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Osteomyelitis of the Jaw Overview

The document discusses osteomyelitis of the jaw, detailing its definition, predisposing factors, etiologies, pathogenesis, clinical presentation, classification, investigations, complications, and management. It highlights the increased incidence in the mandible, the role of systemic and local factors, and the importance of both medical and surgical therapies in treatment. Additionally, it addresses osteoradionecrosis as a related condition resulting from radiation therapy.

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0% found this document useful (0 votes)
48 views79 pages

Osteomyelitis of the Jaw Overview

The document discusses osteomyelitis of the jaw, detailing its definition, predisposing factors, etiologies, pathogenesis, clinical presentation, classification, investigations, complications, and management. It highlights the increased incidence in the mandible, the role of systemic and local factors, and the importance of both medical and surgical therapies in treatment. Additionally, it addresses osteoradionecrosis as a related condition resulting from radiation therapy.

Uploaded by

tegegnegenet2
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

Osteomyelitis of Jaw

Presenter Dr Tegegne, R I
Moderator Dr Tewodros Tefera
(OMFS Consultant )

[Link] G 1
Outlines
• Introduction
• Predisposing factors
• Etiologies & microbiologies
• Pathogenesis
• Clinical presentation
• Classification
• Investigations
• Complications
• Management
• Osteoradionecrosis
[Link] G 2
Introduction
• Osteomyelitis is defined as an inflammation
of the bone marrow that later also involves
adjacent cortical plates& periosteal tissues.
– In the preantibiotics era, osteomyelitis of the
mandible was common.
– With the advent of antibiotics, it became a rare
disease.

[Link] G 3
• In recent years antimicrobials have become
less effective(resistant strain) & is major
diagnostic and therapeutic challenges
• Despite modern therapy it can still remain a
major source of morbidity to the patient that
requires multiple surgeries & resulting in
prolonged treatment duration.

[Link] G 4
• The incidence of osteomyelitis is much higher
in the mandible than maxilla due to
• Less vascularized cortical plate of
mandible
• More dense cortical part of mandible
• More prevalent in male than female
• Affects all age groups infant to elderly

[Link] G 5
Predisposing factors
• Diminished host defenses
• Compromised vascular supply
• Virulent micro organisms are the 3 main risk
factors for osteomyelitis of jaw
• These risk factors can be
• Systemic factors
• Local factors

[Link] G 6
Systemic factors
• Diabetes , anaemia
• Autoimmune states,agranulocytosis
• Malignancies,leukemia ,multiple myeloma
• Malnutrition and aging
• Acquired immunodeficiency syndrome.
• Steroids therapy
• Chemotherapeutic agents
• Bisphosphonates.
[Link] G 7
Local factors
Local conditions that adversely affect the blood supply
can also predispose the host to a bony infection.
• Radiation therapy
• Bone pathology
• Paget diseases
• Fibrous dysplasia
• Osteopetrosis
• Osteoporosis

[Link] G 8
• Trauma
• Odontogenic causes
• Soft tissue injuries
• Soft tissue infections
– Furnuncles
– Carbuncle

[Link] G 9
Etiologies
[Link] causes
Dental caries
Gingival
periodontal diseases
[Link] odontogenic causes
Untreated compound fracture
Gingival or soft tissue lacerations
Bacterial skin infection ( carbuncle ,furnucle)
Hematogenous spread
[Link] G 10
Pathogenesis
• In the maxillofacial region, osteomyelitis primarily
occurs as a result of
• Contiguous spread of odontogenic infections
• Trauma
• Primary hematogenous osteomyelitis is rare in the
maxillofacial region
• It generally occurs in the very young age

[Link] G 11
• The adult process is initiated by an inoculation
of bacteria into the jawbones
• This can occur with the extraction of
teeth,RCT, or fractures of Jaw bones.
• This initial insult results in a bacteria induced
inflammatory cascade

[Link] G 12
• In the normal healthy host, this process is self-
limiting and Is healed
• Occasionally, however, in the normal host, and
certainly in the compromised host, there is
the potential for this process to progress to
the point where it is considered pathologic.
• With inflammation there is hyperemia&
increased blood flow to the affected area.

