OSTEOMYELITIS & OSTEORADIONECROSIS

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Osteomyelitis :
*
Osteon in Greek means bone Myelos in Greek means marrow Itis in Greek means inflammation Osteomyelitis is an inflammation of medullar portion of the bone However, the process is rarely confined to the endosteum. It involves the cortical Master and periosteum as well. Therefore, Click to edit bone subtitle style osteomyelitis may be defined
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as::

* OML is defined as an inflammatory condition of bone primarily

involving soft tissues{ARCHER 1975}

* Extensive inflammation of bone involving cancellous portion{LASKIN

*Inflammatory condition of bone that usually

begins as an infection of the medullary cavity, rapidly involves the haversian system and quickly extends to the periosteum of that area. (TOPAZIAN)

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HISTORY
* SPINOSA VENTOSA
- ARAB PHYSICIANS

* OML OF TIBIA WILLIUM HEY * CHRONIC OML

(1736 1819)

- SAMUEL COPPER ( 1787)

* JOHN HOWSHIP - (1803)

- THE NATURAL AND DISEASED STATES OF BONES (1820)

(1807 1873) 5/21/12

* CHRONIC OML - AUGUSTE NELATON

REES (1847) - OML OF MAXILLA IN NEWBORNS

*
* *

CARL GARRE (1893) - TIBIA

WILENSKY (1932) - OML IN INFANTS HOWARD WALTER FLOREY & COWORKERS - (1941) PENICILLIN THERAPY

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*classification
*Cierny
et al's classification:

*I) Anatomic types: *Stage I : Medullary osteomyelitis *Stage II: Superficial osteomyelitis *Stage III: Localised osteomyelitis *Stage IV: Diffuse osteomyelitis
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*II)Physiological types: 1.Normal host 2.Systemic compromise/local

compromise

3.Treatment is worse than the disease

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* III) Systemic or local factors that affect

immune surveillance, metabolism and local vascularity A) Systemic: i) Malnutrition ii) Renal or hepatic failure iii) Diabetes mellitus iv) Chronic hypoxia v) Immune deficiency or suppression vi) Malignancy vii) Extremes of age viii) Autoimmune disease ix) Tobacco and alcohol abuse

* * * * * * * * * *

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* Local: * i) Chronic lymphedema * ii) Venous stasis * iii) Major vessel disease * iv) Arteritis * v) Extensive scarring * vi) Radiation fibrosis * vii) Small vessel disease * viii) Loss of local sensation.

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* Hudsons classification: * Acute forms of osteomyelitis (suppurative or non- suppurative) * a)contiguous focus : 1) Trauma * 2) Surgery * 3) Odontogenic infection *
b) Progressive : * 1) Burns * 2) Sinusitis * 3) Vascular insufficiency * c) Hematogenous : * 1) Developing skeleton (children)

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* B) Chronic forms of osteomyeliyis * a) Recurrent multifocal : 1) developing skeleton * 2) escalated osteogenic activity * * * b) Garres : 1)unique proliferative subperiosteal reaction * 2)developing skeleton * * c) suppurative or non-suppurative : 1) inadequately treated form * 2) systemically compromised forms * 3) refractory forms * * d) Diffuse sclerosing forms: 1) fastidious organisms * 2)compromised host/pathogen interface. * *
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Topazian's classification : Suppurative osteomyelitis Acute suppurative osteomyelitis Chronic suppurative osteomyelitis 1) Primary 2) Secondary Infantile osteomyelitis
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Non -suppurative osteomy

Diffuse scleroising osteomy

Focal sclerosing osteomye Proliferative perisote itis Osteoradionecrosis

* Predisposing factors:
conditions that alter host defence: diabetes, agranulocytosis,leukaemia,severe anemia,malnutrition,drug abuse,chronic alcoholism,sickle cell disease,typhoid. conditions that alter vascularity of bone:therapeutic radiation, osteoporosis,pagets disease, fibrous dysplasia,bone malignancy, virulence of organisms: lysosomal & enzymatic degradation of host tissues along with microvascular thrombosis brought about by pathogen born bioactive peptides & chemo attracted leukocyte purulence forms a protective barrier for infectious foci,allows organisms to proliferate in an enriched host medium..

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*Disease
Diabetes :

Mechanism facilitating bone infection Diminished leukocyte chemotaxis, phagocytosis,and

lifespan; diminished vascularity of tissue due to vasculopathy, thus reducing perfusion and the ability for an effective inflammatory response; slower healing rate due to reduced tissue perfusion and defective glucose utilization. Leukemia: Deficient leukocyte function and associated anemia Malnutrition: Cancer: Reduced wound healing and reduction of immunological response Reduced wound healing and reduction of immunological response

Osteopetrosis (AlbersSchonberg disease): Reduction of bone vascularization due to enhanced mineralization, replacement of 5/21/12 hematopoietic marrow causing anemia and leukopenia

* Severe anemia (particularly sickle-cell anemia): Systemic

debilitation, reduced tissue oxygenation, bone infarction (sickle cell anemia), especially in patients with a homozygous anemia trait.

