Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine Al-Azhar University. The Pathogenesis of infection in oro-facial region due to odontogenic origin is a common clinical issue. bacterial invasion to deeper tissues usually a spread from diseased dental pulp. Recent evidences indicated a multi-microbial nature. The spread of infection is governed by the thickness of the investing bone and the anatomical relation of the tooth root to the attached muscle. Infection could spread from one facial space to another, and the condition may be aggravated to life threatening situations.

2. Dr. Ahmed M. Adawy
Professor Emeritus, Dep. Oral & Maxillofacial Surg.
Former Dean, Faculty of Dental Medicine
Al-Azhar University

3. Orofacial infections may be odontogenic or non
odontogenic in nature and the vast proportion of
odontogenic infections are caused by the endogenous
bacteria present in the oral cavity . Examples of
odontogenic infections are periapical and periodontal
infections. Most of non-odontogenic infections are
associated with an underlying medical
condition. Examples of non-odontogenic infections
are that of the skin, tonsils, or maxillary sinuses.
Occasionally, infections could develop following an
anesthetic injection or a surgical procedure
(1)

4. One of the most difficult problems to manage in
dentistry is odontogenic infections. These
infections may range from low-grade, well-
localized infections that require only minimal
treatment to severe life-threatening facial space
infections

5. The predisposition of an infection is related to an
interruption of the fine balance between the host,
the micro-organism and the environment. This
imbalance, in turn, may lead to the multiplication
of micro-organisms followed by invasion of
different structures. The severity of infection is
related to the number and virulence of micro-
organisms and resistance of the host

6. Odontogenic infections are typically
Polymicrobial. The most common species of
bacteria isolated in odontogenic infections are the
anaerobic gram-positive cocci Streptococcus
milleri group and Peptostreptococcus, anaerobic
gram-negative rods, such as Bacteroides
(Prevotella) also play an important role. Aerobic
bacteria has little effect
(2)

7. Odontogenic infections progress through 3 stages:
inoculation, cellulitis and abscess . Sinus tract/fistula
may be seen in neglected cases
Inoculation
Is characterized by the entry of pathogenic microbes
into the body without disease occurring.
An infection involves the proliferation of microbes
resulting in triggering of the defense mechanism, a
process manifesting as inflammation
(3)

8. Inflammation
Inflammation is the series of changes which
occurred in the living tissue in response to an
irritant. The manifestation of inflammation is
typical and is characterized by: rubor (redness),
calor (hotness), tumor (swelling or edema), dolor
(pain), and functio laesa (loss of function). This
reaction is protective and aims at limiting or
eliminating the irritant. Depending on the
duration and severity, inflammation is
distinguished as acute, subacute or chronic
.

9. Cellulitis
Is an acute diffuse painful indurated swelling of the soft
tissues resulting from a diffuse spreading of purulent
exudate along the fascial planes with or without
suppuration
Abscess
A collection of pus in a cavity formed by disintegration
of tissue as result of infection

10. Discharging Sinus
Some times abscess ruptures to produce a draining sinus
tract. Usually, infection recur when the site of drainage
closes. Sinus is thus a one side tract of a single
compartment

11. Fistulae
A drainage pathway or abnormal communication
between two epithelium-lined surfaces due to
destruction of the intervening tissue. Fistula is thus an
epithelialized tract opening in both side of two
different compartments

12. The usual cause of odontogenic infections is necrosis of
dental pulp, which is followed by bacterial invasion
through the pulp chamber and into the deeper tissues.
Necrosis of the pulp is the result of deep caries of a
tooth, to which the pulp responds with a typical
inflammatory reaction. Vasodilatation and edema cause
pressure in the tooth and severe pain as the rigid walls
of the tooth prevent swelling. If left untreated the
pressure leads to strangulation of the blood supply to
the tooth through the apex and consequent necrosis

13. The necrotic pulp then provides a
perfect setting for bacterial
invasion into the bone tissue. Pus is
formed in the cancellous bone, and
spreads in various directions by
way of the tissues presenting the
least resistance until a cortical plate
is encountered

14. Clinically, the condition has rapid onset. Radiographically,
changes in bone density may not be noticeable (you have to
wait for approximately 10 days to detect bone rarefaction).
It is characterized by symptoms that are classified as local
and systemic
Local Symptoms
Pain
The severity of the pain depends on the degree of
inflammation. Initially, the pain is dull and continuous and
worsens during percussion of the responsible tooth or when
it comes into contact with antagonist teeth. There is a sense
of elongation of the responsible tooth and slight mobility

