chap-4b osteomyelitis and osteoradionecrosis of jaws jaw.ppt

osteomyelitis and osteoradionecrosis of jaws

1. OSTEOMYELITIS AND ORN
OF THE JAWS
Prepared by Dr Alelign.

2. CONTENT
Introduction
Classification of osteomyelitis
Etiology and predisposing factors
Pathogenesis
Clinical findings
Investigation modality
Management
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3. Learning outcomes
1.Able to know the incidents and risk factors of OML,
ORN,BION of the jaw.
2.Able to understand the current diagnosis and
management of osteomyelitis, osteoradionecrosis,
medication-related osteonecrosis of the jaws.
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4. Introduction to anatomy of jaw bone
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Maxilla
Thin cortex
Limited Spongiosa
excellent blood supply
Mandible
Well developed cortex
Spongiosa is abundant
dense, poorly
vascularized

5. OSTEOMYELITIS:
An inflammatory condition of bone, that begins as an infection of medullary
cavity & haversian systems of the cortex & extends to involve the
periosteum of the affected area.
PERIOSTITIS
Inflammation of periosteum may be due to microbial, traumatic or chemical
Acute Periostitis
Chronic Periostitis
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6. Etiologies
•OML is initiated by a contiguous focus of infection or hematogenous
spread.
•the disease is primarily by contiguous spread from odontogenic
infection like pulpitis or periodontitis tissue
-trauma especially compound fracture
-gingival ulceration ,furuncles or laceration
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7. Predisposing factors
•despite the freqency,and severity of dental infection and
also tooth apex distance from the medulla cavity OML its
infrequent because of host defense
•main risk factors for onset and severity of osteomyelitis of jaw
-Diminished host defenses
-Compromised vascular supply
-Virulent micro organisms
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8. Systemic factors
immunocompromised
•Diabetes , anemia
•Autoimmune states,
•Malignancies ,
•leukemia
•Malnutrition
•Chronic alcoholism
•Sickle cell animia
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9. Local factors
Alteration in the blood supply of the jaw
•Radiation therapy
•Paget diseases
•Fibrous dysplasia
•Osteopetrosis
•Osteoporosis
•Bone necrosis caused by mercury, bismuth, arsenic
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10. microbiology
•in the past OML of the jaw like that of the long bones, was
believed to be caused by staphylococcus(s. aures,
s.epidermidis)
•the prime pathogenic species are found to be
streptococci(ɑ-hemolytic) and anaerobic
Bacteroides(prevotella) or Pepto streptococci species,
fusobacterium
•other organisms like klebsiella , pseudomonas ,proteus ,MTB,
treponema pallidum and actinomyces spp
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11. MICROORGANISM IN OML
More than 500 bacterial species have been identified in the mouth.
staphylococcus(80 to 90%)[aureus & epidermidis]
streptococci(a hemolytic)
oral anaerobes(peptostreptococcus, fusobacterium, prevotella(bacteroids)
pneumococci, actinomyces, nocardia, porphyromonasspp
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13. Trauma, Contagious, Progressive, Hematogenous
Acute inflammation
Tissue necrosis
Vascular thrombosis
Pus accumulation
Vascular collapse
Subperiosteal abscess
infiltration of microorganism
Liberation of proteolytic enzyme & destruction of bacteria,
edema, pus formation
Necrotic tissue + dead bacteria within WBC’s
Venous stasis & Ischemia.& Pus travel through haversian & nutrient canals
In intramedullary pressure
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Further in vascular supply compression of neurovascular bundle
Pathogenesis

14. OML mediated mandibular anesthesia
Mucosal & cutaneous Abscess & fistulae
Formation of sequestra
Involucrum
Penetration of periosteum
Improvtin host defense + AB therapy =Process become chronic
Inflammation of granulation tissue+ new bl .Vs formation=lysis of bone
Cloacae
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through which pus escapes to ep.surface

