This is a presentation on Osteomyelitis of facial skeleton from a point of view of an Oral & Maxillo-Facial Surgeon

1. OSTEOMYELITIS
MODERATOR: Dr (Col) Suresh Menon
PRESENTER : Dr. Rayan M

2. CONTENTS
• DEFINITION
• HISTORY
• PREDISPOSING FACTORS
• PATHOGENESIS
• ETIOLOGY
• CLASSIFICATION
• MICRORGANISMS
• CLINICAL FEATURES AND DISTRIBUTION
• INVESTIGATIONS
• SURGICAL MANAGEMENT
• REFERENCES

3. Osteomyelitis
Osteon means bone; Muelinos means marrow; itis means inflammation
• Extensive inflammation of the bone involving the bone marrow, cortex and
periosteum.
• The term “osteomyelitis” is mostly used to describe a true infection of the bone
induced by pyogenic microorganisms (Marx 1991)

4. History
• The prevalence, clinical course, and management of osteomyelitis of the jawbones
have changed profoundly over the past 50 years.
• This is due to mainly one factor: the introduction of antibiotic therapy, specifically
penicillin.
• In the preantibiotic era, the classical presentation of jawbone osteomyelitis was an
acute onset, usually followed by a later transition to a secondary chronic process
(Wassmund 1935; Axhausen 1934)

5. Predisposing Factors
Systemic, metabolically compromised individuals who can be categorized into the
following subsets:
a. Age of patient
b. Malnutrition
c. Immunosuppression
d.Congenital or acquired pathophysiology disrupting microvascular perfusion of the
calcified tissue structure and investing soft tissue envelope
Osteomyelitis of the Jaws:A 50-Year Perspective; J Oral Maxillolac Surg
51:1294·1301,1993

6. Etiology
• Odontogenic infection – periodontal ,periapical, pericoronal.
• Infection from infected dental cyst.
• Compound fracture of Jaw.
• Traumatic injury.
• Middle ear infection & upper respiratory tract infection through haematogenous route.
• Furuncle of chin by lymphtic route.
• Peritonsillar abscess

7. Local factors
• Long standing carious lesions
• Periodontal diseases (which leads to the breakdown of the periodontal barrier membrane.
• Neonatal, tooth germ associated
• Maxillary sinusitis
• Trauma/ Fracture
• Implant / Foreign body induced
• Radiation
• Other odontogenic infections

8. Pathogenesis
Local and
systemic host
immunity; local
tissue perfusion
Number and
virulence of
pathogens

9. Pathogenesis
Acute inflammation
(edema & pus formation)
Increased intramedullary
pressure
Vascular collapse
(stasis, ischemia of bone)
Avascular bone
Pus, organism extension
Haversian system/ nutrient
canal involvement
Elevation of periosteum
Disrupted blood supply
Avascular infected bone
OSTEOMYELITIS
A
B

10. Infection from the pulp extends into the periapical region
PULPITIS
Acute Chronic
APICAL PERIODONTITIS
PERIAPICAL ABSCESS PERIAPICAL GRANULOMA
Acute Chronic
PERIAPICAL CYST
OSTEOMYELITIS
PERIOSTITIS

11. Effectiveness of host defense
Effectiveness of therapy
Inflammation regresses
Granulation tissue forms
New blood vessels form
Lyse & separate the necrotic
bone
Sequestrum
Large sections of bone gets
embedded within granulation
tissue & encased in a sheath of
new bone – Involucrum
Involucrum is penetrated by
channnels through which pus
escapes to an epithelial surface -
Cloacae

12. MAY BE LYSED
COMPLETELY
MAY BE
REVASCULARISED
REMAIN
QUIESCENT
GET INFECTED
SURGICAL
REMOVAL
Fate of sequestrum

13. Micro organisms
Gram positive organism
• Staphyloccous areus
• Staphyloccous albus
• Haemolytic Streptococci
Gram Negative organism
• Klebsiella
• Pseudomonas
• Proteus
• E. coli

14. Systemic factors altering host immunity
• Diabetes mellitus
• Autoimmune disorders
• AIDS
• Agranulocytosis
• Anemia (especially sickle cell)
• Leukemia
• Malnutrition
•Chemotherapy
• Corticosteroid and other
immunosuppressive therapy
• Alcohol and tobacco
• Drug abuse

