Osteomyelitis is an inflammatory condition of bone that usually begins as an infection of the bone marrow. It can spread rapidly through the bone tissue. There are several classifications of osteomyelitis including acute vs chronic forms and suppurative (pus-forming) vs non-suppurative. Common causes include spread from nearby infected tissues, trauma or surgery, or hematogenous spread from other infections. Staphylococcus aureus is a common cause. Imaging like x-rays, CT and MRI can help identify bone changes. Treatment involves antibiotics, sometimes implanted directly into the bone, along with surgical drainage or debridement of infected tissues.

1. OSTEOMYELITIS
PRESENTED BY: SAILESH KUMAR. R

2. DEFINITION
• “Osteomyelitis is defined as an inflammatory condition of
bone that usually begins as an infection of the medullary cavity,
rapidly involves the haversian system and quickly extends to the
periosteum of the area.”
• Greek word
OSTEON - BONE
MYELOS - MARROW

3. 1970 WALDVOGEL CLASSIFICATION OF
OSTEOMYELITIS
Pathogenesis
1. Hematogenous spread
2. Osteomyelitis secondary to contiguous focus of infection (
soft tissue infection, decubitus ulcer, dental abscess)
3. Osteomyelitis associated with peripheral vascular disease (
diabetes mellitus)

4. WEILAND CLASSIFICATION OF
OSTEOMYELITIS
• Type I osteomyelitis is defined as open exposed bone without evidence
of osseous infection but with evidence of soft tissue infection.
• Type II osteomyelitis consists of circumferential, cortical, and endosteal
infection. Radiograph findings included areas of bony resorption and
often a sequestrum with a surrounding involucrum.
• Type III osteomyelitis consists of cortical and endosteal infection
associated with a segmental bone defect.

5. A) Acute forms of Osteomyelitis(suppurative or non suppurative)
include
1) contiguous focus: trauma, surgery, odontogenic infections
2) progressive : burns ,sinusitis, vascular insufficiency
3) haematogenous: developing children
B) Chronic forms of Osteomyelitis
1) Recurrent multifocal
2) Garres osteomyelities
3) Suppurative or non suppurative
4) Diffuse sclerosing
HUDSONS 1993 CLASSIFICATION OF
OSTEOMYELITIS

6. TOPAZIAN CLASSIFICATION OF OSTEOMYELITIS
BASED ON SUPPURATION
Suppurative
• Acute suppurative
• Chronic suppurative
- Primary
- Secondary
• Infantile
Non suppurative
• Chronic sclerosing
• Focal sclerosing
• Diffuse sclerosing
• Garre’s sclerosing
• Actinomycotic osteomyelitis
• Radiation osteomyelitis and
necrosis

7. ETIOLOGIES
ODONTOGENIC
INFECTIONS
Pericoronitis
Infected socket
Cyst n tumors
TRAUMA-
Compound
fracture,
surgery
INFECTION OF
OROFACIAL REGION
Periostitis
Lacerations
Peritonsillar abscess
HAEMATOGENOUS
INFECTON’S
Furuncle on face
Wound on skin
Middle ear infection
Mastoititis
TB

8. PATHOGENESIS
Acute
inflammation of
marrow tissues
Spread of exudate
along the marrow
spaces
Thrombosis of
vessels due to
compression
Necrosis of bone
Liquefaction of
necrotic tissues
Sequestrum
formation
Involucrum
formation

9. Maxilla
• Extensive blood supply
• Thin cortical plates
• Porous bone
Mandible
• Dense cortical plates
• Less blood supply
OSTEOMYELITIES MORE COMMON IN MANDIBLE –WHY

10. MICROBIOLOGY OF OSTEOMYELITIS
• Staphylococcus aureus & staphylococcus epidermidis
80 -90% due to skin contamination
• A-hemolytic streptococcus is recognized as the primary
organism along with oral anaerobes eg.,
Peptostreptococcus, fusobacterium and prevotela species
• Findings suggestive of pure anaerobic or mixed
aerobic/anaerobic infections

