OSTEOMYELITIS OF THE JAWS
DR.SOORAJ S.
ORAL & MAXILLOFACIAL SURGEON
DEFINITION
Osteomyelitis may be defined as inflammatory condition of the bone ,that begins as an infection of medullary cavity and haversian system of the cortex and extends to involve the periosetum of the affected area
Predisposing factors
1)Condition that alter the host defences
a) Diabetes
b) Agranulocytosis
c) Leukemia
d) Severe anaemia
e) Malnutrition
f) Steroid drug use
g) Cancer chemotheraphy
2)Condition that alters the vascularity of the bone
a) Radiation
b) Osteoporosis
c) Osteopetrosis
d) Paget’s disease of bone
e) Fibrous dysplasia
f) Bone malignancy and bone necrosis caused
by Mercury, Bismuth, Arsenic
3)Virulance of the microorganisms
Certein organisms participatets thrombi formation by virtue of their destructive lysosomal enzymes
Pathogen born bioactive peptides, chemico attacked leukocytic purulance form the protective barrier for the infectious foci
ETIOLOGY AND PATHOGENESIS
Reduced host resistance during surgery or repeated movements of unreduced fractures may contributes to the development of suppurative osteomyelitis
Body
Symphasis, angle
Ramus and condyle
1) Extensive blood supply and significant collateral blood
flow in mid face
2) Porous nature of membranous bone
3) Thin cortical plates
4) Abundent medullary spaces
INFLAMMATION LEADING TO AVASCULAR BONE
Acute inflammation
(edema pus formation )
Increased
Intramedullary pressure
Vascular collapse
(stasis, ischemia of bone )
Avascular bone
EXTENSION OF PUS AND MICROORGANISMS
Pus, organism extension
Haversian system/nutrient
canal involvement
Elevation of periosteum
Disrupted blood supply
Avascular infected bone
MICROBIOLOGY OF OSTEOMYELITIS
Most of the cases caused by aerobic streptococci(alpha hemolytic streptococci,strep viridans),anaerobic streptococci ;and other anaerobes,such as peptostreptococci,fusobacteria and bacteroides
CLASSIFICATION
Suppurative
1)Acute suppurative osteomyelitis
2)Chronic suppurative osteomyelitis
primary – no acute phase preceding
secondary – follows acute phase
3)Infantile osteomyelitis
Non suppurative
1)Diffuse sclerosing osteomyelitis
2)Focal sclerosing osteomyelitis
(condensing osteitis)
3)Proliferative periostitis
(periosteitis ossificans,garries sclerosing osteomyelitis)
4)Osteoradionecrosis
Cierny – Mader classification
stage-1 : Medullary osteomyelitis
stage-2 :Superficial osteomyelitis
stage-3 :Localized osteomyelitis
stage-4 :Diffuse osteomyelitis
A – Host :Normal host
B – Host :Systemic compromise
Local compromise
C – Host :Treatment is worse than disease
ACCUTE SUPPURATIVE OSTEOMYELITIS
Microbiology
The most commonly found organisms in odontogenic OML is staph aureus;step pyogenes
Etiology
1)Odontogenic infections
2)Local traumatic injuries
3)Peritonsillar abscess
4)Furunculosis of the skin
CLINICAL FINDINGS
Involves alveolar process ,angle of mandible ,posterior part of ramus and coronoid process
a) Early cases are characterized by
-Fever ,malaise ,nausea ,vomiting
-Deep seated continuous boring pain in affected area
-Intermittent paraesthesia or anaesthesia of the lower part of the lip
-Indurated swelling of moderated size , which is more confined to periosteal envelop and its content
-Trismus
b) Established cases
-Deep pain , malaise , fever ,dehydration
-Loose teeth , sensitive to percussion
-Purulent discharge through sinuses
-Foetid odour is often present
-Regional lymphadenopathy
If left untreated in such cases osteomyelitis can spread to involve the both side of the mandible .Further spread to TMJ causes septic arithritis
CHRONIC OSTEOMYELITIS
It can be a) Primary
b) Secondary
Clinical features
1)Non healing boney and overlying soft tissue wounds with induration of the soft tissues
2)Intraoral or extraoral draining fistule
3)Thickened and wooden character of the bone
4)Enlargement of the mandible
5) Pathological fracture may occur
6) Teeth in the area becomes loose and sensitive to percussion
Garre’s Sclerosing Osteomyelitis
Etiology
Clinical features
Treatment
IMAGING
ACUTE PHASE
RADIOGRAPHIC EXAMINATION
In early disease, no radiographic change may identifiable
LOCATION – Posterior body of the mandible
PERIPHERY – Ill defined periphery
INTERNAL STRUCTURE – Decrease in density of the involved bone, with loss of sharpness of existing trabeculae
Sequstra can be identified by close inspecting a region of bone
EFFECTS ON THE SARROUNDING STRUCTURES
may result in several lines
(An ONION-SKIN appearance )
This process is referred as
proliferative periostitis
Onion skin appearance
CHRONIC PHASE
RADIOGRAPHIC FEATURES
PERIPHERY –
Gradual transition between
normal trabeculae and sarrounding
bone, when disease is active the
periphery may be radiolucent and
have poorly defined borders