15. GENERAL CLINICAL PRESENTATION
Early sign and symptoms
acute inflammation
Intermittent high fever, malaise, dehydration.
Facial cellulitis , erythematous swelling, necrosis>>accumulation of pus
Trismus
increased intramedullary pressure
Sub acute –sign symptoms
Expansion of bone, Abscess with localisedwarmth
paraesthesia
Regional lymphadenopathy
A foul-smelling, dark exudate accompanying slough of necrotic tissues, gas in soft tissues
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16. classification
•Over the years many ways of classifying osteomyelitis have
been presented
-suppurative or nonsuppurative by Lew and Waldvogel
-into acute and chronic forms by Hudson
-hematogenous or secondary to a contiguous focus of infection
•Hudson is the most advantageous to the clinician, it is divided
into acute or chronic forms based on the presence of the
disease for a 1-month duration
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17. 1. Hudsons classification
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18. 7/20/2024 18
2. Topazian Classification based on clinical picture and radiology.
I. Suppurative osteomyelitis
Acute suppurative osteomyelitis
Chronic suppurative osteomyelitis
–Primary chronic suppurative osteomyelitis
–Secondary chronic suppurative osteomyelitis
Infantile osteomyelitis
II. Nonsuppurative osteomyelitis
Chronic focal sclerosing osteomyelitis
Chronic diffuse sclerosing osteomyelitis
Garrè's chronic sclerosing osteomyelitis
Specific form of OML (Actinomycotic, Tuberculous, Syphilitic..)
Osteoradionecrosis

19. 3. The Zurich Classification System
1) Acute Osteomyelitis
-Acute suppurative
-Subacute suppurative
-Clinically silent with or without suppuration
2) Secondary Chronic Osteomyelitis
3) Primary Chronic Osteomyelitis of the Jaws
-Adult-onset Primary Chronic Osteomyelitis
-Chronic Recurrent Multifocal Osteomyelitis
-Syndrome-associated Primary Chronic Osteomyelitis
-Early-onset Primary Chronic Osteomyelitis (Juvenile
Chronic Osteomyelitis)
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20. Cierny & vibhagool 1993
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Established sign and symptoms
Indurated swelling ,acidosis, toxemia
Penetration>>periosteum>>mucosal/cutaneous abscess
Regional lymphadenopathy
Host resistance>>regression of inflammation
Formation of granulation tissue
Neovascularization>>lysis of bone

22. Investigation modality
Culture & sensitivity
CBC
Imaging
Radiographs
CT Scan
MRI
Scintigraphy
Nuclear medicine
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PRINCIPLES OF TREATMENT OF OML
1. evaluation and supportive therapy
correction of host defence mecha
2. gram stain culture and sensitivity
3. investigation
4. empirical antibiotic therapy
5. removal of loose teeth,foreign body, sequestrum
6. culture guided antibiotics, and HBO therapy
7. possible placement of irrigating drains
8.I&D Sequestrectomy, decortication,
saucerization, resection of jaw, reconstructions.

