orofacial infections.pptx

OROFACIAL INFECTIONS

Group 2

Acute dental alveolar abscessPericoronitisAcute alveolar osteitisCellulitis Ludwig’s Angina Cavernous Sinus Thrombosis Osteomyelitis

Odontogenic Infections

GENERAL CLASSIFICATION-AETIOLOGYOdontogenic

Traumatic

Implant surgery

Reconstructive surgery

Infections from contaminated needles

Others:antrum associated,salivary gland afflictions

Secondary to malignancies

CAUSATIVE MICROORGANISMS Bacterial-odontogenic/non-odontogenic

Fungal

viral

POSSIBLE SPREAD OF INFXN

INFECTIONS

Acute:abscess,cellulitis,fulminating infections

Chronic:

Acute Dento-alveolar Abscess

Def:a circumscribed suppurative type of inflammation involving primarily the tooth and the investing alveolar bone.

This disease entity is a continuation of periapical abscess.

Clinical features

1.Pain:severe throbbing pain

2. Submucosal swelling in the sulcus

Usually on the outer aspect of alveolar process. Fluctuation may be elicited after few days. If left untreated, the swelling bursts and produces sinus tract discharging pus.

3.Tooth is sensitive to touch

4.Fever

5.lymphadenitis:nodes are enlarged, soft and tender

PATHOGENESIS

Bacterial irritation of pulp tissuesPulp hyperemiaPulpitisPulp necrosisAcute periapical periodontitisAlveolitis

PROGNOSIS &TREATMENT

Prognosis depends on virulence and number of microorganisms and patients resistance.It may resolve or progress to chronic dental alveolar abscess then to a periapical granuloma.Treatment:Antibiotics,analgesics,RCT,Extraction.In addition, intra-or extra oral incision and drainage may be required.

Surgical Therapy:

Surgical Technique for Incision and Drainage of an Abscess

Incision and drainage helps :

i. To get rid of toxic purulent material.

ii. To decompress the edematous tissues.

iii. To allow better perfusion of blood, containing antibiotic and defensive elements.

iv. To increase oxygenation of the infected area.

Technique:

1) Topical/Local anesthesia

2) Make a stab incision

3) Closed forceps pushed thru tough deep fascia to pus collection

4) Abscess cavity entered

5) Pus flows along the beaks

6) Placement of a drain; corrugated rubber drain placed and secured

7) Drain left for at least 24 hrs

8) Dressing applied over site of incision

EDEMA,CELLULITIS,ABSCESS

MICROBIOLOGYThe aerobic bacteria found in odontogenic infection are primarily gram positive cocci, most are viridans streptococci species, includeStrep. milleri, Strep. sanguis, Strep. salivarius, strep. mutans.These oral streptococci are also known as α-hemolytic streptococci, which account for about 80 percent of aerobic bacteria found in odontogenic infection.There are two main groups of bacteriodes. First is Oropharyngeal group, which is found in the mouth and contributes to odontogenic infections.The other group found in the gut—the enteric Bacteroides, they include B. Fragilis, B. Vidgatis, B. Distasonis, B. thetaiotaomicron, B. Ovatis. They are rarely seen in oral cavity and mostly do not cause odontogenic infections.Oropharyngeal bacteroides divided into: (a) Porphyromonas, and (b) Prevotella.a. Porphyromonas:It includes P. asacchrolyticus, P.Gingivalis, andP. endodontalis. b. Prevotella:It includes P. melaninogenicus, P. buccae, P. intermedius, P. oralis, P. loescheii, P. ruminocola, andP. denticola. Prevotella intermedius, Porphyromonas gingivalis, andPorphyromonas endodontalis appears to be most pathogenic among them.

These gram negative anaerobic rods, are usually susceptible to most antibiotic, but they are 25 percent resistant to penicillin V and nearly 50 percent resistant to cephalexin, and other first generation cephalosporin.The other group of anaerobic gram negative rod is the genus Fusobacterium. Fusobacterium, like bacteroides are pathogenic and have the ability to destroy tissues through production of proteolytic enzymes and endotoxins. Fusobacterium is usually sensitive to penicillin and penicillin like drugs, but are frequently resistant to erythromycin.

