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 • . • 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- : e.g. in subrnasseteric space. 4- Dysphagia: especially in . 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 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 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 (1 week) remove the drains • Types of Drains • iodoform gauze. • fine mesh gauze • rubber dam • corrugate rubber brain. • penrose drain. • suction drain

N.B: active drains with suction bag are used for suction of blood to avoid haematoms in surgery

• F- Offending tooth: after acute condition subsides a- Extraction of the offending tooth (1st choice) to allow for drainage. b- RCT (2nd choice) Difference between Early & Late Stage Adaa

Late stage Early stage

Site Within bone Soft tissue involvement Pain Sharp throbbing Dull aching Sense of elongation Present Absent Swelling Absent Present Trismus Absent If involves masticatory spaces Dysphagia Absent If involves pharyngeal spaces x-ray Negative iII defined RL Extraction → 1st choice Incision Treatment RCT→ 1st choice and drainage Chronic dentoalveolar abcess

• Causes • 1- periapical infection by non virulent bacteria • 2-after acute infection due to incomplete treatment Signs and symptoms

Asymptomatic Fistula with pus discharging Enlarged lymph node • X ray Periapical radiolucency Treatment 1-Antibiotics Root canal treatment Excision of fistula • Complication of chronic periapical infection • 1-fistula • 2- osteomyelitis • 3- periapical cyst • 4- acute exacerbation • 5- act as a focus of infection leading to arthritis glumerulonephritis Pericoronitis

• Definition : inflammation of soft tissue (operculum) around coronal portion of partially erupted or unerupted tooth.

• Onset:

They can occur through out life time; namely:

1. Infancy and child hood

2. Young adult hood

3. Old age.

• Etiology: • 1- Food impaction below operculum. • 2- Trauma from opposing tooth. • Causative organism: • a. staphylococci and streptococci • b. bacteroids and fusiform bacilli and spirochetes. • Clinical: • I-Acute form: 1- Swelling redness and tenderness. 2. Severe pain 3- Cellulitis and pericoronal abscess may develop. 4-Trismus 5- Dysphagia 6- Lymphadenopathy. 7- Constitutional symptoms as fever and malaise

• II- chronic form: 1. Asymptomatic. 2. Dense fibrous operculum. 3. Dull pain and foul odor Pericoronal infection in infancy and child hood • they are associated with the eruption periods. The soft tissues overlying the tooth follicle may show acute or chronic inflammatory reactions • Acute inflammatory stage: • Acute pericoronitis may occur with formation of a pericoronal abscess with actual fluctuant mass of pus. • Occasionally this abscess may develop a facial cellulitis by the invasion of the infection to the soft tissues, causing local and systemic reactions associated with the general constitutional symptoms of acute infections. • Bacteriology:

It is usually a mixed infection. The causative organisms are many with fusiform bacilli and Vincent's spirochetes more predominant. When pericoronitis occurs in conjunction with a sore throat, streptococcal bacteria are present • Treatment • Acute pericoronitis • Antibiotic • Incision and drainage • Mouth wash • Chronic pericoronitis • Excision of the dense fibrous tissue Pericoronal Infection in Early Adulthood

• Occur around partialy erupted last molar or impacted tooth • Etiology & Predisposing factors: • Traumatic irritation from the opposing tooth • accumulation of food debris • the condition underneath • the operculum is an ideal incubator for bacterial growth; because it permits humidity, warmth, relative deficiency of oxygen, relative immobility and rigidity of the tissue involved, darkness, protection from the washing influence of saliva • Signs and symptoms pain Trismus Dysphagia Submandiular lymphadenitis, Fever malaise anorexia Cellulitis • Treatment • 1- conservative method the aperculectomy a. Daily irrigation beneath the operculum using warm saline, iodine .or hydrogen peroxide. b. Antibiotics. c. Analgesics. d. M.W with warm saline, hydrogen peroxide (every 2 hrs). e. Grinding of the opposing tooth to avoid trauma. • 2-incision and drainage if abcessed • 3-Operculectomy: when acute condition subsides Extraction of the tooth if recurrent if the tooth has chance to erupt in normal position • If not treated adequatly infection can spread to another nearby fascial spaces e.g.submaxillary, submasseteric, pterygomandibular or parapharyngeal space. Pericoronal Infection in Old Age

• For some reasons an impacted tooth may be left unextracted in the jaw of an edentulous patient, assuming that the tooth may stay asymptomatic or because of failure to diagnose the presence of that tooth with X-ray.

• When the patient wears full dentures they cause irritation to the soft tissues overlying that tooth which is affected also with some alveolar resorption and pericoronal infection may occur. - This infection may also occur due to an odontoma embedded in the central portion of the jaw which starts to be symptomatic by pressure and irritation of full dentures worn by the edentulous patients.

- The treatment is to control the acute infection by general and surgical measures till the acute condition subsides then the impaction or odontoma are removed surgically • Routes of spread of infection Natural channels. - Lymphatics. - Blood stream - Nerves e.g. herpes zoster, herpes simplex Factors affecting spread of infection

• I. Factors related to the organisms: • II. Factors related to the host resistance • Resistance spread • Ill. Anatomical factors: • I. Factors related to the organisms: • - Number of M.O: increased Number – increased Spread. • - Virulence of M.O:increased virulence – increased Spread e.g. strep > staph.(depending on enzymes secreted , chemotactic effect, mode of growth) • - Synergism of bacteria e.g. fusobacteria and borrelia. • II. Factors related to the host resistance

• Increased resistance – decrease spread of infection

• Host resistance depends on

.1- Nutritional status of the patients

2. Effecency of immune system

3. Severity of infection =virulence *dosage /host resistance • Factors Associated with Immune System Compromise

• 1. uncontrolled metabolic diseases severe (uncontrolled )Diabetes

Alcoholism

Malnutrition

Chronic renal disease (uremia) • 2. Suppressing diseases: Leukemia Lymphoma Malignant tumors 3. Organ transplants 4. End-stage AIDS 5. suppressing drugs: Chemotherapy Steroid therapy III- ANATOMICAL FACTORS

• 1-THE ANATOMIC LOCATION OF ODONTOGENIC INFECTION • When infection occurs in medulla of maxilla or the mandible it takes the path of least resistance • In rare cases it will transeverse the medullary bones producing thrombosis of the arterioles leading to osteomylitis • More commonly it erodes the cortex and spread into soft tissue • 2- position of the teeth in the alveolus • Maxillary teeth Central,canine and buccal roots of premolars and molars are covered by very thin cortical bone Lateral and palatal roots of of the premolars and molars lie closer to the palatal bone with very thin palatal bone mandibular teeth Central,lateral canine and premolars are covered by very thin cortical buccal plate First,and second molars lie in the centre of the alveolus The third molar usually the lingual cortical plate is much thinner than buccal cortical plates • III- ORGANIZATION OF THE DEEP CERVICAL FASCIA • Cervical fasca is a continuous layer of ct consisting of superfacial , middle and deep layers the Fascial layers envelope separates And supports structures forming fascial spaces which are potential spaces along which infection may spread cellulitis or whithin it infection may become localized • RELATION OF THE ROOT APEX TO TRHE MUSCLE ATTACHEMENT Maxillary teeth: Infection above muscle attachment Extraoral swelling Infection below muscle attachment intraoral swelling Mandibular teeth: Infection below muscle attachmen extra oral swelling. infection above muscle attachment intra oral swelling. • 1. Orblcularis oris • Infection of the upper incisors especially the central is influenced by

• orbicularis oris muscle, if it penetrates the bone below the attachment of the muscle it becomes localized intraoral and it limits its superior spread

• , levator labii suerioris and levator labii superiorly alaque nasi • Tend to localize an infection of the upper canine intraorally if it is below their attachment to bone.

