Osteomyelitis of facial skeleton

This is a presentation on Osteomyelitis of facial skeleton from a point of view of an Oral & Maxillo-Facial Surgeon

1. OSTEOMYELITIS MODERATOR : Dr (Col) Suresh Menon PRESENTER : Dr. Rayan M

2. CONTENTS DEFINITION HISTORY PREDISPOSING FACTORS PATHOGENESIS ETIOLOGY CLASSIFICATION MICRORGANISMS CLINICAL FEATURES AND DISTRIBUTION INVESTIGATIONS SURGICAL MANAGEMENT REFERENCES

3. Osteomyelitis Osteon means bone; Muelinos means marrow; itis means inflammation Extensive inflammation of the bone involving the bone marrow, cortex and periosteum . The term “osteomyelitis” is mostly used to describe a true infection of the bone induced by pyogenic microorganisms (Marx 1991)

4. History The prevalence, clinical course, and management of osteomyelitis of the jawbones have changed profoundly over the past 50 years. This is due to mainly one factor: the introduction of antibiotic therapy, specifically penicillin. In the preantibiotic era, the classical presentation of jawbone osteomyelitis was an acute onset, usually followed by a later transition to a secondary chronic process ( Wassmund 1935; Axhausen 1934)

5. Predisposing Factors Systemic, metabolically compromised individuals who can be categorized into the following subsets: a. Age of patient b. Malnutrition c. Immunosuppression d.Congenital or acquired pathophysiology disrupting microvascular perfusion of the calcified tissue structure and investing soft tissue envelope Osteomyelitis of the Jaws:A 50-Year Perspective; J Oral Maxillolac Surg 51:1294·1301,1993

6. Etiology Odontogenic infection – periodontal ,periapical, pericoronal . Infection from infected dental cyst. Compound fracture of Jaw. Traumatic injury. Middle ear infection & upper respiratory tract infection through haematogenous route. Furuncle of chin by lymphtic route. Peritonsillar abscess

7. Local factors Long standing carious lesions Periodontal diseases (which leads to the breakdown of the periodontal barrier membrane. Neonatal, tooth germ associated Maxillary sinusitis Trauma/ Fracture Implant / Foreign body induced Radiation Other odontogenic infections

8. Pathogenesis

9. Osteomyelitis primarily occurs as a result of contiguous spread of odontogenic infections or as a result of trauma. Primary hematogenous osteomyelitis is rare in the maxillofacial region, generally occurring in the very young.

10. Pathogenesis Acute inflammation (edema & pus formation) Increased intramedullary pressure Vascular collapse (stasis, ischemia of bon e ) Avascular bone Pus, organism extension Haversian system/ nutrient canal involvement Elevation of periosteum Disrupted blood supply Avascular infected bone OSTEOMYELITIS A B

11. Infection from the pulp extends into the periapical region PULPITIS Acute Chronic APICAL PERIODONTITIS PERIAPICAL ABSCESS PERIAPICAL GRANULOMA Acute Chronic PERIAPICAL CYST OSTEOMYELITIS PERIOSTITIS

12. Effectiveness of host defense Effectiveness of therapy Inflammation regresses Granulation tissue forms New blood vessels form Lyse & separate the necrotic bone Sequestrum Large sections of bone gets embedded within granulation tissue & encased in a sheath of new bone – Involucrum Involucrum is penetrated by channnels through which pus escapes to an epithelial surface - Cloacae

13. Fate of sequestrum

14. Micro organisms Gram positive organism Staphyloccous areus Staphyloccous albus Haemolytic Streptococci Gram Negative organism Klebsiella Pseudomonas Proteus E. coli

15. Systemic factors altering host immunity • Diabetes mellitus • Autoimmune disorders • AIDS • Agranulocytosis • Anemia (especially sickle cell) • Leukemia • Malnutrition Chemotherapy • Corticosteroid and other immunosuppressive therapy • Alcohol and tobacco • Drug abuse