Fusobacterium species appears to be the most virulent and when in combination with Strep. milleri, commonly seen in aggressive odontogenic infections

that have descended into the lateral pharyngeal and retropharyngeal spaces and also into the mediastinum.

MAJOR PATHOGENS IN ODONTOGENIC INFXNS.

MEDICAL THERAPY

Supportive care:hydration,soft or liquid diet rich in protein,analgesics,use antiseptic mouthwashes to maintain oral hygiene.

Antibiotic therapy:

PERICORONITIS

Def:inflammation of soft tissues surrounding crown of partially erupted tooth/unerupted tooth EtiologyBacterial growth under flapTraumatic irritation

Common site: impacted/malposedthird molars

TYPES

a)Acuteb)Subacutec)chronic

SIGNS AND SYMPTOMS OF ACUTE PERICORONITIS

Severe painDysphagiaTrismusHalitosisLymphadenitisExtra oral swellingConstitutional symptoms:fever,chills,increased resp. rate, general malaise

SUBACUTE/CHRONIC SIGNS AND SYMPTOMS

Dull painStiffnessPus under flapBad tastelymphadenitis

Spread: The pericoronal infection, if left untreated can spread to the following regions:

i. It can extend submucosally and form a vestibular abscess against mandibular second or third molars; and may discharge as intraoral sinus.

ii. It can extend on the outer surface of buccinator causing buccal space abscess.

iii. It can extend into the submandibular, pterygomandibular and submasseteric spaces.

iv. Rarely, it can extend down to lower border of

mandible behind the depressor anguli oris muscle;

and burst through the skin (if not incise

TREATMENT

Operculectomy

Indicated if

i. Tooth is in good position

ii. 1/3 rd of crown is covered by flap

STEPS

a) LA

b) Irrigation under flap

c) Scalpel/electro scalpel used to remove flap

d) Surgical pack

e) Antibiotics and analgesics

CONSERVATIVE TREATMENT

Selective grinding of opposite toothIrrigation under flapWarm saline and hydrogen peroxide mouthwash antibiotics

ACUTE ALVEOLAR OSTEITIS/DRY SOCKET Def:a complication of XLA in which blood clot disintegrates and patient experiences severe pain.

Causative factors;

Infection:Poor oral hygiene

Trauma:difficult extraction

Immuno-compromised states:HIV,DM

Predisposing factors

Vasoconstrictors in LA

Reduced vascularity- common in the mandible

Smoking

Overinsing mouth

PATHOGENESIS

Inflammation causes release of tissue activator that converts plasminogen to plasmin that causes lysis of fibrinogen causing clot dissolution hence bare bone is left.

Kinogen is also transformed to kinins causing severe pain.

SIGNS AND SYMPTOMS

1. Occur 3rd -4th day after extraction

2. Very severe pain

3. No clot in socket i.e bare bone

4. Bad taste and smell

5. No frank sequestration

6. Rarely pyrexia

7. Lymph node enlargement

TREATMENT

1. Irrigation- with warm saline to remove any debris or foreign material

2. Dressing –zinc-oxide eugenol with some cotton fibers. Dressing is changed every 24-48hrs.

3. Curettage –avoid on the bony walls

4. Antibiotics – not to be used except for guarding against superimposed infection.

It is an acute infection of the skin extending deep into subcutaneous tissues underlying the dermis if abscess is NOT able to establish drainage through the surface of skin or into oral cavity. may spread diffusely through facial planes of soft

tissue. There is edematous spread of acute inflammatory process .

