Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Chronic maxillofacial infections

2,619 views

Published on

Published in: Health & Medicine
  • Be the first to comment

Chronic maxillofacial infections

  1. 1. DR MOHAMMAD AKHEELOMFS PG
  2. 2. Infection – Invasion of the body with organismsthat have the potential to cause disease.Chronic – Lasting a long time. Condition of 3 months duration or longer ( USNational centre for health statastics).Reasons for chronicity – Extremely high host resistance. Sub-virulent microorganisms. Less number of microorganisms.
  3. 3.  Osteo – boneMyelos – marrowItis - inflammation Inflammation of bone involving the cancellousbone, bone marrow, cortical bone &periosteum.
  4. 4.  Noncompliance with health care delivery. Systemic metabolic compromise –-Age-Malnutrition-Immunosuppression-Congenital or acquired pathophysiologicconditions disrupting blood supply Inaccessibility to health care delivery.
  5. 5.  Most are from local causes:1. Acute periapical infection2. Pericoronitis3. Acute periodontal lesions4. Trauma-fractures and extraction of teeth5. Acute infection of the maxillary sinus6. Direct extension of furunculosis of the face7. Hematogenous
  6. 6. • Staph aureus, Staph albus, Strep pyogenes• Bacteriodes, peptostreptococcus.• Arachnia, Actinomyces, Klebsiella,Eikenella etc• Typhoid,Haemophilus, pneumococci,spirochaetes
  7. 7. PulpitisAcute ChronicApical PeriodontitisAcute ChronicPeriapicalAbscessPeriapicalGranulomaPeriapicalCystOsteomyelitisAcute Chronic FocalDiffusePeriostosisCellulitis AbscessBacteraemia Toxaemia Septicemia Dissemination ShockDeathChronicPeriapicalabscess
  8. 8. Mostly occurs in the mandible, rarely in the maxilla. Most odontogenic infections are localised by theproduction of a protective pyogenic membrane orsoft tissue abscess wall. If sufficiently virulent, microorganisms may destroythis barrier.ACUTE Acute inflammation sets in :HyperemiaIncreased capillary permeabilityInfiltration of granulocytes
  9. 9.  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 fromthe cortex, further reducing the blood supply. Compression of the neurovascular bundle acceleratesthrombosis & ischemia. If pus continues to accumulate, the periosteum ispeneterated & mucosal & cutaneous abscesses &fistulae may develop.
  10. 10. 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, thusseparating fragments of necrotic bone from viable bone –Sequestra. Small sections of bone may be completely lysed whilelarger ones may be isolated by a bed of granulationtissue & surrounded in a sheath of new bone –Involucrum Occasionlly , the involucrum is peneterated by channelsthrough which pus escapes to an epithelial surface –Cloacae.
  11. 11. Radiographic evaluation• 30-60% destruction min 4-8 days to 3 wks• Moth eaten appearance, scattered areas of bonedestruction• Islands of sequestrae in radiolucent areassurrounded by involucrum• Stippled granular densification due tosubperiosteal deposition on surface of trabeculaeat the expense of marrow spaces
  12. 12. RADIOGRAPHIC AIDS• Radiographs• Bone imaging - ScintigraphyDetermines presence of reactive boneRadiopharmaceuticals – technetium-99gallium-67indium-111• High resolution Computer tomography• Magnetic Resonance Imaging
  13. 13. Classification & staging system for Osteomyelitis (Ciernyet al, 1985)I. AnatomicStage I : Medullary OM, involves medullary boneusually hematogenousStage II: Superficial OM, < 2cm defect withoutcancellous boneStage III: Localized OM, <2 cm defect, does notinvolve both the corticesStage IV: Diffuse OM, > 2cm, infection, non union,pathologic #
  14. 14. II. Physiological class Host : normal host HostSystemic compromiseLocal compromise Host : treatment worse than disease
  15. 15.  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
  16. 16.  Local factors :• Chronic lymphoedema• Venous stasis• Major vessel disease• Arteritis• Extensive scarring• Radiation fibrosis• Small vessel disease• Loss of local sensation
  17. 17.  Suppurative OM:AcuteChronic – primarysecondaryInfantile
  18. 18.  Non Suppurative :Chronic sclerosing OM: focaldiffuseGarre’s Sclerosing OMActinomycotic OsteomyelitisRadiation Osteomyelitis & Necrosis
  19. 19. I. Acute Suppurative/ Nonsuppurative(A) Contiguous focus: TraumaSurgeryOdontogenic infection(B) ProgressiveBurnsSinusitisVascular insufficiency(C) Haematogenous (metastatic)Developing skeletonDeveloping dentition
  20. 20. II. Chronic forms(A) Recurrent multifocalDeveloping skeletonIncreased osteogenic activity(B) Garre’s OMUnique proliferative subperiosteal reactionDeveloping skeleton(C) Suppurative/ non suppurativeInadequately treatedSystemically compromisedRefractory