[Link] G 13
• Additional leukocytes are recruited to this
area to fight off infection.
• Pus is formed when there is an overwhelming
supply of bacteria and cellular debris
• that cannot be eliminated by the body’s
natural defense mechanisms.

[Link] G 14
• Pus and subsequent inflammatory response
occur in the bone marrow that leads to
• An elevated intramedullary pressure that
decreases the blood supply to this region

[Link] G 15
• The pus can travel via haversian and
Volkmann’s canals to spread throughout the
medullary and cortical bones.
• Pus has perforated the cortical bone and
collects under the periosteum
• the periosteal blood supply is compromised
• That results in avascular necrosis of bone

[Link] G 16
• Finally the pus exits the soft tissues either by
• Intraoral sinuses or fistulas
• Extraoral sinuses or fistulas

[Link] G 17
• Dental caries /trauma → pulpal
involvelvement→ periapical pathologies →
edema and pus→ increase intramedullary
pressure → compromise blood supply→
edema and pus spread by volkman canal and
haversian canal and accumulates under
cortex

[Link] G 18
→ Involves periosteal layer → compromise
periosteal blood supply→ avascular bone
necrosis → involves soft tissue and skin →
fistulas and sinuses

[Link] G 19
[Link] G 20
Microbiology

• In the past, staphylococcal species were


considered the major pathogen in
osteomyelitis of the jaws.
• Now as of microbiologic identification the
prime pathogenic species are streptococci &
anaerobic bacteria.

[Link] G 21
• The anaerobes responsible are Bacteroides or
Pepto streptococci
• Often, the infections are mixed as of final
culture

[Link] G 22
Other bacteria that causes OML
• Actinomycotic bacteria
• Mycobateria
• Spirochetes like treponema pallidum

[Link] G 23
Clinical presentation
 Prevalent in elderly&immuno compromised
and smoker patients.
 Rarely in infant and younger ages
 Presentation differs according to its acute
suppurative ,sub acute ,chronic suppurative
and non suppurative stages

[Link] G 24
Acute suppurative stage
• It is called intramedulary stage that lasts for 10 to 14
days &characterized by
• Deap intense pain
• Fever
• Paresthesia of lower lip
• Identifiable cause
• Minimal swelling
• No teeth mobility
• No fistula
[Link] G 25
• Leukocytosis
• Increased ESR
• Increased CRP
• Positive radionuclide bone scan

[Link] G 26
Sub acute stage(Periosteal OML )
• Un treated acute stage changed to sub acute stage after 14
days to 1 month duration and characterized by:
– Mobility of teeth
– Firm cellulitis of cheek
– Expansion of bone
– Mucsal or cutaneous fistula
– Halitosis
– Lymphadenopathy
– Normal temperature and WBC

[Link] G 27
Secondary chronic stage
• Untreated acute or subacute stage changed to
2ndary chronic after 1month
• Fistula
• Sequestra
• Induration of soft tissues
• Thicken or wooden character of affected area
• Pain and tenderness to palpation

[Link] G 28
Primary chronic stage
• Is also known as chronic suppurative stage where it
may arises from haematogenous spread or rarely
lymphogenous route
• This has no any acute stage
• Mild pain
• Slow increase in bone size
• Sequestra
• No fistula

[Link] G 29
Non suppurative stage
• They are chronic OML that is caused by
• low grade infections
• No pus formation
• They are chronic
• Has bone deposition around the periosteum

[Link] G 30
Classification
• There may ways of classification of OML of jaw
• The two common applicable OML classification are
• Zuric classification &
• literature classification

[Link] G 31
Literature classification
[Link] OML [Link] suppurative OML
[Link] suppurative [Link] oml
[Link] suppurative • Diffuse &
• Primary • Focal/osteotitis
• Secondary [Link] periostitis
[Link] OML • Garres sclerosing
C. Other OML are : [Link]
– Actinomycotic
– TB, Syphilis
– Chemical&cautery