• If above the levator angular oris ext. Canine + infraorbital space between and levator labii superirors alaque Nasi Inner corner of the eye below the skin • 3. Zygomaticus major and minor and levator labii superioris • tend to limit infection of upper premolars intraorally If above these muscles extension canine space. • . Buccinator muscle This muscle limits the spread of infection of upper and lower molars intraorally. Infection of upper molars above buccinator attachment spread . Infection of lower molars below buccinator attachment spread buccal space

• 5. Mentalis muscle • Infection of lower 1,2 above mentalis muscle intraoral localize. • Infection of 1,2 below mentalis muscle extraoral localization below skin (submentalis space) or submental space. • 6. Depressor labii inferioris, depressor anguli oris and platysma Because they are well located below the lower canine apex,infection of lower canine usually localize intraorally. • 7. Mylohyoid muscle • It limits the lingual spread of infection of the lower molars and

• premolars.

• Infection above mylohyoid attachment sublingual space (introaoral).

• Infection below mylohyoid attachment submandib space (extraoroal).

• 8. Masseter and medial pterygoid muscles: • Infected vertically positioned 8 Ext, downwards subamandibular space. • Infected mesiangular or horizonat] 8 Ext. postrolat • Infected mesioangular or horizontal 8 Ext, postromed or parapharyngeal space Fascial spaces

• Fascia: it's continuous .layer of dense C.T. that envelop, support and separate structures • Fascial spaces: • They are Potential spaces between fascial layer. They become true space with pus accumulation or emphysema • Cervical fascia consists of: a- Superficial cervical fascia b- Deep cervical fascia: that is devided into

1-Superficial layer : envelope neck, masseter ms, ,

2- Middle layer --Sterno- hyoid-omohyoid and visceral e.g. around ,larynx, trachea and oesophagus.

3-- Deep layer ---- e.g. prevertebral fascia

N.B Carotid sheath is called (Lincoln's highway).

• Importance of Fascia: • 1- Invest • 2- Support • 3- Protect • 4- Directing the spread of infection • 5- Surgical orientation • Pus-forming infections spread from potential space to potential space by: • 1- Direct expansion and/or • 2- Destruction of boundaries Barriers that control spread of infection are:

• 1- Bone

• 2- Muscles

• 3- Heavy Fascia

• 4- Large vessels / Nerves

• 5-Skin • Fascial spaces Fascial spaces are either

1. Clefts: if they only contain loose alveolar tissue or

2. Compartments: if they contain named neurovascular structures

Primary spaces: are involved directly

Secondary spaces: are involved when infection spreads into them beyond primary spaces and secondarily. 1ry spaces (Direct spread from ADAA 2ry spaces (Indirect spread)

Masticator spaces: Vestibular space / Palatal space →Submasseteric Canine space → Pterygomandibular Buccal space →Temporal (Superficial' and deep) Submental space Lateral pharyngeal Submandibular space Retropharygeal Sublingual space (Space 4) Maxillary spaces infection Abscess of Base of Upper

Anatomic Location. This abscess develops at the loose connective tissue of the base of the upper lip at the anterior region of the maxilla, beneath the pearshaped aperture Etiology. It is usually caused by infected root canals of maxillary anterior teeth. Clinical Presentation. 1-swelling and protrusion of the upper lip, 2-diffuse spreading and obliteration of the depth of the mucolabial fold 3-pain and constitutional symptoms

Treatment. The incision for drainage is made at the mucolabial fold parallel to the alveolar process

• Complication • Cavernus sinus thrombosis, through angular or ophthalmic vein • Differential diagnosis • TRAUMATIC OEDEMA • ALLERGY • NEOPLASM • NORMAL FLESHY LIP • LYMPHANGIOMA Canine Fossa Abscess

• Etiology. Infected root canals of premolars ,canines and occasionaly from the mesial root of the first molar

• Boundaries

• Anteriorly levator labii superioris and orbicularis oris anteriorly

• Posteriorly buccinators muscle

• Lateraly zygomaticus muscle and levator anguli oris

• Clinically

• 1- obliteration of

• 2- swelling of the upper lip

• 3- edema of the upper and lower eye lids

• 4- the entire face is painful to touch • 1. incision and drainage parallel to max. vestibule of affected tooth. • 2- Extraction or R.C.T. • 3- Antibiotics to avoid thrombosis as angular vein (branch of facial vein) courses through canine space

Buccal Space Abscess

• Anteriomedialy : buccinators muscle • Posteromedially : medial ptrygoid, ramus of the mandible and masseter • Laterally skin, superficial fascia. platysma. Deep cervical fascia • Above : zygomatic arch • Below: lower border of the mandible

•Contents

• 1-buccal pad of fat

• 2-facial artery vein nerve

• 3-Buccal lymph nodes

• 4- stensen duct • Pathological development of buccal space • From infected upper 2nd and 3rd molars and lower 1st and 2nd molar • Clinically • 1- intraoral bulging • 2- extraoral swelling confined to the • 3-sever pain • 4- conistitutional symptoms • 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. A hemostat is then used to explore the space thoroughly. An extraoral incision is made when intraoral access would not ensure adequate drainage, or when the pus is deep inside the space. The incision is made approximately 2 cm below and parallel to the inferior border of the mandible

Infratemporal space infection( post zygomatic space) • It is fatal space where infection can be transmitted to the cavernus sinus through inferior and superior ophthalmic vein or directly through foramen oval or lacerum • Boundaries • Anteriorly • Posterior surface of maxilla and that of zygomatic process • Posteriorly • Parotid gland • Laterally • Inner surface of the zygomatic arch • Ramus of the mandible . Coronoid process and temporalis muscle • Medially pterygoid plate , lateral pterygoid muscle, superior constrictor muscle • Superiorly : infratemporal surface of sphenoid bone