  21. 21. (D) Sclerosing OMDiffuseFastidious organismsCompromised hostFocalPredominantly odontogenicChronic localised entry
  22. 22. Etiology – Odontogenic infectionsPeriapical disease caused by pulpal pathosisPeriodontal diseaseLong standing pericoronal infectionInfection of an odontogenic cyst or tumorInfection of an extraction wound Infected fracture site Local trauma to gingiva
  23. 23.  Peritonsillar abscess Furunculosis of chin Hematogenous infectionClinical features –1. Fever, malaise, severe pain.2. Swelling, regional lymphadenopathy.3. Teeth may be loose & sore.4. If the infection involves the mandibular canal, aparaesthesia or anesthesia of the lower lip iscommon.Radiological features –• No evidence till 1 – 2 weeks of diseaseprogression.
  24. 24.  Diffuse lytic changes – fuzziness & increasedtrabacular spaces. Later cortex becomes involved, sequestrum &radiolucent areas.Histologic features – Medullary spaces filled with inflammatoryexudate/pus. Polymorphonuclear leukocytes. Osteoblasts bordering the bony trabeculae aredestroyed
  25. 25. Acute suppurative osteomyelitis
  26. 26.  Primary (infection by subvirulent org.)Secondary to acute infectionClinical Features –• Local tenderness• Swelling• Mild leucocytosis• Low-grade fever• Regional lymphadenopathy• Acute exacerbations - intra and/or extraoralsinuses that intermittently develop and drain asmall amount of pus and then close
  27. 27. • Teeth may not be sore or looseRadiographic Features• Single or multiple radiolucencies ofvariable size and with poorly definedborders• Affected bone becomes moth-eaten inappearance.• Sequestra - irregular calcified areasseparate from remaining bone.• Subperiosteal bone may be deposited.
  28. 28. Sclerotic (L) Body mandible with sequestra
  29. 29. Sclerosis & sequestra (L) Mandible body
  30. 30. Sequestration
  31. 31. Periosteal reaction located at the inferior cortex
  32. 32. • Unusual reaction of bone to infection occurring inextremely high tissue resistance or low gradeinfectionClinical features -• In young adults < 20 yrs.• Mandibular 1stmolars most commonly affected.• Mild pain associated with infected pulp.• No other prominent signs or symptoms.
  33. 33. Radiologic features –• Well circumscribed radiopaque mass ofsclerotic bone surrounding & extendingbelow the apex of one or both roots.• Proliferation more than destruction (infectionacts as a stimulus).Histologic features – Dense mass of bony trabeculae with littleinterstitial marrow tissue. If interstitial soft tissue is present – fibrotic &infiltrated only by a small numbers oflymphocytes.
  34. 34. Chronic focal sclerosing osteomyelitis
  35. 35.  Proliferative reaction of the bone to a low gradeinfection. Infection mostly through diffuse periodontaldisease.Clinical features – More common in older persons, blacks, females &mandibular edentulous areas. Occasional acute exacerbation with resultant mildsuppuration & fistula formation. No other clinical indication of its presence.
  36. 36. Radiological features – Diffuse sclerosis of bone (cotton woolappearance). Indistinct borders between the sclerosis &normal bone. Occasionally bilateral.
  37. 37. Histologic features – Dense irregular trabeculae, some of whichare lined by an active layer of osteoblasts. Focal areas of osteoclastic activity may beseen. Fibrous tissue containing proliferatingfibroblast, lymphocytes & plasma cells ispresent between trabeculae.
  38. 38. Diffuse sclerosis with ® body of mandible
  39. 39.  Rare non-suppurative sclerosingosteomyelitis by the formation of ahard, bony swelling at the periphery Non-tender swelling in the inferiorborder of the mandible below the firstmolar. More frequently in females Affects young individuals before theage of 25 yrs.
  40. 40. Radiologic features –• A focal overgrowth of bone over the cortex(outer surface) may be seen.• Mass of bone is smooth & rather wellcalcified.• No trabecular shadows in the radiolucentspace.• Cortex becomes thickened and laminatedwith alternating radiopaque-radiolucentlayers (onion-peal appearance).
  41. 41. Garre’s osteomyelitis
  42. 42. Garre’s osteomyelitis
  43. 43. 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, subperiostealabscesses on alveolar mucosa & palate, followed bysinus formation.
  44. 44.  Tuberculosis Actinomycosis Syphilis
