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1. The Spread Point of Dental Infection
Odontogenic infection can come from two lines,
o periapical, as a result of pulp necrosis and bacterial invasion into periapical
network,
o and periodontal, as a result of inoculation of bacteria in periodontal pocket.
the most common is through periapical.
Line periapical occur from dental pulp disease, which contains elements of
neurovascular teeth.
Invasion of bacteria in dental pulp is produced necrosis of the neurovascular network.
The infection will spread from the cancellous bone to the cortical plate.
If the cortical plate is thin, then the infection will penetrate the bone and the soft
tissue, and is called the palatal abscess.
While in line periodontal inflammatory process occurs when the virulence of bacteria
exceeds the host's local defense or foreign objects lodged in the groove ginggiva.
Bacteria and inflammatory exudate ginggiva extends from the groove through the
periodontal ligament periapical or tooth radicular area and showed the same reaction
with periapical tooth infection.
These inflammatory products may also cut into supraperiostal field vestibula oral or
cut into the field of space subperiostal mandible body.
Acute or chronic process will evolve.
The chronic process can be a periapical cysts, Granuloma periapical, osteomyelitis, or
fistula formation.
Cysts periapical and Granuloma formation indicates local processes and identified
through dental radiographs as a radiolucent periapical with clear boundaries.
The infection can spread through the alveolar bone or medullary deeper into the
mandible bone basilla or maksilla, producing osteomyelitis.
Some chronic osteomyelitis associated with oral cutaneous fistula in radiographs
showed irregular, blurred shapes.
Periapical chronic infection can also cause paluris formation, fistula formation from
the apex of the teeth through the oral mucosa to vestibula.
The acute process can be either bacterimia, septicemia, cellulitis, dentoalveolar
abscess, and fascial space infections.
Some
combinations of odontogenic manifestation of acute infection can occur when the
infection spreads through the alveolar into the nearest soft tissue.





6. Therapy of Odontogenic Infection

1. Drainage operations
of antibiotics without drainage of pus will not solve the problem of abscess disease
starting antibiotic therapy without gram staining and culture will lead to mistakes in
identifying infectious disease-causing organisms odontogen
important to drain all the primary space especially if the examination, the potential
secondary infection also
CT scans can help identify the spaces that are infected
Panoramic X-rays can help identify when the suspected infection of the teeth involved
1. Treatment or Medication
analgesics and provide care for primary infection if the patient has trismus, swelling or
pain in the mouth.

1. Identification of bacteria responsible
expected to cause the alpha-hemolytic Streptococcus and other anaerobic bacteria
culture should be performed on all patients through incision and drainage and
sensitivity test done when the patient does not visit improved (possibly resistant to
antibiotics)
Results aspiration of the abscess could be sent for culture and sensitivity testing if late
incision and drainage performed

1. Selecting appropriate therapy antibiotic
parenteral penicillin
metronidazole in combination with penicillin can be used in severe infections
Clindamycin for penicillin allergic patients
Cephalosporins (first generation cephalosporins)
antibiotics should not be changed during incisi and drainage in cases of significant
infection odontogen
tooth extraction will cure the infection causes odontogen

2. Fascial space infections
Primary maxillary spaces
Canine
Buccal
Intratemporal
Primary mandibular spaces
Submandibular & Sublingual
Submental
Third molar impacts
Secondary fascial spaces
Mastication (Masseteric, Pterygomandibular, Superficial and deep temporal)
Ludwigs Angina
Lateral pharyngeal
Retropharyngeal
Mediastinitis

1. Primary maxillary
spaces
1. Canine space
a. Canine space is a thin potential space between the levator anguli oris and the levator
labii superi oris muscles. The canine space becomes involved primarily as the result of
infections from the maxillary canine tooth. FIG. 16-2 Canine space infection in
patient's right side resulted from infected canine tooth. The swelling of nasolabial and
infraorbital areas is demonstrated.
b. This is the only tooth with a root
sufficiently long to allow erosion to occur through the alveolar bone superior to the
muscles of facial expression. The infection erodes superior to the origin of the levator
angulioris muscle and below the origin of the levator labii superioris muscle. When
this space is infected, swelling of the anterior face obliterates the nasolabial fold (Fig.
16-2). Spontaneous drainage of infections of this space commonly occurs just inferior
to the medial canthus of the eye.
c. Canine space is the region between the anterior surface of the maxilla and the
overlying levator muscles of the upper lip. Infection of this space manifests as
swelling with obliteration of the nasolabial fold and sometimes pus may drain through
the inner canthus of the eyes.

1. Buccal spaces
a. Buccal spaces are bounded by the overlying skin of the face on the lateral aspect and
the buccinator muscle on the medial aspect (Fig. 16-3). This space may become
infected from extensions of infection from either the maxillary or mandibular teeth.
The posterior maxillary teeth, most commonly the molars, cause most buccal space
infections.
b. The buccal space becomes involved from the teeth when infection erodes through the
bone superior to the attachment of the buccinator muscle. Involvement of the buccal
space usually results in swelling below the zygomatic arch and above the inferior
border of the mandible. Thus both the zygomatic arch and the inferior border of the
mandible are palpable in buccal space infections.














