 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, jaw 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 subcurative Osteomyelitis or non-subcurative 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 periapical, 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 a peritonsular 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. All these are the etiology of jaw Osteomyelitis. The factors that pre-exposed to Osteomyelitis are the conditions affecting host resistance and also conditions that alter the jaw vascularity. For example immunocompromised patients are those who has diabetes mellitus, leukemia, severe anemia, malnutrition, chronic alcoholism, sickle cell anemia and certain fibril conditions. The conditions which alter the jaw vascularity are radiation, osteoporosis, phasic 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, mandibular 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 second way 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 overlaying 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 subperiostial 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 3 weeks after initiation of osteomyelitis process. It is generally accepted that 30-60% 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 4-8 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 mottled 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-vitalyzed. There is gradual resorption around the periphery of the neck coached area and the bone gets separated off. It is called as sequestrum 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 necrosis 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 3 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 micro vascular 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.