Osteomyelitis

Osteomyelitis

1. OSTEOMYELITIS

2. Contents Definition Predisposing factors Classification Suppurative osteomyelitis Non suppurative

3. Definition Inflammation of the bone forming elements with tendency to progression.

4. Severe compromise of blood supply

5. Inadequate blood supply is a main factor as the involved area becomes ischemic and bone becomes necrotic. Bacteria can then proliferate, because normal blood-borne defenses do not reach the tissue, and the osteomyelitis spreads until it is stopped by medical and surgical therapy.

6. Mandible affected more than maxilla

7. Predisposing factors

8. Microbiology Similar to those of odontogenic infections Viridan streptococci Strict anaerobes: Bacteroides Prevotella Fusobacterium Peptostreptococci species

9. Classification Created by Hudson and simple to use 1. Acute osteomyelitis (present for 1 month) Contiguous focus Progressive Hematogenous (present for over 1 month) 2. Chronic osteomyelitis Recurrent multifocal Garré’s Suppurative or nonsuppurative Sclerosing

10. Clinical features of osteomyelitis of facial region Pain Swelling and erythema of overlying tissues Adenopathy Fever Paresthesia of the inferior alveolar nerve Trismus Malaise Fistulas

11. Classification Roughly divided into suppurative and non suppurative based on clinical features. Suppurative Acute Subacute and chronic Infantile osteomyelitis Non suppurative Chronic diffuse sclerosing Garre’s sclerosing

12. SUPPURATIVE OSTEOMYELITIS The dominant form Characterised by pus formation and necrosis of bone Has two distinct forms; Acute ; infection which includes systemic effects Chronic; induce minimal systemic effects Primary chronic; no acute episode Secondary chronic; involves prolonged inflammatory process

13. Pathogenesis Inflammation triggered by bacterial invasion into marrow induces a compromised microcirculation and increased pressure in the intramedullary site. Leads to vascular collaspe , venous stasis and ischaemia and eventually bone necrosis. Further multiplication of microorganisms and the resultant inflammation induce further necrosis of the surrounding bonny tissue and resulting in extensive spread of infection.

14. Clinical features and stages Acute (1-2 weeks) Local symptoms Swelling is minimal and fistulae are absent Deep and intense pain Regional lymph nodes become enlarged and tender.

15. Later purulent exudates erode the cortical bone and periosteum resulting into facial and submandibular cellulitis . If masticatory muscles are affected, trismus may occur. A throbbing pain in the jaw, severe tenderness and a feeling of extrusion of teeth.

16. Vincent’s symptom as the infection affects the inferior alveolar nerve. Subsequently pus discharge from gingival sulcus . Multiple mucosal fistulae become apparent. There is little or no radiographic changes in this stage.

17. Systemic symptoms: High intermittent fever ( 38-40C ) Chills Malaise Headache Decreased appetite With spread of infection systemic toxic symptoms become more severe and sepsis may occur

18. Infection is localized only in the intramedullary site: Adequate antibiotic treatment at this stage may prevent further progression

19. Subacute and Chronic stage If the disease is neglected or does not respond to treatment Some cases primarily develop a chronic form without an acute episode Symptoms disappear or become minimal

20. Locally: Affected teeth are mobile and tender to percusion Swelling becomes localised An involucrum forms In some extreme cases pathologic fracture occurs due to significant bone loss from sequestration

21. Systemically: Temperature falls to the normal range

22. Diagnosis Diagnosis of acute osteomyelitis is based on: History Clinical findings Laboratory workup - Gram stain, culture, sensitivity, and histopathologic evaluations. For chronic osteomyelitis , bony destruction can be confirmed with plain radiographs.

23. Imaging Xrays - OPG Radiographic changes are generally detected after losing 30-50% of bony calcified constituents Changes are detected 1-3 weeks after onset of acute form

24. Once enough bone destruction has set in: Increased radiolucency , uniform pattern or patch with moth-eaten appearance There may also be areas of radiopacity within the radiolucency which represent islands of bone which have not been resorbed ( sequestra ). There may be an area of increased radiodensity surrounding the radiolucency as a result of inflammatory reaction

25. CT Particularly useful in visualizing the actual extent of the lesion MRI Bony changes are detectable earlier Radionuclide scan More sensitive than others Gallium scan images depicts lesions since they tend to accumulate at inflammatory sites

26. Management Diagnose correctly. Evaluate, define and manage the immunocompromised state of the patient first for best response to therapy.

