DR MOHAMMAD AKHEEL OMFS PG

Infection – Invasion of the body with organisms that have the potential to cause disease.

Chronic – Lasting a long time. Condition of 3 months duration or longer

( US National centre for health statastics).

Reasons for chronicity – Extremely high host resistance. Sub-virulent microorganisms. Less number of microorganisms.

Osteo – bone Myelos – marrow Itis - inflammation Inflammation of bone involving the

cancellous bone, bone marrow, cortical bone & periosteum.

Noncompliance with health care delivery. Systemic metabolic compromise – -Age -Malnutrition -Immunosuppression -Congenital or acquired pathophysiologic conditions disrupting blood supply Inaccessibility to health care delivery.

Most are from local causes:1. Acute periapical infection 2. Pericoronitis 3. Acute periodontal lesions 4. Trauma-fractures and extraction of teeth 5. Acute infection of the maxillary sinus 6. Direct extension of furunculosis of the face7. Hematogenous

• Staph aureus, Staph albus, Strep pyogenes

• Bacteriodes, peptostreptococcus.

• Arachnia, Actinomyces, Klebsiella, Eikenella etc

• Typhoid,Haemophilus, pneumococci, spirochaetes

Pulpitis

Acute Chronic

Apical Periodontitis

Acute ChronicPeriapical Abscess

Periapical Granuloma

Periapical Cyst

Osteomyelitis

Acute Chronic Focal

DiffusePeriostosis

Cellulitis Abscess

Bacteraemia Toxaemia Septicemia Dissemination Shock

Death

Chronic Periapical abscess

Mostly occurs in the mandible, rarely in the maxilla.

Most odontogenic infections are localised by the production of a protective pyogenic membrane or soft tissue abscess wall.

If sufficiently virulent, microorganisms may destroy this barrier.

ACUTE Acute inflammation sets in : Hyperemia Increased capillary permeability Infiltration of granulocytes

Proteolytic enzymes liberated due bacteria destruction-tissue necrosis & vascular thrombosis

Pus accumulates - increased intramedullary pressure - vascular collapse, venous stasis & ischemia.

Pus travels through the haversian & nutrient canals & accumulates beneath the periosteum, elevating it from the cortex, further reducing the blood supply.

Compression of the neurovascular bundle accelerates thrombosis & ischemia.

If pus continues to accumulate, the periosteum is peneterated & mucosal & cutaneous abscesses & fistulae may develop.

CHRONIC As natural host defenses & therapy begin to be

effective, it becomes chronic. Inflammation regresses, granulation tissue is

formed. Angiogenesis takes place leading to lysis of bone,

thus separating fragments of necrotic bone from viable bone – Sequestra.

Small sections of bone may be completely lysed while larger ones may be isolated by a bed of granulation tissue & surrounded in a sheath of new bone – Involucrum

Occasionlly , the involucrum is peneterated by channels through which pus escapes to an epithelial surface – Cloacae.

Radiographic evaluation• 30-60% destruction min 4-8 days to 3 wks

• Moth eaten appearance, scattered areas of bone destruction

• Islands of sequestrae in radiolucent areas surrounded by involucrum

• Stippled granular densification due to subperiosteal deposition on surface of trabeculae at the expense of marrow spaces

RADIOGRAPHIC AIDS• Radiographs

• Bone imaging - Scintigraphy

Determines presence of reactive bone

Radiopharmaceuticals – technetium-99

gallium-67

indium-111

• High resolution Computer tomography

• Magnetic Resonance Imaging

Classification & staging system for Osteomyelitis (Cierny et al, 1985)

I. Anatomic

Stage I : Medullary OM, involves medullary bone

usually hematogenous

Stage II: Superficial OM, < 2cm defect without

cancellous bone

Stage III: Localized OM, <2 cm defect, does not

involve both the cortices

Stage IV: Diffuse OM, > 2cm, infection, non union,

pathologic #

II. Physiological class Host : normal host Host Systemic compromise Local compromise Host : treatment worse than disease

Systemic factors affecting immune surveillance , metabolism, local vascularity

• Malnutrition• Renal/ hepatic failure• Diabetes Mellitus• Chronic Hypoxia• Immune deficiency/ suppression• Malignancy• Extremes of ages• Autoimmune disease• Tobacco & Alcohol abuse

Local factors :

• Chronic lymphoedema

• Venous stasis

• Major vessel disease

• Arteritis

• Extensive scarring

• Radiation fibrosis

• Small vessel disease

• Loss of local sensation

Suppurative OM:

Acute

Chronic – primary

secondary

Infantile

Non Suppurative :

Chronic sclerosing OM: focal

diffuse

Garre’s Sclerosing OM

Actinomycotic Osteomyelitis

Radiation Osteomyelitis & Necrosis

I. Acute Suppurative/ Nonsuppurative(A) Contiguous focus: Trauma

Surgery

Odontogenic infection

(B) Progressive

Burns

Sinusitis

Vascular insufficiency

(C) Haematogenous (metastatic)

