odontogenic infections

1. ODONTOGENIC INFECTIONS
Presented By- Dr. Md Mahbubul Hoda
Moderator- Dr. Veerendra Kumar

2. CONTENTS
• INTRODUCTION
• INFECTION & HOST
• PATHOPHYSIOLOGY OF INFECTION
• FACTORS INFLUENCING SPREAD OF INFECTION
• MICROBIOLOGY OF ODONTOGENIC INFECTIONS
• PATHWAY OF SPREAD OF INFECTION
• CLASSIFICATION OF FASCIAL SPACES
• COMPLICATIONS & TREATMENT

3. Introduction
• Odontogenic infections are the most common of all infections of the head and
neck.
• The term infection is defined as the detrimental colonization of a host organism
by a foreign micro organism
• Although most of these infections can be managed successfully with minimal
complications, some can produce serious morbidity and even death.
• Proper and timely treatment like use of antibiotics, early extraction of offending
tooth tends to shorten the usual course of the infection and minimizes the chance
of further complications

4. INFECTION &HOST
Microbial
factors
Host
factors
QUANTITY
VIRULENCE
CELLULAR
HUMORAL
LOCAL

5. • Virulence includes all the factors that make the microbe
detrimental to the host, such as toxins, enzymes that
increase invasiveness , and substance that neutralize the
host defences
• So if the host is normal, infection can occur only under one
of the two circumstances
When host is exposed to a concentration of microbes that
is sufficient to overwhelm normal defences
Pathogen is highly virulent

6. THE PATHOPHYSIOLOGY OF INFECTION
Hyperemia caused by
vasodilatation of
arterioles and capillaries
and increased
permeability of venules
with slowing of the
venous blood flow.
The passage of exudates
rich in plasma proteins,
antibodies, and nutrients
and the escape of
leukocytes into the
surrounding tissues.
Release of a permeability
factor, leucotoxin that
allows migration of
polymorph nuclear
leukocytes(and later
monocytes )into the area.
Precipitation of a
network of fibrin from
the exudates
Phagocytosis of bacteria
and other organisms as
well as of dead cells.
Disposal by
macrophages of necrotic
debris.

7. Factors influencing the spread
General factors
• Patient resistance: Humoral (Antigen antibody action) & cellular(Leucocyte
action)
• Bacterial quantity & virulence
Local factors
• Type of bone whether trabecular or cortical
• Relation of tooth apices to the muscle attachments
• Tissue spaces

8. Microbiology of odontogenic infections
• Most are by opportunistic pathogens present in the oral cavity. It is
usually a synergistic role of streptococci & anaerobes. Early infections
are predominated by aerobic streptococci whereas long standing
infections are predominated by anaerobic Gram positive cocci and
Gram negative rods
• Peptostreptococcus, staphylococcus, lactobacillus, prevotella,
treponema, Fusobacterium, Veillonella, Actinomyces, Bacteroides,
oral Streptococcus species are most commonly seen in case of severe
odontogenic infection that can results in life threatening condition.

9. • These microorganism produce enzyme like
• Streptokinase (fibrinolysin),
• Hyaluronidase
• Streptodornase
These results in breakdown of fibrin and connective tissue ground
substance and lyse cellular debris, thus facilitating rapid spread of
bacterial invaders.

11. INFECTIONS OF ODONTOGENIC ORIGIN ACUTE AND CHRONIC
Infections of dental origin are every common and
may present as pain, swelling, trismus,
lymphadenopathy, facial sinuses.
ACUTE ALVEOLAR ABSCESS
• An abscess is a collection of pus that has accumulated in a cavity
formed by the tissue on the basis of an infectious process. It is a
defensive reaction of the tissue to prevent the spread of infections to
other parts of the body.