11. IMAGING IN OSTEOMYELITIS
• Plain radiograph
• Technetium bone scan – accumulates in areas of increased
osteoblast activity
• Ga scan & 111 In WBC scan - accumulates at sites of
inflammation or infection and in the bone marrow
• CT scan - detecting cortical destruction, intraosseous gas,
periosteal reaction, and soft tissue extension.
• MRI

12. RADIOGRAPHIC FINDINGS
- 30- 60% of mineralised bone must be destroyed for significant
radiographic
changes.
Established osteomyelitis demonstrate following changes –
• scattered areas of bone destruction with “moth eaten appearance”
because of enlargement of medullary space and widening of
volkmann’s canal.
• Presence of sequestra with evidence of trabecular pattern and marrow
space.
• A sheath of new bone called as involucrum is often found separated
from sequestra by a zone of radiolucency.
• The central sequestra usually present in osteomyelitis help to
distinguish from fibrous dysplasia.

13. Moth eaten Appearence Focal Sclerosing Osteomyelitis

14. CBCT

15. ACUTE OSTEOMYELITIS
Results – from highly virulent organisms
Clinical features–
- Deep intense pain
- High intermittent fever
- Paraesthesia of lower lip.
- Fetid odour
- pus
- Teeth in affected area begin to loosen and become sensitive
to percussion.
- Regional lymphadenopathy.

16. CHRONIC SUPPURATIVE OSTEOMYELITIS
Primary – resulting from organism which are less virulent.
Secondary – after acute osteomyelitis.
Clinical features –
- seen in incompletely treated cases of acute osteomyelitis.
- Pain & tenderness.
- Intraoral or extra oral draining fistula.
- Thickened or wooden character of bone.
- Enlargement of mandible, because of deposition of subperiosteal new
bone.
- Pathologic fracture may occur.
- Loosening of teeth & tender on percussion.

17. Chronic Suppurative Osteomyelitis

18. NON SUPPURATIVEOSTEOMYELITIS
Chronic focal sclerosing osteomyelitis-
• Is an unusual reaction of bone to infection, occurring in instances of
extremely high tissue resistance or in cases of a low grade infection.
• Young persons below 20yrs , tooth most commonly involved is first
molar
• Well-circumscribed radio-opaque mass of sclerotic bone surrounding
and extending below the apex of involved tooth

19. CHRONIC FOCAL SCLEROSING OSTEOMYELITIS

20. CHRONIC DIFFUSE SCLEROSING OSTEOMYELITIS
• Represents a proliferative
reaction of bone to low
grade infection.
• Here the portal of entry of
infection is mainly through
the periodontium.
• More common in females.
• Is of insidious in nature.

21. GARRE’S CHRONIC NONSUPPURATIVE SCLEROSING
OSTEOMYELITIS / PERIOSTEITIS OSSIFICANS
• First described by CARL GARRE in 1893 as a focal gross
thickening of the periosteum of long bones, with peripheral
reactive bone formation resulting from mild irritation or
infection.

22. OSTEOMYELITIS DUE TO NON PYOGENIC
ORGANISMS
ACTINOMYCOTIC OSTEOMYELITIS:
• Is a chronic infection manifests both with granulomatous
and suppurative features involving soft tissues and bone
of cervicofacial region.
• It is caused by actinomycosis israelii.

23. TUBERCULOUS OSTEOMYELITIS
• Mycobacterium tuberculosis is usually brought about by
hematogenous spread and is almost always secondary to
a primary focus in respiratory or alimentary tract.
• Localised osteomyelitis may follow tooth extraction
performed on tuberculous patient. Active tuberculosis
infection of the tooth socket

24. DIFFERENTIAL DIAGNOSIS
Osteogenic sarcoma
• Permeative lesion borders,
• stippled bone pattern,
• destruction of cortical outlines,
• perpendicular spiculations of periosteal
new bone,
• destruction of lamina dura, and widening
of the entire periodontal ligament space

