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MINISTRY of PUBLIC HEALTH of UKRAINE VINNITSYA NATIONAL PIROGOV MEMORIAL MEDICAL UNIVERSITY It is "confirmed" on a methodical meeting of department of pediatric dentistry head-chair doc.Filimonov Yu.V._____ "____ " ___________ in20 Methodical recommendation for 4d year students of dental faculty Educational discipline Module ¹ Rich in content module ¹ Topic Course Faculty Autor Pediatric surgery 1 1 Odontogenic acute osteomyelitis. pathogenesis, manadement 4 Dental Isakova N.M. Vinnitsya 2012 Etiology, Actuality of theme: 1. Concrete aims: Osteomyelitis of jaws is an infectiously-allergic festering-necrotizing process which develops in a bone under the action of both external (physical, chemical, biological) and internal factors on a background previous sensitization of organism.This definition is confirmed by the results of morphologic investigations of foci purulent infiltration of the bone marrow , thrombosis and purulent infiltration of the bone. 3.Educator aims: To develop sense of professional responsibility for the timeliness of diagnostics of osteomyelitis jaws in children and rightness of determination of medical tactics of doctor-stomatology. 3 Base knowledges, abilities, habits which are necessary for study the topic. Names of previous disciplines Skills are got 1. General anatomy The structure of the maxillofacial region, the blood and nerve supply 2. Gistology Histological structure of the oral mucous cavity. The mechanism of development and phase of inflammation 3. Therapy, pediatrics Know the features of a child's body. Know the basic diseases of importance in conducting the diagnosis of major dental diseases 4. Task for independent work during preparation to employment. 4.1. List of basic terms, parameters, descriptions which a student must master at preparation to employment : Term Determination 1. Preventive means Sanation of the oral cavity, radical treatment of all forms of chronic periodontitis with toothextraction 2. Chronic periostitis Excessive formation of periosteal stack layering, which are to be removed surgically due to indications 3. Granulomatous periodontitis Formed on the area of the root apex granulomais detected only radiographically. 4.2. Theoretical questions to employment: 1. Able to diagnose sharp serous and purulent osteomyelitis of children and define medical tactics them. 2. Able to conduct differential diagnostics of sharp osteomyelitis children with tumours and inflammatory diseases of jaws on the intensifying. 3. Able to conduct differential diagnostics of chronic osteomyelitis children with tumours and inflammatory diseases of jaws. jaws for jaws for stage of jaws for 4.3 Practical works (tasks) To conduct the different types of the local anaesthetizing on phantoms. 5. A plan and organizational structure of lesson in discipline. № Stages of Distribution Types of control employment of time 1. practical tasks, Preparatory stage 15 min situatioonal tasks, 1.11.1OThe organizational verbal crossquestions. 1.2 Forming of examination at motivation. standart list of 1.3 Control of questions. initial level of preparation. 2. 55 min Basic stage. 3. 3.1. 3.2. 3.3 20 min Final stage Control of eventual level of preparation. General estimation of studing activity of student. Informing of students about the theme of next employment. test tasks Maintenance of theme Facilities of studies Text-books, methodical recommendations. The words, ossews in Latin means bony, andosteon in Greek means bone, and myelos means marrow; and in Greek means inflammation. By meaning OML is an inflammation of medullary portion of bone or bone marrow or cancellous bone. However, the process is rarely confined to medulla. It involves cortical bone and periosteum as well. Therefore, OML may be defined as an inflammatory condition of bone, that begins as an infection of medullary cavity and haversian systems of the cortex and extends to involve the periosteum of the affected area. The inflammation may be acute, subacute or chronic. It may be localized; or may involve a larger portion of bone. It may besuppurative or nonsuppurative. OML of the jaws was once a common and dreaded disease; because of its prolonged therapy and the resultant disfigurement and dysfunction, due to loss of major portion of the jaw bone. In the contemporary world, the incidence of OML of the jaws has become less, because of the worldwide avail-ability of newer antimicrobials, better awareness, and