1. Infratemporal space
a. The infratemporal space lies posterior to the maxilla. It is bounded medially by the
lateral plate of the pterygoid process of the sphenoid bone and superiorly by the base
of the skull. Laterally, the infratemporal space is continuous with the deep temporal
space.

b. The infratemporal space is rarely infected, but when it is, the cause is usually an
infection of the maxillary third molar (Fig. 16-4). Maxillary odontogenic infections
may also spread superiorly to cause secondary periorbital or orbital cellulitis or
cavernous sinus thrombosis. Periorbital or orbital cellulitis rarely occurs as the result
of odontogenic infection, but when either does occur, the presentation is typical:
redness and swelling of the eyelids and involvement of both the vascular and neural
components of the orbit. This is a serious infection and requires aggressive medical
and surgical intervention from multiple specialists.

c. Cavernous sinus thrombosis may also occur as the result of superior spread of
odontogenic infection via a hematogenous route (Fig. 16-5). Bacteria may travel from
the maxilla posteriorly via the pterygoid plexus and emissary veins or anteriorly via
the angular vein and inferior or superior ophthalmic veins to the cavernous sinus. The
veins of the face and orbit lack valves, which permits blood to flow in either direction.
Thus bacteria can travel via the venous drainage system and contaminate the
cavernous sinus, which results in thrombosis.


d. Cavernous sinus thrombosis is an unusual occurrence that is rarely the result of an
infected tooth. Like orbital cellulitis, cavernous sinus thrombosis is a serious, life-
threatening infection that requires aggressive medical and surgical care. Cavernous
sinus thrombosis has a high mortality even today.


1. Primary mandibular spaces
1. Sublingual &
submandibular spaces
a. The sublingual and submandibular spaces have the medial border of the mandible as
their lateral boundary. These two spaces are involved primarily by lingual perforation
of infection from the mandibular molars, although they may be involved by premolars,
as well. The factor that determines whether the infection is submandibular or
sublingual is the attachment of the mylohyoid muscle on the mylohyoid ridge of the
medial aspect of the mandible (Fig. 16-7).

b. If the infection erodes through the medial aspect of the mandible above this line, the
infection will be in the sublingual space and is most commonly seen with premolars
and the first molar. If the infection erodes through the medial aspect of the mandible
inferior to the mylohyoid line, the submandibular space will be involved. The
mandibular third molar is the tooth that most commonly involves the submandibular
space primarily.


c. The second molar may involve either the sublingual or submandibular space,
depending on the length of the individual roots, and may involve both spaces
primarily. The sublingual space lies between the oral mucosa of the floor of the mouth
and the mylohyoid muscle (Fig. 16-8, A). Its posterior border is open, and therefore it
freely communicates with the submandibular space and the secondary spaces of the
mandible to the posterior aspect. Clinically little or no extraoral swelling is produced
by an infection of the sublingual space, but much intraoral swelling is seen in the floor
of the mouth on the infected side (Fig. 16-8, B). The infection usually becomes
bilateral, and the tongue becomes elevated.

d. The submandibular space lies between the mylohyoid muscle and the overlying skin
and superficial fascia (Fig. 16-9). The posterior boundary of the submandibular space
communicates with the secondary spaces of the jaw posteriorly. Infection of the
submandibular space causes swelling that begins at the inferior border of the mandible
and extends medially to the digastric muscle and posteriorly to the hyoid bone (Fig.
16-10).

1. Submental space infection
1. Infection can result directly due to infected mandibular incisor or indirectly
from the submandibular space
2. Space located between the anterior bellies of the digastric muscle laterally,
deeply by the mylohyoid muscle, and superiorly by the deep cervical fascia,
the platysma muscle, the superficial cervical fascia, and the skin











MICROBIOLOGY OF ODONTOGENIC INFECTIONS
Usually caused by endogenous bacteria
Aerobic bacteria alone rarely causative agents
Streptococcus species are usually the etiologic organisms if aerobic bacteria present
Half odontogenic infections: anaerobes
Most odontogenic infections due to mixed flora
Mixed infections may have 5-10 organisms present
Bacterial composition
1. 5%-aerobic bacteria
2. 60%-anaerobic bacteria
3. 35% mixed aerobic and anaerobic bacteria
Commonly cultured organisms: alpha-hemolytic Streptococcus, Peptostreptococcus,
Peptococcus, Eubacterium, Bacteroides (Prevotella)
melaninogenicus, and Fusobacterium.
Common symptoms
oral, neck, and dental pain
neck swelling
Odynophagia
Dysphagia
Dysphonia
Trismus
tongue swelling
Airway patency is the main concern
Diagnosis
Clinical findings
Bacterial culture
CT scan

Treatment
Maintenance of airway patency
Surgical incision and drainage
Antibiotics active against oral flora
Penicillin
Erythromycin
Clindamycin
Cefadroxil
Metronidazole
Tetracycline

3. Infection of third molar impaction

Pericoronitis
Infection due to complication of partial bony impaction.
The flap of gum tissue which partially covers the erupting third molar, creates a pocket
where bacteria that are present in the mouth can grow.
The swelling and infection can become very serious.

Symptoms
spontaneous pain
localized swelling
purulence/drainage
foul taste
difficulty swallowing
enlarged lymph nodes
fever
limited mouth opening
facial cellulitis/infection
In most instances the symptoms will recur and the only definitive treatment is
extraction.
If left untreated, however, recurring infections are likely, and the infection can
eventually spread to other areas of the mouth.

