OMFS III Notes 2024-2025 PDF

ORAL & MAXILLOFACIAL SURGERY III 2024-2025 ‫جامعة حورس‬-‫رؤية ورسالة كلية طب األسنان‬ ‫جامعة حورس‬-‫رؤية كلية طب األسنان‬ ‫التميز والريادة في مجال طب األسنان محليا ً وإقليميا ً ودوليا ً من حيث التعليم والبحث العلمي وخدمة‬ ‫المجتمع‬ Vision of the Faculty of Dentistry - Horus University Excellence and leadership in the field of dentistry locally, regionally and internationally in terms of education, scientific research and community service. ‫جامعة حورس‬-‫رسالة كلية طب األسنان‬ ‫إعداد خريجين مؤهلين بالمعرفة النظرية والمهارات العمليه والسلوكيات اإلنسانية التي تمكنهم من‬ ‫المنافسه في سوق العمل ونقل المعرفة من خالل إجراء الدراسات والبحوث العلمية وتقديم الخدمات‬.‫المجتمعيه المتميزه للمواطنين‬ Mission of the Faculty of Dentistry - Horus University Preparing qualified graduates with theoretical knowledge, practical skills and human behaviors that enable them to compete in the labor market and transfer knowledge through conducting studies and scientific research and providing distinguished community services to citizens. ‫عميد الكليه‬ ‫مديروحدة ضمان الجوده‬ ‫ محمد حامد غازي‬/‫د‬.‫ا‬ ‫ ريهام محمد عبد للا‬/‫د‬.‫ا‬ [email protected] ‫وحدة ضمان الجوده‬ 1  Overall Aim of Course: The aims of this course are to provide students with an appropriate foundation of knowledge covering oral and maxillofacial surgery infection and common lesion in the oral and maxillofacial region in children and adults with various surgical interventions.  Intended Learning Outcomes (ILO's): a- Knowledge and understanding: By the end of this course, the student should be able to: a.1. Label the clinical symptoms and signs of the oral soft & hard tissues infections. a.2. Recognize the maxillary sinus and its dental implications List the clinical symptoms and signs of the oral cavity cysts and tumors of the oral a.3. cavity. a.4. List the differential diagnosis of different lesions affecting oral & maxillofacial region. a.5. Label the different disease and lesion of salivary glands b- Intellectual skills: By the end of this course, the student should be able to: Differentiate between normal and abnormal features that is particularly relevant to b.1. dental practice. b.2. Organize maxillofacial emergencies. b.3. Construct the line of management of facial trauma. Assess the role of oral surgery and its interface with other dental and medical b.4. specialties in the management of head and neck tumors. c- Professional and practical skills: By the end of this course, the student should be able to: c.1. Practice the necessary procedures for controlling complications of oral surgery both general (medical) and local (surgical) intra-operatively and post-operatively c.2. Apply different anesthetic techniques for oral and maxillofacial region. c.3. Use the needed surgical armamentarium. c.4. Preform teeth simple extraction. c.5. Preform removal of fractured teeth and remaining roots. c.6. Apply current infection control guidelines. 1 d- General and transferable skills: By the end of this course, the student should be able to: d.1. Communicate with colleagues, staff and patient d.2. Manage time set priorities work to prescribed time limits. d.3. Utilize infection control measures in dental practice. d.4. Develop appropriate professional behavior with management of stress in workplace d.5. Communicate with other specialty to improve the medical services. 2 LIST OF CONTENTS TOPIC PAGE  Management of Odontogenic infection 1  Management of Complex odontogenic infections: 23 Fascial spaces infection  Management of Complex odontogenic infections: 42 Osteomyelitis  Management of Cysts of the oral cavity. 52  Management of Odontogenic tumors 70  Management of Non-odontogenic tumors 95 Management of ODONTOGENIC INFECTIONs 1 MANAGEMENT OF ORO-FACIAL INFECTIONS Infection Involves the proliferation of microbes resulting in triggering of the defense mechanism, a process manifesting as inflammation. Incidence 90–95% of infections that manifest in the orofacial region are odontogenic The majority of infections in orofacial and neck regions belong to this group. approximately 70% present as periapical inflammation, principally the acute dentoalveolar abscess, with the periodontal abscess following ETIOLOGY: Odontogenic Non-vital teeth Pericoronitis Tooth extraction Periapical granulomas and infected cysts. Others Postoperative trauma, defects due to fracture, salivary gland disease, and infection as a result of local anesthesia (Rare causes) Signs of infection -Redness : due to vasodilatation. - Hotness : due to inflow of warm blood. - Pain : due to pressure on the nerve ending by edema. - Loss of function :due to reflex inhibition of muscle movement associated with pain 1 2 PATHWAYS OF ODONTOGENIC INFECTION when inadequately managed, an infection will progress and spread through the path of least resistance The periapical infection progress can vary according to the: Host resistance. The number and virulence of the organism. Anatomy of the involved area Host Defense Mechanisms Innate immunity Intact Anatomic Barrier Neutrophils. Macrophages. Dendritic cells. Natural killer cells. Lymphoid cells. Complement system Acquired immunity HUMORAL DEFENSES CELLULAR DEFENSES Immunoglobulins Phagocytes Complement Granulocytes Monoytes Lymphocytes 2 3 MICROBIOLOGY OF ODONTOGENIC INFECTIONS The most commonly isolated aerobic bacteria from odontogenic infections are the viridans-type Streptococci. The most isolated anaerobic bacteria from odontogenic infections include Bacteroides spp Approximately 50% to 60% of all odontogenic infections involve a combination of both aerobic and anaerobic bacteria Anatomy of involved area (local factors) The thickness of bone The type of muscle attachment The faciolingual location of the source of the infection 3 4 Phases and fates of oral infection: Resolution Acuteness Chronicity Phases and fates of oral infection: 1. Acuteness Once the periodontal or periapical tissues get inoculated with bacteria, the infection may spread equally in all directions within bone. At this stage, if an intervention such as an endodontic or periodontal procedure or dental extraction is done, the further spread may be arrested or even abolished with judicious antibiotics When left untreated, the infection continues to spread follows the path of least resistance depending principally on the thickness of bone,the faciolingual location of the source of the infection and the type of muscle attachment When infections reach the soft tissues, it generally manifests in three stages The inoculation (edema) stage refers to the stage in which the invading bacteria begin to colonize and typically occurs in the first 3 days of onset of symptoms. This stage is characterized by diffuse, soft, doughy red swelling that is mildly tender 4 5 The cellulitis stage occurs between days 3 and 5 and represents the intense inflammatory response elicited by streptococci infection. This stage is characterized by poorly defined diffuse firm red swelling that is exquisitely painful to palpation. Indurated (consistency of a taught muscle/wooden like/ brawny hard). Streptococci produce enzymes such as streptokinase (fibrinolysin), hyaluronidase, and streptodornase. These enzymes break down fibrin and connective tissue ground substance and lyse cellular debris, thus facilitate rapid spread of bacteria along the tissue planes indurated (consistency of a taught muscle/wooden like/ brawny hard) The abscess stage as the infection evolves and anaerobes begin to predominate, liquefaction of tissues occurs with the formation of purulence. As purulence is formed, the swelling and redness become better defined and localized, and the consistency changes from firm to fluctuant. The suppurative infections are characteristic of staphylococci, often with anaerobes, such as bacteroides, and are usually associated with large accumulation of pus, which require immediate drainage. These microorganisms produce coagulase, an enzyme, that may cause fibrin deposition. In addition, the pressure from the expanding abscess, preventing compromising blood flow leading to ischemia, and thereby further increasing the zone of necrosis within the abscess cavity. 5 6 Abscess: The odontogenic abscesses present in the following forms: a) Acute periapical abscess: An abscess arises and remains in the confines of alveolar bone i.e. the pus is contained in a thick-walled cavity. b) Acute dentoalveolar abscess: Once the infection has crossed the confines of alveolar bone and comes to lie in the neighbouring soft tissues, and it gets localized. c) Acute periodontal abscess. d) Acute pericoronal abscess. 2.The chronicity With long standing infection of non-virulent organisms, the infection becomes chronic with production in localized area of necrosis These infections may occasionally rupture and drain spontaneously, which results in temporary resolution, preventing spread to deeper potential spaces. Spontaneously draining infections may continue to drain and form a fistula to the oral cavity or a sinus tract to skin, or reclose and result in the reforming of an abscess 3.The resolution When an infection is drained, either spontaneously or via surgery, the host defense mechanism destroys the involved bacteria and healing begins to occur; this is the hallmark of the resolution stage. 6 7 Pathway of Odontogenic infection Acute Dentoalveolar Abscess Definition An acute purulent inflammation of the periapical tissues, presenting at nonvital teeth, when microbes exit the infected root canals into periapical tissue. Stages 1. Early stage: ADAA without soft tissue involvement. 2. Late stage: ADAA with soft tissue involvement Signs & Symptoms Early stage: ADAA without soft tissue involvement (Central Bone Abscess) 1. A feeling of elongation of the tooth. 2. severe throbbing pain 3. Systemic Symptoms (fever, chills, malaise with pain in muscles and joints and lymphadenitis) 7 8 Signs & Symptoms Late stage: ADAA with soft tissue involvement (Subperiosteal Abscess) 1. As pus break through the cortical plates and escape into the soft tissues immediate relief of the severe throbbing pain occurs. 2. Edema appears intraorally or extraorally 3. Trismus and dysphagia are common. 