 Hello and welcome back to OMFS lecture series. The topic for today's lecture is Osteomyelitis of Jaws. Osteomyelitis was and still is a challenging disease for the clinicians and patients. In the past, Osteomyelitis was frequently encountered and had an uncertain outcome. Whereas today, Jaws Osteomyelitis is less common due to improved nutrition, dental care, availability of antibiotic therapy, early diagnosis and intervention. Osteon in Latin means bone. Myelos means marrow. Itis means inflammation. Therefore, by meaning, Osteomyelitis is an inflammation of medullary portion of bone or bone marrow or cancerless bone. However, the process of Osteomyelitis is rarely confined to only medulla. It involves cortical bone and periosteum as well. Therefore, Osteomyelitis may be defined as an inflammatory condition of bone that begins as an infection of medullary cavity and havation systems of the cortex and extends to involve the periosteum of the affected area. Due to the long-standing existence of Osteomyelitis as a clinical entity, a variety of classifications of various forms of the disease are given. Based upon the present or absence of separation or PUS, Osteomyelitis may be classified as sub-puretive Osteomyelitis or non-subpuretive Osteomyelitis. Historically accepted classification is based on its clinical course, that is acute, sub-acute or chronic form of Osteomyelitis. Sierney et al. and Vibhagur developed a classification and staging system based on anatomic location of infectious process, the physiologic status of the host, systemic or local factors affecting the immune system, metabolism and local vascularity. Classification based on pathogenesis of altered vascular perfusion as a factor to the presence and persistence of Osteomyelitis was given by Vibhagur in the year 1993. There are three types. Hematogenous Osteomyelitis, Osteomyelitis secondary to a contiguous focus of infection and Osteomyelitis associated with or without peripheral vascular disease. Osteomyelitis of jaw may be caused due to many factors. Autontogenic infections are the common local cause of Osteomyelitis. These infections may be due to periapycle, periodontal or pericoronal diseases. Infected autontogenic cyst as well as an infected extraction socket or a fracture site can also lead to jaw Osteomyelitis. Local traumatic injuries like injuries of gingiva which are usually insignificant but they may become serious in patients with low resistance or in immunocompromised patients. Also instruments used for extraction of teeth can also cause a local injury which leads to Osteomyelitis. Infections of orophacial regions, for example apetitonsular abscess or a skin infection. All these have been reported as a cause of Osteomyelitis especially of the ascending ramus region. Hematogenous infection may cause multiple sites of Osteomyelitis. The microorganisms enter the blood through a minor wound in the skin or infection of the respiratory tract or even infection of middle ear. So all these are the etiology of jaw Osteomyelitis. The factors that pre-disposed to Osteomyelitis are the conditions affecting host resistance and also conditions that alter the jaw vascularity. For example immunocompromised patients are those who has diabetic melitis, leukemia, severe anemia, malnutrition, chronic alcoholism, sickle cell anemia and certain fibril conditions. The conditions which alter the jaw vascularity are radiation, osteoporosis, phasitic disease, fibrous dysplasia, bone malignancy and bone necrosis. Therefore these are the pre-disposing factors to jaw Osteomyelitis. Moving on to the pathogenesis of Osteomyelitis. The important factor in establishment of Osteomyelitis is the compromise in the blood supply. The primary blood supply to the mandible is by inferior alveolar artery and the secondary supply is the periosteal supply which is parallel to the cortical surface of the bone. The process leading to Osteomyelitis is initiated by acute inflammation which may arise as a result of an odontogenic infection, a mandibular fracture or a facial infection. Acute inflammation is characterized by factors like hypremia, increased capillary permeability and infiltration of granulocytes. All these factors will lead to tissue necrosis. The necrotic tissue along with white blood cells and bacteria comprise the pus. The pus accumulates and the local edema that results lead to an increase in the intramedullary pressure resulting in vascular collapse. Vascular collapse is characterized by venous stasis, ischemia and local thrombosis. The pus travels through the havation canal and the nucleon canals and accumulates beneath the periosteum thus elevating it from the cortex and thereby further reducing the vascular supply. So all these events jointly result in a compromised local blood supply to the bone. The bone eventually becomes avascularized and finally results in sequestra formation which is otherwise called the necrosed bone. The microbial flora present in osteomyelitis is considered to be of a mixed nature with both aerobic and anaerobic bacteria present. A few of the relevant organisms present in osteomyelitis are mentioned here. Hence an established case of osteomyelitis is usually a polymytrobial disease. As far as the involvement of maxilla and mandibular considered in osteomyelitis, mandible is affected more because of the dense poorly vascularized cortical plates and also the single blood supply from the inferior alveolar bundle. The extensive blood supply of the maxilla makes it less prone to osteomyelitis when compared to mandible. Also the maxilla has a thin cortical plate and the medullary portion of maxilla is more porous. Therefore it avoids the infection from