24. ANTIBIOTIC REGIMEN
Inpatient treatment
Penicillin 2 million u iv qid+ metronidazole 500mg qid
improved for 48 to 72 hours switch to penicillin v 500mg po qidfor additional 4 to 6 weeks
Or ampicillin/sulbactam 1.5-3g iv qid
improved for 48 to 72 hours switch to Augmentin 1000mg po bid for additional 4 to 6 weeks
Outpatient treatment
Penecillinv 2gm +metronidazole 500mg tidfor 2 to 4 weeks after the last sequestrum
removed and pt without symptoms Or
Clindamycin 600mg to900mg iv qidthen clindamycin 300 mg qidpo
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25. HBO THERAPY
100% O2 at 2.4 atmospheric absolute pressure
1 dive----90 min
5 days a week
30 to 60 dives
Given in monoplace / large chambers
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26. HYPERBARIC OXYGEN THERAPY
Increases arterial & venous tension
Additional O2 being carried in plasma
Direct bacteriostatic effect on micro.Org
Bactericidal and bacteriostatic
Increases leukocyte bactericidal activity
Fibroblastic activity
Neovascularisation
Proliferation of granulation tissue
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27. Acute osteomyelitis
Defined the time element as being 1 month after onset of symptoms.
Clinical Features:
Pain is the primary feature of this inflammatory process.
Pyrexia, painful lymphadenopathy, leucocytosis
A fetid oral oudor
trismus
Teeth mobility and decreased or loss of sensitivity.
paraesthesia or anaesthesia of the lower lip is described (Vincent’s symptom)
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28. laboratory
Elevated c reactive protein level and ESR
Leucocytosis
Thrombocytosis
Positive blood culture
Culture
Staphylococcus aureus, Staphylococcus epidermidis.
Histopathologic Features
Pressure in the medullary space is increased and blood vessels are destroyed.
Inflammatory exudate occupies the marrow spaces.
Necrotic bony trabeculae show:
-loss of osteocytes from lacunae from 2 weeks onward. .
-Trabeculae are surrounded by bacterial colonization and acute inflammatory infiltrate
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29. Conventional Radiology
1 to 2 weeks
A normal radiographic appearance.
Radiolucency
Loss of trabecular structure
Lose of counter of the mandibular canal
Erosion of the cortical bone
3 to 4 weeks
Radiolucent line around cortical bone with increase radiopacity
Calcified periosteal reaction
linear irregular radiolucency Fracture/ fistula
Scintigraphy
Detection of increased bone turnover activity 2−3 days after the onset of symptoms.
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30. CT scan
With in 2 weeks
Loss of cancellous bone trabeculae
Demineralization, thinning of endosteal cortical plate
Lose of counter of the mandibular canal
3 to 4 weeks
Sequester formation
Calcified periosteal reaction
MRI FINDING
With in 2 weeks
Replacement of marrow fat by inflammation
enlargement of marrow space and thinning of cortical plate
Subperiosteal; extension of inflammation
3 to 4 weeks
Sequestrum
Non calcified periosteal reaction
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31. Principles of treatment of acute osteomyelitis of the jaws
Establish correct diagnosis, based on history, clinical evaluation, and imaging
Biopsy in unclear cases to rule out other pathology (e.g., malignancy)
Removal of source of infection
Local incision and drainage of pus
Local curettage with removal of superficial sequestra
Collection of specimens for Gram stain, culture and sensitivity, histopathology
Begin with empiric broad-spectrum antibiotic therapy
change to culture-guided antibiotics
More extensive surgical debridement if necessary
Possible adjunctive hyperbaric oxygen therapy
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32. Primary chronic osteomyelitis
The disease tends to a rise de novo without an actual acute phase
Syndrome-associated primary chronic osteomyelitis SAPHO syndrome
The term SAPHO synovitis; acne and pustulosis; hyperostosis; and osteitis.
Three diagnostic criteria characterize sapho syndrome:
1. Multifocal osteomyelitis with or without skin manifestations
2. Joint inflammation associated either pustular psoriasis or palmoplantar pustulosis,
acne
3. Sterile osteitis in the presence of one of the skin manifestations
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33. Clinical Features
swelling and, regional lymphadenopathy
Sinus formation and purulent discharge.
Sequestrum formation (dead bone).
Tooth loss, pathologic fracture.
limitation of jaw opening and/or myofacialpain
reduced sensation of the inferior alveolar nerve (Vincent’s symptom)
Histopathologic Features:
Bone marrow spaces are occupied with fibrous connective tissue and chronic
Inflammatory cells
Culture
Propionibacterium acnes
Actinomyces spp. and E. corrodens7/20/2024 33

