Osteomyelitis is an inflammatory condition of bone tissue that is typically caused by bacterial infection. It begins in the bone marrow and can spread to involve the cortical bone and periosteum if left untreated. Key factors in its progression include impaired blood flow and immune function. It is classified as either suppurative (characterized by pus formation) or non-suppurative. Suppurative osteomyelitis may be acute or chronic, while non-suppurative types include chronic diffuse sclerosing osteomyelitis and Garre's sclerosing osteomyelitis. Treatment involves long-term antibiotic therapy along with surgical debridement to improve blood supply and support healing.

1. OSTEOMYELITIS

2. Contents
• Definition
• Predisposing factors
• Classification
• Suppurative osteomyelitis
• Non suppurative

3. Definition
• Inflammation of the bone forming elements
with tendency to progression.
Begins in
medullary
cavity
Extends +
spreads to
cortical
bone
Eventually
reaches
the
periostium

4. Invasion of bacteria into cancellous
bone
Inflammation + edema in marrow
spaces
Compression of blood vessels
Severe compromise of blood supply

5. • 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.

6. Mandible
Less perfusion
from inferior
alveolar artery
only
Overlying cortical
bone is dense and
prevents penetration
of periosteal blood
vessels
Maxilla
Blood supply much
richer and derived from
several arteries, which
form a complex network
of feeder vessels.
Less dense than mandible
Mandible affected
more than maxilla

7. Predisposing factors
Osteomyelitis
Radiation
exposure
Fracture
of
mandible
Impaired
blood
flow
Impaired
immunity
Poor
nutrition
Odontogenic
infections

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

9. 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

10. 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

11. Classification
• Roughly divided into suppurative and non
suppurative based on clinical features.
• Suppurative
1. Acute
2. Subacute and chronic
• Infantile osteomyelitis
• Non suppurative
1. Chronic diffuse sclerosing
2. Garre’s sclerosing

12. SUPPURATIVE OSTEOMYELITIS
• The dominant form
• Characterised by pus formation and necrosis of
bone
• Has two distinct forms;
a) Acute ; infection which includes systemic effects
b) Chronic; induce minimal systemic effects
• Primary chronic; no acute episode
• Secondary chronic; involves prolonged
inflammatory process

13. 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.

14. 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.

15. –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.

16. –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.

17. • 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

18. • Infection is localized only in the intramedullary
site:
–Adequate antibiotic treatment at this stage
may prevent further progression

19. 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

20. • 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

21. • Systemically:
–Temperature falls to the normal range

22. 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.

23. 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

24. –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

25. • 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

26. Management
• Diagnose correctly.
• Evaluate, define and manage the
immunocompromised state of the patient first
for best response to therapy.

27. • Antibiotics, surgery and supportive care
–Antibiotic Therapy
• Penicillins
• Clindamycin
• Metronidazole

28. • 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.

29. Surgery
Improves blood supply in
the involved area -> allowing
adequate penetration of
antibiotics
Maximizes the host defense
mechanisms and self healing
ability

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

31. 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.

32. • 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.

33. • 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.

34. • 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

35. • 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.

36. • 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.

37. • 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.

38. • 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.

39. 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.

40. Infantile osteomyelitis
• Occur few days after birth
• Commonly involves the maxilla
Etiology
• Remains unclear
• Thought to involve;
Perinatal trauma
Infection of the maxillary sinus
Hematogenous spread

41. • 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.

42. 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

43. Treatment
• Prompt and aggrassive
• Use of intravenous antibiotics and drainage of
abscesses
• S. aureus is the most common pathogen
involved

44. NON SUPPURATIVE OSTEOMYELITIS
CHRONIC DIFFUSE SCLEROSING.
• Usually affects mandible
• Characterised by;
Recurrent pain and swelling
No suppuration or abscess formation
paraesthesia

45. Etiology
• Unclear
• Possibly due to;
Hyperactive immunologic response
hyperostosis

46. Radiography;
• Intermingled sclerotic and osteolytic lesion
with a solid periosteal reaction
• External bone resorption
Treatment
• Difficult to eradicate- may persist for years
• Asymptomatic; NSAIDs, corticosteroids

47. Garre’s sclerosing osteomyelitis
• Named after a Swiss surgeon, Dr Carl Garre
• Characterized by;
Active periosteum proliferation
Formation of subperiosteal bone
No purulent exudate

48. • Believed to result from over inflammatory
reaction of the periosteum
• Commonly in children and adults
• Usually on the lateral surface of body of
mandible

49. Etiology
• Periapical abscess
• Post extraction infection
Clinical features
• Localized, unilateral and hard mandibular
swelling with little tenderness
• Pain can be episodic
• No apparent systemic signs

50. Radiological findings
• Thickened cortical bone
• Onion skin appearance due to new bone
formation
Treatment
• Elimination of cause

51. References
• Oral and maxillofacial surgery, L Andersson, KE
Kahnberg, MA Pogrel
• Textbook of Oral and Maxillofacial Surgery 3rd
ed, NA Malik