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DR MOHAMMAD AKHEEL
OMFS PG
Infection – Invasion of the body with organisms
that have the potential to cause disease.
Chronic –
 Lasting a long time.
 Condition of 3 months duration or longer ( US
National centre for health statastics).
Reasons for chronicity –
 Extremely high host resistance.
 Sub-virulent microorganisms.
 Less number of microorganisms.
 Osteo – bone
Myelos – marrow
Itis - inflammation
 Inflammation of bone involving the cancellous
bone, bone marrow, cortical bone &
periosteum.
 Noncompliance with health care delivery.
 Systemic metabolic compromise –
-Age
-Malnutrition
-Immunosuppression
-Congenital or acquired pathophysiologic
conditions disrupting blood supply
 Inaccessibility to health care delivery.
 Most are from local causes:
1. Acute periapical infection
2. Pericoronitis
3. Acute periodontal lesions
4. Trauma-fractures and extraction of teeth
5. Acute infection of the maxillary sinus
6. Direct extension of furunculosis of the face
7. Hematogenous
• Staph aureus, Staph albus, Strep pyogenes
• Bacteriodes, peptostreptococcus.
• Arachnia, Actinomyces, Klebsiella,
Eikenella etc
• Typhoid,Haemophilus, pneumococci,
spirochaetes
Pulpitis
Acute Chronic
Apical Periodontitis
Acute Chronic
Periapical
Abscess
Periapical
Granuloma
Periapical
Cyst
Osteomyelitis
Acute Chronic Focal
Diffuse
Periostosis
Cellulitis Abscess
Bacteraemia Toxaemia Septicemia Dissemination Shock
Death
Chronic
Periapical
abscess
Mostly occurs in the mandible, rarely in the maxilla.
 Most odontogenic infections are localised by the
production of a protective pyogenic membrane or
soft tissue abscess wall.
 If sufficiently virulent, microorganisms may destroy
this barrier.
ACUTE
 Acute inflammation sets in :
Hyperemia
Increased capillary permeability
Infiltration of granulocytes
 Proteolytic enzymes liberated due bacteria destruction-
tissue necrosis & vascular thrombosis
 Pus accumulates - increased intramedullary pressure -
vascular collapse, venous stasis & ischemia.
 Pus travels through the haversian & nutrient canals &
accumulates beneath the periosteum, elevating it from
the cortex, further reducing the blood supply.
 Compression of the neurovascular bundle accelerates
thrombosis & ischemia.
 If pus continues to accumulate, the periosteum is
peneterated & mucosal & cutaneous abscesses &
fistulae may develop.
CHRONIC
 As natural host defenses & therapy begin to be effective,
it becomes chronic.
 Inflammation regresses, granulation tissue is formed.
 Angiogenesis takes place leading to lysis of bone, thus
separating fragments of necrotic bone from viable bone –
Sequestra.
 Small sections of bone may be completely lysed while
larger ones may be isolated by a bed of granulation
tissue & surrounded in a sheath of new bone –
Involucrum
 Occasionlly , the involucrum is peneterated by channels
through which pus escapes to an epithelial surface –
Cloacae.