Diagnosis
history test
clinical examination
radiographic examination
total and differential counts of leucocytes
bacteriological examinations done to determine the nature of causative organisms so
that it is helpful to confirm the sensitivity to various antibiotics.

Treatment
Antibiotics (penicillin, metronidazole)
Warm salt water rinses
Analgesics
Extraction
It should go away in about one week. However, if the tooth does not completely enter
the mouth and food and bacteria keep building up under the gum, pericoronitis will
more than likely return.
Pericoronitis does not cause any long-term effects. If the affected tooth is removed or
erupts fully into the mouth, the condition cannot return.




3. Secondary fascial
spaces
1. Mastication spaces
a. Masseteric spaces
The masseteric space exists between the lateral aspect of the mandible and the medial
boundary of the masseter muscle (see Fig. 16-4). It is involved by infection most commonly
as the result of spread from the buccal space or from soft tissue infection around the
mandibular third molar. When the masseteric space is involved, the area overlying the angle
of the jaw and ramus becomes swollen. Because of the involvement of the masseter muscle,
the patient will also have moderate-to-severe trismus caused by inflammation of the masseter
muscle.
b. Pterygomandibular space
The pterygomandibular space lies medial to the mandible and lateral to the medial pterygoid
muscle (see Fig. 16-4). This is the space into which local anesthetic solution is injected when
an inferior alveolar nerve block is performed. Infections of this space spread primarily from
the sublingual and submandibular spaces. When the pterygomandibular space alone is
involved, little or no facial swelling is observed; however, the patient almost always has
significant trismus. Therefore trismus without swelling is a valuable diagnostic clue for
pterygomandibular space infection. The most common occurrence of this clinical picture is
caused by needle tract infection from a mandibular lock.
c. Temporal space
The temporal space is posterior and superior to the masseteric and pterygomandibular spaces
(see Fig. 16-4). It is divided into two portions by the temporalis muscle:
(1) a superficial portion that extends to the temporal fascia
(2) a deep portion that is continuous with the infratemporal space
Rarely are the superficial and deep temporal spaces secondarily involved and usually only
in severe infections. When these spaces are involved, the swelling that occurs is evident in
the temporal area, superior to the zygomatic arch and posterior to the lateral orbital rim.
1. Ludwigs Angina
An acute, toxic cellulitis, beginning usually in the submandibular space and
secondarily involving the sublingual and submental space as well.
Commonly a disease of dental origin.
A.k.a Angina Ludovici.
Usually affect second and third molars.
Ludwigs angina is rare and sometimes fatal.
Morbidity and mortality primarily result from airway compromise from swelling.
Streptococci and staphylococci are
the most common bacteria associated with Ludwigs angina.

Source of infection :-
Involvement of a mandibular molar, either periapical or periodontal.
Submandibular gland sialadenitis.
Oral soft tissue lacerations.
A penetrating injury of the floor of mouth (stab wound).
Osteomyelitis in a compound jaw fracture.

Clinical features
Swelling of the floor of mouth
Swelling is firm, painful and diffuse, showing no evidence of localization and paucity
of pus.
Elevation of tongue
Dysphagia (difficulty in swallowing)
Stridor (difficulty in breathing)
High fever
Rapid pulse, fast respiration
Moderate leukocytosis
As the disease continues, the swelling involve neck and edema may occur.
The infection may spread to parapharyngeal spaces, to the carotid sheath or to
pterygopalatine fossa.

Diagnosis
A CT scan of the neck may be recommended.
Culture of fluid from the tissues may show bacteria.

Differential Diagnosis in Cases of Ludwigs
Angina
Angioneurotic edema
Cellulitis
Lingual carcinoma
Lymphadenitis
Peritonsillar abscess
Salivary gland abscess
Sublingual hematoma

Laboratory findings
Stretococci (mostly found)
Fusiform bacili and spiral form
Staphylococci
Diphteroids
Prevotella melaninogenicus
Prevotella oralis
Prevotella corrodens

Treatment
Management :-
Early recognition of incipient cases
Maintenance of airway
Intense and prolonged antibiotic therapy
Extraction of affected tooth
Surgical drainage
For edema of glottis, do the tracheotomy that creates an opening through the neck into
the windpipe to prevent suffocation.

Commonly Used Antibiotic Agents in Cases of Ludwigs Angina :-
Ampicillin/sulbactam
Cefoxitin
Clindamycin*
Gentamicin
Penicillin G plus metronidazole
Piperacillin/tazobactam
Ticarcillin/clavulanate
*Administer if patient is allergic to penicillin.

