11. DIAGNOSIS
A- Patient’s 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
ikassem@dr.com
12. 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.
ikassem@dr.com
15. Clinical Features Of Suppuration
(stage of abscess formation)
*Pain: .dull aching-throbbing
*Temp: .hectic fever
*Swelling: .fluctuant
.+ve paget’s
*Skin: .pitting edema
*Aspiration test pus
ikassem@dr.com
16. Principles of Treatment of Acute Odontogenic
Infections
1st: Control of infection:
A- Stage of cellulitis.
B- Stage of suppuration
2nd: Support the patient
3rd:Removal of the cause
4th:Treatment of complications
ikassem@dr.com
17. Control of Infection
Stage of cellulitis:
-Antibiotic therapy
1- Broad spectrum
2- Bactericidial
3- Combination
-Hot fomentation
- Warm mouth wash
-Control any predisposing factor
ikassem@dr.com
18. Stage of Suppuration
(Abscess Formation)
.Incision + Drainage,,,,When??? And How???
.Culture and sensitivity
.Antibiotics according to the culture& sensitivity.
.Anti-anaerobic chemotherapy:
*Metronidazole
ikassem@dr.com
19. 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)
ikassem@dr.com
20. AIR WAY OBSTRUCTION
1- Ludwig’s angina
2- Impending Ludwig’s angina
3-Panfacial spaces infection
4-Retropharyngeal abscess
5-Extremes of age (very young&
very old)
6- Acute necrotizing fascitis.
ikassem@dr.com
21. Clinical Features of suppuration
(Stage of Abscess formation)
Paindull aching Throbbing
Temp. Hectic fever
Swelling Fluctuation,+Ve
Paget’s test.
Skin Pitting edema
Aspiration test- Pus
ikassem@dr.com
22. 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.
ikassem@dr.com
23. Incision for drainage of a sublingual abscess. The
incision is performed parallel to the Incision for drainage of a palatal
submandibular duct abscess, parallel to the greater palatine
and the lingual nerve vessels
ikassem@dr.com
24. 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
ikassem@dr.com
25. Diagrammatic illustrations showing the incision of an
intraoral abscess and the
placement of a hemostat to facilitate
the drainage of pus
ikassem@dr.com
26. Diagrammatic
illustrations showing the placement
of a rubber drain in the cavity
and stabilization with a suture
on one lip of the incision
ikassem@dr.com
27. 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.
ikassem@dr.com
28. 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.
ikassem@dr.com
29. 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.
ikassem@dr.com
30. 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,
ikassem@dr.com
31. 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.
ikassem@dr.com
32. 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:
ikassem@dr.com
33. 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.
ikassem@dr.com
34. Clinical Implications
1.The microbiology of cellulitis-type
infections, that don’t 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. ikassem@dr.com
35. 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.
ikassem@dr.com
36. 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.
ikassem@dr.com
37. 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.
ikassem@dr.com
38. 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
ikassem@dr.com
39. Patient Monitoring
1. Response to treatment.
2. Development of adverse reactions
3. Superinfection and Recurrent infection.
ikassem@dr.com
40. AIR WAY OBSTRUCTION
1- Ludwig’s angina
2- Impending Ludwig’s angina
3-Panfacial spaces infection
4-Retropharyngeal abscess
5-Extremes of age(very young&
very old)
6- Acute necrotizing fascitis.
ikassem@dr.com
41. 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…..
ikassem@dr.com
43. 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….
ikassem@dr.com
44. Natural History of Dental infection
ِ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.
ikassem@dr.com
45. 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
ikassem@dr.com
46. Spread Through Tissue Spaces and
Planes
This is the commonest route of
spread
ikassem@dr.com
47. 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
ikassem@dr.com
48. 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
ikassem@dr.com
49. 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
ikassem@dr.com
50. Subperiosteal abscess with lingual
localization. a Diagrammatic illustration; b
clinical photograph
ikassem@dr.com
51. Submucosal abscess with buccal localization.
a Diagrammatic illustration; b clinical
photograph
ikassem@dr.com
52. 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
ikassem@dr.com
54. Treatment of Acute Dento-Alveolar
Infection
• * Medical: Antibiotics ????
• * Dental:
R.C.T.,
Extraction,
Periodontal
• * Surgical: Incision and
Drainage, Bone fenestration
ikassem@dr.com
55. 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.
ikassem@dr.com
58. 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
ikassem@dr.com
59. LUDWING’ANGINA
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 2nd,and 3rd 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.
ikassem@dr.com
60. BACTERIOLOGY
Mixed infections; mainly hemolytic streptoccoci
and mixture of aerobic gm –ve micro-
organisms including fusiform bacilli,vincent’s
organism and various staphyloccus.
ikassem@dr.com
61. 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. Patient’s Mouth; is usually opened because of
elevation of the floor of mouth and swelling of
the tongue.
ikassem@dr.com
62. 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.
ikassem@dr.com
63. 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.
ikassem@dr.com
64. Air Way Management
1.Anethesia; No Anethesia??
