Osteomylitis and osteoradionecrosis of...

Osteomyelitis and

osteoradionecrosis of jaw DR PRAJESH DUBEY

DEPARTMENT OF ORAL AND MAXILLOFACIAL SURGERY

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Dr. Prajesh Dubey, Subharti Dental College, SVSU

Content

Osteomyelitis

Incidence

Factors predisposing osteomyelitis

Etiology

Pathogenesis

Microbiology

Classifications

Clinical presentations

Imaging

Treatment

Types of osteomyelitis

Osteoradionecrosis

Etiopathogensis

Clinical features

Treatment

Prevention of

osteoradionecrosis

Postirradiation dental care

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OESTEOMYLITIS

It is defined as an inflammation of the bone marrow with a

tendency to progression.

This is what differentiates it in the jaw from the dentoalveolar

abscess, “dry socket” and “osteitis,” seen in infected fractures.

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It is described as an inflammatory condition of bone that usually

begins as an infection of medullary cavity rapidly involves the

haversian system and quickly extends to periosteum of that area.

Pus that formed in this area thereby compromise its periosteal

blood supply.

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Incidence

Much higher in the mandible due to poorly vascularized cortical

plates and the blood supply primarily from the inferior alveolar

vessels.

Diminished host defenses, both local or systemic like diabetes,

autoimmune states, malignancies, malnutrition, and acquired

immunodeficiency syndrome.

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Factors-

predisposing

osteomyelitis

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ETIOLOGY

Odontogenic infections

Trauma

Infections derived from periostitis following gingival ulceration

Infections derived by hematogenous route—furuncle on face,

wound on the skin, upper respiratory tract infection, middle ear

infection

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Pathogenesis

Osteomyelitis primarily occurs as a result of contiguous spread

of odontogenic infections or as a result of trauma.

Primary hematogenous osteomyelitis generally occurs in the

very youngs.

Whereas in adults, process is initiated by inoculation of bacteria

into the jawbones that can occur with the extraction of teeth,

root canal therapy, or fractures of the maxilla or mandible.

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Inflammation

Hyperemia and increased blood

flow

Additional

leukocytes

Pus is formed

If it is formed in bone marrow it causes decreased blood supply of

the region due to elevated intramedullary pressure

Pus spread via haversian and Volkmann’s canals to medullary

and cortical bones.

Perforation of the cortical

bone

Collection of the pus under the periosteum

Compromised periosteal blood supply

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Microbiology

Earlier said to be S. aureus and S. epidermidis ranged between 80 to 90%;

remaining bacteria are mainly streptococci, pneumococci, typhoid and

acid fast bacilli.

Now osteomyelitis is recognized as a disease caused primarily by

streptococci and oral anaerobic bacteria present in oral cavity.

Clinician must begin antibiotic treatment, includes penicillin and

metronidazole as dual-drug therapy or clindamycin as a single-drug

treatment.

And definitive therapy should be based on the final culture and

sensitivities.

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FINDINGS HELPFUL IN PURE AEROBIC/MIXED

AEROBIC ANAEROBIC INFECTION

Foul smelling exudate

Slouging necrotic tissue

Gas & black discharge

Gram stain revealing multiple organism of diff morphological characters

Presence of sequestra

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Classification

BASED UPON DURATION OF 1 MONTH

-ACUTE

A) Contiguous focus B). Progressive

c). Hematogenous

-SUB ACUTE

-CHRONIC

A) Recurrent multifocal

B) Garré’s

C) Suppurative or nonsuppurative

D) Sclerosing

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Waldvogel classification system for

osteomyelitis:

Hematogenous osteomyelitis

Osteomyelitis secondary to a contiguous focal infection.

Osteomyelitis with or without associated peripheral vascular

disease.

Chronic osteomyelitis.

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ON THE BASIS OF PRESENCE OF PUS

SUPPURATIVE

• ACUTE SUPPURATIVE

• CHRONIC SUPPURATIVE

• (PRIMARY- No acute phase

preceding)

• (SECONDARY- follows acute

phase)

• INFANTILE OSTEOMYELITIS

• NON SUPPURATIVE

• DIFFUSE SCLEROSING

• FOCAL SCLEROSING

(CONDENSING OSTEITIS)

• PROLIFERATIVE PERIOSTITIS

(GARRE’S SCLEROSING OM)

• OSTEORADIONECROSIS

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Classification based on clinical picture

and radiology

Hjorting-Hansen E, Decortication in treatment of osteomyelitis of the mandible. Oral Surg Oral Med