15. Disease Mechanism facilitating bone infection
Diabetes Diminished leukocyte chemotaxis, phagocytosis; diminished vascularity of tissue
due to vasculopathy, thus reducing perfusion and the ability for an effective
inflammatory response; slower healing rate
Leukemia Deficient leukocyte function and associated anaemia
Malnutrition Reduced wound healing and reduction of immunological response
Cancer Reduced wound healing and reduction of immunological response
Osteopetrosis Reduction of bone vascularization due to enhanced mineralization, replacement of
hematopoietic marrow causing anaemia & leukopenia
Severe anemia Systemic debilitation, reduced tissue oxygenation, bone infarction (sickle cell),
especially in patients with a homozygous anaemia trait
AIDS Impaired immune response
Immunosuppr-
ession
Impaired immune response

16. Classifications
• Classification based on pathogenesis – Waldvogell
• Dual classification based on pathological anatomy and pathophysiology - Cierny
• Classification based on clinical picture, radiology, pathology, and etiology - Topazian RG
• Clinical appearance and course of the disease, as well as on radiological features - Zurich
Classification System

17. Waldvogell
• Hematogenous osteomyelitis
• Osteomyelitis secondary to a contiguous focus of infection
• Osteomyelitis associated with or without peripheral vascular disease
Waldvogell, F.A., Medoff, G. and Swartz, M.N.Osteomyelitis: a review of clinical
features, therapeutic considerations and unusual aspects. N Engl J Med
282:198–266, 316–322, 1970.

18. Cierny
• Anatomic Types
Stage I: medullar osteomyelitis –involved medullary bone without cortical
involvement; usually hematogenous
Stage II: superficial osteomyelitis –less than 2 cm bony defect without cancellous bone
Stage III: localized osteomyelitis– less than 2 cm bony defect on radiograph, defect
does not appear to involve both cortices
Stage IV: diffuse osteomyelitis – defect greater than 2 cm. Pathologic fracture,
infection, nonunion
• Physiological class
A host: normal host
B host: systemic compromised host, local compromised host
C host: treatment morbidity worse than disease,low prognosis
Ciney G, Mader JT, Pennick H : A clinical staging system of adult osteomyelitis, Contemp Orthop 10:17, 1985

19. Topazian
I. Suppurative osteomyelitis
1. Acute suppurative osteomyelitis
2. Chronic suppurative osteomyelitis
– Primary chronic suppurative osteomyelitis
– Secondary chronic suppurative osteomyelitis
3. Infantile osteomyelitis
II. Non suppurative osteomyelitis
1. Chronic sclerosing osteomyelitis
– Focal sclerosing osteomyelitis
– Diffuse sclerosing osteomyelitis
2. Garre's sclerosing osteomyelitis
3. Actinomycotic osteomyelitis
4. Radiation osteomyelitis and necrosis
Topazian RG Osteomyelitis of the Jaws. In Topizan RG, Goldberg MH (eds): Oral and Maxillofacial Infections.Philadelphia, WB Saunders
1994,Chapter 7, pp 251-88

20. Zurich
1. Acute Osteomyelitis (AO)
2. Secondary Chronic Osteomyelitis (SCO)
3. Primary Chronic Osteomyelitis (PCO)
Acute
Osteomyelitis
Secondary Chronic
Osteomyelitis
Primary Chronic
Osteomyelitis
• Neonatal, tooth germ associated
• Trauma/fracture related
• Odontogenic
• Foreign body, transplant/implant induced
• Associated with bone pathology and/ or systemic disease
•Early onset
(juvenile chronic osteomyelitis)
• Adult onset
• Syndrome associated

21. Hudson’s
I. Acute forms of osteomyelitis (suppurative or nonsuppurative)
A. Contagious focus
1. Trauma
2. Surgery
3. Odontogenic Infection
B. Progressive
1. Burns
2. Sinusitis
3. Vascular insufficiency
C. Hematogenous (metastatic)
Developing skeleton (children)

22. II. Chronic forms of osteomyelitis
A. Recurrent multifocal
1. Developing skeleton (children)
2. Escalated osteogenic (activity< age 25 years)
B. Garrè's
1. Unique proliferative subperiosteal reaction
2. Developing skeleton (children and young adults)
C. Suppurative or non suppurative
1. Inadequately treated forms
2. Systemically compromised forms
3. Refractory forms (chronic recurrent multifocal osteomyelitis CROM)
D. Diffuse sclerosing
1. Fastidious micro organisms
2. Compromised host/pathogen interface