Developing skeleton

Developing dentition

II. Chronic forms(A) Recurrent multifocal

Developing skeleton

Increased osteogenic activity

(B) Garre’s OM

Unique proliferative subperiosteal reaction

Developing skeleton

(C) Suppurative/ non suppurative

Inadequately treated

Systemically compromised

Refractory

(D) Sclerosing OM

Diffuse

Fastidious organisms

Compromised host Focal

Predominantly odontogenic Chronic localised entry

Etiology – Odontogenic infections Periapical disease caused by pulpal

pathosis Periodontal disease Long standing pericoronal infection Infection of an odontogenic cyst or tumor Infection of an extraction wound Infected fracture site Local trauma to gingiva

Peritonsillar abscess Furunculosis of chin Hematogenous infectionClinical features – 1. Fever, malaise, severe pain. 2. Swelling, regional lymphadenopathy. 3. Teeth may be loose & sore.4. If the infection involves the mandibular

canal, a paraesthesia or anesthesia of the lower lip is common.

Radiological features – • No evidence till 1 – 2 weeks of disease

progression.

Diffuse lytic changes – fuzziness & increased trabacular spaces.

Later cortex becomes involved, sequestrum & radiolucent areas.

Histologic features – Medullary spaces filled with inflammatory

exudate/pus. Polymorphonuclear leukocytes. Osteoblasts bordering the bony

trabeculae are destroyed

Acute suppurative osteomyelitis

Primary (infection by subvirulent org.) Secondary to acute infectionClinical Features – • Local tenderness• Swelling • Mild leucocytosis• Low-grade fever • Regional lymphadenopathy • Acute exacerbations - intra and/or extraoral

sinuses that intermittently develop and drain a small amount of pus and then close

• Teeth may not be sore or looseRadiographic Features • Single or multiple radiolucencies of

variable size and with poorly defined borders

• Affected bone becomes moth-eaten in appearance.

• Sequestra - irregular calcified areas separate from remaining bone.

• Subperiosteal bone may be deposited.

Sclerotic (L) Body mandible with sequestra

Sclerosis & sequestra (L) Mandible body

Sequestration

Periosteal reaction located at the inferior cortex

• Unusual reaction of bone to infection occurring in extremely high tissue resistance or low grade infection

Clinical features -

• In young adults < 20 yrs.

• Mandibular 1st molars most commonly affected.

• Mild pain associated with infected pulp.

• No other prominent signs or symptoms.

Radiologic features –

• Well circumscribed radiopaque mass of sclerotic bone surrounding & extending below the apex of one or both roots.

• Proliferation more than destruction (infection acts as a stimulus).

Histologic features – Dense mass of bony trabeculae with

little interstitial marrow tissue. If interstitial soft tissue is present –

fibrotic & infiltrated only by a small numbers of lymphocytes.

Chronic focal sclerosing osteomyelitis

Proliferative reaction of the bone to a low grade infection.

Infection mostly through diffuse periodontal disease.

Clinical features – More common in older persons, blacks,

females & mandibular edentulous areas. Occasional acute exacerbation with

resultant mild suppuration & fistula formation.

No other clinical indication of its presence.

Radiological features – Diffuse sclerosis of bone (cotton wool

appearance). Indistinct borders between the

sclerosis & normal bone. Occasionally bilateral.

Histologic features – Dense irregular trabeculae, some of

which are lined by an active layer of osteoblasts.

Focal areas of osteoclastic activity may be seen.

Fibrous tissue containing proliferating fibroblast, lymphocytes & plasma cells is present between trabeculae.

Diffuse sclerosis with ® body of mandible

Rare non-suppurative sclerosing osteomyelitis by the formation of a hard, bony swelling at the periphery

Non-tender swelling in the inferior border of the mandible below the first molar.

More frequently in females Affects young individuals before the age

of 25 yrs.

Radiologic features –• A focal overgrowth of bone over the

cortex (outer surface) may be seen.• Mass of bone is smooth & rather well

calcified.• No trabecular shadows in the

radiolucent space.• Cortex becomes thickened and

laminated with alternating radiopaque-radiolucent layers (onion-peal appearance).

Garre’s osteomyelitis

Garre’s osteomyelitis

Etiology – Infection during delivery. Trauma to oral mucosa. Hematogenous.Clinical features - Sudden onset & runs an acute course. High fever, rapid pulse, vomiting, delirium &

prostration. Local signs – edema with eyelids,

subperiosteal abscesses on alveolar mucosa & palate, followed by sinus formation.

Tuberculosis Actinomycosis Syphilis

Disrupt the infectious foci. Debride any foreign bodies necrotic tissue, or

sequestra. Culture and identify specific pathogens for

eventual definitive antibiotic treatment. Drain and irrigate the region. Begin empiric antibiotics based on Gram

stain. Stabilize calcified tissue regionally.

Supportive therapy Consider adjunctive treatments to

enhance microvascular reperfusion (usually reserved for refractory forms only).

Sequestrectomy Saucerization  Trephination Decortication Vascular flaps Hyperbaric oxygen therapy Reconstruction as necessary following

resolution of the infection.