4. Systemic Symptoms( fever, chills, malaise with pain in muscles and joints and lymphadenitis). Radiographic appearance 1. Early stage of ADAA has a negative radiographic picture as no changes can be noticed apart from a slight widening of the periodontal space in the periapical region. 2. Late stage of ADAA there is widening of the periodontal space with interruption of the lamina dura and a localized ill-defined area of radiolucency may be seen in the periapical region. Treatment Early stage of ADAA 1. Evacuate the imprisoned pus at the periapical area (access opening). 2. Removal of the cause of the infection. 3. Raising the body resistance and helping it to overcome the invading organisms (e.g. antibiotics) Treatment Late stage of ADAA 1. General supportive measures (Bed rest , Adequate fluid intake, Adequate nourishment). 2. Antibiotics to help body to overcome the invading microorganisms. 3. Analgesics to help in alleviating the pain. 4. Heat application to increase the circulation and enhance body defense. 8 9 5. Incision and drainage when indicated. 6. Elimination of the cause through RCT or extraction Complications of ADAA 1. Fascial space infection. 2. Ludwig’s angina. 3. Osteomyelitis. 4. Septicemia. 5. Fatal complications: meningitis, brain abscess or cavernous sinus thrombosis Periodontal Abscess Definition An acute or chronic purulent inflammation, which develops in an existing periodontal pocket. Clinically Characterized by edema located at the middle of the tooth, dull pain, and redness of the gingiva. Symptoms are not as severe as those observed in the acute dentoalveolar abscess. 9 10 Treatment Simple and entails incision, through the gingival sulcus with a probe or scalpel, of the periodontal pocket that has become obstructed. Incision may also be performed at the gingiva; more specifically, at the most bulging point of the swelling or where fluctuation is greatest. Periodontal abscess VS Acute dentoalveolar abscess Chronic Dentoalveolar Abscess Definition Acute odontogenic infections, if not treated in time, develop into chronic infections, resulting in spontaneous drainage intraorally or on the skin. Asymptomatic , mild intermittent pain or mild edema and redness of the tissues of the periapical region. The tooth is sensitive to percussion and the pulp of the offending tooth tests nonvital 10 11 Radiographic picture irregular radiolucent area surrounding the apex of the root is observed in cases of chronic dentoalveolar abscesses, which is due to bone destruction Treatment Eliminating the infection from the responsible tooth with endodontic therapy or in conjunction with surgical treatment (apicoectomy) Fistulectomy ( Extraoral fistula) Periapical Granuloma A small mass of well-defined granulation tissue developing in the periodontal tissues around the apex of the tooth. Radiographically, a small well-defined radiolucent area surrounded by radiopaque line around the root apex. Treatment a. RCT with apicoectomy and apical curettage. b. Extraction of the offending tooth, usually the granuloma comes out attached to the root apex. If not, the socket has to be curetted. 11 12 Management of odontogenic infections (1)controlling (3) mobilizing (2) establishing the source of the host drainage the infection defense system Management of Infection 1. Determine the cause and the severity of the infection 2. Evaluate the host defense 3. Decide on setting of care 4. Treat surgically (Incision and Drainage) 5. Support medically 6. Choose and prescribe antibiotics appropriately 7. Evaluate patient frequently 1. Determine the cause and the Severity of Infection Odontogenic infections can range from routine and localized to severe and life-threatening. Determination of severity begins with a complete history, followed by physical examination, and any necessary testing (e.g., radiographic imaging studies, laboratory studies) Complete History The patient’s chief complaint. A thorough history of the chief complaint (history of present illness). This provides the clinician with valuable clues that could help determine the origin and etiology of the infection. Changes in the character and location of pain History of extraction or any other trauma to the site Duration of the symptoms Previous treatment history Past medical and social history Physical Examination The clinician should avoid examining the oral cavity first, which makes it easy to miss obvious yet extremely important findings that have a direct impact upon management. It is recommended that the clinician begin from “big to small,” or “outside then inside.” a.General examination (The patients may present with fatigue, fever, and malaise or so-called toxic appearance) Vital signs (temperature, blood pressure, heart rate, and respiratory rate) Head and neck examination Palpation of swellings should be done to know the tenderness Generalized lymph node examination 12 13 b.Extraoral examination Skin changes—swelling, redness, ulcers, etc. Bony enlargements Lymph node swellings Presence of any sinus openings, fistula, etc C.Intra-oral examination Mandibular mouth opening Oral cavity examination Swelling (consistency, fixity), discharge, dental caries, deviation of tissues (tongue, uvula) Imaging Studies periapical (IOPA) or orthopantomogram (OPG) depending on the symptomatology and clinical examination. CT scan may be required in severe cases to assess the pathway Laboratory Studies The most used laboratory study is the complete blood count, with focus on the white blood cell (WBC) count, and more specifically, the WBC differential count. 2. Evaluate State of Patient’s Host Defense Mechanisms two main categories of medical comorbidities that adversely affect the host defense system are inadequately controlled metabolic diseases and conditions that directly affect the immune system 3.Decide on setting of care When infection detected early, the vast majority of odontogenic infections may be safely managed by the general dentist. Based upon location, severity, surgical access, and status of host defenses. The decision to refer to oral & maxillofacial surgeon for hospital admission a) Anatomic location Graded in severity by level to which the airway and vital structures are threatened Low Buccal, Vestibular, Subperiosteal Moderate Masticator space Severe Lateral pharyngeal Retropharyngeal Danger Space of infection 13 14 b) Severity of infection c) Surgical Access The need for GA or not d) Status of Host Defenses Many patients with or without underlying conditions are often dehydrated and have elevated blood glucose, which could further compromise the host defense system. 4. Treat Infections Surgically (Definitive treatment) “the most important therapeutic action in the management of orofacial infections is the drainage of pus, and antibiotics are merely an adjunct…” (Pogrel, A; OMFS Clinics of North America.Feb 1993) incision and drainage three factors involved in the management of odontogenic infections—eliminating the source of the infection, establishing surgical drainage, and mobilizing the host defense system—it is easy to understand the central role of surgical management because the first two factors can only be achieved surgically 14 15 Drainage of pus, is achieved (1) By way of the root canal. (2) Scaling and root planing with debridement (3) With an intraoral incision. (4) With an extraoral incision. (5) Through the extraction socket ▪ Incision and drainage of the abscess should be performed at the appropriate time. This is when the pus has accumulated in the soft tissues and fluctuates during palpation, that is when pressed between the thumb and middle finger, there is a wave-like movement of the fluid inside the abscess. Heat application a. Increase the blood supply to the area. b. Stimulate phagocytosis. c. Has some analgesic effect. d. Help liquefaction and pus formation Indications a. Space infections (primary) that has localized pus collection with a clinically evident point of fluctuance. Example: buccal space infection with point of fluctuance on face. b. Space infections (secondary) that has pus collection with no clinical sign of fluctuance but requires immediate drainage to prevent progression. Example: masseteric space infection—only clinical sign is trismus. c. Non-suppurative space infection such as Ludwig’s angina, where I&D serves as a method of decompression of the tissue planes, but could be lifesaving. The goal of surgical drainage Incision and drainage facilitates healing by two main mechanisms. The first and most important mechanism is decreasing the bacterial load. Lowering the bacterial load with elimination of the source and drainage of the infection allows the host defense system (third component of management) to remove any residual infection. The second mechanism of surgical drainage is decreasing the pressure of the infected tissues. When the hydrostatic pressure of the infected tissues is decompressed with surgical drainage, the local blood supply is improved, and this allows the host defense system, and adjunctive antibiotics, to better reach the infected. Incision and drainage is not solely reserved for abscesses, but can facilitate healing of cellulitis without waiting for the localization of the infection (abcess formation), via the same mechanism 1. It reduces pressure of edematous tissues on the airway reducing respiratory embarrassment. 15 16 2. Adequate culture specimen can be obtained, so an empirical antibiotic therapy may be continued or changed a. Blunt dissection into the tissue spaces breaks the pus locules and fibrous barrier, thus facilitating reach of the antibiotics into the infective site. 3. It allows placement of drains, which may be valuable to drain pus collection as time progresses, and irrigation of the tissues at regular intervals. 