Radiographic evaluation
• 30-60% destruction min 4-8 days to 3 wks
• Moth eaten appearance, scattered areas of bone
destruction
• Islands of sequestrae in radiolucent areas
surrounded by involucrum
• Stippled granular densification due to
subperiosteal deposition on surface of trabeculae
at the expense of marrow spaces
RADIOGRAPHIC AIDS
• Radiographs
• Bone imaging - Scintigraphy
Determines presence of reactive bone
Radiopharmaceuticals – technetium-99
gallium-67
indium-111
• High resolution Computer tomography
• Magnetic Resonance Imaging
Classification & staging system for Osteomyelitis (Cierny
et al, 1985)
I. Anatomic
Stage I : Medullary OM, involves medullary bone
usually hematogenous
Stage II: Superficial OM, < 2cm defect without
cancellous bone
Stage III: Localized OM, <2 cm defect, does not
involve both the cortices
Stage IV: Diffuse OM, > 2cm, infection, non union,
pathologic #
II. Physiological class
 Host : normal host
 Host
Systemic compromise
Local compromise
 Host : treatment worse than disease
 Systemic factors affecting immune surveillance ,
metabolism, local vascularity
• Malnutrition
• Renal/ hepatic failure
• Diabetes Mellitus
• Chronic Hypoxia
• Immune deficiency/ suppression
• Malignancy
• Extremes of ages
• Autoimmune disease
• Tobacco & Alcohol abuse
 Local factors :
• Chronic lymphoedema
• Venous stasis
• Major vessel disease
• Arteritis
• Extensive scarring
• Radiation fibrosis
• Small vessel disease
• Loss of local sensation
 Suppurative OM:
Acute
Chronic – primary
secondary
Infantile
 Non Suppurative :
Chronic sclerosing OM: focal
diffuse
Garre’s Sclerosing OM
Actinomycotic Osteomyelitis
Radiation Osteomyelitis & Necrosis
I. Acute Suppurative/ Nonsuppurative
(A) Contiguous focus: Trauma
Surgery
Odontogenic infection
(B) Progressive
Burns
Sinusitis
Vascular insufficiency
(C) Haematogenous (metastatic)
Developing skeleton
Developing dentition
II. Chronic forms
(A) Recurrent multifocal
Developing skeleton
Increased osteogenic activity
(B) Garre’s OM
Unique proliferative subperiosteal reaction
Developing skeleton
(C) Suppurative/ non suppurative
Inadequately treated
Systemically compromised
Refractory
(D) Sclerosing OM
Diffuse
Fastidious organisms
Compromised host
Focal
Predominantly odontogenic
Chronic localised entry
Etiology –
 Odontogenic infections
Periapical disease caused by pulpal pathosis
Periodontal disease
Long standing pericoronal infection
Infection of an odontogenic cyst or tumor
Infection of an extraction wound
 Infected fracture site
 Local trauma to gingiva
 Peritonsillar abscess
 Furunculosis of chin
 Hematogenous infection
Clinical features –
1. Fever, malaise, severe pain.
2. Swelling, regional lymphadenopathy.
3. Teeth may be loose & sore.
4. If the infection involves the mandibular canal, a
paraesthesia or anesthesia of the lower lip is
common.
Radiological features –
• No evidence till 1 – 2 weeks of disease
progression.
 Diffuse lytic changes – fuzziness & increased
trabacular spaces.
 Later cortex becomes involved, sequestrum &
radiolucent areas.
Histologic features –
 Medullary spaces filled with inflammatory
exudate/pus.
 Polymorphonuclear leukocytes.
 Osteoblasts bordering the bony trabeculae are
destroyed
Acute suppurative osteomyelitis
 Primary (infection by subvirulent org.)
Secondary to acute infection
Clinical Features –
• Local tenderness
• Swelling
• Mild leucocytosis
• Low-grade fever
• Regional lymphadenopathy
• Acute exacerbations - intra and/or extraoral
sinuses that intermittently develop and drain a
small amount of pus and then close
• Teeth may not be sore or loose
Radiographic Features
• Single or multiple radiolucencies of
variable size and with poorly defined
borders
• Affected bone becomes moth-eaten in
appearance.
• Sequestra - irregular calcified areas
separate from remaining bone.
• Subperiosteal bone may be deposited.
Sclerotic (L) Body mandible with sequestra
Sclerosis & sequestra (L) Mandible body
Sequestration
Periosteal reaction located at the inferior cortex
• Unusual reaction of bone to infection occurring in
extremely high tissue resistance or low grade
infection
Clinical features -
• In young adults < 20 yrs.
• Mandibular 1st
molars most commonly affected.
• Mild pain associated with infected pulp.
• No other prominent signs or symptoms.
Radiologic features –
• Well circumscribed radiopaque mass of
sclerotic bone surrounding & extending
below the apex of one or both roots.
