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Odontogenic infection


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Odontogenic infection

  1. 1. Odontogenic infection Islam Kassem
  2. 2. CLASSIFICATION OF ODONTOGENIC INFECTIONSAre classified into:A- Iatrogenic infectionB- Non-iatrogenic infection
  3. 3. Non-Iatrogenic Infection• Pericoronal infections(Pericoronitis& Operculitis) Impacted or unerupted tooth.• Periodontitis• Acute Alveolar Abscess• Soft Tissue Abscess• Facial Cellulitis• Facial Spacess Abscess• Panfacial spaces infection• Acute necrotizing infection• Complicated odontogenic infection
  4. 4. IATROGENIC ODONTOGENIC INFECTIONI- post-injection infectionII- Post-extraction infectionIII- post- surgical infection
  5. 5. TYPES OF INFECTIONBacterial: Endogenous or Exogenous
  6. 6. PREDISPOSING FACTORSTraumaDebilitating conditionsImmuno compromised states
  7. 7. AETIOLOGY OF IMMUNODEFICIENCYA- Systemic conditions: AIDS Diabetes mellitus End-stage renal disease Leukemia/lymphoma Systemic lupus erythematous Advanced age
  8. 8. AETIOLOGY OF IMMUNODEFICIENCY, cont.B- Primary immunodeficienciesX-linked severe combined immunodeficiencyWiskott-Aldrich syndromeChediak-Higashi syndromeDiGeorge syndrome
  9. 9. AETIOLOGY OF IMMUNODEFICIENCY, contC- Iatrogenic causes: Immunosuppressive drugsBroad-spectrum antibioticsChemotherapyRadiation therapyBone marrow transplantation
  10. 10. AETIOLOGY OF IMMUNODEFICIENCY, cont D- Social Factors; * Alcoholism * IIIicit drug use * Morbid Obesity.
  11. 11. DIAGNOSISA- Patient’s history.B- Clinical ExaminationC- Radiographically; in the acute phase , no signs are observed at the bone, may be observed 1- 2 weeks later, unless there is recurrence of a chronic condition
  12. 12. RADIOGRAPHIC DIAGNOSIS.There may be :1.A deeply carious tooth ,or2. Restoration very close to the pulp,3. As well as thickening of the periodontal ligament.These data indicate a causative tooth.
  13. 13. Presentations• Pain• Lymphadenopathy• Swelling• Facial sinuses• Trismus• Symptoms secondary to complications
  14. 14. •Clinical Features• A-Local: B-systemic extra-oral *Fever Intra-oral *Headache• Manifestations *Tachycardia• Trismus * Malaise• Teeth• Discharge
  15. 15. Clinical Features Of Suppuration (stage of abscess formation)*Pain:  .dull aching-throbbing*Temp:  .hectic fever*Swelling: .fluctuant .+ve paget’s*Skin:  .pitting edema*Aspiration test  pus
  16. 16. Principles of Treatment of Acute Odontogenic Infections1st: Control of infection: A- Stage of cellulitis. B- Stage of suppuration2nd: Support the patient3rd:Removal of the cause4th:Treatment of complications
  17. 17. Control of InfectionStage of cellulitis: -Antibiotic therapy 1- Broad spectrum 2- Bactericidial 3- Combination -Hot fomentation - Warm mouth wash -Control any predisposing factor
  18. 18. Stage of Suppuration (Abscess Formation).Incision + Drainage,,,,When??? And How???.Culture and sensitivity.Antibiotics according to the culture& sensitivity..Anti-anaerobic chemotherapy: *Metronidazole
  19. 19. Support of the patient.• Hospitalization in the following conditions:1.Risk of airway obstruction2. Immunocompromised States3. Difficulty in swallowing4. Patient very ill5. Underlying systemic disease6. Patient unable to manage at home.7. Extremes of age( very young & very old)
  20. 20. AIR WAY OBSTRUCTION1- Ludwig’s angina2- Impending Ludwig’s angina3-Panfacial spaces infection4-Retropharyngeal abscess5-Extremes of age (very young& very old)6- Acute necrotizing fascitis.