3. Lateral pharyngeal space
Boundaries
One of the parapharyngeal space, is bounded anteriorly by the buccopharyngeal aponeurosis,
the parotid gland and the pterygoid muscles, posteriorly by the prevertebral fascia, laterally by
the carotid sheath and medially by the lateral wall of the pharynx.
Clinical feature
Source infection is from 3
rd
molar, sometimes 2
nd
molar, particularly by way of
selection in the submandibular space or by direct extension from the tooth.
Infection of this space with abscess formation may impinge on the pharynx, causing
difficulties in swallowing and even in breathing. Pain may also be referred to the ear.
Trismus is usually present.
Anesthetic may be required to confirm the diagnosis.
The tonsillar pillar and tonsil are displaced medially, and so is the uvula.
In latter condition, the trismus is less severe or absent and the tonsil, instead of being
normal, is enlarged and inflamed.
Lateral pharyngeal space infections have the potential to spread upwards through
various foramina at the base of the skull and cause cavernous sinus thrombosis,
meningitis, and brain abscess.
Spread posteriorly to the retropharyngeal space or invade the carotid sheath.
Lateral pharyngeal space communicate with the mediastinum by the prevertebral
fascia so that the infection may reach this area by direct extension.

4. Retropharyngeal Space
Boundries
Anteriorly by the wall of the pharynx
Posteriorly by the prevertable fascia
Laterally by the lateral pharyngeal space and carotid sheath
Clinical features
Infection here may result from medial extension of infection on the lateral pharyngeal space,
and an abcess may form, displacing or pressing the buccopharyngeal fascia foward and
impinging on the pharynx.
Patient with retropharygeal space will have:
I. Pain
II. Dysphagia
III. Dyspnea
IV. Nuchal rigidity
V. Bulging of the posterior pharyngeal wall is seen is prominent on one side because
of adherence of the median raphe of the prevertable fascia.
Downward extension of a retropharyngeal space infection will result in mediastinitis may
cause thrombosis of the internal jugular vein and erosion of the internal carotid
artery resulting in fatal hemorrhage.
Radiographs of lateral soft tissue can be helpful in establishing a diagnosis by permitting
visualization of the widened retropharyngeal space
A computed tomography can also be used.


Treatment
Retropharyngeal abscesses often need to be drained surgically.
A vertical incision is made in the upper neck to drain the pus.
Tracheotomy is often required to prevent upper airway obstruction caused by oedema
in the neck.
Antibiotics are also given.

1. Mediastinitis
Mediastinitis is inflammation of the tissues in the mid-chest, or
mediastinum. It can be either acute or chronic.
Acute mediastinitis is usually bacterial and due to rupture of organs in the
mediastinum.
As the infection can progress rapidly, this is considered a serious condition.
Chronic sclerosing (or fibrosing) mediastinitis, while potentially serious, is
caused by a long-standing inflammation of the mediastinum, leading to
growth of acellular collagen and fibrous tissue within the chest and around
the central vessels and airways.
Symptoms
Chest pain
Chills
Coughing up blood
Fever
Malaise
Shortness of breath
Causes and Treatment
Acute
Before the development of modern cardiovascular surgery, cases of acute
mediastinitis usually arose from either perforation of the esophagus or from
contiguous spread of odontogenic or retropharyngeal infections.
However, in modern practice, most cases of acute mediastinitis result from
complications of cardiovascular or endoscopic surgical procedures.
Treatment usually involves aggressive intravenous antibiotic therapy and
hydration.
If discrete fluid collections (such as abscesses) have formed, they may have
to be surgically drained.

Chronic
Chronic mediastinitis is usually a radiologic diagnosis manifested by diffuse
fibrosis of the soft tissues of the mediastinum.
This is sometimes the consequence of prior granulomatous disease, most
commonly histoplasmosis.
Other identifiable causes include tuberculosis and radiation therapy.
Fibrosing mediastinitis most frequently causes problems by constricting
blood vessels or airways in the mediastinum.
This may result in such complications as superior vena cava syndrome or
pulmonary edema from compression of pulmonary veins.
Treatment for chronic fibrosing mediastinitis is somewhat controversial, and
may include steroids or surgical decompression of affected vessels.

3. Osteomyelitis of the jaws
1. Acute osteomyelitis of the jaws
1. Osteomyelitis of the jaws is mainly a disease of adults with several potential sources
of infection:
Periapical infection
A periodontal pocket involved in a fracture
Acute necrotizing gingivitis or pericoronitis( even more rarely)
Penetrating, contaminated injuries (open fractures or gunshot wounds)
2. Important predisposing causes are:
a. Local damage to or disease of the jaws
Fractures including gunshot wounds
Radiation damage
Pagets disease or osteoporosis
b. Impaired immune defences
Acute leukemia
Poorly controlled diabetes mellitus
Sickle cell anemia
Chronic alcoholism or malnutrition
3. The effect of immunodefiency is variable and acute osteomyelitis of the jaw is
uncommon in HIV infection.