15. Local Symptoms
Edema
Edema appears intraorally or extraorally and it usually has
a buccal and more rarely palatal or lingual localization.
This swelling presents before suppuration, particularly in
areas with loose tissue, such as the sublingual region, lips,
or eyelids. Usually the edema is soft with redness of the
skin. During the final stages, the swelling fluctuates,
especially at the mucosa of the oral cavity. This stage is
considered the most suitable for incision and drainage of
the abscess

16. Systemic Symptoms
The systemic symptoms usually observed are: fever,
chills, malaise with pain in muscles and joints,
insomnia, nausea, and vomiting. Laboratory tests
usually show leukocytosis, an increased erythrocyte
sedimentation rate, and a raised C-reactive protein
(CRP) level
Treatment
Extraction of the tooth (or removal of the necrotic
pulp by an endodontic procedure) results in resolution
of the infection

17. Routes of Spread of Odontogenic Infection:
a. By direct continuity via the tissue
b. Via the lymphatics into the regional lymph nodes and
subsequently into the blood stream
c. Haematogenous spread leading to thrombophlebitis,
bacteremia or septicemia. Thrombus may propagate
along the veins, entering the cranial cavity via emissary
veins to produce cavernous sinus thrombosis

18. Whether the pus spreads buccally, palatally or lingually
depends mainly on the position of the tooth in the dental
arch, the thickness of the bone, and the distance it must
travel

19. The length of the root and the relationship between the
apex and the proximal and distal attachments of
various muscles also play a significant role in the
spread of pus

20. Sometimes, infection may spreads towards the fascial
spaces, forming serious abscesses called fascial space
infection. The fascial spaces are potential areas and do
not exist in healthy individuals. Bone, muscle, fascia,
neurovascular bundles, and skin can all act as barriers
to the spread of infection. It should be remembered
however, that no tissue barrier or boundary is so
restrictive to universally prevent spread of infection
into contiguous anatomical spaces

21. Facial spaces have been classified as either primary or
secondary spaces infection
Primary maxillary spaces
 Canine
 Buccal
 Infratemporal
Primary mandibular spaces
 Submental
 Buccal
 Submandibular
 Sublingual
(4)

22. Secondary fascial spaces
•Masseteric
•Pterygomandibular
•Superficial and deep temporal
•Lateral pharyngeal
•Retropharyngeal
•Prevertebral

23. Infection at the base of the upper lip typically originates from
the upper anterior teeth. It spreads to the orbicularis oris
muscle, from the labial sulcus between the levator labii
superioris muscle and the levator angularis oris muscle

24. Spread of infection to the canine
fossa usually originates from
maxillary canine or upper
premolar teeth, often presenting
above the buccinator muscle
attachment. These swellings
usually obliterate the nasolabial
fold and may extend to the lower
eyelid

25. The attachment of the buccinator muscle to the base of the
alveolar process can control the spread of infection in the
region of the mandibular and maxillary molars. An
infection spreads intraorally, superficial to the buccinator
muscle, in front of the anterior border of the masseter
muscle. Thus, the clinical manifestations of infection in this
space are characterized by swelling confined to the cheek

26. The palate is usually involved in infections originating
from the maxillary lateral incisor or the palatal roots of the
posterior teeth. The infection spreads from the apices of
these teeth, perforating the palatal alveolar bone, and pus
accumulates below the palatal mucoperiosteum

27. Extension of infection from maxillary molars can pass into
the infratemporal space. The space is located behind the
zygomatic bone posterior to the maxilla and medial to the
insertion of the medial pterygoid muscle. The
infratemporal space is bounded superiorly by the greater
wing of the sphenoid and is in close proximity to the
inferior orbital fissure, with a possible risk of spread of
infection to the orbit. Infection may ascend into the
cavernous sinus (through venous plexus in the ovale and
spinosum foramen)

28. Infratemporal space

29. The submental space lies between the two anterior
bellies of the digastric muscle. Anteriorly and laterally
this space is bounded by the body of the mandible. It is
contained, superficially, by the platysma muscle and,
deeply and superiorly, by the mylohyoid muscle.
Infection of this space usually arises from mandibular
anterior teeth, where the infection perforates the
lingual cortex; swelling of the submental region is a
characteristic clinical feature. The skin over the
swelling is stretched and hardened, and the patient
experiences considerable pain and difficulty with
swallowing

