1. DR MOHAMMAD AKHEEL
OMFS PG

2. 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.

4.  Osteo – bone
Myelos – marrow
Itis - inflammation
 Inflammation of bone involving the cancellous
bone, bone marrow, cortical bone &
periosteum.

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

6.  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 face
7. Hematogenous

7. • Staph aureus, Staph albus, Strep pyogenes
• Bacteriodes, peptostreptococcus.
• Arachnia, Actinomyces, Klebsiella,
Eikenella etc
• Typhoid,Haemophilus, pneumococci,
spirochaetes

8. Pulpitis
Acute Chronic
Apical Periodontitis
Acute Chronic
Periapical
Abscess
Periapical
Granuloma
Periapical
Cyst
Osteomyelitis
Acute Chronic Focal
Diffuse
Periostosis
Cellulitis Abscess
Bacteraemia Toxaemia Septicemia Dissemination Shock
Death
Chronic
Periapical
abscess

9. 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

10.  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.

11. 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.

12. 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

13. 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

14. 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 #

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

16.  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

17.  Local factors :
• Chronic lymphoedema
• Venous stasis
• Major vessel disease
• Arteritis
• Extensive scarring
• Radiation fibrosis
• Small vessel disease
• Loss of local sensation

18.  Suppurative OM:
Acute
Chronic – primary
secondary
Infantile

19.  Non Suppurative :
Chronic sclerosing OM: focal
diffuse
Garre’s Sclerosing OM
Actinomycotic Osteomyelitis
Radiation Osteomyelitis & Necrosis

20. I. Acute Suppurative/ Nonsuppurative
(A) Contiguous focus: Trauma
Surgery
Odontogenic infection
(B) Progressive
Burns
Sinusitis
Vascular insufficiency
(C) Haematogenous (metastatic)
Developing skeleton
Developing dentition

21. 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

22. (D) Sclerosing OM
Diffuse
Fastidious organisms
Compromised host
Focal
Predominantly odontogenic
Chronic localised entry

23. 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

24.  Peritonsillar abscess
 Furunculosis of chin
 Hematogenous infection
Clinical 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.

25.  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

26. Acute suppurative osteomyelitis

27.  Primary (infection by subvirulent org.)
Secondary to acute infection
Clinical 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

28. • Teeth may not be sore or loose
Radiographic 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.

29. Sclerotic (L) Body mandible with sequestra

30. Sclerosis & sequestra (L) Mandible body

31. Sequestration

32. Periosteal reaction located at the inferior cortex

33. • 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.

34. 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.

35. Chronic focal sclerosing osteomyelitis

36.  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.

37. Radiological features –
 Diffuse sclerosis of bone (cotton wool
appearance).
 Indistinct borders between the sclerosis &
normal bone.
 Occasionally bilateral.

38. 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.

39. Diffuse sclerosis with ® body of mandible

40.  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.

41. 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).

42. Garre’s osteomyelitis

43. Garre’s osteomyelitis

44. 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.

45.  Tuberculosis
 Actinomycosis
 Syphilis

46.  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.

47.  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.

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

49. Resection of the jaw with immediate or
delayed reconstruction.
 Hyperbaric oxygen therapy

50. A B
C
Saucerization

51. A B
C
Decortication

52. Closed wound irrigation &suction

53.  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

54.  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

56.  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).

57. RADIATION
BONE
FORMATION OF HYPOXIC – HYPOVASCULAR –
HYPOCELLULAR TISSUE
TISSUE BREAKDOWN
CHRONIC NONHEALING WOUNDS

58. 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

59. 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.

60. 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

61. MOTH EATEN APPEARANCE ®
BODY

62. 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

63. 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.

64. 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.

65. 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.

66. 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.

67. 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.

68. Thank you