23. Distribution
• Mandible > maxilla
• Mandible – body > symphysis > angle > ascending ramus > condyle

24. Clinical features
Acute suppurative osteomyelitis
• Deep intense pain
• High intermittent fever
• Hypoesthesia
• Clinical abscess/pus formation
• Clearly identifiable cause
• Exposure of bone
• Swelling is minimal
• Lymphadenopathy

25. •Subacute suppurative osteomyelitis
• Deep pain, malaise, fever, anorexia
• Teeth loosen – sensitive to percussion
• Pus exudes around gingival sulcus/fistula
• Fetid odour
• Firm cellulitis of cheek
• Expansion of bone from increased periosteal activity
• Erythema, abscess formation, tenderness on palpation
• Paresthesia
• Trismus – not always present
• Regional lymphadenopathy

26. • Chronic suppurative Osteomyelitis
• Multiple fistulae
• Induration of soft tissues
• Thickened /wooden character of the affected area with pain & tenderness on palpation
• In primary chronic osteomyelitis – no acute phase of infection
• Insidious in onset
• Slight pain
• Slow increase in jaw size
• Gradual development of sequestrum
• Often without fistulae

27. Infantile osteomyelitis

28. • Osteomyelitis Maxillaries Neonatarum, Maxillitis of infancy
• Osteomyelitis in the jaws of new born infants occurs almost exclusively in
maxilla.
• First described by Rees in 1847.
• Wilensky (1932) described it in comprehensive manner.
• McCash & Rowe – less common after introduction of antibiotics.
29

29. Etiology
• Trauma – through break in mucosa cause during delivery.
• Infection involving maxillary sinus
• Infection from the nose.
• Hematogenous spread through streptococci & pneumococci.
• Infected nipple – infected human or artificial nipple
30

30. Pathogenesis
• Main cause is said to be infection – especially with S. aureus.
• Hematogenous spread has been suggested from either a skin injury or pyogenic
infection of the middle ear, mastoid process, tonsils & even umbilical cord.
• Local causes may be small abrasions suffered at the time of delivery
31

31. Clinical features
• Illness is ushered in by fever, anorexia & intestinal disturbances.
• First sign is swelling or redness below the inner canthus of the eye.
• Followed by marked edema of the eyelids
• Alveolus & palate become swollen.
• In a day or so, this is followed by a pus discharge.
• Sinus formation below the inner canthus of the eye.
• Intraorally, swelling spreads across the palate with multiple draining sinuses along
the alveolar margin on affected side.
• With establishment of free drainage, a chronic stage ensues.
32

32. • Persists until sequestra & affected tooth buds are extruded or surgically removed.
• Among the extruded sequestra maybe the outer 1/3rd or 2/3rd of the inferior orbital
margin.
• Chronic suppuration may lead to residual permanent deformity of the maxilla, loss
of teeth & adherent scars below the eyelid.
• When recognized early and appropriate therapy instituted, the results are good.
33

33. Treatment
• Intravenous antibiotics, preferably penicillin.
• Culture & sensitivity testing
• Incision & drainage of fluctuant areas
• Sequestrectomy
• Supportive therapy
34

34. Acute osteomyelitis

35. Clinical features:
• Patient experiences deep seated, boring, continuous pain.
• Moderate sized indurated swelling forms over the affected region of jaw involving the
cheek.
• When mandible involved, loss of sensation occurs on lower lip on affected side due to
involvement of inferior alveolar nerve.
• Teeth become loose, tender on percussion
• Pus discharged through multiple sinuses in the alveolus or exudes along the necks of
teeth.
• Trismus – may be severe & serious in children.
• Fetid odour
• Regional lymphadenopathy usually present.
36

36. General features:
• Temperature of approx 100ºF.
• Following establishment of drainage, pain eases and temperature falls.
• If left untreated, death may occur due to septicemia, pneumonia, meningitis and
cavernous sinus thrombosis.
• Area of bone deprived of its blood supply becomes dead, sequestrum formation occurs
followed by pathologic fractures.
• New bone is produced alongside osteomyelitic area, rapid in children.
• Sometimes the entire jaw may be reconstituted in spite of massive death of original
bone.
• Other cases, jaw may fail to grow and permanent deformity ensues, especially if
condylar area affected.
37

