Infection of oral nd maxillofacial surgery • Inflammation: It's tissue reaction to noxious stimuli e.g. thermal, chemical, mechanical, ....etc .In order to repair or replace the damaged tissues. • Infection: It's invasion of tissue by pathogenic micro-organisms or its toxins. • Abscess: pus accumulation in newly formed pathological cavity. • Mechanism of inflammation: • Vascular phase : Vasodilatation of the arterioles - causing hyperaemia • Extravasation of plasma rich in plasma proteins, antibodies and nutrients into the surrounding tissues • Cellular phase : • Collection of leucocytes • Leucotoxin, increases permeability allowing polymorphs into the area. •Exudate forming fibrin, walling off the region • Macrophages — phagocytosis of bacteria, dead cells. • Cardinal signs of inflammation: • Redness - Hotness - Tenderness - Swelling - Loss of function Classification of infection • According to origin • Odontogenic infection • Periapical acute dentoalveolar abscess • Pericoronitis. • Periodontitis • • Non-odontogenic • sinusitis • Sialadenitis • lymphadenitis • Trauma. • Haematogenous • iatrogenic • According to the causative organisms: • Viral • Bacterial (specific-non-specific) • Fungal infection. • According to onset, duration and severity: • Acute. • Subacute. • Chronic. • Oral cavity provides an optimum environment for microorganism growth and colonization: - • Moisture. • - Warmth. • - Protected crypts e.g. fissures, gingival crevices • Oral flora • Number of species 200 .. Number of M.O 106 109MO/cc of saliva • It contains: aerobic, anaerobic, facultative anaerobes. • Aerobic M.O 30% Anaerobic M.O 70% cocci BACILLI aerobic nonaerobic Aerobic nonaerobic GRAM+ PEPTOSTREPTOCOCCI Cornebacterium clostrdium Streptococci diphteria Staphylococci Peptococci Gram - Neisseria Veilonella H. influenza Bacterioid melaninogenicus - Fusobacterium Odontogenic Gram + cocci (Streptococci and peptostreptococci) Gram - anaerobic bacilli Infection pathogens Difference between Streptococci and Staphylococci Staphylococci Streptococci Mode of growth Chain clusters Flbrinolysin Hyaluronidase Enzymes secreted Streptolysin Coagulase Chemotaxls Less More Spread & virulence More spread Localized Infection • Antibiotics affect on bacterial cell rather than the human cell Due to Difference between bacterial cell and human cell Human cell Bacterial cell Cell wall Thick thin Nuclear membrane Present Absent (only DNA aggregates) Golgi and endoplasmic Present Absent reticulum Stages of infection • 1- inoculation stage (0-3days) aerobes inoculate the host resulting in a soft doughy and mildly tender swelling • 2- cellulitis stage 3-5 days intense inflammatory response hard red tender swelling • 3- abcess stage 5-7days anaerobes predominate ,lequified abcess in the center of a swelling • Resolution stage spontaneous drainageor surgical drainage Abscess Cellulitis Cause Bacteria induce inflammation Bacteria induce suppuration Duration Occurs 1st Occurs after localization localization Large Diffuse Small Circumscribed Palpation Indurated Fluctuant Pus accumulation No but with inflammatory exudates Yes Seriousness More Less A cute dento alveolar abscess • It's an acute circumscribed non-specific suppurative infection involving the apex and investing alveolar bone. • Etiology: Non- vital tooth • Microbiology: Aerobic M.O,streptococci- staphylococcus aureus Anaerobic M.O , peptostreptococd- Bacteroid- fusobacterium • Pathogenesis (mechanism of Invasion) • Pulp hyperaemia (reversible) Transient pain with hot and cold that disappears after removal of stimulus)-Pulpitis (irreversible) (persistent pain even after removal of stimulus) - Pulp necrosis (Liquefaction and disintegration of pulp tissue as B.V can not expand) → Apical periodontitis (Due to escape of bacteria to periapical area) →ADAA → Suppuration Surrounded by Pyogenic membrane (Dead & alive WBC+ dead &alive Bacteria + necrotic tissues + inf. exudate) • Stages of Acute Dento-Alveolar abscess : I-early stage: Confined within bone with no soft tusse involvement. II-Late stage: perforate bone with soft tissue involvement - Early stage- (Intra-alveolar abscess) • Definition: It's confined within periapical bone without S.T involvement. Clinical: signs & symptoms 1- Sense of elongation on-occlusion due to edema pressure in periodontal ligament 2- Severe tenderness on percussion or mastication 3- Severe throbbing pain provoked by heat: Due to pressure on nerve endings of the surrounding tissues. • 4- Slight mobility of the tooth due to edema of periodontal ligament. 5- Regional lymphadenopathy e.g. submandibular, submental, jugulodiga lymph node 6- Constitutional symptoms: - Fever - Headache - Malaise. • X-ray: Negative or widening of periodontal membrane space with interrupted lamina dura. • Treatment: • 1- General supportive measures: a. bed rest b. high protein diet c. fluid intake • 2- Antibiotics: i- Penicillin → 1st choice. 