1. CLINICAL FEATURES
1. Most patients with osteomyelitis are adult males with infection of the mandible.
2. Osteomyelitis of the maxilla is a rare disease of neonates or infants after either birth
injuries or uncontrolled middle ear infection.
3. Early complaints are severe, throbbing, deep-seated pain, and swelling with external
swelling due to inflammatory oedema. Later, distension of the periosteum with pus,
and finally subperiosteal bone formation cause the swelling to become firm. The
overlying gingival is red, swollen and tender.
4. Associated teeth are tender. They may become loose and pus may exude from an open
socket or gingival margins. Muscle oedema causes difficulty in opening the mouth and
swallowing.
5. Regional lymph nodes are enlarged and tender and anaesthesia or paraaesthesia of the
lower lip is characteristics.
6. Frequently the patient remains well but in the acute phase there may be fever and
leukocytosis. A severe ill, or very pale patient suggests underlying disease which
requires investigation.
7. Radiographic changes do not appear until after at least 10 days.
8. Later, in young person particularly, subperiosteal new bone formation causes a buccal
swelling and appears as thin, curved strip of new bone below the lower border of the
jaw in lateral radiographs.
1. PATHOLOGY
1. Oral bacteria, particularly anaerobes such as Bacteroides, Porphyromonas or
Prevotella spesies are important causes but the infection is often mixed. Staphylococci
may be responsible when they enter from the skin via an open fracture.
2. The mandible has a relatively limited blood supply and dense bone with thick cortical
plates. Infection causes acute inflammation in the medullary soft tissues and
inflammatory exudates spreads infection through the marrow space. It also compresses
blood vessels confined in the rigid boundaries of the vascular canals.
3. Thrombosis and obstruction then lead to further bone necrosis. Dead bone is
recognizable microscopically by lacunae empty of osteocytes but filled with
neutrophils and colonies of bacteria which proliferates in the dead tissue.
4. Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced
along the medulla and eventually reaches the subperiosteal region by resorption of
bone. Distension of the periosteum by pus and formation of sinuses on the skin or oral
mucosa are rarely seen now.
5. At the boundaries between infected and healthy tissue, osteoclasts resorb the periphery
of the dead bone which eventually becomes separated as a sequestrum. Once infection
starts to localize, new bone forms around it, particularly subperiosteally.
6. Where bone has died and been removed, healing is by granulation with formation of
coarse fibrous bone in the proliferating connective tissue. After resolution, fibrous
bone is gradually replaced by compact bone and remodeled to restore normal
morphology.
1. MANAGEMENT
1. The main requirement:
a. Essential measures
Bacterial sampling and culture
Vigorous (empirical) antibiotic treatment
Drainage
Give specific antibiotics based on culture and sensitivities
Give analgesic
Debridement
Remove source of infection, if possible
b. Adjunctive treatment
Sequestrectomy
Decortications if necessary
Hyperbaric oxygen
Resection and reconstruction for extensive bone destruction
2. Bacteriological diagnosis a specimen of pus or swab from the depths of the lesion
must first be taken for culture and sensitivity
3. Antimicrobial treatment Immediately a specimen has been obtained, vigorous
antibiotic treatment should be started. Initially, penicillin, 600-1200 mg daily can be
given by injection, with metronidazole 200-400mg 8-hourly. Clindamycin penetrates
avascular tissue better and is frequently effective. \
4. Debridement- removal of foreign or necrotic material and immobilization of any
fracture are necessary if there has been a gunshot wound or other contaminating
injury.
5. Removal of sequestra- dead bone should not be forcibly separated and vigorous
curetting is inadvisable, but in the late stages a loosened sequestrum may have to be
removed. Teeth should be extracted only if loosened by tissue destruction.
6. Adjunctive treatment- decortication or hyperbaric oxygen therapy or both may be
required, particularly in radiation-associated osteomyelitis.
1. COMPLICATIONS
1. Anaesthesia of the lower lip usually recovers with elimination of the infection.
2. Rare complications include pathological caused by extensive bone destruction, chronic
osteomyelitis after inadequate treatment, cellulitis due to spread of exceptionally
virulent bacteria or septicemia in an immunodeficient patient.
1. Chronic osteomyelitis
1. Rarely, inadequately treated acute osteomyelitis may lead to chronic suppurative
osteomyelitis, which may also be a complication of irradiation.
2. Persistent low-grade infection is associated with bone destruction and granulation
tissue formation, but little suppuration.
3. Chronic osteomyelitis can also arise de novo as a result of infection by weakly virulent
bacteria or in avascular bone.

1. CHRONIC FOCAL SCLEROSING OSTEOMYELITIS(
CONDENSING OSTEITIS)
1. This is an uncommon bony reaction to exceptionally low-grade periapical
inflammation or, alternatively, to unusually strong local tissue resistance.
2. Patients are typically under 20 years. Infection is most frequently related to a
mandibular first permanent molar which is typically grossly carious and non-vital, but
causes little or no symptoms.


1. Pathology
1. The main features are dense compact bone with few lacunae, many of which are
empty of osteocytes.
2. Prominent resting and reversal lines give it a pagetoid appearance. Scanty fibrous
interstitial tissue is infiltrated by a few lymphocytes.
3. Removal of the offending tooth is followed by slow resolution. An area of sclerotic
bone may remain indefinitely.
1. DIFFUSE SCLEROSING OSTEOMYELITIS
1. Diffuse sclerosing osteomyelitis is usually seen in the elderly and most commonly in
black people.
2. The main symptoms are vague pain or an unpleasant taste with occasional episodes of
mild suppuration and fistula formation. Radiographs show patchy diffuse or nodular
sclerosis, resembling the cotton-wool radiopacities of cement-osseous dysplasia or
Pagets disease, often bilaterally.
1. Pathology
1. Dense, irregular bone shows a pagetoid pattern of reversal lines. Connective tissue in
the marrow spaces is patchily infiltrated by variable numbers of chronic inflammatory
cells.
2. During acute exacerbations, neutrophils become numerous.
3. Removal of any infected teeth and antibiotic therapy are the initial treatment. Often
the sclerotic masses form sequestra and if so, the affected are should be guttered and
the dense masses removed. Healing may then follow but because of the bony sclerosis
a chronic relapsing course is common.