12. ACUTE PERIAPICAL ABSCESS
• They arises when organisms from an infected necrotic tooth pulp invade the
periodical tissues.
• They usually gain access to the periradicular tissues through the apical foramina
so that the infection is truly periodical, but on perforation, or an opening in the
floor of the pulp chamber of a primary molar resulting from resorption or a
fractured root.
• Under these circumstances the abscess develops on the lateral aspect of the root
or at the root furcation. Infection from a split root characteristically presents as a
mid-root sinus or a longitudinal area of resorption along the lateral border of the
root.

14. • PERIODONTAL ABSCESS
• It is infection of periodontium, with collection of pus within
periodontal space. It may present as an inflamed tender swelling over
gums in region of the involved tooth. Often discharge of pus from the
gingival crevice of the involved tooth can be seen.
• Pericoronal abscess arises around the crown of a partially erupted vital
tooth, usually the 3rd molar, and therefore, resembles a periodontal
abscess.

15. INFLAMMATION
• Inflammation is the localized reaction of vascular and connective
tissue of the body to an irritant, resulting in the development of an
exudate rich in proteins and cells.
• This reaction is protective and aims at limiting or eliminating the
irritant with various procedures while the mechanism of tissue repair
is triggered.
• Depending on the duration and severity, inflammation is
distinguished as acute, subacute or chronic.

16. • Acute Inflammation: This is characterized by rapid progression and
is associated with typical signs and symptoms. If it does not regress
completely, it may become subacute or chronic.
• Subacute Inflammation :This is considered a transition phase
between acute and chronic inflammation.
• Chronic Inflammation: This procedure presents a prolonged time
frame with slight clinical symptoms and is characterized mainly by
the development of connective tissue.

17. Clinical signs and symptoms:
• Rubor (redness),
• Calor (heat),
• Tumor (swelling or edema),
• Dolor (pain), and
• Functio laesa (loss of function).

18. The natural progression of inflammation is distinguished into various phases
• Serous Phase: This is a procedure that lasts approximately 36 hours, and is
characterized by local inflammatory edema, hyperemia or redness with
elevated temperature, and pain. Serous exudate is observed at this stage,
which contains proteins and rarely polymorphonuclear leukocytes.
• Cellular Phase: This is the progression of the serous phase. It is
characterized by massive accumulation of polymorphonuclear leukocytes,
especially neutrophil granulocytes, leading to pus formation. If pus forms in
a newly developed cavity, it is called an abscess. If it develops in a cavity
that already exists, e.g., the maxillary sinus, it is called an empyema.

19. • Reparative Phase: During inflammation, the reparative phenomena
begin almost immediately after inoculation. With the reparative
mechanism of inflammation, the products of the acute inflammatory
reaction are removed and reparation of the destroyed tissues.

20. Characteristic Inoculation Cellulitis Abscess
Duration 0–3 days 3–7 days Over 5 days
Pain Mild–moderate Severe and generalized Moderate–severe, localized
Size Small Large Small
Localization Diffuse Diffuse Circumscribed
Palpation Soft, doughy, mildly
tender
Hard, exquisitely tender Fluctuant, tender
Appearance Normal Reddened Peripherally reddened
Skin quality Normal Thickened Centrally undermined and
shiny
Surface temperature Slightly heated Hot Moderately heated

21. Characteristic Inoculation Cellulitis Abscess
Loss of function Minimal or none Severe Moderately severe
Tissue fluid Edema Serosanguineous,
flecks of pus
Pus
Level of malaise Mild Severe Moderate–severe
Degree of
seriousness
Mild Severe Moderate–severe
Predominant
bacteria
Aerobic Mixed Anaerobic

22. PROGRESSION OF ODONTOGENIC INFECTION
• Dental disease is the underlying cause of most of the inflammatory
swellings occurring in and around the jaws.
• Inflammation may begin at root apex or the gingival margins or the
soft tissue overlying the crown of an unerupted or partially erupted
teeth.

