Osteomyelitis 12.01.16

1/28/2016
OSTEOMYELITIS
Dr. Ibtisam Briek SENUSSI
PHD in Oral Pathology
Master Orthodontic treatment
Master Industrial and Environmental Toxicology
28/11/2013
OSTEOMYELITIS
 WHAT IS OSTEOMYELITIS ?
 FACTORS PREDISPOSING TO OSTEOMYELITIS
 PATHOGENESIS OF OSTEOMYELITIS
 TYPES OF OSTEOMYELITIS
 PATHOGENESIS
 CLINICAL FEATURES
 HISTOLOGY
 RADIOLOGY
 MANAGEMENT
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OSTEOMYELITIS
 OSTEOMYELITIS WHAT’S IN THE NAME ?

The word “ osteomyelitis ” originates from the ancient
Greek words osteon (bone) and muelinos (marrow) that
means infection of medullary portion of the bone.
 WHAT IS IT?
It is an acute and chronic inflammatory process in the
medullary spaces or cortical surfaces of bone that extends
away from the initial site of involvement.
PREDISPOSING FACTORS
LOCAL FACTORS SYSTEMIC FACTORS

Decreased vascularity / (impaired host defense)
vitality of bone
 Trauma.  Immune deficiency states.

 Radiation injury.  Immuno-suppression.
 Paget’s disease.  Diabetes mellitus.
 Osteopetrosis.  Extremes of age.
 Major vessel disease.  Malnutrition (Sickle cell
disease).
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PATHOGENESIS OF OSTEOMYELITIS
TYPES OF OSTEOMYELITIS
 SUPPURATIVE OSTEOMYELITIS
Acute
Chronic
 FOCAL SCLEROSING OSTEOMYELITIS
 DIFFUSE SCLEROSING OSTEOMYELITIS
 OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS
 RADAITION ASSOCIATED OSTEOMYELITIS

(osteoradionecrosis).
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SUPPURATIVE OSTEOMYELITIS
ONSET OF DISEASE 4 WEEKS
Acute suppurative Chronic suppurative

osteomyelitis osteomyelitis
t
Onset of disease Deep
bacterial invasion into
medullary & cortical
bone
 Source of infection is usually an adjacent focus of

infection associated with teeth or with local trauma.
 It is a polymicrobial infection, predominating anaerobes
such as Bacteriods, gram (– ve).
 Staphylococci may be a cause when an open fracture is
involved.
 Mandible is more prone than maxilla as vascular supply is
readily compromised.
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ACUTE SUPPURATIVE OSTEOMYELITIS
Acute inflammation of the bone & bone marrow
Causes
 Extension of periapical abscess .
 Physical injury ( fracture or surgery).
 Bacteremia.
 The most of acute osteomyelitis are infectious.
 Any organism may be part of the etiologic picture,
(staphylococci & streptococci are identified the most).
Organisms entry into the jaw, mostly mandible, compromising the vascular
supply
Medullary infection spreads through marrow spaces
Thrombosis in vessels leading to extensive necrosis of bone
Lacunae empty of osteocytes but filled with pus ,bacteria proliferate in

the dead tissue
Suppurative inflammation extend through the cortical bone to involve the

periosteum
Stripping of periosteum comprises blood supply to cortical plate, predispose

to further bone necrosis
Sequestrum is formed bathed in pus, separated from surrounding vital bone

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CLINICAL FEATURES
 EARLY :
Severe throbbing, deep- seated pain.
Swelling due to inflammatory edema.
Gingiva appears red, swollen & tender.
Teeth are tender, loose in severe case
Trismus, anasthesia, parasthesia lower
lip, lymph nodes enlargement
 LATE :
Distension of periosteum with pus.
 FINAL:
Subperiosteal bone formation cause swelling to become firm.
HISTOLOGY
 Submitted material for biopsy predominantly consists of
necrotic bone & is diagnosed as Sequestrum

 Bone shows:
Loss of osteocytes from lacunae.

Peripheral resorption.
Bacterial colonization.
Acute inflammatory infiltrate consisting of
poly-morphonuclear leukocytes in haversian
canals & peripheral bone.
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Sequestrum
RADIOGRAPHIC FEATURES
 May be normal in early stages of disease .
 Do not appear until after at least 10 days.
 Radiograph may demonstrate ill-defined radiolucency.