1. CHRONIC OSTEOMYELITIS WITH PRODUCTIVE
PERIOSTITIS (NONSUPPURATIVE OSTEOMYELITIS,
GARRES OSTEOMYELITIS)
1. This uncommon response to low-grade chronic periapical or perifollicular infection is
characterized by reactive subperiosteal new bone formation.
2. Typically, the lower first permanent molar region of the mandible in young adults is
affected. There may be mild pain before a non tender, bony, hard swelling forms,
usually along the lower border or lateral aspect of the jaw.
3. A radiograph shows a carious tooth and a related periapical area of radiolucency or,
less commonly, folliculitis round an unerupted tooth. A smooth, convex overgrowth of
cortical bone results. The remainder of the jaw may appear normal or radiolucent or
osteosclerotic.
1. Pathology
1. Osteoid and woven bone forms in fibrous connective tissue.
2. It shows parallel, concentric laminations. Patchy infiltration by chronic inflammation
cells may be found in deep biopsy.
3. Removal of the infection leads to gradual remodeling of the jaw.
4. CANCRUM ORIS
1. Definition
A gangrenous stomatitis, usually beginning in the mucous membrane of the corner of the
mouth or cheek, and then progressing fairly rapidly to involve the entire thickness of the lips
or cheek (or both), Noma is a type of gangrene that destroys mucous membranes of the mouth
and other tissues. It occurs in malnourished children in areas of poor cleanliness. Noma means
to devour (a spreading sore), is rapidly a spreading mutilating diseases usually occurring n the
debilitated or nutritionally deficient persons.
2. Epidemiology
It is seen chiefly in children, but also found in adults under certain conditions. The disease is
rare today North America and Western Europe. Most cases occur in Africa, Southeast Asia,
and South America.
3. Causes
The exact cause is unknown, but may be due to bacteria called fusospirochetal organisms.
Predisposing factors play an important role in the development of the condition. Often they
have had an illness such as diphtheria, dysentery, measles, pneumonia, scarlet fever, syphilis,
tuberculosis, and blood dyscrasias. Thus noma may be considered a secondary complication
of systemic disease rather than a primary disease.

Diagram 1 (Source: http://health.allrefer.com/health/noma-mouth-sores.html)
4. Symptoms and Pathogenesis
Cancrum oris appears to originate as a specific infection by, acute necrotizing
gingivostomatitis, which is soon complicated by secondary invasion of many other
microbial forms including streptococci, staphylococci, and diphtheria bacilli. Noma
causes sudden, rapidly worsening tissue destruction. The gums and lining of the
cheeks become inflamed and develop ulcers. The ulcers develop a foul-smelling
drainage, causing breath odor and an odor to the skin. The initial site is a
commonly an area of stagnation around fixed bridge or crown. The infection
spreads to the skin, and the tissues in the lips and cheeks die. The process can
eventually destroy the soft tissue and bone. Eventual destruction of the bones
around the mouth causes deformity and loss of teeth.
5.
Diagram 1.1
(Source: http://grassrootsmile.org/html/Funding/funding.html)
1. Diagnostic Tests
Physical examination shows inflamed areas of the mucous membranes, mouth
ulcers, and skin ulcers. These ulcers have a foul-smelling drainage. There may be
other signs of malnutrition.
2. Treatment
Antibiotics and proper nutrition helps stop the disease from getting worse. Plastic surgery
may be necessary to remove destroyed tissues and reconstruct facial bones. This will improve
facial appearance and the function of the mouth and jaw. Immediate treatment of any existing
malnutrition further improves the probability of saving the patient.
3. Expectations (Prognosis)
In some cases, this condition can be deadly if left untreated. Other times, the condition may
heal over time even without treatment. However, it can cause severe scarring and deformity.
1. Complications
a. Disfigurement
b. Discomfort (Gangrenous Stomatitis - Overview, 2009)







Diagram 1.2 Patient who has undergone reconstructive surgery in Bolivia
(Source:
http://www.itg.be/itg/DistanceLearning/LectureNotesVandenEndenE/imagehtml/i
mages/prevs/CD_1055_034c.jpg)
6. Maxillary Sinusitis
1. Definition
An acute or chronic inflammation of the maxillary sinus
Due to
o A direct extension of dental infection (odontogenic sinusitis)
o Infectious diseases due to bacteria, fungus, or virus such as the common cold
influenza and exanthematous diseases from local spread of infection in the
adjoining frontal or paranasal sinuses, or from traumatic injury of the sinuses
with a superimposed infection
o Foreign bodies, tumors and granulomatous lesions of the nasomaxillary
complex.
Organism involves Streptococcus pneumoniae, Hemophilus influenza, Moraxella
catarrhalis in children, gram negative bacilli, anaerobic organism, rhinovirus and
parainfluenza and etc.
1. Acute Maxillary Sinusitis
Predisposing Factors
o An acute periapical abscess or
o An acute exacerbation of a chronic inflammatory periapical lesion which
involves the sinus through direct extension or
o Extraction of a maxillary bicuspid or molar and perforation of the sinus
(awaken a latent chronic sinusitis)
o Organism involved are S. pneumoniae, H. influenzae,and Moraxella
catarrhalis
Clinical Features
o Moderate to severe pain with swelling overlying the sinus
o May have headache
o Pressing over the maxilla (check, posterior teeth, ear) increases the pain, which
is due to pressure.
o Numbness in maxillary molars and premolars
o Discharge of pus into the nose and fetid breath
o Fever & malaise
1. Chronic Maxillary Sinusitis
Sinusitis of more than 3 months duration
May develop as the acute lesion subsides or may represent a chronic lesion from the
onset
Common predisposing factors
o Upper respiratory viral infections
o Allergic sinusitis
o Phycomycosis infection ( especially in diabetic patients
Oraganisms involved are anaerobes and streptococcus such as bacteroides or
veillonella
Clinical Features
o Genrerally lacking and condition may only be discovered during routine
examination
o Headache, fever, vague facial expression or upper toothache
o Stuffy sensation on the affected side of the face
o Mild discharge of pus into the nose
o Fetid breath
o RARELY have dystrophic calcification termed antrolith which may be
detected radiographically


