Odontogenic infection

Islam Kassem
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CLASSIFICATION OF ODONTOGENIC
INFECTIONS

Are classified into:

A- Iatrogenic infection

B- Non-iatrogenic infection
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Non-Iatrogenic Infection
Pericoronal infections(Pericoronitis& Operculitis)
Impacted or unerupted tooth.
Periodontitis
Acute Alveolar Abscess
Soft Tissue Abscess
Facial Cellulitis
Facial Spacess Abscess
Panfacial spaces infection
Acute necrotizing infection
Complicated odontogenic infection
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IATROGENIC ODONTOGENIC
INFECTION
I- post-injection infection
II- Post-extraction infection
III- post- surgical infection
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TYPES OF INFECTION
Bacterial: Endogenous or
Exogenous


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PREDISPOSING FACTORS
Trauma
Debilitating conditions
Immuno compromised states

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AETIOLOGY OF IMMUNODEFICIENCY
A- Systemic conditions:
AIDS

Diabetes mellitus

End-stage renal disease

Leukemia/lymphoma

Systemic lupus erythematous

Advanced age
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AETIOLOGY OF IMMUNODEFICIENCY,
cont.
B- Primary immunodeficiencies
X-linked severe combined immunodeficiency
Wiskott-Aldrich syndrome
Chediak-Higashi syndrome
DiGeorge syndrome
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AETIOLOGY OF IMMUNODEFICIENCY,
cont
C- Iatrogenic causes:
Immunosuppressive drugs
Broad-spectrum antibiotics
Chemotherapy
Radiation therapy
Bone marrow transplantation

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AETIOLOGY OF IMMUNODEFICIENCY,
cont
D- Social Factors;
* Alcoholism
* IIIicit drug use
* Morbid Obesity.
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DIAGNOSIS
A- Patients history.
B- Clinical Examination
C- Radiographically; in the acute phase , no signs
are observed at the bone, may be observed 1-
2 weeks later, unless there is recurrence of a
chronic condition

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RADIOGRAPHIC DIAGNOSIS
.There may be :
1.A deeply carious tooth ,or
2. Restoration very close to the pulp,
3. As well as thickening of the periodontal
ligament.
These data indicate a causative tooth.
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Presentations

Pain
Lymphadenopathy
Swelling
Facial sinuses
Trismus
Symptoms secondary to complications



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Clinical Features

A-Local: B-systemic
extra-oral *Fever
Intra-oral *Headache
Manifestations *Tachycardia
Trismus * Malaise
Teeth
Discharge
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Clinical Features Of Suppuration
(stage of abscess formation)
*Pain: .dull aching-throbbing
*Temp: .hectic fever
*Swelling: .fluctuant
.+ve pagets
*Skin: .pitting edema
*Aspiration test pus



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Principles of Treatment of Acute Odontogenic
Infections
1
st
: Control of infection:
A- Stage of cellulitis.
B- Stage of suppuration
2
nd
: Support the patient

3
rd
:Removal of the cause

4
th
:Treatment of complications
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Control of Infection
Stage of cellulitis:
-Antibiotic therapy
1- Broad spectrum
2- Bactericidial
3- Combination
-Hot fomentation
- Warm mouth wash
-Control any predisposing factor
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Stage of Suppuration
(Abscess Formation)
.Incision + Drainage,,,,When??? And How???
.Culture and sensitivity
.Antibiotics according to the culture& sensitivity.
.Anti-anaerobic chemotherapy:
*Metronidazole
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Support of the patient.
Hospitalization in the following conditions:
1.Risk of airway obstruction
2. Immunocompromised States
3. Difficulty in swallowing
4. Patient very ill
5. Underlying systemic disease
6. Patient unable to manage at home.
7. Extremes of age( very young & very old)
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AIR WAY OBSTRUCTION
1- Ludwigs angina
2- Impending Ludwigs angina
3-Panfacial spaces infection
4-Retropharyngeal abscess
5-Extremes of age (very young&
very old)
6- Acute necrotizing fascitis.
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Clinical Features of suppuration
(Stage of Abscess formation)

Paindull aching Throbbing
Temp. Hectic fever
Swelling Fluctuation,+Ve
Pagets test.
Skin Pitting edema
Aspiration test- Pus
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Drainage of Pus

* Anesthesia ????
*Incision; should fulfill the
following:
1.Over the most fluctuant site
2.Large and adequate
3. Independent
4. Includes all loculi
5. Avoids important structures
6. Cosmetic, if possible.




