the external ocular muscles,
exophthalmos, fixation of the eyeball,
intraocular hemorrhage and even blindness
can occur.
• Massive swelling of the nose and forehead
areas.
• Complete paralysis of the third, fourth and
sixth cranial nerves common.
• Pain above the eye and diminished sensation
over the forehead.
• The condition is initially unilateral but, it often
becomes bilateral within 2 to 3 days.
• Death may occur due to brain abscess, meningitis,
septicemia, toxemia or pyemia, etc
. TREATMENT
• Maintenance of airway in cases of respiratory
distress
• High doses of antibiotic therapy
• Drainage
• Anticoagulant therapy