• Proliferation more than destruction (infection
acts as a stimulus).
Histologic features –
 Dense mass of bony trabeculae with little
interstitial marrow tissue.
 If interstitial soft tissue is present – fibrotic &
infiltrated only by a small numbers of
lymphocytes.
Chronic focal sclerosing osteomyelitis
 Proliferative reaction of the bone to a low grade
infection.
 Infection mostly through diffuse periodontal
disease.
Clinical features –
 More common in older persons, blacks, females &
mandibular edentulous areas.
 Occasional acute exacerbation with resultant mild
suppuration & fistula formation.
 No other clinical indication of its presence.
Radiological features –
 Diffuse sclerosis of bone (cotton wool
appearance).
 Indistinct borders between the sclerosis &
normal bone.
 Occasionally bilateral.
Histologic features –
 Dense irregular trabeculae, some of which
are lined by an active layer of osteoblasts.
 Focal areas of osteoclastic activity may be
seen.
 Fibrous tissue containing proliferating
fibroblast, lymphocytes & plasma cells is
present between trabeculae.
Diffuse sclerosis with ® body of mandible
 Rare non-suppurative sclerosing
osteomyelitis by the formation of a
hard, bony swelling at the periphery
 Non-tender swelling in the inferior
border of the mandible below the first
molar.
 More frequently in females
 Affects young individuals before the
age of 25 yrs.
Radiologic features –
• A focal overgrowth of bone over the cortex
(outer surface) may be seen.
• Mass of bone is smooth & rather well
calcified.
• No trabecular shadows in the radiolucent
space.
• Cortex becomes thickened and laminated
with alternating radiopaque-radiolucent
layers (onion-peal appearance).
Garre’s osteomyelitis
Garre’s osteomyelitis
Etiology –
 Infection during delivery.
 Trauma to oral mucosa.
 Hematogenous.
Clinical features -
 Sudden onset & runs an acute course.
 High fever, rapid pulse, vomiting, delirium &
prostration.
 Local signs – edema with eyelids, subperiosteal
abscesses on alveolar mucosa & palate, followed by
sinus formation.
 Tuberculosis
 Actinomycosis
 Syphilis
 Disrupt the infectious foci.
 Debride any foreign bodies necrotic tissue, or
sequestra.
 Culture and identify specific pathogens for
eventual definitive antibiotic treatment.
 Drain and irrigate the region.
 Begin empiric antibiotics based on Gram stain.
 Stabilize calcified tissue regionally.
 Supportive therapy
 Consider adjunctive treatments to enhance
microvascular reperfusion (usually reserved for
refractory forms only).
 Sequestrectomy
 Saucerization 
 Trephination
 Decortication
 Vascular flaps
 Hyperbaric oxygen therapy
 Reconstruction as necessary following
resolution of the infection.
 General management
 Antibiotic therapy
 Surgical management –
Incision & drainage
Extraction of teeth
Closed wound irrigation & drainage
Intra-arterial antibiotics
Sequestrectomy
Sequestrectomy with saucerization
Decortication
Resection of the jaw with immediate or
delayed reconstruction.
 Hyperbaric oxygen therapy
A B
C
Saucerization
A B
C
Decortication
Closed wound irrigation &suction
 Regimen 1: for hospitalized /medically compromised
patient or when IV therapy indicated:
aqueous penicillin , 2 million U IV q4th , plus metronidazole ,
500 mg , q6H
When improved for 48 to 72 hrs , swtich to :
Penicillin V , 500 mg PO q6h, for additional 4 to 6 weeks
or ampicillin /sulbactum ( unasyn),1.5 to 3 g iv q6h
When improved swtich to :
Amoxicillin/clavunate ( augmentin) , 875 /125 mgPO bid ,
for additional 4 to 6 weeks
 Regimen 2 :
 penicillinV 2g, plus metronidazole ,0.5 gq8h PO,for 2 to 4 weeks
after last sequestrum removed and patient without symptoms
 Or clindamycin , 600to 900 mg q6h IV , then
 Clindamycin, 300to 450mg mg q6h PO
 Or cefoxitin ( mefoxin) , 1g q8h IV or 2 g q4h IM/IV until no
symptoms , then swtich to
 Cephalexin ( keflex) , 500mg q6h PO, for 2 to 4 weeks
 For penicillin allergic patients :
 Clindamycin
 Cefoxitin as above , if allergy not of anaphylactoid type
 Exposure of nonviable bone which fails to heal
without intervention following exposure to
intense irradiation >5000mGy.