37. Radiographic features
• Early stages mandible appears normal.
• Earliest radiographic change is that trabeculae in involved area are thin, of poor density
& slightly blurred.
• Subsequently multiple radiolucencies appear which become apparent on radiograph.
• In some cases there is saucer shaped area of destruction with irregular margins.
• Loss of continuity of lamina dura, seen in more than one tooth.
38

38. Chronic suppurative ostoemyelitis

39. • Commences as the acute condition subsides.
• In acute phase, degree of destruction of cortical plate depends on:
- Extent to which pus has spread beneath periosteum
- Virulence of the organisms concerned
• As soon as pus drains intra or extraorally, condition ceases to spread and chronic phase
commences.
• Infection is localized but persistent as bacteria are able to grow in dead bone inaccessible
to body’s defenses.

40. Clinical features
• Pain is mild and intermittent, temperature rarely elevated and WBC count may be
normal.
• Acute exacerbations occur at regular intervals; intense pain and swelling
accompanied by pyrexia.
• Lasts for 3 – 4 days, relieved when pus discharges.
• New bone formation leads to thickening causing facial asymmetry.
41

41. • Thickened or “wooden” character of bone.
• Self limiting, eventually cures itself as the last sequestra is discharged.
• Patient may be left with residual deformity of the jaw and multiple facial scars
where sinuses have discharged.
42

42. Radiographic Features
• Depends on the stage; early stage no changes seen.
• Trabeculae in the involved area become thin or appear fuzzy & then lose their
continuity.
• Eventually areas of bone destruction appear giving rise to characteristic mottling.
• After some time “moth eaten” appearance is seen
• Sequestra appear denser on radiographs.
43

43. Management
• 3D: Debridement, Drainage and Drug
• Sequestrum : if small exfoliates through mucosa
If large surgical removal

44. Chronic non-suppurative ostoemyelitis

45. Garre’s Osteomyelitis (Chronic Osteomyelitis with
Proliferative Periostitis)
• Chronic Non Suppurative Sclerosing Osteitis/ Periostitis Ossificans.
• Non suppurative productive disease characterized by a hard swelling.
• The infectious agent localizes in or beneath the periosteal covering of the cortex.
• Occurs primarily in young persons who possess great osteogenic activity of the
periosteum.
46

46. Clinical Features
• Uncommonly encountered, described in tibia and in the head and neck region, in the
mandible.
• Typically involves the posterior mandible & is usually unilateral.
• Patients present with an asymptomatic bony, hard swelling with normal appearing overlying
skin and mucosa.
• On occasion slight tenderness may be noted
47

47. • The increase in the mass of bone may be due to mild toxic stimulation of periosteal
osteoblasts by attenuated infection.
• Hypertrophy may represent an exuberant attempt at repair.
• When the existing cause becomes quiescent, the resultant mass undergoes remodelling.
• Boyd & Bell state the permanent thickening of bone.
48

48. Radiographic features
• Radiopaque laminations of bone that roughly parallel each other & the underlying
cortical surface.
• Laminations vary from 1 – 12 in number, radiolucent separations often are present
between new bone and original cortex. (“onion skin appearance”)
49

49. Management
• Consists of removal of the offending teeth or endodontic treatment
• Administration of an antibiotic.
• Regression of the periosteal reaction is expected over a period of time without any need for
surgical intervention.
• Bone curettage.
Kaushal Mahendra Shah, Amol Karagir, Shridevi Adaki: Chronic non- supperative osteomylities with proliferative periostitis or garre`s
osteomyelitis: BMJ (2013) 10, 114-115

50. Chronic diffuse sclerosing osteomyelitis

51. • Analogous to the focal form.
• Represents a proliferative reaction of bone to low grade infection.
• Portal of entry is not through carious infection but rather through diffuse
periodontal disease.

