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MANAGEMENT OF MANAGEMENT OF OSTEOMYELITIS OF JAWOSTEOMYELITIS OF JAW

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DEFINITIONDEFINITION

The word “osteomyelitis” originates from the

Ancient Greek words osteon (bone) and

muelinos (marrow) and means infection of

medullary portion of the bone.

Osteomyelitis is defined as an inflammationof the bone marrow with a tendency to progression. (Peterson’s)

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CLASSIFICATIONCLASSIFICATION

BY HUDSON JW (J Oral Maxillofac Surg 1993 Dec;51(12):1294-301)

1. Acute osteomyelitis a. Contiguous focus b. Progressive c. Hematogenous 2. Chronic osteomyelitis a. Recurrent multifocal b. Garre's c. Suppurative or non-suppurative d. Sclerosing

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CLASSIFICATION BASED ON CLINICAL PICTURE AND RADIOLOGY (Osteomyelitis of the jaws. J Can Dent Assoc 1995 May;61(5):441-2,445-8 ) I. Suppurative osteomyelitis 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis II. Nonsuppurative osteomyelitis 1. Chronic focal sclerosing osteomyelitis 2. Chronic diffuse sclerosing osteomyelitis 3. Garrè's chronic sclerosing osteomyelitis (proliferative osteomyelitis) III. Osteoradionecrosis

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BY LEW & WALDVOGELBY LEW & WALDVOGEL

1.1. SuppurativeSuppurative

2.2. Non suppurativeNon suppurative

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MODIFEID BY TOPAZIANMODIFEID BY TOPAZIAN1. Suppurative Osteomyelitis1. Suppurative Osteomyelitis - Acute Suppurative osteomyelitis- Acute Suppurative osteomyelitis - Chronic Suppurative osteomyelitis- Chronic Suppurative osteomyelitis a. Primarya. Primary b. Secondaryb. Secondary - Infantile osteomyelitis- Infantile osteomyelitis2. Nonsuppurative Osteomyelitis2. Nonsuppurative Osteomyelitis - Chronic Sclerosing osteomyelitis- Chronic Sclerosing osteomyelitis a. Focala. Focal b. Diffuseb. Diffuse - Garre’s sclerosing osteomyelitis- Garre’s sclerosing osteomyelitis - Actinomycotic osteomyelitis- Actinomycotic osteomyelitis - Radiation osteomyelitis- Radiation osteomyelitis

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The Zurich Classification System

1. Acute Osteomyelitis (AO)

2. Secondary Chronic Osteomyelitis (SCO)

3. Primary Chronic Osteomyelitis (PCO)

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Osteomyelitis is divided into Acute or

Chronic forms based on the presence of the disease for a 1-month duration.

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PREDISPOSING FACTORSPREDISPOSING FACTORS

1. Local and systemic factors altering the vascularity altering the vascularity of boneof bone

- radiation- radiation - osteoporosis- osteoporosis - osteopetrosis- osteopetrosis - bone malignancy- bone malignancy - paget’s disease- paget’s disease - Smoking - Diabetes mellitus - Bisphosphonate induced osteochemonecrosis

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2. Systemic factors altering host defenses2. Systemic factors altering host defenses - - Diabetes mellitus - Autoimmune disorders - AIDS - Agranulocytosis - Anemia (especially sickle cell) - Leukemia - Malnutrition - Chemotherapy - Corticosteroid and other immunosuppressive therapy - Alcohol and tobacco - Drug abuse

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Mechanisms of systemic diseases/conditions Mechanisms of systemic diseases/conditions predisposing to osteomyelitispredisposing to osteomyelitis (Adapted from Marx 1991)(Adapted from Marx 1991)

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 anemiaDeficient leukocyte function and associated anemia

Malnutrition Reduced wound healing and reduction of immunological responseReduced wound healing and reduction of immunological response

Cancer Reduced wound healing and reduction of immunological responseReduced wound healing and reduction of immunological response

Osteopetrosis Reduction of bone vascularization due to enhanced mineralization Reduction of bone vascularization due to enhanced mineralization replacement of hematopoietic marrow causing anemia and replacement of hematopoietic marrow causing anemia and leukopenialeukopenia

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Severe anemia (particularly sickle-cell anemia)

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

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

Immuno-suppression (steroids, cytostatic drugs)

Impaired immune response

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ETIOLOGY

1) Odontogenic infection1) Odontogenic infection - Periodontal- Periodontal - Periapical- Periapical - Pericoronal- Pericoronal2) Infection from infected dental cyst3) Compound fracture of Jaw. 4) Traumatic injury5) Middle ear infection & upper respiratory tract infection

through haematogenous route. 6) Furuncle of chin by lymphtic route 7) Peritonsillar abscess

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PATHOGENESISPATHOGENESIS Osteomyelitis primarily occurs

as a result of contiguous spread of odontogenic infections or as a result of trauma.