 Dose rates > 0.55 mGy/hr – elevated risk.
 Triad of Irradiation, trauma, infection.
 Hypoxia, hypocellularity, hypovascular
tissues,associated with parenchymal
breakdown & chronic wound manifestation
secondary to radiation exhaustion of reparative
process (Marx-1983).
RADIATION
BONE
FORMATION OF HYPOXIC – HYPOVASCULAR –
HYPOCELLULAR TISSUE
TISSUE BREAKDOWN
CHRONIC NONHEALING WOUNDS
Clinical Staging:
• Stage I Exposed bone, non-healing wound
• Stage II Stage I non-responders, after 30 HBO
dives
• Stage III ORN cutaneous fistula, pathological
#s, inferior border resorption
Clinical features –
 Mandible more commonly affected.
 Loss of epithelial covering & exposure of bone.
 Pathological # may occur.
 Sequestrum formation.
 Intense pain, with intermittent swelling &
drainage.
 Sometimes painless.
Radiological features –
 Periphery is ill defined & similar to that in
chronic osteomyelitis.
 Irregular bony resorption – Moth eaten
appearance.
 Radiopaque or sclerotic appearance.
 Scattered regions of radiolucency , with or
without sequestrum.
Radiographic Aids –
 High resolution CT.
 Scintigraphy 99m Tc MDP shows regional
perfusion,bone turnover.
 MRI
MOTH EATEN APPEARANCE ®
BODY
Treatment of Osteoradionecrosis
• Rule out neoplastic disease
• Stabilise nutritional & metabolic condition
• Administer preoperative hyperbaric oxygen
• Debride soft & bony necrotic tissues as necessary
• Provide post operative hyperbaric oxygen
• Consider soft tissue vascular flap support
• Perform bony reconstruction if warranted
Surgical: sequestrectomy, resection intra/
extraorally
Hyperbaric oxygen therapy:
• 20-40 sessions 2.8-3.0 ATA , 100%, 2 times
daily for 90 minutes followed by 20
postoperative sessions.
Physiologic parameters augmented by
hyperbaric oxygen therapy:
• Increased oxygen diffusion to tissues.
• Revascularises irradiated tissues.
• Enhanced leucocytic lysosomal activity.
• Neutralisation of bacterial toxins.
• Free Oxygen radical Bactericidal activity against
anaerobes.
• Aerobic augmentation of wound healing cycle ,
collagen synthesis fibroblastic cellular density.
• Neoangiogenesis stimulation.
• Limits amount of nonvital tissues.
Pre Radiotherapy
 All teeth with questionable prognosis should be extracted
 All restorable teeth should be restored.
 Thorough prophylaxis & topical fluoride application.
 Oral hygiene measures & instructions should be
demonstrated & reinforced.
 Any sharp cusps should be rounded to prevent
mechanical irritation.
 Impressions for fabrication of custom fluoride trays to be
used during treatment.
 Stop habits like tobacco use & alcohol consumption.
During Radiotherapy –
 Pt should rinse mouth at least 10 time a day
with saline.
 Chlorhexidine mouth rinses twice daily to
minimize bacterial/ fungal levels within
mouth.
 Weekly oral hygiene evaluation by dentist.
 If overgrowth of candida albicans – nystatin or
clotrimazole topical application.
 Monitor mouth opening.
 Monitor nutritional status.
Post Radiotherapy –
 Dental evaluation every 3 – 4 months.
 Oral prophylaxis.
 Topical fluoride application should be done using
custom trays.