31. The submandibular space is located below the mylohyoid
muscle, medial to the ramus and the body of the mandible.
It is bounded anteriorly by the attachments of the anterior
belly of the digastric muscle and posteriorly by the
posterior belly of digastric muscle and the stylomandibular
ligament. Infection from the posterior mandibular teeth
may pass lingually, below the attachment of the
mylohyoid muscle, into this space. Clinically, swelling of
the submandibular region tends to obliterate the angle of
the mandible, causing pain and redness of the skin
overlying this region. Dysphagia is also usually a marked
symptom

33. Infection spreads into this space as the result of
perforation of the lingual cortex, above the attachment of
the mylohyoid muscle. This space is bounded superiorly
by the mucous membranes and inferiorly by the
mylohyoid muscle. The genioglossus and geniohyoid
muscles form the medial boundary. Laterally, this space is
bounded by the lingual surface of the mandible. Infection
in this space will raise the floor of the mouth and displace
the tongue, medially and posteriorly. Such tongue
displacement may compromise the airway and immediate
intervention may be required. Dysphagia and difficulty
with speech are also common

35. The most common source of infection in the submasseteric
space is from lower third molar pericoronitis. This space is
bound laterally by the masseter muscle and medially by the
outer surface of the ramus of the mandible. It is in direct
communication with the lateral pharyngeal space posteriorly.
The temporalis muscle divides the superior part of this space
into two portions, the superficial temporal space and the
deep temporal space. Severe trismus due to spasm of the
masseter muscle is a characteristic feature of involvement of
this fascial space

36. Temporal
space
Massetric
space

37. Infection in this space is manifested by trismus, due to
the involvement of the pterygoid muscles. This space
is bounded medially by the medial pterygoid muscle
and laterally by the medial surface of the mandible,
anteriorly by the pterygomandibular raphe, and
posteriorly by the deep lobe of the parotid gland. The
lateral pterygoid muscle forms the roof of this space

38. Pterygomandibular
space

39. This space is located on the lateral side of the neck,
bounded medially by the superior constrictor muscle of
the pharynx and posterolaterally by the parotid space. The
lateral pharyngeal space contains the carotid sheath,
glossopharyngeal nerve, accessory nerve, and the
hypoglossal nerve, as well as the sympathetic trunk. Thus,
spread of infection into this space carries a significant
danger of spreading into a descending neck infection and
involvement of the mediastinum. Clinically, stiffness of
the neck, swelling of the lateral wall of the pharynx,
medial displacement of the tonsils, dysphagia, and trismus
are among the characteristic clinical features of
involvement of this space

41. This space is located between the posterior wall of the
pharynx and the prevertebral fascia. This space is in
direct communication with the base of the skull,
superiorly, and the mediastinum, inferiorly. It has the
same characteristic clinical features as infection of the
lateral pharyngeal space and carries a significant
complication risk of a descending neck infection

42. Patients with dentofacial infections may present with various
signs and symptoms, ranging from less important to extremely
serious. Quick assessment of the patient’s situation is essential
as the first step of therapy. If the patient shows central nervous
system changes, airway compromise, or toxification, then
immediate hospitalization, aggressive medical treatment, and
surgical intervention may be necessary. Basic principles of
patient evaluation must be followed. A complete patient history,
physical examination, laboratory investigation, radiological
investigation, and accurate and appropriate interpretation of
findings must be made. Following these basic principles
provides the best chance of accurate diagnosis and treatment (5)

43. 1- Proper knowledge of anatomy, anatomical landmarks
and vital structures of the face and neck is necessary to
predict pathways of spread of infections and to drain these
spaces
2- Remove the cause (i.e. extract the tooth, open &
extirpate the pulp)
3- Incision & Drainage (never let the sun set on undrained
pus)
4- Antibiotics

44. For intraoral abscess, stab incision is done through the
mucosa down deep to the underlying bone. Incisions
for extra-oral abscesses should be placed in a skin
crease to leave the least evident scar. Once the skin
incision is made, blunt evacuation of pus might be
done using a curved haemostat. The abscess cavity
should be kept open to allow continuous drainage.
Corrugated rubber, ribbon gauze, or tubular plastic
drain might be used

45. Incision and drainage helps to get rid of toxic purulent
material, to decompress edematous tissues, to allow
better perfusion of blood, which contains antibiotic
and defense elements, and to increase oxygenation of
the infected area

46. Antibiotics is generally indicated when the swelling is
diffuse and spreading, and especially if fever is
present and infection spreads to the fascial spaces,
regardless of whether there is an indication of the
presence of pus. Antibiotic therapy is usually empiric,
given the fact that it takes time to obtain the results
from a culture sample. Odontogenic infections are
polymicrobial. Historically, penicillins have been used
to treat odontogenic infections.