52. Clinical features
• May occur at any age, most common in older persons, especially in edentulous
mandibles.
• No gender predilection
• Insidious nature, presents no clinical indications of its presence.
• Acute exacerbation – vague pain, unpleasant taste, mild suppuration.
• Many times spontaneous formation of fistula seen opening onto mucosal surface
to establish drainage
53

53. Radiographic features
• Diffuse patchy, sclerosis of bone – “cotton wool” appearance
• Radiopacity may be extensive and bilateral.
• Due to diffuse nature, border between sclerosis & normal bone is often indistinct.
54

54. Actinomycotic osteomyelitis
• Cervicofacial actinomycosis is a slowly progressive infection with both
granulomatous and suppurative features.
• In secondary chronic osteomyelitis, infection with Actinomyces is mostly of
endogenous origin, since the pathogen is known to be an oral saprophyte,
present in periodontal pockets, carious teeth, tonsillar crypts.
• Spontaneous drainage of serous fluid containing granular material may occur.

55. Management
• Tretment should be vigorous.
• Removal of foci of infection.
• Resection of the sequestrated bone.
• Excision of all the granulation tissue until healthy tissue is exposed.
• Prolonged administration of antibiotics, preferably penicillin.
• Additional exposure time to antibiotic is necessary because lysis of Actinomyces species occurs at
slow rate.
Bahar Sezer et al: Actinomycosis osteomyelitis of the jaw: report of four cases and a review of the literature: Journal of Dental Sciences
(2017) 12, 301-307

56. Osteomyelitis associated with tuberculosis
• Osteomyelitis of the jaws can be caused by infection with Mycobacterium
tuberculosis
• The mechanisms of spread of infection are, in analogy to other osteomyelitis cases,
caused by other bacteria, by direct inoculation, through tooth-extraction sockets,
through any breach in the mucosa during tooth eruption, spread from adjacent soft
tissue sites, or by hematogenous spread.

57. Management
• Resection of the sequestrated bone.
• Anti tubercular therapy ( four conventional drug rifampicin, isoniazid, pyrazinamide and
ethambutol initially as an intensive regiment followed by rifampicine and isoniazid for a
period of 9-12 months)
• However WHO recommends a short course therapy of 6 months because of the pauci –
bacillary nature of the disease.
Parvaiz a. Koul et al: Tubercular osteomyelitis of the mandible in a young female: International journal of Mycobacteriology 3 (2014)
155 -157)

58. Principles of treatment
• Evaluation and correction of host defense
• Gram staining, culture and sensitivity
• Imaging
• Administration of empirical antibiotics
• Removal of loose teeth and sequestrum
• Culture guided antibiotics
• Possible placement of irrigating drains/antibiotic beads
• Surgical procedures

59. Investigations
• Hemogram
• Pus - Culture & Antibiotic sensitivity
• E.S.R. & C reactive protein may be seen.

60. Conventional radiographs
• 30-60% bone destruction required
• The orthopanoramic view is not useful in the initial evaluation of osteomyelitis.
• The ‘moth-eaten’ appearance of bone or sequestrum of bone, is the classic
appearance of osteomyelitis.

61. Imaging
• Radionuclide imaging – provides information based on reactive bone
• 99mTc – gets distributed in areas of increased blood flow
• 99mTc - confirms acute osteomyelitis
• Additional 67Ga study – distinguish from
neoplastic diseases.

62. CT and MRI
• CT shows increased attenuation in medullary cavity, destruction of cortical bone, new
bone formation and appearance of sequestra.

63. Investigations
Conventional Radiograph
+ve
Osteomyelitis
-ve
Osteomyelitis highly suspected
Technitium bone scan
+ve
Osteomyelitis
-ve
Osteomyelitis highly suspected
-ve
Osteomyelitis highly suspected
Ga scan
+ve
Osteomyelitis
MRI & CT
+ve
Osteomyelitis
-ve

64. • Complete bed rest
• Supportive therapy
Nutritional support High protein diet
High caloric diet
Adequate multivitamins
• Rehydration
Hydration orally
Administration of I.V fluids
• Blood transfusion
If RBC , Hb % are low
• Control of Pain
Analgesic and sedation
• Antibiotic therapy
Treatment

65. Antibiotic Regimen for Osteomyelitis of Jaw
Regimen 1: For in patients/ medically compromised patients
Aqueous penicillin, 2 million U IV q4h, plus metronidazole, 500mg, q6h
When improved for 48 to 78 hours, switch to:
Penicillin V, 500mg PO q4h, plus metronidazole 500mg PO q6h for 4 to 6 weeks
Or
Augmentin 1gm PO bid for 4 to 6 weeks

66. Regimen 2: For outpatients
Penicillin V, 2 g, plus metronidazole, 0.5g, q8h PO for 2 to 4 weeks after last
sequestrum removed and patient without symptoms
Or
Clindamycin 600 to 900 mg q6h IV, then:
Clindamycin 300 to 450 mg q6h PO