* IV drug abuse: Repeated septic injections, spreading of septic emboli

(especially with harboring septic vegetation on heart valves, in skin or within veins).

* AIDS: Impaired immune response. * Immunosuppression (steroids, cytostatic drugs): Impaired immune
response

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*Etiology
* Odontogenic infections : * pulpal or periodontal tissues * pericoronitis * infected socket * infected cyst and tumor. * Trauma : * compound fractures * surgery- iatrogenic

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* Infection of orofacial region: * Periosteitis - gingival ulceration * Infected lymph nodes furuncles * Lacerations * Peritonsillar abcess . * Infections by hematogenous route: * furuncle of face * skin wound * middle ear infection * mastoiditis * systemic TB * upper respiratory tract infection. *
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*Odontogenic infections *Trauma *Gingival infections *Lymph node infections *Hematogenous origin.

Osteomyelitis of jaws predisposing factors, etiology JOMS (34) 2006

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Click to edit Master subtitle style

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* Caries * Necrotic pulp * * * Trauma

Periapical abscess Acute Apical periodontitis Chronic Periapical granuloma

Osteomyelitis

Periapical cyst

Interrelationship of possible results of periapical inflammation

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Uncontrolled Diabetes

Decreased immunity

Delayed wound healing

Microangiopathy & atherosclerosis

Fungal sinusitis
Direct invasion

Fungus invades from the sinus into blood vessels

Non healing extraction socket invades more vessels

Fungi forms thrombi within blood vessels

Reduces vascularity

Bone necrosis

pathophysiology of bone necrosis secondary to mucormycotic infection in a diabetic patient 5/21/12 Med Oral Patol Oral Cir Bucal 2007;12:E360-4

*Microbiology
* Primarily * S.aureus
Streptococci (-hemolytic), Peptostreptococcus, Fusobacterium and Prevotella. skin wounds and fistulas.

* Eikenella corrodens- perimandibular

space infections. Occasionally Klebsiella, pseudomonas and proteus are found.

* Specific forms of osteomyelitis- Mycobacterium tuberculosis,

Treponema pelladium, Actinomyces.

* Staphylococcal extra oral trauma with soft tissue involvement.

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Findings helpful in recognition of pure anerobic or mixed aerobic and anerobic infection in osteomyelitis of jaws are presence of

Foul smelling exudate

Sloughing of the necrotic tissue Gas in soft tissue Black discharge from the wound

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*Clinical findings:
*Clinical findings: *4 clinical types: 1.Acute suppurative 2.Secondary chronic 3.Primary chronic 4.Non suppurative
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Acute pyogenic osteomyelitis(acute suppurative oml)

*Aetiology: odontogenic infections, local traumatic injuries,

peritonsillar abscess, furunculosis,haematogenious infection *Clinical features: In adults it occurs most commonly in mandible, alveolar process, angle, post part of ramus and coronoid process., condyle is reported rarely(linsey 1953) .. *Early cases: high intermittent fever, malaise, nausea, vomiting, anorexia, deep seated boring high intense continous pain, intermittent paraesthesia or anaesthesia of IAN, facial cellulitis, trismus,.

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*Eastablished cases: deep pain malaise, fever, dehydration,

teeth become loose, sensitive to percussion, purulent discharge through sinuses, intraorally around gingival sulcus, buccal vestibule, extra orally around face through cutaneous fistulae, foetid odour, trismus, dehydration, acidosis, toxemia, regional lymphadenopathy..

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ACUTE SUPPURATIVE OML

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Primary chronic osteomyelitis (results from organisms which are

less virulent) 1. Insidious onset 2. Slight pain 3. Slow increase in jaw size 4. Gradual development of sequestra.

Secondary chronic osteomyelitis (occurs when treatment did not

succed in eliminating acute osteomyelitis) 1. Fistulas 2. Induration of soft tissue 3. Thick/wooden character 4. Pain and tenderness.

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CHRONIC SUPPURATIVE OML

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*Imaging:
* Imaging of suspected osteomyelitis of the mandible is accomplished by
conventional radiography, supplemented as needed by CT,MRI and radionucleiotide bone scanning. * Proper imaging aids in determining the extent and degree of disease ,location of sequestra and in planning to approach and extent of surgery. * As estimated 30% to 60% of the mineralized portion of the bone must be destroyed before significant radiographic changes can be distinguished *

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* 1) Conventional radiograph * Radiographic changes described by worth : * Moth eaten appearance * Sequestra seperated by zone of radiolucency * Stippled or granular densification of bone.

with new bone involucrum.

* Moth eaten appearance is because of enlargement of medullary spaces and widening

of volkmans canal resulting from destruction by lysis and replacement with granulation tissue.