  21. 21. Clinical Features of suppuration (Stage of Abscess formation)Paindull aching Throbbing Temp. Hectic fever Swelling Fluctuation,+Ve Paget’s test. Skin Pitting edema Aspiration test- Pus
  22. 22. Drainage of Pus * Anesthesia ???? *Incision; should fulfill the following:1.Over the most fluctuant site 2.Large and adequate 3. Independent 4. Includes all loculi5. Avoids important structures 6. Cosmetic, if possible.
  23. 23. Incision for drainage of a sublingual abscess. Theincision is performed parallel to the Incision for drainage of a palatalsubmandibular duct abscess, parallel to the greater palatineand the lingual nerve vessels
  24. 24. Incisions for drainage of a submandibular or parotid (a), and asubmasseteric (b) abscess. During cutaneousincisions, the course of the facial artery andvein must be taken into consideration (a),as well as that of the facial nerve (b
  25. 25. Diagrammatic illustrations showing the incision of anintraoral abscess and theplacement of a hemostat to facilitatethe drainage of pus
  26. 26. Diagrammaticillustrations showing the placementof a rubber drain in the cavityand stabilization with a sutureon one lip of the incision
  27. 27. Indications of Antibiotic Therapy* After incision and Draniage;*?? Is it necessary to give antibiotics to all patients??????*Of course NO.*Minor infections in patients with intact host defenses may not require antibiotic therapy.* Even, some moderately severe infections can be treated without antibiotics.
  28. 28. The Decision To Use Antibiotic Therapy1.Depressed host defenses, even, in minor infections.2.In treating minor infections that donot lend themselves to surgical intervention, such as a diseased tooth that must be retained but doesnot drain when the pulp chamber is opened.3.If the infection in stage of cellulitis.4. If the abscess is sourrended by an area of cellulitis.
  29. 29. 5. If there is lymphangitis or lymphadenitis.6. If the infection is complicated; septecemia, paeymia,…7. If there is specific infection, Tuberculosis.8. In Patients with Prosthetic appliances.9. Patients with systemic manifestations of infections.
  30. 30. Principles of Choosing the Appropriate AntibioticThe Following guidelines are useful in selecting the proper antibiotic:1.Identification of the causative organism,2. Determination of the antibiotic sensitivity.3. Use of specific narrow spectrum antibiotic4. Use of least toxic antibiotic,
  31. 31. 5. Patient drug history.6. Use of bactericidal rather than bacteriostatic drugs.7. Use of antibiotic with proven history of success.8.Cost of the antibiotic.
  32. 32. Identification of the Causative OrganismThis can be achieved either by:1. Isolating the organism from pus, blood or tissues, in the laboratory; or2. Empirically, based on knowledge of the pathogenesis, and clinical presentation of the specific infectionAntibiotic therapy is then either initial or definitive:
  33. 33. Microbiology of Odontogenic Infections** The typical odontogenic infection is caused by a mixture of aerobic and anaerobic bacteria  70 %.* Anerobic bacteria causes  25%* Aerobic bacteria Causes only 5% of cases.
  34. 34. Clinical Implications1.The microbiology of cellulitis-type infections, that don’t have abscess formation, shows almost exclusevely, aerobic bacteria.2. As the infection becomes more severe, the microbiology becomes a mixed flora of aerobic and anaerobic bacteria,3. If the infection process becomes contained and controlled by the body defenses, the aerobic bacteria are no longer able to survive, in the hypoxic acidotic environment, and only anaerobic bacteria are found.
  35. 35. Therapeutic ImplicationsAerobic Bacteria of Odontogenic Infection:* Primarily Gram-Positive Cocci, mainly streptococcistrept. Viridans &Alpha-hemolytic  all of which are susceptible to penicillin and other antibiotics with similar antimicrobialspectrum.* The streptococci Accounts for 85 % of the aerobic bacteria found in odontogenic infections.
  36. 36. Therapeutic Implications, cont.Anerobic bacteria of odontogenic infection;1. Their number is greater than that of aerobic bacteria.2. There are two main groups of anerobic bacteria:A- Anaerobic gram positive cocci,B-Anaerobic gram-negative rods.
  37. 37. Culture and SensitivityIndications:1. If the infection has compromised the host defenses.2. If the patient had received appropriate treatment for three days without improvement.3. If the infection is a post-operative wound infection.4. If the infection is recurrent.5. If actinomycosis is suscepected.6. If osteomyleitis is present.NB; in these situations deviation from the normal bacterial pattern is likely.