16. Disease Mechanism facilitating bone infection Diabetes Diminished leukocyte chemotaxis , phagocytosis ; diminished vascularity of tissue due to vasculopathy , thus reducing perfusion and the ability for an effective inflammatory response; slower healing rate Leukemia Deficient leukocyte function and associated anaemia Malnutrition Reduced wound healing and reduction of immunological response Cancer Reduced wound healing and reduction of immunological response Osteopetrosis Reduction of bone vascularization due to enhanced mineralization, replacement of hematopoietic marrow causing anaemia & leukopenia Severe anemia Systemic debilitation, reduced tissue oxygenation, bone infarction (sickle cell), especially in patients with a homozygous anaemia trait AIDS Impaired immune response Immunosuppr-ession Impaired immune response

17. Classifications Classification based on pathogenesis – Waldvogell Dual classification based on pathological anatomy and pathophysiology - Cierny Classification based on clinical picture, radiology, pathology, and etiology - Topazian RG Clinical appearance and course of the disease, as well as on radiological features - Zurich Classification System

18. Waldvogell Hematogenous osteomyelitis Osteomyelitis secondary to a contiguous focus of infection Osteomyelitis associated with or without peripheral vascular disease Waldvogell , F.A., Medoff , G. and Swartz, M.N. Osteomyelitis : a review of clinical features, therapeutic considerations and unusual aspects. N Engl J Med 282:198–266, 316–322, 1970.

19. Cierny Anatomic Types Stage I: medullar osteomyelitis –involved medullary bone without cortical involvement; usually hematogenous Stage II: superficial osteomyelitis – less than 2 cm bony defect without cancellous bone Stage III: localized osteomyelitis – less than 2 cm bony defect on radiograph, defect does not appear to involve both cortices Stage IV: diffuse osteomyelitis – defect greater than 2 cm. Pathologic fracture, infection, nonunion Physiological class A host: normal host B host: systemic compromised host, local compromised host C host: treatment morbidity worse than disease,low prognosis Ciney G, Mader JT, Pennick H : A clinical staging system of adult osteomyelitis, Contemp Orthop 10:17, 1985

20. Topazian I. Suppurative osteomyelitis 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis – Primary chronic suppurative osteomyelitis – Secondary chronic suppurative osteomyelitis 3. Infantile osteomyelitis II. Non suppurative osteomyelitis 1. Chronic sclerosing osteomyelitis – Focal sclerosing osteomyelitis – Diffuse sclerosing osteomyelitis 2. Garre's sclerosing osteomyelitis 3. Actinomycotic osteomyelitis 4. Radiation osteomyelitis and necrosis Topazian RG Osteomyelitis of the Jaws. In Topizan RG, Goldberg MH ( eds ): Oral and Maxillofacial Infections.Philadelphia , WB Saunders 1994,Chapter 7, pp 251-88

21. Zurich 1. Acute Osteomyelitis (AO) 2. Secondary Chronic Osteomyelitis (SCO) 3. Primary Chronic Osteomyelitis (PCO) Acute Osteomyelitis Secondary Chronic Osteomyelitis Primary Chronic Osteomyelitis • Neonatal, tooth germ associated • Trauma/fracture related • Odontogenic • Foreign body, transplant/implant induced • Associated with bone pathology and/ or systemic disease •Early onset (juvenile chronic osteomyelitis) • Adult onset • Syndrome associated

22. Hudson’s I. Acute forms of osteomyelitis (suppurative or nonsuppurative) A. Contagious focus 1. Trauma 2. Surgery 3. Odontogenic Infection B. Progressive 1. Burns 2. Sinusitis 3. Vascular insufficiency C. Hematogenous (metastatic) Developing skeleton (children)

23. II. Chronic forms of osteomyelitis A. Recurrent multifocal 1. Developing skeleton (children) 2. Escalated osteogenic (activity< age 25 years) B. Garrè's 1. Unique proliferative subperiosteal reaction 2. Developing skeleton (children and young adults) C. Suppurative or non suppurative 1. Inadequately treated forms 2. Systemically compromised forms 3. Refractory forms (chronic recurrent multifocal osteomyelitis CROM) D. Diffuse sclerosing 1. Fastidious micro organisms 2. Compromised host/pathogen interface