 Pt to be instructed in daily self administration of
topical fluoride administration.
 Salivary substitutes should be prescribed.
 Restore teeth developing post-radiotherapy caries
using amalgam or composites.
 Extraction of teeth can be carried out with the use of
- Hyperbaric oxygen before & after extraction
- Prophylactic antibiotic
 Evaluate artificial dentures.
Thank you

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Chronic maxillofacial infections

  • 2. Infection – Invasion of the body with organisms that have the potential to cause disease. Chronic –  Lasting a long time.  Condition of 3 months duration or longer ( US National centre for health statastics). Reasons for chronicity –  Extremely high host resistance.  Sub-virulent microorganisms.  Less number of microorganisms.
  • 3.
  • 4.  Osteo – bone Myelos – marrow Itis - inflammation  Inflammation of bone involving the cancellous bone, bone marrow, cortical bone & periosteum.
  • 5.  Noncompliance with health care delivery.  Systemic metabolic compromise – -Age -Malnutrition -Immunosuppression -Congenital or acquired pathophysiologic conditions disrupting blood supply  Inaccessibility to health care delivery.
  • 6.  Most are from local causes: 1. Acute periapical infection 2. Pericoronitis 3. Acute periodontal lesions 4. Trauma-fractures and extraction of teeth 5. Acute infection of the maxillary sinus 6. Direct extension of furunculosis of the face 7. Hematogenous
  • 7. • Staph aureus, Staph albus, Strep pyogenes • Bacteriodes, peptostreptococcus. • Arachnia, Actinomyces, Klebsiella, Eikenella etc • Typhoid,Haemophilus, pneumococci, spirochaetes
  • 8. Pulpitis Acute Chronic Apical Periodontitis Acute Chronic Periapical Abscess Periapical Granuloma Periapical Cyst Osteomyelitis Acute Chronic Focal Diffuse Periostosis Cellulitis Abscess Bacteraemia Toxaemia Septicemia Dissemination Shock Death Chronic Periapical abscess
  • 9. Mostly occurs in the mandible, rarely in the maxilla.  Most odontogenic infections are localised by the production of a protective pyogenic membrane or soft tissue abscess wall.  If sufficiently virulent, microorganisms may destroy this barrier. ACUTE  Acute inflammation sets in : Hyperemia Increased capillary permeability Infiltration of granulocytes
  • 10.  Proteolytic enzymes liberated due bacteria destruction- tissue necrosis & vascular thrombosis  Pus accumulates - increased intramedullary pressure - vascular collapse, venous stasis & ischemia.  Pus travels through the haversian & nutrient canals & accumulates beneath the periosteum, elevating it from the cortex, further reducing the blood supply.  Compression of the neurovascular bundle accelerates thrombosis & ischemia.  If pus continues to accumulate, the periosteum is peneterated & mucosal & cutaneous abscesses & fistulae may develop.
  • 11. CHRONIC  As natural host defenses & therapy begin to be effective, it becomes chronic.  Inflammation regresses, granulation tissue is formed.  Angiogenesis takes place leading to lysis of bone, thus separating fragments of necrotic bone from viable bone – Sequestra.  Small sections of bone may be completely lysed while larger ones may be isolated by a bed of granulation tissue & surrounded in a sheath of new bone – Involucrum  Occasionlly , the involucrum is peneterated by channels through which pus escapes to an epithelial surface – Cloacae.