Oral Pathol 1970 May;29(5):641-55

I. Acute/subacute osteomyelitis

II. Secondary chronic osteomyelitis

III. Primary chronic osteomyelitis

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Classification based on clinical picture,

radiology, etiology, and pathophysiology

Acute osteomyelitis

1. Associated with Hematogenous spread

2. Associated with intrinsic bone pathology or peripheral vascular disease

3. Associated with odontogenic and nonodontogenic local processes

Marx RE Chronic Osteomyelitis of the Jaws Oral and Maxillofacial Surgery Clinics of North America, Vol 3, No 2,

May 91, 367-81

Mercuri LG Acute Osteomyelitis of the Jaws Oral and Maxillofacial Surgery Clinics of North America, Vol 3, No 2, May 91, 355-65

Chronic osteomyelitis 1. Chronic recurrent multifocal osteomyelitis of children

2. Garrè's osteomyelitis

3. Chronic suppurative osteomyelitis – Foreign body related – Systemic disease related

– Related to persistent or resistant organisms

4. True chronic difuse sclerosing osteomyelitis

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CIERNY-MADER STAGING SYSTEM (1985)

Classification and staging for osteomyelitis

1ANATOMIC TYPE: STAGING SYSTEM:

Stage 1: Medullary osteomyelitis –no cortical

involvement , usually hematogenous

Stage2: Superficial osteomyelitis-less than 2cm

bony defect without cancellous bone.

Stage3: Localized osteomyelitis –less than 2cm

bony defect, without involving both cortices.

Stage4: Diffuse osteomyelitis-Larger than 2 cm

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2.PHYSIOLOGIC TYPE:

A. Host: Normal host

B. Host

Systemic compromise

Local compromise.

Systemic and local compromise.

C. Host: Treatment worse than disease.

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Clinical Presentation

4 types can be observed clinically-

1) Acute suppurative osteomyelitis- Deep pain, high fever,

paresthesia and anesthesia of the lower lip, usually deep carious

associated teeth,

Swelling is minimal, tooth are not loose and fistulas are usually

not present.

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2) Sub acute suppurative- After 10 to 14

days of acute form, pus extends through

haversian canals to accumulate under

the periosteum.

Pain, fever, malaise are present, teeth

begins to loose and tender, pus exudes

around gingival sulcus, fistula formation

and fetid odor.

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3) Secondary chronic ( begins as acute phase)- clinical findings are fistulas, induration of soft tissue and thickened or ‘wooden’ character to the affected area.

4) Primary chronic- (Not preceded by acute) slight pain, slow increase in jaw size, and gradual development of sequestra, often without fistulas.

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Maxillofacial imaging for osteomyelitis

Radiographic presentation lag behind the clinical presentation since cortical involvement is

required for any change to be evident. Therefore, it takes several weeks before bony

changes appear.

Orthopanoramic view

CBCT

CT scans

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• Worth’s Criteria (1969)

• ‘Moth-eaten’ appearance (enlargement of medullary spaces and widening of Volkmann’s

canals)

• Islands that is ‘seqeustrum’ evidence of trabecular pattern and marrow spaces

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MRI can help in early diagnosis by loss of the marrow appears

before cortical erosion or sequestrum of the bone.

The technetium 99 with the addition of gallium 67 or indium

111 as contrast agents, differentiate areas of infection from

trauma or postsurgical healing as these agents specifically

bind to white blood cells.

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Conventional radiograph

Positive Negative (suspected)

Technetium bone scan

Positive Negative

Ga 67 or WBC scan

Positive Negative

Drainable abscess- MRI, Sequestrum- CT

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Treatment

Usually medical and surgical interventions required.

Overall treatment plan includes-

Evaluation and correction of host defense deficiencies

Gram staining, culture and sensitivity

Administration of antibiotics

Removal of loose teeth and sequestra,

Administration of culture guided antibiotics

Sequestrectomy, saucerization, debridement, direct placement of

antibiotic, HBO therapy, resection of infected bone, reconstruction.

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Inhitial management is administration of high dose intravenous antibiotic

therapy.

Identify and correct host compromise factors, and treat the cause.

For hospitalized pt-

Aqueous penicillin, 2 million U IV 4 hourly, plus metronidazole, 500mg 6 hourly, when improved for 48 to 72 hours- switch to- penicillin V, 500mg PO 6 hourly, plus metronidazole 500mg PO 6 hourly for an additional 4-6 weeks.

For outpatients- Penicillin V 2g, plus metronidazole 400mg 8hourly PO, for 2-4 weeks.