Primary hematogenous

osteomyelitis is rare in the maxillofacial region, generally occurring in the very young.

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1) Virulent Organasim get entry winto medullary cavity via many routes.

2) Localization of infection (Most infection are localized by a pyogenic membrane & soft tissue abscess wall).

3) Disorganization of pyogenic membrane by micro organism & by chronic movement of unreduced fracture of Jaw.

4) Due to chronic movement of unreduced fracture or disorganization of pyogenic membrane there will be ischemia & this will introducing the bacteria & microbes deep into under lying cavity.

5) Accumulation of Pus & there will be increased pressure in Medullary cavity.

6) Pus travel through haversion & volkaman's canal & accumulation beneath the periosteum & elevating it from cortex & there by reducing the blood supply.

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7) Reduced blood supply causes necrosis of bone.

8) Then pus penetrate the periosteum & mucosal & cutaneous fistulae develop & thereby discharging the purulent pus.

9) Small section of necrotic bone may get completely lysed while large get localized & get separated from the shell of new bone by bed of grannulation tissue. The dead bone is surrounded by the new viable bone this is called involucrum.

10) Involucrum contain one or more holes on the surface pus find its way from these orifices.

11) Beside all this microganism precipitate the thrombi formation these thrombi provided isolating barrier from the immune response & further proliferation of microbes :- Thrombi can cause systemic spread of infection

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CLINICAL PRESENTATION

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SIGNS & SYMPTOMS

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

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- - The The painpain in osteomyelitis is often described as a deep and in osteomyelitis is often described as a deep and boring pain, which is often out of proportion to the clinical boring pain, which is often out of proportion to the clinical picturepicture

- Fever often accompanies acute osteomyelitis, whereas it is relatively rare in chronic osteomyelitis.

- Paresthesia of the inferior alveolar nerve is a classic sign of a pressure on the inferior alveolar nerve from the inflammatory process within the medullary bone of the mandible.

- Trismus may be present if there is inflammatory response in the muscles of mastication of the maxillofacial region.

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GOALS OF MANAGEMENT

1) Attenuate and eradicate proliferating

pathological organisms.

2) Promote healing.

3) Reestablish vascular permeability

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TREATMENT GUIDELINES

- Disrupt infectious foci - Debride any foreign bodies, necrotic tissues or sequestra. - Culture and identify specific pathogens for definitive antibiotic treatment - Drain and irrigate the region - Consider adjunctive treatment to enhance microvascular reperfusion

1 Trephination 2 Decortication 3 Vascular flaps 4 Hyperbaric oxygen therapy

- Reconstruction

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SUCCESSFUL TREATMENT IS BASED ON FOLLOWING FUNDAMENTAL PRINCIPLES

Early diagnosis

Bacterial culture and sensitivity testing

Adequate, appropriate and prompt antibiotic therapy.

Adequate pain control

Proper surgical intervention

Reconstruction

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LAB INVESTIGATIONS

- Hemogram- Hemogram

- Pus Culture & Antibiotic sensitivity- Pus Culture & Antibiotic sensitivity

- - In the acute phase of osteomyelitis it is common to see a leukocytosis with left shift.

- E.S.R. & C reactive protein may be seen but they are non specific

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IMAGING - - The orthopanoramic view is indispensable in the

initial evaluation of osteomyelitis.

- One must bear in mind that radiographic images lag behind the clinical presentation since cortical involvement is required for any change to be evident.

- However, one can often see the appearance of “moth-eaten” bone or sequestrum of bone, which is the classic appearance of osteomyelitis.

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- The CT scan can give very detailed images as to early cortical erosion of bone in ostemyelitis.

- CT scanning, like plain films, requires 30 to 50% demineralization of bone before changes can be seen, thus presenting an essential delay in diagnosis of osteomyelitis.

- MRI can assist in the early diagnosis of osteomyelitis by loss of the marrow signal before cortical erosion or sequestrum of the bone appears

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A 63-year-old woman 2.5 weeks after extraction of carious left lower molar with new onset of left mandibular swelling.

Panoramic view does not provide any clue to the presence of osteomyelitis.

The axial high-resolution bone-window CT image displays slight thinning, demineralization and endosteal resorption of lingual cortical plate.