  38. 38. Principles of Antibiotic adminstration1. Proper dose2. Proper time interval3.Proper route of adminstration4.Consistency of route of adminstration.5. Combination antibiotic therapy
  39. 39. Patient Monitoring1. Response to treatment.2. Development of adverse reactions3. Superinfection and Recurrent infection.
  40. 40. AIR WAY OBSTRUCTION1- Ludwig’s angina2- Impending Ludwig’s angina3-Panfacial spaces infection4-Retropharyngeal abscess5-Extremes of age(very young& very old)6- Acute necrotizing fascitis.
  41. 41. Removal of Underlying CauseA- Local Factors:1.Remaining Root(s)2.Dead Tooth3. Apical or residual cysts.4. Periodontal disease5. Bad Oral hygiene.6- forigen body; broken needle, file…..
  42. 42. Removal of Underlying Cause(cont.)B- Underlying Systemic Causes;1.Diabetes Mellitus2. Blood Dyscrasias3. Chronic deblitating Diseases4. Immuno-Suppressed Patients.
  43. 43. FATE OF ACUTE ODONTOGENIC INFECTIONDepend on the following factors;1- Virulence of the micro-organism2- Host Resistance3- Anatomic Geography.4- Management: a. Timing b. Line of treatment c.Antibiotic; type,dosage,duration….
  44. 44. Natural History of Dental infectionِAcute odontogenic infection:1-Resolution; When???2-Chronicity Trismus,if the mastcatory muscles are involved which may last for years.3- Spread : Acute soft tissue Abscess  Deep facial spaces abscess Bacteremia&Septicemia Ascending facial-cerebral infection.  Descending  To the neck,Chest4- Complications: a-Fistulae; cutaneous or mucosal. b- Osteomyelitis.
  45. 45. SPREAD OF INFECTION. Infection may spread in three ways:1. By continuity through tissue spaces and planes,2. By way of lymphatic system3. By way of blood circulation
  46. 46. Spread Through Tissue Spaces and PlanesThis is the commonest route of spread
  47. 47. Diagrammatic illustrations showing spread of infection (propagation of pus) of an acute dent alveolar abscess, depending on the position of the apex of the responsible tooth. a Buckle root: buccal direction. b Palatal root: palatal direction Diagrammatic illustration showing the localization of infection above or below the mylohyoid muscle, depending on the position of the apices of the responsible toothSpreadof pus towards the maxillarysinus, due to thecloseness of the apicesto the floor of the antrum
  48. 48. Spread of pus depending on thelength of root and attachment of buccinatormuscle. a Apex above attachment: accumulation of pus in the buccalspace. b Apex beneath the buccinator muscle intraoral pathwaytowards the mucobuccal fold
  49. 49. Intraalveolar abscess of maxilla (a) and mandible (b)Diagrammatic illustrations showing accumulation of pus at a portion of thealveolar bone in relation to theperiapical region
  50. 50. Subperiosteal abscess with linguallocalization. a Diagrammatic illustration; bclinical photograph
  51. 51. Submucosal abscess with buccal localization.a Diagrammatic illustration; b clinicalphotograph
  52. 52. Subcutaneous abscess originating from amandibular tooth. a Diagrammatic illustration. bClinical photograph. The swelling mainly involves theregion of the angle of the mandible
  53. 53. Fascial abscess (submandibular). aDiagrammatic illustration. b Clinicalphotograph
  54. 54. Treatment of Acute Dento-Alveolar Infection• * Medical: Antibiotics ????• * Dental: R.C.T., Extraction, Periodontal• * Surgical: Incision and Drainage, Bone fenestration
  55. 55. Causes of failure of treatment• 1- Failure to drain an abscess• 2-Obstruction of a duct (salivary gland)• 3-Presence of a foreign body or stone• 4-Presence of an open portal (I.v,urinary catheter)• 5-Poor host resistance• 6-failure of antibiotic to reach the site (osteomyelitis)• 7-Inadeqate antibiotic dosage,duration,type• 8-wrong bacteriologic diagnosis e.g. specific infection.