  45. 45.  Disrupt the infectious foci. Debride any foreign bodies necrotic tissue, orsequestra. Culture and identify specific pathogens foreventual definitive antibiotic treatment. Drain and irrigate the region. Begin empiric antibiotics based on Gram stain. Stabilize calcified tissue regionally.
  46. 46.  Supportive therapy Consider adjunctive treatments to enhancemicrovascular reperfusion (usually reserved forrefractory forms only). Sequestrectomy Saucerization  Trephination Decortication Vascular flaps Hyperbaric oxygen therapy Reconstruction as necessary followingresolution of the infection.
  47. 47.  General management Antibiotic therapy Surgical management –Incision & drainageExtraction of teethClosed wound irrigation & drainageIntra-arterial antibioticsSequestrectomySequestrectomy with saucerizationDecortication
  48. 48. Resection of the jaw with immediate ordelayed reconstruction. Hyperbaric oxygen therapy
  49. 49. A BCSaucerization
  50. 50. A BCDecortication
  51. 51. Closed wound irrigation &suction
  52. 52.  Regimen 1: for hospitalized /medically compromisedpatient or when IV therapy indicated:aqueous penicillin , 2 million U IV q4th , plus metronidazole ,500 mg , q6HWhen improved for 48 to 72 hrs , swtich to :Penicillin V , 500 mg PO q6h, for additional 4 to 6 weeksor ampicillin /sulbactum ( unasyn),1.5 to 3 g iv q6hWhen improved swtich to :Amoxicillin/clavunate ( augmentin) , 875 /125 mgPO bid ,for additional 4 to 6 weeks
  53. 53.  Regimen 2 : penicillinV 2g, plus metronidazole ,0.5 gq8h PO,for 2 to 4 weeksafter 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 nosymptoms , 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
  54. 54.  Exposure of nonviable bone which fails to healwithout intervention following exposure tointense irradiation >5000mGy. Dose rates > 0.55 mGy/hr – elevated risk. Triad of Irradiation, trauma, infection. Hypoxia, hypocellularity, hypovasculartissues,associated with parenchymalbreakdown & chronic wound manifestationsecondary to radiation exhaustion of reparativeprocess (Marx-1983).
  55. 55. RADIATIONBONEFORMATION OF HYPOXIC – HYPOVASCULAR –HYPOCELLULAR TISSUETISSUE BREAKDOWNCHRONIC NONHEALING WOUNDS
  56. 56. Clinical Staging:• Stage I Exposed bone, non-healing wound• Stage II Stage I non-responders, after 30 HBOdives• Stage III ORN cutaneous fistula, pathological#s, inferior border resorption
  57. 57. 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.
  58. 58. Radiological features – Periphery is ill defined & similar to that inchronic osteomyelitis. Irregular bony resorption – Moth eatenappearance. Radiopaque or sclerotic appearance. Scattered regions of radiolucency , with orwithout sequestrum.Radiographic Aids – High resolution CT. Scintigraphy 99m Tc MDP shows regionalperfusion,bone turnover. MRI
  59. 59. MOTH EATEN APPEARANCE ®BODY
  60. 60. 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
  61. 61. Surgical: sequestrectomy, resection intra/extraorallyHyperbaric oxygen therapy:• 20-40 sessions 2.8-3.0 ATA , 100%, 2 timesdaily for 90 minutes followed by 20postoperative sessions.
  62. 62. Physiologic parameters augmented byhyperbaric oxygen therapy:• Increased oxygen diffusion to tissues.• Revascularises irradiated tissues.• Enhanced leucocytic lysosomal activity.• Neutralisation of bacterial toxins.• Free Oxygen radical Bactericidal activity againstanaerobes.• Aerobic augmentation of wound healing cycle ,collagen synthesis fibroblastic cellular density.• Neoangiogenesis stimulation.• Limits amount of nonvital tissues.
  63. 63. 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 bedemonstrated & reinforced. Any sharp cusps should be rounded to preventmechanical irritation. Impressions for fabrication of custom fluoride trays to beused during treatment. Stop habits like tobacco use & alcohol consumption.
  64. 64. During Radiotherapy – Pt should rinse mouth at least 10 time a daywith saline. Chlorhexidine mouth rinses twice daily tominimize bacterial/ fungal levels withinmouth. Weekly oral hygiene evaluation by dentist. If overgrowth of candida albicans – nystatin orclotrimazole topical application. Monitor mouth opening. Monitor nutritional status.
  65. 65. Post Radiotherapy – Dental evaluation every 3 – 4 months. Oral prophylaxis. Topical fluoride application should be done usingcustom trays. Pt to be instructed in daily self administration oftopical fluoride administration. Salivary substitutes should be prescribed. Restore teeth developing post-radiotherapy cariesusing amalgam or composites. Extraction of teeth can be carried out with the use of- Hyperbaric oxygen before & after extraction- Prophylactic antibiotic Evaluate artificial dentures.
  66. 66. Thank you

×