23. Pathways of odontogenic infection
Acute – Chronic
periapical infection
Fistula
Cellulitis
Intra oral
soft tissue
abscess
Ascending
facial – cerebral
infection
Deep fascial
space infection
Bacteremia-
septicemia
Osteomyelitis

24. SPREAD OF INFECTION FROM INDIVIDUAL
TEETH
• There are many different routes by which apical infection may spread
from individual teeth and the more common are described below :
UPPER CENTRAL INCISOR
• This tooth most commonly drains into the labial sulcus and produces
oedema of the upper lip. Spread into the palate and extension into the
floor of the nose are unusual, particularly the latter. The palate is more
likely to be involved where the incisor is very proclined and palatal
infection may track posteriorly so that abscess formation occurs near
the junction of the hard and soft palates.

25. UPPER LATERAL INCISOR
• Spread is similar to the central incisor except that, as the root apex is
more deeply placed, palatal infection is more common and nasal spread
even less common.
Spread of periapical infections from maxillary incisors can be
into (a) labial sulcus (b) nasal floor (c) palatally

26. UPPER CANINE
• The maxillary canine has a long
root and, when fully erupted, its
apex is quite high and may be
situated a little lateral to the curved
junction of the lateral and inferior
margins of the anterior bony
aperture of the nose.

27. • Apical infection is likely to spread into the canine space, a subdivision
of the superficial facial compartment situated between the levator labii
superioris muscle and the underlying maxillary labial plate of bone.

28. UPPER PREMOLARS
• Spread from the apex of the second premolar is more likely to be
buccal than palatal. Occasionally the apices may be close to the
maxillary antrum so that apical infection may extend there.
• Infection spreading buccally may penetrate the labial plate and enter
the sulcus or spread superiorly into the soft tissues. When it goes
upwards and laterally it may then pass from under the lateral borders
of levator anguli oris and zygomaticus minor to enter the superficial
facial space, continuing upwards or posteriorly.

29. The attachment of buccinator muscle superior to the apices of maxillary molars regulates the spread of
periapical infection. If the periapical infection erodes the buccal bone below the attachment of buccinator
(A), it results in buccal vestibular abscess. If it perforates above the buccinator (B), it leads to buccal space
infection.

30. UPPER FIRST AND SECOND MOLARS
• Infection from the palatal apices of any of the upper molar teeth tends to
track either into the palate or superiorly into the maxillary antrum. From
observations on dried skulls there is often no bone separating the molar
apices from the antral cavity, only the soft tissue of the periodontal
membrane and adjacent thin antral mucosa.
• The buccal apices are likely to point buccally. Infection may then spread
either above the origin of the buccinators to enter the superficial facial
compartment or, less commonly, into the buccal sulcus.
• From the buccal apices of the first molar it may pass anteriorly or
posteriorly to the malar buttress, which forms a bony barrier that
sometimes is very prominent and has its lower point over the distobuccal
root of this tooth

31. • UPPER THIRD MOLAR
• The spread of infection from the apices of the third molar is similar
to that of the second molar except that buccally it is more likely to
go posteriorly and superiorly. This is due to the curvature
downwards of the posterior part of the buccinators origin lying
between the tuberosity and the upper part of the anterior border of
the pterygomandibular ligament
• From the tuberosity infection can readily track medially into the
paratonsillar space, medially then upwards along the tensor palate
tendon into the hard and soft palates, superiorly into the pterygo-
palatine fossa and deep pterygoid space, and posteriorly and then
inferiorly into the parapharyngeal space.

32. • From the pterygopalatine fossa it may pass superiorly into the orbit
anteriorly or cranium posteriorly, both very dangerous sites. The
lateral spread of infection from the buccal apices is likely to be above
the origin of buccinators directly into the superficial facial
compartment rather than into the vestibular space.

33. A) Posterior relations of maxillary third molar, (B) periapical
infection from maxillary third molar may spread to vestibule,
maxillary sinus, buccal space or palatally.