4. Serves to abort the spread of the infection into deeper anatomic spaces. Type of anaethesia ✓ Regional nerve block anesthesia is always preferred over infiltration techniques for two reasons: (1) penetration of the local anesthetic is difficult when the agent is injected directly into an infected area because the acidic (low pH) local environment (2) infiltration anesthesia carries the risk of seeding infection to neighboring uninfected sites or tissue spaces ✓ Oro/ nasal tracheal intubation ✓ Fiber-optic intubation or tracheostomy may be considered in; patients with limited mouth opening (trismus) or in patients having intra-oral and pharyngeal infections (sub-lingual, lateral/retropharyngeal spaces) where the chances of aspiration is high in the event of oro/naso-tracheal intubations 16 17 Guidelines for placement of incisions in infected cases: 1. Incisions should be placed in the most dependent areas. 2. Incisions should be parallel to the skin creases. 3. Incisions should lie in an esthetically acceptable site as far as possible. 4. Incisions should be supported by healthy underlying dermis and subcutaneous tissue. Placing the incision through the thin, often shiny skin directly overlying the abscess, which normally gets undermined by an abscess burrowing its way to the surface; results in a puckered contracted scar which gets collapsed into abscess cavity. 5. Incisions placed intraorally, should not crossfrenal attachments, and should be placed parallel to nerve fibers in the region of mental nerve. 6. The removal of the cause; such as an infected tooth, a segment of necrotic bone, a foreign body, if not already done, then should be done at the time of incision and drainage procedure. Hilton’s Method of Abscess Drainage Antisepsis of the area with an antiseptic solution before the incision. Anesthesia of the area where incision and drainage of the abscess are to be performed, with the block technique together, in order to avoid the risk of existing microbes spreading into deep tissues. Stab incision with the help of 11 number blade is made at the most dependent area along the skin crease through skin and subcutaneous tissue. The length of the incision must be sufficient—at least 10 to 15 mm Closed forceps are pushed through the tough deep fascia and advanced towards the pus collection. Abscess cavity is entered, and forceps opened in a direction parallel to vital structures. Pus flows along sides of the beaks. Explore the entire cavity for additional loculi Pus collected and sent for culture and sensitivity test. Abscess cavity is irrigated with antiseptic solution. 17 18 Corrugated rubber drain is inserted deep into the abscess cavity and secured to the edge of the incision and the drain is removed once there are no active exudates. Dressing placed over the incision Purpose of keeping the drain: The purpose of drain is to allow the discharge of tissue fluids and pus from the wound by keeping it patent. The drain allows for debridement of the abscess cavity by irrigation. Tissue fluids flow along the external surface of a latex drain. Hence, it is not always necessary to make perforations in the drain, which could weaken and perhaps cause fragmentation within the tissues Removal of drains: Drains should be removed when the drainage has nearly completely ceased. Thus, drains are usually left in infected wounds for 2–7 days 5.Supportive therapy It involves those modalities which aid the patient’s own body defenses. It consists of the following: 1. Adequate control of systemic diseases that may affect treatment ( blood glucose control) 2. Administration of antibiotics. 3. Hydration of patient as Patients with infection and fever present a considerable loss of body fluids—250 mL for every degree (centigrade) temperature rise. Ambulatory patients must drink 8–10 glasses of water or any other liquid. Intravenous fluids can be given to those patients who are hospitalized to improve hydration. 4. Maintain adequate nutritional status-high protein intake. The daily calorie requirement also increases by up to 13% for each degree (centigrade) above normal body temperature 5. Analgesic. 6. Bed rest. 7. Application of heat in the form of moist pack, advice mouth rinses. 8. Frequent wound irrigation and change of dressings, and removal of drain. 8. Dental management by extraction or root-canal treatment for drainage 18 19 6.Antibiotic administration Involves the empiric administration of the most appropriate antibiotic, which is based on knowledge of antimicrobial effectiveness, side-effects, adverse reactions, contraindications, and the cost Odontogenic infections are almost invariably caused by normal oral flora (predominantly facultative oral streptococci, anaerobic streptococci, and Prevotella and Fusobacterium species) and typically have a predictable bacterial composition. This predictability makes the routine use of culture and sensitivity testing unnecessary and impractical because the causative organisms are already known. The predictable nature of the causative organisms in odontogenic infections also favors the use of a limited number of antibiotics, when indicated. These include penicillin, amoxicillin, clindamycin, and azithromycin, which are effective against aerobic and facultative streptococci and oral anaerobes Antibiotic classification II.Bacteriostatic antibiotics Drug merely retards the growth of the bacteria by attaching to the ribosomes and DNA inside the cell. 19 20 Narrow spectrum versus Broad spectrum antibiotic Narrow-spectrum antibiotics are active against a select group of bacterial types. Broad-spectrum antibiotics are active against a wider number of bacterial types and, thus, may be used to treat a variety of infectious diseases. Indications for antibiotics Presence of cellulitis (with or without concomitant abscess) Swelling extending beyond the alveolar process Trismus Lymphadenopathy Fever (>101°F [38.3°C]) Severe pericoronitis Osteomyelitis Immunocompromised patient (with appropriate surgical management of infection 20 21 Indications for Culture and Antibiotic Sensitivity Testing ✓ Rapidly progressive infection ✓ Previous, multiple antibiotic therapy ✓ Nonresponsive infection (after >48 h) ✓ Recurrent infection ✓ Compromised host defenses Administer Antibiotic Properly ❖ The proper dose, timing, route and duration of administration of antibiotics are as important as proper antibiotic selection. The goal is to achieve a high-enough plasma level to kill or halt the bacteria that are sensitive to the antibiotic while minimizing adverse side effects ❖ Use of antimicrobial with least toxicity and side effects- prevents vital organ damage and Use of bactericidal rather than bacteriostatic drug prevents residual infection. ❖ Duration of administration can vary depending on the patient’s response to surgical treatment and antibiotic therapy, but the typical regimen consists of a 4- to 5-day course ❖ On the other hand, a prescribed course of antibiotics must be completed, regardless of symptoms, to minimize the risk of increasing antibiotic resistance 7. Evaluate Patient Frequently The swelling normally decreases by 48–72 hours postoperatively, allowing for a temporary rise in swelling because of surgical trauma. Trismus and WBC count, usually tend to reduce by 24– 48 hours after surgery. A review of the case does not show any improvement by 48–72 hours postoperatively, then a re-evaluation should be done for the following: Effectiveness of the wound drainage, Antibiotic therapy, and A search for a previously undetected source of infection 21 22 Management of Complex odontogenic infections: Fascial spaces infection 23 OROFascial spaces INFECTION infections Fascia: A sheet of connective tissue covering or binding together body structures Fascial spaces: Fascia lined tissue compartments filled with loose, areolar connective tissue that can be inflamed when invaded by microorganisms. CLASSIFICATION OF FASCIAL SPACES Direct involvement (Primary spaces) Indirect involvement (Secondary spaces) A. Primary maxillary spaces: 1) Masticatory spaces: (Masseteric, 1) Upper lip pterygomandibular, superficial and 2) Canine. deep temporal). 3) Buccal. 2) Lateral pharyngeal. 4) Infratemporal spaces. 3) Retropharyngeal. B. Primary mandibular spaces: 4) Prevertebral spaces 1) Buccal 5) Parotid space. 2) Submental. 3) Submandibular. 4) Sublingual spaces. Abscess of Base of Upper Lip Anatomic It is a vestibular abscess, at the base of the upper lip, on the oral Location: side of orbicularis oris muscle. Etiology: It is usually caused by infected root canals of maxillary anterior teeth. Clinical Swelling and protrusion of the upper lip, which is accompanied by Presentation: diffuse spreading and obliteration of the depth of the mucolabial fold. Treatment:  The incision for drainage is made at the mucolabial fold parallel to the alveolar process. A hemostat is then inserted inside the cavity, which reaches bone, aiming for the apex of the responsible tooth, facilitating the evacuation of pus. After drainage of the abscess, a rubber drain is placed until the clinical symptoms of the infection subside.  Removal of the cause, either RCT or extraction. Complications  Orbital cellulitis  Cavernous sinus thrombosis 24 Figure 1 Muscles related to base of upper lip & canine fossae Figure 2 Drainage of abscess of base of upper lip Canine Fossa Abscess (Infraorbital Space) Anatomic The canine fossa is a small space between the levator labii Location: superioris and the levator anguli oris Etiology: Infected root canals of maxillary canine or premolars. Clinical Localized, tender edema in the infraorbital region, which spreads Presentation: towards the medial canthus of the eye, lower eyelid, and side of the nose as far as the corner of the mouth. Later on the skin becomes reddish, taut and shiny due to suppuration There is also obliteration of the nasolabial fold, and somewhat of the mucolabial fold. Treatment: The incision for drainage is performed intraorally at the mucobuccal fold (parallel to the alveolar bone), in the canine region. A hemostat is then inserted, which is placed at the depth of the purulent accumulation until it comes into contact with bone, while the index finger of the nondominant hand palpates the infraorbital margin. Finally, a rubber drain is placed, which is stabilized with a suture on the mucosa. Figure 3 Canine fossa abscess 25 Buccal Space Abscess Boundaries: Superiorly: the zygomatic arch. Inferiorly the inferior border of the mandible. Medially: buccinators muscle. Laterally: covered by skin , superficial fascia. Posteriorly: anterior border of the Masseter. Anteriorly: corner of the mouth. Etiology: From infected root canals of posterior teeth of the maxilla and mandible. Clinical Swelling of the cheek, which extends from the zygomatic arch as far Presentation: as the inferior border of the mandible, and from the anterior border of the ramus to the corner of the mouth. The skin appears taut and red, with or without fluctuation of the abscess, which if neglected, may result in spontaneous drainage. Treatment: Access to the buccal space is usually intraoral for three main reasons: 1. Because the abscess fluctuates intraorally in the majority of cases. 