1) Osteomyelitis and osteoradionecrosis of the jaw bones are inflammatory conditions that can develop due to infections, trauma, radiation therapy or bisphosphonate use. 2) They are characterized by necrosis of bone tissue which fails to heal properly and can lead to exposed bone, pain, swelling and draining fistulas. 3) Treatment involves controlling infections, relieving pain, removing devitalized bone tissue surgically if needed, and reconstructing the affected area with grafts or flaps. Preventing these conditions involves minimizing invasive dental procedures for those at high risk.

1. OROFACIAL INFECTION
CHAPTER 3
OSTEOMYELITIS OF THE JAW
BONES
DR. HAYDAR MUNIR SALIH
BDS, PHD (BOARD CERTIFIED)

2. Osteomyelitis
 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. Predisposing Factors
1. Conditions that alter host defenses such as
diabetes mellitus and severe anemia
2. Conditions that alter vascularity of bone
therapeutic irradiation, osteoporosis, Paget’s disease
3. Virulence of organisms

4. Etiology
1. primary Odontogenic infections: originating from
pulpal or periodontal tissues
2. Trauma: It is the second leading cause: (a)
Especially, compound fracture, and (b) Surgery-
iatrogenic
3. Infections of orofacial regions : Periostitis
following gingival ulceration
4. Infections derived by hematogenous route:
wound on the skin

5. Blood supply of mandible
mandibular vascular
support as being provided
through multiple arterial
loops from a single major
vessel, which renders
large portion of bone
susceptible to necrosis
with the occurrence of
major vessel infectious
thrombosis.

6. Osteomyelitis in maxilla is rare!
(i) Extensive blood supply and
significant collateral blood flow in
midface,
(ii) Porous nature of membranous
bone,
(iii) Thin cortical plates, and
(iv) Abundant medullary spaces

8. Hudson’s classification of Osteomyelitis of
the jaws
1. Acute forms of OML
a. Contiguous focus
b. Progressive
c. Hematogenous
2. Chronic forms of OML
a. Recurrent multifocal
b. Garre’s
c. Suppurative or nonsuppurative
d. Diffuse sclerosing

9. Acute Pyogenic OML (Acute
Suppurative OML)
 It may have the appearance of a typical odontogenic
infection.
 It can be localized and widespread, with extensive
sequestration and possible pathological fracture
 Occurrence: In adults, it is more common in mandible
and involves alveolar process, angle of mandible,
posterior part of ramus and coronoid process

10. Clinical features
 Deep seated boring, continuous intense pain in
the affected area
 Intermittent paresthesia or anesthesia of the
lower lip
 Teeth in involved area begin to loosen and
become sensitive to percussion
 Trismus
 Alveolar abscess

11. Clinical features

12. Chronic Osteomyelitis
It can be
(a) primary: resulting from organisms which are
less virulent, and
(b) secondary: occurring after acute OML,
when the treatment did not succeed in
eliminating the infection.

13. Clinical Features
(1) Pain and tenderness: the pain is minimal,
(2) Non- healing bony and overlying soft tissue wounds with
induration of soft tissues,
(3) Intraoral or extraoral draining fistulae,
(4) Thickened or “wooden” character of bone,
(5) Enlargement of mandible, because of deposition of
subperiosteal new bone.
(6) Pathological fractures may occur,
(7) Teeth in the area tend to become loose and sensitive to
palpation and percussion.

14. Clinical Features

15. Radiographic findings
occur only 3 weeks after initiation of OML
process. It is generally accepted that 30 to 60
percent of mineralized portions of bone must
be destroyed before significant radiographic
changes are noted. Therefore, in early stages,
history and clinical features constitute the sole
data upon which diagnosis can be made.

16. In early stage, there is
widening of marrow
spaces, and enlargement
of Volkmann’s canals,
which imparts a
“mottled appearance”.

17.  The granulation tissue between living and dead bone produces
irregular lines and zones of radiolucency. This results in
characteristic “moth-eaten appearance” of established OML.

18.  The gradual resorption around periphery of infarcted area of bone
separates it off as a sequestrum. Such a devitalized piece of bone
appears sclerosed and becomes a foreign body which is called as
sequestrum.

19.  Subperiosteal new bone, can be seen as a fine linear opacity, or as a
series of laminated opacities, like an onion skin, parallel to surface of
cortex. This is seen at the lower border. This adds to loss of radiological
definition of original underlying bone structure. Where new bone is
superimposed upon that of jaw, a delicate “fingerprint” or “orange-
peel” appearance is seen.

20. Conservative management
(1) Complete bed rest,
(2) Supportive therapy,
(3) Dehydration,
(4) Blood transfusion,
(5) Control of pain,
(6) IV antimicrobial agents,
(7) Postoperative care,
(8) Hyperbaric oxygen (HBO therapy), and
(9) Special treatment for specific needs.

21. Surgical management:
Saucerization & decortication

22. Surgical management:
Sequestrectomy

23. Surgical management: resection of
the jaw with or without bone graft

24. OSTEORADIONECROSIS OF THE
FACIAL BONES
Osteoradionecrosis (ORN) is an exposure
of nonviable, non- healing, non septic
lesion in the irradiated bone, which fails to
heal without intervention.

25. Marie Curie
1898

26. Wonder cure

27. Wonder cure

28. Etiopathology (Pathological Changes)
The ‘Three H’ principle of irradiated tissue.
(i) Hypocellularity,
(ii) Hypovascularity of the irradiated tissues and
(iii) Hypoxia.
This comprises of all the elements of bone; including
marrow and periosteum, as well as the investing soft
tissues.