  • 12. Radiographic evaluation • 30-60% destruction min 4-8 days to 3 wks • Moth eaten appearance, scattered areas of bone destruction • Islands of sequestrae in radiolucent areas surrounded by involucrum • Stippled granular densification due to subperiosteal deposition on surface of trabeculae at the expense of marrow spaces
  • 13. RADIOGRAPHIC AIDS • Radiographs • Bone imaging - Scintigraphy Determines presence of reactive bone Radiopharmaceuticals – technetium-99 gallium-67 indium-111 • High resolution Computer tomography • Magnetic Resonance Imaging
  • 14. Classification & staging system for Osteomyelitis (Cierny et al, 1985) I. Anatomic Stage I : Medullary OM, involves medullary bone usually hematogenous Stage II: Superficial OM, < 2cm defect without cancellous bone Stage III: Localized OM, <2 cm defect, does not involve both the cortices Stage IV: Diffuse OM, > 2cm, infection, non union, pathologic #
  • 15. II. Physiological class  Host : normal host  Host Systemic compromise Local compromise  Host : treatment worse than disease
  • 16.  Systemic factors affecting immune surveillance , metabolism, local vascularity • Malnutrition • Renal/ hepatic failure • Diabetes Mellitus • Chronic Hypoxia • Immune deficiency/ suppression • Malignancy • Extremes of ages • Autoimmune disease • Tobacco & Alcohol abuse
  • 17.  Local factors : • Chronic lymphoedema • Venous stasis • Major vessel disease • Arteritis • Extensive scarring • Radiation fibrosis • Small vessel disease • Loss of local sensation
  • 18.  Suppurative OM: Acute Chronic – primary secondary Infantile
  • 19.  Non Suppurative : Chronic sclerosing OM: focal diffuse Garre’s Sclerosing OM Actinomycotic Osteomyelitis Radiation Osteomyelitis & Necrosis
  • 20. I. Acute Suppurative/ Nonsuppurative (A) Contiguous focus: Trauma Surgery Odontogenic infection (B) Progressive Burns Sinusitis Vascular insufficiency (C) Haematogenous (metastatic) Developing skeleton Developing dentition
  • 21. II. Chronic forms (A) Recurrent multifocal Developing skeleton Increased osteogenic activity (B) Garre’s OM Unique proliferative subperiosteal reaction Developing skeleton (C) Suppurative/ non suppurative Inadequately treated Systemically compromised Refractory
  • 22. (D) Sclerosing OM Diffuse Fastidious organisms Compromised host Focal Predominantly odontogenic Chronic localised entry
  • 23. Etiology –  Odontogenic infections Periapical disease caused by pulpal pathosis Periodontal disease Long standing pericoronal infection Infection of an odontogenic cyst or tumor Infection of an extraction wound  Infected fracture site  Local trauma to gingiva
  • 24.  Peritonsillar abscess  Furunculosis of chin  Hematogenous infection Clinical features – 1. Fever, malaise, severe pain. 2. Swelling, regional lymphadenopathy. 3. Teeth may be loose & sore. 4. If the infection involves the mandibular canal, a paraesthesia or anesthesia of the lower lip is common. Radiological features – • No evidence till 1 – 2 weeks of disease progression.
  • 25.  Diffuse lytic changes – fuzziness & increased trabacular spaces.  Later cortex becomes involved, sequestrum & radiolucent areas. Histologic features –  Medullary spaces filled with inflammatory exudate/pus.  Polymorphonuclear leukocytes.  Osteoblasts bordering the bony trabeculae are destroyed
  • 27.  Primary (infection by subvirulent org.) Secondary to acute infection Clinical Features – • Local tenderness • Swelling • Mild leucocytosis • Low-grade fever • Regional lymphadenopathy • Acute exacerbations - intra and/or extraoral sinuses that intermittently develop and drain a small amount of pus and then close
  • 28. • Teeth may not be sore or loose Radiographic Features • Single or multiple radiolucencies of variable size and with poorly defined borders • Affected bone becomes moth-eaten in appearance. • Sequestra - irregular calcified areas separate from remaining bone. • Subperiosteal bone may be deposited.
  • 29. Sclerotic (L) Body mandible with sequestra
  • 30. Sclerosis & sequestra (L) Mandible body
  • 32. Periosteal reaction located at the inferior cortex
  • 33. • Unusual reaction of bone to infection occurring in extremely high tissue resistance or low grade infection Clinical features - • In young adults < 20 yrs. • Mandibular 1st molars most commonly affected. • Mild pain associated with infected pulp. • No other prominent signs or symptoms.