34. Chronic Non-suppurative Osteomyelitis
A more heterogenic group which lacks the formation of pus and fistula.
Chronic osteomyelitis with proliferative periostitis (garré's osteomyelitis)
Diffuse sclerosing osteomyelitis
Actinomycotic
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35. Chronic Osteomyelitis with Proliferative Periostitis (Garré's Osteomyelitis)
Subtype of osteomyelitis that has a prominent periosteal inflammatory reaction .
Clinical Features
Asymptomatic bony, hard swelling with normal appearing overlying skin and mucosa.
On occasion, slight tenderness may be noted
Radiographic features
Onion skin appearance
Histopathology
Sub periosteal reactive new bone formation
Marrow spaces contain fibrous tissue with scattered lymphocytes and plasma cells.
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36. SCLEROSING OSTEOMYELITIS
Focal and diffuse types
Diffuse Sclerosing Osteomyelitis
-An inflammatory reaction in response to a microorganism of low virulence.
-Clinical Features
-Pain, swelling, and limitation of mouth opening, as well as occasional lymphadenopathy,
The mandible may be tender to palpation, particularly at the buccal cortex.
Radiographic features
-prominent endosteal sclerosis without prominent cortical bone loss and with minimal or no periosteal
bone formation
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37. Focal Sclerosing osteomyelitis bony scar
condensing osteitis, and sclerotic bone.
focal bony reaction to a low-grade inflammatory stimulus. It
is usually seen at the apex of a tooth with long-standing
pulpitis.
Clinically:
Asymptomatic
Radiographic
In X-RAY: sclerotic area related to apex of dead tooth.
Histopathology
these lesions are masses of dense sclerotic bone.
Treatment –
the lesion itself need not to be removed.
The inflamed pulp that stimulated the focal sclerosing
osteomyelitis should be treated.
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38. Actinomycotic COML
A slowly progressive infection with both granulomatous and suppurative features.
Clinical feature
Firm soft tissue masses are present on the skin with purplish to dark-red oily areas and
occasionally small zones of fluctuance
Spontaneous drainage of serous fluid containing granular material may occur. When placed on a
piece of gauze, these granular, yellowish substances, also called sulfurgranules, can be seen
clearly and represent colonies of bacteria.
Radiological
Zones of osteolysis, sclerosis on radiographs.
Occasionally sequester formation is also noted.
Culture
A.Israelii, A.Naeslundii, A. Odontolyticus, and A. Meyeri
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39. TB OSTEOMYELITIS
Osteomyelitis of the jaws caused by infection with Mycobacterium tuberculosis is uncommon and, in most
described instances, the tuberculosis infection is rarely confined to the bone.
Adults are predominantly affected
The clinical and radiological picture
may resemble secondary chronic osteomyelitis with features similar to a dento-alveolar abscess; however,
cervical lymphadenopathy, producing discrete or matted masses which are usually nontender, may be a
distinctive presenting feature.
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40. 7/20/2024 40
Chronic osteomyelitis conventional radiography
area of increased opacity with loss of trabeculae
sequester formation
calcified periosteal reaction
pathological fracture
scintigraphy and positron emission tomography
scintigraphy and positron emission tomography (PET) belong to the diagnostic procedures that use
radionuclides to assess the presence and activity of chronic osteomyelitis.
Scintigraphy is the diagnostic procedure of choice in detecting saphosyndrome

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CT scan
Opacification + cortical plate thickness
Gross defects on cortical plate
Calcified periosteal reaction
TMJ involvment
MRI
Replacement of marrow by fat
Bone marrow enlargement
Periosteal thinning
Periosteal extension of inflammatory tissue

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Principles of treatment of chronic osteomyelitis of the jaws
Establish correct diagnosis, based on history, clinical evaluation, and imaging studies
Biopsy in unclear cases to rule out other pathology (e.g., malignancy)
Determine extent of infected bone and soft tissue
Evaluation and correction of host defensedeficiencies when possible
Surgical debridement of infected tissue dictated by extent of the lesion
sequestrectomy, local curettage, saucerization, decortication, resection)
Collection of specimens for Gram stain, culture and sensitivity, histopathology
Begin with empiric broad-spectrum antibiotic therapy
culture-guided antibiotics as soon as possible
Possible adjunctive hyperbaric oxygen therapy
More extensive surgical debridement if necessary (e.g., repeated decortication, resection)
surgery followed by 2 weeks of intravenous antibiotics, followed by 6 weeks of oral antibiotics,

43. BIONJ
Bisphosphonates (bps) are the most widely used and effective anti-resorptiveagent
for the treatment of diseases in which there is an increase in osteoclastic
resorption, including post-menopausal osteoporosis, paget’sdisease, and tumor
associated Osteolysis.
Etidronate(didronel)
Pamidronate(aredia)
Alendronate (fosamax)
Risedronate(actonel)
Ibandronate(boniva)
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44. 7/20/2024 44
Pathogenesis
Act by inhibition of osteoclast-mediated
bone turnover and renewal.
Incorporated into the hydroxyl-apatite
matrix at sites of active bone
remodelling and into periodontal
structures.
Prolonged secondary mineralization,
increase in mineral density and mild
augmentation of bone matrix.