becoming contained within the bone and it facilitates spread of edema and pus into adjacent tissues. Therefore involvement of maxilla is less in osteomyelitis when compared to that of mandible. Now let's see what are the features of acute separative osteomyelitis. The involvement of the disease will be in maxilla or mandible, though the involvement or spread in mandible is more wider due to the reasons mentioned earlier. Again the infection is of mixed nature and the patient will present with generalized constitutional symptoms like high intermittent fever, malice, nausea, vomiting and anorexia. There is regional lymph adenopathy or inflammation of the regional lymph nodes. There is elevated WBC count which is suggestive of an acute infection. The teeth are tender to percussion and are loose or sore. A rise in pressure from the local edema in inferior alveolar canal can cause parastasia or anesthesia of lip. Christmas may be also present. So these are the clinical signs and symptoms associated with acute pyogenic or acute separative osteomyelitis. Moving on to chronic osteomyelitis. It can be primary meaning resulting from organisms which are less virulent and secondary occurring after acute osteomyelitis when the treatment did not succeed in eliminating the infection. The clinical features of chronic osteomyelitis are usually limited to pain and tenderness where the pain is minimal. A non-healing, bony and overlying soft tissue wounds with induration of the soft tissues. That means the soft tissues are indurated. Intraoral or extraoral reigning fistulae as you can see in the diagram. A thickened or wooden characteristic of the bone. Enlarged mandible because of the deposition of subperiosteal new bone. A pathological fracture may be present. A sterile abscess may be present. Which is usually common in the long bones but rarely it occurs in jaws also. The teeth in the area tend to be loose and also sensitive to palpation and percussion. So these are the clinical features of chronic osteomyelitis. The radiological examination of chronic osteomyelitis can be accomplished by the use of conventional radiography as well as specialized imaging techniques. The radiographic changes occur only three weeks after initiation of osteomyelitis process. It is generally accepted that 30 to 60 percentage of mineralized portions of bone must be destroyed before any significant radiographic changes are noted. And this degree of bone alteration requires a minimum of 4 to 8 days after the onset of acute osteomyelitis. Therefore in early stages or in acute osteomyelitis history and clinical features constitute the only data upon which diagnosis can be made. In early stage there is widening of marrow spaces and also enlargement of workman's canals which imparts a mortal appearance. The granulation tissue which is formed between the living and dead bone produces irregular lines and zones of radiolucency. This results in characteristic moth-eaten appearance of established osteomyelitis. In later stages of the disease when the cortex get involved due to ischemia a portion of the cortical bone becomes de-vitalized. There is gradual resorption around the periphery of the necrosed area and the bone gets separated off. It is called as sequestrone or sequestra. There is again subperiosteal new bone formation which is called the involucrum. It can be seen as a fine linear opacity which is usually present at the lower border. So this sheet of new bone called involucrum is often separated from the sequestra or the necrosed bone by a zone of radiolucency. Therefore in a mandible where the new bone is superimposed upon that of the jaw, a delicate fingerprint or orange peel appearance is seen. So this is regarding the radiographic findings within conventional radiographic images. The specialized radiographic techniques employed in diagnosis of osteomyelitis are computer tomography, radioisotopes and positron emission tomography. Computerized tomography or CT. It gives more definite picture of calcified tissue involvement. Radioisotope scanning can identify occult areas of involvement but due to poor resolutions this technique is not very effective. Positron emission tomography uses radioisotopes of physiologically active compounds like glucose, ammonia and fluoride. Petscan can identify the changes in bone as early as three days after the onset of symptoms of osteomyelitis. This enables confirming the diagnosis at a very early stage of osteomyelitis as well as early interceptive antibiotic and supportive therapy can be started. After obtaining clinical and radiographic findings diagnosis of this condition is made on basis of presence of sequestra, areas of separation that involves the tooth bearing area of jaw bone and also the regional or systemic compromise of immune response of the patient as well as the microvascular decomposition of the area is identified. So this is how diagnosis of osteomyelitis is made based upon all these three factors. The management aspect of osteomyelitis will be discussed in the upcoming lecture. That's all for this lecture. Thank you. Hello everyone. Welcome back to OMFS lecture series. In this lecture we shall discuss the management of jaw osteomyelitis. So there are a certain goals that we need to achieve while managing a case of osteomyelitis. Those goals are to attenuate and eradicate proliferating pathological organisms to promote healing and to reestablish the vascular permeability. You know that the vascular supply to the infected bone is compromised. So it is important to reestablish the blood supply to the bone. The Marx protocol for treatment of osteomyelitis include the following to disrupt the infectious foci, debridement, culture