  56. 56. Complications of Acute• Odontogenic Infection 1-Chronicity• 2-Dead teeth• 3-periapical abscess• 4-Periodontal abscess• 5-Sinuses(cutaneous&/or mucosal)• 6-Chronic dental granuloma• 7-Periostitis
  57. 57. Complications of Acute Odontogenic Infection ) (cont• 7-osteomyelitis• 8-Extra-articular TMJ ankylosis• 9-Cutaneous scars• 10-Fistulae: cutaneous muscosal• 11-Mediastinits, meningitis• 12-Death ?????
  58. 58. Persistance of infectionTo be suspected in the following conditions:1. Prolonged period of treatment2. Increasing amount of pus3. Bad odour of pus4. Unexplained severe pain5. Spreading infection6. Persistance of fever Any or all of the above means Onset of complications
  59. 59. LUDWING’ANGINADefinition; acute and diffuse cellulitis involving bilaterally the submental,submandibular and sublingual spaces.Aetiology:1.Acute odontogenic infections which open below the mylohyoid attachment, usually from the mandibular 2nd,and 3rd molars.2. Penetrating injuries of the floor of the mouth.3. Osteomyleitis of the mandible.4. Compound mandibular fractures especially of the angle.5. Suppurative submandibular sialadenitis.
  60. 60. BACTERIOLOGYMixed infections; mainly hemolytic streptoccoci and mixture of aerobic gm –ve micro- organisms including fusiform bacilli,vincent’s organism and various staphyloccus.
  61. 61. CLNICAL FEATURES1. Swelling; rapidly developing brawny hard involving floor of the mouth and three subs- spaces starting unilaterally and ending bilaterally. The swelling is localization.Later the swelling may extend to the neck.2. Patient’s Mouth; is usually opened because of elevation of the floor of mouth and swelling of the tongue.
  62. 62. CLNICAL FEATURES, cont.3. The tongue; is elevated and protruded from the mouth, with a wooden appearance and limited movement.4. Glottic edema; severe edema of the glottis and larynx which cause airway obstruction.5. Stridor, difficult respiration and dysphagia.6.Constitutional symptoms.
  63. 63. MANAGEMENT1.Maintain a patent airway.2.Incision and Drainage Decompression of the airway??3. Antibiotics.4. General Supportive Measures.5.Treatment of the Underlying Cause , if possible.6 . Post-operative Care.
  64. 64. Air Way Management1.Anethesia; No Anethesia?? Local?? Or General??2. Intubation; Oral or Nasal?3. Tracheostomy
  65. 65. Infections of the Oral Mucosa
  66. 66. • Viral infections• Bacterial infections• Fungal infections• HIV infection and AIDS
  67. 67. Herpes Viradae• Herpes Simplex 1• Herpes Simplex 2• Varicella Zoster• Epstein-Barr• Cytomegalovirus (HHV5)• Herpes 6• Herpes 7• Herpes 8
  68. 68. Herpes Simplex Virus• Most frequent cause of viral infections of the mouth• Primary HSV I Infectious (Acute Herpetic Gingivostomatitis) – 5 days incubation, then 2 days of prodromal symptoms – Acute onset of malaise, fever, and lymphadenopathy. – Multiple vesicles and ulcers can occur any part in the oral mucosa and lips – 10-14 days to resolve – Spread by droplets or lesion contact – Majority of cases are subclinical
  69. 69. Mild circumoral
  70. 70. Herpes Simplex Virus– Extraoral spread of infection: skin, fingers, nail bed, eyes Herpetic whitlow
  71. 71. • Treatment – Supportive – Acyclovir in extreme cases• Prognosis: – self-limited – resolves in 10-14 days
  72. 72. • HSV remain latent in trigeminal sensory ganglia• Virus reactivation associated with: – Ultraviolet radiation – Trauma – Immunosuppression
  73. 73. Recurrent Herpetic Stomatitis• Prodrome: • tingling • burning • paresthesia• Vesicles and ulcers recur: most common herpes labialis – Intraorally: hard palate and gingiva – In small clusters
  74. 74. Varicella-Zoster Virus Chickenpox and herpes zoster (shingles)Primary Infection: Varicella (Chicken pox) – Prodrome: malaise, fever, lymphadenopathy – Macules, papules, vesicles, ulcers on skin and oral mucosa • Especially soft palate – Skin lesions are pruritic.