http://en.wikipedia.org/wiki/File:Illu09_sinuse
s.jpg

http://hcd2.bupa.co.uk/images/factsheets/Sinus_427
x240.jpg

http://www.sinusinfocenter.com/images/InflammationInfectionMaxillaryLarge.jpg


1. Diagnosis
A doctor makes the diagnosis based on the typical symptoms and, sometimes, on x-ray
studies.
X-rays may show fluid in the sinuses, but a computed tomography (CT) scan is
better able to determine the extent and severity of sinusitis. If a person has maxillary
sinusitis, the teeth may be x-rayed to check for tooth abscesses.
Sometimes a doctor passes a thin viewing scope (endoscope) into the nose to inspect
the sinus openings and to obtain samples of fluid for culture. This procedure, which
requires a local anesthetic (to numb the area), can be done in the doctor's office.
Predisposing factors in the patient's history may help confirm the diagnosis or
indicate underlying conditions that require therapy. The two most common
predisposing factors are a recent upper respiratory tract viral infection (lasting more
that seven to 10 days) and allergic disease.
Sinusitis in children is suspected when a pus-filled discharge from the nose
persists for more than 10 days along with extreme tiredness (fatigue) and
cough. Pain or discomfort in the face may be present. Fever is uncommon.
When examining the nose, a doctor sees pus-filled drainage. A CT scan can
confirm the diagnosis.
1. Treatment
Treatment of acute sinusitis is aimed at improving sinus drainage and curing
the infection.
Nasal sprays (constrict the blood vessels and shrink the sinus and nasal
membranes, thus, reducing stuffiness in the sinuses and nasal passageways):
Phenylephrine
Antihistamines ( Drugs used for sinus infection treatment when the cause is
allergy): Claritin (loratadine), Chlor-
Trimeton (chlorpheniramine), Benadryl (diphenhydramine).
Pain relievers: After consulting your doctor, you may use stronger
prescribed drugs like Tylenol (acetaminophen), Aspirin or Ibuprofen.
A relatively new procedure known as Balloon Sinuplasty is also gaining
popularity.
Surgical methods: Functional endoscopic sinus surgery (FESS) has become
the accepted standard approach and technique when surgical treatment of
sinusitis is indicated. Surgery for sinus infection treatment should only be
considered when other medical treatments have failed.
For fungal sinus infection treatment, there is a need for anti-fungal
medicines. But if the case is severe enough where fungal balls are present,
surgery seems to be the best alternative.
1. Prevention method:
Reduce exposure to allergens.
Improve household ventilation by opening windows whenever possible.
Use a humidifier in the home or office when the person has a cold.
Sleep with the head of the bed elevated. This promotes sinus drainage.
Use decongestants with caution.
Avoid air pollutants (such as smoke) that irritate the nose.
Eat a balanced diet and exercise.
Minimize exposure to persons with known infections.

7. SEPSIS AND SIRS (systemic inflammatory Response Syndrome)
1. DEFINITION OF SEPSIS AND SIRS
1. Sepsis-Sepsis is a serious medical condition that is characterized by a whole-body
inflammatory state (called a systemic inflammatory response syndrome or SIRS) and
the presence of a known or suspected infection. The body may develop this
inflammatory response to microbes in the blood, urine, lungs, skin, or other tissues.
An incorrect layman's term for sepsis is blood poisoning, more aptly applied to
Septicemia.
2. Severe sepsis-Severe sepsis occurs when sepsis leads to organ dysfunction, low blood
pressure (hypotension), or insufficient blood flow (hypoperfusion) to one or more
organs (causing, for example, lactic acidosis, decreased urine production, or altered
mental status). Sepsis can lead to septic shock, multiple organ dysfunction syndrome
(formerly known as multiple organ failure), and death.
3. Oral sepsis- A condition occurring within the mouth and adjacent areas characterized
by the presence of pathogens.
4. SIRS-inflammatory state affecting the whole body, frequently in response to infection,
but not necessarily so. It is related to sepsis, a condition in which individuals both
meet criteria for SIRS and have a known or highly suspected infection.
1. CRITERIA OF SIRS
1. The manifestations of SIRS include, but are not limited to:
1. Body temperature less than 36C or greater than 38C
2. Heart rate greater than 90 beats per minute
3. Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or,
an arterial partial pressure of carbon dioxide less than 4.3 kPa (32 mmHg)
4. White blood cell count less than 4000 cells/mm (4 x 10
9
cells/L) or greater
than 12,000 cells/mm (12 x 10
9
cells/L); or the presence of greater than 10%
immature neutrophils (band forms)
SIRS can be diagnosed when two or more of these criteria are present.

