2. OSTEORADIONECROSIS (ORN)
Ewing was the first to use the term ‘radiation
osteitis’ to describe changes in bone after
radiotherapy.
In the following years, several terms were used to
name these changes in bone, such as radiation
osteitis, ORN and avascular bone necrosis.
3. In 1974, Guttenberg proposed the term ‘septic
ORN of the mandible’ to describe the stage of
necrosis when irradiated bone becomes
superficially infected, ending up with a high risk
of involvement of deeper structures.
4. In 1983, Marx defined ORN as ‘an area >1 cm of
exposed bone in a field of irradiation that failed
to show any evidence of healing for at least 6
months’. Marx also reported that superficial
contamination and no interstitial infection was
present.
In 1987, Marx and Johnson suggested the
definition of ORN as: ‘The exposure of nonviable
bone which fails to heal without intervention’.
5. Epstein et al. defined ORN as ‘an ulceration or
necrosis of the mucous membrane, with exposure
of necrotic bone for more than 3 months’.
Widmark et al. described ORN as ‘a non-healing
mucosal or cutaneous ulcer with denuded bone,
lasting for more than 3 months’.
6. Wong et al. defined ORN as ‘a slow-healing
radiation-induced ischemic necrosis of variable
extent occurring in the absence of local primary
tumor necrosis, recurrence or metastatic disease’.
7. Classification system of osteoradionecrosis (ORN)
The Notani classification, is quickly applicable to
all cases of mandibular osteoradionecrosis (ORN)
after clinical examination and orthopantogram:
Notaniclass Clinical features
Stage I ORN confined to dentoalveolar bone
Stage II
ORN limited to dentoalveolar bone or mandible above
the inferior dental canal, or both
Stage III
ORN involving the mandible below the inferior dental
canal, or pathological fracture, or skin fistula
8. Epstein et al. classification of osteoradionecrosis
Type I
Resolved, healed
(A) No pathologic fracture
(B) Pathological fracture
Type II
Chronic persistent (nonprogressive)
(A) No pathologic fracture
(B) Pathological fracture
Type III
Active progressive
(A) No pathologic fracture
(B) Pathological fracture
9. Lyons et al. classification of osteoradionecrosis
Stage Description
1
<2.5 cm length of bone affected (damaged or exposed);
asymptomatic. Medical treatment only.
2
>2.5 cm length of bone; asymptomatic, including pathological
fracture or involvement of inferior dental nerve or both.
Medicaltreatment only unless there is dental sepsis or obviously
loose, necrotic bone.
3
>2.5 cm length of bone; symptomatic, but with no other features
despite medical treatment. Consider debridement of loose or
necroticbone, and local pedicled flap.
4
2.5 cm length of bone; pathological fracture, involvement of
inferior dental nerve, or orocutaneous fistula, or a combination.
Reconstruction with free flap if patient’s overall condition allows
10. Clayman introduced a classification of ORN related
to the integrity of the overlying mucosa. According
to this classification:
Type I includes cases of ORN in which bone lysis
occurs under intact gingiva or mucosa.
Type II includes more aggressive cases of ORN in
which soft tissues break down and the bone is
exposed to saliva, causing secondary
contamination. This is defined as radiation
osteomyelitis.
11. Coffin divided cases of ORN into two groups:
Minor.
Major.
Morton and Simpson subdivided ORN into three
groups –
Minor.
Moderate.
Major.
12. In 1983, Marx proposed a three-stage system
for ORN:
Stage I- If they exhibit exposed bone in a field of
radiation that has failed to heal for at least 6
months and do not have a pathological fracture,
cutaneous fistula or osteolysis to the inferior
border.
13. In Stage I, all patients receive 30 sessions of HBO at
2.4 atmospheres absolute for 90 minutes at depth.
Patients who respond to HBO alone demonstrate a
softening of the radiated tissues and spontaneous
sequestration of exposed bone with formation of
granulation tissue.