ACUTE OSTEOMYELITIS

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Three months later, the patient presents with sudden onset of pain and marked malocclusion. The panoramic view discloses an irregular osteolytic area, a fracture traversing the remaining basilar bone and suspicion of multiple sequester with some degree of bone radiopacity.

The presence of two buccal sequesters, partial cortical plate resorption, irregular calcified periosteal apposition and cancellous bone osteolysis and distal sclerosis is shown by the axial high-resolution bone-window CT image.

CHRONIC OSTEOMYELITIS

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- Nuclear medicine has evolved to aid in the diagnosis of osteomyelitis.

- The technetium 99 bone scan is very sensitive in highlighting areas of increased bone turnover; however, the scan is not very specific to areas of infection.

- With the addition of gallium 67 or indium 111 as contrast agents, one can differentiate areas of infection from trauma or postsurgical healing as these agents specifically bind to white blood cells.

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Odontogenic secondary chronic osteomyelitis (axial CT view).

Corresponding bone scan

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TREATMENT

- The management of osteomyelitis of the maxillofacial region requires both medical and surgical interventions.

- The tentative diagnosis is made from clinical evaluation, radiographic evaluation, and tissue diagnosis.

- Medical evaluation and management in defining and treating any immunocompromised state is indicated

and often helpful.

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Medical Management

1. Complete bed rest

2. Supportive therapy

Nutritional support – High protein diet

High caloric diet

Adequate multivitamins

3. Rehydration

- Hydration orally

- Administration of I.V. fluids

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4. Blood transfusion

- If RBC, Hb% are low

5. Control of Pain

- Analgesic and sedation

6. Antibiotic therapy

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SURGICAL OPTIONS

1) Incision and drainage

2) Extraction of offending teeth

3) Sequestrectomy

4) Saucerisation

5) Decortication (Mowlem’s decorticotomy)

6) Resection and Reconstruction:

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The aim is to debride the necrotic or poorly vascularized bony sequestra in the infected area and improve blood flow.

Sequestrectomy involves removing infected and avascular pieces of bone—generally the cortical plates in the infected area.

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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 (Mowlem 1945) 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.

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- The key element in the above procedures is

determined clinically by cutting back to good

bleeding bone

- It is often necessary to remove teeth adjacent

to an area of osteomyelitis.

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Secondary chronic osteomyelitis of the left mandible: The Infection originated from the decayed lower left second molar and spread anteriorly to the second left premolar; posteriorly the affected bone reaches the ascending ramus

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Buccal incision along the gingival margin with vestibular extensions distally and mesiallyb). Note that the subperiosteal newly formed bone

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Subperiosteal dissection and exposure of the affected

region

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Removal of the odontogenic focus and the teeth in the

affected region and removal of sequestrum

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The margins of the intended area of

decortication are marked with a burr.

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A long burr is used to perform multiple monocortical decortication osteotomies on the buccal cortex When performing the osteotomies it should be stressed that they are strictly limited to the buccal cortex of the mandible to avoid damage to the inferior alveolar nerve

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The buccal cortical bone and the inferior border are then

removed with a chisel, until bleeding bone is

encountered.

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Mobilization of the interior alveolar nerve is performed to allow access to the surrounding deeper areas of affected bone.

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Meticulous removal of affected bone and granulation

tissue is performed. The curettage is completed when

vital bone is visible.

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Mandible after completed decortication and surgical debridement. The remaining bone represents the remaining vital bone tissue

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If necessary, additional burr holes and perforations can

be performed to facilitate contact better in vascularized

deeper bone compartments or to the lingual periosteum

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Resection of affected buccal periosteum with

areas of neoosteogenesis

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The remaining bone is suspected to be prone to fracture, appropriate stabilization and reconstruction should beperformed.

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Primary closure is achieved to ensure close contact of the bone bed to the well-vascularizedsoft tissue.

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The maxillary−mandibular fixation for 6 weeks with wire stents was additionally performed for sufficient Stabilization and immobilization of the operated left mandible to ensure healing without complication

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HYPERBARIC OXYGEN THERAPY

- Hyperbaric oxygen (HBO is defined in the European Code of Good Practice as the inhalation of pure oxygen (FiO2=1) under a pressure above the ambient pressure.

- In medicine,HBO is used within the range of 100–300 kPa. Above this pressure, oxygen presents an increased risk of central nervous toxicity

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Multiplace hyperbaric oxygen chamber

Monoplace hyperbaric oxygen chamber

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The purpose of HBO in chronic refractory

Osteomyelitis of the jaws is

- It reverses the hypoxic state of the infected bone.

- It enhances leukocyte killing of microorganisms.

- Survival and toxin production of certain anaerobes and facultative anaerobes