•Contents of infratemporal fossa -Lateral pterygoid muscle -Ptrygoid plexus of vein -Mandibular nerves and its branches -Lingual nerve - • Long buccal nerve •-Mylohyoid nerve •-Maxillary artery and vein •Otic ganglion and its roots •Chorda tympani nerve

• Pathological development of infratemporal abcess

• 1- infection from maxillary molars specially 3rd molar

• 2-osteomyelitis of the assending ramus ,condyle or coronoid process

• 3- local anaesthesia of maxillary nerve or posterior superior alveolar nerve

• 4-ascending infection from ptrygomandibular space • Signs and symptoms • 1-sever pain on opening

• 2- trismus

• 3-swelling of the pharynx

• 4-deviation of the mandible to the affected site on opening

• 5- if the cause is the upper molars there is swelling of the upper eye lids

• 6- if untreated the whole side of the face is involved , the eye closed

• 7- constitutional symptoms

• Treatment. The incision for drainage of the abscess can be made intraorally or extraorally by performing a superficial incision followed by blunt evacuation of pus using hemostat • Intraoral incision • 1- Incision is performed medial and parallel to the medial aspect of the ascending ramus • 2-or incision is made in the mucobuccal fold lateral to upper 3rd molar and curved hemostat is introduced and advanced behind the tuberosity and the directed medially and superiorly into the abcess cavity then drains inserted

• Extra oral incision • 3 cm long incision is performed at the angle formed by the fontal and temporal processes of the zygomatic bone the incisions carried in the hair line through the skin and superfacial and deep temporal fascia the blunt dissection completed by curved hemostat into infratempral space then rubber dam drain is inserted

Temporal space infection

• Superficial temporal space Superficial to temporalis muscle • Deep to temporalis muscle Pathogenesis Infected maxillary molars Sign and symptoms Swelling tenderness above temporal region Trismus

• Incision and drainage • Hair line of temporal region palatal Abcess

• Pathogenesis infected roots lateral incisor or palatal roots of upper posterior teeth infected cyst • Signs and symptoms • Globular tender swelling slightly elevated ,factuation is difficult to elicit due to thick firmly attached mucoperiostium • Incision and drainage Must be in anteroposterior palatal direction and at the alveolar rather than palatal mucosa to avoid injury to greater palatine artery

Mandibular abcesses Submandibular space infection

• it lies below mylohyoid muscle and it is located below and medial to the posteror part of the mandible • Boundaries • Medially Mylohyoid muscle and hyoglossus muscle superior laterally Medial aspect of the mandible and mylohyoid ridge Inferolaterally Investing layer of deep cervical fascia ,platysma, superfacial facia skin • Inferiorly

The hyoid bone ,intermediate tendon of digastric muscle

Anterior

Anterior belly of digastric

Posteriorly

Posterior-belly of digastric , stylohyoid muscle , and stylomandibular ligament that separate submandibular space from parotid space

• Pathological development of submandibular space

• 1- infected mandibular molars with roots below mylohyoid muscle

• 2- mandibular fracture

• 3-osteomyelitis

• Contents lymph nodes وsubmandibular gland ,warton,s duct 1- •

• 2-Facial artery

• 3- facial vein

• Clinical signs and symptoms

• 1- swelling and obliterating the angle of the mandible

• 2-pain and tenderness on palpation

• 3- dysphagia

• 4- trismus

• 5-severe cases show systemic signs and symptoms as fever malaise ,tachycardia • Differential diagnosis

• 1- submandibular sialadenitis

• 2- submandibular tumor

• 3- branchial cleft cyst

• 4-lymphoma

• 5-leukemia

• • Treatment

• Incision 2 cm below the lower border of the mandible , through the skin superfacial facia then followed by blunt dissection using hemostat then drain is inserted

Submasseteric space infection

• Anatomy • Medially • Lateral surface of the ramus of the mandible • Lateral • • Posteriorly • parotid gland

• Pathologucal development • 1- periapical infection from lower third molar • 2- pericoronitis • 3- ramus fracture • 4- posterior spread of infection from buccal abcess • Signs and symptoms

• 1-deeply seated' severe throbbing pain over the mandibular ramus of sudden onset

• 2-, swelling of the soft tissues of the face

• 3-trismus.

• 4-The temperature remains high until drainage is established,

• 5-patient becomes toxic-

• Treatment: • Through an intra-oral incision not less than 3 cm down the anterior border of the ramus , starting from the coronoid process , till the buccal sulcus opposite the second molar, a curved hemostat is inserted and passed backward and upward while keeping in close contact with the external surface of the bone

• 2-an extraoral incision • is made beneath the angle of the mandible and the ramus is exposed . The lower part of the masseter muscle is then detached which allows pus to drain A rubber drain is inserted next and attached to the skin of the wound'

Abscess of sublingual spaces:

• The sublingual spaces are separated in the mid-line by a dense fascia median raphe they are situated

above the mylohyoid muscle. • Boundaries

• Above: The of the floor of the mouth.

• Below: Mylohyoid muscle.

• Medially: Fascia median raphe.

• Antro-laterally: the lingual surface of the body of the mandible. Posteriorly: The hyoid bone • Each space is divided into two spaces:

• 1. Superficial: situated between mylohyoid and geniohyoid muscles' 2.Deep: Beteen geniohyoid and genioglossus muscles.

• contents:

• - Deep part of submandibular gland

• -Submandibular gland duct (Wharton's duct).

• - .

• - Lingual nerve. • Hypoglossal nerve

• hyoglossus muscle

• Genioglossus muscle

• Terminal branches lingual artery

• Pathologic development of sublingual abscess

• 1-from an infected tooth, progressing toward the lingual side of the jaw, the infection emerges above the mylohyoid muscle.

• 2-infection extended from other spaces primarily the submandibular space. • Signs and symptoms –

• Firm, painful swelling which raises the floor of the mouth

• . The is displaced medially and backwards.

• - The sublingual glands are prominent

• - Painful difficult swallowing (dysphagia).

• - Systemic signs and symptoms in severe cases. - Little evidence of swelling of the face unless the submandibular space involved

• Treatment: • - The incision should be made at the base of the alveolar process of the mandible in the lingual sulcus so that the sublingual gland, the lingual nerve, and the will not be injured

Abscess of sub-mental space

• Boundaries • Superior: • Mylohyoid muscle. • Inferior: Investing layer of deep cervical fascia, platysma, superficial fascia and skin • Lateral: Anterior belly of digastric muscle, separating the sub-mental space from the submandibular space. • Antro-laterally: lingual surface of the mandible • Posteriorly hyoid bone

• Contents of sub-mentat space: -

Sub-mental lymph nodes.

- Anterior jugular vein.