34. LOWER INCISORS
As the apices of these teeth are slightly closer to
the labial than to the lingual cortical plate of the
mandible, infection is likely to drain into the
labial sulcus or spread into the soft tissues of the
chin
When extension lingually does occur, this will
either be subgingival or into the sublingual space
above the origin of the mylohyoid. From the
sublingual space, the infection may descend to
enter the submental space

35. LOWER CANINES
As the root of this tooth is longer than those of the incisors, spread is likely to be deep to the labial sulcus, into the
superficial facial compartment. Interiorly it is slightly impeded by the origin of the depressor labii inferiors and by the
more superficial depressor anguli oris and overlying platysma, as the last two muscles are attached to the mandible rather
more distally than is the depressor labii inferiors, they lie below the level of the premolar apices. The insertion of platysma
extends posteriorly along the inferior border of the mandible opposite the molar teeth.
.

36. LOWER PREMOLARS
From these teeth buccally, infection enters the vestibular space and may then pass
below or through the buccinators to enter the superficial facial compartment. Oedema
on the mental nerve, which emerges from the foramen below or between the premolars,
may cause altered sensation in the skin covering the side of the chin and lower lip.
Extension lingually involves the floor of the mouth. Initially this may enter the
sublingual space and then perforate the mylohyoid to gain the submandibular space,
the later being slightly more likely with the second premolar

37. LOWER FIRST AND SECOND MOLARS
The first molars tend to be symmetrically placed in the mandible with equal
thickness of buccal and lingual bone covering the roots.
The second molar is more lingually placed with thicker buccal bone. Hence
apical infection is more likely to track buccally from the first than the second
molar. When this occurs, the direction of spread will be related to the length of
the roots as it may perforate the buccal plate either above or below origin of
buccinator to enter either the vestibular superficial facial spaces.

38. The distal apex of the second molar is usually
situated below the level of the buccinators
attachment.
Lingually, the apices of the first molar lie above
the mylohyoid, whereas those of the second
molar lie below it so that infection from the
latter tends to involve the submandibular space

39. LOWER THIRD MOLAR
The bone covering the third molar apices is much thicker buccally than lingually.
Examination of dried mandibles shows that often there is little or no bone over the
lingual aspect of these roots allowing infection to spread easily into the submandibular
space, and then posteriorly to beyond the free margin of the mylohyoid to enter the
sublingual space.
Posteriorly infection may track from the third molar region into the paratonsillar,
parapharyngeal, superficial pterygoid, and occasionally the submasseteric spaces.

40. Lateral to the distal part of the paratonsillar space are the carotid artery and
internal jugular vein so that pus in this space is adjacent to the major vessels of
the head and neck.
The submasseteric space infection, although uncommon, appears to be more
likely with a distoangular third molar, especially if part of the pericoronal
space is situated outside the origin of the buccinators muscle.

41. The lower third molar lies at such a critical anatomical site that posterior spread of
infection, in particular, may extend into any of several important tissue spaces.
Involvement of the parapharyngeal space is a serious complication owing to possible
extension downwards into the thorax, and similarly infection of its upper recess, the
deep pterygoid space, may be hazardous because of spread upwards to the base of the
skull.

42. SITES OF LOCALIZATION OF ACUTE DENTAL INFECTIONS13
Involved Teeth Usual Exit From Bone Relation Of Muscle
Attachment To Root
Apices
Site Of Localization
Upper central incisor Labial Above Oral vestibule
Upper lateral incisor Labial
Palatal
Above Oral vestibule
Palate
Upper canine Labial Above
Below
Oral vestibule
Canine space
Upper premolars Buccal
Palatal
Above Oral vestibule
Palate
Upper molars Buccal
Palatal
Above
Below
Oral vestibule
Buccal space
Palate

43. Lower incisors Labial Above
Below
Submental space
Oral vestibule
Lower canine Labial Below Oral vestibule
Lower premolars Buccal Below Oral vestibule
Lower first molar Buccal
Lingual
Below above
Below
Oral vestibule
Buccal space
Sublingual space
Lower second molar Buccal
Lingual
Below
Above
Below
Above
Oral vestibule
Buccal space
Sublingual space
Submandibular space
Lower third molar Lingual Above Submandibular
pterygomandibular space