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Incision for drainage of a sublingual abscess. The
incision is performed parallel to the
submandibular duct
and the lingual nerve
Incision for drainage of a palatal
abscess, parallel to the greater palatine
vessels
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Incisions for drainage of a submandibular or parotid (a), and a
submasseteric (b) abscess. During cutaneous
incisions, the course of the facial artery and
vein must be taken into consideration (a),
as well as that of the facial nerve (b
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Diagrammatic illustrations showing the incision of an
intraoral abscess and the
placement of a hemostat to facilitate
the drainage of pus
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Diagrammatic
illustrations showing the placement
of a rubber drain in the cavity
and stabilization with a suture
on one lip of the incision
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Indications of Antibiotic Therapy
* After incision and Draniage;
*?? Is it necessary to give antibiotics to all
patients??????
*Of course NO.
*Minor infections in patients with intact host defenses
may not require antibiotic therapy.
* Even, some moderately severe infections can be
treated without antibiotics.
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The Decision To Use Antibiotic Therapy
1. Depressed host defenses, even, in minor
infections.
2.In treating minor infections that donot lend themselves
to surgical intervention, such as a diseased tooth
that must be retained but doesnot drain when the
pulp chamber is opened.
3.If the infection in stage of cellulitis.
4. If the abscess is sourrended by an area of cellulitis.
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5. If there is lymphangitis or
lymphadenitis.
6. If the infection is complicated;
septecemia, paeymia,
7. If there is specific infection,
Tuberculosis.
8. In Patients with Prosthetic
appliances.
9. Patients with systemic
manifestations of infections.


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Principles of Choosing the Appropriate
Antibiotic
The Following guidelines are useful in
selecting the proper antibiotic:
1.Identification of the causative
organism,
2. Determination of the antibiotic
sensitivity.
3. Use of specific narrow spectrum
antibiotic
4. Use of least toxic antibiotic,
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5. Patient drug history.
6. Use of bactericidal rather than
bacteriostatic drugs.
7. Use of antibiotic with proven history of success.
8.Cost of the antibiotic.

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Identification of the Causative
Organism
This can be achieved either by:
1. Isolating the organism from pus, blood or
tissues, in the laboratory; or
2. Empirically, based on knowledge of the
pathogenesis, and clinical presentation of
the specific infection
Antibiotic therapy is then either initial or
definitive:
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Microbiology of Odontogenic
Infections
** The typical odontogenic infection is
caused by a mixture of aerobic and anaerobic
bacteria 70 %.
* Anerobic bacteria causes 25%
* Aerobic bacteria Causes only
5% of cases.
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Clinical Implications
1.The microbiology of cellulitis-type
infections, that dont have abscess formation, shows
almost
exclusevely, aerobic bacteria.
2. As the infection becomes more severe, the microbiology
becomes a mixed flora of aerobic and anaerobic
bacteria,
3. If the infection process becomes contained and
controlled by the body defenses,
the aerobic bacteria are no longer able to
survive, in the hypoxic acidotic
environment, and only anaerobic bacteria
are found.
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Therapeutic Implications
Aerobic Bacteria of Odontogenic Infection:
* Primarily Gram-Positive Cocci, mainly streptococcistrept.
Viridans &Alpha-hemolytic all of which are susceptible
to penicillin and other antibiotics with similar
antimicrobialspectrum.
* The streptococci Accounts for 85 % of the aerobic bacteria
found in odontogenic infections.
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Therapeutic Implications, cont.
Anerobic bacteria of odontogenic infection;
1. Their number is greater than that of aerobic
bacteria.
2. There are two main groups of anerobic
bacteria:
A- Anaerobic gram positive cocci,
B-Anaerobic gram-negative rods.
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Culture and Sensitivity
Indications:
1. If the infection has compromised the host defenses.
2. If the patient had received appropriate treatment for three
days without improvement.
3. If the infection is a post-operative wound infection.
4. If the infection is recurrent.
5. If actinomycosis is suscepected.
6. If osteomyleitis is present.
NB; in these situations deviation from the normal bacterial
pattern is likely.
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Principles of Antibiotic adminstration

