Endo-Mail
 



Young Bui, D.D.S.
Osteomyelitis of the Jaw, Part Two
Young Bui

Young Bui

THE FOLLOWING explanation of osteomyelitis of the jaw is excerpted from, “Osteomyelitis of the Jaws,” by Richard G. Topazian, Chapter 10 of Oral and Maxillofacial Infections.
OSTEOMYELITIS is an inflammation of the medullary portion of the jaw bone which extends to involve the periosteum of the affected area.  The infection becomes established in the calcified portion of bone when pus in the medullary cavity or beneath the periosteum obstructs the blood supply.  The infected bone becomes necrotic once ischemia sets in.  An underlying alteration of host defenses is present in the majority of patients with osteomyelitis of the jaw.  Conditions altering the vascularity of bone predispose the patient to the onset of osteomyelitis and include radiation, osteoporosis, osteopetrosis, Paget’s disease of bone, and bone malignancy. 
     Osteomyelitis of the maxilla is much less frequent than that of the mandible because the maxillary blood supply is far more extensive.  Compromise of the blood supply is a critical factor in the establishment of osteomyelitis.  The mandible receives its major blood supply from the inferior alveolar artery.  A secondary source is the periosteal supply giving off nutrient vessels that penetrate the cortical bone and anastomose with branches of the inferior alveolar artery. 
     Most periapical and periodontal infections are localized by the production of a protective pyogenic membrane or soft tissue abscess wall.  If sufficiently virulent, microorganisms may destroy this barrier.  The process leading to osteomyelitis is initiated by acute inflammation.  Tissue necrosis occurs as proteolytic enzymes are liberated and as destruction of bacteria and vascular thrombosis ensue.  When pus accumulates, intramedullary pressure increases, resulting in vascular collapse, venous stasis, and ischemia.  Pus accumulates beneath the periosteum, elevating it from the cortex and thereby further reducing the vascular supply.  If pus continues to accumulate, the periosteum is penetrated and mucosal and cutaneous abscesses and fistulae may develop. 
     Early acute suppurative osteomyelitis of the mandible is usually characterized by deep intense pain, high intermittent fever, parasthesia of the mental nerve and a clearly identifiable cause.  In the initial phase of the acute form, teeth are not loose, swelling is minimal, and fistulae are not present.  At this juncture, the process is true intramedullary osteomyelitis.  Immediate aggressive antibiotic therapy may prevent progression to involvement of the periosteum. 
     In established suppurative osteomyelitis, symptoms include deep pain, malaise, fever, and anorexia.  Within 10 to 14 days after onset, teeth in the involved area begin to loosen and become sensitive to percussion.  Pus exudes around the gingival sulcus or through mucosal and cutaneous fistulae.  Firm cellulitis of the cheek, enlargement of the dimensions of the bone from increased periosteal activity, abscess formation with localized warmth, erythema, tenderness to palpation, and mental nerve paresthesia also may be noted.
     Osteomyelitis of the jaws usually requires both medical and surgical treatment.  An underlying alteration of host defenses is present in many patients with osteomyelitis of the jaws.  Steps should be taken to identify and correct factors that may delay recovery.  Whenever possible, specimens should be obtained for Gram staining, aerobic and anaerobic cultures and sensitivity testing.  Conventional radiographs and possibly bone scanning should be obtained to determine the extent of the disease, the existence of causative factors such as periapical abscesses and fractures, and the presence and location of sequestra.  Extremely loose teeth and sequestra that are readily accessible should be removed early in the course of the disease.  After the acute stages of the disease have subsided with intravenous or parenteral antibiotics and supportive measures, other treatment options include sequestrectomy, debridement, decortication, resection of infected bone, and immediate or late bone graft reconstruction.
Excerpted from “Osteomyelitis of the Jaws” by Richard G. Topazian, Chapter 10 of Oral and Maxillofacial Infections, Copyright © 2002 by W. B. Saunders publishers.


OSTEOMYELITIS of the jaws does not occur often these days.  We can reduce the incidence further by using a rubber dam and apex locator during root canal therapy.  Without a rubber dam, saliva can contaminate the tooth and our gloves, which in turn will transfer bacteria onto the reamers.  Without an apex locator, we can over-instrument the canal and introduce bacteria on the reamer deep into the medullary portion of the jaw bone.  This continuous introduction of bacteria into the medullary region can cause osteomyelitis in an immune-compromised patient.
 

July - August 2006
Without a rubber dam, saliva can contaminate the tooth and our gloves, which in turn will transfer bacteria onto the reamers.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 


FEEDBACK?

We welcome your responses and questions. 
Please feel free to visit the Endo Forum and add your comments about any of the articles in Endo-Mail.

Do not force the Peeso drill when removing gutta percha to make a post hole. Gutta percha is really soft, so running the drill at full speed with gentle pressure should melt the gutta percha away. If you have to push hard, then you are drilling into the tooth structure and are going to perforate out through the root.


Essential Dental Seminars
© Copyright 2004 by Musikant, Deutsch, Kase, Dukoff, Bui, & Hoffman. All rights reserved.