* Stippled or granular densification of bone is caused by subperiosteal deposition of

new bone obscuring the intrinsic bone structure or deposition of new bone on surface of existing trabeculae at the expense of marrow spaces. The central sequestra present in osteomyelitis helps to differentiate it from fibrous dysplaia.

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* It is useful in determining the presence of reactive bone. * Radiopharmaceuticals that are absorbed by the bone provide useful

Radio nucleotide imaging

information based on the presence of reactive bone formation rather than demineralization. * Changes are seen as early as 3 days after the onset of clinical symptoms of osteomyelitis. * Tecnitum labelled methylene disphosphonate administered IV. The radioisotope is distributed to the entire skeleton and concentrated in the areas of increased blood flow and osteoblastic activity. * A rectilinear scanner or scintillation camera ,both of which contain sodium iodide, a crystal nucleotide that emits light is used to take isotope containing areas.

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* The complete Tc bone scan has three phases. * First phase: (flow study) consists of 3-4 sec
images during 1to 2 min after injecting the drug.

* Second phase: (blood pool study) single image

obtained 5 to 10 min after injection.

* Third phase: (delayed phase) multiple views

obtained 2to 4 hrs after injection.

* Addition of Ga to Tc scan aids in distinguishing

osteomyelitis from malignancy and trauma
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* Positive findings with both the tests usually * Tc- scan positive , Ga scan negative

confirm the infectious nature of the disease.

,osteomyelitis probably is not the cause . Ga uptake that exceeds Tc- uptake indicate active inflammatory disease.

* In chronic osteomyelitis , reduced Ga- uptake in

the followup scan is useful indicator for termination of therapy in osteomyelitis.

* CT scan special value than plain radiography in

revealing the extent of the lesion, extension of cortical erosion and identification of sequestra.
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*Treatment:
* Principles of treatment : * 1) Evaluation and correction of compromised host defense. * 2) Gram staining, culture and sensitivity * 3) Imaging * 4) Administration of stain guided empirical antibiotics * 5) Removal of loose teeth and sequestra * 6) Administration of culture guided antibiotics, repeated cultures * 7) Placement of irrigation drains / antibiotic impregnated beads * 8) Sequestrectomy, debridement, decortication, resection,
reconstruction.

* IMF should be considered when continuity of the mandible is

questionable and possibility of pathologic fracture.
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*Antibiotic regimen:
* Regimen I: hospitalised/medically compromised/IV indicated * Aqueous penicillin 2 million U IV /4hr + metronidazole 500mg
IV/6 hr * When improved for 48-72 hrs * Penicillin V 500mg 4 hr + metronidazole 500mg 6 hr for 4-6 weeks OR * Ampicillin /sulbactum 1.5 -3.0 g IV/6 hr * Amoxicillin / clavulanate 875/125 mg 12 hr for 4-6 weeks.

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* Regimen II : Out Patient Treatment * Penicillin V 2gm + metronidazole 500mg 8hr

for 2 4 weeks after last seqestrum removed and patient without symptoms . OR * Clindamycin 600-900 mg IV/6hr Clindamycin 300-450 mg 6hr * OR * Cefoxitin 1.0 gm IV/8 hr until no symptoms Cephalexin 500mg 6hr 2-4 weeks. *

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Acute suppurative osteomyelitis

Extraction of teeth

Removal of accessible sequestra Evacuation of pus *After acute stage has subsided Sequestrectomy, saucerization, debridemnet,
direct placement of antibiotics, resection of infected bone and immediate or late reconstruction
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* Sequestrectomy * Removal of foreign bodies * Repeated cultures and improvement of host defenses * Local antibiotic therapy * Closed wound irrigation- suction :- Neosporin irrigant

Chronic suppurative osteomyelitis

or 1% neosprin with 0.1% polymixin B in equal volumes /12 hrly. * Antibiotic impregnated beads : Tobramycin or gentamycin contained in acrylic resin(poly methyl methacrylate). * HBO therapy.

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*Closed wound irrigation and suction : *After intra oral debridement ,saucerisation or decortication ,

small pediatric nasogastric tubes ,french catheters, or polyethelene irrigation tubes 3 to 4 mm in diameter and 6-10 inches in length are perforated along the distance of 3-4 cm from tip. *Tubes are placed into the bone bed through separate skin incisions along lateral bony surface and are affixed to the bone with catgut sutures through holes drilled in the bone. The drains are held to the skin with sutures or tapes

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* After tube placement water tight closure of the wound is achieved,

tubes are flushed with saline solutions, irrigation solution is introduced through one tube while other tube is connected to low pressure suction. * Irrigation solutions contain antibiotics, wetting agents, and proteolytic enzymes. 1-2 lit of solution every hourly. * Irrigation is continued for 1 week and until three successive cultures are sterile.