1. Proper dose
2. Proper time interval
3.Proper route of adminstration
4.Consistency of route of adminstration.
5. Combination antibiotic therapy

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Patient Monitoring
1. Response to treatment.
2. Development of adverse reactions
3. Superinfection and Recurrent infection.
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AIR WAY OBSTRUCTION
1- Ludwigs angina
2- Impending Ludwigs angina
3-Panfacial spaces infection
4-Retropharyngeal abscess
5-Extremes of age(very young&
very old)
6- Acute necrotizing fascitis.
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Removal of Underlying Cause
A- Local Factors:
1.Remaining Root(s)
2.Dead Tooth
3. Apical or residual cysts.
4. Periodontal disease
5. Bad Oral hygiene.
6- forigen body; broken needle, file..
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Removal of Underlying Cause(cont.)
B- Underlying Systemic Causes;
1.Diabetes Mellitus
2. Blood Dyscrasias
3. Chronic deblitating Diseases
4. Immuno-Suppressed Patients.
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FATE OF ACUTE ODONTOGENIC INFECTION
Depend on the following factors;
1- Virulence of the micro-organism
2- Host Resistance
3- Anatomic Geography.
4- Management:
a. Timing b. Line of treatment
c.Antibiotic; type,dosage,duration.
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Acute odontogenic infection:

1-Resolution; When???
2-Chronicity Trismus,if the mastcatory muscles are
involved which may last for years.
3- Spread : Acute soft tissue Abscess
Deep facial spaces abscess
Bacteremia&Septicemia
Ascending facial-cerebral infection.
Descending To the neck,Chest
4- Complications:
a-Fistulae; cutaneous or mucosal.
b- Osteomyelitis.


Natural History of Dental infection
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SPREAD OF INFECTION
. Infection may spread in three ways:
1. By continuity through tissue
spaces and planes,
2. By way of lymphatic system
3. By way of blood circulation
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Spread Through Tissue Spaces and
Planes
This is the commonest route of
spread
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Diagrammatic
illustrations showing spread
of infection (propagation of pus)
of an acute dent alveolar abscess,
depending on the position of the
apex of the responsible tooth.
a Buckle root: buccal direction.
b Palatal root: palatal direction
Diagrammatic
illustration showing the
localization of infection
above or below
the mylohyoid muscle,
depending on the position
of the apices of the
responsible tooth
Spread
of pus towards the maxillary
sinus, due to the
closeness of the apices
to the floor of the antrum
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Spread of pus depending on the
length of root and attachment of buccinator
muscle. a Apex above attachment: accumulation of pus in the buccal
space. b Apex beneath the buccinator muscle intraoral pathway
towards the mucobuccal fold
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Intraalveolar abscess of maxilla (a) and mandible (b)
Diagrammatic illustrations showing accumulation of pus at a portion of the
alveolar bone in relation to the
periapical region
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Subperiosteal abscess with lingual
localization. a Diagrammatic illustration; b
clinical photograph
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Submucosal abscess with buccal localization.
a Diagrammatic illustration; b clinical
photograph
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Subcutaneous abscess originating from a
mandibular tooth. a Diagrammatic illustration. b
Clinical photograph. The swelling mainly involves the
region of the angle of the mandible
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Fascial abscess (submandibular). a
Diagrammatic illustration. b Clinical
photograph
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Treatment of Acute Dento-Alveolar
Infection
* Medical: Antibiotics ????
* Dental:
R.C.T.,
Extraction,
Periodontal
* Surgical: Incision and
Drainage, Bone fenestration
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Causes of failure of treatment

1- Failure to drain an abscess
2-Obstruction of a duct (salivary gland)
3-Presence of a foreign body or stone
4-Presence of an open portal (I.v,urinary catheter)
5-Poor host resistance
6-failure of antibiotic to reach the site (osteomyelitis)
7-Inadeqate antibiotic dosage,duration,type
8-wrong bacteriologic diagnosis e.g. specific infection.