- Communications:

- Submental abscess may extend to the sub_mandibular space and infection may travel from one to the other • Clinical signs and symptoms : -

• general cellulitis of the sub-mental region first this board like and stiff until suppuration

• Dysphagia. –

• The infection may extend to the epiglottis and causes difficulty in breathing.

• - General signs of sepsis as fever, malaise etc

• Treatment • Sub-mental abscesses incised below the mandible. Generally, a transverse incision which follows the normal folds of the skin

• Differential diagnosis of submental abscess: • - Dermoid cyst. • - Thyroglossal duct cyst • - Chronic inflammatory lymph nodes 5. Abscess Pterygomandibular space.

• It is the lowest part of the infra temporal space • Boundaries . • Laterally: Medial surface of the ramus • Medially: Medial pterygoid muscle. • Above: lateral pterygoid muscle. • Anteriorly: the • Posteriorly: the deep lobe of the parotid gland

• Contents:

• Lingual nerve.

• Inferior dental nerve.

• Inferior dental vessels.

• Internal maxillary artery.

• Posterior temporal artery.

• Pterygoid plexus of veins surrounding the inferior head of the lateral pterygoid muscle AN: inferior alveolar nerve, LN: lingual nerve, LPM: lateral pterygoid muscle, MA: maxillary artery, MPA: medial pterygoid muscle, NM: nerve to mylohyoid Pathologic development of Pterygomandibular space abscess:

- Septic mandibular nerve block"

- Acute pericoronitis around mandibular third molar.

- Apical infection of mandibular molar teeth

- Gun shot wounds or compound fracture of the angle of the mandible.

- Inferior dissection of pus from the infratemporal space • Signs and symptoms: - Severe trismus

- Moderate extra-oral swelling over the submandibular region.

- Swelling of the oral mucous membrane overlying the space with medial displacement of the lateral pharyngeal wall • Tenderness and pain on palpation over the medial aspect of the ramus.

• - Dysphagia.

• - General constitutional symptoms.

• - Air hunger posture if bilateral infection 0ccurs

• - May be displacement of the edematous uvula to the opposite side. • Treatment (lncision and drainage): Incision and drainage can be carried out through intra-oral approach or extra_oral approach.

• lntra-oral approach

• Incision is made just medial to the anterior border of the ramus. The tissues medial to the ramus is bluntly dissected with curved hemostat. rubber dam drain is inserted loosely and sutured in place with (000) black si1k.

• Extra-oral approach Skin • incision 4 cm long is carried out through skin and sub cutaneous tissue in a curved fashion below and behind the angle of the mandible. Blunt dissection with a hemostat. Rubber dam drain is inserted.

6. Abscess of parapharyngeal space:

• Shape: • The space is inverted cone; its base is the skull and its apex at ihe hyoid bone. • Laterally: Medial pterygoid muscle. • Medially: superior conistrictor muscle. • Posteriorly: parotid gland, prevertebral and visceral layers of the deep cervical fascia. • Superiorly: base of the skull base of the sphenoid • Inferiorly: the parapharyngeal space is bounded by the attachment of the capsule of the submandibular gland to the sheath of the stylohyoid muscle and posterior belly of digastric muscle • Communications: • 1-The pterygomandibular space communicates with the parapharyngeal space around the anterior and posterior borders of the medial pterygoid muscle. • 2-infection of this space may disseminate upward through various foramina at the base of the skull, producing brain abscess, meningitis or cavernous sinus thrombosis. • 3- Infection may travel downward along the carotid sheath toward the mediastinum and may descend to the lungs causing lung abscess • 4- ThromboPhlebitis‘ • 5 - Arterial erosion'

• Contents: - • Deep cervical lymph nodes' • - Facial artery. • - Ascending Pharyngeal artery‘ • - Carotid -sheath (internal carotid artery' internal jugular vein and vagus nerve)' • - GlossoPharyngeal nerve' • - Hypoglossal nerve' • - Acessory nerve‘ • - Cervical sympathetic trunk' • Pathotogic development: . – • 1-acute infection around a mandibular third molar

• 2- - Extention from a pterygomandibular abscess.

• 3 - peri-tonsillar suppurailon may erode the superior pharyngeal constrictor the lateral pharyngeal space • Clinical signs and symptoms: • 1- severe pain in the affected side his referred to the ear, face or neck‘

• 2- (dysphagia)'

• 3-- Severe trismus

• 4-Swelling of the lateral wall of the pharynx and medial displacement of the tonsils' tonsillar Pillar and the uvula‘

• 5- firm, tender and indurated external swelling may be observed beneath the angle of the mandible

• -6- the constitutional symptoms are generally present such as fever' malaise' rapid Pulse .. etc

• Treatment:

• The treatrnent consists of antibiotics' surgical drainage and tracheostomy' Incision and drainage may be carried out extra-or intra- orally

• lntra-oral lncision: Vertical incision is made in the retromolar ang1e, lateral and parallel to the pterygomandibular fold, A curved hemostat is introduced medial to the medial. pterygoid muscle to evacuate the pus present in the para pharyngeal space' A drain is then inserted

• Extra-oral incision: Extra-oral incision is considered safer since there is no danger of aspiration of pus and pulmonary complication' The extra-oral incision is the same as that used for drainage of the submandibular space 7. :

• The retro pharyngeal space , lies between the posterior wall of the pharynx and the prevertebal fascia. The loose areolar cornective tissue which exists here not only permits pharyngeal movement, but allows infection to travel inferiorly to to the posterior mediastinum as far as the diaphragm 'and superiorly to the base of the skull adequate drainage of the retro-pharyryngeal spaces are together considered as parapharyngeal space'

8. Abscess of Parotid space

• Boundaries • It is surrounded medially and laterally by deep servical fascia that form parotid capsule

• Etiology: • a- Retrograde infection through the duct. • b- Blood born infection. • c- Posterior spread from submasseteric or pterygomand Spaces • d- Mastoiditis and otitis media • E- fracture of assending ramus • Contents: - • -superficial and deep portion of the parotid gland. • - Stenson's duct. • - Portion of the facial nerve' • - Posterior facial vein' • - AuriculotemPoral nerve‘ • - Superficial temporal artery‘ • - External carotid artery • - Parotid lymph nodes' • - Internal maxillary artery'

• Signs and symptoms • Swelling of the parotid region with eversion of ear lobules • The patient complains of. pain in the parotid region which is referred to the ear and temporal area' • -pain on eating or swallowing • Pus oozing from parotid papilla • Lymphadenitis • Fever malaise

• Differential diagnosis • Mumps. • sialolithiasis, • cyst and tumors affecting the Parotid gland' – • submassetenc space' – • Fracture of the ascending ramus of the mandible • Treatment: Abscess of the parotid space requires an extra oral approach ,is best drained by Blair incision, this extends around the angle of the jaw from behind the posterior border of the and forward 2 cm below the bone 9. Abscess of carotid sheath:

• Carotid sheath is fascial condensation surrounding IJV, vagus nerve, ECA, ICA. It lies below the sterno-mastoid muscle, and the part most commonly affected lies above the posterior belly of the omohyoid Muscle.