* Antibiotics in high concentrations can be placed in direct contact

with bone manually or with implantable pump.

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Closed wound irrigation and suction

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* Neosporin

irrigant (bacitricin zinc neomycin sulphate polymixin-B sulphate solution for iirgation)or a solution of .1% polymixin-B in equal volumes may be instilled every 12 hrly.

* Wound must not be over filled. The volume should be gradually

reduced to allow for the filling of the wound by healthy granulation tissue.

* Systemic antibiotics should be continued and for atleast 2 months

after cessation of clinical evidence of disease.

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Antibiotic impregnated beads:

* Antibiotic is leached from the beads , producing high local

concentrations but low systemic concentrations thus reducing the risk of toxicity. * Used especially in chronically infected bone associated with fractures and in chronic sclerosing osteomyelitis refractory to systemic antibiotics. * In chronic sclerosing osteomyelitis after decortcation beads are applied against fresh bleeding surface , a drain is inserted and wound is closed . Beads and drain are left in place for 10-14 days. * In fracture associated cases, foreign bodies are removed , bone ends are debrided , rigid reconstruction plate is placed, string of antibiotic impregnated beads is placed against the bone.

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Antibiotic impregnated beads:

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* HBO therapy: * It is used to promote healing in refractory chronic osteomyelitis or

osteoradionecrosis. * This method works by increasing tissue oxygenation levels that would help fight off nay aerobic bacteria present in their wounds. * HBO therapy consists of 100% oxygen delivered in apressurized manner. * Increased levels of oxygen which has negative effects on bacteria and positive effect on angiogenisis, and increased blood flow to thw area. * It consist of treatment sessions for 90 min based at 2.4 atm of pressure 20 -30 dives post operatively in case of osteoradionecrosis.

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* Surgical management
Adjuvant to medical treatment, In acute stage surgery should be limited to removal of loose
teeth,bone fragments,incision and drainage of fluctuant areas,& may proceed if necessary to sequestrectomy, with or with out saucerization,decortication,resection,reconstruction,..

Treatment of any systemic diseases & supportive therapy consisting of

high protein & vitamin diet, with adequate hydration. once chronic infection has been established decision has to be taken concerning further surgical management.

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* Sequestrectomy
*:
Sequestra usually are cortical but may be cancellous or corticocancellous and generally are not seen until atleast 2 weeks after the onset of infection. * Sequestra are avascular and therefore poorly penetrated by antibiotics.in the chronic stage the involucrum or shell of bone produced by periosteum may be perforated by tracts(cloacae) through which pus escapes in to epithelial surfaces..pathological fractures occurs in this region.rarely sterile abscess brodies abscess occurs in jaws.

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* Sequestrectomy and saucerization:

* Unroofing
bone to expose medullary cavity for debridement.

* Useful in chronic osteomyelitis because it permits the removal of

formed and forming sequestra.

* Should be performed intraorally whenever possible, provides direct

access to bone and avoids facial scaring.

* The defect is packed open to allow subsequent exfoliation of

unrecognised sequestra

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* Steps: * A buccal mucoperiosteal flap is reflected to expose the infected

bone .extensive tissue reflection should be avoided to preserve the blood supply . * Loose teeth and bony segments and particles are removed . * Lateral cortex of the mandible is reduced until bleeding is encountered at all margins approximately to the level of unattached mucosa thus producing saucer lie defect. * Granulation tissue and loose bone fragments are removed from the bone bed using curettes and the area is thoroughly irrigated, the region is usually hyperaemic , but bleeding is readily controlled by packing

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* The buccal falp is trimmed and a medicated -1/2 inch pack

(idoform)is inserted for hemostasis and to maintain the flap in retracted position until initial healing occours. * Pack is retained by sutures for 3-6 days and may be replaced several times until the surface of the bed of granulation tissue is epithelialised and the margins have healed. * Reduction of the lingual cortex rarely is necessary except to remove necrotic bone and sharp crestal margin. Mylohyoid muscle attachment provides rich vascular supply and maintains the vascularity of the bone lingually. * When performed extra orally the defect also may be packed open. However the soft tissue is closed primarily and closed irrigation suction is used.

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* Decortication: * Removal of chronically infected cortex of bone. The lateral and

inferior border cortex is removed 1-2 cm beyond the affected area thus providing access to the medullary cavity.

* It can be used in primary and secondary osteomyelitis or when

initial conservative regimens failed.

* First advocated in 1917 and further discussed by Mowlem.

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* Steps:

1.creation of a buccal flap by a crestal incision extending along the necks of teeth, 2.reflection of mucoperiosteum to the inferior border, 3.removal of teeth in involved area, 4.removal of lateral cortical plate & inferior border with chisels. * Bone bend is debrided thoroughly ,the flap is closed primarly & dead space is eliminated by reapproximation of flap and use of a pressure bandage for 24-48hrs, irrigation tubes or closed suction drains may be used. * Antibiotic impregnated acrylic beads may be used for 10-14 days.