Local?? Or
General??
2. Intubation; Oral or Nasal?
3. Tracheostomy
ikassem@dr.com
68. 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
ikassem@dr.com
73. Recurrent Herpetic Stomatitis
• Prodrome:
• tingling
• burning
• paresthesia
• Vesicles and ulcers recur: most common herpes
labialis
– Intraorally: hard palate and gingiva
– In small clusters
ikassem@dr.com
74. 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.
ikassem@dr.com
75. Zoster (Shingles)
• Multiple recurrence is rare
– Same latent state as HSV, in sensory ganglia
– Predisposing factors:
• Decreased immunocompetence
– Elderly patients
– Immunosuppressive drugs
ikassem@dr.com
76. 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
ikassem@dr.com
78. 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
ikassem@dr.com
79. 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.
ikassem@dr.com
80. 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
ikassem@dr.com
82. Measles (Rubeola)
• Paramyxovirus
• Children
• Prodromal symptoms
• Koplik spots disappear as
skin rash starts
ikassem@dr.com
83. 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
ikassem@dr.com
84. 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
ikassem@dr.com
85. Noma (cancrum oris)
• Orofacial gangrene
• Malnourished children
• Immunosuppressed individuals
• Usually preceded by NUG
ikassem@dr.com
86. 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
ikassem@dr.com
88. 6 weeks later
• Secondary syphilis: skin rash and mucous patch
– Snail track ulcers, flat areas of ulceration that
coalesced
ikassem@dr.com
89. 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
ikassem@dr.com
90. 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 ikassem@dr.com
91. Tuberculosis
• Mycobacterium tuberculosis
• Oral infection is not common
– Primary oral infection
– Secondary oral infection: infected sputum from
pulomonary TB
ikassem@dr.com
98. 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. ikassem@dr.com
99. B) Local:
1) Ill-fitting dentures.
2) Reduced vertical dimension.
3) Lip-licking habit.
4) Overuse of antiseptic and antibiotic
rinses.
ikassem@dr.com
100. -Mucocutaneous. -Pseudomembranous.
-Syndrome associated.
Systemic Local
-Atrophic.
-Hypertrophic.
Pseudomembranous (Thrush): in the form of white plaques which can
be scraped off small hemorrhagic areas.
ikassem@dr.com
101. Atrophic Candidiasis:
• Atrophic glossitis due to loss of filiform
papillae.
• Angular cheilitis due to loss of vertical occlusal
dimension.
• Median rhomboid glossitis.
ikassem@dr.com
103. 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.
ikassem@dr.com
104. 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.
ikassem@dr.com
105. 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.
ikassem@dr.com
106. 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.
ikassem@dr.com
107. Coccoidioidomycosis and
Blastomycosis:
Are both uncommon in Egypt and can be
diagnosed after histological examination of
the oral ulcers.
ikassem@dr.com
108. 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.
ikassem@dr.com
109. 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.
ikassem@dr.com
110. 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.
ikassem@dr.com
113. 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
ikassem@dr.com
114. 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 Paget’s disease of bone
• Hypercalcemia of malignancy
• Bone metastases of solid tumors
– breast and prostate carcinoma; other solid tumors
• Osteolytic lesions of multiple myeloma
ikassem@dr.com
115. History of Bisphosphonate
Development
• Mid-19th Century German chemists
– Anti-corrosive in pipelines
• 20th Century - Clinical applications
– Tc99 Bone scans
– Toothpaste
• Anti-tartar, anti-plaque effects
– Osteopathies
• Anti-resorptive effect
ikassem@dr.com
116. 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
ikassem@dr.com
117. Medical Indications for Oral BPs
• Paget’s 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
ikassem@dr.com
118. Pharmacokinetics
• Oral BP’s
– 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”
ikassem@dr.com
119. 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…………………
ikassem@dr.com
120. 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
ikassem@dr.com
121. 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
ikassem@dr.com
122. BRONJ: Clinical Presentation
• Subclinical Form
– asymptomatic
– radiographic signs
• Sclerosis of lamina
dura
• Widening of PDL space
ikassem@dr.com
124. 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
ikassem@dr.com
125. BRONJ: IV BPs
More frequently
Lesions more
extensive
All stages
II, III more
common
Lower success with
Tx
Patients generally
sicker
ikassem@dr.com
126. Stage 0 Lesions
• Spontaneous onset numbness
and pain
• No exposed bone
• No prior dental antecedent
• Positive image findings:
– Sclerosis
– Positive bone scan
ikassem@dr.com
127. 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)
ikassem@dr.com
128. 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
ikassem@dr.com
129. Similar Clinical Entities
• Closely resembles
Osteopetrosis
– Loss of osteoclastic
function
– Hypermineralization
– Fractures, nonunions,
open oral wounds
– Endpoint: bone necrosis,
+/- infection
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130. 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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131. 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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132. 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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133. 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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134. 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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135. 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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136. 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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