[Link] G 32
Zuric classification
• This classification is widely accepted and classify
OML interms of etiology ,pathogenesis ,clinical
features ,radiology and histopathological features
• So OML is classified as
• Acute osteomyelities
• Secondary chronic
• Primary chronic

[Link] G 33
[Link] G 34
[Link] G 35
Diagnosis &Investigations
• laboratorical and imagings are used to investigate OML .
• Laboratorical investigations are very sensitive & non specific
• Shows acute stages & clinical progression
• These includes :
– WBC……leukocytosis
– Gram stain , culture
– ESR
– CRP &Biopsy

[Link] G 36
• In acute stage 4 to 14 days , history taking clinical
features & bone scan are more important for
investigation of OML
• In established cases ,radiograph are more useful

[Link] G 37
Maxillofacial imagings
• Imagings are used to show destructed parts of bone ,
the location of OML , risk factors like trauma and
predisposing bone pathologies
• However , at least 30 % to 50% of cortical bone has
to be destructed to be seen on radiograph
• They are less important for acute stage than clinical
presentations

[Link] G 38
• OPG,IOPA
• CT
• MRI….. Bone marrow inflammation
• Nuclear Bone scan (Tc 99, Ga 67 ,In 111) contains
labeled methylene diphosphonate
• Show bone turn over
• Non specific and are sensitive
• Used as contrast media
• Bind to WBC that shows infection
[Link] G 39
Radiologic features
[Link] eaten appearance
• Shows scattered area of bone destructions
[Link] and involucrum
[Link] or granular densification of bon
• Sclerosing OML
[Link] skin appearance
• Garres oml

[Link] G 40
[Link] G 41
[Link] G 42
[Link] G 43
[Link] G 44
[Link] G 45
[Link] G 46
DDx
• Fibrous dysplasia
• Paget diseases
• Osteoporosis & osteopetrosis
• Leukemia
• Multiple myeloma
• Ewings sarcoma
• Osteosarcoma

[Link] G 47
Complication
• Osteonecrosis
• Pathologic fracture of bone
• Septicemia &thromboembolism
• Continuity defects
• Septic arthritis
• Impaired growth
• Skin cancer & osteosarcoma

[Link] G 48
Treatment
• Medical therapy
• Surgical therapy
• Supportive therapy
– Analgesics and bed rest
– High protein diet
– Vitamin diet
– High fluid intake
– Treat the underlying causes

[Link] G 49
Medical therapy
Systemic antibiotics
[Link] G 2million units IV 6x/ day plus
metronidazole #2 to 3 day& then continues :
– Pencillin V 6x/day po plus metronidazole 500mg
tid po for 2 to 6 weeks

[Link] G 50
[Link] allergic pt
[Link] 600mg iv QID for 2 to 3 days &then
– Clindamycin 300mg po QID for 2 to 6 weeks or
[Link] 1g iv tid for 2 to 3 days and then
– Cephalexin 500mg po tid or
D. Vancomycine 1G iv bid

[Link] G 51
• Resistant and recurrent OML that is caused by
methiline resistant staphylococus and vancomycine
resistant enterococci are treated by
• Tigecycline
• Linezolid

[Link] G 52
Surgical therapy
• There 6 options of surgical management of OML
depending on its extent of involvement
• Exodontia
• I&D
• Sequestrectomy
• Saucerization
• Decortication
• Resection & reconstruction

[Link] G 53
• Sequestreomy ,saucerization and decortication are
basically the same procedure that differs by
invasiveness of the procedure.
• Sequestrectomy is removal of sequestrum that is
localized only at the center of the bone

[Link] G 54
• Saucerization is removal of sequetrum along with
lateral portion of cortical part of the bone
• Decortication is more extensive procedure that
involves removal of sequestrum ,lateral and inferior
part of the cortex

[Link] G 55
[Link] G
56
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
megavoltage which is felt to be kinder to the bone
&soft tissues..