67. Local Antibiotic Therapy
Closed wound irrigation-suction
• Placement of tubes against the bone maybe
desirable to allow drainage of pus and
provide a route of irrigation
• Afferent tube is used to introduce irrigating
solutions into the desired area
• Efferent tube is used to suction out the pus
and fluids
• Irrigations are continued for one week until
three successive cultures are sterile

68. Antibiotic impregnated beads
• Polymethylmethacrylate acrylic resins
impregnated with antibiotics
• Used to deliver high concentration of
antimicrobials
• The beads and drain are left in place for 10 to 14
days.

69. Surgical management
• Incision and drainage
• Extraction of offending teeth
• Sequestrectomy
• Sequestrectomy and saucerization
• Decortication
• Resection and reconstruction

70. Sequestrectomy
• It involves removing infected and avascular pieces of bone generally
the cortical plates in the infected area.
• Incision: maxilla
mandible
• Removal of the sequestrum
• Closure

71. 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.

72. Decortication
Mowlem
• 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.

73. Resection
• Approach
• Intra oral

74. • Extra oral

75. Hyperbaric Oxygen Therapy
• Involves intermittent, usually daily, inhalation of 100% humidified oxygen under
pressure greater than 1 absolute atmospheric pressure
• Patient is placed in a chamber, oxygen is given by mask or hood
• Each session, or dive, is 90 minutes in length.
• Treatment given 5 days per week for 30, 60 or more dives at 2.4 ATA for 90
minutes while breathing 100% oxygen twice daily
76

76. Beneficial aspects of hyperbaric oxygen
• Enhancement of lysosomal degradation potential of PMLs and oxygen radicals.
• Free radicals of oxygen are bactericidal to many pathogens.
• Many exotoxins liberated by microorganisms are rendered inert by exposure to
elevated partial pressure of oxygen.
• Tissue hypoxia intermittently reversed by HBO mimicking tissue level during wound
healing
• Positive enhancement of neo-angiogenesis
77

77. HBO chamber
78

78. References
• Topazian RG Osteomyelitis of the Jaws. In Topizan RG, Goldberg MH (eds): Oral and Maxillofacial
Infections.Philadelphia, WB Saunders 1994,Chapter 7, pp 251-88
• Textbook of Oral & Maxillofacial Surgery – Daniel M. Laskin
• Osteomyelitis of the Jaws:A 50-Year Perspective; J Oral Maxillolac Surg 51:1294·1301,1993
• Waldvogell, F.A., Medoff, G. and Swartz, M.N.Osteomyelitis: a review of clinical features, therapeutic
considerations and unusual aspects. N Engl J Med282:198–266, 316–322, 1970.
• Ciney G, Mader JT, Pennick H : A clinical staging system of adult osteomyelitis, Contemp Orthop 10:17, 1985
• Marx, Cillo, and Ulloa. Oral Bisphosphonate-Induced Osteonecrosis. J Oral Maxillofac Surg 2007.
• Osteomyelitis after bilateral sagittal split osteotomy: case report and a review of the management. Oral
SurgOral Med Oral Pathol Oral Radiol Endod 2011;111:442-448)

79. • Lyons A, Ghazali N: Osteoradionecrosis of the jaws: Current understanding of its
pathophysiology and treatment. Br J Oral Maxillofac Surg 46:653, 2008
• Feldmeier JJ: Hyperbaric Oxygen 2003: Indications and Results— Hyperbaric Oxygen Therapy
Committee Report. Kensington, MD, Undersea & Hyperbaric Medical Society, 2003
• Notani K, Yamazaki Y, Kitada H, et al. Management of mandibular osteoradionecrosis
corresponding to the severity of osteoradionecrosis and the method of radiotherapy. Head Neck
2003;25:181–6.
• A. Lyons et al;Osteomyelitis of the jaw: British Journal of Oral and Maxillofacial Surgery 52
(2014) 392–395
• Tibbles PM, Edelsberg JS: Hyperbaric oxygen therapy. N Engl J Med 334:1642, 1996
• Delanian S, Lefaix JL. The radiation-induced fibroatrophic process:therapeutic
perspective via the antioxidant pathway. Radiother Oncol 2004;73:119–31.