• Source of infection :- from - Submandibular space - Infratemporal space - Parapharyngeal space ,parotid space • Clinical features :- • 1- pain along the course of carotid sheath • 2- Intermittent bleeding episodes from nose or pharynx due to erosions of carotid artery or IJV. • 2- Palsies of cranial nerves X, XI, XII • 3- Enlarging hematoma in neck • 4- Pyrexia, chills, malaise. • treatment

• incision and Drainage through incision along anterior border of sternocleidomastoid muscle. Extern al jugular vein can be explored. .if .it shows evidence of being indurated and thrombosed, it should be ligated below the lowest limit of its involvment to prevent further descent of the infection Ludwig’s angina

• Definition:- • It is indurated board like fascial cellulitis that involving submandibular, submental, and sublingual spaces bilaterally • Etiology - infection of the mandibular molars. - Compound fracture of the mandibular angle or body. - Penetrating injury of the floor of the mouth. - Osteomyelitis of the mandible • Types:- • (1) Non Suppurative: --Induration board like. -No tendency for localization of pus. - Poor prognosis. (2) Suppurative:- - Have few drops of pus. - Tendency for localization of pus. - Better prognosis. • True Ludwig's Angina:

• There is bilateral involvement of submandibular, sublingual and sub- mentaL spaces.

• Pseudo-Ludwi g's An gina:

• There is unilateral involvement of submandibular sublingual and sub- mental spaces. • Bacteriology:

• Ludwig's Angina caused by mixed infection, mainly hemolytic streptococci and mixture of aerobic gram -ve microorganisms including fusiform bacilli, Vincent's organisms and various staphylococci. • Clinical signs and symptoms • 1-brawny non-fluctuant, tender swelling which spreads to the sub- mental region involving either the sub-mental or the sublingual space or both • 2-The patient has open mouth appearance due to swelling and elevation of the floor of the mouth, 3-and wooden raised hard tongue • 4-- Displace epiglottis posteriorly • 5 difficult breathing. • 6- Dysphagia and • 7-difficult speech. – 8-Difficulty of breathing due to :

- a- elevated tongue b- laryngeal edema c- epiglottic edema

9 Lymphadenopathy

10- Fever, malaise

GENERAL THERAPEUTIC PROCEDURES OF PATIENT WITH ACUTE INFECTION INCLUDING LUDWIG'S ANGINA: • - General supportive measures • - Massive antibiotics' • - Sedative. • - Heat therapy • - Incision and drainage‘ • - Removal of the cause' • - Post operative care‘ • - Tracheostomy, if there is respiratory embarrassment • 1-General supportive measures include - hospitalization. - Complete bed rest' - Adequate fluid intake to compensate dehydration. It should be remembered that the patient may be dehydrated because of the fever and inability to swallow - Hydration can be done by oral rout or by intravenous infusion - 2-Adequate nourishment - Diet must be rich in carbohydrate ,proteins and vitamins if - oral rout is difficult drip methods can be used using IV PROTEINS AS PANAMINES or amigens • 3-Antibiotics • 1- empirical dose • 2- antibiotics after culture sensitivity tests • 4-Sedatives: Sedatives and analgesics should be administered because the relieve the pain dfecrease anxiety of the patient and help fast recovery • 4-Heat therapy • Heat is applied intra-orally and extraorally • 5-lncision and drainage Surgical treatment (I &D) must be instituted without delay 1-to avoid: - mediastinitis. - Suffocation due to Laryngeal compression or glottic edema. -Considerable tissue loss due to pressure necrosis • 2-It must be done early for • a- Release tension and pressure of edema on airway. • b- Allow for drainage. • c- To obtain a specimen for culture and sensitivity test to give proper antibiotic • Technique:- • 1- Disinfection of site of incision. • 2- IV analgesia and field block LA at incision site avoid GA because of laryngeal edema and elevated tongue cause occlusion of airway. If the patient is debilitated or comatosed trachaeostomy can be done • 3- 2 submanidular incisions 2 cm below the inferior border of mandible. • - 1 submental skin incision at 1 cm below chin. 4- Insert haemestate to evacuate pus in spaces. • 5- Insert penrose fenestrated drain from submandibular to submental space bilaterally (through and through drainage) • Post-operative treatment:,

• external drainage the wound and drain should be kept covered with an adequate dressing held in place by a bandage.

• 2- irrigation by means of a syringe with saline solution one or more times a day

• 3-and the dressing must be large enough to hold the heat because hot dressing increases the blood supply to the area involved and thus stimulate phagocytosis and the elimination of toxic material

Periapical infection OSTEOMYLITIS • Definition:

• Osteomyelitis is an inflammation of bone generally produced by pyogenic organisms' It involves the cancellous bone and the bone marrow

• Onset and Phases:

• The infection starts by invasion of the medullary portion of bone, it may invade the cortex, portion of the periosteum and soft tissue causing facial edema and cellulitis' • Bacteriology: • Osteomyelitis is a pyogenic infection mainly caused by

• staphylococcus aureus‘

• , staphylococcus albus,

• streptococcus haemolyticus,

• pneumococci

• and micrococcus tetragenus • Osteomyelitis more commonly affects the mandible than the maxilla due to the following factors. • - The mandible has less blood supply and less resistance to the infection than the maxilla.

• - The mandible possesses a dense cortical bone which is not easily penetrated with the infection and has more wide spongious portion where the infection usually starts and travels more, destroying more extensive areas.

• - The mandible is much more exposed to trauma than the maxilla, more and high incidence of fracture. •Pathogenesis • : 1-The necrotic process

• A-starts in the spongiosa. large areas of bone are destroyed by infection and become devitalized due to loss of their blood supply caused by septic thrombosis of the blood vessels.

• B- Also raising the periosteum in acute osteomyelitis invaded with the infecion lead to cutting of the periosteal blood supply . to the bone leading to necrosis, destruction and de-vitalization of more extensive areas of bone • 2- formation of the sequestra

• there is a line of separation formed of granulation tissue between the dead and living bone.

• the necrotic devitalized areas of bone detached from the living bone called sequestrae. Osteoclastic resorption seem to take part also in the process of necrosis • 3-The reparative mechanism of the body is manifested by

• A-forming granulation tissue between the sequestrated parts and sound bone.

• B- reparative process , takes place by new deposition of periosteal bone by the inner side of the periosteum. This newly formed bone is termed the involucrum which occurs in chronic cases osteomyelitis in order to strengthen the jaw, • 4-The involucrum is perforated with holes (Cloacae) through which pus drains from the infected sequestrum

• 5-The sequestrum is hard rough, porous and lighter in color than the normal bone due to the ionized calcium which is mobilized by the. surrounding osteolytic process and precipitated in the islands of dead. bone (sequestrae).