2. To avoid injuring the facial nerve. 3. For esthetic reasons. The intraoral incision is made at the posterior region of the mouth, in an anteroposterior direction and very carefully in order to avoid injury of the parotid duct or the mental nerve. A hemostat is then used to explore the space thoroughly. Figure 4 Buccal space abscess 26 Infratemporal Abscess The space in which this abscess develops is the superior extension of the pterygomandibular space Anatomic Laterally: the ramus of the mandible and the temporalis muscle. Location: Medially: the medial and lateral pterygoid muscles, and is continuous with the temporal fossa. Contents The mandibular nerve, mylohyoid nerve, lingual nerve, buccal nerve, chorda tympani nerve, and the maxillary artery &part of the pterygoid venous plexus. Etiology: Infected buccal roots of maxillary molars. Septic posteior superior alveolar nerve & inferior alveolar nerve block. Ascending infection from pterygomandibular space. Clinical Trismus and pain during opening of the mouth with lateral deviation Presentation: towards the affected side. Edema at the region anterior to the ear which extends above the zygomatic arch &edema of the eyelids are observed. Treatment: Intraoral incision: at the depth of the mucobuccal fold, and, more specifically, laterally (buccally) to the maxillary third molar and medially to the coronoid process, in a superoposterior direction. A hemostat is inserted into the suppurated space, in a superior direction. Extraoral incision: in certain cases, the incision is performed on the skin in a superior direction, and extends approximately 3 cm. The starting point of the incision is the angle created by the junction of the frontal and temporal processes of the zygomatic bone. Drainage of the abscess is achieved with a curved hemostat, which is inserted through the skin into the purulent accumulation. Figure 5 Temporal space (superficial & deep, including infratemporal space), Submasseteric & pterygomandibular spaces. 27 Temporal Abscess Anatomic The temporal space is the superior continuation of the Location: infratemporal space. This space is divided into superficial and deep temporal spaces. The superficial temporal space is bounded laterally by the temporal fascia and medially by the temporalis muscle, while the deep temporal space is found between the medial surface of the temporalis muscle and the temporal bone. Etiology: Spread of infection from the infratemporal space, with which it communicates. Clinical Painful edema of the temporal region, trismus (the temporalis and Presentation: medial pterygoid muscles are involved), and pain during palpation of the edema. Treatment: Extraoral incision: the incision for drainage is performed horizontally, at the margin of the scalp hair and approximately 3 cm above the zygomatic arch. It then continues carefully between the two layers of the temporal fascia as far as the temporalis muscle. Palatal Space Etiology: Maxillary teeth whose roots lie close to it e.g. Maxillary lateral incisors (causing anterior palatal abscess) Palatal roots of molars (causing posterior palatal abscess). Clinical This infection perforates the palatal alveolar bone and pus accumulates Presentation: beneath the palatal mucoperiosteum. A well-defined fluctuant swelling confined to one side of the palate, adjacent to the offending tooth. Treatment: Intraoral incision done along the palatal mucoperiosteum down to the bone. The incision is made at right angles of to the long axis of the teeth carried out anteroposteriorly carefully on the alveolar mucosa rather the palatal mucosa to avoid injury of the palatal arteries. Figure 6 Incision for drainage of a palatal abscess, parallel to greater palatine vessels 28 Mental Abscess Anatomic The accumulation of pus in this space is located at the anterior Location: region of the mandible, near the bone, and, more specifically, underneath the mentalis muscle, with spread of the infection towards the symphysis menti. Etiology: infected mandibular anterior teeth (incisors). Clinical Firm and painful swelling in the area of the chin is observed, while Presentation: later the skin becomes shiny and red. Treatment: The incision for drainage of the abscess may be performed at the depth of the mucobuccal fold, if the abscess fluctuates intraorally. If the pus has spread extraorally, though, an incision is made on the skin, parallel to the inferior border of the chin, 1–1.5 cm posteriorly. After drainage is complete, a rubber drain is placed. Submental Abscess Anatomic This space is situated in the midline just behind the chin Location: Boundaries: Superiorly: Mylohyoid muscle. Inferiorly By skin, superficial fascia, platysma and deep cervical fascia. Laterally: The anterior belly of digastric muscle. Contents The anterior jugular vein and the submental lymph nodes. Etiology: The mandibular anterior teeth or is the result of spread of infection from other anatomic spaces (sublingual, submandibular). Clinical Indurated and painful submental edema, which later may fluctuate or Presentation: may even spread as far as the hyoid bone Treatment: After local anesthesia is performed around the abscess, an incision on the skin is made beneath the chin, in a horizontal direction and parallel to the anterior border of the chin. The pus is then drained in the same way as in the other cases. 29 Sublingual Abscess There are two sublingual spaces above the mylohyoid muscle, to the right and left of the midline. Boundaries: Superiorly: the mucosa of the floor of the mouth. Inferiorly the mylohyoid muscle.. Medially: the lingual septum Anteriorly the inner surface of the body of the mandible. & Laterally: Posteriorly: the hyoid bone. Contents the submandibular duct (Wharton’s duct), the sublingual gland, the lingual nerve, terminal branches of the lingual artery, and part of the submandibular gland. Etiology: mandibular anterior teeth, premolars and the first molar, whose apices are found above the attachment of the mylohyoid muscle. Also, infection may spread to this space from other contiguous spaces with which it communicates (submandibular, submental, lateral pharyngeal). Clinical The abscess of the sublingual space presents with characteristic Presentation: swelling of the mucosa of the floor of the mouth, resulting in elevation of the tongue towards the palate and laterally. The mandibular lingual sulcus is obliterated and the mucosa presents a bluish tinge. The patient speaks with difficulty, because of the edema, and movements of the tongue are painful. Treatment: The incision for drainage is performed intraorally, ½ inch from lingual plate to avoid injury to Wharton’s duct and the lingual nerve. In order to locate the pus, a hemostat is used to explore the space inferiorly, in an anteroposterior direction and beneath the gland. After drainage is complete, a rubber drain is placed. 30 31 Submandibular Abscess This space is one on each side of the submental space. Boundaries: Superiorly: The mylohyoid muscle. Inferiorly Superficial layer of deep cervical fascia. Medially: Anterior belly of digastric. Laterally: Medial surface of the mandible below the mylohyoid ridge. Posteriorly: Stylohyoid ligament and posterior belly of digastric muscle. Contents the submandibular salivary gland, the submandibular lymph nodes and facial artery and vein. Etiology: the mandibular second and third molars, if their apices are found beneath the attachment of the mylohyoid muscle. It may also be the result of spread of infection from the sublingual or submental spaces. Clinical moderate swelling at the submandibular area, which spreads, creating Presentation: greater edema that is indurated and redness of the overlying skin. Also, the angle of the mandible is obliterated, while pain during palpation and moderate trismus due to involvement of the medial pterygoid muscle are observed as well. Treatment: The incision for drainage is performed on the skin, approximately 1 cm beneath and parallel to the inferior border of the mandible. During the incision, the course of the facial artery and vein (the incision should be made posterior to these) and the respective branch of the facial nerve should be taken into consideration. A hemostat is inserted into the cavity of the abscess to explore the space and an attempt is made to communicate with the infected spaces. Blunt dissection must be performed along the medial surface of the mandibular bone, because pus is often located in this area as well. After drainage, a rubber drain is placed. 32 Submasseteric Abscess The space in which this abscess located between Boundaries: Anteriorly: the mucosa of the retromolar area. Posteriorly the parotid gland. Medially: the lateral surface of the ramus of the mandible. Laterally: the masseter muscle Etiology: Infection of this space originates in the mandibular third molars (pericoronitis). Clinical A firm edema that is painful to pressure in the region of the Presentation: masseter muscle, severe trismus. Intraoral edema presents at the retromolar area and at the anterior border of the ramus. Rarely fluctuates. Treatment:  Intraoral incision that begins at the coronoid process and runs along the anterior border of the ramus towards the mucobuccal fold, approximately as far as the second molar. Extraoral skin incision beneath the angle of the mandible. 