Odontogenic infection
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Transcript of Odontogenic infection
CLASSIFICATION OF ODONTOGENIC INFECTIONS
Are classified into:
A- Iatrogenic infection
B- Non-iatrogenic infection
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
IATROGENIC ODONTOGENIC INFECTION
I- post-injection infection
II- Post-extraction infection
III- post- surgical infection
AETIOLOGY OF IMMUNODEFICIENCY
A- Systemic conditions:
AIDS
Diabetes mellitus
End-stage renal disease
Leukemia/lymphoma
Systemic lupus erythematous
Advanced age
AETIOLOGY OF IMMUNODEFICIENCY, cont.
B- Primary immunodeficiencies
X-linked severe combined immunodeficiency
Wiskott-Aldrich syndrome
Chediak-Higashi syndrome
DiGeorge syndrome
AETIOLOGY OF IMMUNODEFICIENCY, cont
C- Iatrogenic causes: Immunosuppressive drugs
Broad-spectrum antibiotics
Chemotherapy
Radiation therapy
Bone marrow transplantation
AETIOLOGY OF IMMUNODEFICIENCY, cont
D- Social Factors;
* Alcoholism
* IIIicit drug use
* Morbid Obesity.
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
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.
Presentations
• Pain
• Lymphadenopathy
• Swelling
• Facial sinuses
• Trismus
• Symptoms secondary to complications
•Clinical Features
• A-Local: B-systemic extra-oral *Fever
Intra-oral *Headache
• Manifestations *Tachycardia
• Trismus * Malaise
• Teeth
• Discharge
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
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
Control of Infection
Stage of cellulitis:
-Antibiotic therapy
1- Broad spectrum
2- Bactericidial
3- Combination
-Hot fomentation
- Warm mouth wash
-Control any predisposing factor
Stage of Suppuration (Abscess Formation)
.Incision + Drainage,,,,When??? And How???
.Culture and sensitivity
.Antibiotics according to the culture& sensitivity.
.Anti-anaerobic chemotherapy:
*Metronidazole
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)
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.
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
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.
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
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
Diagrammatic illustrations showing the incision of an intraoral abscess and the placement of a hemostat to facilitate the drainage of pus
Diagrammatic illustrations showing the placement of a rubber drain in the cavity and stabilization with a suture on one lip of the incision
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.
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.
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.
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,
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.
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:
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.
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. [email protected]
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.
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.
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.
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
Patient Monitoring
1. Response to treatment.
2. Development of adverse reactions
3. Superinfection and Recurrent infection.
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.
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…..
Removal of Underlying Cause(cont.)
B- Underlying Systemic Causes; 1.Diabetes Mellitus
2. Blood Dyscrasias
3. Chronic deblitating Diseases
4. Immuno-Suppressed Patients.
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….
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
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
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
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
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
Subperiosteal abscess with lingual localization. a Diagrammatic illustration; b clinical photograph
Submucosal abscess with buccal localization. a Diagrammatic illustration; b clinical photograph
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
Fascial abscess (submandibular). a Diagrammatic illustration. b Clinical photograph
Treatment of Acute Dento-Alveolar Infection
• * Medical: Antibiotics ????
• * Dental:
R.C.T.,
Extraction,
Periodontal
• * Surgical: Incision and
Drainage, Bone fenestration
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.
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
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 ?????
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
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.
BACTERIOLOGY
Mixed infections; mainly hemolytic streptoccoci and mixture of aerobic gm –ve micro-organisms including fusiform bacilli,vincent’s organism and various staphyloccus.
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.
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.
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.
Air Way Management
1.Anethesia; No Anethesia??
Local?? Or
General??
2. Intubation; Oral or Nasal?
3. Tracheostomy
• Viral infections
• Bacterial infections
• Fungal infections
• HIV infection and AIDS
Herpes Viradae
• Herpes Simplex 1
• Herpes Simplex 2
• Varicella Zoster
• Epstein-Barr
• Cytomegalovirus (HHV5)
• Herpes 6
• Herpes 7
• Herpes 8
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
Herpes Simplex Virus
– Extraoral spread of infection: skin, fingers, nail bed, eyes
Herpetic whitlow
• Treatment
– Supportive
– Acyclovir in extreme cases
• Prognosis:
– self-limited
– resolves in 10-14 days
• HSV remain latent in trigeminal sensory ganglia
• Virus reactivation associated with:
– Ultraviolet radiation
– Trauma
– Immunosuppression
Recurrent Herpetic Stomatitis
• Prodrome:
• tingling
• burning
• paresthesia
• Vesicles and ulcers recur: most common herpes labialis
– Intraorally: hard palate and gingiva
– In small clusters
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.