• 6- the sequestrum,tends to be expelled although occasionally a small sequestrum is lysed, absorbed, during effective antibiotic therapy.

• Etiology: • l. Odontogenic causes: • a) Periapical infections

• b) Periodontal infection

• c) -Pericoronal infections around impacted or partially erupted teeth

• d) Infections of odontogenic cysts or tumors'

• e) Residual infections.

• f) lnfection through the teeth sockets after extraction causing localized osteitis (dry socket)

• • ll. Chemical Poisoning • lll. Traumatic: - • Excessive traumatization of tissues during difficult extractions

• Compound fracures of the jaws

• Pressure types of local anesthesia such as intra-osseous anesthesia

• Local traumatic injuries

• Improper use of surgical burs • V. Haematogenous infection

Wounds

Furuncles or boils

Chicken pox lesions

Vl. Fevers:

Such as typhoid, pneumonia, measles, influenza

Vll. Infectious granulomatous diseases: Such as syphilis" tuberculosis and actinomycosis

Vlll. Peri-tonsillar abscess: Can cause osteomyelitis of the ascending ramus Classification of Osteomyelitis

1- according to the clinical course of the disease into: a. Acute b. b. Sub-acute c. c. Chronic • according to the histo-pathological findings into • I. Suppurative. where pus formation occurs in instances of low body resistance. • II. Sclerosing (Nou-suppurative). • according to the distribution of the disease. • into: • a) Localized • b) Generalized • The following classification is of a clinical value:

• 1- Osteotmyelitis in infants and nursing (osteomyelitis maxillaris neonatum)

• 2- Acute osteomyelitis in children

• 3- Suppurative osteomylitis in adults:

• a. Acute b. Sub-acute c. Chronic • 4- Chronic sclerosing osteomylitis

• a. Focal sclerosing (condensing ostitis).

• b. Diffuse sclerosing.

• 5- Chronic sclerosing osteomyelitis with proliferative periostitis (Garre's osteomyelitis, periostitis ossificans) • 6- osteomyelitis caused by specific factors • A-as syphilis, tuberculosis,actinomycosis • B-osteoradionecrosis • C-Chemical osteomyelitis • D-Electrocoagulation osteomyelitis Osteomyelitis in infants (osteomyelitis maxlllaries neonatorum)

• Causative microorganism • In most cases, it is caused by Staphylococcus aureus. • The microorganisms are believed to enter wounds made during delivery if the finger must be inserted into the child's mouth, or through injuries of the made by sucking a foreign body. caused by infections of the nose. • Haematogenous invasion by streptococci or pneumococci • Clinical findings:

• constitutional reactions such as high fever rapid pulse, vomiting,

• In some instances.

• swelling of the face with edema of the eyelids, sub-periosteal abscesses developing on the alveolar mucosa and are followed by fistulas draining pus. Lowered resistance plays an important part in this disease, protein and poly vitamins should be supplied abundantly

• , the disease may run a chronic course with a slow onset, slight fever, and moderate pain

• 2l Acute osteomyelitis in children

• Characterized bY:-

• 1-It is usualiy fulminating and can be very serious. –

• Mandible or maxilla may be involved'

• - It is complicated by the presence of unerupted teeth

• - The involvement the condyle and the temporomandibular joint cause serious secondary deformities during the period of skeletal growth. The downward and forward growth of the jaw can be arrested on the affected side, causing asymmetry of the face‘ 3) Suppurative osteomyelitis in adults

May be acute ,subacute and chronic a. Acute suppurative osteomyelitis This is an invasive, aggressive clinical picture: 1-- occurs quite rapidly with a sudden onset. - The first symptom is pain which is deep, persisting and usually referred to the ear’ - All the teeth in the involved area are loose, mobile and tender to Percussion - Pus seeps around the necks and the interproximal spaces of teeth • 3-Edema of the overlying soft tissues, the gingiva becomes red and edematous' • 4- Elevated temperature- The patient is feverish, frustrated, dehydrated and has a • Toxic appearance and malaise • Increased white blood count which reach to 20.000mm3 • lntermittent numbness or paresthesia of the • Laboratory studies for acute osteomyelitis • 1-leukocytosis 12000-20000cell/cc • 2-There is increase in polymorph-nuclear leucocytes. • 3- Increased of immature cells (neutrophils) as a result of toxaemia • 4-In long standing cases associated with toxaemia, anemia may result leading to decreased hemoglobin % and RBC • 5- Blood culture should be made if the patient is very ill and should be repeated • 6-Dehydration and acidosis • 7- albuminurea • 8-If there is pus it should be cultured for antibiotic sensitivity test • Radiographic findings: • Usually negative unless the condition is an outcome of a chronic osteomyeitis, the only radiographic finding may be enlargement of the marrow spaces" • b. Sub-acute suppurative osteomyelitis • The symptoms are generally the same as in the acute phase but are less severe' The sub-acute phase may continue to decrease until it becomes chronic but may revert to the acute stage of the disease c. Chronic suppurative osteomyelitis

• Occurs after 2-3 weeks in an untreated case, the clinical signs an symptoms are the same as with the acute phase but are very much milder, in addition there are • 1. Sinus tracks • 2-sequestration • 3- lnvolucrum: • 4. Laboratory studies for chronic osteomyelitis: • 1 - Normal leucocytic count but there is slight increase in acute exacerbation • 2- Smears, culture, antibiotic sensitivity tests should be done Periodically • 3 - Blood cultures to rule out evidence of blood stream infection • 4- Bacterial smear for sulfur granules if actinomycosis is expected • 5-Serological tests and biopsy examination to exclude syphilis • 6- Laboratory test and biopsy for tuberculosis (t.B.). • 7 - Tests for anemia . • Radiographic findings: • - There are irregular alternative radiolucent areas together with radio opacitis-. • At this stage the irregular radiolucent areas appear as if the bone was eaten by a warm (moth eaten appearance ) If sequestrae is formed, it will appear irregular and more radiopaque than normal bone due to the calcium deposition from the osteoclastic resorption

• - A line of radiolucency (granulation tissue) separate the sequestrum -- Sub-periosteai bone formation (involucrum)

• DifferentiaI diagnosis • 1. Actinomycosis ; It is gram positive nonaerobic bacteria infection characterizecl by multiple sinuses oozing yellowish masses containing sulpher granules which are investigated with bacteriological smears • 2. Tuberculosis; • Invasive osteomylitis may occur due to tuberculous infection. The tuberculous bacilli in saliva form ulcers or invade the bone through extraction wounds. • Diagnosis • chest X-rays,(enlarged hillarl ymph nodes , pleural effusion) • laboratory examinations ( tuberculin test) • sputum culture and microscopic examination • PCR WITH NUCLEIC ACID AMPLIFICATION • 3-Syphilis:

• Tertiary syphilitic lesions ( GUMMA) produce syphilitic periosteitis and osteomyelitis. It should be differentiated with serologic tests and biopsy. Wasserman. khan's tests and biopsy

• Rapid plasma reagin (RPR), a syphilis blood test that looks for antibodies to the syphilis bacteria.