33 Pterygomandibular Abscess Boundaries: Laterally: the medial surface of the ramus of the mandible. Medially: the medial pterygoid muscle Superiorly: the lateral pterygoid muscle Posteriorly: the parotid gland. Anteriorly the pterygomandibular raphe Contents the mandibular neurovascular bundle, lingual nerve, and part of the buccal fat pad. Etiology: Pericoronitis related to mandibular third molars or the result of an inferior alveolar nerve block, if the penetration site of the needle is infected. Clinical Severe trismus and slight extraoral edema beneath the angle of the Presentation: mandible are observed. Intraorally, edema of the soft palate of the affected side is present, as is displacement of the uvula and lateral pharyngeal wall, while there is difficulty in swallowing. Treatment: The incision for drainage is performed on the mucosa of the oral cavity and, more specifically, along the medial and anterior aspect of ramus. The incision must be 1.5 cm long and 3–4 mm deep. A curved hemostat is then inserted, which proceeds posteriorly and laterally until it comes into contact with the medial surface of the ramus. The abscess is drained, permitting the evacuation of pus along the shaft of the instrument. 34 Lateral Pharyngeal Abscess Anatomic It is bounded by the lateral wall of the pharynx, the medial Location pterygoid muscle, the styloid process and the associated attached muscles and ligaments, and the parotid gland. Contents The internal carotid artery, the internal jugular vein with the respective lymph nodes, the glossopharyngeal nerve, hypoglossal nerve, vagus nerve, and accessory nerve. Communications: It communicates directly with the submandibular space, as well as with the brain by way of foramina of the skull. Etiology: originate in the region of the third molar or due to spread of infection from the submandibular and pterygomandibular spaces. Clinical Extraoral edema at the lateral region of the neck that may spread Presentation: as far as the tragus of the ear, Displacement of the pharyngeal wall, tonsil and uvula towards the midline. Pain that radiates to the ear. Trismus, difficulty in swallowing, significantly elevated temperature, and generally malaise are noted. Treatment: Drainage is performed extraorally (similar to that of the submandibular abscess) with an incision 2 cm long, inferior to or posterior to the posterior part of the body of the mandible. Drainage of the abscess may also be performed intraorally, although it is difficult and risky, because there is a great chance of aspiration of pus, especially if the procedure is carried out under general anesthesia Retropharyngeal Abscess Anatomic The retropharyngeal space is located posterior to the soft tissue Location: of the posterior wall of the pharynx. Boundaries: Anteriorly: the superior pharyngeal constrictor muscle and the associated fascia Superiorly: the base of the skull. Inferiorly the posterior mediastinum. Posteriorly: the prevertebral fascia. Etiology: originate in the lateral pharyngeal space Clinical The same symptoms as those present in the lateral pharyngeal abscess Presentation: appear clinically, with even greater difficulty in swallowing though, 35 due to edema at the posterior wall of the pharynx. If it is not treated in time, there is a risk of: 1. Obstruction of the upper respiratory tract, due to displacement of the posterior wall of the pharynx anteriorly. 2. Rupture of the abscess and aspiration of pus into the lungs, with asphyxiation resulting. 3. Spread of infection into the mediastinum. Treatment: Therapy entails drainage through the lateral pharyngeal space, which is where the infection usually begins Parotid Space Abscess Anatomic The space in which this abscess develops is located in the area Location: of the ramus of the mandible and, more specifically, between the layers of the fascia investing the parotid gland. Communication It communicates with the lateral pharyngeal and the submandibular spaces. Contents the parotid gland and its duct, the external carotid artery, the superficial temporal and facial artery, the retromandibular vein, the auriculotemporal nerve, and the facial nerve Etiology: originates from odontogenic migratory infections of the lateral pharyngeal and submandibular spaces Clinical It presents with characteristic edema of the retromandibular and Presentation: parotid region. Difficulty in swallowing and pain mainly during chewing, which radiates to the ear and temporal region. In certain cases there is redness of the skin and subcutaneous fluctuation (. Also, a purulent exudate may be noted from the papilla of the parotid duct after pressure is applied. Treatment: Depending on the margins of the edema, therapy entails a broad incision posterior to the angle of the mandible, extending from the level of the inferior aspect of the lobule of the ear to just above the mandible, taking particular care not to injure the respective branch of the facial nerve. Drainage of pus is achieved after blunt dissection using a hemostat to explore the purulent collection 36 37 Possible Life Threatening Complications of Orofacial Infection Related to the upper jaw Related to the lower jaw a) Intracranial complications, with a) Ludwig‘s angina. possibilities of cavernous sinus b) Descending deep cellulitis of the thrombosis, brain abscess, dural neck, resulting in mediastinitis meningitis and osteomyelitis of the skull. c) Carotid sheath invasion. b) Retrobulbar cellulitis with possibility of blindness. Ludwig’s AnginA Definition: Ludwig’s angina is a grave acute cellular infection and is characterized by bilateral involvement of the submandibular and sublingual spaces, as well as the submental space. In the past this condition was fatal, although today adequate surgical treatment and antibiotic therapy have almost eliminated fatal episodes. Etiology: 1. Dental infection which opens below the mylohyoid attachment usually from lower second & third molars. 2. Iatrogenic: Use of a contaminated needle for giving local anaesthesia. 3. Traumatic injuries to orofacial region:Mandibular fracture. 4. Osteomyelitis of the mandible. 5. Submandibular and sublingual sialadenitis. Microbiology Mixed infection, mainly hemolytic streptococci and mixture of aerobic gram –ve microoragnisms. Types: a) Septic non-suppurative type: suppuration doesn’t occur, the infection has no tendency for localization and drainage is difficult or impossible. This type has a bad prognosis because of edema of the larynx and glottis which might cause suffocation and death if not promptly controlled; the patient must be hospitalized for fast treatment. b) Septic suppurative type: adequate drainage can be obtained as the localization of pus occurs and prognosis is much more favorable. 38 Signs and Symptoms: 1. Swelling: a) Rapidly developing brawny hard swelling of the floor of the mouth and submandibular area involving sublingual, submandibular and submental spaces bilaterally. b) The swelling is firm, painful and diffuse with no evidence of localization and does not pit on pressure. c) Later the swelling may extend to the neck with sharp demarcation and it may even reach the clavicle. 2. Patient’s mouth is opened because of the elevation of the floor of the mouth which has a reddish or bluish coloration. 3. The tongue: a) Elevated and protruded from the mouth. b) Has a wooden appearance. c) Has a stiff movement. 4. Edema of the glottis leading to difficulty in breathing and suffocation if treatment is delayed. 5. Difficulties in swallowing and respiration. 6. Constitutional symptoms: fever, rapid pulse, rapid respiration, malaise, excessive salivation, dehydration and leukocytosis. Treatment 1. General supportive measures. 2. Antibiotics. 3. Heat therapy. 4. Surgery. 5. Treatment or removal of the cause. 6. Postoperative care. 1. General supportive measures: a) Hospitalization. b) Complete bed rest. c) Fluid intake to compensate for dehydration and to restore electrolyte balance, if the patient can’t swallow 1000 cc. of 5% glucose solution or lactated ringer’s solution should be given by continuous i.v. drip method every 12 hours. d) Adequate nourishment with high caloric and vitamin diet. 2. Antibiotics: Antibiotics play a vital role in managing Ludwig‘s angina.  Usually, IV antibiotics with proper dosage and frequency are necessary.  IV penicillin can be given empirically in combination with metronidazole or clindamycin.  Pus evacuated should be cultured and sent for AB sensitivity test. 39  AB should be given at appropriate doses at appropriate intervals. 3. Heat therapy: Hot water bags are applied to the jaw and neck to increase local circulation in the area and may affect fluctuation. Hot saline mouth wash is also used. 4. Surgery includes: A. Tracheostomy: Is done when there are any respiratory difficulties and performed before any surgery to ensure free airway. B. Incision and Drainage: Aim of incision: a) Release tissue tension. b) Drin any drop of pus which may be present deep in tissue spaces. c) Decompress submandibular region and to release the tension within it. Procedures: a. Preparation of the surgical field: skin cover submandibular region is washed with detergent soap and scrubbed with alcohol. b. Anaesthesia: 1st IV sedation with short acting barbiturate. 2nd use of ring block L.A. G.A. is contraindicated due to: i. Patient is only able to maintain the airway with assistance of accessory muscles of respiration when patient is conscious. So with G.A. this voluntary control over airway is lost. ii. When the patient is unconscious, there is a massive increase in the edema and airway becomes occluded. N.B if G.A. is necessary, it should be followed by an endotracheal tube while the patient is conscious. C. No. 10 BP is used to perform 2 cm long incision 2 cm below the chin in the midline. The incision is made through skin, subcutaneous tissue and platysma muscle. D. Hemostat is directed to submandibular space, then advanced until the tip is felt under the skin 1 cm below the angle where submandibular incision is made. E. Make culture of specimen of pus evacuated from submandibular space. F. The mylohyoid muscle fibers are separated by blunt dissection to gain entrance to sublingual space or by intraoral approach. A drain is grasped by hemostat and pulled to project from submental incision, the ends of the drain are sutured together. 