  75. 75. Zoster (Shingles)• Multiple recurrence is rare – Same latent state as HSV, in sensory ganglia – Predisposing factors: • Decreased immunocompetence – Elderly patients – Immunosuppressive drugs
  76. 76. Zoster (Shingles)• Unilateral vesicular eruptions• Prodromes of pain and parasthesia for up to 2 weeks• Trigeminal Nerve: – Ophthalmic division is most frequently involved – Intra or extra oral or both• Complications – Post herpetic neuralgia – Ramsay Hunt syndrome: involvement of geniculate ganglion
  77. 77. Coxsackievirus Enteroviradae• Over 30 types• Ones worth mentioning – Herpangina – Hand-foot and mouth – Acute lymphonodular pharyngitis
  78. 78. Herpangina– Coxsackie Viruses, Group A, RNA– Children– Sudden onset of • fever, sore throat, nausea, vomiting, diarrhea and lymphadenopathy.– Vesicles and ulcers in posterior oral cavity– D/D: primary herpes– Treatment is symptomatic
  79. 79. Hand foot and mouth disease• Coxsackie A16• Spread in households – Oral lesions almost always present – Oral lesions resemble herpangina but can be larger – 7-10 days.
  80. 80. Infectious Mononucleosis (glandular fever)• EBV• Young adults• Transmitted by saliva• Clinically: pharyngitis, LN enlargement• Fever, prolonged malaise• Non specific oral manifestation• Petechei on juncetion of hard and soft palate• Serology: atypical peripheral lymphocytes
  81. 81. Infectious mononucleosis (glandular fever)• EBV – Nasopharyngeal carcinoma – Hairy leukoplakia – Burkitt’s lymphoma – Oral squamous cell carcinoma?
  82. 82. Measles (Rubeola)• Paramyxovirus• Children• Prodromal symptoms• Koplik spots disappear as skin rash starts
  83. 83. Measles (Rubeola)• Skin rash: start on face, go to trunk• FeverComplications• Otitis media, pneumonia, encephalitis, brain damage• Noma may be a complication in malnourished patients
  84. 84. Cytomegalovirus• Herpes group• Rarely causes disease in immunocompetent• Subclinical infection is common 40-60% of population• Affects immunocompromised individuals – Neonatal, transplant, immunosuppressant• Affect salivary glands common but asymptomatic• Cause non specific oral ulceration – Atypical peripheral lymphocytes
  85. 85. Noma (cancrum oris)• Orofacial gangrene• Malnourished children• Immunosuppressed individuals• Usually preceded by NUG
  86. 86. Actinomycosis• Chronic and endogenous, anaerobic, Gram positive• Actinomyces israelli predominate• Soft tissues of the submandibular region – Source of infection: infected root canal or third molar• Firm swelling (painless) that suppurate• Multiple sinuses pointing to skin• sulphur granules
  87. 87. Syphilis• Treponema pallidum• Primary: chancre : shallow ulcer – Indurated base – Associated with lymphadenopathy – Heals spontanously
  88. 88. 6 weeks later• Secondary syphilis: skin rash and mucous patch – Snail track ulcers, flat areas of ulceration that coalesced
  89. 89. Years laterTertiary :• Gumma: – Necrosis and type IV hypersensitivity – Perforation of palate• Atrophic glossitis: – due to endarteritis obliterance – Followed by:• Syphilitic leukoplakia – Hyperkeratosis – Followed by:• Squamous cell carcinoma
  90. 90. Congenital Syphilis• Miscarriage, still birth or neonatal infection• Collapse of nasal bridge• Hutchinson triad: blindness, deafness, dental anomalies – Hutchinson incisors (notched teeth) • Screw driver teeth – Peg shaped laterals – Mulberry molars • Constricted atrophic cusps • Globular masses of hard tissue
  91. 91. Tuberculosis• Mycobacterium tuberculosis• Oral infection is not common – Primary oral infection – Secondary oral infection: infected sputum from pulomonary TB
  92. 92. Classical TB ulcer:• Painless• Undermind• On the tongue
  93. 93. Gingival involvement:• Granulomatous inflammation
  94. 94. Tuberculosis• Diagnosis: Biopsy, granulomatous inflammation – Granulomas with central necrosis – Identification of Acid Fast Bacilli• Treatment: – 2 antimicrobial agents: isoniazide and rifampicin, 4-8 months
  95. 95. Leprosy• Mycobacterium leprae• Endemic in tropical areas• 2 forms of infection: – Tuberculoid – Lepromatous• Oral lesions in lepromatous – Secondary to nasal involvement – Maxillary gingiva, palate
  96. 96. Gonorrhoea• Neisseria gonorrhea• Mainly tonsillar and soft palatal lesions• Erythema, vesicles, ulcers, pain
  97. 97.
