OSTEOMYELITIS

Contents

• Definition• Predisposing factors• Classification• Suppurative osteomyelitis• Non suppurative

Definition

• Inflammation of the bone forming elements with tendency to progression.

Begins in

medullary

cavity

Extends +

spreads to

cortical bone

Eventually reaches the periostium

Invasion of bacteria into cancellous bone

Inflammation + edema in marrow spaces

Compression of blood vessels

Severe compromise of blood supply

• Inadequate blood supply is a main factor as the involved area becomes ischemic and bone becomes necrotic.

• Bacteria can then proliferate, because normal blood-borne defenses do not reach the tissue, and the osteomyelitis spreads until it is stopped by medical and surgical therapy.

Mandible

Less perfusion from inferior alveolar artery only

Overlying cortical bone is dense and prevents penetration of

periosteal blood vesselsMandible affected more than maxilla

Predisposing factors

Osteomyelitis

Radiation exposure

Fracture of mandible

Impaired blood flow

Impaired immunity

Poor nutrition

Odontogenic infections

Microbiology

• Similar to those of odontogenic infections–Viridan streptococci– Strict anaerobes:• Bacteroides• Prevotella• Fusobacterium• Peptostreptococci species

Classification • Created by Hudson and simple to use• 1. Acute osteomyelitis (present for 1 month)– Contiguous focus – Progressive– Hematogenous (present for over 1 month)

• 2. Chronic osteomyelitis– Recurrent multifocal – Garré’s – Suppurative or nonsuppurative– Sclerosing

Clinical features of osteomyelitis of facial region

• Pain• Swelling and erythema of overlying tissues• Adenopathy• Fever• Paresthesia of the inferior alveolar nerve• Trismus• Malaise• Fistulas

Classification

• Roughly divided into suppurative and non suppurative based on clinical features.

• Suppurative1. Acute2. Subacute and chronic

• Infantile osteomyelitis• Non suppurative

1. Chronic diffuse sclerosing2. Garre’s sclerosing

SUPPURATIVE OSTEOMYELITIS

• The dominant form• Characterised by pus formation and necrosis of

bone• Has two distinct forms;a) Acute ; infection which includes systemic effectsb) Chronic; induce minimal systemic effects• Primary chronic; no acute episode• Secondary chronic; involves prolonged

inflammatory process

Pathogenesis

• Inflammation triggered by bacterial invasion into marrow induces a compromised microcirculation and increased pressure in the intramedullary site.

• Leads to vascular collaspe, venous stasis and ischaemia and eventually bone necrosis.

• Further multiplication of microorganisms and the resultant inflammation induce further necrosis of the surrounding bonny tissue and resulting in extensive spread of infection.

Clinical features and stages

Acute (1-2 weeks)• Local symptoms– Swelling is minimal and fistulae are absent– Deep and intense pain– Regional lymph nodes become enlarged and

tender.

– Later purulent exudates erode the cortical bone and periosteum resulting into facial and submandibular cellulitis.– If masticatory muscles are affected, trismus

may occur.–A throbbing pain in the jaw, severe

tenderness and a feeling of extrusion of teeth.

–Vincent’s symptom as the infection affects the inferior alveolar nerve.– Subsequently pus discharge from gingival

sulcus.–Multiple mucosal fistulae become apparent.– There is little or no radiographic changes in

this stage.

• Systemic symptoms:– High intermittent fever ( 38-40C )– Chills– Malaise– Headache– Decreased appetite– With spread of infection systemic toxic symptoms

become more severe and sepsis may occur

• Infection is localized only in the intramedullary site:–Adequate antibiotic treatment at this stage

may prevent further progression

Subacute and Chronic stage

• If the disease is neglected or does not respond to treatment

• Some cases primarily develop a chronic form without an acute episode

• Symptoms disappear or become minimal

• Locally:–Affected teeth are mobile and tender to

percusion – Swelling becomes localised–An involucrum forms– In some extreme cases pathologic fracture

occurs due to significant bone loss from sequestration

• Systemically:– Temperature falls to the normal range

Diagnosis

• Diagnosis of acute osteomyelitis is based on:–History–Clinical findings– Laboratory workup - Gram stain, culture,

sensitivity, and histopathologic evaluations.

• For chronic osteomyelitis, bony destruction can be confirmed with plain radiographs.

Imaging • Xrays - OPG–Radiographic changes are generally detected

after losing 30-50% of bony calcified constituents–Changes are detected 1-3 weeks after onset

of acute form

–Once enough bone destruction has set in:• Increased radiolucency, uniform pattern

or patch with moth-eaten appearance• There may also be areas of radiopacity

within the radiolucency which represent islands of bone which have not been resorbed (sequestra).• There may be an area of increased

radiodensity surrounding the radiolucency as a result of inflammatory reaction

• CT–Particularly useful in visualizing the actual

extent of the lesion• MRI–Bony changes are detectable earlier

• Radionuclide scan–More sensitive than others–Gallium scan images depicts lesions since

they tend to accumulate at inflammatory sites

Management

• Diagnose correctly.• Evaluate, define and manage the

immunocompromised state of the patient first for best response to therapy.