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Complications of Acute
Odontogenic Infection
1-Chronicity
2-Dead teeth
3-periapical abscess
4-Periodontal abscess
5-Sinuses(cutaneous&/or mucosal)
6-Chronic dental granuloma
7-Periostitis

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Complications of Acute Odontogenic
Infection(cont)
7-osteomyelitis
8-Extra-articular TMJ ankylosis
9-Cutaneous scars
10-Fistulae: cutaneous
muscosal
11-Mediastinits, meningitis
12-Death ?????
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Persistance of infection
To be suspected in the following conditions:
1. Prolonged period of treatment
2. Increasing amount of pus
3. Bad odour of pus
4. Unexplained severe pain
5. Spreading infection
6. Persistance of fever
Any or all of the above means
Onset of complications
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LUDWINGANGINA
Definition; acute and diffuse cellulitis involving bilaterally the
submental,submandibular and sublingual spaces.
Aetiology:
1.Acute odontogenic infections which open below the mylohyoid
attachment, usually from the mandibular 2
nd
,and 3
rd
molars.
2. Penetrating injuries of the floor of the mouth.
3. Osteomyleitis of the mandible.
4. Compound mandibular fractures especially of the angle.
5. Suppurative submandibular sialadenitis.
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BACTERIOLOGY
Mixed infections; mainly hemolytic streptoccoci
and mixture of aerobic gm ve micro-
organisms including fusiform bacilli,vincents
organism and various staphyloccus.
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CLNICAL FEATURES
1. Swelling; rapidly developing brawny hard
involving floor of the mouth and three subs-
spaces starting unilaterally and ending
bilaterally. The swelling is localization.Later the
swelling may extend to the neck.
2. Patients Mouth; is usually opened because of
elevation of the floor of mouth and swelling of
the tongue.

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CLNICAL FEATURES, cont.
3. The tongue; is elevated and protruded from the
mouth, with a wooden appearance and limited
movement.
4. Glottic edema; severe edema of the glottis and
larynx which cause airway obstruction.
5. Stridor, difficult respiration and dysphagia.
6.Constitutional symptoms.
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MANAGEMENT
1.Maintain a patent airway.
2.Incision and Drainage
Decompression of the airway??
3. Antibiotics.
4. General Supportive Measures.
5.Treatment of the Underlying
Cause , if possible.
6 . Post-operative Care.

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Air Way Management
1.Anethesia; No Anethesia??
Local?? Or
General??
2. Intubation; Oral or Nasal?
3. Tracheostomy
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Infections of the Oral Mucosa

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Viral infections
Bacterial infections
Fungal infections
HIV infection and AIDS
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Herpes Viradae
Herpes Simplex 1
Herpes Simplex 2
Varicella Zoster
Epstein-Barr
Cytomegalovirus (HHV5)
Herpes 6
Herpes 7
Herpes 8

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Herpes Simplex Virus
Most frequent cause of viral infections of the mouth

Primary HSV I Infectious (Acute Herpetic Gingivostomatitis)
5 days incubation, then 2 days of prodromal symptoms
Acute onset of malaise, fever, and lymphadenopathy.
Multiple vesicles and ulcers can occur any part in the oral mucosa and
lips
10-14 days to resolve
Spread by droplets or lesion contact
Majority of cases are subclinical



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Mild circumoral crusting
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Herpes Simplex Virus
Extraoral spread of infection:
skin, fingers, nail bed, eyes
Herpetic whitlow
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Treatment
Supportive
Acyclovir in extreme cases
Prognosis:
self-limited
resolves in 10-14 days

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HSV remain latent in trigeminal sensory
ganglia
Virus reactivation associated with:
Ultraviolet radiation
Trauma
Immunosuppression
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Recurrent Herpetic Stomatitis
Prodrome:
tingling
burning
paresthesia
Vesicles and ulcers recur: most common herpes
labialis
Intraorally: hard palate and gingiva
In small clusters
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Varicella-Zoster Virus
Chickenpox and herpes zoster (shingles)
Primary Infection: Varicella (Chicken pox)
Prodrome: malaise, fever, lymphadenopathy
Macules, papules, vesicles, ulcers on skin and oral
mucosa
Especially soft palate
Skin lesions are pruritic.
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Zoster (Shingles)