and identification of specific pathogens, drainage and irrigation of the region, adjunctive treatments like profanation and decortication in order to enable microvascular reperfusion and reconstruction. These are the treatment guidelines given by Marx in the year 1992. Therefore for a successful treatment, following principles are considered. Early diagnosis, a bacterial culture and sensitivity testing, adequate antibiotic therapy and pain control, proper surgical intervention followed by reconstruction. Management of osteomyelitis can be divided into conservative and surgical management. Complete bed rest is advised to the patient followed by supportive therapy which includes nutritional support in the form of high protein and high caloric diet and also adequate multivitamins has to be supplemented. The patient has to be kept rehydrated orally or through administration of IV fluids. Blood transfusion is performed in case the RBCs and hemoglobin count is low. Pain is controlled with analgesics. Sedation may be also employed for keeping the patient comfortable and to allow to sleep. Here is the recommended antibiotic regimens for osteomyelitis of jaws. Antibiotic of first choice or regimen one is penicillin which is considered as an empirical therapy. So you may administer aqueous penicillin 2 million units intravenously every 4 hours or oxacillin 1 gram IV every 4 hours. Once the patient has been asymptomatic for 48 to 72 hours then you may switch to penicillin V orally 500 mg which is given every 4 hours. Also Dytaloxacillin 250 mg orally every 4 hours for 2 to 4 weeks may be administered. Regimen 2 is based on the culture and sensitivity results. Penicillin is resistant to penicillins like oxacillin, cloxacillin, Dytaloxacillin or Fluoxoxacillin may be given. Glendamycin is the second choice antibiotics which is effective against penicillinase producing cephalococci, streptococci and anaerobic bacteria including bacteroids. This is used because of its ability to diffuse widely in the bone. It is not recommended as first choice because it is bacterostatic and can cause diarrhea due to pseudo membranous colitis. Cifazoline or Cifalexin is the third choice of antibiotics in osteomyelitis. It is effective against most cocci including penicillinase producing cephalococci and gram-negative aerobic bacillae. For example E. coli, Clepsilla and Proteus. Cifalosporins are not recommended as first choice because they are moderately effective against anaerobes and also because of broad spectrum coverage. This increases the antibiotic complications like bacterial resistance and super infection. Therefore Cifalosporins are third choice of antibiotics and not considered as first choice antibiotic. The fourth choice is erythromycin. Again these drugs cannot be used as first choice because they are bacterostatic and rapidly develop resistance strains. So this is regarding the antibiotic regimen used for osteomyelitis of jaw. In a non-healing case of osteomyelitis where it doesn't respond to antibiotics you may consider hyperbaric oxygen therapy. We know that the tissues are hypoxic as the blood supply has been cut off due to vascular collapse. So basically HPO is supplying oxygen to the tissues devoted of it. How is HPO given? Hyperbaric oxygen therapy involves the intermittent usually daily inhalation of 100% humidified oxygen under pressure which is greater than one atmospheric absolute pressure. The patient is placed in a chamber and oxygen is given by mask. Each dive or exposure is 90 minutes in length. The treatment is given 5 days per week for 30 to 60 or more dives in a monoplace chamber. So understand that hyperbaric oxygen therapy is administering a 100% age oxygen at 2.488 for 90 minutes twice daily for 5 days per week. So over the last several decades HPO therapy has emerged as a potential alternative to surgical reperfuration. What are the beneficial aspects of hyperbaric oxygen therapy? HPO therapy enhances the lysosomal degradation by the defense mechanism of the body like the leukocytes and oxygen radical. The free radicals of oxygen which are supplied during the HPO therapy are toxic to many pathogenic anaerobes that means it is bactericidal. The exotoxins liberated by these organisms are also made inert by exposure to a high partial pressure of oxygen. The tissue hypoxia which is present at the site is intermittently reversed by HPO therapy. This will enhance the wound healing and the positive enhancement of neo-angiogenesis is another beneficial aspect of HPO therapy. Neo-angiogenesis is nothing but the formation of new blood vessels. Therefore the tissue hypoxic condition within the wound can be reversed and thus the wound healing is promoted. This is regarding the hyperbaric oxygen therapy. Moving on to the surgical management of jaw osteomyelitis. Surgical intervention is done under antibiotic coverage started at least one to two days prior to the procedure. The first step is incision and drainage. Incision and drainage should be done as soon as possible. It relieves the pressure and pain caused by the pus accumulation. Incision of abscess can be carried out intra-orally or extraordinarily depending upon the location. Evacuation of pus by drainage lessens absorption of toxic products and prevents further spread of infection in the bone thus helping in its localization. The second step is to extract the offending teeth. Sometimes the drainage is achieved by extraction of the offending teeth. The third step is debridement followed by incision and drainage thorough debridement of affected area should be carried out. The area may be irrigated with hydrogen peroxide and normal saline. Any foreign body necrotic