Aetiology:Streptococcus pyogenes

Cellulitis

two dangerous forms:

Ludwig’s Angina

Cavernous Sinus Thrombosis

Cellulitis

named after German physician who described the seriousness of disorder in 1836

Angina comes from Latin word angere

strangle

Ludwig’s Angina

AETIOLOGY

1.Odontogenic infections:abcesses2.Iatrogenic: Use of contaminated

needles3.Traumatic injuries to orofacial

region: mandibular fractures,deep penetrating wounds

4.Osteomyelitis5.Submandibular/sublingual

sialadenitis6.Secondary infections of oral

malignancies

70% of cases, develop from spread of an acute infection from lower molar teeth

prevalence in patients who are immunocompromised secondary to disorders such as:

diabetes mellitus organ transplantation acquired immunodeficiency syndrome (AIDS) aplastic anemia

Ludwig’s Angina

Clinical Features

massive swelling on neck

often extends close to clavicle

involvement of sublingual space results in

• elevation Woody Tongue• posterior enlargement can compromise• protrusion of tongue airway

Ludwig’s Angina

Ludwig’s Angina

Clinical Features

involvement of submandibular space results in

• enlargement• tenderness of neck above

level of hyoid bone Bull Neck• pain in neck + floor of mouth• restricted neck movement

Ludwig’s Angina

Clinical Features

involvement of submandibular space results in

• dysphagia• dysphonia• dysarthria• drooling• sore throat

Ludwig’s Angina

Clinical Features

involvement of lateral pharyngeal space

• respiratory obstruction secondary to laryngeal edema

• tachypnea• dyspnea• tachycardia• patient needs to maintain erect position

Ludwig’s Angina

Treatment & Prognosis

centers around 4 activities

• maintenance of airway• incision + drainage• antibiotic therapy• elimination of original focus

of inflammation

Ludwig’s Angina


initial observation many clinicians administer

• systemic corticosteroid medications such as intravenous (IV) dexamethasone

attempt to reduce cellulitis

Ludwig’s Angina


if signs or symptoms of impending airway obstruction:

• fiber-optic nasotracheal intubation

• tracheostomy

• cricothyroidotomy

Ludwig’s Angina


if signs or symptoms of impending airway obstruction:


sometimes performed instead of tracheostomy

perceived lower risk of spreading infection to mediastinum

Ludwig’s Angina



Ludwig’s Angina

Treatment & Prognosis high dose of penicillin(penicillin G, 2 to 4 million

units, IV 4 to 6 hourly; or 500 mg six hourly orally). Amoxycillin; 500 mg 6 and 8 hourly, IV and orally Cloxacillin; 500 mg orally, 8 hourly. In case of allergy to penicillin; Erythromycin 600 mg

6 to 8 hourly. Gentamicin has activity against some resistant

staphylococci and pseudomonas. 80 mg I.M, B.D. Clindamycin IV 300 to 600 mg 8 hourly, orally and

intravenously. Its spectrum of activity includes gram positive cocci including penicillinase resistant staphylococci, and Bacteroides.

Ludwig’s Angina

TREATMENT CTD

Metronidazole: It is a useful antibiotic against anaerobic flora found in oral infections. It is administered in the form of 400 mg 8 hourly orally or intravenously.

Cephalosporins: These are closely related to penicillin and have similar spectrum of their activity. These are usually reserved for resistant infections.

Usually, a combination of antibiotic therapy is indicated for aggressive management of Ludwig’s angina, a penicillin or it’s derivative alongwith metronidazole or gentamicin.

Note: Antibiotics should be changed subsequent to the result of bacterial culture and sensitivity testing


if infection remains:

diffuse surgical intervention indurated is at discretion of clinician brawny + often governed by patient’s

response to noninvasive therapy

Ludwig’s Angina


complications:

• Pericarditis• Pneumonia• Mediastinitis• Sepsis• Empyema• Respiratory Obstruction

Ludwig’s Angina

edematous periorbital enlargement

with involvement of eyelids + conjunctiva. Aetiology:StaphylococciStreptococci and some gram –vebacteria


in cases, involving canine space

swelling along lateral border of nose

may extend up to medial aspect of eye + periorbital area

protrusion + fixation of eyeball



induration + swelling of adjacent forehead + nose

pupil dilation lacrimation may also photophobia occur loss of vision



pain over eye + along distribution of:

• opthalmic Trigeminal • maxillary branches Nerve



surgical drainage + high-dose antibiotic medication similar to those administered for patient’s with Ludwig’s Angina


OML may be defined as an inflammatory condition of bone, that begins as an infection of medullary cavity and haversian systems of the cortex and extends to involve the periosteum of the affected area.

an acute or chronic inflammatory process in extends

medullary spaces OR away from cortical surfaces of bone initial site of

involvement

Osteomyelitis

caused by bacterial infections

result in expanding lytic destruction of involved bone

with suppuration sequestra formation

Osteomyelitis

PREDISPOSING FACTORS 1. Conditions that alter host defenses would include chronic debilitating systemic diseases—such as diabetes mellitus, agranulocytosis, leukemia, severe anemia, malnutrition, drug abuse, chronic alcoholism, sickle cell disease, and febrile illnesses such as typhoid.

2. Conditions that alter vascularity of bone, include—therapeutic irradiation, osteoporosis, Paget’s disease, fibrous dysplasia, bone malignancy, metallic bone necrosis (caused by mercury, bismuth, and arsenic). An intrinsic and extrinsic vascular component has a more profound influence, both in onset of occurrence as well as in resolution outcome.

3. Virulence of organisms: Certain organisms precipitate thrombi formation by virtue of their destructive lysoso`mal enzymes (Hudson 1993).

ETIOLOGY 1.odontogenic infections

2. Trauma: It is the second leading cause: (a) Especially, compound fracture, and (b) Surgery-iatrogenic

3. Infections of oro-facial regions derived from:

a. Periostitis following gingival ulceration,

b. Lymph nodes infected from furuncles, and

c. Lacerations

d. Peritonsillar abscess.

4. Infections derived by hematogenous route: Furuncle on face, wound on the skin, upper respiratory tract infection, middle ear infection, mastoiditis, systemic tuberculosis.

PATHOGENESIS The process leading to osteomyelitis is initiated by acute inflammation, hyperemia, increased capillary permeability and infiltration of granulocytes. Tissue necrosis occurs, as proteolytic enzymes are liberated and as destruction of bacteria and vascular thombosis continues, there is a pus formation. The pus is a combination of necrotic tissue and dead bacteria and WBC accumulate. When pus accumulates, the intramedullary pressure increases resulting in vascular collapse, venous stasis, and ischemia. Subsequently, pus travels through haversian and nutrient canals and accumulates beneath the periosteum, elevating it from the cortex; and thereby further reducing vascular supply. Compression of neurovascular bundle accelerates thrombosis, ischemia, and infarction, later resulting in paresthesia and sequestrum formation. As natural host defenses and therapy begin to be effective, the process may become chronic, inflammation regresses, granulation tissue is formed; new blood vessels cause lysis of bone, thus separating fragments of necrotic bone (sequestrum) from viable bone. Small sections of bone may be completely lyzed, whereas larger ones may be isolated by a bed of granulation tissue encased in a sheath of new bone (Involucrum). Sequestra, may be revascularized, remain quiescent, or continue to be chronically infected and require surgical removal. Occasionally, involucrum gets penetrated by channels, known as cloacae, through which pus escapes from sequestrum to an epithelial surface.

CLASSIFICATION

MICROBIOLOGY

Most of the cases are caused by aerobic streptococci (α-hemolytic streptococci, Streptococcus viridans), anaerobic streptococci; and other anaerobes, such as Peptost-reptococci, Fusobacteria, and Bacteroides (Peterson 1999). Sometimes, anaerobic or microaerophilic

cocci, Gram negative organisms such as Klebsiella,

Pseudomonasand Proteusare also found. Other organisms

such as M. tuberculosis, T. pallidum, and Actinomyces species

produce their respective specific forms of OML.

patients of all ages can be affected

strong male predominance

most cases involves mandible

Osteomyelitis

Acute Supporative Osteomyelitis

Chronic Suppporative Osteomyelitis

Osteomyelitis

acute inflammatory process spreads through medullary spaces of bone

insufficient time has passed for body to react to presence of inflammatory infiltrate