40 G. Heavy dressing of several layers of gauze is applied to hide the free end of the drain and to keep the area warm. 5. Removal of cause: After the acute stage subsides, the offending tooth if present should be extracted or treated endodontically. 6. Postoperative care: a) Hot application is indicated. b) Irrigation is done by fenestrated drain every 24-48 hours, the drain and the dressing are changed. c) Complete drainage occurs in 7-10 days, after which the drain is removed the dressing is continued until complete healing of incision. d) IV fluid intake should be continued until the patient is able to swallow, then soft and fluid diet with high caloric and vitamin content is given. e) Antibiotic is continued until complete recovery. REFERENCES  Contemporary Oral & Maxillofacial Surgery, Seventh Edition  Peterson’s Principles of Oral & Maxillofacial Surgery, 2nd Edition  Head,neck and orofacial infections: An Interdisciplinary Approach. James R. Hupp. Elie M. Ferneini 41 Management of Complex odontogenic infections: Osteomyelitis of the jaws 42 1 Osteomyelitis of the jaws Definition - An inflammatory condition of the bone, it usually begins in the medullary cavity, involving the cancellous bone; then it extends and spreads to the cortical bone and eventually to the periosteum. Incidence - Osteomyelitis more commonly affects the mandible than maxilla due to the following factors: 1- The blood supply to the maxilla is much richer and is derived from several arteries, which form a complex network of feeder vessels. 2- The mandible has less blood supply, its primary blood supply from the inferior alveolar artery and so mandible has less resistance to infection than the maxilla. 3- The dense overlying cortical bone of the mandible prevents penetration of periosteal blood vessels; the mandibular cancellous bone is more likely to become ischemic and therefore infected. 4- The mandible is more exposed to trauma than the maxilla. Etiological factors I- Odontogenic infection The most common odontogenic causes are: 1- Periapical infection of the medullary portion of bone through the apical foramina of decayed and infected or devitalized teeth. 2- Periodontal infection reaching the spongiosa of bone through the gingival crevices. 3- Pericoronal infection around impacted or partially erupted teeth. 4- Residual infection and infection of odontogenic cyst or tumors. 5- Post extraction localized alveolar osteitis (dry socket) 6- Spread of infection from the paranasal sinuses, by way of continuity through tissue spaces and planes. II- Chemical Poisoning 1- Poisonous substance such as arsenic used for devitalization may reach the medullary bone causing infection and bone destruction. 2- Medications linked to osteomyelitis are steroids, chemotherapeutic agents, and bisphosphonates (BRONJ). 43 2 III- Traumatic injuries 1- Excessive traumatization of tissues during difficult extraction caused by excessive uncontrolled force, large segments of alveolar bone maybe broken resulting in infection and osteomyelitis. 2- Compound fractures of the jaws which gets infected by contamination or nonunion fracture due to improper treatment. 3- Pressure type local anaesthesia such as intraosseous anaesthesia which may cause stripping and rising of the periosteum with subsequent cutting of the periosteal blood supply to the bone. 4- Local traumatic injuries like blow to the tooth and hard object to gingiva may be complicated with infection, especially in patients with low resistance. 5- Improper use of surgical burs resulting in overheating of the bone and subsequent necrosis. 6- Curetting the socket of acutely infected teeth will break the tissue barrier and cause spreading of infection and invasion of the bone marrow. IV- Radiation therapy (Osteoradionecrosis) Sclerosis of blood vessels occur with diminished or cut blood supply to the radiated bone (endarteritis obliterans).Surgery following radiotherapy often complicated by infection and necrosis which may lead to extensive incidence of osteomyelitis. V- Hematogenous infection Osteomyelitis of the jaw bones may be caused by infection from distant infected lesions such as: 1- Wound: the infection may enter the blood stream from minor wound or cut on the skin 2- Furuncle or boils anywhere in the body are suppurative focci loaded with staphylococci that may invade the mandible causing necrosis and osteomyelitis. Predisposing factors include: 1- Compromised host defenses due to compromised local blood supply (Paget’s disease, radiotherapy, bone malignancy, osteoporosis), or systemic disease (e.g., alcoholism, diabetes mellitus, leukemia, AIDS, malnutrition). 2 - Infection from microorganisms with great virulence. 44 3 Pathogenesis - Invasion of bacteria into the cancellous bone, which causes inflammation and edema in the marrow spaces, results in compression of the blood vessels in the bone and subsequent severe compromise of the blood supply. - The failure of microcirculation in the cancellous bone is a critical factor in the establishment of osteomyelitis, because 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. Bacteriology - The microbiology of osteomyelitis of the mandible have demonstrated that the primary bacteria of concern are similar to those causing odontogenic infections, that is, streptococci, anaerobic cocci such as Peptostreptococcus spp., and gram-negative rods such as those of the genera Fusobacterium and Prevotella. - Osteomyelitis of the mandible differs substantially from osteomyelitis of other bones in which staphylococci are the predominant bacteria. Classification 1- Based on pathogenesis I. Hematogenous II. Peripheral vascular disease III. Focus of infection 2- Duration and severity I. Acute II. Chronic 3- Clinical type I. Acute suppurative II. Primary chronic III. Secondary chronic IV. Non suppurative 45 4 4- Presence of pus I. Suppurative osteomyelitis 1. Acute suppurative osteomyelitis 2. Chronic suppurative osteomyelitis 3. Infantile osteomyelitis II. Nonsuppurative osteomyelitis 1. Chronic sclerosing osteomyelitis – Focal sclerosing osteomyelitis – Diffuse sclerosing osteomyelitis 2. Garrè's sclerosing osteomyelitis 3. Osteoradionecrosis and Medication-related osteonecrosis of the jaw (MRONJ) Acute suppurative osteomyelitis Clinical features  Piercing, deep, and constant pain and usually referred to the ear  Low or moderate fever, facial cellulitis, lymphadenitis, or even trismus.  Intermittent paresthesia or dysesthesia of the lower lip may accompany the disease.  A firm painful edema of the overlying soft tissues  The tooth becomes loose and tender to percussion.  Discharge of pus from the periodontium around the neck and interproximal space of teeth  Increased white blood count which may reach to 20,000/mm3 Radiographic Finding Shows little or no radiographic change, because 10 to 12 days are required for lost bone to be detectable radiographically. Treatment 1- Pharmaceutical treatment with antibiotics. Antibiotics must be administered intravenously, in large doses, for at least 3–4 days after the fever ceases. Treatment may then continue orally for another 2–4 weeks, depending on the extent of the disease, the causative pathogen, and the clinical response. The antibiotic of choice is penicillin (3x106 units every 4 hours, i.v.), and in the case of allergy to penicillin, clindamycin is administered (600 mg every 6 h, i.v.). 46 5 2- The precipitating event, condition, or both must also be carefully managed. 3- Medical consultation for correction of host defense deficiency preferably prior to surgical intervention. 4- Patient has a serious acute osteomyelitis; hospitalization may be required for administration of IV antibiotics. Clindamycin is preferred because it is an excellent drug for both streptococci and the usual causative anaerobes. 5- Surgical treatment is usually limited. It consists primarily of removing obviously nonvital teeth in the area of the infection, wires or bone plates that may have been used to stabilize a fracture in the area. 6- Local incision, and drainage of pus and occasionally local curettage with removal of superficial sequestra are necessary to ensure an environment for healing. 7- For acute osteomyelitis that results from jaw fracture, the surgeon must stabilize the mobile segments of the mandible with tight intermaxillary fixation or some other technique. Chronic suppurative osteomyelitis - Characterized by a clinical course lasting over a month. It may occur after the acute phase, or it may be a complication of odontogenic infection without a preceding acute phase. Clinical features - Clinical presentation is milder, with painful exacerbations and discharge of pus, or sinus tracts. - Diagnosis is often difficult to make, while Radionuclide scans (scintigraphy with 99mTc) helps to reveal latent sites and confirm the infection. Radiographic Finding - Usually demonstrates bony destruction in the area of infection. The appearance is one of increased radiolucency, which may be uniform in its pattern or patchy, with a "moth-eaten" appearance. - There may also be areas of radiopacity within the radiolucency. These radiopaque areas represent islands of bone that have not been resorbed and are known as sequestra. - In long-standing chronic osteomyelitis there may actually be an area of increased radiodensity surrounding the area of radiolucency. This is the result of an osteitis type of reaction in 47 6 which bone production increases as a result of the inflammatory reaction; this newly formed bone is termed involucrum Treatment Requires not only aggressive antibiotic therapy but also aggressive surgical therapy. 1- Hospitalization and high-dose IV Clindamycin antibiotics to control the initial symptoms. 2- For severe chronic osteomyelitis that has been difficult to control, antibiotic administration may continue for up to 6 months. 3- Cultures and antibiotic sensitivity test is the drug of choice, so that the selection of an antibiotic can be based on the specific microbiology of the infection. 4- The underlying systemic disease or general illness should be diagnosed and treated medically. 