• Antibiotics, surgery and supportive care

–Antibiotic Therapy• Penicillins• Clindamycin•Metronidazole

• Acute osteomyelitis– The course of antibiotic should be

continued until clinical signs have disappeared completely.

• Chronic osteomyelitis –Adminstration is recommended after

surgery until evidence of wound healing is seen.

Surgery

Improves blood supply in the involved area -> allowing

adequate penetration of antibiotics

Maximizes the host defense mechanisms and self healing ability

Sequestrectomy• Involves removing infected and avascular

pieces of bone—generally the cortical plates in the infected area.

Saucerization• Involves the removal of the adjacent bony

cortices and open packing to permit healing by secondary intention after the infected bone has been removed.

• Decortication – Involves removal of the dense, often

chronically infected and poorly vascularized bony cortex and placement of the vascular periosteum adjacent to the medullary bone to allow increased blood flow and healing in the affected area.

• The key element in the above procedures is determined clinically by cutting back to good bleeding bone.

• Clinical judgment is crucial in these steps but can be aided by preoperative imaging that shows the bony extent of the pathology.

• It is often necessary to remove teeth adjacent to an area of osteomyelitis.

• In removing adjacent teeth and bone the clinician must be aware that these surgical procedures may weaken the jaw bone and make it susceptible to pathologic fracture

• Supporting the weakened area with a fixation device (external fixator or reconstruction type plate) and/or placing the patient in maxillomandibular fixation is frequently used to prevent pathologic fracture.

• Hyperbaric oxygen (HBO) treatment has also been advocated for the treatment of refractory osteomyelitis.

• This treatment method works by increasing tissue oxygenation levels that would help fight off any anaerobic bacteria present in these wounds.

• The widespread use of HBO treatment of osteomyelitis still remains controversial.

• Resection of the jaw bone has traditionally been reserved as a last-ditch effort, generally after smaller debridements have been performed or previous therapy has been unsuccessful or to remove areas involved with pathologic fracture.

• This resection is generally performed via an extraoral route, and reconstruction can be either immediate or delayed based on the surgeon’s preference.

• We believe that early resection and reconstruction shorten the course of treatment.

• Indicated once the patient develops paresthesia in mandibular osteomyelitis.

• At this point preservation of the mandible is highly unlikely and one should attempt to shorten the course of the disease and treatment.

Supportive care

• Patients should be hospitalized for any aggressive surgery.

• Provided with intravenous antibiotic therapy and managed for correct fluid balance and nutrition.

• As mentioned previously, the patient is likely to have an underlying compromise of their host defenses.

Infantile osteomyelitis

• Occur few days after birth• Commonly involves the maxillaEtiology• Remains unclear• Thought to involve;Perinatal traumaInfection of the maxillary sinusHematogenous spread

• Disease could spread to involve the eye and brain

• Potential risk for serious optic and cerebral sequelae, facial deformities, serious damage to jaw growth and loss of teeth.

Sign and symptoms

• Swelling of the face and eye lid• Subperiosteal abscesses on the alveolar

mucosa and palate• High fever• Rapid pulse rate• Vomiting delirium and postration

Treatment

• Prompt and aggrassive• Use of intravenous antibiotics and drainage of

abscesses• S. aureus is the most common pathogen

involved

NON SUPPURATIVE OSTEOMYELITIS

CHRONIC DIFFUSE SCLEROSING.• Usually affects mandible• Characterised by;Recurrent pain and swellingNo suppuration or abscess formationparaesthesia

Etiology

• Unclear• Possibly due to;Hyperactive immunologic responsehyperostosis

Radiography;• Intermingled sclerotic and osteolytic lesion

with a solid periosteal reaction• External bone resorptionTreatment• Difficult to eradicate- may persist for years• Asymptomatic; NSAIDs, corticosteroids

Garre’s sclerosing osteomyelitis

• Named after a Swiss surgeon, Dr Carl Garre• Characterized by;Active periosteum proliferationFormation of subperiosteal boneNo purulent exudate

• Believed to result from over inflammatory reaction of the periosteum

• Commonly in children and adults• Usually on the lateral surface of body of

mandible

Etiology

• Periapical abscess• Post extraction infectionClinical features• Localized, unilateral and hard mandibular

swelling with little tenderness• Pain can be episodic• No apparent systemic signs

Radiological findings

• Thickened cortical bone• Onion skin appearance due to new bone

formationTreatment • Elimination of cause

References

• Oral and maxillofacial surgery, L Andersson, KE Kahnberg, MA Pogrel

• Textbook of Oral and Maxillofacial Surgery 3rd ed, NA Malik