Each Stage I responder undergoes an additional 10
HBO sessions and then the tissues are allowed to
heal completely.
14. Stage II patients are those who do not respond to
the 30 sessions of HBO. This group is characterised
by a large amount of non-viable bone that makes
resorption and sequestration from HBO-induced
angiogenesis alone impossible.
Stage III patients are characterised by having a
large quantity of non-viable bone and/or soft tissue
unable to be managed by HBO-induced angiogenesis
alone or HBO combined with local sequestrectomy.
15. Factors that affect the development of ORN
Primary site of tumor.
Posterior mandible is more commonly affected
by ORN because of its compact and dense nature.
Proximity of tumor to bone.
Extent of mandible included in primary radiation
field.
State of dentition—odontogenic and periodontal
disease.
Poor oral hygiene.
Radiation dose>60 Gy.
16. Use of brachytherapy.
Nutritional status.
Concomitant chemo-radiation.
Ill-fitting tissue borne prosthesis resulting in
chronic trauma.
Acute trauma from surgical procedures to the
jaw.
Advanced stage tumors.
17. Pathogenesis of ORN
ORN affects the small blood vessels of bone,
inducing inflammation (endarteritis), which favors
the generation of small thrombi that obliterate the
vascular lumen and thus interrupt tissue
perfusion.
Radiation therapy produces an increase in free
radicals and alters collagen synthesis.
18. The bone loses its normal cellularity and undergoes
fibrosisatrophy with impairment of its repair and
remodeling capacity.
Under such conditions even minimal external
trauma causes ulceration, facilitating
contamination and infection and thus favoring bone
necrosis.
19. Clinical features of ORN
Mandible more commonly affected than maxilla due
to:
Maxilla rich vascular supply.
Absence of dense cortical plates in maxilla.
Most lesions are perimandibular.
20. Posterior mandible affected more readily than
anterior because posterior part of mandible is more
frequently in the direct field of radiation.
Initially: Trismus, fetid breath, increased
temperature.
Discomfort or tenderness at the site.
Bad taste.
Paresthesia and anesthesia.
Loss of mucosal covering and exposure of bone.
Exposed bone is gray to yellow in colour.
21. Exposed bone has a rough surface texture that
abrades the adjacent soft tissues and causes
further discomfort.
Necrosis of exposed bone.
Tissues surrounding the exposed bone may be
indurated and ulcerated from infections or
recurrent tumors.
Formation of sequestra.
Intense pain with intermittent swelling and
drainage extraorally.
22. Radiological findings
ORN is not usually detectable radiographically in
early stages.
The described radiographic features range from
normal appearance, to localised osteolytic areas,
extensive osteolytic areas, sequestra and fracture.
23. The most definitive radiographic alterations in early
disease are increased radiodensity, as well as a
mixed radioopaque/radiolucent lesion in which
radiolucent areas represent bone destruction.
In Orthopantomogram (OPT) ORN is depicted as an
undefined radiolucency, without sclerotic
demarcation, which surrounds necrotic zone.
24. Radiopaque areas can be identified when bone
sequestra are formed. In order to be visible in an
OPT, a substantial alteration in mineral content and
extensive involvement of bone is required and this
only occurs in later stages of ORN.
CT shows osseous abnormalities, such as focal lytic
areas, cortical interruptions and loss of the
spongiosa trabeculation on the symptomatic side,
frequently accompanied by soft-tissue thickening.
25. In MRI with gadolinium administration, an abnormal
marrow signal, cortical destruction and slight-to-
mild irregular enhancement is demonstrated. MRI
has the advantage of excellent tissue contrast and
high spatial resolution.
Scintigraphy using 99mTc- marked diphosphonates
(99mTc-MDP) allows highly sensitive depiction of
mandibular lesions as a result of their altered
phosphate metabolism.
26. Dental management of ORN
Pre- irradiation dental care:
The non-restorable teeth should be extracted a
traumatically under antibiotic coverage.