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* Resection and reconstruction:

* Pathological fracture * Persistent infection * Marked infection of both cortical plates * Extra oral approach * Debrided until bleeding surfaces are encountered distally and

proximally * Autologous corticocancellous bone secured to reconstruction plate * Split ribs packed with cancellous bone * Metallic or other alloplastic trays.

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*Types of osteomyelitis
* Osteomyelitis associated with fractures: * Inadequate reduction, fixation and immobilization * Over zealous use of intraosseous wiring, bone plates and screws. * Treatment : * IMF * Loose teeth and foreign material to * Reconstruction plate * Antibiotic therapy.

be removed

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* Infantile osteomyelitis: * Causes: * Hematogenus * Perinatal trauma * Infection of maxillary sinus * Contaminated human/artificial nipples. * Clinically: * Cellulitis around the orbit * Irritability and malaise * Hyperpyrexia * Anorexia and dehydration * Convulsions and vomiting * Inner and outer canthal swelling
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* Palpebral edema * Closure of eye * Subperiosteal abscess - ethmoiditis * Purulent discharge - nose or inner canthal sinus * Buccal and palatal swelling of maxilla * Fistulas * Treatment : * IV antibiotics * Supportive treatment * Drainage * Conservative sequestrectomy * Antibiotics for 2-4 weeks
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* Proliferating periosteitis (Garres sclerosing osteomyelitis): * 1893 Carl Garre * Irritation induced focal thickening of periosteum and cortical bone of
the Tibia. * 1955 Pell mandible * Young individuals,children

* Clinically: localized, hard, nontender, bony swelling, associated with

carious tooth

* Radiographically : onion peel appearance, periapical radiolucency.

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Garres Osteitis

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* Treatment :
1) removal of the source of infection,extraction or RCT. 2) antibiotic therapy 3) surgical recountouring 4) follow up

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* Chronic sclerosing osteomyelitis: * 1) Chronic diffuse sclerosing osteomyelitis * 2) Florid osseous dysplasia * 3) Focal sclerosing osteomyelitis * Chronic diffuse sclerosing osteomyelitis : * Cause: controversial ,infectious or non infectious
due to over usage of jaw ,malocclusion, abnormal jaw positioning ..

Affects both basal bone and alveolar process,entire height of mandible, unilateral. * Angle,ramus,condyle is also involved. * Bone is expanded and tender

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* Episodes of recurrent swelling and pain * Inflammatory ,nonsuppurative,painful disease. * 3rd decade of life.women, * RADIOGRAPHICALLY:Diffuse intramedullary sclerosis with poorly
defined margins with occasional radioopacity

focal areas of radiolucency &

Treatment : Antibiotic therapy Decortication ,rescection,reconstruction, HBO therapy

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Florid osseous dysplasia :

* Multiple small exuberant, lobulated, densely

opaque masses restricted to alveolar process. * Black women,infection results from bacterial invasion by periapical infection,advanced periodontal disease,extraction,surgical incisions,ulcerations. * Fistulas and sequestra may form . * 2nd rly infected is suppurative,mildiy painful,withoutnexpansion of mandible.. * Masses, sequestra & associated granulation tissue are excised & wound debridement ,irrigation, followed by primary or secondary closure..

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* Actinomycotic osteomyelitis : * * Endogenous oral saprophytes * Soft tissue swelling, purpilish, dark red ,oily areas * External sinuses - sulfur granules Dense bone and scar tissue -

lumpy jaw * Delay in healing of extraction sockets * Radiolucencies of varying size , marked scleorosis * Slowly progressive with granulomatous & suppurative features

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* Actinomyces israelii , A naselundii, A odontolyticus, * Occasionally affects bone * Cervicofacial involvement is 2/3rd of total cases,direct extension
or hematogenous. * Cervicofacial disease affects mandible & overlying soft tissues , parotid, tongue, sinuses * Established infection does not respect tissue planes * purplish , dark red , oily soft tissue masses are present * Sulphur granules through sinuses, spreads unimpeded by anatomical barriers

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* Treatment: * Irrigation solutions - For 72 hrs. * th strength Dakins solution(2.5% NaOCl 10% NaHCO3) * 9- Aminoacridine * strength of 3% H2O2 * Saline solution for next 3-5 days . * Penicillin G 10 -20 million units/ day IV for 4-6 weeks * * Penicillin V 1g /6 hr for 6-12 months orally OR * * Ampicillin 50mg/kg /day/IV 4-6 weeks * Amoxicillin 5oomg/8hr 6-12 months. OR * * Doxycycline 100mg/12hr 6 months * If confined only to soft tissue 2-4 months treatment * Ceftriaxone 1g /IV/24hr. * Imaging to monitor bone healing
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*Nocardial osteomyelitis: *Soil saprophyte *Access inhalation or direct inoculation to skin *In jaw- acute necrosis and abscess formation *Treatment : * Pus drainage * Sulfisoxazole 2g /PO/6hr

or Trimethoprim/Sulfametoxazole PO/12hr - 6 months.