  98. 98. CandidiasisPredisposing factors:A) Systemic:1) Immunological immaturity in infants.2) Immunological exhaustion in elderly.3) Systemic corticosteroids.4) Systemic antibiotics.5) Systemic immune suppression therapy.6) Chemotherapy.7) Disease-induced xerostomia.8) Drug-induced xerostomia.9) Diabetes Mellitus.10) HIV and AIDS.
  99. 99. B) Local:1) Ill-fitting dentures.2) Reduced vertical dimension.3) Lip-licking habit.4) Overuse of antiseptic and antibiotic rinses.
  100. 100. -Mucocutaneous. -Pseudomembranous. -Syndrome associated.Systemic Local -Atrophic. -Hypertrophic.Pseudomembranous (Thrush): in the form of white plaques which canbe scraped off small hemorrhagic areas.
  101. 101. Atrophic Candidiasis:• Atrophic glossitis due to loss of filiform papillae.• Angular cheilitis due to loss of vertical occlusal dimension.• Median rhomboid glossitis.
  102. 102. Hypertrophic Candidiasis:This can mimic lichen planus, leukoplakia,verrucous carcinoma or a squamous cell carcinoma.
  103. 103. Treatment of Candidiasis:1. Removal of the concomitant underlying factors.2. Nystatin oral suspention or as vaginal suppositories.3. In chronic Candidiasis: Nystatin + Fluconazole (Diflucan).4. In disseminated Candidiasis: Amphotericin B infusion.
  104. 104. Benign Migratory Glossitis (Stomatitis) (Geographic Tongue)Alternating areas of rough keratinized areas and smooth red dekeratinized areas.It is asymptomatic except on occasions when spicy foods or citrus acidic products are used.Treatment: non-specific, sometimes Nystatin gives response in symptomatic cases.
  105. 105. Histoplasmosis The classic presentation of the disease is the appearance of single or multiple oral ulcers in an older person with chronic obstructive pulmonary disease (COPD).Differential diagnosis:1. Other deep fungal infections such as coccidioidomycosis and blastomycosis.2. Squamous cell carcinoma.3. Syphilitic chancre.4. T.B. ulcers.Diagnosis: Biopsy is mandatory.
  106. 106. Treatment:a) Oral : Itraconazole 200-400 mg daily for 7 months, or:b) I.V. : Amphotericin B :in individuals non-responsive to oral treatment, are immunocompromised or have histoplasmosis meningitis.
  107. 107. Coccoidioidomycosis and Blastomycosis:Are both uncommon in Egypt and can be diagnosed after histological examination of the oral ulcers.
  108. 108. RhinoscleromaIn the mouth , this can present as a granulomatous mass in the palate.Differential diagnosis:1. Nasopharyngeal angiofibroma.2. Antral squamous cell carcinoma.3. Lymphoepithelioma.4. Rhinophyma.Rhinoscleroma is not specifically related to diabetes or immune suppression as is mucormycosis.Diagnosis: Depends on biopsy.
  109. 109. MucormycosisThe most common presentation is maxillary and orbital cellulitis in a person with uncontrolled D.M. with ketoacidosis . Immunocompromised patients also are susceptible.The maxillary sinuses are usually filled with black necrotic bone and granulation tissue.Palatal ulcers frequently occur and will often progress to large oro-naso-antral and orbital communications.
  110. 110. AspergillosisBesides its usual clinical presentations in the form of external otitis and maxillary sinusitis, it can involve the skin of the face as a black-coloured ulcer.