24. Distribution Mandible > maxilla Mandible – body > symphysis > angle > ascending ramus > condyle

25. Clinical features Acute suppurative osteomyelitis Deep intense pain High intermittent fever Hypoesthesia Clinical abscess/pus formation Clearly identifiable cause Exposure of bone Swelling is minimal Lymphadenopathy

26. Subacute suppurative osteomyelitis Deep pain, malaise, fever, anorexia Teeth loosen – sensitive to percussion Pus exudes around gingival sulcus /fistula Fetid odour Firm cellulitis of cheek Expansion of bone from increased periosteal activity Erythema , abscess formation, tenderness on palpation P aresthesia Trismus – not always present Regional lymphadenopathy

27. Chronic suppurative Osteomyelitis Multiple fistulae Induration of soft tissues Thickened /wooden character of the affected area with pain & tenderness on palpation In primary chronic osteomyelitis – no acute phase of infection Insidious in onset Slight pain Slow increase in jaw size Gradual development of sequestrum Often without fistulae

28. Infantile osteomyelitis

29. Osteomyelitis Maxillaries Neonatarum , Maxillitis of infancy Osteomyelitis in the jaws of new born infants occurs almost exclusively in maxilla. First described by Rees in 1847. Wilensky (1932) described it in comprehensive manner. McCash & Rowe – less common after introduction of antibiotics. 29

30. Etiology Trauma – through break in mucosa cause during delivery. Infection involving maxillary sinus Infection from the nose. Hematogenous spread through streptococci & pneumococci. Infected nipple – infected human or artificial nipple 30

31. Pathogenesis Main cause is said to be infection – especially with S. aureus. Hematogenous spread has been suggested from either a skin injury or pyogenic infection of the middle ear, mastoid process, tonsils & even umbilical cord. Local causes may be small abrasions suffered at the time of delivery 31

32. Clinical features Illness is ushered in by fever, anorexia & intestinal disturbances. First sign is swelling or redness below the inner canthus of the eye. Followed by marked edema of the eyelids Alveolus & palate become swollen. In a day or so, this is followed by a pus discharge. Sinus formation below the inner canthus of the eye. Intraorally, swelling spreads across the palate with multiple draining sinuses along the alveolar margin on affected side. With establishment of free drainage, a chronic stage ensues. 32

33. Persists until sequestra & affected tooth buds are extruded or surgically removed. Among the extruded sequestra maybe the outer 1/3 rd or 2/3 rd of the inferior orbital margin. Chronic suppuration may lead to residual permanent deformity of the maxilla, loss of teeth & adherent scars below the eyelid. When recognized early and appropriate therapy instituted, the results are good. 33

34. Treatment Intravenous antibiotics, preferably penicillin. Culture & sensitivity testing Incision & drainage of fluctuant areas Sequestrectomy Supportive therapy 34

35. Acute osteomyelitis

36. Clinical features: Patient experiences deep seated, boring, continuous pain. Moderate sized indurated swelling forms over the affected region of jaw involving the cheek. When mandible involved, loss of sensation occurs on lower lip on affected side due to involvement of inferior alveolar nerve. Teeth become loose, tender on percussion Pus discharged through multiple sinuses in the alveolus or exudes along the necks of teeth. Trismus – may be severe & serious in children. Fetid odour Regional lymphadenopathy usually present. 36

37. General features: T emperature of approx 100ºF. Following establishment of drainage, pain eases and temperature falls. If left untreated, death may occur due to septicemia, pneumonia, meningitis and cavernous sinus thrombosis. Area of bone deprived of its blood supply becomes dead, sequestrum formation occurs followed by pathologic fractures. New bone is produced alongside osteomyelitic area, rapid in children. Sometimes the entire jaw may be reconstituted in spite of massive death of original bone. Other cases, jaw may fail to grow and permanent deformity ensues, especially if condylar area affected. 37

38. Radiographic features Early stages mandible appears normal. Earliest radiographic change is that trabeculae in involved area are thin, of poor density & slightly blurred. Subsequently multiple radiolucencies appear which become apparent on radiograph. In some cases there is saucer shaped area of destruction with irregular margins. Loss of continuity of lamina dura, seen in more than one tooth. 38

39. Chronic suppurative ostoemyelitis

40. Commences as the acute condition subsides. In acute phase, degree of destruction of cortical plate depends on: Extent to which pus has spread beneath periosteum Virulence of the organisms concerned As soon as pus drains intra or extraorally , condition ceases to spread and chronic phase commences. Infection is localized but persistent as bacteria are able to grow in dead bone inaccessible to body’s defenses.