better dental health care. However, we do come across a few cases of OML; the causes can be attributed to the following: (i) development of certain strains of organisms, which are resistant to certain antibiotics, and (ii) presence of more cases of medically handicapped individuals in the present population. It is an opportunistic disease, as presented by the host to the pathogenic microbe. Predisposing Factors The factors that predispose to OML are as follows: (i) conditions affecting host resistance or defences, (ii) compromised vascular integrity and perfusion in the host bone, at the local, regional or systemic level, and (iii) virulence of microorganisms. These factors play an important role in the onset and severity of OML. 1. Conditions that alter host defences would include chronic debilitating systemic diseases: such as diabetes mellitus, agranulocytosis, leukaemia, severe anaemia, malnutrition, drug abuse, chronic alcoholism, sickle cell disease, and febrile illnesses such as typhoid. 2.Conditions that alter vascularity of bone include therapeutic irradiation, osteoporosis, Paget's disease, fibrous dysplasia, bone malignancy, metallic bone necrosis (caused by mercury, bismuth, and arsenic). An intrinsic and extrinsic vascular component has a more profound influence, both in onset of occurrence as well as in resolution outcome. 3. Virulence of organisms certain organisms precipitate thrombi formation by virtue of their destructive lysosomal enzymes (Hudson 1993) (Table 1). Lysosomal and enzymatic degradation of host tissue, along with microvascular thrombosis brought about by pathogen borne bioactive peptides and chemo attracted leukocytic purulence, forms a protective barrier for the infectious foci, allowing organisms to proliferate in anenriched host medium while protected from the host immunity. Brodie's abscess of long bone osteomyelitis is the classic example of this isolational phenomenon, which can also occur in osteomyelitis of tooth bearing bone, but to a lesser extent. 1. Non-compliant patients refractory to health care delivery, 2. Systemic, metabolically compromised individuals who can befurther categorized into the following subsets; (a) age of patients,(b) malnutrition, (c) immunosuppression, (d) congenital oracquired pathophysiology disrupting microvascular perfusion of the calcified tissue structure and investing soft tissue envelope. 3. Inaccessibilty to health care delivery The process of OML is initiated by invasion of bacteria into the cancellous bone, followed by acute inflammation:hyperaemia, increased capillary permeability; and infiltration of granulocytes. The failure of microcirculation in the cancellous bone is a critical factor in the establishment of the osteomyelitis. The infection spreads along the path of least resistance. Since the involved area becomes ischaemic and bone becomes necrotic, bacteria can then proliferate, because normal blood-borne defences do not reach the tissue and osteomyelitis spreads, until it is stopped by medical and surgical therapy. Etiology Osteomyelitis of the jaws is caused by the following: 1. Odontogenic infections Primarily odontogenic infections originating from pulpal or periodontal tissues, pericoronitis, infected socket, infected cyst, tumour, etc. 2.Trauma It is the second leading cause: (a) especially, compound fracture, and (b) surgery-iatrogenic 3. Infections of orofacial regions—derived from (a) periostitis following gingival ulceration, (b) lymph nodes infected from furuncles, and (c) lacerations (d) peritonsillar abscess. 4. Infections derived by hematogenous route Furuncle on face, wound on the skin, upper respiratory tract infection, middle ear infection, mastoiditis, systemic tuberculosis. The infections from the last two groups account for a small percentage of cases. Pathogenesis Osteomyelitis is initiated from a contiguous focus of infection or by hematogenous spread. Osteomyelitis is an infectious process of the medullary myeloid cavity of bone. In the craniofacial skeleton only the mandible and the calvarium have myeloid compartments. The important factor in establishment of OML is the compromise in the blood supply. It is worth considering the blood supply and venous drainage of mandible. 1. Blood supply (a) Primary supply: The mandible is supplied by inferior alveolar artery, except coronoid process, which is supplied by temporalis muscle vessels, (b) Secondary Supply: It is the periosteal supply, which generally runs parallel to cortical surface of bone, giving off nutrient vessels those penetrate cortical bone and anastomose with the branches of inferior alveolar artery. 