General management Antibiotic therapy Surgical management – Incision & drainage Extraction of teeth Closed wound irrigation & drainage Intra-arterial antibiotics Sequestrectomy Sequestrectomy with saucerization Decortication

Resection of the jaw with immediate or delayed reconstruction.

Hyperbaric oxygen therapy

A B

C

Saucerization

A B

C

Decortication

Closed wound irrigation &suction

Regimen 1: for hospitalized /medically compromised patient or when IV therapy indicated:

aqueous penicillin , 2 million U IV q4th , plus metronidazole , 500 mg , q6H

When improved for 48 to 72 hrs , swtich to : Penicillin V , 500 mg PO q6h, for additional 4 to 6

weeks or ampicillin /sulbactum ( unasyn),1.5 to 3 g iv q6h When improved swtich to : Amoxicillin/clavunate ( augmentin) , 875 /125

mgPO bid , for additional 4 to 6 weeks

Regimen 2 : penicillinV 2g, plus metronidazole ,0.5 gq8h PO,for 2 to 4

weeks after last sequestrum removed and patient without symptoms

Or clindamycin , 600to 900 mg q6h IV , then Clindamycin, 300to 450mg mg q6h PO Or cefoxitin ( mefoxin) , 1g q8h IV or 2 g q4h IM/IV until no

symptoms , then swtich to Cephalexin ( keflex) , 500mg q6h PO, for 2 to 4 weeks For penicillin allergic patients : Clindamycin Cefoxitin as above , if allergy not of anaphylactoid type

Exposure of nonviable bone which fails to heal without intervention following exposure to intense irradiation >5000mGy.

Dose rates > 0.55 mGy/hr – elevated risk. Triad of Irradiation, trauma, infection. Hypoxia, hypocellularity, hypovascular

tissues,associated with parenchymal breakdown & chronic wound manifestation secondary to radiation exhaustion of reparative process (Marx-1983).

RADIATION

BONE

FORMATION OF HYPOXIC – HYPOVASCULAR – HYPOCELLULAR TISSUE

TISSUE BREAKDOWN

CHRONIC NONHEALING WOUNDS

Clinical Staging:• Stage I Exposed bone, non-healing

wound

• Stage II Stage I non-responders, after 30 HBO dives

• Stage III ORN cutaneous fistula, pathological #s, inferior border resorption

Clinical features – Mandible more commonly affected. Loss of epithelial covering & exposure of

bone. Pathological # may occur. Sequestrum formation. Intense pain, with intermittent swelling &

drainage. Sometimes painless.

Radiological features – Periphery is ill defined & similar to that in

chronic osteomyelitis. Irregular bony resorption – Moth eaten

appearance. Radiopaque or sclerotic appearance. Scattered regions of radiolucency , with or

without sequestrum.

Radiographic Aids – High resolution CT. Scintigraphy 99m Tc MDP shows regional

perfusion,bone turnover. MRI

MOTH EATEN APPEARANCE ® BODY

Treatment of Osteoradionecrosis• Rule out neoplastic disease

• Stabilise nutritional & metabolic condition

• Administer preoperative hyperbaric oxygen

• Debride soft & bony necrotic tissues as necessary

• Provide post operative hyperbaric oxygen

• Consider soft tissue vascular flap support

• Perform bony reconstruction if warranted

Surgical: sequestrectomy, resection intra/ extraorally

Hyperbaric oxygen therapy:

• 20-40 sessions 2.8-3.0 ATA , 100%, 2 times daily for 90 minutes followed by 20 postoperative sessions.

Physiologic parameters augmented by hyperbaric oxygen therapy:

• Increased oxygen diffusion to tissues.• Revascularises irradiated tissues.• Enhanced leucocytic lysosomal activity.• Neutralisation of bacterial toxins.• Free Oxygen radical Bactericidal activity

against anaerobes.• Aerobic augmentation of wound healing

cycle , collagen synthesis fibroblastic cellular density.

• Neoangiogenesis stimulation. • Limits amount of nonvital tissues.

Pre Radiotherapy All teeth with questionable prognosis should be

extracted All restorable teeth should be restored. Thorough prophylaxis & topical fluoride application. Oral hygiene measures & instructions should be

demonstrated & reinforced. Any sharp cusps should be rounded to prevent

mechanical irritation. Impressions for fabrication of custom fluoride trays to

be used during treatment. Stop habits like tobacco use & alcohol consumption.

During Radiotherapy – Pt should rinse mouth at least 10 time a

day with saline. Chlorhexidine mouth rinses twice daily to

minimize bacterial/ fungal levels within mouth.

Weekly oral hygiene evaluation by dentist. If overgrowth of candida albicans – nystatin

or clotrimazole topical application. Monitor mouth opening. Monitor nutritional status.

Post Radiotherapy – Dental evaluation every 3 – 4 months. Oral prophylaxis. Topical fluoride application should be done

using custom trays. Pt to be instructed in daily self administration

of topical fluoride administration. Salivary substitutes should be prescribed. Restore teeth developing post-radiotherapy

caries using amalgam or composites. Extraction of teeth can be carried out with the

use of - Hyperbaric oxygen before & after extraction - Prophylactic antibiotic Evaluate artificial dentures.

Thank you