[Link] G 57
• Collimation&shielding of tissues in conjunction with
careful dental evaluation preoperatively have greatly
decreased the incidence of ORN.
• The effects of radiation last a lifetime and do not
decrease over time.
• ORN is generally caused by trauma to the radiated
area usually by dental extraction
• But it can also occur spontaneously

[Link] G 58
• Radiation above 5,000 to 6,000 rads is generally felt
to make the mandible susceptible ORN

[Link] G 59
Clinical features
• Severe ,deep boring pain in irradiated area
• Trismus
• Swelling
• Soft tissue abscess
• Draining sinuses and fistulas
• Halitosis
• Induration&ulceration of surrounding tissues

[Link] G 60
• Evidence of exposed bone
• Pathological fracture
• Other radiation effects
• Radiation caries
• Mucositis
• Xerostomia
• Food lodgment

[Link] G 61
Investigation &Diagnosis
• History of radiation
• Clinical features
• Radiographs
• Early stage … no bone changes
• Late stage …sequestrum and pathological #
– OPG
– CT
– MRI

[Link] G 62
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

[Link] G 63
• Tissue removed in a prior cancer patient should be
sent to pathology
• To rule out occult or recurrent malignant diseases
that masquerade as a bony infection

[Link] G 64
Medical therapy
• Pain alleviation by narcotics and nerve blocks
• Local wound debridement and packing every 7days
by neomycine and ZOE
• Antiobiotis therapy
• HBO
• U/S Therapy
• Adequate nutrition

[Link] G 65
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 and or 10 dives

[Link] G 66
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

[Link] G
67
Clinical applications
• ORN
• OML
• Air embolism
• CO poisoning
• Mucormycosis
• Promote bone graft healing and flap uptake

[Link] G 68
Contraindication
• Optic neuritis
• Immunosuppressive disorder
• COPD
• Claustrophobia

[Link] G 69
Complication
• Oxygen toxicity
• Seizures
• Tooth and sinus pain
• Visual changes
• High pressure nervous syndromes
• Decompression sickness
• pneumothorax

[Link] G 70
Marx protocol of HBO
Stage I
30 dives
examine exposed bone

Response no response cutaneous fistula

10 dives stage II pathologic #


surgery resorption of bone
10 dives

response no response

stop stage III


surgery and fixation,reconstruction,10 dive

[Link] G 71
Surgical therapy
• Sequestrectomy
• Bone resection
• Intraoral and extraoral approaches

[Link] G 72
Prevention
• Extraction before radiation therapy
• All teeth in line of radiation
• Carious and periodontally involved teeth
• Good oral hygiene maintenance
• Fluoride therapy

[Link] G 73
• Atraumatic extraction after radiation therapy can be
treated by :
• Pentoxifylline 400mg bid that ( ↑Blood supply )

• Tocopherol1ooIU daily – anti oxidant


• Clodronate – antiresorbitive drug

[Link] G 74
Top tips
• Osteomyelitis &ORN present an ongoing%potentially
difficulty clinical scenario to manage.
• Many patients will receive a combination of surgery
and medical management
• Some patients will ben required to undergo extensive
and potentially disfiguring surgery

[Link] G 75
• The medical management includes antibiotic therapy
and HBO treatment
• Medical therapy may expensive, longer duration &
disruptive to the patient’s life.
• Both of these conditions can be started with simple
dental extraction treatment .

[Link] G 76
• Clinicians must always be vigilant for post-treatment
complications -osteomyelitis and osteoradionecrosis.
• Despite advances in both medical management and
surgical therapy, the absolute answer to the
prevention is the simplest and most effective

[Link] G 77
References
• Baltensperger –Eyrich jaw osteomyelitis 2009
• Peterson principle of maxillofacial surgery ,2nd
edition

[Link] G 78
Thank you

[Link] G 79

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