27. Antibiotics, surgery and supportive care Antibiotic Therapy Penicillins Clindamycin Metronidazole

28. Acute osteomyelitis The course of antibiotic should be continued until clinical signs have disappeared completely. Chronic osteomyelitis Adminstration is recommended after surgery until evidence of wound healing is seen.

29. Surgery Improves blood supply in the involved area -> allowing adequate penetration of antibiotics Maximizes the host defense mechanisms and self healing ability

30. Sequestrectomy Involves removing infected and avascular pieces of bone—generally the cortical plates in the infected area.

31. 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.

32. Decortication 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.

33. The key element in the above procedures is determined clinically by cutting back to good bleeding bone. Clinical judgment is crucial in these steps but can be aided by preoperative imaging that shows the bony extent of the pathology.

34. It is often necessary to remove teeth adjacent to an area of osteomyelitis . In removing adjacent teeth and bone the clinician must be aware that these surgical procedures may weaken the jaw bone and make it susceptible to pathologic fracture

35. Supporting the weakened area with a fixation device ( external fixator or reconstruction type plate) and/or placing the patient in maxillomandibular fixation is frequently used to prevent pathologic fracture.

36. Hyperbaric oxygen (HBO) treatment has also been advocated for the treatment of refractory osteomyelitis . This treatment method works by increasing tissue oxygenation levels that would help fight off any anaerobic bacteria present in these wounds. The widespread use of HBO treatment of osteomyelitis still remains controversial.

37. Resection of the jaw bone has traditionally been reserved as a last-ditch effort, generally after smaller debridements have been performed or previous therapy has been unsuccessful or to remove areas involved with pathologic fracture. This resection is generally performed via an extraoral route, and reconstruction can be either immediate or delayed based on the surgeon’s preference.

38. We believe that early resection and reconstruction shorten the course of treatment. Indicated once the patient develops paresthesia in mandibular osteomyelitis . At this point preservation of the mandible is highly unlikely and one should attempt to shorten the course of the disease and treatment.

39. Supportive care Patients should be hospitalized for any aggressive surgery. Provided with intravenous antibiotic therapy and managed for correct fluid balance and nutrition. As mentioned previously, the patient is likely to have an underlying compromise of their host defenses.

40. Infantile osteomyelitis Occur few days after birth Commonly involves the maxilla Etiology Remains unclear Thought to involve; Perinatal trauma Infection of the maxillary sinus Hematogenous spread

41. Disease could spread to involve the eye and brain Potential risk for serious optic and cerebral sequelae , facial deformities, serious damage to jaw growth and loss of teeth.

42. Sign and symptoms Swelling of the face and eye lid Subperiosteal abscesses on the alveolar mucosa and palate High fever Rapid pulse rate Vomiting delirium and postration

43. Treatment Prompt and aggrassive Use of intravenous antibiotics and drainage of abscesses S. aureus is the most common pathogen involved

44. NON SUPPURATIVE OSTEOMYELITIS CHRONIC DIFFUSE SCLEROSING . Usually affects mandible Characterised by; Recurrent pain and swelling No suppuration or abscess formation paraesthesia

45. Etiology Unclear Possibly due to; Hyperactive immunologic response hyperostosis

46. Radiography ; Intermingled sclerotic and osteolytic lesion with a solid periosteal reaction External bone resorption Treatment Difficult to eradicate- may persist for years Asymptomatic; NSAIDs, corticosteroids

47. Garre’s sclerosing osteomyelitis Named after a Swiss surgeon, Dr Carl Garre Characterized by; Active periosteum proliferation Formation of subperiosteal bone No purulent exudate

48. Believed to result from over inflammatory reaction of the periosteum Commonly in children and adults Usually on the lateral surface of body of mandible

49. Etiology Periapical abscess Post extraction infection Clinical features Localized, unilateral and hard mandibular swelling with little tenderness Pain can be episodic No apparent systemic signs

50. Radiological findings Thickened cortical bone Onion skin appearance due to new bone formation Treatment Elimination of cause

51. References Oral and maxillofacial surgery, L Andersson , KE Kahnberg , MA Pogrel Textbook of Oral and Maxillofacial Surgery 3 rd ed , NA Malik