  111. 111. Lesions mimicking fungal orofacial lesions:1.Leukoplakia :
  112. 112. Bisphosphonate RelatedOsteonecrosis of the Jaws
  113. 113. Bisphosphonates – what are they?• Class of drugs• High affinity for calcium – Binds to bone surfaces – Nitrogen: increased affinity, potency• Prevent bone resorption and remodeling• IV and oral formulations – IV: tx for bone resorption 2° metastatic tumors, osteolytic lesions – Oral: tx for osteoporosis, osteopenia
  114. 114. Bisphosphonates: Common uses• Prevention and treatment of osteoporosis inpostmenopausal women• Increase bone mass in men with osteoporosis• Tx of glucocorticoid-induced osteoporosis• Tx of Paget’s disease of bone• Hypercalcemia of malignancy• Bone metastases of solid tumors – breast and prostate carcinoma; other solid tumors• Osteolytic lesions of multiple myeloma
  115. 115. History of Bisphosphonate Development• Mid-19th Century German chemists – Anti-corrosive in pipelines• 20th Century - Clinical applications – Tc99 Bone scans – Toothpaste • Anti-tartar, anti-plaque effects – Osteopathies • Anti-resorptive effect
  116. 116. Medical Indications for IV BPs• Bone metastasis, hypercalcemia – RANKL-mediated osteoclastic resorption • Multiple myeloma, breast CA, prostate CA • Paracrine-like effect – PTH-like peptide osteoclastic resorption • Small cell carcinoma, oropharyngeal cancers • Endocrine-like effect
  117. 117. Medical Indications for Oral BPs• Paget’s Disease of bone – Accelerated bone turnover • Reduced compressive strength, increased vascularity • Bone pain • Elevated AP levels• Osteoporosis – Effects of estrogen loss: • Decreased bone turnover/renewal – Adipocyte differentiation > osteoblastic differentiation – increased fibrofatty marrow – Progressively porotic bone – DEXA scan for BMD values
  118. 118. Pharmacokinetics• Oral BP’s – Absorbed in small intestine • Less if taken with meal – 1-10% available to bone• Circulating half-life: 0.5-2 hrs – Rapid uptake into bone matrix – 30-70% of IV/oral dose accumulates in bone – Remainder excreted in urine• Repeated doses accumulate in bone – Removed only by osteoclast- mediated resorption – “Biologic Catch 22”
  119. 119. Bisphosphonate Side Effects•Upset stomach •Inflammation/erosions of esophagus•Fever/flu-like symptoms•Slight increased risk for electrolyte disturbance•Uveitis•Musculoskeletal joint pain•And of course…………………
  120. 120. BRONJ • Exposed, devitalized bone in maxillofacial region • Prior history or current use of BP • Vague pain, discomfort • Spontaneous occurrence, or… • 2° surgery or trauma to oral soft tissue/
  121. 121. BRONJ: Clinical Presentation• Exposed alveolar bone – Open mucosal wound – Necrotic bone – Spontaneous or Traumatic • Extractions, periodontal surgery, apicoectomy, implant placement• Infection – Purulence, bone pain – Orocutaneous fistula
  122. 122. BRONJ: Clinical Presentation• Subclinical Form – asymptomatic – radiographic signs • Sclerosis of lamina dura • Widening of PDL space
  123. 123. Clinical Presentation (cont)…• Soft tissue abrasions – Tissues rubbing against bone• AND………
  124. 124. Staging of BRONJ• Proposed by AAOMS: – Patients at risk (Subclinical) • No apparent exposed/necrotic bone in pts treated w/ IV or oral BPs – Patients with BRONJ • Stage 1: Exposed/necrotic bone, asymptomatic, no infection • Stage 2: Exposed/necrotic bone, pain, clinical evidence of infection • Stage 3: Exposed/necrotic bone, pain, infection, one or more of the following: – Pathologic fracture, extra-oral fistula, osteolysis extending to inferior border
  125. 125. BRONJ: IV BPsMore frequently Lesions moreextensiveAll stages  II, III more commonLower success withTxPatients generallysicker
  126. 126. Stage 0 Lesions• Spontaneous onset numbness and pain• No exposed bone• No prior dental antecedent• Positive image findings: – Sclerosis – Positive bone scan