  • 34. Radiologic features – • Well circumscribed radiopaque mass of sclerotic bone surrounding & extending below the apex of one or both roots. • Proliferation more than destruction (infection acts as a stimulus). Histologic features –  Dense mass of bony trabeculae with little interstitial marrow tissue.  If interstitial soft tissue is present – fibrotic & infiltrated only by a small numbers of lymphocytes.
  • 35. Chronic focal sclerosing osteomyelitis
  • 36.  Proliferative reaction of the bone to a low grade infection.  Infection mostly through diffuse periodontal disease. Clinical features –  More common in older persons, blacks, females & mandibular edentulous areas.  Occasional acute exacerbation with resultant mild suppuration & fistula formation.  No other clinical indication of its presence.
  • 37. Radiological features –  Diffuse sclerosis of bone (cotton wool appearance).  Indistinct borders between the sclerosis & normal bone.  Occasionally bilateral.
  • 38. Histologic features –  Dense irregular trabeculae, some of which are lined by an active layer of osteoblasts.  Focal areas of osteoclastic activity may be seen.  Fibrous tissue containing proliferating fibroblast, lymphocytes & plasma cells is present between trabeculae.
  • 39. Diffuse sclerosis with ® body of mandible
  • 40.  Rare non-suppurative sclerosing osteomyelitis by the formation of a hard, bony swelling at the periphery  Non-tender swelling in the inferior border of the mandible below the first molar.  More frequently in females  Affects young individuals before the age of 25 yrs.
  • 41. Radiologic features – • A focal overgrowth of bone over the cortex (outer surface) may be seen. • Mass of bone is smooth & rather well calcified. • No trabecular shadows in the radiolucent space. • Cortex becomes thickened and laminated with alternating radiopaque-radiolucent layers (onion-peal appearance).
  • 44. Etiology –  Infection during delivery.  Trauma to oral mucosa.  Hematogenous. Clinical features -  Sudden onset & runs an acute course.  High fever, rapid pulse, vomiting, delirium & prostration.  Local signs – edema with eyelids, subperiosteal abscesses on alveolar mucosa & palate, followed by sinus formation.
  • 46.  Disrupt the infectious foci.  Debride any foreign bodies necrotic tissue, or sequestra.  Culture and identify specific pathogens for eventual definitive antibiotic treatment.  Drain and irrigate the region.  Begin empiric antibiotics based on Gram stain.  Stabilize calcified tissue regionally.
  • 47.  Supportive therapy  Consider adjunctive treatments to enhance microvascular reperfusion (usually reserved for refractory forms only).  Sequestrectomy  Saucerization   Trephination  Decortication  Vascular flaps  Hyperbaric oxygen therapy  Reconstruction as necessary following resolution of the infection.
  • 48.  General management  Antibiotic therapy  Surgical management – Incision & drainage Extraction of teeth Closed wound irrigation & drainage Intra-arterial antibiotics Sequestrectomy Sequestrectomy with saucerization Decortication
  • 49. Resection of the jaw with immediate or delayed reconstruction.  Hyperbaric oxygen therapy
  • 53.  Regimen 1: for hospitalized /medically compromised patient or when IV therapy indicated: aqueous penicillin , 2 million U IV q4th , plus metronidazole , 500 mg , q6H When improved for 48 to 72 hrs , swtich to : Penicillin V , 500 mg PO q6h, for additional 4 to 6 weeks or ampicillin /sulbactum ( unasyn),1.5 to 3 g iv q6h When improved swtich to : Amoxicillin/clavunate ( augmentin) , 875 /125 mgPO bid , for additional 4 to 6 weeks
  • 54.  Regimen 2 :  penicillinV 2g, plus metronidazole ,0.5 gq8h PO,for 2 to 4 weeks after last sequestrum removed and patient without symptoms  Or clindamycin , 600to 900 mg q6h IV , then  Clindamycin, 300to 450mg mg q6h PO  Or cefoxitin ( mefoxin) , 1g q8h IV or 2 g q4h IM/IV until no symptoms , then swtich to  Cephalexin ( keflex) , 500mg q6h PO, for 2 to 4 weeks  For penicillin allergic patients :  Clindamycin  Cefoxitin as above , if allergy not of anaphylactoid type
  • 55.