600,000 I.U penicillin (G) I.M or ii- 500mg Penicillin V oral + 500mg metronidazole (flagyl 500mg). iii- Augmentin (amoxicillin + Clavulenate) or Unasyn 1500mg (Ampicillin + sulbactam) are suitable for Staph. Resistant bacteria (B- lactamase) iv- In allergy to penicillin : give a- Clindamycin 300-600 mg (Dalacin-c) → aerobic + anaerobic • b- 500mg erythromycin + metronidazole 500mg (flagyl 500mg). • 2- Analgesics: Aspirin or paracetamol (in gastric upsets) • 4- Removal of the cause by Proper drainage through: A. RCT→ 1st choice B. Extraction (avoid curettage → Dry socket) Indications of extractions: 1- Endoddntic ttt can not be done e.g. in curved canals. 2- Tooth related to maxillary sinus. 3- Loose tooth. 4- Deciduous tooth to avoid injury to underlying tooth germ. 5- Medically compromised persons • Time of extraction: 2 schools - During acute phase - to allow early drainage. - Or After acute phase subsides. Technique of anaesthesia: 1- Nerve block with sedation (short acting barbiturate). 2- general anaesthesia • Infiltration is contraindicated: a- To avoid spread of infection. b- It's not potent at the site of infection because: ACIDIC medium , prevent liberation of free active base. - Fibrin deposition around infection acts as a barrier for LA - Vasodilatation at inflamed area lead to rapid absorption of LA - Inflammation of myelin sheath. Late stage dentoalveolar abcess • Definition • Pus passes through spongy bone then perforate cortical bone to form subperiosteal abcessa • . Pain: decrease after perforation of the periosteum dull aching pain Tenderness as pressure-on nerve endings is released. 3- Trismus: e.g. in subrnasseteric space. 4- Dysphagia: especially in parapharyngeal space. 5- Difficult breatheing: e.g. Ludwig’s-angina 6- Regional lymphadenopathy: enlarged- Tender- soft. 7- Constitutional symptoms: - Fever, Malaise, Dehydration, Toxic appearance • Treatment: Hospitalization and airway management in severe infection • a- supportive treatment for Increasing the body resistance:. a. Bed rest. b. High protein diet c. Multivitamins. d. Fluid intake. b- Antibiotics: I- Empirical antibiotics: as before II- According to Culture and sensitivity test specific antibiotics: c- Analgesics: as aspirin or paracetamol,….etc. • D- Hot fomentation (hydrotherapv) localization of infection Aim: V.D increase circulation. increase leucocytes + antibiotics at infection area Wall off the infection. Fasten suppuration Fasten localization either I.O or E.O (depending on anatomy) Analgesic effect. Technique: use moist heat not dry heat Extra oral -hot fomentation Intraoral -warm saline M.W • E- Incision and Drainage: Def.: is the surgical evacuation of pus. Aim: 1- Outlet for pus and toxic materials. 2- Promote tissue defense mechanism and healing. 3- Relief of tissue distension. 4- Relief of Pain caused by histamine and bradykinins 5- Prevents spontaneous drainage through skin fistula. 6- Prevents further spread to other fascial spaces or to blood • Optimum time (signs of localization of pus): 1- Pointing and development of erythematous halo. 2- Fluctuation test: (Bi-digital palpation) - Press by index finger of one hand over abscess at one side felt by index finger of the other hand. - The test is performed at 2 planes at right angle to each others. 3- Pitting on pressure: - Done in deep abscess. - Slight depression on pressure that returns slowly. 4- Aspiration pus. • Principles of l & D (Technique): 1. Anesthesia to the, area: • Topical ethyl chloride. • Nerve block, Field block distant from infected area to avoid spreading of M C • GA 2. Use lancet number 11 /or 15. 3. Incision passes through healthy tissues. 4. In esthetically acceptable area, it made in skin crease. 5. Incision should avoid injury to important structures: • E.O incision is 1-2 cm // to the inferior border of the mandible to avoid injury to marginal mandibular nerve (Branch of facial nerve). - I.O incision should run in posteroanterior direction not transversally to: a. avoid injury to parotid duct b.avoid injury to greater palatine nerve and vessels, c. avoid mental nerve injury d.avoid, injury to lingual nerve • 6. At the lowest point to Obtain dependent drainage (Gravitational drainage 7. Blunt evacuation of pus: .insert haemostat closed into abscess cavity , then withdrawal of haemostate outside while it's slightly opened. • 8. Insertion of Drains e.g, rubber drain or penrose drain to avoid reapproximation of wound edges that interfere with further drainage. Suture the drain to one end of incision using non-resorbable suture Every 48 hrs , remove the drain, irrigation & put shorter drain After complete drainage