2. Venous drainage of mandible There are two routes: (i) Via inferior alveolar vein; it runs upwards, and joins pharyngeal plexus, and (ii) It runs downwards, and joins external jugular veins. Waldron (1943) gave an exhaustive morphologic description of vascular morphology of mandible and associated structures to account for spread of OML. He described mandibular vascular support as being provided through multiple arterial loops from a single major vessel, which renders large portion of bone susceptible to necrosis with the occurrence of major vessel infectious thrombosis. Waldervogel (1970) described, its relationship to vascular support of long bones of developing and adult human skeleton. He made several conclusions: i. These tend to be segregation of vascular channels, which act like "end organs," due to lack of terminal collateral anastomosis, ultimately, leading to vascular plugging by bacteria, microthrombi or both. ii. When afferent vessels anastomose with medullary channels, there is a possibility of a decrease in venous flow with associated areas of greater turbulence. iii. There may be a reduction in host immune defense mechanism associated with these vascular channels in calcified tissue. A true osteomyelitic infectious process does not occur in the maxilla despite the presence of tooth follicle or anatomic respiratory sinus cavities, including the nose. Osteomyelitis in Maxilla Osteomyelitis in maxilla is rare; due to: (i) extensive blood supply and significant collateral blood flow in midface, (ii) porous nature of membranous bone, (iii) thin cortical plates, and (iv) abundant medullary spaces. These preclude confinement of infections within bone; and permit dissipation of edema and pus into soft tissues and paranasal air sinuses. The mechanism of formation and accumulation of pus is worth understanding. The process leading to osteomyelitis is initiated by acute inflammation, hyperaemia, increased capillary permeability and infiltration of granulocytes. Tissue necrosis occurs as proteolytic enzymes are liberated and as destruction of bacteria and vascular thombosis continues, there is a pus formation. The pus is a combination of necrotic tissue and dead bacteria and WBC accumulate. When pus accumulates, the intramedullary pressure increases resulting in vascular collapse, venous stasis, and ischaemia. Subsequently, pus travels through haversia and nutrient canals and accumulates beneath the periosteum, elevating it from the cortex; and thereby further reducing vascular supply. Compression of neurovascular bundle accelerates thrombosis, ischaemia, and infarction, later resulting in paraesthesia and sequestrum formation. Extensive periosteal elevation is seen more frequently in children, since periosteum is presumed to be less firmly bound to bone. If pus continues to accumulate, the periosteum is penetrated; mucosal and cutaneous abscesses and fistulae develop. As natural host defences and therapy begin to be effective, the process may become chronic, inflammation regresses, granulation tissue is formed; new blood vessels cause lysis of bone, thus separating fragments of necrotic bone (sequestrum) from viable bone. Small sections of bone may be completely lysed, whereas larger ones may be isolated by a bed of granulation tissue encased in a sheath of new bone (Involucrum). Sequestra, may be revascularized, remain quiescent, or continue to be chronically infected and require surgical removal. Occasionally, involucrum gets penetrated by channels, known as "cloacae", through which pus escapes from sequestrum to an epithelial surface. Radiographically, the bone surrounding sequestrum appears less densely mineralized than sequestrum itself, since vascularity of vital bone creates relative demineralization. Ischaemia causes increase in C02 level, which attracts Calcium due to change in pH. The calcium deposition leads to increase in mineralization of the sequestrum. Microbiology In the past, the etiology of OML was associated with skin surface bacteria, S aureus; and to a lesser extents epidermidis, or hemolytic streptococci. However, the picture of S.aureus as primary offending pathogen does not hold true with regard to OML of toothbearing bone. Sinus tractculture results, especially in the jaws, are often misleading, as they are usually contaminated with Staphylococcus