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Clinical feature
Exposed bone
Supra alveolar sclerosis
Bony expansion
Imaging
Areas of sclerosis,
Thickening of the lamina dura
Cortical bone prominence

46. Staging of BIONJ
Stage 0; no clinical evidence of necrotic bone but have nonspecific findings.
Stage 1; Patients have exposed and necrotic bone who are asymptomatic
Stage 2; Patients have exposed and necrotic bone who are symptomatic.
Stage 3; stage 2 and one or more of the following:
Exposed and necrotic bone extending beyond the alveolar bone.
Pathologic fracture.
Extraoral fistula.
Oral-antral or oral-nasal communication.
Osteolysis extending to the border of the mandible or maxillary sinus floor.
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47. PREVENTION OF OFBIONJ
Initiation of bisphosphonate therapy
Therapy should be delayed until oral/dental health is optimized.
Non restorable teeth and teeth with poor prognoses should be extracted.
Bisphosphonate therapy allowed 14–21 days after procedure.
Patients receiving bisphosphonates
Maintain good oral and dental hygiene
Dental procedures that involve bony surgery should be avoided.
Placement of dental implants should be avoided.
Stop the medication 2 months before dentoalveolar surgery.
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48. TREATMENT BIONJ
In stage 0 patients conservative treatment.
In stage 1 patients, oral anti-microbial rinses, such as chlorhexidine
0.12%, are indicated.
In stage 2 patients Oral antimicrobial rinses + antibiotic therapy
In stage 3 patients, surgical debridement, including resection, is used
in conjunction with antibiotic treatment.
Stopping oral bisphosphonate treatment ????
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49. OSTEORADIONECROSIS
Osteoradionecrosisisaslowhealingradiationinducedischemicnecrosis
ofthebonewithassociatedsofttissuenecrosisofvariableextent
occurringinabsenceoftumornecrosis,recurrenceormetastaticdisease
Below50gy----uncommon
Above60below70---occursfrequently
Above75gychancesincrease10times
Timeperiod---meanof7.5yearsto20years
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50. Predisposing factors
Total dose of radiation therapy
Method of delivery of radiation
Advanced stage tumors
Poor nutritional status
Use of alcohol and tobacco
Volume of mandible in field of radiation
Individual patient sensitivity
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51. RADIATION > 5000 Rads
NON HEALING WOUND
DEMANDS EXCEED SUPPLY
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Pathogenesis
3 HYPO
TISSUE BREAKDOWN
Hypocellularity
Hypovascularity
Hypoxia