1. SYMPTOM OF SEPSIS
Fever, sometimes,body temperature may be normal or even low
Chills and severe shaking
The heart beating very fast, breathing may be rapid, low blood pressure is often
observed in septic patients
Confusion, disorientation, and agitation may be seen as well as dizziness and
decreased urination
Rash on their skin may be a reddish discoloration or small dark red dots throughout
the body
Pain in the joints at your wrists, elbows, back, hips, knees, and ankles
1. SYMPTOM OF SIRS
Temperature > 38C or < 36C
Heart rate > 90 beats/min
Respiratory rate > 20 breaths/min or PaCO
2
< 32 mm Hg
WBC count > 12,000/mm
3
, < 4000/mm
3
, or > 10% immature (band) forms

1. MANAGEMENT FOR SEPSIS
Resuscitate: ABCs
o Airway: AMS, unable to protect airway
o Breathing: Respiratory failure
o Circulation: Restoration of blood pressure to levels which perfuse core organs.
Sphygmomanometer unreliable
Arterial catheter
CVP
Mixed Venous O2 sat
Restore tissue perfusion
Causes of poor tissue perfusion
Leaky vessels
Decreased vascular tone
Myocardial depression
Interventions
o Volume infusion
Intravenous fluids
Administered in well-defined, rapidly infused boluses
Continued until blood pressure, tissue perfusion, and oxygen
delivery acceptable or presence of pulmonary edema
Colloid vs. Crystalloid: No evidence to recommend one over
the other
PRBCs
o Vasopressors
Second-line agents
Hypotensive despite fluid resuscitation, Cardiogenic pulmonary edema,
or elevated wedge pressure (>18)
Vascoconstrictors
Phenylephrine, Norepinephrine, Dopamine, Epinephrine, Vasopressin
Increase peripheral vascular resistance
Increase arterial blood pressure
Important compensatory mechanism for restoring blood
pressure in hypovolemic shock such as hemmorrhage
o Inotropes
Identify and eradicate source of infection
Empiric broad spectrum antibiotics
o ASAP after blood cultures collected
o Modify as culture results dictate
Remove infectious source
o Remove catheter, Drain abscess/fluid collections, Divert gut
Assure adequate tissue oxygenation
Goal: Maintain oxygen delivery (DO2) at levels that match tissue O2 needs (VO2)
o Supratherapeutic oxygenation not consistently shown to be effective
Detection of tissue hypoxia--Lactate
o May be difficult to interpret
Treatment of tissue hypoxia
o Maximize arterial oxygen content
o Keep SaO2 >97%
o Augment cardiac output
o Support hematocrit
Activated Protein C
o Known inflammatory and procoagulant host responses to infection.
o TNF-alpha, IL-1, IL-6, thrombin
o Diffuse endovascular injury, multiorgan dysfunction and death
o Activated Protein C
anticoagulant, modulates the inflammatory response
reduced levels of protein C found in majority of patients with sepsis
and are associated with increased risk of death
Glucose Control
o Recs are to keep serum glucose levels < 150
Nutrition
o Route: preferably enteral
o Nutritional support improves wound healing and decreases susceptibility to
infection.
o Nutritional support results in higher lymphocyte counts and higher serum
albumin (surrogate markers of immune competency)
8.
9.
10.
11.
12.
13.
14.
15.
16. Bibliography
1. Surveillance for dental caries, dental sealants, tooth retention, edentulism, and enamel
fluorosis. Beltran-Aguilar, ED, et al. 2005.
2. systemic diseases caused by oral infection. Li, X, Kolltveit, KM, Tronstad, L, Olsen,
I. 2000.
3. Oral infections and systemic diseases. Holmstrup, P, Poulsen, AH, Andersen, L, et
al. 2003.
4. periodontal therapy reduces the rate of preterm low birth wight in women with pregnancy-
associated gingivitis. Lopez, NJ. 2005.
5. Association between periodontal disease and risk for atherosclerosis, cardiovascular
disease, and stroke. . Scannapieco, FA, Bush, RB, Paju, S. 2003.
6. Peterson's principles of oral and maxillofacial surgery, Chapter 1. Miloro, Michael, et al.
7. Topazian, Richard G., Goldberg, Morton H. and Hupp, James R. Oral and
maxillofacial infections . 2002.
8. Gangrenous Stomatitis - Overview. (2009, December 5). Retrieved February 2010, from
Kosmix: http:/www.health.allrefer.com/health/noma-info.html
9. http://grassrootsmile.org/html/Funding/funding.html
10.http://www.itg.be/itg/DistanceLearning/LectureNotesVandenEndenE/imagehtml/ppages/C
D_1055_034c.htm
11. http://health.allrefer.com/health/noma-mouth-sores.html