5- Surgical debridement of infected tissue dictated by extent of the lesion [removal of affected teeth and foreign bodies/implants, sequestrectomy, local curettage, saucerization (means unroofing of the oral-faced jawbone to expose the medullary cavity for subsequent thorough debridement).] 6- Adjunctive hyperbaric oxygen therapy has been used to successfully treat difficult cases Mechanism in osteomyelitis therapy  Reverse the hypoxic state of the infected bone.  Enhancing leukocyte killing potential.  Direct toxic effect on strict anaerobes and facultative anaerobes.  promotes angiogenesis in the tissue and hence increasing local tissue perfusion - More extensive surgical debridement if necessary (e.g., repeated decortication by surgical removal of all investing cortical bone on the buccal side of mandible or resection of the diseased part of mandible) Infantile osteomyelitis - Neonatal osteomyelitis arises as a consequence of hematogenous spread of microorganisms results from directly inoculated bacteria (wounds made during delivery or through injuries of oral mucosa). The most common bacterial pathogen causing osteomyelitis in children is Staphylococcus aureus - Clinically, the disease have rapid onset, with sever constitutional reactions such as high fever, rapid pulse and vomiting. ( may run a chronic course with slow onset in some cases) - Local signs are swelling of the face, edema of the eyelid, subperiosteal abscess developing on the alveolar mucosa and palate followed by fistula draining pus. 48 7 - Treatment by antibiotic therapy after culture and sensitivity test. Surgical interference should be conservative because the loss of bone and teeth often cause marked deformities Sclerosing Osteomyelitis Chronic focal sclerosing osteomyelitis - An unusual bone reaction, with normal defense mechanisms, to an infection caused by microorganisms of low virulence. It occurs in persons under 20 years old with significant carious lesions, especially the first molar. - Either endodontic therapy or extraction of the tooth is required. Chronic diffuse sclerosing osteomyelitis. - Mainly occurs in elderly people, and is exhibited in edentulous areas of the mandible. - The symptoms are mild, and include episodes of recurrent pain, edema, and/or trismus. - Upon radiographic examination, depending on the phase of the disease, osteolytic or diffuse sclerosing zones at the posterior region of the mandible are observed. - Treatment consists of muscle relaxants, nonsteroidal anti-inflammatory drugs, antibiotics Chronic osteomyelitis with proliferative periostitis ( Garre’s osteomyelitis) - Characterized by the formation of new bone beneath the periosteum at the surface of the cortex, which covers an inflammatory area of spongiosa, caused by mild irritation and infection. Common pathogens include staphylococci and streptococci. - The lesion is seen in persons less than 30 years of age, usually children, and - characterized by non-tender swelling at the inferior border of the mandible. The skin as well as the mucosa has a normal appearance. - Radiographic finding show the affected portion of the bone with an area of increased density and in a peripheral view show cortical thickening. -Treatment consists of extraction of the tooth, Remission of the lesion is expected within 2–6 months. 49 8 Osteoradionecrosis - A severe disease that is observed after high radiation doses resulting in ischemia, devitalization of the bone and loss of large bone segment. - The cause of the disease is tooth extraction or surgery a short while after the radiotherapy, a period during which the body cannot achieve satisfactory healing. - The clinical presentation includes pain and rapid spread of the lesion to a large part of the bone. - Management consists of combined surgical and pharmaceutical treatment, while the use of hyperbaric oxygen is beneficial. Bisphosphonate-induced osteonecrosis of the jaws (BIONJ) - Exposed non-healing bone in the mandible or maxilla that persists for more than 8 weeks in a person who received a systemic bisphosphonate but has not undergone local radiation to the jaws - Result from potent intravenous bisphosphonates (Zometa) used for the treatment of hypercalcemia of malignancy and stabilization of metastatic malignancies in bone Or oral bisphosphonate (Fosamax) used for the treatment of osteoporosis. - bisphosphonates prevent the normal renewal of bone in the lamina dura and the edentulous alveolar crest, which results in retention of old bone that dies off and is not replaced. Such necrotic bone fails to support the blood supply of the overlying mucosa and therefore results in loss of mucosa and bone exposure. - Manifested as spontaneous bone exposure (25%), but 75% of cases are initiated by some type of trauma (tooth removal, active periodontitis, periodontal surgery, and dental implant placement) - Treatment: chlorhexidine oral mouth wishes three times daily, antibiotic therapy (Penicillin VK, 500 mg by mouth four times daily, if the patient is allergic to penicillin, reasonable alternatives are doxycycline, 100 mg once daily). Surgeries must be extensive and take the form of alveolectomies or continuity resections to resolve intravenous BIONJ. 50 9 Differential diagnosis Osteomyelitis should be differentiated by clinical pathological radiographic means, laboratory and microscopic examination from simulating conditions Actinomycosis - A chronic bacterial infection caused by the Gram- positive, anaerobic bacteria Actinomyces israelii. This microorganism lies dormant in the oral cavity and may become activated under certain circumstances. - Portals of entryof include root canals of infected teeth, postextraction sockets. - A hard, slightly painful lesion characterizes the clinical presentation, with reddish overlying skin, on which sinus tracts are often observed. Sulfur granules are found in the pus discharged from the sinus tracts, which are composed of colonies of the microorganism. Either the skin alone or the bone as well may be involved in the infection. - Treatment consists of surgical incision and drainage with excision of sinus tracts, and administration of penicillin for several months (up to a year), depending on the severity of the disease.  Tuberculosis - Invasive osteomyelitis caused by tuberculous infection. The tuberculous bacilli in saliva invade the bone through extraction wound. - Diagnosis made by chest x-ray, laboratory examination and microscopic examination - Management involve Anti tubercular drugs and radical surgical resection.  Syphilis - Tertiary syphilitic lesions produce syphilitic periosteitis and osteomyelitis, can be differentiated with serologic test and biopsy.  Malignant neoplasm - History of lesion, Clinical, radiological examination and biopsy are aids for differential diagnosis. 51 Management of Cysts of the oral cavity. 52 Cysts of The Jaws Definition: A true cyst constitute a pathologic cavity or sac filled with fluid or semi-fluid material or gaseous contents, lined by epithelium and surrounded by a definite connective tissue wall. TYPES OF CYSTS TRUE CYSTS: that which is lined by epithelium e.g dentigerous cyst, radicular cyst etc. PSEUDO CYSTS: not lined by epithelium, e.g. Solitary bone cyst, Aneurismal bone cyst etc Cyst has following parts: WALL (made of connective tissue) EPITHELIAL LINING LUMEN OF CYST Pathogenesis 1. Cyst initiation Initiation results in the proliferation of the epithelial cells and the formation of small cavity. a. Cell Rests of Malassez : Remanants of Hertwigs epithelial root sheath in the PDL after the root formation is completed.(lateral peridontal cyst) b. Reduced Enamel Epithelium : Residual epithelial cells surrounds the crown of the tooth after enamel formation is complete.(dentigerous cyst) 53 c. Cell Rests of Serres (Remanants of Dental Lamina) : Islands of epithelial cells that originate from the oral epithelium and remain in the tissue after inducing tooth development.(odontogenic keratocyst) 2.Cyst enlargement or expansion 1.Increase in hydrostatic pressure inside the cyst 2.Because of large number of osmotically active molecules in cyst fluid, the cyst contents are hypertonic (high osmotic Pressure) compared with serum 3.Cyst lining release bone resorbing factor Which stimulate osteoclastic activity Like prostaglandin E2&E3 and collagenase also released by the inflammatory cells of the capsule. 54 I) Odontogenic cysts The odontogenic cysts are derived from epithelium associated with the development of dental apparatus usually the epithelium associated with odontogenic cyst is Derived from: 1) A tooth germ. 2) Reduced enamel epithelium of the tooth crown 3) Epithelial rests of Malassez 4) Remnants of the dental lamina. ODONTOGENIC CYSTS (General Considerations) Odontogenic cysts are true cysts occurring in the jaws. They arise from stimulation of epithelium left over from tooth development. Well-Defined / Corticated Usually Radiolucent :Exception is Gorlin Cyst which may be Mixed Uni-locular / Sometimes Multilocular Types of Odontogenic cysts  Developmental cysts: Dentigerous Primordial Eruption Gingival Odontogenic keratocyst Calcifying epithelial odontogenic cyst  Inflammatory: Radicular cyst Residual cyst Inflammatory lateral periodontal cyst 55 II) Non-odontogenic cysts (Fissural cysts): The epithelium of these cysts are derived from entrapped epithelium between embryonic process of bones at the union lines. These cysts are classified into: Fissural cysts Nasopalatine Nasolabial Median Palatine Globulo-maxillary Median mandibular Pseudocysts 1. Aneurysmal bone cyst 2. Traumatic bone cyst 3. Salivary gland inclusion disease (stafen bone cyst or developmental lingual depression of the mandible). 56 Soft tissue cysts Salivary cysts (mucocele) Gingival cysts (odontogenic) Dermoid, Epidermoid Branchial cleft cyst Thyroglossal duct cyst Recent classification I Cysts of the jaws II Cysts associated with the maxillary antrum III Cysts of the soft tissues of the mouth, face, neck and salivary glands Diagnosis of Cysts of the Jaws A) Clinically: 1. Main complaint. 57 2. Examination of the teeth. 3. Vitality tests. 4. The site: a) In cases of non-odontogenic cysts. b) In cases of odontogenic cysts. 