osteomyelitis of jaw- Abhijeet kamble

1. By-“abhijeet kamble”
Final year

2. The word “osteomyelitis” originates from the
ancient
• Greek words osteon (bone) and muelinos (marrow)
• and literally means infection of medullary portion of
the bone.
• DEFINED AS..;
• .. an inflammatory condition of bone that begins as
an infection of medullary cavity and haversian
systems of the cortex and extends to involve the
periosteum of the affected area.

3. Acute suppurative osteomyelitis
Chronic suppurative osteomyelitis
 Chronic focal sclerosing osteomyelitis (pseudo-paget, condensing osteomyelitis)
 Chronic diffuse sclerosing osteomyelitis
Chronic osteomyelitis with proliferative periostitis (Garre's chronic nonsuppurative
sclerosing osteitis, ossifying periostitis)
 Specific osteomyelitis:
1. Tuberculosis osteomyelitis
2. Syphilitic osteomyelitis
3. Actinomycotic osteomyelitis

4. • LOCAL
• FACTORS
• (decreased
vascularity/v
itality of
bone)
Trauma.
Radiation
injury.
Paget’s
disease.
Osteoporosis.
Major vessel
disease.
SYSTEMIC
FACTORS
(impaired host defense)
Immune deficiency
states.
Immunosuppression
Diabetes mellitus.
Malnutrition.
Extremes of age.

5. Inflammatory process of entire bone
including cortex & periosteum
Increased medullary pressure
Vascular collapse
Avascular bone

6. • More common in adult with
mandibular infection
• Osteomyelitis of Maxilla more
common in neonate .
• Sever throbbing pain , deeply sited
pain .
• Swelling ,malaise and pyrexia
• Gingiva red swollen and tender
• Involved teeth tender and mobile .
• Intra and extra-oral pus discharge
• Regional L.N enlargement
• Paresthesia of lower lips .
• Trismus

7. • 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
polymorphonuclea
r leukocytes in
haversian canals &
peripheral bone

8. 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.

9. Acute
inflamman of
marrow
tissues
Spread of
exudate
along the
marrow
spaces
Thrombosi
s of
vessels
due to
compressi
on
Necrosi
s of
bone
Liquefation
of necrotic
tissues
Lifting of
periosteu
m causing
further
necrosis
Finally,Osteoclastic activity >> SEQUESTRUM

10. ESSENTIAL MEASURES
• Bacterial sampling & culture.
• Emperical antibiotic treatment.
• Drainage.
• Analgesics.
• Specific antibiotics based on
culture & sensitivity.
• Debridement.
• Remove source of infection, if
possible.
ADJUNCTIVE TREATMENT
• Sequestrectomy.
• Decortication (if necessary)
• Hyperbaric oxygen.
• Resection & reconstruction for
extensive bone destruction.

11. CHRONIC
OSTEOMYELITIS
CHRONIC
SUPPURATIVE
OSTEOMYELITIS
SCLEROTIC
CEMENTAL
MASSES
CHRONIC DIFFUSE
SCLEROING
OSTEOMYELITIS
CHRONIC FOCAL
SCLEROSING
OSTEOMYELITIS

12. Low grade
inflammation with
associated with
bone destruction ,
granulation tissue
formation with
little suppuration
Causes :
1. Inadequate
treatment of acute
osteomyelitis.
2. Infection by weak
bacteria .
3. Infection of avscular
bone .
4. Irradiation

13. Swelling
Pain
Sinus formation
Purulent discharge
Sequestrum formation
Tooth loss
Pathologic fracture

14. Inflammed connective tissue
filling inter-trabecular areas
of bone.
Scattered sequestra.
Pockets of abscess.

15. Patchy, ragged & ill defined
radiolucency.
Often contains radiopaque
sequestra.
• Sequestra lying close to the
peripheral sclerosis &
lower border.
• New bone formation is
evident below lower border.

16. 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
Curretage, 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 jawbones must be immobilized.

17. 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.

18. 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.
Dense sclerotic bone.
Scanty connective tissue.
Inflammatory cells.

19. 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

20. 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.

21. It is an ill-defined, highly controversial, evolving
area of dental medicine.
Exact etiology is unknown.
Chronic intraosseous bacterial infection creates
a smoldering mass of chronically inflammed
granulation tissue.

22. Arises exclusively in adult-hood
with no sex pre-dominance.
Primarily occurs in mandible.
No pain.
No swelling.
Bone sclerosis and remodling.
Scanty marrow spaces.
Necrotic bone separates from vital
bone & become surrounded by
granulation tissue.
Secondary bacterial colonization
often is visible.

23. • Increased radiodensity
may be seen
surrounding areas of
lesion.
Diffuse area of
increased
radiodensity of Rt.
Side of mandible

24. Diffuse or nodular sclerosis resembling
cotton wool

25. Elimination of
originating
sources of
inflammation
via extraction &
endodontic
treatment.
Sclerotic area
remain
radiographicall
y.