Multiple recurrence is rare
Same latent state as HSV, in sensory ganglia
Predisposing factors:
Decreased immunocompetence
Elderly patients
Immunosuppressive drugs

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Zoster (Shingles)
Unilateral vesicular eruptions
Prodromes of pain and parasthesia for up to 2 weeks
Trigeminal Nerve:
Ophthalmic division is most frequently involved
Intra or extra oral or both
Complications
Post herpetic neuralgia
Ramsay Hunt syndrome: involvement of
geniculate ganglion


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Coxsackievirus
Enteroviradae
Over 30 types
Ones worth mentioning
Herpangina
Hand-foot and mouth
Acute lymphonodular pharyngitis

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Herpangina
Coxsackie Viruses, Group A, RNA
Children
Sudden onset of
fever, sore throat, nausea, vomiting, diarrhea and
lymphadenopathy.
Vesicles and ulcers in posterior oral cavity
D/D: primary herpes
Treatment is symptomatic

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Hand foot and mouth disease
Coxsackie A16
Spread in households
Oral lesions almost
always present
Oral lesions resemble
herpangina but can
be larger
7-10 days.

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Infectious Mononucleosis
(glandular fever)
EBV
Young adults
Transmitted by saliva
Clinically: pharyngitis, LN enlargement
Fever, prolonged malaise
Non specific oral manifestation
Petechei on juncetion of hard and soft palate
Serology: atypical peripheral lymphocytes
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Infectious mononucleosis
(glandular fever)
EBV
Nasopharyngeal carcinoma
Hairy leukoplakia
Burkitts lymphoma
Oral squamous cell carcinoma?

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Measles (Rubeola)
Paramyxovirus
Children
Prodromal symptoms
Koplik spots disappear as
skin rash starts
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Measles (Rubeola)
Skin rash: start on face, go to
trunk
Fever
Complications
Otitis media, pneumonia,
encephalitis, brain damage
Noma may be a complication in
malnourished patients

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Cytomegalovirus
Herpes group
Rarely causes disease in immunocompetent
Subclinical infection is common 40-60% of
population
Affects immunocompromised individuals
Neonatal, transplant, immunosuppressant
Affect salivary glands common but asymptomatic
Cause non specific oral ulceration
Atypical peripheral lymphocytes
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Noma (cancrum oris)
Orofacial gangrene
Malnourished children
Immunosuppressed individuals
Usually preceded by NUG
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Actinomycosis
Chronic and endogenous, anaerobic, Gram positive
Actinomyces israelli predominate
Soft tissues of the submandibular region
Source of infection: infected root canal or third molar
Firm swelling (painless) that suppurate
Multiple sinuses pointing to skin
sulphur granules
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Syphilis
Treponema pallidum
Primary: chancre : shallow ulcer
Indurated base
Associated with lymphadenopathy
Heals spontanously

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6 weeks later
Secondary syphilis: skin rash and mucous patch
Snail track ulcers, flat areas of ulceration that
coalesced

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Years later
Tertiary :
Gumma:
Necrosis and type IV hypersensitivity
Perforation of palate
Atrophic glossitis:
due to endarteritis obliterance
Followed by:
Syphilitic leukoplakia
Hyperkeratosis
Followed by:
Squamous cell carcinoma

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Congenital Syphilis
Miscarriage, still birth or neonatal infection
Collapse of nasal bridge
Hutchinson triad: blindness, deafness, dental
anomalies
Hutchinson incisors (notched teeth)
Screw driver teeth
Peg shaped laterals
Mulberry molars
Constricted atrophic cusps
Globular masses of
hard tissue
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Tuberculosis
Mycobacterium tuberculosis
Oral infection is not common
Primary oral infection
Secondary oral infection: infected sputum from
pulomonary TB

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Classical TB ulcer:
Painless
Undermind
On the tongue

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Gingival involvement:
Granulomatous
inflammation