41. Clinical features Pain is mild and intermittent, temperature rarely elevated and WBC count may be normal. Acute exacerbations occur at regular intervals; intense pain and swelling accompanied by pyrexia. Lasts for 3 – 4 days, relieved when pus discharges. New bone formation leads to thickening causing facial asymmetry. 41

42. Thickened or “wooden” character of bone. Self limiting, eventually cures itself as the last sequestra is discharged. Patient may be left with residual deformity of the jaw and multiple facial scars where sinuses have discharged. 42

43. Radiographic Features Depends on the stage; early stage no changes seen. Trabeculae in the involved area become thin or appear fuzzy & then lose their continuity. Eventually areas of bone destruction appear giving rise to characteristic mottling. After some time “moth eaten” appearance is seen Sequestra appear denser on radiographs. 43

44. Management 3D: Debridement, Drainage and Drug Sequestrum : if small exfoliates through mucosa If large surgical removal

45. Chronic non- suppurative ostoemyelitis

46. Garre’s Osteomyelitis ( Chronic Osteomyelitis with Proliferative Periostitis ) Chronic Non Suppurative Sclerosing Osteitis/ Periostitis Ossificans. Non suppurative productive disease characterized by a hard swelling. The infectious agent localizes in or beneath the periosteal covering of the cortex. Occurs primarily in young persons who possess great osteogenic activity of the periosteum. 46

47. Clinical Features Uncommonly encountered, described in tibia and in the head and neck region, in the mandible. Typically involves the posterior mandible & is usually unilateral. Patients present with an asymptomatic bony, hard swelling with normal appearing overlying skin and mucosa. On occasion slight tenderness may be noted 47

48. The increase in the mass of bone may be due to mild toxic stimulation of periosteal osteoblasts by attenuated infection. Hypertrophy may represent an exuberant attempt at repair. When the existing cause becomes quiescent, the resultant mass undergoes remodelling . Boyd & Bell state the permanent thickening of bone. 48

49. Radiographic features Radiopaque laminations of bone that roughly parallel each other & the underlying cortical surface. Laminations vary from 1 – 12 in number, radiolucent separations often are present between new bone and original cortex. (“onion skin appearance”) 49

50. Management Consists of removal of the offending teeth or endodontic treatment Administration of an antibiotic. Regression of the periosteal reaction is expected over a period of time without any need for surgical intervention. Bone curettage. Kaushal Mahendra Shah, Amol Karagir , Shridevi Adaki : Chronic non- supperative osteomylities with proliferative periostitis or garre`s osteomyelitis: BMJ (2013) 10, 114-115

51. Chronic diffuse sclerosing osteomyelitis

52. Analogous to the focal form. Represents a proliferative reaction of bone to low grade infection. Portal of entry is not through carious infection but rather through diffuse periodontal disease.

53. Clinical features May occur at any age, most common in older persons, especially in edentulous mandibles. No gender predilection Insidious nature, presents no clinical indications of its presence. Acute exacerbation – vague pain, unpleasant taste, mild suppuration. Many times spontaneous formation of fistula seen opening onto mucosal surface to establish drainage 53

54. Radiographic features Diffuse patchy, sclerosis of bone – “cotton wool” appearance Radiopacity may be extensive and bilateral. Due to diffuse nature, border between sclerosis & normal bone is often indistinct. 54

55. Actinomycotic osteomyelitis Cervicofacial actinomycosis is a slowly progressive infection with both granulomatous and suppurative features. In secondary chronic osteomyelitis, infection with Actinomyces is mostly of endogenous origin, since the pathogen is known to be an oral saprophyte, present in periodontal pockets, carious teeth, tonsillar crypts. Spontaneous drainage of serous fluid containing granular material may occur.