52. Grading
•Grade 1–alveolar bone exposed
•Grade 2---does not respond to hyperbaric oxygen therapy,
sequestrectomy and saucerization
•Grade 3–pathological fractures
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53. Clinical features
Pain
Exposed bone with gray to yellow color
Fetid breath and elevated temperature
Intraoral and extraoral fistulae
Pathologic fractures
Trismus
Induration & ulceration
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54. INVESTIGATIONS
Radiographs
Computed tomography
Magnetic resonance imaging
Nuclear isotope technitium99 methylene diphosphate bone scanning
Technetium 99m isotope scanning
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55. Prevention
Presurgical
Infected non vital and periodontally compromised teeth to be extracted
Teeth in line of radiation
Alveoloplastywith removal of sharp bony margins
Restorations and periodontal therapy
Prophylactic hyperbaric oxygen therapy
Prevention by surgery
Preservation of periosteum
Closure with adequate blood supply
Mandibular osteotomies in midline
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56. prevention by oncoradiologist
exposure to lowest dose
CT guided irradiation
ultra potential radiation source
brachytherapy
patient duties
maintain oral hygiene
maintaining healthy periodontium
regular flossing /use of gel tray
chlorohexidine containing tooth paste and oral rinse
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57. TREATMENT
•Conservative treatment
Initially control of infection
Irrigation
Exposed bone debridement
Pack with zinc peroxide and neomycin
•Ultrasound therapy
•Surgical
•Hyperbaric oxygen
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58. •Holes drilled into lingual cortical plate to
encourage revascularisation
Ultrasound therapy
•Promotes neovascularity and neocellularity
•Protocol was 40 to 50 ten minute sessions
•Increases fibroblast and osteoblast proliferation
•Collagen production
•Stimulates growth of blood vessels
•Deeper bone penetration
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59. Surgical
Indications for bone resection
Oro cutaneous fistula
Pathological fractures
Segmental bony resorption on radiographs
Hyperbaric oxygen not successful
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60. HYPERBARICOXYGENTHERAPY
HBOtherapyconsistsof100%oxygendeliveredfor90minbasedat2.4
atmofpressure.
20to30divesaregivenpreoperativelybeforeanysurgicalinterventionis
performed.
TheareaofORNisthendebridedandfollowedwith10additionalHBO
treatments.
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61. ORN
•Osteoradionecrosis is a chronic nonhealing wound that is hypoxic,
hypocellular & hypovascular
•In years past, the radiation therapist used ortho voltage therapy &
there was a high incidence of ORN.
•However, the modern radiation therapists use megavoltagewhich is
felt to be kinder to the bone &soft tissues..
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62. •Collimation & shielding of tissues in conjunction with careful dental
evaluation preoperatively have greatly decreased the incidence of
ORN.
ethiology
•when caused by trauma to the radiated area usually its by dental
extraction
•one third cause is spontaneous
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63. Clinical features
•Severe ,deep boring pain in irradiated area
•Trismus
•Swelling
•Soft tissue abscess
•Draining sinuses and fistulas
•Halitosis
•Induration & ulceration of surrounding tissues
•Evidence of exposed bone
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64. Investigation &Diagnosis
•History of radiation
•Clinical features
•Radiographs
•Early stage … no bone changes
•Late stage …sequestrum and pathological #
•OPG
•CT
•MRI
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65. Management
•The main aim of treatment of radionecrosis is to restore vascular
supply and removal of affected by there by restore revascularization
that promote the body to heal itself
•They can be
•Medical and surgical therapy
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66. Medical therapy
•Pain alleviation by narcotics and nerve blocks
•Local wound debridement and packing with neomycineand Zinc
peroxide weekly
•Antibiotic pencillinand meterondazole or clindamicin alone
•HBO
•U/S Therapy
•Adequate nutrition
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67. Surgical therapy
•Sequestrectomy
•Bone resection
•Intraoral and extraoral approaches
67
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68. Hyperbaric oxygen therapy
•HBO is one dive therapy that consists of 100 % oxygen at 2.4
Atmospheric pressure in 90 minutes
•Frequency of therapy is 5 times per week
•Duration of therapy 30 dives or 10 dives
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70. Beneficial effects
•Enhances WBC lysosomal activity
•Neutralize bacterial toxins
•Bactericidal and anti oxidant to anaerobes
•Promote wound healing and collagen synthesis
•Neoangiogenesis effect
•Increased oxygen perfusion to hypoxic areas
70
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71. Clinical applications
•ORN
•OML
•Air embolism
•CO poisoning
•Mucormycosis
•Promote bone graft healing and flap uptake
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72. Contraindication
•Optic neuritis
•Immunosuppressive disorder
•COPD
•Claustrophobia
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73. Complication
•Oxygen toxicity
•Seizures
•Tooth and sinus pain
•Visual changes
•High pressure nervous syndromes
•Decompression sickness
•pneumothorax
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74. Prevention
•Extraction before radiation therapy
•All teeth in line of radiation
•Carious and periodontally involved teeth
•Good oral hygiene maintenance
•Fluoride therapy
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75. Take home massage
OML, is an inflammatory condition of the bone, beginning in the medullar cavity and haversian
systems and extending to involve the periosteum of the affected area.
Imaging is a crucial diagnostic tool in the assessment of acute and chronic osteomyelitis of the
jaws.
The principles of osteomyelitis therapy of the jaws are focus eradication by meticulous
debridement including removal of dead bone and unstable internal fixation devices, combined
with correct empirical and adequate antibiotics
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REFERENCE

77. THANK YOU
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