 After sufficient bone resorption irregular, moth eaten
areas of radiolucency may appear.
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The panoramic radiograph of suppurative osteomyelitis

at the right side of mandible.
moth eaten appearance

MANAGEMENT
ESSENTIAL MEASURES
 Bacterial sampling & culture.
 Empirical antibiotic treatment.
 Drainage.
 Analgesics.
 Specific antibiotics based on culture & sensitivity test.
 Debridement.
 Remove source of infection, if possible.
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MANAGEMENT
 Difficult to manage medically.
 Surgical intervention is mandatory, depends on spread of process.
 Antibiotics are same as in acute condition but are given through IV
in high doses.
SMALL LESIONS
Curettage, removal of necrotic bone and decortication are sufficient.
EXTENSIVE OSTEOMYELITIS
Decortication combined with transplantation of cancellous bone chips.
PERSISTANT OSTEOMYELITIS
Resection of diseased bone followed by immediate reconstruction with
an autologous graft is required. Weakened jaw bones must be
immobilized.
COMPLICATIONS
 Rare but include:
Pathological fracture Extensive bone destruction.
Chronic osteomyelitis Inadequate treatment.
Cellulitis Spread of virulent bacteria.
Septicemia Immuno-compromised patient.
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DIFFERENTIAL DIAGNOSIS
 This lesion must be distinguished from

1. Osteosarcoma
2. Fibrous dysplasia
CHRONIC SUPPURATIVE OSTEOMYELITIS
Inadequate treatment of acute osteomyelitis
• Periodontal diseases
• Pulpal infections
• Extraction wounds
• Infected fractures
Infection in the medullary spaces spread and form granulation tissue
Granulation tissue forms dense scar to wall off the infected area
Encircled dead space acts as a reserviour for bacteria & antibiotics

have great difficulty reaching the site
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CLINICAL FEATURES
 Swelling
 Pain
 Sinus formation
 Purulent discharge
 Tooth loss
 Sequestrum formation
 Pathologic fracture
HISTOLOGY
 Inflammed connective tissue filling inter-trabecular areas of bone.
 Scattered Sequestra.
 Pockets of abscess.
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HISTOLOGY
Sequestra Dr. Ibtisam Briek SENUSSI
RADIOLOGY
 Patchy, ragged & ill defined radiolucency (moth eaten pattern).

 Often contains radiopaque sequestra.
 Sequestra lying close to the peripheral sclerosis & lower border.
 New bone formation is evident below lower border.
(moth eaten pattern)

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RADIOLOGY
MANAGEMENT
ESSENTIAL MEASURES
 Bacterial sampling & culture.
 Empirical antibiotic treatment.
 Drainage.
 Analgesics.
 Specific antibiotics based on culture & sensitivity test.
 Debridement.
 Remove source of infection, if possible.
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MANAGEMENT
ADJUNCTIVE TREATMENT
 Sequestrectomy
 Decortication (if necessary)
 Hyperbaric oxygen
 Resection & reconstruction for extensive bone destruction.
 Immobilization is required in some cases.

1. Osteosarcoma
2. Fibrous dysplasia
3. Paget’s disease of bone
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FOCAL SCLEROSING OSTEOMYELITIS
Condensing osteitis
 Also known as “Condensing osteitis”.

 Localized areas of bone sclerosis.
 Bony reaction to low-grade peri-apical infection or
unusually strong host defensive response.
 Association with an area of inflammation is critical.
CLINICAL FEATURES
 Children & young adults are affected.

 In mandible, premolar & molar regions are affected.
 Bone sclerosis is associated with non-vital or pulpitic
tooth.
 No expansion of the jaw.
HISTOLOGY
 Dense sclerotic bone.
 Scanty connective tissue.
 Inflammatory cells.
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RADIOLOGY
 Localized but uniform increased radiodensity related to
tooth.
 Widened periodontal ligament space or peri-apical area.
 Sometimes an adjacent radiolucent inflammatory lesion
may be present.
 Increased areas of radiodensity surrounding apices of
nonvital mandibular first molar
RADIOLOGY
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MANAGEMENT
 Elimination of the source of inflammation by extraction
or endodontic treatment.
 If lesion persists and periodontal membrane remains
wide, reevaluation of endodontic therapy is considered.
 After resolution of lesion, inflammatory focus is termed
as bone scar.
28/11/2013

1. Focal cemento osseous dysplasia: it shows a
radiolucent border.
2. Idiopathic osteosclerosis: here, the lesion is
separated from the tooth apex.
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DIFFUSE SCLEROSING OSTEOMYELITIS
 Chronic intra-osseous bacterial infection creates a

smoldering mass of chronically inflammed granulation
tissue.
 Characterized by pain, inflammation, varying degrees of
periosteal hyperplasia, sclerosis and radiolucency of
affected bone.
CLINICAL FEATURES
 Arises exclusively in adult-hood with no sex pre-

dominance.
 Primarily occurs in mandible.
 No pain.
 No swelling.
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HISTOLOGY

 Bone sclerosis.
 Fibrous replacement of marrow Scanty marrow spaces.
 Chronic inflammatory cells infiltration & neutrophiles are also seen.
 Secondary bacterial colonization often is visible.
 Bony trabeculae exhibit irregular size and shape may be lined by
osteoblasts. (focal osteoclastic activity is present)
Scleroting osteomyelitis of the mandible. Biopsy show thick trabeculae, fibrous marrow,scattered
lymphocytes / sclerotic masses are composed of dense bone also exhibiting numerous reversal lines.
RADIOLOGY
 Increased radiodensity may be seen surrounding areas of
lesion.
 Diffuse area of increased radiodensity of the mandible
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RADIOLOGY
MANAGEMENT
 Elimination of originating sources of inflammation via
extraction & endodontic treatment.
 Sclerotic area remain radiographically.
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 Can be confused clinically and radiologically

with certain other intra-bony pathoses like
 Florid cemento-osseous dysplasia.