Clindamycin should be prescribed if pt is allergic to penicillin.

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Whenever possible, specimens should be obtained for gram

staining, aerobic and anaerobic cultures, and antibiotic

sensitivity testing.

A foul- smelling, dark exudate- suggest anaerobic osteomyelitis.

A thick creamy pus from a localized abscess indicates a

staphylococcal infection.

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Local antibiotic therapy

Closed wound irrigation- suction-

Irrigation without surgical debridement to the point of bleeding bone is unlikely to be effective, prolongs the process, and delays definitive treatment.

Various agents containing antibiotics, proteolytic enzymes, wetting agents may be used.

Antibiotics may be placed in direct contact with the bone manually or with an implantable pump.

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Antibiotic-impregnated Beads- They can be used to

deliver high concentrations of antibiotics into the

wound bed.

Antibiotic leaches from the beads, and produce high

local concentrations and low systemic

concentrations.

Tobramycin or gentamycin is generally used as AIB.

Beads and drain are left in place for 10 to 14 days.

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Surgical management

Necessary with medical therapy.

Surgical management is removal of loose teeth, bone fragments, I&D

of fluctuant areas and if necessary sequestrectomy, saucerization,

decortication, or resection and then reconstruction.

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Sequestrectomy

Sequestra are generally seen after 2 weeks of onset of infection.

Once fully formed, sequestra persists for several months before they

are resorbed.

Once the sequestra has formed completely, it can be removed with

the minimum of the surgical trauma.

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Saucerization

Saucerization is “Unroofing” of the bone to expose

medullary cavities for thorough debridement.

The margins of necrotic bone overlying the focus of

osteomylities are excised allowing visualization of sequestra

and exision of affected bone.

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Steps- 1) Buccomucoperioseteal flap is reflected.

2) loose teeth and bone segment are removed.

3) lateral cortex of the mandible is reduced using

burs.

4) All granulation tissue and loose bone fragments

are removed from the bone bed using curettes.

5) buccal flap is trimmed and a medicated ¼ or ½

inch pack is inserted for hemostasis and to

maintain the flap in a retracted position until initial

healing occurs.

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Decortication

First described for jaw osteomyelitis in 1917 by Mowlem.

It refers to the removal of chronically infected cortical bone.

Lateral and inferior cortex is removed 1 to 2 cm beyond the

affected area thus providing access to the medullary cavity.

Usually granulation tissue and pus exists within the medullary cavity

that antibiotics cannot penetrates.

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Steps- 1) Creation of a buccal flap by

a crestal incision extending along the

neck of teeth.

2) Reflection of the mucoperiosteal

flap to inferior border.

3) Removal of the teeth of the

involved area.

4) Removal of the lateral cortical

plate and the inferior border with

chisels.

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Resection and reconstruction-

Used in cases of-

Pathological fracture

Persistent infection after decortications

Marked closure of both cortical plates.

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Types of osteomyelities

1) Osteomyelitis associated with fractures-

Develops when failure to use effective methods of reduction,

fixation and immobilization, as debris and microorganisms gain

access to the fracture site.

Overzealous use of intraosseous wiring, bone plates, screws that

devascularize bone segment.

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2)- Infantile Osteomyelitis

Occurs most often a few weeks after birth and usually affects

maxilla.

It believed to occur by hematogenous route or from perinatal

trauma of the oral mucosa.

Have risk of involvement of eye, extension to dural sinuses, and

the potential for facial deformities and loss of teeth.

Clinically patient has cellulitis centered around the orbit.

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3)- Proliferative periostitis (garre’s

sclerosing osteomyelitis)

Resembles infectious osteomyelitis and affects mainly children.

First described by Carl Garre in 1893.

Characterized clinically by-

Localized, hard, non tender, unilateral bony swelling of the lateral

and inferior aspects of the mandible.

Skin appears normal,

Associated with carious first molar with a history of past toothache.

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Radiographically- laminated or Onion skin appearance.

It is considered a response to a low grade infection or

irritation that influence the potentially active periosteum of

young individual to lay down new bone.

D/D- Ewing’s Sarcoma, Osteosarcoma, cortical hyperostosis.

T/t- removal of identifiable source of inflammation.

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CHRONIC SCLEROSING OSTEOMYELITIS

1)- Chronic diffuse sclerosis osteomyelitis-

Inflammatory, non-suppurative, painful disease with a protracted

course.

It occurs only in the mandible and affects the both the basal

bone and the alveolar process, involve the entire height of the

mandible.

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Bone is often mildly expanded and tender.

Episodes of recurrent swelling and pain occur.