56. Management Tretment should be vigorous. Removal of foci of infection. Resection of the sequestrated bone. Excision of all the granulation tissue until healthy tissue is exposed. Prolonged administration of antibiotics, preferably penicillin. Additional exposure time to antibiotic is necessary because lysis of Actinomyces species occurs at slow rate. Bahar Sezer et al: Actinomycosis osteomyelitis of the jaw: report of four cases and a review of the literature: Journal of Dental Sciences (2017) 12, 301-307

57. Osteomyelitis associated with tuberculosis Osteomyelitis of the jaws can be caused by infection with Mycobacterium tuberculosis The mechanisms of spread of infection are, in analogy to other osteomyelitis cases, caused by other bacteria, by direct inoculation, through tooth-extraction sockets, through any breach in the mucosa during tooth eruption, spread from adjacent soft tissue sites, or by hematogenous spread.

58. Management Resection of the sequestrated bone. Anti tubercular therapy ( four conventional drug rifampicin, isoniazid, pyrazinamide and ethambutol initially as an intensive regiment followed by rifampicine and isoniazid for a period of 9-12 months) However WHO recommends a short course therapy of 6 months because of the pauci – bacillary nature of the disease . Parvaiz a. Koul et al: Tubercular osteomyelitis of the mandible in a young female: International journal of Mycobacteriology 3 (2014) 155 -157)

59. Principles of treatment Evaluation and correction of host defense Gram staining, culture and sensitivity Imaging Administration of empirical antibiotics Removal of loose teeth and sequestrum Culture guided antibiotics Possible placement of irrigating drains/antibiotic beads Surgical procedures

60. Investigations Hemogram Pus - Culture & Antibiotic sensitivity E.S.R. & C reactive protein may be seen.

61. Conventional radiographs 30-60% bone destruction required The orthopanoramic view is not useful in the initial evaluation of osteomyelitis. The ‘moth-eaten’ appearance of bone or sequestrum of bone, is the classic appearance of osteomyelitis.

62. Imaging Radionuclide imaging – provides information based on reactive bone 99m Tc – gets distributed in areas of increased blood flow 99m Tc - confirms acute osteomyelitis Additional 67 Ga study – distinguish from neoplastic diseases.

63. CT and MRI CT shows increased attenuation in medullary cavity, destruction of cortical bone, new bone formation and appearance of sequestra .

64. Investigations Conventional Radiograph + ve Osteomyelitis - ve Osteomyelitis highly suspected Technitium bone scan + ve Osteomyelitis - ve Osteomyelitis highly suspected - ve Osteomyelitis highly suspected Ga scan + ve Osteomyelitis MRI & CT + ve Osteomyelitis - ve

65. Complete bed rest Supportive therapy Nutritional support High protein diet High caloric diet Adequate multivitamins Rehydration Hydration orally Administration of I.V fluids Blood transfusion If RBC , Hb % are low Control of Pain Analgesic and sedation Antibiotic therapy Treatment

66. Antibiotic Regimen for Osteomyelitis of Jaw Regimen 1: For in patients/ medically compromised patients Aqueous penicillin, 2 million U IV q4h, plus metronidazole, 500mg, q6h When improved for 48 to 78 hours, switch to: Penicillin V, 500mg PO q4h, plus metronidazole 500mg PO q6h for 4 to 6 weeks Or Augmentin 1gm PO bid for 4 to 6 weeks

67. Regimen 2: For outpatients Penicillin V, 2 g, plus metronidazole, 0.5g , q8h PO for 2 to 4 weeks after last sequestrum removed and patient without symptoms Or Clindamycin 600 to 900 mg q6h IV, then: Clindamycin 300 to 450 mg q6h PO

68. Local A ntibiotic T herapy Closed wound irrigation-suction Placement of tubes against the bone maybe desirable to allow drainage of pus and provide a route of irrigation Afferent tube is used to introduce irrigating solutions into the desired area Efferent tube is used to suction out the pus and fluids Irrigations are continued for one week until three successive cultures are sterile

69. Antibiotic impregnated beads Polymethylmethacrylate a crylic resins impregnated with antibiotics Used to deliver high concentration of antimicrobials The beads and drain are left in place for 10 to 14 days.