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Tuberculosis
Diagnosis: Biopsy, granulomatous
inflammation
Granulomas with central necrosis
Identification of Acid Fast Bacilli
Treatment:
2 antimicrobial agents: isoniazide and rifampicin,
4-8 months

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Leprosy
Mycobacterium leprae
Endemic in tropical areas
2 forms of infection:
Tuberculoid
Lepromatous
Oral lesions in lepromatous
Secondary to nasal involvement
Maxillary gingiva, palate
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Gonorrhoea
Neisseria gonorrhea
Mainly tonsillar and soft palatal lesions
Erythema, vesicles, ulcers, pain
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Candidiasis
Predisposing factors:

A) Systemic:

1) Immunological immaturity in infants.
2) Immunological exhaustion in elderly.
3) Systemic corticosteroids.
4) Systemic antibiotics.
5) Systemic immune suppression therapy.
6) Chemotherapy.
7) Disease-induced xerostomia.
8) Drug-induced xerostomia.
9) Diabetes Mellitus.
10) HIV and AIDS.

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B) Local:
1) Ill-fitting dentures.
2) Reduced vertical dimension.
3) Lip-licking habit.
4) Overuse of antiseptic and antibiotic
rinses.

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-Mucocutaneous.
-Syndrome associated.
-Pseudomembranous.
-Atrophic.
-Hypertrophic.
Pseudomembranous (Thrush): in the form of white plaques which can
be scraped off small hemorrhagic areas.
Systemic Local
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Atrophic Candidiasis:
Atrophic glossitis due to loss of filiform
papillae.
Angular cheilitis due to loss of vertical occlusal
dimension.
Median rhomboid glossitis.
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Hypertrophic Candidiasis:
This can mimic lichen planus,
leukoplakia,verrucous carcinoma or a
squamous cell carcinoma.

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Treatment of Candidiasis:
1. Removal of the concomitant underlying
factors.
2. Nystatin oral suspention or as vaginal
suppositories.
3. In chronic Candidiasis:
Nystatin + Fluconazole (Diflucan).
4. In disseminated Candidiasis:
Amphotericin B infusion.
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Benign Migratory Glossitis (Stomatitis)
(Geographic Tongue)
Alternating areas of rough keratinized areas and
smooth red dekeratinized areas.
It is asymptomatic except on occasions when spicy
foods or citrus acidic products are used.
Treatment: non-specific, sometimes Nystatin
gives response in symptomatic cases.
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Histoplasmosis
The classic presentation of the disease is the appearance of
single or multiple oral ulcers in an older person with
chronic obstructive pulmonary disease (COPD).

Differential diagnosis:
1. Other deep fungal infections such as coccidioidomycosis
and blastomycosis.
2. Squamous cell carcinoma.
3. Syphilitic chancre.
4. T.B. ulcers.
Diagnosis: Biopsy is mandatory.


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Treatment:
a) Oral : Itraconazole 200-400 mg daily for 7 months, or:
b) I.V. : Amphotericin B :in individuals non-responsive to
oral treatment, are immunocompromised or have
histoplasmosis meningitis.
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Are both uncommon in Egypt and can be
diagnosed after histological examination of
the oral ulcers.
Coccoidioidomycosis and
Blastomycosis:
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Rhinoscleroma
In the mouth , this can present as a granulomatous mass in the
palate.
Differential diagnosis:
1. Nasopharyngeal angiofibroma.
2. Antral squamous cell carcinoma.
3. Lymphoepithelioma.
4. Rhinophyma.
Rhinoscleroma is not specifically related to diabetes or immune
suppression as is mucormycosis.
Diagnosis: Depends on biopsy.
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Mucormycosis
The most common presentation is maxillary and orbital
cellulitis in a person with uncontrolled D.M. with
ketoacidosis . Immunocompromised patients also
are susceptible.
The maxillary sinuses are usually filled with black
necrotic bone and granulation tissue.
Palatal ulcers frequently occur and will often progress
to large oro-naso-antral and orbital
communications.

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Aspergillosis
Besides its usual clinical presentations in
the form of external otitis and maxillary
sinusitis, it can involve the skin of the
face as a black-coloured ulcer.