29. Etiopathology (Pathological Changes)
 The hypoxic tissue, when damaged, is unable to
respond metabolically to the injury.
 Due to hypoxia, the injured tissue macrophages are
unable to phagocytose bacteria or dead tissue in
wounds, fibroblasts fail to lay down new collagen and a
chronic non healing wound develops. (Wound, whose
oxygen and metabolic requirements for healing exceed
the available supply).

30. Clinical features
(1) Severe, deep, boring pain which may continue for weeks or
months. (2) Swelling of face when infection develops,
(3) Soft tissue abscesses and persistently draining sinuses,
(4) Exposed bone; in association with intraoral or extraoral fistulae,
(5) Trismus,
(6) Fetid odor,
(7) Pyrexia,
(8) Pathological fracture may be present.

31. Clinical features

32. Treatment
1. Debridement.
2. Control of infection:
3. Hospitalization.
4. Other supportive treatment: e.g. Hydration
5. Analgesics:
6. Good oral hygiene:
7. Frequent irrigations of wounds.
8. Exposed dead bone:
9. Treatment of small areas by drilling multiple holes into vital bone is
recommended
10. Sequestrectomy,
11. Hyperbaric oxygen therapy is a useful adjunct

33. Osteoradionecrosis: Surgical
management

34. Osteoradionecrosis: Surgical
management

35. Hyperbaric oxygen therapy

36. Treatment
 12. In advanced or refractory cases of ORN
(pathological fracture, orocutaneous fistula)
surgical treatment, at present, remains the
only treatment option available

37. Osteoradionecrosis case report :
clinical presentation case

38. Osteoradionecrosis case report:
radiograph

39. Osteoradionecrosis case report:
surgical management

40. Free flap
reconstruction of
osteoradionecrosis

43. Prevention of ORN
Pre-irradiation Dental Care
1. Extraction of teeth: The teeth in direct beam of radiation should be
extracted; which include:
(i) nonrestorable teeth, (ii) teeth with considerable periodontal disease,
(iii) patients with poor oral health and motivation. The radiation therapy
is delayed by 10 to 14 days to allow for initial healing.
2. The prominent interdental septa, sharp socket margins should be
trimmed
3. Unerupted and deeply buried teeth are best left in situ.
4. Restoration of teeth: The remaining teeth should be restored and
periodontal therapy should be completed in this two week period

44. Post-irradiation Dental Care
1. Avoidance of dentures: The dentures should not be worn in the
irradiated jaw for one year after therapy.
2. Maintenance of oral hygiene.
3. Application of topical fluoride as for pre-irradiation care.
4. Extraction as a last resort: The number of necessary extraction
should be limited to a minimum of one or two per appointment.
Teeth should be removed a traumatically. Sharp bony margins should
be trimmed off, without raising extensive flaps. Extractions to be done
under antibiotic prophylaxis.

45. Bisphosphonates
 Bisphosphonates are a class of agents used to treat
osteoporosis and malignant bone metastases.
Bisphosphonates inhibit bone resorption and, thus,
bone renewal by suppressing the recruitment and
activity of osteoclasts thereby shortening their life
span
 Besides osteoporosis, bisphosphonates are used to
manage Paget’s disease of bone and hypercalcemia
of malignancy. Bisphosphonates are given to patients
with cancer to help control bone loss resulting from
metastatic skeletal lesions

46. Bisphosphonates

47. Bisphosphonates
 The mechanism of action of bisphosphonates is
that they bind to bone mineral, where they are
concentrated and accumulate over time.
Bisphosphonates are potent inhibitors of
osteoclastic activity, and this is why they are
usually prescribed
 Depending on the duration of the treatment
and the specific bisphosphonate prescribed, the
drug may remain in the body for years

48. BISPHOSPHONATE
OSTEORADIONECROSIS
OF THE JAW

49. Mechanism of BOJ
As a result, bone turnover becomes profoundly
suppressed, and over time, bone shows little
physiologic remodeling Bone becomes brittle and
unable to repair physiologic microfractures that
occur in the human skeleton with daily activity
Patients receiving bisphosphonates intravenously
clearly are more susceptible to BOJ than are those
receiving the drug orally.

50. Clinical Signs and Symptoms of BOJ
 The most common clinical presentation associated with BOJ is an
ulcer with exposed bone in a patient who has had a dental extraction
 Similar to osteoradionecrosis, in the early stages of oral BOJ, no
radiographic manifestations can be seen
 Patients may be asymptomatic but may have severe pain because of
the necrotic bone becoming infected secondarily after it is exposed
to the oral environment
 The osteonecrosis often is progressive and may lead to extensive
areas of bony exposure and dehiscence
 Often, a purulent discharge and local swelling occur in adjacent soft
tissue, with trismus and regional lymphadenopathy.

52. Dental Care for Patients Who Are
Taking Bisphosphonates
 The treatment of patients receiving oral or intravenous
bisphosphonate therapy is principally preventive
 Extraction of teeth should be avoided, when possible.

53. Role of Orally Administered
Alendronate
 At this time, it appears that the incidence of BOJ
manifesting in patients taking alendronate for
osteoporosis is 1 : 1000 to 1 : 1,700
 One thing that can be done when contemplating an
invasive procedure on a patient taking an oral
bisphosphonate is withdrawing the medication for a
period (“drug holiday”).

54. Dental Care for Patients with BOJ
 For patients with established lesions of BOJ, the goal is
to get the patient comfortable because it is likely the
patient will have to live with the exposed bone. T
 reatment should be directed at eliminating or
controlling pain and preventing progression of the
exposed bone
 If the exposed bone has sharp edges that are irritating
adjacent soft tissue, the sharp edges of bone may be
eliminated by using a rotating diamond bur