organisms. Most of the cases are caused by aerobic streptococci (a hemolytic streptococci, Strep viridans), anaerobic streptococci; and other anaerobes, such as peptostreptococci, fusobacteria, and Bacteroides (Peterson 1999). Sometimes, anaerobic or microaerophilic cocci, Gram-negativeorganisms such as Klebsiella, Pseudomonas and Proteus are also found. Other organisms such as M tuberculosis, T.pallidum, and Actinomyces species produce their respective specific forms of OML. Hence, established acute OML is usually a polymicrobial disease and includes: streptococci, bacteroides, peptostreptococci and fusobacteria, as well as other opportunistic bacteria. Marx et al (1992) identified Actinomycoses, Eikenella and Arachnia as pathogens in some of the more refractory forms of OML of jaws. Other unusual organisms such as Coccidioides, tuberculous bacilli, Treponema and Klebsiella have also been implicated as causative agents. The change in bacterial pattern is not because of ecology. It is attributable to the employment of more sophisticated culture methods. Classification and Staging Due to the long-standing existence of OML as a clinical entity, a variety of classifications of this disease process have evolved. A variety of classifications of various forms of the disease are given, which are as follows: 1. Historically accepted classification It is based on clinical course: (a) acute, and (b) chronic. The arbitrary time limit,to identify acute from chronic forms, is of one month Hudson's classification of OML of the jaws Acute forms of OML (Suppurative or non-suppurative) include: a. Contiguous focus: (i) Trauma, (ii) Surgery, and (iii) Odontogenic infections. b. Progressive: (i) Burns, (ii) Sinusitis, and (iii) Vascular insufficiency. c. Hematogenous (Metastatic): Developing skeleton (children) Chronic forms of OML a. Recurrent multifocal: (i) Developing skeleton (children), (ii) Escalated osteogenic activity ( age < 25 years) b. Garre's: (i) Unique proliferative subperiosteal reactior (ii) Developing skeleton (children to young adults) c. Suppurative or non-suppurative: (i) Inadequately treated forms, (ii) Systemically compromised forms, and (iii) Refractory forms (CROM: Chronic refractory OML). d. Diffuse sclerosing: (i) Fastidious organisms, and (ii) Compromised host/pathogen interface 2. Classification based on pathogenesis of altered vascular perfusion as a major contributing factor to the presence and persistence of OML as a clinical disease. (Vibhagool et al 1993): There are three types: • Hematogenous OML • OML secondary to a contiguous focus of infection • OML associated with or without peripheral vascular disease 3. Classification based on presence or absence of suppuration 4. Cierny et classification location status al and of of the (1985) staging and Vibhagool (1993) system; based infectious process, and host systemic (iii) or on (i) (ii) local developed a anatomic physiological factors affecting immune system, metabolism, and local vascularity. Acute Pyogenic OML (Acute suppurative OML) Acute pyogenic OML may have the appearance of a typical odontogenic infection. It can be localised and It involved medullary bone without cortical involvement; usually hematogenous Less than 2 cm of bony defect without cancellous bone. Less than 2 cm bony defect seen on radiograph, defect does not appear to involve both cortices. The defect is less than 2 cm, pathological fracture, infection, and nonunion II. Physiological types A host: Normal host В host: Systemic compromise (Bs); local compromise (Bl) C host: Treatment is worse than the disease. HI. Systemic or local factors that affect immune surveillance, metabolism, and local vascularity (i) Malnutrition, (ii) Renal or hepatic failure, (iii) Diabetes mellitus, (iv) Chronic hypoxia, (v) Immune deficiency or suppression, (vi) Malignancy, (vii) Extremes of age, (viii) Autoimmune disease, and (ix) Tobacco and alcohol abuse: (i) Chronic lymphedema, (ii) Venous stasis, (iii) Major vessel disease,(iv) Arteritis, (v) Extensive scarring, (vi) Radiation fibrosis, (vii) Small vessel disease, and (viii) Loss of local sensation widespread, with extensive sequestration and possible pathological fracture. Microbiology It is caused by pyogenic organisms. OML in the toothbearing area is polymicrobial in nature. The most commonly found organisms found in odontogenic OML is Staph aureus; and also Strep pyogenes. Vincent's Spirochaetes may also be present. Gram-negative bacilli may also be present (E. coli) Etiology 1. Odontogenic infections These are the common local causes of OML. These infections may result from (i) periapical disease secondary to pulp pathosis, (ii) periodontal disease, (iii) pericoronitis of long duration, (iv) infected odontogenic cyst, and (v) infection of an extraction wound or fracture site. 2. Local traumatic injuries (a) Injuries of gingiva, are usually insignificant; however, may become serious in patients with low resistance (Ivy and Cook 1942), and (b) Instruments used for extraction of teeth. 