47. With the ever-increasing bacterial resistance to penicillin-
based antibiotics with dental pathogens and concurrent
clinical failures with penicillins, other agents have become
increasingly attractive. Amoxicillin/clavulanate,clindamycin,
and metronidazole are useful alternatives in combating the
anaerobic bacteria involved in dentoalveolar infection .
Clindamycin has more recently become a drug of choice for
the management of odontogenic infections because of the
bacterial susceptibility to this drug, great oral absorption,
low emergence of bacterial resistance and good antibiotic
levels in bone.
(6)

48. 1. Rapidly progressive cellulitis
2. Dyspnea (shortness of breath or difficult breathing)
3. Dysphagia (difficulty in swallowing)
4. Spread to deep facial spaces
5. Fever of more than 38º C
6. Intense trismus ( inter-incisal distance less than 10 mm)
7. Failure of initial treatment
8. Severe involvement of general health status
9. Immunocompromised patients (diabetes, alcoholism or
drug addiction, malnutrition, treatment with corticoids,….)
(7)

49. Ludwig's Angina is a massive indurated brawny
cellulites, occurs bilaterally in the submandibular,
sublingual & submental spaces. Infection is propagated by
lymphatic spread or directly through submandibular space.
Cellulitis is then rapidly spread to involve bilaterally the
parapharyngeal and pterygoid spaces

50. Clinically, the condition is characterized by:
1. Painful bilateral swelling of floor of mouth and
elevation of tongue.
2. Bilateral firm, brawny painful, diffuse swelling of upper
part of neck
3. Difficulty in swallowing and breathing
4. Rapid pulse, high fever, fast respiration
5. Leucocytosis
Patient should be hospitalized. Conservative treatment
includes intravenous antibiotic therapy and close airway
observation . Pus is evacuated, when indicated, by
through & through drainage
(8)

51. Infections may spread via hematogenous route to the
cavernous sinus occurs from:
1- Anteriorly: a) Superior labial venous plexus to
b) Anterior facial vein, then via c) Superior or inferior
ophthalmic vein into the cavernous sinus
2- Posteriorly: from retromandibular vein to the ptrygo-
mandibular venous plexus, the emissary vein passing
through foramen ovale, spinosum, to cavernous sinus
3- Superior petrosal sinus (inside the ear)
(9)

52. Anterior
pathway
ophtalmic v.
infraorb. v.
deep facial v.
Posterior
pathway
pterygoid plx.
→ oval or
spinosum for.

53. Never squeeze infection
boil in the dangerous
area

54. Osteomylitis is defined as an inflammation of the
bone marrow with a tendency to progression to
involve adjacent cortical plates and often periosteal
tissues. The incidence of osteomyelitis is much
higher in the mandible due to the dense cortical bone
that prevents the penetration of periosteal blood
supply, and the inferior alveolar artery is the only
supply to the mandible. It is much less common in
the maxilla due to the excellent blood supply from
number of different arteries. In addition the maxillary
bone is much less dense than the mandible
(10)

55. 1- Acute suppurative
2- Subacute
3- Chronic suppurative
4- Rarely, a sclerotic nonpurulent form of osteomylitis
occurs; this is termed Garrès sclerosing osteomylitis.
Other related disorders are chronic recurrent
multifocal osteomylitis; tuberculous osteomylitis
Acute and chronic osteomylitis is distinguished by the
development of dead bone sequestra. Sequestra is an
island of dead bone that have not been resorbed

56. The appearance of “moth-eaten” bone or sequestrum
of bone, is the classic feature of chronic osteomylitis

57. Classic treatment is sequestrectomy and saucerization.
The aim is to débride the necrotic bony sequestra in
the infected area and improves blood flow
Decortication involves removal of the dense, often
chronically infected and poorly vascularized bony
cortex till reaching good bleeding bone, and
placement of the vascular periosteum adjacent to the
medullary bone to allow increased blood flow and
healing in the affected area

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