  • 56.  Exposure of nonviable bone which fails to heal without intervention following exposure to intense irradiation >5000mGy.  Dose rates > 0.55 mGy/hr – elevated risk.  Triad of Irradiation, trauma, infection.  Hypoxia, hypocellularity, hypovascular tissues,associated with parenchymal breakdown & chronic wound manifestation secondary to radiation exhaustion of reparative process (Marx-1983).
  • 57. RADIATION BONE FORMATION OF HYPOXIC – HYPOVASCULAR – HYPOCELLULAR TISSUE TISSUE BREAKDOWN CHRONIC NONHEALING WOUNDS
  • 58. Clinical Staging: • Stage I Exposed bone, non-healing wound • Stage II Stage I non-responders, after 30 HBO dives • Stage III ORN cutaneous fistula, pathological #s, inferior border resorption
  • 59. Clinical features –  Mandible more commonly affected.  Loss of epithelial covering & exposure of bone.  Pathological # may occur.  Sequestrum formation.  Intense pain, with intermittent swelling & drainage.  Sometimes painless.
  • 60. Radiological features –  Periphery is ill defined & similar to that in chronic osteomyelitis.  Irregular bony resorption – Moth eaten appearance.  Radiopaque or sclerotic appearance.  Scattered regions of radiolucency , with or without sequestrum. Radiographic Aids –  High resolution CT.  Scintigraphy 99m Tc MDP shows regional perfusion,bone turnover.  MRI
  • 62. Treatment of Osteoradionecrosis • Rule out neoplastic disease • Stabilise nutritional & metabolic condition • Administer preoperative hyperbaric oxygen • Debride soft & bony necrotic tissues as necessary • Provide post operative hyperbaric oxygen • Consider soft tissue vascular flap support • Perform bony reconstruction if warranted
  • 63. Surgical: sequestrectomy, resection intra/ extraorally Hyperbaric oxygen therapy: • 20-40 sessions 2.8-3.0 ATA , 100%, 2 times daily for 90 minutes followed by 20 postoperative sessions.
  • 64. Physiologic parameters augmented by hyperbaric oxygen therapy: • Increased oxygen diffusion to tissues. • Revascularises irradiated tissues. • Enhanced leucocytic lysosomal activity. • Neutralisation of bacterial toxins. • Free Oxygen radical Bactericidal activity against anaerobes. • Aerobic augmentation of wound healing cycle , collagen synthesis fibroblastic cellular density. • Neoangiogenesis stimulation. • Limits amount of nonvital tissues.
  • 65. Pre Radiotherapy  All teeth with questionable prognosis should be extracted  All restorable teeth should be restored.  Thorough prophylaxis & topical fluoride application.  Oral hygiene measures & instructions should be demonstrated & reinforced.  Any sharp cusps should be rounded to prevent mechanical irritation.  Impressions for fabrication of custom fluoride trays to be used during treatment.  Stop habits like tobacco use & alcohol consumption.
  • 66. During Radiotherapy –  Pt should rinse mouth at least 10 time a day with saline.  Chlorhexidine mouth rinses twice daily to minimize bacterial/ fungal levels within mouth.  Weekly oral hygiene evaluation by dentist.  If overgrowth of candida albicans – nystatin or clotrimazole topical application.  Monitor mouth opening.  Monitor nutritional status.
  • 67. Post Radiotherapy –  Dental evaluation every 3 – 4 months.  Oral prophylaxis.  Topical fluoride application should be done using custom trays.  Pt to be instructed in daily self administration of topical fluoride administration.  Salivary substitutes should be prescribed.  Restore teeth developing post-radiotherapy caries using amalgam or composites.  Extraction of teeth can be carried out with the use of - Hyperbaric oxygen before & after extraction - Prophylactic antibiotic  Evaluate artificial dentures.