3. Peritonsillar abscess It has been reported as a cause of OML of ascending ramus. 4. Furunculosis ofskinlt is a rare cause of OML. Hoenigef al (1931) have reported such a case. 5. Hematogenous infection It may cause multiple sites of OML. The organisms enter the blood stream through a minor wound in the skin, or infection of upper respiratory tract, or infection of middle ear. The predisposing factors include: (i) undernourished children, (ii)lowered general resistance of body, (iii) generalised body diseases: such as; diabetes, leukaemia, and agranulocytosis, and (iv) acute illnesses, such as influenza, measles, scarlet fever, pertussis and pneumonia, etc.Blair et al (1931) reported one case following tonsillitis, one following measles, and one following diphtheria. Galli (1926) reported a case of OML of maxilla associated with renal complication. Recently, with the use of newer antibiotics and early institution of antibiotics hematogenous spread is not commonly seen. 6. Infected compounded odontome(Romer 1955). 7. Compound fractures of jaws are complicated by OML. Clinical features Occurrence In adults, it is more common in mandible and involves alveolar process, angle of mandible, posterior part of ramus and coronoid process. OML of condyle is reportedly rare (Linsey 1953). A. Early cases are characterised by: 1. Generalised constitutional symptoms: High inter mittent fever, malaise, nausea, vomiting, anorexia. 2. Deep seated boring, continuous intense pain in the affected area. 3. Intermittent paraesthesia or anaesthesia of the lower lip, which helps the clinician to differentiate this condition from alveolar abscess. 4. Facial cellulitis, or indurated swelling of moderate size, which is more confined to the periosteal envelop and its contents: (i) thrombosis of inferior alveolar vasa nervorum, (ii) rise in pressure from edemain inferior alveolar canal, (iii) teeth are tender to percussion and loose 5. Trismus: In children: (i) fulminating, (ii) severe and serious, (iii) involvement of maxilla or mandible, (iv) complicated by the presence of unerupted developing teeth buds, which become necrotic and act as foreign bodies and prolong the disease process. Long-term involvement of TMJ can cause ankylosis of TMJ and subsequently affect the growth and development of facial structures. Laboratory Studies: show mild leucocytosis (PMNL) and albuminuria. B. Established cases are characterized by: 1. Deep pain, malaise, fever, dehydration, anorexia. 2. Teeth in involved area begin to loosen and become sensitive to percussion. 3. Purulent discharge through sinuses: (a) intra-orally; (i) around gingival sulcus: or (ii) through buccal vestibule, and (b) extra-orally on the face, through cutaneous fistulae. 4. Foetid odour is often present. 5. Trismus may be present. 6. Dehydration, acidosis and toxaemia. 7. Regional lymphadenopathy is usually pesent. Laboratory studies show (i) moderate leucocytosis (PMNL), and (ii) slightly elevated ESR, (iii) anaemia, and (iv) albuminuria. Blood cultures, wound culture and sensitivity, and complete blood count along with peaks and troughs on any antimicrobial prescribed should be assessed on a regular basis. Radiological changes are absent initially. Literature. Basic: 1.Lectures which are read on the department of pediatric dentistry. 2. Pinkham J.R. Pediatric dentistry. – 2nded.- W.B. Sounders Company. – 1994.647 p. 3. Pediatric dentistry /Ed. R.R.Welbury.- Oxford, 1997 – 584p. Additional: 1. Хирургическая стоматология.: Учебник /Т.Г.Робустовой. - М.: Medicine, 1990, 327. 2. Стоматология детского возраста: Учебник / А.А.Колесова. - М.: Medicine, 1991. 3. Танфильев Д.Е. Удаление зубов. - Л.: Medicine. 1976. - 160 с. 4. Соловьев М. М., Игнатов Ю.Д., Конобевцев О. Ф. Обезболивание at лечении зубов in детей. - М.: Medicine, 1985. - 184 с. 5. Рузин Г.П., Бурых М. М. Основы технологии операций в хирургической стоматологии и челюстно-лицевой хирургии. - Харьков, 2000. - 291 с.