70. Surgical management Incision and drainage Extraction of offending teeth Sequestrectomy Sequestrectomy and saucerization Decortication Resection and reconstruction

71. Sequestrectomy It involves removing infected and avascular pieces of bone generally the cortical plates in the infected area. Incision: maxilla mandible Removal of the sequestrum Closure

72. Saucerization Involves the removal of the adjacent bony cortices and open packing to permit healing by secondary intention after the infected bone has been removed.

73. Decortication Mowlem Involves removal of the dense, often chronically infected and poorly vascularized bony cortex and placement of the vascular periosteum adjacent to the medullary bone to allow increased blood flow and healing in the affected area.

74. Resection Approach Intra oral

75. Extra oral

76. Hyperbaric Oxygen Therapy Involves intermittent, usually daily, inhalation of 100% humidified oxygen under pressure greater than 1 absolute atmospheric pressure Patient is placed in a chamber, oxygen is given by mask or hood Each session, or dive, is 90 minutes in length. Treatment given 5 days per week for 30, 60 or more dives at 2.4 ATA for 90 minutes while breathing 100% oxygen twice daily 76

77. Beneficial aspects of hyperbaric oxygen Enhancement of lysosomal degradation potential of PMLs and oxygen radicals. Free radicals of oxygen are bactericidal to many pathogens. Many exotoxins liberated by microorganisms are rendered inert by exposure to elevated partial pressure of oxygen. Tissue hypoxia intermittently reversed by HBO mimicking tissue level during wound healing Positive enhancement of neo-angiogenesis 77

78. HBO chamber 78

79. References Topazian RG Osteomyelitis of the Jaws. In Topizan RG, Goldberg MH ( eds ): Oral and Maxillofacial Infections.Philadelphia , WB Saunders 1994,Chapter 7, pp 251-88 Textbook of Oral & Maxillofacial Surgery – Daniel M. Laskin Osteomyelitis of the Jaws:A 50-Year Perspective; J Oral Maxillolac Surg 51:1294·1301,1993 Waldvogell , F.A., Medoff , G. and Swartz, M.N. Osteomyelitis: a review of clinical features, therapeutic considerations and unusual aspects. N Engl J Med282:198–266, 316–322, 1970. Ciney G, Mader JT, Pennick H : A clinical staging system of adult osteomyelitis, Contemp Orthop 10:17, 1985 Marx, Cillo , and Ulloa . Oral Bisphosphonate -Induced Osteonecrosis . J Oral Maxillofac Surg 2007. Osteomyelitis after bilateral sagittal split osteotomy : case report and a review of the management. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2011;111:442-448)

80. Lyons A, Ghazali N: Osteoradionecrosis of the jaws: Current understanding of its pathophysiology and treatment. Br J Oral Maxillofac Surg 46:653, 2008 Feldmeier JJ: Hyperbaric Oxygen 2003: Indications and Results— Hyperbaric Oxygen Therapy Committee Report. Kensington, MD, Undersea & Hyperbaric Medical Society, 2003 Notani K, Yamazaki Y, Kitada H, et al. Management of mandibular osteoradionecrosis corresponding to the severity of osteoradionecrosis and the method of radiotherapy. Head Neck 2003;25:181–6. A. Lyons et al;Osteomyelitis of the jaw: British Journal of Oral and Maxillofacial Surgery 52 (2014) 392–395 Tibbles PM, Edelsberg JS: Hyperbaric oxygen therapy. N Engl J Med 334:1642, 1996 Delanian S, Lefaix JL. The radiation-induced fibroatrophic process:therapeutic perspective via the antioxidant pathway. Radiother Oncol 2004;73:119–31.