tissue or small sequestrum also should be removed at this stage. The next step you may consider is a decortigation which is removal of chronically infected lateral and inferior cortical plates of bone one to two centimeter beyond the area of involvement. Thus you gain access to the bone medulla. Once the cortical plate is removed you gain access to the medullary bone. So what are the steps in decortication? You first create a buckle flap by placing a crystal incision along the necks of the teeth. A mucoperiostal flap is reflected up till the inferior border of mandible. The teeth in the involved area are removed followed by removal of cortical plates lateral and inferior to the involved area preferably with a chisel. The bony bed is then thoroughly debrided and the flap is closed primarily. Any dead space can be eliminated by applying pressure bandage and also by placing irrigation tubes. So this is how decortication is performed. After decortication two small tubes are placed against the bony bed through separate skin incisions and secured with sutures. One tube is connected to the low pressure section to allow drainage of pus and the other is kept patent to provide a route through which locally antibiotics may be installed. So daily first saline irrigation has to be performed followed by antibiotic insulation and this is repeated until negative cultures are obtained. Systemic antibiotics are also continued for at least two to three months following cessation of evidence of disease. The next step is sequestromy which is the removal of sequestra or the necrosis bone. This is an integral part of definitive therapy. This method helps in establishing a local micro vascular proliferation. This is undertaken through an intraoral or extraoral approach depending upon the site of sequestrum. So sequestra are usually cortical and may be cancellous or corticocancelous. These are avascular and therefore poorly penetrated by antibiotics. Pathological fractures can also occur in the region of sequestrum due to bone loss. So once a proper access has been gained through an intraoral or extraoral approach the contents are carefully cuted from the site until healthy bone is exposed to the view. So this is the method of sequestromy. Saucerization is the excision of margins of necrotic bone overlying a focus of osteomyelitis. This is useful in chronic form because it permits removal of the sequestra and enables a vector visualization. It is performed with a large round bar and the buccal cortex is reduced to the level of unattached mucosa. Thus producing a saucer-like defect. So here the defect formed is a saucer-like and not a deep hollow cavity. Both sequestromy and saucerization are to be carried out after the acute face has subsided. This enables a better defence mechanism of host and the host can overcome the virulence of organisms. Refination or fenestration is the creation of bony holes or windows in the overlying cortical bone adjacent to the infectious process. This is performed for the decompression of the medullary compartment. Drilling of holes into the cortex and thus reaching the medulla allow vascular communication between the pediosteum and the medullary cavity. When extensive portion of the bone is involved in the disease process then resection of the jaw bone is advocated. Following resection reconstruction is performed to maintain the continuity of the fragments to prevent pathological fracture to prevent facial deformity and to provide attachment of the soft tissues. So this is regarding the surgical management of osteomyelitis. Following all the surgical steps post-operative care has to be considered. This includes continued use of antibiotics analgesics and warm saline moutherinsins. Adequate hydration, complete rest, removal of sequestra in case there are any in the alveolar part of the bone. The wound is then closed preferably primarily with a drain. So this is all about the surgical management of jaw osteomyelitis. Here is an extraordinary clinical picture of a patient with uncontrolled diabetes mellitus. There are multiple draining sinuses with pus discharge for 2 years. This is the closer view of one of the draining sinuses. Incri-oral picture showing the exposed sequestrum in the oral cavity. So after controlling the disease surgical resection was plant, hemimandabilitomy was plant. And this is the surgical picture of resection of the hemimandabil. And this is the resected specimen. Several complications can occur as a result of osteomyelitis of jaw. With chronic osteomyelitis neoplastic conversion of inflammatory metoplesia to squamousal carcinoma is noted. Therefore neoplastic transformation is one of the complications of osteomyelitis. Another one is the discontinuity defect. The defects can be spontaneous or surgically induced. So this will necessitate jaw reconstruction once the infection is resolved. A third complication is the progressive diffuse sclerosis. This condition involves the cortical and medullary portion of the maxillofacial skeleton over a period of time. So these are the complications associated with jaw osteomyelitis. Considering the prognosis of the condition. If proper, aggressive and comprehensive therapy is instituted on time. Then the recovery of acute and chronic osteomyelitis is always good. But in cases of certain chronic osteomyelitis which is associated with regional or systemic disease like microvascular or immunosuppressive disorders. Then the treatment itself may be worse than the disease. So in these cases the attempt should be done to provide a long term conservative therapy than any major surgical debridement. So that's all regarding the management of osteomyelitis of jaw. Thank you.