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Lesions mimicking fungal orofacial lesions:
1.Leukoplakia :
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Bisphosphonate Related
Osteonecrosis of the Jaws
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Bisphosphonates what are they?
Class of drugs
High affinity for calcium
Binds to bone surfaces
Nitrogen: increased affinity, potency
Prevent bone resorption and
remodeling
IV and oral formulations
IV: tx for bone resorption 2
metastatic tumors, osteolytic lesions
Oral: tx for osteoporosis, osteopenia

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Bisphosphonates: Common uses
Prevention and treatment of osteoporosis in
postmenopausal women
Increase bone mass in men with osteoporosis
Tx of glucocorticoid-induced osteoporosis
Tx of Pagets disease of bone
Hypercalcemia of malignancy
Bone metastases of solid tumors
breast and prostate carcinoma; other solid tumors
Osteolytic lesions of multiple myeloma
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History of Bisphosphonate
Development
Mid-19
th
Century German chemists
Anti-corrosive in pipelines
20
th
Century - Clinical applications
Tc99 Bone scans
Toothpaste
Anti-tartar, anti-plaque effects
Osteopathies
Anti-resorptive effect






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Medical Indications for IV BPs
Bone metastasis,
hypercalcemia
RANKL-mediated
osteoclastic resorption
Multiple myeloma, breast
CA, prostate CA
Paracrine-like effect
PTH-like peptide
osteoclastic resorption
Small cell carcinoma,
oropharyngeal cancers
Endocrine-like effect
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Medical Indications for Oral BPs
Pagets Disease of bone
Accelerated bone turnover
Reduced compressive strength,
increased vascularity
Bone pain
Elevated AP levels
Osteoporosis
Effects of estrogen loss:
Decreased bone
turnover/renewal
Adipocyte differentiation >
osteoblastic differentiation
increased fibrofatty marrow
Progressively porotic bone
DEXA scan for BMD values




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Pharmacokinetics
Oral BPs
Absorbed in small intestine
Less if taken with meal
1-10% available to bone
Circulating half-life: 0.5-2 hrs
Rapid uptake into bone matrix
30-70% of IV/oral dose
accumulates in bone
Remainder excreted in urine
Repeated doses accumulate in bone
Removed only by osteoclast-
mediated resorption
Biologic Catch 22

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Bisphosphonate Side Effects
Upset stomach
Inflammation/erosions of esophagus
Fever/flu-like symptoms
Slight increased risk for electrolyte disturbance
Uveitis
Musculoskeletal joint pain
And of course
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BRONJ
Exposed, devitalized bone in
maxillofacial region
Prior history or current use of
BP
Vague pain, discomfort
Spontaneous occurrence, or
2 surgery or trauma to oral
soft tissue/bone
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BRONJ: Clinical Presentation
Exposed alveolar bone
Open mucosal wound
Necrotic bone
Spontaneous or
Traumatic
Extractions,
periodontal surgery,
apicoectomy, implant
placement
Infection
Purulence, bone pain
Orocutaneous fistula

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BRONJ: Clinical Presentation
Subclinical Form
asymptomatic
radiographic signs
Sclerosis of lamina
dura
Widening of PDL space




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Clinical Presentation (cont)
Soft tissue abrasions
Tissues rubbing against bone








AND
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Staging of BRONJ
Proposed by AAOMS:

Patients at risk (Subclinical)
No apparent exposed/necrotic bone in pts treated w/ IV or oral BPs

Patients with BRONJ
Stage 1: Exposed/necrotic bone, asymptomatic, no infection

Stage 2: Exposed/necrotic bone, pain, clinical evidence of infection

Stage 3: Exposed/necrotic bone, pain, infection, one or more of the
following:
Pathologic fracture, extra-oral fistula, osteolysis extending to
inferior border

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More frequently
Lesions more
extensive
All stages
II, III more
common
Lower success with
Tx
Patients generally
sicker