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*Condensing osteitis:
Localized area of bone sclerosis Associated with apex of the carious

tooth

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Severe Osteomyelitis Following Immediate Placement of a Dental Implant

spread of infection from an adjacent tooth to the site of an implant and causing an extensive localized osteomyelitis ,the presence of plaque in the gingival sulci of the extracted teeth, is considered a risk factor for infection and failure of immediate implants.

INT J ORAL MAXILLOFAC IMPLANTS 2008;23:137142 5/21/12

Osteonecrosis of the mandible associated with bisphosphonate therapy:

the exact mechanism of bisphosphonate mediated osteoclast inhibition has not been completely elucidated, it is known that these compounds affect bone remodelling at various levels. The inhibiting function of osteoclasts results in disruption of normal bone homeostasis. Through inhibition of endothelial proliferation, intraosseous circulation and bone blood flow are interrupted, which might induce avascular bone.

Oral Surgery (1752-2471), Aug2009, Vol. 2 Issue 3, p153-157 5/21/12

*History of intravenous bisphosphonate therapy

with: *Multiple myeloma *Metastatic bone disease with breast or prostate cancer *Osteogenesis imperfecta *Dental comorbidities *Active periodontitis *Dental caries *Dental abscesses *Failing root canal treatment *Any elective surgery in the oral cavity

5/21/12 Bisphosphonate-Associated Osteonecrosis of the Jaws

Common orofacial findings associated with BON

*Poor wound healing * Spontaneous or postsurgical softtissue *breakdown leading to intraoral or extraoral *bone exposure * Bone necrosis * Osteomyelitis

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* Bisphosphonate use < 3 years with no clinical or radiographic risk

factors * CTx level must be > 150 pg/mL. * Proceed with planned surgery but with informed consent regarding the increased risk of possible future BON with surgical treatment. * Establish a regular recall schedule; contact physician to discuss alternative treatment and intermittent drug holidays.

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*Bisphosphonate use < 3 years with 1 or more

clinical or radiographic risk factors

* Stop bisphosphonate therapy for 3-month drug

holiday. * If CTx level < 150 pg/mL, delay surgery and stop bisphosphonate therapy for at least 3 more months * recheck CTx level 3 months later. * If CTx level > 150 pg/mL then proceed with surgery. * If CTx remains < 150 pg/mL then no surgery and *check CTx level again in 3 months. * 3-month drug holiday post-surgery

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*Bisphosphonate use > 3 years

* Contact physician to discontinue bisphosphonate

3 months before surgery and for at least 3 months postoperatively, but preferably for 1 year. * Determine serum CTx level at time of consultation and immediately before surgery. CTx must be 150 pg/mL before proceeding with surgery. * Detail informed consent regarding risk of bisphosphonate-associated osteonecrosis (BON). * Use an alternative to bisphosphonate for long-term treatment, if possible.

JCDA June 2007, Vol. 73, No. 5

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Journal of Indian Academy of Oral Medicine and Radiology, OctoberDecember 2010;22(4):221-224

Maxillary Necrosis: A Sequelae of Fungal Osteomyelitis

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*CONTENTS. * *Introduction *Definition *Classification *Pathophysiology *Etiology *Clinical features *Radiological feature *Culture test *Diagnosis *Complications *Treatment
* Conservative * HBO therapy * Surgical treatment
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Marx protocol for HBO therapy

* . The current prevalence rate is less than 4%, where as the

frequency was about 15% 20 years ago. Although the risk is low, it increases dramatically if a local surgical procedure is performed within 21 days of radiation therapy initiation or between 4 and 12 months after therapy.

* Definition:* Osteoradionecrosis is a non healing nonseptic lesion of radiated

bone in which bone volume and density cannot be maintained by the hypocellular, hypovascular, hypoxic tissue which cannot adequately meet its metabolic demands.

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* Definitions: * * Beumer : when bone in the radiation field was exposed

for at least

2 months in the absence of local neoplastic disease. * * Marx: an area greater than 1 cm of exposed bone in a field of irradiation that had failed to show any evidence of healing for at least 6 months. * * Hutchinson : an area of exposed bone present for longer than 2 months in a previously irradiated field, in the absence of recurrent tumour. * Epstein : an ulceration of the mucous membrane with exposure of necrotic bone * Harris: irradiated bone becomes devitalised and exposed through the overlying skin or mucosa, persisting without5/21/12 for 3 healing months in the absence of tumour recurrence.

Sl Yea Defined No r by . 1. 197 Meyer 0

Definition

2.