 Paget's disease of bone.
OSTEOMYELITIS WITH PROLIFERATIVE

PERIOSTITIS (Garré’s osteomyelitis)
 Also called Periostitis ossificans & Garré’s Osteomyelitis.

 It represents a periosteal reaction to the presence of
inflammation.
 It is a type of osteomyelitis associated with periosteal bone
formation.
 Affected periosteum forms several rows of reactive vital
bone that parallel each other & expand surface of altered
bone.
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PERIOSTITIS
PATHOGENESIS
The spread of low-grade, chronic apical inflammation through

cortical bone
Periosteal reaction occurs
Stimulates proliferative reaction of periosteum

PERIOSTITIS
CLINICAL FEATURES
 Affected patients are primarily children & young adults.

 Incidence is mean age of 13 years.
 No sex predominance is noted.
 Most cases arise in the premolar & molar area of mandible.
 Hyperplasia is located most commonly along lower border of
mandible.
 Most cases are uni-focal, multiple quadrants may be
affected. Dr. Ibtisam Briek SENUSSI
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PERIOSTITIS
HISTOLOGY

 (A) Parallel rows of highly cellular & reactive woven bone
 (A) Trabeculae are frequently oriented perpendicular to
surface.
 (B) Tissue form the central mandible is minimally inflammed &
has fibrous appearance.
 (C) Periosteal tissue shows sclerotic lamination.
A B C
BIBLIOGRAPHY
 Soames JV, Southam JC. Oral pathology/. 4th ed. Oxford 2007-2008.
 Shafer WG, Hine MK, Levy BM. A text book of oral pathology. 6 th
ed. W.B. Saunders Company. Phil, London, Toronto, 2005.
 Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial
pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007.
 Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology
and oral medicine, 8th Ed, Churchill Livingstone, 2008.
 Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic
Correlations. 4th ed. Saunders Company, 2003.
 Google Image
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1/28/2016

Dr. Ibtisam Briek SENUSSI

Dr. Ibtisam Briek SENUSSI

 OSTEOMYELITIS WHAT’S IN THE NAME ?

Dr. Ibtisam Briek SENUSSI

LOCAL FACTORS SYSTEMIC FACTORS

 Trauma.  Immune deficiency states.

Dr. Ibtisam Briek SENUSSI

Dr. Ibtisam Briek SENUSSI

 FOCAL SCLEROSING OSTEOMYELITIS

 DIFFUSE SCLEROSING OSTEOMYELITIS

 OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS

 RADAITION ASSOCIATED OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

ONSET OF DISEASE 4 WEEKS

Acute suppurative Chronic suppurative

 Source of infection is usually an adjacent focus of

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

Acute inflammation of the bone & bone marrow

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

Medullary infection spreads through marrow spaces

Thrombosis in vessels leading to extensive necrosis of bone

Lacunae empty of osteocytes but filled with pus ,bacteria proliferate in

Suppurative inflammation extend through the cortical bone to involve the

Stripping of periosteum comprises blood supply to cortical plate, predispose

Sequestrum is formed bathed in pus, separated from surrounding vital bone

ACUTE SUPPURATIVE OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

necrotic bone & is diagnosed as Sequestrum

Loss of osteocytes from lacunae.

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

 Do not appear until after at least 10 days.

 Radiograph may demonstrate ill-defined radiolucency.

Dr. Ibtisam Briek SENUSSI

The panoramic radiograph of suppurative osteomyelitis

moth eaten appearance

ACUTE SUPPURATIVE OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

ACUTE SUPPURATIVE OSTEOMYELITIS

ACUTE SUPPURATIVE OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

 This lesion must be distinguished from

Dr. Ibtisam Briek SENUSSI

CHRONIC SUPPURATIVE OSTEOMYELITIS

Inadequate treatment of acute osteomyelitis

Infection in the medullary spaces spread and form granulation tissue

Encircled dead space acts as a reserviour for bacteria & antibiotics

CHRONIC SUPPURATIVE OSTEOMYELITIS

Dr. Ibtisam Briek SENUSSI

CHRONIC SUPPURATIVE OSTEOMYELITIS

 Inflammed connective tissue filling inter-trabecular areas of bone.

Dr. Ibtisam Briek SENUSSI

CHRONIC SUPPURATIVE OSTEOMYELITIS

Sequestra Dr. Ibtisam Briek SENUSSI

CHRONIC SUPPURATIVE OSTEOMYELITIS

 Patchy, ragged & ill defined radiolucency (moth eaten pattern).

(moth eaten pattern)