44. Classification of Fascial Spaces
Primary Fascial spaces
• Maxillary
Canine
Buccal
Infratemporal
• Mandibular
Submental
Buccal
Sublingual
Submandibular
Secondary Fascial Spaces
Masseteric
Pterygomandibular
Superficial & deep temporal
Retropharyngeal
Lateral pharyngeal
Prevertebral
Parotid

45. Classification of fascial spaces :Grondinsky & Holyoke
Deep neck spaces
• Space 1: superficial to the superficial fascia – subcutaneous space
• Space 2: group of spaces surrounding the strap muscles lying superficial to the first 2
divisions of middle layer
• Space 3: lying superficial to the visceral division – contains pretracheal, retropharyngeal
& lateral pharyngeal
• Space 3A: is the carotid sheath
• Space 4: lies between the alar & prevertebral division – danger space
• Space 4A: is in posterior triangle of the neck, posterior to carotid sheath
• Space 5: prevertebral space
• Space 5A: enclosed by the the prevertebral fascia, posterior to the transverse processes
of the vertebrae, as it surrounds the scalene and spinal postural muscles.

46. General principles of therapy
1. Surgical therapy
The primary goal in surgical management of infection is to remove the
cause of the infection, which is most commonly a necrotic pulp or
deep periodontal pocket.
A secondary goal is to provide drainage of accumulated pus and
necrotic debris.
2.Supportive care:
Antibiotics, hydration of the patient, analgesics
46

47. Need for antibiotic administration
• The first factor is the seriousness of the infection when the patient
comes to the dentist. If the infection has modest swelling, has
progressed rapidly, or is a diffuse cellulitis, the evidence would
support the use of antibiotics in addition to surgical therapy.
• The second factor is whether adequate surgical treatment can be
achieved. In many situations extraction of the offending tooth may
result in rapid resolution of the infection.
• The third consideration is the state of the patient's host defenses.

48. Techniques of Incision and Drainage
• Most dependant part
• Sufficiently large opening
• Esthetically acceptable areas
• Little or no visible scarring
48

49. Complications of odontogenic
infection
Odontogeinc infections can spread towards adjacent areas or enter the
bloodstream and cause systemic complications.
1) Ludwigs angina
2) Mediastinitis
3) Necrotizing fascitis
4) Cavernous sinus thrombosis
5) Cerebral abscess
6) Meningitis
7) Acute Orbit

50. Ludwig’s angina
• Ludwig’s angina is a firm, acute, toxic cellulitis of the submandibular,
submental and sublingual spaces bilaterally.
• Etiology-
• Dental infection
• compound mandibular fracture
• oral soft tissue laceration
• Pharyngeal infection/ tonsillitis

51. Clinical feature-
Bilateral brawny swelling is observed, non fluctuating and
painful on palpation, mouth hangs somewhat open and tongue
in contact with the palate, with clear edema on floor of the
mouth.
Difficulty in breathing, chills, fever, increased salivation with
restricted tongue movements.
Airways obstruction
Swallowing difficulty

52. Diagnosis-
• Can be made on clinical findings and radiographs like lateral neck or
CT is helpful in confirmation in later stage .
Management-
• Maintenance of airway
• Intense and prolonged antibiotic therapy
• Extraction of the affected teeth
• Hydration
• Surgical decompression

53. Principles of Treatment
• It should be taken as a life threatening condition. So best
treated by aggressive intervention
• The treatment is based on the combination of following factors
1)early diagnosis
2)Maintanence of patent airway
3)intense and prolonged antibiotic therapy
4)extraction of offending tooth
5)surgical drainage/decompression of the fascia spaces
53

54. Complications
• Septicemia
• Obstruct airways and provoke edema of epiglottis
• Can spread to pharyngeal spaces from there can spread to mediastinum,
producing thoracic emphysema