ORN is a classic triad of Radiation, Trauma and Infection. 197 Tittering Osteomyelitis secondary to 1 ton radiation. 198 R. E.An area of exposed bone > 1 3 Marx cms in a field of irradiation that had failed to show any evidence of healing for at least 6 months. 5/21/12 198 Brumer Exposure of bone of the

3.

4.

Sl Yea Defined N r by o. 6.

Definition

7.

198 Marx &Exposure of non-viable 7 Johnso irradiated bone which fails n to heal without intervention. 198 Epstein An ulceration or necrosis of 7 et al the mucous membrane with exposure of necrotic bone for more than 3 months. 198 Epstein 7 et al Resolving chronic or acute necrotic lesion with or 5/21/12 without pathologic fracture

8.

Sl Yea Defined N r by o. 11. 199 Harris 2

Definition

Exposed irradiated bone that has failed to heal over a period of 3 months in the absence of local tumor

12. 199 Mirante 3 et al

ORN is loss of viable bone resulting from radiation therapy 13. 199 Van ORN is defined as bone and 5 Merkes soft tissue necrosis of 6 5/21/12 tyn months duration excluding radiation induced

* 1922 Regaud published first report. * Terms used: * Radiation osteitis * Radio- osteonecrosis * Radiation osteomyelitis * Osteomyelitis of irradiated bone * Osteonecrosis * Radio- osteomyelitis * Septic osteoradionecrosis * Post-radiotherapy osteonecrosis.

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* Classification of Osteoradionecrosis:

* Two types: * Type I:- In this type bone lysis occurs under intact gingiva/ mucosa.
When the soft tissue breaks down, the bone becomes exposed to saliva and secondary contamination occurs. It tends to heal with conservative therapy.

* Type II:- in this type sepsis is directly introduced by trauma of dental

extraction or surgery. This is an aggressive form of Osteoradionecrosis and is better described as radiation osteomyelitis. It doesnt heal with conservative therapy.

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Classification of Post radiation Osteonecrosis 1.By Epstein et al (1987)

Stage I Ia Ib II IIa IIb III IIIa IIIb Description Resolved, healed No pathologic fracture Past pathologic fracture Chronic, nonprogressive No pathologic fracture Pathologic fracture Active, progressive No pathologic fracture Pathologic fracture Local wound care HBO and surgery if indicated Treatment Prevention of recurrence

Local wound care; HBO if indicated

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* 2.Marx et al (1983) * Based on the time of occurrence since radiation and also based
on traumatic episodes.

* Type I Develops shortly after radiation; is due to synergistic effects

of surgical trauma and radiation closely coupled in time. * Type II Develops years after radiation and follows a traumatic event; rarely occurs before 2 years after treatment; most commonly occurs after 6 years; due to progressive endarteritis and vascular occlusion of the nutrient vessels in the bone. . * Type III (Spontaneous ORN) Occurs spontaneously without a preceding traumatic event; usually occurs between 6 months and 3 years after radiation. ; due to immediate cellular damage and death due to radiation treatment. This occurs when the radiation dose exceeds 7000 Rads or the fraction doses are greater than 200 Rads per day.
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* Anatomical considerations
Although Osteoradionecrosis occurs in other bones like sternum, skull, pelvis it is most commonly seen mandible because: * * Increased incidence of head and neck cancers * Frequent and successful use of radiation therapy in this area. * Presence of teeth in dense bone * Most oral tumors are perimandibular. * * * Maxilla is less commonly affected because: * The absence of dense cortical plate (decreased bone density) * Increased vascularity
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* Etiology:

* 1.Radiation and trauma

Trauma due to: * Tooth extraction (most common factor) * Mucosal ulcer (eg: denture sore) * Lacerations * Scaling of teeth * Compound fractures * Periodontal diseases * Injudicious root canal instrumentation * 2. About 1/3 of the instances of Osteoradionecrosis occurs spontaneously 5/21/12

* Theories of pathophysiology
Watson and scarborough : reported 3 factors based on clinical observation. * Exposure to radiotherapy above a critical dose * Local injury * Infection

* Mayer : radiation ,trauma and infection theory. * He suggested that injury provided the opening for invasion of oral
microbial flora in to the underlying irradiated bone.

* Referred osteoradionecrosis as secondary infection after injury to

devitalised bone and even radiation induced osteomyelitis

* Marks : hypoxic-hypocellular hypovascular theory. * Concluded that osteoradionecrosis is not a primary infection of

5/21/12 irradiated bone but a complex metabolic and hemostatic deficiency of tissues that is created by radiation induced cellular injury.