Subperiosteal new bone formation
fingerprint or orange peel
appearance
INTERNAL STRUCTURE
Lesion usually composed of the
more radiopaque or sclerotic
bone pattern
A close inspection of the radiolucent region may reveal an island of bone or sequstrum within the center
EFFECTS ON SARROUNDING STRUCTURE
Periosteal new bone formation ,which is radiographically single or series of radiopaque lines
Over a time the radiolucent strip that seperates this new bone from the outer cortical bone surface may be filled with granular sclerotic bone
Chronic lesions may develop
a draining fistula
Radionuclide imaging
Radionucleotide scanning or skeletal scintigraphy is usefull in determining the presence of the reactive bone
Tc – labelled methylene diphosphonate administrated intravenously . The radioisotope is distrubuted to the entire skeleton and concentrated in the areas of increased blood flow and osteoblastic activety
OML OF MANDIBULAR POSTERIOR REGION
Advantages
Magnetic resonance imaging
When bone scan findings are negative or equivocal and osteomyelitis is still highly suspected MRI provides usefull information in selected cases
ADVANTAGES
DISADVANTAGES
Distinction between soft tissue changes as a secondary reactive inflammation and primary soft tissue changes involvement in cases of OML is not possible
CONE BEAM CT-SCAN
Predominant radiographic pattern of osteomyelitis from computed tomograms (Yoshero et al)
1)Most common presentation of OML is mixed pattern in which osteosclerosis is combined with equal or less amounts of osteolysis, not associated with teeth
2)Sclerotic pattern, in which osteosclerosis is dominant
3)Lytic pattern, in which osteolysis is predominant
4)Sequestration seen with or without bony changes
information in volume, rather
than a slice providing three
dimensional images
MANAGEMENT
A) Conservative management
1)Complete bed rest
2)Supporative therapy
3)Dehydration
4)Blood transfusion
5)Control of pain
6.Antimicrobial theraphy
MICRO ORGANISMS | ANTIBIOTIC OF CHOICE | ALTERNATIVE |
STAPHYLOCOCCUS AUREUS | Naficillin sodium or oxacillin sodium 1.2-2.0g i.v 4 to 6th hrly Or Cefazolin(or other first generation cephalosporinin equalant dosage) 1g i,.v every 8th hrly | vancomycin |
METHACILLIN RESISTANT | Vancomycin 30mg/kg i.v in two equally devided doses.Not to exceed 2gm/hr unless serum levels are monitored for 4-6 weeks | |
Penicillin sensitive streptococci or pneumococci or entrococci | Ampicillin sodium 12g/24hrs i.v continously or in 6 equally divided doses(The addition of Gentamycin sulfate 1mg/kg i.v or i.m every 8th hrly for 1-2 week is option) Ceftriaxone 2g i.v every day for 4-6 weeks | Ciprofloxicin 500-750mg orally 4-6th hrly |
ANTIBIOTIC IMPREGNATED BEADS
7) Special treatment for specific needs
-Anaemia
-Diabetes mellitus
- Malnutrition
Hyperbaric O2 in treatment of OML
Hyperbaric oxygen therapy consists of breathing 100% oxygen through a face mask or hood in a monoplace or a large chamber at 2.4 absolute atmospheres pressure for 90 min session or dives for as many as 5 days a week totaling 30 or more sessions often followed by another 10 or more sessions
Action of HBO
1)Enhancement of lysosomal degradation potential of polymorphonuclear leukocytes and O2 radicals
2)Exotoxin liberated by microorganisms are rendered inert by exposure to elevated partial pressure of O2
3)Tissue hypoxia is reversed by HBO
4)Postive enhancement of neoangiogenesis
Clinical effects
Marx protocol
Stage – 1
Response
Stage-2
Response
Stage-3
|
|
|
ATA) (stage 1 responder) |
Healing without exposed bone (stage 2 responder) |
CONTRAINDICATIONS
Pneumothorax
COPD
Optic neuritis
Acute viral infection
Congenital spherocytosis
Malignancy
Pregnancy
SURGICAL MANAGEMENT
A.Incision and drainage
B. Extraction of loose offending tooth
C.Decortication
Steps in decortication
1)Creation of buccal flap by crestal incision extending along the neck of the teeth
2)Reflection of mucoperiosteal flap
3)Removal of lateral and inferior border of cortical plate
4)Debride, flap should be primerly closed
5)Irrigation tubes are placed
E .Continuous or intermittent indwelling closed catheter irrigation
gastric tube catheter or
Polyethylene drain tubes
3-4mm in diameter and
6-10 inch long
drainage and other for
local antibiotic delivery
F. Sequestrectomy
a) Small and accessible – Intraoral approach
b) Large and inaccessible – Extraoral approach
G . Saucerization
Saucerization is unroofing of the bone to expose the medullary cavity for through debridement
to expose infected bone, loose teeth are
removed and superior aspect of buccal
cortical plate is excised.The bone is
trimmed until bleeding is noted from all
margin
saucer, mucosa is trimmed,suture tied
over the pack
covered by normal mucosa