55. • Bilateral incision into the submandibular space with blunt dissection to
the midline suffices, if a through and through drain or bilateral drain
meeting in midline are placed.
• Platysma suprahyoid fascia
fascia of submandibular gland is entered
mylohyoid muscles should be divided enter in sublingual space and
advance the dissection till hyoid bone

56. Mediastinitis
• Mediastinum is a space which Looks like a Greek temple.

57. • Acute purulent mediastinitis occasionally develops as a complication
of odontogenic infection, in which case it is termed descending
necrotizing mediastinitis (DNM).
• The organisms most commonly implicated include Prevotella,
Peptostreptococcus, Fusobacterium, Veillonella, Actinomyces, and
oral Streptococcus.
• When gas production is found in DNM, the condition is sometimes
referred to as gas gangrene. Gram-positive cocci (Streptococcus,
Peptostreptococcus, and Peptococcus) and gram-negative rods such
as Fusobacterium can cause tissue damage through their gas
production; in this case, the term used is nonclostridial gas gangrene
Sakamoto H,Aoki T,Kise Y;Descending necrotizing mediastinitis due to odontogenic infections;
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:412-9

58. • The criteria for the diagnosis of DNM, which were clearly defined by
Estrera et al,1 include (1) clinical evidence of severe oropharyngeal
infection, (2) characteristic roentgenographic features of mediastinitis,
(3) documentation of necrotizing mediastinal infection at the operation
or postmortem (or both), (4) and establishment of the relationship
between DNM and the oropharyngeal process
Sakamoto H,Aoki T,Kise Y;Descending necrotizing mediastinitis due to odontogenic infections;
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:412-9

59. • Because DNM progresses rapidly, early diagnosis is extremely
important. At present, CT scanning is more reliable as a diagnostic
tool than chest radiography
Sakamoto H,Aoki T,Kise Y;Descending necrotizing mediastinitis due to odontogenic infections;
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:412-9

60. Clinical features-
Dysphagia with oesophageal regurgitation
Dyspnoea
Stiff neck
Swelling in the side of the neck below sternocleidomastoid
Retrosternal pain
Non productive cough
Oedema in upper throax
High fever and chills

61. Diagnosis-
AP chest X-ray shows broadening of the mediatianal space.
Lateral neck X rays shows displacement of posterior wall of the
pharynx .
Potential complications-
Septicemia
Pleural effusion
Empyema
Compression of blood vessels
Pericarditis , shock and death

62. Management
• Medical management-
1) Antibiotics at its maximum doses supportive case in intensive care
units are mandatory.
2) Association of Penicillin G or cephalosporin and Metronidazol is
often consider in shock therapy and in presence of gram negative
organism Gentamycin has to be added.

63. Surgical management-
• Transcervical approach has been recommended, performing a wide
incision in the area of anterior edge of sternocleidomastoid muscles
and reaching all the way to the mediastinum by means of blunt
dissection.
• After proper irrigation, continuous suction drain are placed, during
post operative period, the patient must be placed in the
Trendelenberg position.
• In case of mediastinitis mortality rate is very high, its around 42%.

64. Necrotizing fasciitis
• NF was first described by Hippocrates in the 5th century
• In the late 18th century, Sir Gilbert Blane, a British naval surgeon, and
Thomas Trotter and Leonard Gillespie, both British physicians,
described NF in detail
• This term 1st suggested by Wilson in 1952.
Whitesides L;Cervical Necrotizing Fasciitis of Odontogenic Origin: A Case Report and Review of 12 Cases;J Oral
Maxillofac Surg 58:144-151, 2000

65. • Necrotizing fasciitis of the head and neck is a multifactorial, soft tissue
infection that spreads very quickly and is characterized by the
formation of large necrotic lesion and gas located in the subcutaneous
tissue and superficial fascia.
• Deep plane infection caused by bacterial toxins can results in
thrombosis, ischemia and tissue necrosis which finally can results in
multi organ failure and death.