• Venereal disease research laboratory (VDRL) test, which also checks for syphilis antibodies PRIMARY SYPHYLIS( CHANCRE ) 2RY SYPHYLIS ( SKIN RASHES) 3RY SYPHYLIS( GUMMA) • 4. Osteitis fibrosa cystica: ( hyperparathyroidism) • The diffrential diagnosis is made by the clinical symptomatology, pathological examinations and specific blood analysis

• e.g. there is increase in parathyroid hormone

• , increase in ionized serum calcium

• decrease ln serum phosphorous,

• there is increase in calcium in urine

• increase in alkaline phosphatase • 5. Malignant neoplasm • Can be differentiated by • History of the lesion, • clinical x-ray • biopsy examination Treatment of acute and chronic supportive osteomyIitis :

• l. General supportive measures (acute and chronic): • 1- - Bed rest or hospitalization. • 2 - Diet should be of soft nature to prevent pressure on the weakened bone • 3-diet should be of high caloric and protein value • 4- Adequate doses of fluids to compensate dehydration and restore the fluid balance. • 5- Sedative and analgesics. • 6- The underlying systemic diseases or general illness should be diagnosed and treated medically • ll. Heat therapy: • May be extra-orally with hot bags and intra-orally by frequent irrigation of the drained area using warm sterile normal saline. The patient is also instructed to use warm mouth washes frequently to help localization of the infection and drainage • lll. Effective antiblotic therapy is given upon making cultures and antibiotic sensitivity tests • Sometimes it is necessary to continue antibiotic for 4-6 weeks in severe cases of osteomyeiitis in order to prevent recurrence

• IV. Drainage of suppurative areas: • Sometimes the pus is confined in the cancellous bone, because the cortical bone is too dense and can not be perforated. Holes are drilled in the compact cortical bone using surgical burs for evacuation of this pus.

• Decortication

• sucerization • V. Sequestrectomy:

• - the sequestrum tends to be expelled • -sometimes the sequestrum is resorbed (lysed)

• The sequestrum should not be removed too early

• the sequestrae which became detached and completely loose. are lifted gently with a hemostat from its bed.

• No curetting is made after removal of the sequestrae • Vl. Removal of the etiological teeth:

• Vll. lmmobilization of the jaws: • With intermaxillary fixation in case of a pathological fracture. or a fracture which may occur during operative procedures. • VIII. Decorticectomy • lX. Remodeling of jaw 4) Chronic sclerosing osteomyelitis

• a. Focal sclerosing (condensing osteitis)

• Definition: • It is unusual reaction of bone to infection occurring in instances of extremely high tissue resistance or in cases of low grade infection • Clinical signs and symptoms: • - May be asymptomatic.

• - Mild pain

• associated with an infected pulp.

• - Young age goup before the age af 20 years usually affected

• - The tooth most commonly involved is the mandibular first molar which present a large carious cavity. • Radiographic findings ):

• The lesion appears as well circumscribed radio-opaque mass of sclerotic bone surrounding or extending below the apex of the affected tooth.

• DifferentiaI dignosis,'

• benign cementoblastoma

• Treatment:

• - Root canal treatment or extraction of the affected tooth.

b. Chronic diffuse sclerosing osteomyelitis

• Chronic diffuse osteomyelitis is a condition similar to the focal form of

the disease and also represents a prolifrative reaction of the bone to

a low grade infection,

• The portal of through a diffuse periodontal disease. • Clinical signs and symptoms: • - age group most common in older patients especially in edentulous areas. • - Sex predilection" females most commonly affected than males. • - Race, in blacks, but the disease may be seen in any race. • - • -Acute exacerbation may occur resulting in mild suppuration" spontaneous formation of a fistula ,vague pain • a bad taste in the mouth • Radiographic findings

• It appears as radio-opaque lesion with indistinct border

• In occasional cases there is bilateral involvement of both the maxilla and the mandible in the same patient.

• Differential diagnosis :

• Paget's disease (has cotton wool appearance ) • Treatment:

• - Antibiotic to treat the acute episode.

• - If a tooth is present in one of these sclerotic areas and must be extracted, utilize surgical approach with removal of liberal amount of bone to facilitate extraction and increase bleeding to accelerate healing. 5) Garre's osteomyelitis, (chronic osteomyelitis with proliferative periostitis, periostitis ossificans, Garre's chronic sclerosing osteitis

• Definition: It is a non suppurative osteomyelitis characterized by a peripheral periosteal bone apposition • Etiology: - • badly decayed tooth. • - Cellulitis or infection of the overlying soft tissue • .- Hematogenous • - lmproper management of acute or chronic dento-alveolar infection in children • Bacteriology: • - Staphylococcus aureus, the most common • - Hemolytic streptococci • - Actinomyces may be found in mixed culture

• Clinical signs and symptoms: • - Young age group is commonly affected (before the age of 25 years). - The anterior surface of the tibia is the commonest site, • the oral lesion usually affects the mandible, seldom the maxilla is affected • Treatment: • - Antibiotics. • - Extraction of the affected tooth. • - Shaving of bone in case of facial disfigurement. • Prognosis:

• Usually the condition will gradually subside after removal of the cause

• Differential diagnosis:

• -Infantile cortical hyperostosis

• - Ewing's sarcoma.

• - (osteopetrosis or marble bone disease).

• -chronic focal sclerosing osteomyelitis. -Hypervitaminosis A. -Syphilis. - Leukemia.