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* Clinical features:

* Pain and evidence of exposed bone (main clinical feature) * Trismus, fetid breath and elevated body temp in the initial

stage * Acute infections usually absent * Exposed bone with a gray to yellowish color is seen in association with intra and extra oral fistulae. * Pathologic fracture may be present * The exposed bone often has a rough surface texture that abrades adjacent soft tissues and causes further discomfort. * The tissue surrounding the exposed bone may be indurated or ulcerated from infection or recurrent tumor (if induration persists after infection has been controlled by irrigation and antibiotics, if needed, or if ulceration is present, biopsy 5/21/12 should be performed). The exposed bone not necessarily be radiation compromised

* Radiographic features:* * Little radiographic changes in the early stages * The characteristic changes seen in osteomyletis of non irradiated

bone, that is formation of sequestra or involucra, occurs late or not at all in irradiated bone because of severely compromised blood supply. * Radiographically Osteoradionecrosis appears as radiolucent modeling with indefinite nonsclerotic borders and occasional areas of radio opacity associated with bony sequestrum. * Often there is an appearance of moth-eaten bone present on these films * CT scan is better than MRI in terms of resolution * Nuclear isotope technetium-99 methylene diphosphate (99m Tc MDP) bone scanning may show areas of bone turnover, but poor resolution limits its diagnostic usefulness where margins of the 5/21/12 lesion are concerned. However initial blood flow assay with 99m

* Culture and sensitivity test *

Culture of the bone involved shows no organisms deeply; the surface organisms being predominantly streptococci, candida species and gram-negative organisms. Staphylococci can be seen if there is a communication with skin. * When irradiated bone becomes involved in infection derived from overlying skin, the organism most commonly found are staphylococcus aureus and streptococous epidermidis.

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* Diagnosis of Osteoradionecrosis.

* History * Clinical features * Histological and radiographic assessment to rule out

recurrent/metastatic disease. (Therefore diagnosis of Osteoradionecrosis is a diagnosis of exclusion

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* Complications of Osteoradionecrosis. * Intractable pain * Drug dependency * Trismus * Nutritional deficiency * Pathological fracture * Oral and cutaneous fistula * Loss of large areas of soft tissue and bone. * These patients also lose time from work and family
and suffer the psychologic stigma of having a nonhealing wound. Osteoradionecrosis can have a tremendous in put in quality of life.

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* Treatment: * Control of frank infection: Penicillin +metronidazole OR clindamycin * * Irrigation of soft tissue margins * Mechanical debridement and smoothening of bone * Saturated zinc peroxide and neomycin pack * Lingual cortical plate drilled to encourage
revascularization. * Ultra sound therapy: promote s neovascularity and neocellularity. * Bone resection.

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* HBO therapy: * 100% oxygen

at 2.4 absolute pressure for 90 min for 5 days a week totaling 30 or more sessions. * oxygen under increased tension enhances neo angiogenisis, fibroblastic proliferation,collagen synthesis, bacteriostatic action and phagocytic killing.

* Indications: * Osteitis and osteomyelitis of the maxilla and

mandible * Osteoradionecrosis * Osteopetrosis of mandible
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* Contra indications: * Pneumothorax * Optic neuritis * COPD * Acute viral infection * Congenital spherocytosis * Uncontrolled , acute seizures * Upper respiratory tract infections * Uncontrolled high fever * History of prior thoracic and ear surgery * Psychiatric problems * Pregnancy
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* Complications: * Eustachian tube dysfunction * Tympanic membrane rupture * Oxygen toxicity * Ear, sinus or tooth pain * Decompression sickness * Pneumothorax * Arterial gas embolism * Middle ear hemorrhage * Deafness * Change in vision * Fire hazard * Nausea, fatigue, claustrophobia * Nitrogen emboli to CNS, lungs or joints * Certain types of hemolytic anemia * Equipment malfunction

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The Marx -University of Miami protocol

[1983]

-For treatment of Osteoradionecrosis.

Stage I 30X (100% O2 for 90 minutes at 2.4 ATA) Examine the exposed bone

No surgery No antibiotics Saline rinsing only

Response
10x (100% O2 for 90 minutes at 2.4 ATA) (Stage I responder)

No response

Cutaneous fistula Pathologic fracture Resorption of inferior border of the mandible

Stage II Surgery (maintain inf erior border of the mandible) 10x (100% O2 for 90 minutes at 2.4 ATA)

Response No response He aling without exposed bone (Stage II responder)

Stage III Excision of non -viable bone Fixation of mandibular segments 10x (100% O2 for 90 minutes at 2.4ATA) Reconstruction after 10 months No further HBO required

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* ROYAL ADELAIDE HOSPITAL, AUSTRALIA, MODIFICATION OF MARX

PROTOCOL

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* Prevention: * Pre radiation dental care: * Extractions, restorations and periodontal teratment10-14 days before radiation. * Custom trays for fluoride application

* Post irradiation dental care: * Dentures not to be used for 1 yr * Fluoride application * Saliva substitute- pilocarpine * Pulpitis- restoration/ endodontic therapy with care * Atraumatic extractions Suggested regimen: * Penicillin V 2g + metronidazole 500mg 1hr before
surgery.

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