66. • Close inspection of the patient with fully developed cervical NF shows
a rapidly enlarging swelling about the head and neck, with 3 zones of
demarcation: a wide peripheral zone of erythema outside a zone of
tender purple skin surrounding a central black necrotic area.A fetid
odor signaling dead tissue often is present.
Whitesides L;Cervical Necrotizing Fasciitis of Odontogenic Origin: A Case Report and Review of 12 Cases;J Oral
Maxillofac Surg 58:144-151, 2000

67. • Clinical features-
1) Dental infection with soft tissue involvement producing gangrene
of the subcutaneous cell producing swelling
2) With initial stage of severe pain followed by parasthesia or even
anesthesia may develop.
3) Skin will become purple dark with poorly defined edges with foul
smell and purulent exudate.
4) Cutaneous necrosis on 4th to 5th day noted
5) Fever, chills and crepitation are common feature.

68. Diagnosis-
Computerised axial tomography and magnetic resonance are the most
useful imaging studies for early diagnosis of necrotising fasciitis.
Management-
•Diseases must be recognized at its early course.
•Maintenance of airways.
•Treatment is based on early start of broad spectrum antibiotics with
intravenous route.
•Immediately surgical treatment is obligatory, with incision and
drainage, in addition to vigrous debridement of fasciae.

69. • Whitesides L;Cervical Necrotizing Fasciitis of Odontogenic Origin:
A Case Report and Review of 12 Cases;J Oral Maxillofac Surg
58:144-151, 2000
• HBO has been gaining support as an adjunctive treatment for NF
• The benefits of HBO include enhanced lysosomal degradation potential;
formation of free radicals of oxygen, which are pathogenic to many anaerobes;
elevated tissue partial pressures of oxygen, inactivating many exotoxins
produced by microorganisms; temporary reversal of tissue hypoxia to encourage
wound healing; and stimulation of neoangiogenesis
• The increase in oxygen tension also improves the killing potential of leukocytes
and inhibits growth of anaerobes

70. Cavernous sinus thrombosis
• Cavernous sinus thrombosis is one of the major complications of infection in
the maxillofacial region, which occurs rarely (7%).
• Potential odontogenic source- Buccal, infratemporal space
• The microbiology of CST is well documented. The most commonly isolated
organisms are Staphylococcus aureus (about 70%) and Streptococcus species
(about 20%). Other reported organisms include Pneumococcus, Bacteroides,
Fusobacterium, Proteus, Haemophilus, Pseudomonas, and Corynebacterium
species.
• Bacteria stimulate the formation of a thrombus by the release of a
procoagulative substance and through toxins that cause tissue damage
Valmont Desa; Cavernous Sinus Thrombosis: Current Therapy; J Oral Maxillofac Surg 70:2085-2091,
2012

71. Clinical feature
1) Pain in the eye with tenderness on pressure
2) High fluctuating fever, chills and rapid pulse
3) Venous obstruction subsequently causes oedema of eyelid
4) Chemosis, proptosis and retinal hemorrhage may be noted.
5) Terminal stage can results in meningitis.

72. Eagleton’s Criteria:
1. Known site of infection
2. Bloodstream infection evidenced by chills, high fever, and toxicity
3. Signs of venous obstruction in the retina, conjunctiva, eyelids and
orbits on one or both sides
4. Paresis of third, fourth, and sixth nerves
5. Semi comatose condition

73. • CURRENT THERAPY
Surgery
• Surgical intervention should be directed at the primary source of the
infection and the surrounding areas of involvement. Incision and
drainage of the involved sites should be accomplished as soon as
possible.
• Antibiotic therapy should consist of a third-generation cephalosporin,
nafcillin, and metronidazole. Vancomycin can be substituted for nafcillin
if the risk of methicillin resistance is high
• Steroids
• The benefits of decreasing orbital inflammation, cranial nerve edema,
vasogenic edema, and intracerebral hemorrhage must be weighed against
the potential immunosuppressive effects and possible prothrombotic
properties.
Valmont Desa; Cavernous Sinus Thrombosis: Current Therapy; J Oral Maxillofac Surg 70:2085-2091,
2012