• -Metastatic neuroblastoma Osteoradionecrosis

• Definition: Bone necrosis as a result of radiotherapy. Etiology: High dose of radiotherapy, • Pathogenesis: Radiotherapy leads to:Hypovascularity ,Hypoxia ,Hypocelluarity this leads to Decrease blood supply and subsequent bone necrosis • Clinical: • 1-Exposed necrotic dead sequestrated bone. • 2. Radiation caries due to xerostomia. • 3. Fistula and pus oozing • Incidence: Mandible > maxilla X-ray: Moth eaten • Prevention during radiotherapy: • 1- Chlorhexidine 1% M-.W to control mucositis. • 2- Protection against caries sodium fluoride gel 1% • 3- RCT rather than Extraction to avoid osteoradionecrosis. • 4- Extraction is done before radiotherapy • Treatment • 1- Hyperbaric oxygen; • Marx protocol for HBO Prophylactic ORN= 20 dives pre-op and 10 dives post-op • Active ORN = 30 dives pre-operative and 10 dives post-op • 2. Sequestrectomy & Saucerization. • 3. Extraction of the offending tooth. Bisphosphanate psteomylitis Fatal complications of odontogenic infection (Serious sequlae) • Ascending complications: include • 1- Orbital cellulitis. 2- Brain abscess. 3- Cavernous sinus thrombosis. 4- Dural meningitis. 5- Ankylosis of TMJ. • Descending complications: included 1- Ludwig’s angina. 2- Airway obstruction. 3- Mediastenitis. 4- Necrotizing fascitis. 5- Carotid sheath involvement 6- Pulmonary abscess • . (1) Orbital Cellulitis • Etiology :- Infection spread from: • - 1- Infratemporal or pterygopalatine abscesses through the pterygoid plexus of veins of the inferior opthalmic vein.

• 2- Infection of ant. Teeth of maxilla can spread directly or via communication of the non-valved angular facial vein and opthalmic veins.

• 3- Extension of odontogenic infection across the maxillary sinus into the through the inferior orbital fissure • Clinical features:- • - Proptosis • - painful eye movement • - Opthalmoplegia • Affection of extraocular mobility. • - Change and loss of visual acuity. • N.B : all due to involvement cranial nerves 3, 4, 5d

• Complications:- • 1- Loss of visual acuity. • 2- Cavernous sinus thrombosis. • 3- Meningitis and brain abscess e neurologic impairment or death. (2) Brain abscess and dural Meningitis

• Mode of spread infections:- • 1- Direct spread: • - Through erosion of base of skull • -Through foramina of the skull. • -Through infraorbital fissure. • -Through fracture floor of maxillary sinus lead to spread infection from sinus to frontal sinus. • Through injection of L.A solution • a) Contaminated needle • b) Needle passed from infected space. • 2- Indirect: (hematogenous spread) through septic thrombus spread through valveless veins.

• Clinical features :- • - Headache • - Low-grade fever • - Nausea • - Vomiting • - Neurologic deficit • - Nuchal rigidity • - Mental status change • - Seizures

• Laboratory investigations : • - - CT scan, MRI. • - Neurologic tests. • - Blood test • TTT :- Chloramphenicol,sulphonamides ceftriaxone may be used

(3) Cavernous sinus thrombosis • Applied anatomy :- • - 2 sinuses are located on each side of sphenoid bone and connected by intercavernous sinuses. • Communications:- • - Direct from face: - through angular vein to superior and inferior ophthalmic veins, which drain directly into cavernous sinuses. • Indirect :- through pterygoid venous plexus which communicate cavernous sinus by way of the sphenoid emissary vein which drains into posterior aspect of inferior ophthalmic vein

• Drainage: It drains into inferior and superior petrosal sinuses. - Related structures • a- ICA • b- Oculomotor nerve (III) • c- Trochlear nerve (IV) • d- Ophthalmic and maxillary nerves • e- Abducent nerve (VI • Etiology: Source of infection - • All veins of face are valveless • - Ant. teeth infection and Ant. facial vein and angular vein – --- superior and inferior opthalmic veins -- cavernous sinus. • - Posterior teeth infection pterygoid venous plexus ---emissary veins cavernous sinus ------or inferior orbital fissure---- inferior ophthalmic vein ------cavernaus • Clinical manifestations:- • Ptosis • inability to open eye. • Dilated pupil. • Ophthalmoplegia due to affection of III, IV, VI cranial n • Numbness fore head and face (V1, V2). • Swelling and redness around one or both eyes. • Retinal hemorrhage due to venous congestion • vision loss or diplopia. • Severe headache due to intracranial pressure. High fever, fatigue and seizures and coma and death. • Treatment • Hospitalization and intensive care • 1- Removal of infection focus. • 2- Antibiotic: broad spectrum antibiotic e.g., penicillin and sulfonamides is better choice due to they are brain transmitter. • 3- Anticoagulant therapy: to prevent extension of the thrombus and interference with venous drainage of the brain. • 4- Heparin is most common use. • 5- Reference to neurosurgeon for craniotomy

• (4) TMJ Ankylosis • Infection of TMJ can produce prolonged limitation of motion, disturbance and destruction of articular surfaces and alteration of normal physiological process of TMJ. Destruction of articular surface with limitation of motion will lead to ankylosis. • (5) Ludwig’s angina • It is indurated broad like fascial cellulitis that involving submandibular, submental, and sublingual spaces bilaterally. • (6) Airway obstruction • May occur related to:- • - Ludwig’s angina • - Pharyngeal space • - Peritonsilitis • Airway obstruction may necessitate emergency tracheostomy or cricothyroidotomy rather than intubation. • (7) Mediastenitis • It is spread of infection to chest cavity down to diaphragm including major BVs and heart.

• Etiology:- - Downward spread of retropharyngeal and danger space. Complications: - pericarditis, pulmonary abscess.

• Treatment :-

• Hospitalization and airway security

• -Surgical drainage

• -Antibiotics

• -Supportive measures (8) Pulmonary abscess • It may occur as complication of mediastinitis.

• Clinical features of mediastinitis and pulmonary abscess include - Fever - Tachycardia - Leucocytosis - Pain in chest, back or neck

•(9) Necrotizing fasciaitis • - It is an aggressive bacterial infection of the fascia resulting in necrosis and loss of large area of skin. • - Predisposing factors: • - Immunocompromized pt. • -Diabetics • -Allocholics • -Cancer • - Radiotherapy • - Chemotherapy • Immunosuppressive drugs intake. • Clinical features:- • Skin begins with smooth, tense, shiny skin no clear demarcation between normal and affected areas. • When infection progresses, dusty, purplish discoloration of skin with balloon filled with bad smiling exudate.

• Complications:

• death due to extension to mediastinum and acidosis, fluid and electrolyte disturbance, haemolysis. -

• Treatment

• - Fasciatomy

• irrigation and dressed with packs impregnated with zinc peroxide, hydrogen peroxide

• Antibiotic

• supportive methods. • (10) Carotid sheath involvement • (10) Carotid sheath involvement • Carotid sheath is fascial condensation surrounding IJV, vagus nerve, CCA, ICA. • Source of infection :- from • - Submandibular space • - Infratemporal space • - Parapharyngeal space • Clinical features :- • 1- Intermittent bleeding episodes from nose or pharynx due to erosions of carotid artery or IJV. • 2- Palsies of cranial nerves X, XI, XII • 3- Enlarging hematoma in neck • 4- Pyrexia, chills, malaise. • TTT: - I, D through incision along anterior border of sternocleidomastoid muscle. • Control of bleeding from vessels • Supportive care • Antibiotic