5. Bony expansion, rate of growth , pain  Cysts rarely cause any symptoms, unless they become secondarily infected.The signs depend mostly upon the size and location of the cyst.  If the cyst has not expanded beyond the normal anatomical boundaries of the bone, then there will be no palpable lump outside or inside the mouth.  Cysts that have expanded beyond the normal anatomic boundaries of a bone are still often covered with a thin layer of new bone. At this stage, there may be a sign termed "eggshell cracking", where the thinned cortical plate cracks when pressure is applied.  A lump may be felt, which may feel hard if there is still bone covering the cyst, or fluctuant if the cyst has eroded through the bone surrounding it. A cyst may become acutely infected, and discharge into the oral cavity via a sinus.  Adjacent teeth may be loosened, tilted or even moved bodily. Rarely, roots of teeth are resorbed, depending upon the type of cyst.  The inferior alveolar nerve runs through the mandible and supplies sensation to the lower lip and chin. As most cysts expand slowly, there will be no altered sensation (anesthesia or paraesthesia), since the inferior alveolar canal is harmlessly enveloped or displaced over time. More aggressive cysts, or acute infection of any cyst may cause altered sensation. Sometimes, they cause higher risk of pathological fracture of lower jaw, especially around angle of mandible. 58 B) Radiologically a) Intra-oral. b) Extra-oral: Panoramic view. Lateral oblique sinus view. Posterior-anterior C.T scan C) Aspiration: Pale straw-colored fluid with few cholesterol crystals. Odontogenic cyst. Blood fills the syringe. Central hemangioma and aneurysmal bone cyst. Golden-yellow fluid which will coagulate on standing. Solitary bone cyst. Mucous. Retention cyst. Pale, yellow material like pus (dirty-white material without pus odor). Odontogenic keratocyst. Pus and cystic fluid. Infected cyst. Air. Maxillary sinus. -ve aspiration. Solid lesions. D) Histopathology (1) Odontogenic Cyst (Radicular Cyst)  also known as Apical Periodontal Cyst; Periapical Cyst; Root End Cyst  common  not inevitable sequela of periapical granuloma originating as a result of:  bacterial infection  necrosis of dental pulp  following carious involvement of tooth 59 Pathogenesis The phase of initiation Epithelial cell rests of Malassez in the PDL proliferated by inflammation via endotoxins The phase of cyst formation Epithelialium proliferates and covers the bare connective tissue surface of an abscess cavity A cyst cavity forms within a proliferating epithelial mass in an apical granuloma by degeneration and death of cells in the center. The phase of Growth and enlargement Osmosis makes a contribution to the increase in the size of cysts. The radicular cyst is the most common cyst and is frequently classified as an inflammatory cyst. It has its origin from the cell rests of Malassez which are present in periodontal and periapical ligament, and in periapical granulomas. The main cause of the cyst is infection from the crown of a carious tooth producing an inflammatory reaction at the tooth apex and sensitivity to percussion, forming a granuloma. The liquefaction of the apical granuloma produces a radicular cyst. Clinically: At first it presents as hard swelling, but with time the swelling enlarge and an egg shell crack can be felt M=F It may occur in deciduous as well as permanent teeth. In adult it may occur at the fourth decades. Teeth mobility are seen in some cases.  Clinical Features  asymptomatic  present no clinical evidence of their presence  seldom painful or even sensitive to percussion  represents chronic inflammatory process develops only over a long period of time Radiographic Features  identical with periapaical granuloma  since the lesion is a chronic progressive one developing in a pre-existing granuloma 60 cyst may be of greater size than granuloma due to longer duration  occasionally, exhibits thin, radioopaque line around the periphery of radiolucent area indicates reaction of bone to slowl expanding mass Histologic Features  epithelium lining apical periodontal cyst is usually stratified squamous in type Treatment & Prognosis  similar to periapical granuloma involved tooth may be removed periapical tissue carefully curetted under some condition; root canal therapy with apicoectomy and enucleation of cystic lesion (2) Residual Cysts A Residual cyst is a cyst that develops after incomplete removal of the original cyst. Usually asymptomatic, small size (less than 1 cm in diameter). Unilocular, round or oval, well-defined, usually well-corticated. It can cause bone expansion and displacement of the adjacent teeth. 61 (3) Periodontal cyst This may be either apical periodontal cyst “appear as radiolucent area at the apex of the tooth”, or lateral periodontal cyst “appear as radiolucent area along the lateral surface of the root”. The mandibular premolar-canine-incisor region is the most frequent location  Treatment & Prognosis  local excision (4) Botryoid Odontogenic Cyst The botryoid odontogenic cyst was recognized by Weathers and Waldron (1973), which is thought to arise from odontogenic epithelial rests. It is probable that the botryoid cyst is a variant of the lateral periodontal cyst. The gross appearance of the largest lesion was described as resembling a bunch of grapes, hence the term botryoid. Multicystic form of the lateral periodontal cyst radiographic appearance is that of a multilocular Radiolucency Age range of 23-85 years premolar- canine-incisor segment being the most common site. Treatment and Prognosis: Conservative complete removal is the most appropriate treatment (5) Dentigerous Cyst  also known as Follicular Cyst  2nd most common type of odontogenic cyst  most common developmental cyst of the jaws  attached to tooth cervix (enamel-cementum junction) 62  encloses crown of unerupted permanent teeth but may be associated with a supernumerary teeth or a complex or composite odontome  Etiology  develops from proliferation of enamel organ remnant or reduced enamel epithelium  related to epithelial proliferation  release of bone-resorbing factors  increase in cyst fluid osmolality  Clinical Features  commonly seen in association with most commonly impacted teeth (3rd molars and maxillary canines)  greater incidence in males  symptoms are generally absent  delayed eruption being the most common indication of dentigerous cyst formation  Radiographic Features  well-defined 63  unilocular or ocassionally mutilocular radiolucency with coricated margins  associated with crown of unerupted tooth  resorption of roots of adjacent erupted teeth may occasionally be seen Potential complication: The developmental of ameloblastoma (mural ameloblastoma) from the lining epithelium, or from the rest of odontogenic epithelium. The developmental of epidermoid carcinoma from the lining epithelium 64 (5) Eruption Cyst (eruption hematoma) Cyst Associated with Erupting Tooth Soft Tissue Swelling Over Crown filled with fluid or blood Histology Same as Dentigerous Cyst infants and young children appears as a smooth, bluish, firm or fluctuant swelling of the alveolar ridge overlying the erupting tooth Excise or unroof with no Recurrence (6) Odontogenic keratocyst Clinically: Swelling and bone expansion may be present. It may occur at any age and the mandible is more susceptible than maxilla. exhibit aggressive clinical behavior peak incidence within 2nd-3rd decades of life Multiple keratocysts occurs with some frequency in basal cell nevus bifid rib syndrome. Male > female. Very rarely cause resorption of the roots. Swelling, bone expansion and displacement of the adjacent teeth. Expansion is delayed until the cortex is perforated, because it tend to extend into the medullary cavity. 65 If the cyst occur in the maxilla, considerable enlargement into the maxillary sinus may occur before noticeable jaw enlargement takes place. The lesion is not painful (asymptomatic) unless secondary infected. Age: Any age can be affected, but some specified the period during the second and third decades to have a peak incidence. Site: Mandible is more affected than maxilla. Most lesions (50%) occur in the angle and ramus of the mandible and may extend for varying distances into the ascending ramus, but any other site may be involved including the midline and any part of the maxilla. Radiographic appearance well circumscribed radiolucent area (round or ovoid, unilocular or multilocular) with sclerotic border in place of normal tooth The cyst, however may enlarge and envelop un-erupted tooth and produce a dentigerous appearance The multilocular primordial cyst can not be distinguished from ameloblastoma on radiological examination only and biopsy is necessary before treatment is planned The cyst content is very diagnostic as it contains keratin, aspiration using a wide bore needle. Total protein may be estimated in this keratin and will be found to be below 4 gm /100 ml. Recurrence of this cyst is very high which may result from failure to remove active epithelial residues. Recurrence may be 40% or as high as 60%. Because the Due to thin lining , daughter cyst in the cyst lining 66 cyst penetrate the cortex and the sub-periosteal new bone, any attempt to remove the periosteum from the fragile cyst lining result in perforation of the wall and tear in the lining and fragment may be left behind recurrence may occur. This is a non-inflammatory odontogenic cyst that arises from the dental lamina. 11% of jaw cysts Well-Defined / Corticated,Radiolucent Any Location: posterior portion of body, angle and ramus maxilla at 3rd molar region Gorlin-Goltz Syndrome Bifid Rib-Basal Cell “Nevus” Syndrome Features: Multiple OKC’s of Jaws Multiple Basal Cell “Nevi” / Carcinomas Skeletal Anomalies including Bifid Ribs and intracranial Calcification may demonstrate frontal and temporoparietal bossing and mandibular prognathism Risk of Other Tumors: Meduloblastomas Same Recurrence Problem as other OKC’s (7) Primordial Cyst Cyst Arising in place of a Tooth Recurrence Potential Low Unless OKC 67 This cyst develops through cystic degeneration of the stellat

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