74. • Anticoagulants
• The role of anticoagulation for the treatment of CST has been
debated The proposed benefit is the cessation of progression of the
thrombus in the septic CST. Bacteria may reside within a thrombus
for a period until canalization of the thrombus occurs, allowing for
the penetration of antibiotics.
Valmont Desa; Cavernous Sinus Thrombosis: Current Therapy; J Oral Maxillofac Surg 70:2085-2091,
2012

75. Cerebral Abscess
Cerebral abscess is a rare complication of odontogenic
infection, which can occurs as a complication of Cavernnous
sinus thrombosis or following trauma.
Most common site- Temporal lobe and cerebellum.
Clinical features-
1) Clinical signs will necessarily depend on the location of the
infectious site in the brain

76. • 2) Most commonly symptoms arises because of increased intracranial
pressure.
Intense headache
Nausea
Vomiting
• 3) Convulsion, aphasia, change in character and behavior occurs in
case of frontal lobe involvement.
• Diagnosis-
• CT scan and papillary stasis can be checked with ophthalmoscope

77. Treatment-
Antibiotics (IV Chloramphenicol or 3rd generation
cephalosporin to be used.
Steroids and Mannitol to reduce cerebral edema.
Surgery to be done for drainage.

78. Meningitis
Meningitis is the most common neurologic complication
resulting from infections in the Oral & Maxillofacial region.
Clinical features-
Headache, confusion, comatose
Fever
Stiffness of neck
Vomiting
Positive Kernig’s sign – Strong passive resistance when an
attempt is made to extend knee from flexed position

79. Brudzinski’s sign- abrupt flexion of neck in supine position
results in involuntary flexion of knees are frequently present.
Diagnosis- can be made by lumber puncture and examination
of CSF.
Management-
Neurological complications requires hospital care
Antibiotic 1gm Chloramphenicol 6th hourly recommended
with Penicillin G at 24 million units/day till culture and
sensitivity reports not come.
Use of Mannitol and steroids to control cerebral oedema and
vascular collapse and shock.

80. ACUTE ORBIT
Orbital infections of odontogenic origin are the rarest sequelae, with a
prevalence of 1.3%. Correct diagnosis, adequate antibiotic therapy, and
surgical drainage are the keys to success.
Blake FAS, Siegert J; The Acute Orbit: Etiology, Diagnosis, and Therapy;J Oral Maxillofac Surg 64:87-
93, 2006

81. • Surgical incision and drainage of the subperiosteal or intraorbital
abscess.
• Antibiotic therapy, initially intravenously.
• Eradication of the primary source, ie, revision of the paranasal sinuses
and extraction of decayed teeth or other osseous infections

82. References
• Oral and maxillofacial infections- Topazian 4th edition
• Textbook of oral and maxillofacial surgery- Kruger 6th edition
• Oral and maxillofacial surgery- volume two Daniel.M.Laskin
• Anatomy for surgeons vol.1 Henry Hollinshead
• Essentials of human anatomy
• Peterson s principles of oral and maxillofacial surgery, vol.1
• Valmont Desa; Cavernous Sinus Thrombosis: Current Therapy; J Oral
Maxillofac Surg 70:2085-2091, 2012

83. • Blake FAS, Siegert J; The Acute Orbit: Etiology, Diagnosis, and
Therapy;J Oral Maxillofac Surg 64:87-93, 2006
• Sakamoto H, Aoki T,Kise Y;Descending necrotizing mediastinitis due
to odontogenic infections;Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2000;89:412-9
• Whitesides L;Cervical Necrotizing Fasciitis of Odontogenic Origin: A
Case Report and Review of 12 Cases;J Oral Maxillofac Surg 58:144-
151, 2000
• Sharma M, Patil K, Guledgud MV. Ultrasonographic evaluation of
fascial space infections of odontogenic origin. J Oral Maxillofac
Radiol 2014;2:8-14