BRONJ: IV BPs
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Stage 0 Lesions
Spontaneous onset numbness
and pain
No exposed bone
No prior dental antecedent
Positive image findings:
Sclerosis
Positive bone scan
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BRONJ: Historical Context
Rare reports prior to 2001
2003: Marx reported 36 patients
2004: Ruggiero et al reported 63 pts (from 2001-2003)
2005: Migliorati reported 5 cases
2005: Estilo et al reported 13 cases
Sept. 2004: Novartis (manufacturer of Aredia & Zometa) altered
labeling to include cautionary language concerning osteonecrosis of
the jaws
2005: FDA issued warning for entire drug class (including oral
bisphosphonates)
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Phossy-Jaw: A Historical Entity
Lorinser, 1845: first reported cases

Industrial laborers working w/ white phosphorus powder
Matchmaking, fireworks factories
Missile factories

Clinical presentation
Nonhealing mucosal wound following extraction
Pain
Fetid odor
Suppuration
Necrosis w/ bony sequestra
Extra-oral fistulae

Miles, Hunter: 20% mortality due to infections
Pre-antibiotic era

Conservative treatment
Selective debridement
Minimal mucosal manipulation
Topical agents: copper sulfate
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Similar Clinical Entities
Closely resembles
Osteopetrosis
Loss of osteoclastic
function
Hypermineralization
Fractures, nonunions,
open oral wounds
Endpoint: bone necrosis,
+/- infection


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NOT to be confused with these other entities:

Osteoradionecrosis (ORN):
avascular bone necrosis 2 radiation
Osteomyelitis:
thrombosis of small blood vessels leading to
infection within bone marrow
Steroid-induced osteonecrosis:
more common in long bones
exposed bone very rare

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Estimated Incidence of BRONJ 2 IV BPs
Limited to retrospective studies with limited
sample sizes
Marx:
Zometa: exposed bone within 6-12
months
Aredia: 10-16 months
Estimates of cumulative incidence of BRONJ
range from 0.8% to 12%
Marx: 5-15%
Including Subclinical osteonecrosis
Incidence will rise:
Increased recognition
Increased duration of exposure
Increased followup


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Why Only in the Jaws?
Dixon et al 1997
Alveolar crest has high remodeling rate
10x tibia
5x mandible at level of IA canal
3.5x mandible at inferior border
Greater uptake of Tc 99m in bone scans
Occlusal forces
Compression at root apex and furcations
Tension on lamina dura and periodontal ligament
Remodeling of lamina dura in response
Reduced remodeling with BP uptake hypermineralization
Sclerotic appearance of Lamina dura
Widening of periodontal ligament space

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Risk Factors for Development of BRONJ
Drug-related factors
Potency of BP
Zoledronate > pamidronate > oral BPs
Duration of therapy
Local factors
Dentoalveolar surgery
Extractions, implants, periapical surgery, periodontal surgery w/ osseous
injury
7-fold risk for BRONJ with IV BPs
5 to 21-fold risk in some studies
Local anatomy
lingual tori, mylohyoid ridge, palatal tori
Mandible > maxilla (2:1)
Concomitant oral disease
7-fold risk for BRONJ with IV BPs


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Risk factors (continued)
Demographic/systemic factors
Age: 9% increased risk for every passing decade
Multiple myeloma patients treated w/ IV BPs
Race: Caucasian
Cancer diagnosis
multiple myeloma > breast cancer > other cancers
Osteopenia/osteoporosis diagnosis concurrent w/ cancer diagnosis

Additional risk factors:
Corticosteroid therapy
Diabetes
Smoking
EtOH
Poor oral hygiene
Chemotherapeutic drugs
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Subclinical Risk Assessment
Early signs of BP toxicity:
Radiographs
Panoramic, PA films
Sclerosis of alveolus, lamina dura
Widening of PDL space
Clinical exam
Tooth mobility
Unrelated to alveolar bone loss
Deep bone pain with no apparent etiology
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Treatment Strategies
Stage III disease
Pathologic fractures, refractory
cases
Preservation of function
Airway, speech
compromise with large
mandible resections
Segmental resections, titanium
plate reconstruction, external
fixation.
All infections must be
cleared first
Delay reconstruction
up to 3 months
Avoid bone grafting

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Study source?
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Contemporary Oral &
maxillofacial surgery
Page 291 -316
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