25. Fibrous dysplasia
• Superior displacement of
the mandibular canal and
• In the absence of these
findings, displacement of
the sinus cortex, alteration
of the lamina dura to the
abnormal bone pattern,
and narrowing of the
periodontal ligament space

26. PRINCIPLES OF TREATMENT OF
OSTEOMYELITIS
1.) Evaluation & correction of host defense.
2.) Gram staining, culture & sensitivity.
3.) Imaging to determine extent of lesion & also rule out bone
tumors.
4.) Administration of empirical antibiotics.
5.) Removal of loose teeth & sequestra.
6.) Administration of culture guided specific antibiotics.
7.) Possible placement of irrigating drains –antibiotics beads.
8.) Sequestrectomy, debridement, decortication, resection &
reconstruction.

27. ANTIBIOTIC REGIMEN FOR
OSTEOMYELITIS
Regimen I – in patient ( hospitalised )
• Aqueous pencillin 2 million U IV 4th hourly + metronidazole 500 mg 6th hourly
( When improved for 48-72 hrs switch to)
• Pencillin V 500mg PO 4th hourly + metronidazole 500 mg PO 6th hourly for 4-6
weeks
Or
• Ampicillin / sulbactam 1.5 -3.0 gms IV 6th hourly
( when improved for 48-72hrs switch to)
Amoxicillin clavulanate 875/125 mg po 12th hourly for 4- 6 weeks

28. REGIMEN II - FOR OUT PATIENT TREATMENT
• Pencillin V 2g + metronidazole 0.5 g 8th hourly PO 2-4
weeks after last sequestrum removed
Or
• Clindamycin 600 -900mg 6th hourly IV then
• Clindamycin 300- 450 mg 6th hourly PO
Or
• Cefoxitin 1gm iv 8th hourly / 2gm 4th hourly until no
symtoms then switch to
• Cephalexin 500mg 6th hourly PO for 2-4weeks

29. LOCALANTIBIOTIC THERAPY
Closed wound irrigation with suction
• Antibiotic in high concentrations placed in direct contact with bone
manually or implantable pump.
• Neosporin irrigant ( bacitracin zn – neomycin sulfate- polymixin b )
instilled on 12 hr cycle. Drug left in place for 3 hrs & low intermittent
suction used for 9hrs followed by culture of specimens

30. LOCALANTIBIOTIC THERAPY
Antibiotics is leached from the beads producing high local concentration
but low systemic concentration thus reducing the risk of toxicity.
Antibiotic impregnated beads
After decortication Tobramycin or Gentamycin
contained in acrylic resin bone cement beads left
in place for 10-14 days & then removed.

31. Saucerization followed by sequestrectomy
It is the excision of the margins of the necrotic bone over a focus of
osteomyelitis, which allows visualization of the sequestra and excision of
the affected bone.
The defect is packed open to allow exfoliation of unrecognized sequestra.
Saucerization Sequestrectomy

32. DECORTICATION
OBWEGESSER (1960) Advocated this method, which include
removal of chronically infected lateral and inferior cortical
plates of bone 1-2 mm beyond the area of involvement,
to gain access to medullary cavity.

33. Trephination
Creation of bony holes or windows in the overlying
cortical bone.
Drilling of holes allow vascular communication b/w
periosteum & medullary cavity.
Resection
done in case of massive destruction of bone.

34. Reconstruction
- To maintain continuity of fragment.
- To prevent fracture.
- To provide attachment of soft tissue.
- In cases of pathological fracture.
- Persistent infection after decortication.
Post operative care
- Use of antibiotics, analgesics, saline mouth
Rinses & complete bed rest.

35. REFERENCES
• Oral maxillofacial infections – topazian
• Acute osteomyelitis of the jaws, oral and maxillofacial surgery
clinics of north america- vol. 3, 2: 355- 365, 1991. Louis G
mercuri
• Chronic osteomyelitis of the jaws, oral and maxillofacial
surgery clinics of north america- vol. 3, 2: 367- 381, 1991.
Robert E marx
• Osteomyelitis of head and neck, J laryngology and otology, 99
(11) 1059-1065, 1985.

36. THANK YOU