Osteomyelitis (Acute Suppurative Osteomyelitis)

Clinical Features

symptoms of acute inflammatory process less than1 month in duration

fever

leukocytosis

Osteomyelitis (Acute Supporative Osteomyelitis)

Clinical Features

lymphadenopathy

soft tissue swelling of affected area

on occasion, paresthesia of lower lip


Histopathologic Features

biopsy material from patients

• liquid content• lack of soft tissue component• consist predominantly of

necrotic bone


Histopathologic Features

necrotic bone

• loss of osteocytes• peripheral resorption• bacterial colonization• acute inflammatory infiltrate

consists of polymorphonuclear leukocytes


Radiographic Features

ill- defined radioluscency

periosteal new bone formation may be seen

• response to subperiosteal spread of infection

• proliferations more common in young patients



periosteal new bone formation may be seen

• single-layered radioopaque line

• separated from normal cortex by an intervening radiolucent band



on occasion, exfoliation of fragments of necrotic bone

fragment of necrotic bone that has separated from adjacent vital bone is teremed sequestrum



on occasion, fragments of necrotic bone may become surrounded by new vital bone, known as involucrum


Treatment

if obvious abscess formation,

• antibiotics penicillin clindamycin cephalexin cefotaxime gentamicin

• drainage


defensive response leads to production of granulation tissue

subsequent forms dense scar tissue

• attempt to wall off infected area

Osteomyelitis (Chronic Supporative Osteomyelitis)


subsequent forms dense scar tissue

• encircled dead space acts as reservoir for bacteria

• antibiotic medications have great difficulty reaching the site


Clinical Features

if acute osteomyelitis is not resolved expeditiously

entrenchment of chronic osteomyelitis occurs

sometimes may arise without previous acute episode


Clinical Features

swelling pain sinus formation purulent discharge sequestrum formation tooth loss pathologic fracture


Clinical Features

may experience acute exacerbations or periods of decreased pain associated with chronic smoldering progression


Histophathologic Features

biopsy material from patient• soft tissue component

• consists of chronically or subacutely inflammed connective tissue filling the intertrabecular areas of bone

• scattered sequestra + pockets of abscess formation



patchy ragged ill-defined radiolucency

• often contains central radiopaque sequestra




Treatment

difficult to manage medically

• pockets of dead bone• organisms are protected

from antibiotic drugs

due to surrounding wall of fibrous connective tissue


Treatment

surgical intervention is mandatory

antibiotic medications are similar to those used in acute form

• but must be given intravenously in high doses


COMPLICATIONS

Complications:Several sequalae/complications can

occur as a result of OML of jaws.

1. Neoplastic transformation:With chronic OML,

neoplastic conversion of inflammatory metaplasia

to squamous cell carcinoma is noted. The incidence

reported is 0.2 to 1.5 percent.

2. Discontinuity defects:The defects can be (a) spontaneous or (b) surgically induced; necessitating

jaw reconstruction; once infection is resolved

(Figs 41.11A to D).

3. Progressive diffuse sclerosis:It involves the medullary

and cortical portions of maxillofacial skeleton;

especially mandible, over a period of time.

HBO THERAPY

SURGICAL THERAPY

The surgical treatment

modalities include: (1) Incision and drainage

(2) Extraction of loose or offending teeth (3) Debridement (4) Decortication (5) Continuous or

Intermittent indwelling closed catheter irrigation

(6) Sequestrectomy (7) Saucerization (8) Resection

of jaw (9) Trephination (10)

Immediate or delayed reconstruction with bone

graft.

Surgical intervention is done under antibiotic cover,

started at least, 1 to 2 days prior to the procedure.

ANTIBIOTIC PROPHYLAXIS

DISADVANTAGES OF AB PROPHYThey may alter host natural flora

Development of antibiotic resistant microorganisms

They may provide no benefit

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orofacial infections.pptx