Osteon

OSTEOMYELITIS & OSTEORADIONECROSIS

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

bone and periosteum as well. Therefore, osteomyelitis may be defined

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)

HISTORY

*SPINOSA VENTOSA - ARAB PHYSICIANS

*OML OF TIBIA – WILLIUM HEY (1736 – 1819)

*CHRONIC OML - SAMUEL COPPER ( 1787)

* JOHN HOWSHIP - (1803)

- THE NATURAL AND DISEASED STATES OF BONES (1820)

*CHRONIC OML - AUGUSTE NELATON

(1807 – 1873)

* REES (1847) - OML OF MAXILLA IN NEWBORNS

* CARL GARRE (1893) - TIBIA

* WILENSKY (1932)

- OML IN INFANTS

* HOWARD WALTER FLOREY & COWORKERS - (1941) PENICILLIN THERAPY

*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

*II)Physiological types:

1. Normal host

2. Systemic compromise/local compromise

3. Treatment is worse than the disease

*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

*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.

*Hudson’s classification:

*Acute forms of osteomyelitis (suppurative or nonsuppurative)

*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)

*B) Chronic forms of osteomyeliyis

* a) Recurrent multifocal :

* 1) developing skeleton

* 2) escalated osteogenic activity

*

* b) Garre’s :

* 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.

*

Topazian's classification:

Suppurative osteomyelitis Non-suppurative osteomyelitis

Acute suppurative osteomyelitis Diffuse scleroising osteomyelitis

Chronic suppurative osteomyelitis Focal sclerosing osteomyelitis

1) Primary Proliferative perisoteitis

2) Secondary Osteoradionecrosis

Infantile osteomyelitis

*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..

*Disease Mechanism facilitating bone infection

Diabetes : 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: Reduced wound healing and reduction of

immunological response

Cancer: Reduced wound healing and reduction of

immunological response

Osteopetrosis (Albers–Schonberg disease): Reduction of bone vascularization due to enhanced mineralization, replacement of

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

*Etiology*Odontogenic infections :

* pulpal or periodontal tissues

* pericoronitis

* infected socket

* infected cyst and tumor.

*Trauma :

* compound fractures

* surgery- iatrogenic

*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.

*

*Odontogenic infections

*Trauma

*Gingival infections

*Lymph node infections

*Hematogenous origin.

Osteomyelitis of jaws predisposing factors,

etiology JOMS (34) 2006

pathogenesis

* Caries Periapical abscess Osteomyelitis

* Acute

* Necrotic pulp Apical periodontitis

* Chronic

* Trauma Periapical granuloma Periapical cyst

Interrelationship of possibleresults of periapical inflammation

* pathophysiology of bone necrosis secondary to mucormycotic infection in a diabetic patient

Med Oral Patol Oral Cir Bucal 2007;12:E360-4

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

*Microbiology*Primarily - Streptococci (α-hemolytic), Peptostreptococcus,

Fusobacterium and Prevotella.

*S.aureus – 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.

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

*Clinical findings:*Clinical findings:

*4 clinical types:

1. Acute suppurative

2. Secondary chronic

3. Primary chronic

4. Non suppurative

*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,.

Acute pyogenic osteomyelitis(acute

suppurative oml)

*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..

ACUTE SUPPURATIVE OML

Primary chronic osteomyelitis (results from organisms which are less virulent)

1. Insidious onset2. Slight pain3. Slow increase in jaw size4. Gradual development of sequestra.

Secondary chronic osteomyelitis (occurs when treatment did not succed in eliminating acute osteomyelitis)

1. Fistulas2. Induration of soft tissue3. Thick/wooden character 4. Pain and tenderness.

* CHRONIC SUPPURATIVE OML

*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

*

*1) Conventional radiograph

*Radiographic changes described by worth :

*Moth eaten appearance

*Sequestra seperated by zone of radiolucency with new bone involucrum.

*Stippled or granular densification of bone.

*Moth eaten appearance is because of enlargement of medullary spaces and widening of volkman’s 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.

Radio nucleotide imaging*It is useful in determining the presence of reactive bone.

*Radiopharmaceuticals that are absorbed by the bone provide useful 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.

*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

*Positive findings with both the tests usually confirm the infectious nature of the disease.

*Tc- scan positive , Ga –scan negative ,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.

*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.

* The role of adjunctive hyper baric oxygen treatment for non radiation osteomyelitis and patient who are medically compromised with no HBO contraindications.

*

*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.

*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.

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

* Acute suppurative osteomyelitis

* Chronic suppurative osteomyelitis

*Sequestrectomy

*Removal of foreign bodies

*Repeated cultures and improvement of host defenses

*Local antibiotic therapy

*Closed wound irrigation- suction :- Neosporin irrigant 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.

*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

*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.

* Closed wound irrigation and suction

*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.

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.

* Antibiotic impregnated beads:

*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.

*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.

* 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.

* 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

*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

*The buccal falp is trimmed and a medicated ¼ -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.

*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.

*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.

* 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.

*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 be removed

*Reconstruction plate

*Antibiotic therapy.

*Types of osteomyelitis

*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

*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

*Proliferating periosteitis (Garre’s 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.

Garre’s Osteitis

*Treatment :

1) removal of the source of infection,extraction or RCT.

2) antibiotic therapy

3) surgical recountouring

4) follow up

*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

*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 focal areas of radiolucency & radioopacity

Treatment : Antibiotic therapyDecortication ,rescection,reconstruction,HBO therapy

* 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..

*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

*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

*Treatment:

* Irrigation solutions - For 72 hrs.