Zoster (Shingles)
• Multiple recurrence is rare – Same latent state as HSV, in sensory ganglia
– Predisposing factors:
• Decreased immunocompetence – Elderly patients
– Immunosuppressive drugs
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
Coxsackievirus Enteroviradae
• Over 30 types
• Ones worth mentioning
– Herpangina
– Hand-foot and mouth
– Acute lymphonodular pharyngitis
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
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.
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
Infectious mononucleosis (glandular fever)
• EBV
– Nasopharyngeal carcinoma
– Hairy leukoplakia
– Burkitt’s lymphoma
– Oral squamous cell carcinoma?
Measles (Rubeola)
• Paramyxovirus
• Children
• Prodromal symptoms
• Koplik spots disappear as skin rash starts
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
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
Noma (cancrum oris)
• Orofacial gangrene
• Malnourished children
• Immunosuppressed individuals
• Usually preceded by NUG
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
Syphilis
• Treponema pallidum
• Primary: chancre : shallow ulcer – Indurated base
– Associated with lymphadenopathy
– Heals spontanously
6 weeks later
• Secondary syphilis: skin rash and mucous patch
– Snail track ulcers, flat areas of ulceration that coalesced
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
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 [email protected]
Tuberculosis
• Mycobacterium tuberculosis
• Oral infection is not common
– Primary oral infection
– Secondary oral infection: infected sputum from pulomonary TB
Tuberculosis
• Diagnosis: Biopsy, granulomatous inflammation
– Granulomas with central necrosis
– Identification of Acid Fast Bacilli
• Treatment:
– 2 antimicrobial agents: isoniazide and rifampicin, 4-8 months
Leprosy
• Mycobacterium leprae
• Endemic in tropical areas
• 2 forms of infection: – Tuberculoid
– Lepromatous
• Oral lesions in lepromatous – Secondary to nasal involvement
– Maxillary gingiva, palate
Gonorrhoea
• Neisseria gonorrhea
• Mainly tonsillar and soft palatal lesions
• Erythema, vesicles, ulcers, pain
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.
B) Local:
1) Ill-fitting dentures.
2) Reduced vertical dimension.
3) Lip-licking habit.
4) Overuse of antiseptic and antibiotic rinses.
-Mucocutaneous.
-Syndrome associated.
-Pseudomembranous.
-Atrophic.
-Hypertrophic.
Pseudomembranous (Thrush): in the form of white plaques which can
be scraped off small hemorrhagic areas.
Systemic Local
Atrophic Candidiasis:
• Atrophic glossitis due to loss of filiform papillae.
• Angular cheilitis due to loss of vertical occlusal dimension.
• Median rhomboid glossitis.
Hypertrophic Candidiasis:
This can mimic lichen planus,
leukoplakia,verrucous carcinoma or a
squamous cell carcinoma.
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.
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.
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.
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.
Are both uncommon in Egypt and can be
diagnosed after histological examination of
the oral ulcers.
Coccoidioidomycosis and Blastomycosis:
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.
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.
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.
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
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
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
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
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
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”
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…………………
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
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
BRONJ: Clinical Presentation
• Subclinical Form
– asymptomatic
– radiographic signs
• Sclerosis of lamina dura
• Widening of PDL space
Clinical Presentation (cont)…
• Soft tissue abrasions
– Tissues rubbing against bone
• AND………
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
More frequently Lesions more extensive All stages II, III more
common Lower success with Tx Patients generally sicker
BRONJ: IV BPs
Stage 0 Lesions
• Spontaneous onset numbness and pain
• No exposed bone
• No prior dental antecedent
• Positive image findings:
– Sclerosis
– Positive bone scan
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)
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
Similar Clinical Entities
• Closely resembles Osteopetrosis
– Loss of osteoclastic function
– Hypermineralization
– Fractures, nonunions, open oral wounds
– Endpoint: bone necrosis, +/- infection
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
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
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
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
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
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
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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