  127. 127. BRONJ: Historical Context• Rare reports prior to 2001• 2003: Marx reported 36 patients• 2004: Ruggiero et al reported 63 pts (from 2001-2003)• 2005: Migliorati reported 5 cases• 2005: Estilo et al reported 13 cases• Sept. 2004: Novartis (manufacturer of Aredia & Zometa) altered labeling to include cautionary language concerning osteonecrosis of the jaws• 2005: FDA issued warning for entire drug class (including oral bisphosphonates)
  128. 128. Phossy-Jaw: A Historical Entity• Lorinser, 1845: first reported cases• Industrial laborers working w/ white phosphorus powder – Matchmaking, fireworks factories – Missile factories• Clinical presentation – Nonhealing mucosal wound following extraction – Pain – Fetid odor – Suppuration – Necrosis w/ bony sequestra – Extra-oral fistulae• Miles, Hunter: 20% mortality due to infections – Pre-antibiotic era• Conservative treatment – Selective debridement – Minimal mucosal manipulation – Topical agents: copper sulfate
  129. 129. Similar Clinical Entities• Closely resembles Osteopetrosis – Loss of osteoclastic function – Hypermineralization – Fractures, nonunions, open oral wounds – Endpoint: bone necrosis, +/- infection
  130. 130. NOT to be confused with these other entities:– Osteoradionecrosis (ORN): • avascular bone necrosis 2° radiation– Osteomyelitis: • thrombosis of small blood vessels leading to infection within bone marrow– Steroid-induced osteonecrosis: • more common in long bones • exposed bone very rare
  131. 131. Estimated Incidence of BRONJ 2° IV BPs• Limited to retrospective studies with limited sample sizes• Marx: – Zometa: exposed bone within 6-12 months – Aredia: 10-16 months• Estimates of cumulative incidence of BRONJ range from 0.8% to 12% – Marx: 5-15% • Including Subclinical osteonecrosis• Incidence will rise: – Increased recognition – Increased duration of exposure – Increased followup
  132. 132. Why Only in the Jaws?• Dixon et al 1997 – Alveolar crest has high remodeling rate • 10x tibia • 5x mandible at level of IA canal • 3.5x mandible at inferior border• Greater uptake of Tc 99m in bone scans – Occlusal forces • Compression at root apex and furcations • Tension on lamina dura and periodontal ligament • Remodeling of lamina dura in response • Reduced remodeling with BP uptake  hypermineralization – Sclerotic appearance of Lamina dura – Widening of periodontal ligament space
  133. 133. Risk Factors for Development of BRONJ• Drug-related factors – Potency of BP • Zoledronate > pamidronate > oral BPs – Duration of therapy• Local factors – Dentoalveolar surgery • Extractions, implants, periapical surgery, periodontal surgery w/ osseous injury • 7-fold risk for BRONJ with IV BPs • 5 to 21-fold risk in some studies – Local anatomy • lingual tori, mylohyoid ridge, palatal tori • Mandible > maxilla (2:1) – Concomitant oral disease • 7-fold risk for BRONJ with IV BPs
  134. 134. Risk factors (continued) Demographic/systemic factors  Age: 9% increased risk for every passing decade  Multiple myeloma patients treated w/ IV BPs  Race: Caucasian  Cancer diagnosis  multiple myeloma > breast cancer > other cancers  Osteopenia/osteoporosis diagnosis concurrent w/ cancer diagnosis Additional risk factors:  Corticosteroid therapy  Diabetes  Smoking  EtOH  Poor oral hygiene  Chemotherapeutic drugs
  135. 135. Subclinical Risk Assessment• Early signs of BP toxicity: – Radiographs • Panoramic, PA films – Sclerosis of alveolus, lamina dura – Widening of PDL space – Clinical exam • Tooth mobility – Unrelated to alveolar bone loss • Deep bone pain with no apparent etiology
  136. 136. Treatment Strategies• Stage III disease – Pathologic fractures, refractory cases • Preservation of function – Airway, speech compromise with large mandible resections • Segmental resections, titanium plate reconstruction, external fixation. – All infections must be cleared first » Delay reconstruction up to 3 months – Avoid bone grafting
  137. 137.
  138. 138. Study source?
  139. 139. • Contemporary Oral & maxillofacial surgery• Page 291 -316
  140. 140. • You can get it form•
  141. 141. •Thank you