*¼ th strength Dakin’s solution(2.5% NaOCl 10% NaHCO3)

*9- Aminoacridine

*½ 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

*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.

*Condensing osteitis:

Localized area of bone sclerosis

Associated with apex of the carious tooth

Severe Osteomyelitis Following Immediate Placement of a Dental Implant

INT J ORAL MAXILLOFAC IMPLANTS 2008;23:137–142

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

Osteonecrosis of the mandible associated with bisphosphonatetherapy:

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

the exact mechanism of bisphosphonate mediatedosteoclast inhibition has not been completelyelucidated, it is known that these compounds affectbone remodelling at various levels. The inhibitingfunction 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.

* Bisphosphonate-Associated Osteonecrosis of the Jaws

*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

* Common orofacial findings associated with BON

*Poor wound healing

*• Spontaneous or postsurgical soft-tissue

*breakdown leading to intraoral or extraoral

*bone exposure

*• Bone necrosis

*• Osteomyelitis

*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.

*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

*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

* Maxillary Necrosis: A Sequelae of Fungal* Osteomyelitis

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

* CONTENTS.

*

* Introduction

* Definition

* Classification

* Pathophysiology

* Etiology

* Clinical features

* Radiological feature

* Culture test

* Diagnosis

* Complications

* Treatment* Conservative

* HBO therapy

* Surgical treatment

* Marx protocol for HBO therapy

* Royal Adelaide hospital modification of HBO therapy

* Complications of HBO therapy

* Prevention of Osteoradionecrosis

* Technique for extraction of teeth prior to radiation therapy

* Review of literature

* Conclusion

* Bibliography.

*. 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.

*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 without healing for 3 months in the absence of tumour recurrence.

Sl No.

Year

Defined by

Definition

1. 1970

Meyer ORN is a classic triad of Radiation, Trauma and Infection.

2. 1971

Titterington

Osteomyelitis secondary to radiation.

3. 1983

R. E. Marx

An area of exposed bone > 1 cms in a field of irradiation that had failed to show any evidence of healing for at least 6 months.

4. 1983

Brumer et al

Exposure of bone of the maxilla or mandible within the radiation treatment volume persisting for 3 months or longer.

5. 1986

Morton & Simpson

Loss of soft tissue integrity and exposure of irradiated and damaged bone.

Sl No.

Year

Defined by

Definition

6. 1987

Marx & Johnson

Exposure of non-viable irradiated bone which fails to heal without intervention.

7. 1987

Epstein et al

An ulceration or necrosis of the mucous membrane with exposure of necrotic bone for more than 3 months.

8. 1987

Epstein et al

Resolving chronic or acute necrotic lesion with or without pathologic fracture

9. 1989

Widmark et al

Non healing mucous or cutaneous ulcers with denuded bone lasting for more than 3 months.

10. 1990

Koka et al

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

Sl No.

Year

Defined by

Definition

11. 1992

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

12. 1993

Mirante et al

ORN is loss of viable bone resulting from radiation therapy

13. 1995

Van Merkestyn

ORN is defined as bone and soft tissue necrosis of 6 months duration excluding radiation induced periodontal breakdown.

14. 1997

Lewis clayman

ORN is a non-healing nonspecific lesion of bone in which the bone volume and density cannot be maintained by hypoxic, hypovascular and hypocellular tissues which cannot meet adequately its metabolic demands.

*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.

*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 doesn’t heal with conservative therapy.

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

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

*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.

*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

*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

*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

*Mark’s : hypoxic-hypocellular – hypovascular theory.

*Concluded that osteoradionecrosis is not a primary infection of irradiated bone but a complex metabolic and hemostatic deficiency of tissues that is created by radiation induced cellular injury.

*Microorganisms,contaminats, trauma may or may not be the intiating factor.

*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 should be performed).

* The exposed bone not necessarily be radiation compromised or dead. The soft tissue envelope may be the only structure insulted and if conservatively treated it may heal over the exposed bone areas with out bone debridement. This is usually seen in cases where radiation dose was below 500 μGy.

*Glabrous skin is a reliable sign of at least radiation-induced soft tissue injury and should promote suspicion of underlying bony sequela.

*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 lesion are concerned. However initial blood flow assay with 99m Tc MDP isotope scanning can be of some benefit in assessing regional perfusion of the affected side

*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’.

*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

*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 non-healing wound. Osteoradionecrosis can have a tremendous in put in quality of life.

*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.

*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

* Severe maxillofacial trauma and / or crush injuries.

*Orthognathic surgery (to salvage a failing case of multipiece maxillary osteotomies)

*Necrotizing infections of soft tissues of the head and neck

* Implantological rehabilitation in irradiated oncological patients

* In healing of grafted bone.

*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

* 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

The Marx-University of Miami protocol [1983]

-For treatment of Osteoradionecrosis.

No surgery No antibiotics Saline rinsing only

Response No response

Response No response

Stage I ▪30X (100% O2 for 90 minutes

at 2.4 ATA) ▪Examine the exposed bone

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

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

Healing 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

▪Cutaneous fistula ▪Pathologic fracture ▪Resorption of inferior border of the mandible

*ROYAL ADELAIDE HOSPITAL, AUSTRALIA, MODIFICATION OF MARX PROTOCOL

*Prevention:

* Pre radiation dental care:

* Extractions, restorations and periodontal teratment-

10-14 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.

* 500mg of both 6hrly for 1 week.

*OR

*Clindamycin 600 mg 1hr before and

* 300 mg 8hrly for 1 week.

Osteon

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