Mainly seen in adult in their 3rd decade.

2/3rd times in females.

Radiographically, a diffuse intramedullary sclerosing with poorly

defined margins defect can be seen.

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2)- Florid osseous dysplasia-

Multiple, exuberant, lobulated densely opaque masses, restricted to the

alveolar process in either or both jaw.

Most often in black women.

Focal sclerosing osteomyelitis- Localized area of bone sclerosing

associated with the apex of a carious tooth and peripheral periodontitis.

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Actinomycotic osteomyelitis-

Chronic, slowly progressive infection with both granulomatous and

suppurative features,

Affects soft tissue only and occasionally, bone.

It forms external sinuses that discharge distinctive sulfur granules

and spreads unimpeded by anatomical structures.

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Actinomyecitis are not fungi but rather gram positive,

microaerophilic, non spore forming, non acid-fast bacteria.

Firm, soft tissue masses are present on the skin, they have

purplish, dark red, oily areas with occasional small zone of

fluctuance.

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Fungal Osteomyelitis

Very rare and generally presents in an indolent fashion.

Fungal infections are opportunistic infections and devastating to

patients if it is invasive in nature.

These frequently enter the body due to a decrease in host defense

or through an invasive gateway, such as a dental extraction.

Candidal infection is more often encountered when compared to

other fungal infection, i.e. mucormycosis, aspergillosis etc.

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The clinical presentations of fungal osteomyelitis are similar to the

bacterial osteomyelitis (e.g. Exposed bone with varying pain).

Involvement of maxillary sinus with a complaint of sinusitis in maxillary

fungal osteomyelitis has been seen more.

The fungus invades the arteries leading to thrombosis that

subsequently causes necrosis of hard and soft tissues. Mucormycosis

is frequent in diabetic patients because a favorable environment is

created due to an excess of ketone bodies in diabetic patients.

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It is extremely rare to find candidal osteomyelitis in the

maxilla and because of nonspecific symptoms,

diagnosis is very challenging.

Aspergillosis is the second most common fungal

infection after candida. It is usually invasive in nature

when involving maxillary sinus though noninvasive forms

have also been reported and does not cause bone

destruction when compared to mucormycosis.

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OSTEORADIONECROSIS

Osteoradionecrosis is a radiation

induced non –healing, hypoxic

wound rather than true

osteomyelitis of irradiated bone.

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Infection is usually initiated by injury to irradiaated tissue

According to Marx it is a chronic, nonhealing wound caused

by hypocellularity , hypovascularity and hypoxia of the

irradiated tissue.

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Etiopathogenesis of osteoradionecrsis

Radiation

Trauma

Infection

Effect of irradiation depends upon:

Quality and quality of radiation

Size of the portals used

Location and extent of the lesion

Condition of teeth and peridontium

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Mandible is more commonly affected than maxilla.

Radiation often has serious effects: -Mucositis

-Atrophic mucosa

-Xerostomia

-Radiation caries etc.

Breakdown occur because the tissue cannot maintain normal cellular

turnover and collagen synthesis such tissue is susceptible to spontaneous

breakdown, breakdown from other trauma especially tooth extraction.

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Clinical features of osteoradionecrosis

Pain and evidence of exposed bone (grey to yellow color)

Trismus

Elevated temperature

Pathological fractures

Tissue surrounding the exposed bone may be indurated and ulcerated.

Nutritional deficiencies

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Treatment:

1) Hospitalized to allow parental antibiotic and fluids.

2) Penicillin plus metronidazole or clindamycin alone is recommended.

3) Gentle, pulsating irrigation of the soft tissue margin is useful in

removing debris and reducing inflammation. But high pressure

irrigation should be avoided because debris might be pushed

deeply into the tissue.

4) Supportive treatment with fluids and a liquid or semiliquid diet, high

in protein and vitamin is desirable.

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6)- Exposed bone then is mechanically debrided and smoothened

with large round or barrel shaped burs and covered with a pack

saturated with zinc peroxide and neomycin.

7) Irrigation and packing repeated weekly until sequestration

occurs or the bone is penetrated by granulation tissue.

Pentoxyfylline and tocopherol (Vit E) are the usually used medical

treatment for ORN.

Pentoxyfylline- 400mg TDS, Improves blood flow by decreasing its

viscosity.

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Ultrasound therapy:

Promotes neo-vascularity and neo-cellularity of ischemic tissue.

Bone resection:

Patient who are not candidates for extensive treatment because

of their medical condition may achieve pain relief by resection

of the segment of the involved bone.