26. Also known as “ Periostitis ossificans” & “Garre’s osteomyelitis”.
It represents a periosteal reaction to the presence of inflammation.
Affected periosteum forms several rows of reactive vital bone that
parallel each other & expand surface of altered bone.
The spread of low-grade, chronic apical inflammation through cortical
bone
Periosteal reaction occurs
Stimulates proliferative reaction of periosteum

27. Periostitis

29. 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.

30. Parallel rows of highly
cellular & reactive woven
bone .
Trabeculae are
frequently oriented
perpendicular to surface.
Trabeculae sometimes
form an interconnecting
meshwork of bone.
Between trabeculae,
uninflammed fibrous
tissue is evident.

31. Radiopaque laminations
of bone roughly parallel
each other & underlying
cortical surface.
Laminations may vary
from 1-12 in number.
Radiolucent separations
often are present between
new bone & original
cortex.

32. • Histopathology:
Fibro-osseous microscopic
feature

33. Removal of
infection.
After infection
has resolved,
layers of bone
will consolidate
in 6-12 months .

34. • Definition :
• Osteoradionecrosis is defined as an exposure of
nonviable,nonhealing,nonseptic lesion in
irradiated bone which fails to heal with out
intervention.
• It is characterized by presence of exposed bone
for a period of at least 3 months occurring at
any time after delivery of radiation therapy.

35. • Osteoradionecrosis (ORN), also known as post
radiation osteonecrosis (PRON).
• Doses above 50Gy usually are required to cause
irreversible damage.

36. Therapeutic doses of irradiation
Endothelial death, thrombosis &
hyalinsation of blood vessels .
Progressive obliterative endarteteritis
hyalinisation & fibrosis & thrombosis of vessels

37. Decreased microcirculation
Osteoblasts & osteocytes are destroyed & marrow spaces in
bone become filled with fibrous tissue .
Decrease of cellularity & vascularity
Hypoxia in irradiated tissue
CONT.

38. PATHOPHYSIOLOGY OF OSTEORADIONECROSIS
 Marx 1983 …...
Osteoradionecrosis - cumulative tissue damage
induced by radiation rather than trauma or
bacterial invasion of bone.
Complex metabolic and tissue homeostatic
deficiency seen in hypocellular, hypovascular, and
hypoxic tissue.
Three "H" principle.

39. WHY MANDIBLE AT AN INCREASED RISK?
 Generally a bone – with more tenuous blood supply and more
mechanically stress - more susceptible to the development of
osteoradionecrosis.
 The craniofacial skeleton receives its blood supply in three
distinct manners:
1. vessels that enter the bone via direct muscular attachments,
2. periosteal perforators, and
3. intramedullary vessels

40. Types of osteoradionecrosis
 SPONTANEOUS ORN (39%) – degradative function
exceeds new bone production.
 TRAUMA INDUCED ORN (61%) – reparative capacity of
bone is insufficient to overcome an insult.
 Bone injury can occur through direct trauma -
1. tooth extraction [84%],
2. related cancer surgery or biopsy [12%],
3. denture irritation [1%]) or
4. by exposure of the oral cavity to the environment
secondary to overlying soft tissue necrosis.
Remy H Blanchaert, Jr, MD, DDS, Osteoradionecrosis of the Mandible
eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Head
And Neck Oncology

41.  By Marx(1983)
Type I – Develops shortly after radiation,
Due to synergistic effects of surgical
trauma and radiation injury.
Type II – Develops years after radiation and follows a trauma
Rarely occurs before 2 year after treatment &
commonly occurs after 6 years.
Due to progressive endarteritis and vascular effusion.

42.  Type III
Occurs spontaneously without a preceding a traumatic event.
Usually occurs between 6 months and 3 years after radiation.
Due to immediate cellular damage and death due to radiation
treatment.

43.  Radiation factors
 Tumor factors
 Dental factors
 Others

44.  Severe , deep , boring pain which
may continue for weeks or
months .
 Swelling of face when infection
develops
 Soft tissue abscesses &
persistently draining sinuses .
 Exposed bone ; in association with
intraoral or extraoral fistulae .
 Trismus .

45.  Foetid odour .
 Pyrexia .
 Pathological fracture
Radilucent area with indefinite
nonsclerotic border
Radioopacity usually associated with
sequestrum

46. Bone necrosis follow irradiation
of oral malignancy
Endarteritis obliterans and thrombosis
of inferior dental artery
Bone sterile and more susceptible for
infection
Osteo-radionecrosis

47. Debridement
Antibiotics
Hydration of the patient
High protien & vitamin diet
 Analgesics
 Maintenance Of Good Oral hygiene-oral rinse

48.  Frequent irrigation of wounds
 Loose exposed dead bone is removed
 Sequestrectomy
 Bone resection if there is persistant infection or
pathologic #
 Hyperbaric o2 therapy

49. HYPERBARIC OXYGEN THERAPY
 DEF:Breathing of 100% oxygen through a face mask or hood
in a monoplace or large chamber @ 2.4ATP , for 90 min
session/dives for as many as 5 days a week totaling 30 more
sessions often followed by another 10 or more session.

50. REFRENCES:
• J.V. SOAMS 4TH EDITION.
• NEVILLE & DAM 3RD
EDITION.
• R.A. CAWSON 8TH EDITION.
• GOOGLE FOR IMAGES.