Sufficient time to be given for proper healing 7-14
days.
Judicious alveoloplasty to be done to permit linear
closure of mucoperiostium.
All sharp bony margins to be contoured because the
irradiated bone does not remodel spontaneously.
27. All restorable teeth to be restored.
Periodontal therapy to be completed within this 2
weeks interval.
Oral hygiene maintenance instructions.
Application of fluoride in custom made trays:
1- 0.4% Stannous fluoride gel.
2- 1% sodium fluoride gel.
3- 1% acidulated fluorophosphate gel.
28. Post- irradiation dental care:
Denture not to be used in irradiated arch for 1 year
after radiotherapy.
Saliva substitute to lubricate the mouth because of
decrease flow from irradiated mucous and salivary
gland.
Pilocarpine used to stimulate flow if residual
salivary gland function present.
29. If pulpitis develops, endodontic therapy to be
started, care taken during instrumentation.
Necessary extraction, limited to 1 or 2 teeth per
appointment.
30. Management of ORN
When ORN develops:
Avoid mucosal irritants.
Discontinue the use of dental appliances.
Maintain nutritional status.
Stop smoking and alcohol consumption.
Topical antibiotic (tetracycline) and Antiseptic
(chlorhexidine) rinses may reduce the potential local
irritationfrom the microbial flora.
31. For chronic persisting ORN:
Local wound care:
Penicillin V 500 mg QID X 7 days with
Metronidazole 400 mg QID X 7 days.
or
Clindamycin 300 mg TID X 7days.
Topical tetracycline rinses.
Antiseptic mouthwashes (Chlorhexidine).
Hyperbaric oxygen if needed.
32. For active progressive ORN:
Appropriate analgesia should be provided.
HBO (hyperbaric oxygen)therapy: 20 to 30dives at
100% oxygen and 2 to 2.5 atmospheres of pressure
for 90 minute sessions, five times a week followed by
additional 10 dives.
33. Bone resection:
Sequestra managed by resectioning of the segment
of involved bone to prevent occurrence of radiation
compromised skin.
Mandible reconstructed to provide continuity for
esthetic and function.
34. Ultrasound Therapy:
Non thermal effects used in the stimulation of tissue
regeneration, healing of varicose ulcers, pressure
sores, blood flow in chronically ischemic muscles,
protein synthesis in fibroblasts and tendon repair.
35. Hyperbaric Oxygen?
It is the oxygen under increased tension.
HBO therapy consist of breathing 100% oxygen
through a face mask or hood in a monoplace or a
large chamber at 2.4 absolute atmospheric pressure
for 90 minutes sessions (dive) for as many as 5 days
a week totaling 30 or more sessions often followed by
10 additional dives, post surgically.
36. Effects of Hyperbaric Oxygen (HBO)
Increased arterial and venous oxygen tension. The
additional O2 is carried in physical solution in the
plasma.
O2 at high tension enhances the healing by a direct
bacteriostatic effect on the microorganisms that
renders them susceptible to lower antibiotic
concentrations and also enhancing the phagocytic
killing.
37. Hyperbaric Oxygen (HBO) stimulates:
Neoangiogenesis.
Fibroblastic proliferation
Collagen synthesis.
Proliferation of granulation tissues increases and
advances from increased O2 tension from the non-
diseased periphery into the necrotic bone.
As resorption and replacement of devitalized bone
with healthy tissue progress, formation of sequestra
that may undergo resorption is enhanced.
38. Indications for prophylactic use of HBO
When surgery is required after radiotherapy.
When patient is at high risk due to high dose
radiation to the bone with a high biologic effect
(Time-Dose Fraction>109).
When extensive surgery is required.
39. Limitations of HBO therapy
Limited facilities.
Expensive
O2toxicity.
Seizures.
High pressure nervous syndrome.
Trigger Point Injections.
Decompression sickness.
Pneumothorax.
Arterial gas embolism.
Tooth and sinus pain.
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