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HYPERBARIC OXYGEN THERAPY:

The therapeutic principle of HBOT lies in its ability to drastically increase in

the oxygen transport capacity of the blood.

At normal atmospheric pressure, oxygen transport is limited by the oxygen

binding capacity of hemoglobin and very little oxygen is transported

by blood plasma.

Oxygen transport by plasma, however, is significantly increased using

HBOT because of the higher solubility of oxygen as pressure increases.

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HBO therapy causes an increase in the

arterial and venous oxygen tension; the

additional oxygen is carried in physical

solution in the plasma.

HBO therapy consists of breathing 100%

oxygen through a face mask or a large

chamber at 2.4 absolut atmospheres

pressure for 90 minute sessions for as many

as 5 days a week, totaling 30 or more

sessions often fallowed by another 10 more

sessions.

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Oxygen under increased tension enhances healing by a direct

bacteriostatic effect on micro-organisms and by enhancing

phagocytic activity.

Neoangiogenesis, fibroblastic changes and collagen synthesis

also occurs.

Osteomyelitis and osteoradionecrosis patients may be

candidates for HBO treatment in conjunction with antibiotic and

surgical care.

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Marx-University of Miami Protocol Stage-I

- 30 X (100% O2for 90 mins at 2.4 ATA)

- Examine exposed bone

Responder (Formation of healthy granulation tissue)

- 10 X (100% O2for 90 mins at 2.4 ATA)

Nonresponders

Stage- II

Decortication sequestretomy, saucirization etc till bleeding margins

- 10 X (100% O2for 90 mins at 2.4 ATA)

Responder

Healing without exposed bone

Nonresponders

Stage III

Excision of the nonvital bone,

Fixation of the mandibular segments,

10 X (100% O2for 90 mins at 2.4 ATA)

Reconstruction after 3 months

No further HBO required

Cutaneous fistula,

Pathological fracture

Resorption of inferior border of mandible

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PREVENTION OF OSTEORADIONECROSIS:

Preirradiation dental care:

Preventive dental measures are effective in reducing the risk of

osteoradionecrosis.

The radiotherapist should seek dental consultation sufficiently

early before initiation of radiation therapy to allow achievement

of optimal oral health.

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1. All non-restorable teeth in the direct beam of radiation and

teeth with significant periodontal disease should be extracted

10 to 14 days before radiation therapy begins.

2. Judicious alveoplasty should performed to permit a liener

closure of the mucoperiosteum.

3. All remaining teeth should be restored and periodontal

therapy be completed within 2 weeks interval.

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Postirradiation dental care:

Dentures should not be used in the irradiated arch for 1 year after

radiotherapy .

A saliva substitute may be used to lubricate the mouth.

(Pilocarpine).

If postirradiated pulpitis develops endodontic treatment should be

provided.

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Necessary extraction should be limited to one or two teeth per

appointment. Removal of teeth should be performed as atraumatic

as possible. No attempt should be made to raise mucoperiosteal flap

or linear closure.

A plain local anesthecis should be used.

A suggested regimen is 2 grm penicillin V plus 500mg metronidazole

orally 1 hour before surgery and 500mg of both drugs given four

times a day for 1 week after extraction.

Alternatively 600mg of clindamycin 1 hour before surgery and 300mg

three times a day for a week is recommended.

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Thankyou

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Classification of osteomyelitis:

1. Acute form of osteomyelitis ( suppurative or nonsuppurative)

A. Contignuous focus

I. 1.Trauma

II. 2.Surgery

III. 3.Odontogenic infection

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B) Progressive

I. 1.Burns

II. 2.Sinusitis

III. 3.Vascular insufficiency

C) Hematogenous (metastatic)

i. Developing skeleton (children)

ii. Developing dentition (children)

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2) Chronic forms of osteomyelitis

A) Recurrent multifocal

i. Developing skeleton (children)

ii. Escalated osteogenic activity (

C). Suppurative nonsuppurative

i. Inadequately treated forms

ii. Systemically compromised forms.

iii. Reractory forms (chronc refractory osteomyelitis (CROM))

D). Sclerosing:

i. Diffuse-

a) Fastidious microorganisms

b) Compromised host and pathogen interface.

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ii) Focal

a predominantly odontogenic

B. Chronic localized injury.

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APPLIED SURGICAL ANATOMY

The bone has essentially three structures, a cortical bone, a cancellous

bone and the periosteum. The cortical bone is present outside and is

covered by the periosteum, while the cancellous bone lies within the

cortical bone

Figs 18.1A to D: Haversian system of the bone

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