infections of oro facial & neck region a

8/2/2019 Infections of Oro Facial & Neck Region A

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ODONTOGENIC INFECTIONSOF ORO FACIAL & NECK

REGION


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ETIOLOGY1

General classification: Odontogenic:

Pulp disease. Periodontal disease. Secondarily infected cysts or odontomes.

Remaining root fragment. Residual infection. Pericoronal infection.

Traumatic: Penetrating soft & hard tissue wounds.

Implant & reconstructive surgery Others:

Infected antrum. Salivary gland afflictions. Secondary to oral malignancies.


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Odontogenic infections1

Acute.

Chronic.

In the acute stage infection may remain intra bony

or spread into soft tissues in following clinicalforms:

1.Abscess.1.Circumscribed collection of pus in a pathological tissue

space.

2.It is a thick walled cavity containing pus.

3.Suppurative infections characteristic of staphylococci &anaerobes--- large accumulation of pus--- pointing &drainage.


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Abscess


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2.Cellulitis.1.This is spreading infection of loose CT.

2.It is a diffuse, erythematous, mucosal or

cutaneous infection.3.It is result of streptococci & does not result in largeaccumulation of pus.

4.Streptococci produce streptokinase (fibrinolysin),hyaluronidase & streptodornase.

5.These break down fibrin & CT ground substanceand lyse cellular debris, thus spread of exudationalong the tissue planes.


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Cellulitis


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3.Fulminating infections.1.Spread of infection in various primary spaces in

the orofacial region.

2.Here secondary spaces along the pathway of leastresistance are involved.

3.Spread of deep cervical spaces and beyond.


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Acute Peri Apical Abscess1

An abscess arises and remains in the confinesof space between the root apex & the alveolarbone.

This is due to vascular dilatation, an exudate ofneutrophil leucocytes & oedema in the peri apicalregion.

it is due to persistent irritation from chronic pulpor acute virulent infection, or less hostresistance.


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ETIOLOGY:

Main cause is infective necrosis of pulp whichis due to;

Caries.

Traumatic exposure of pulp.

Sterile necrosis apical vessels are torn by blowon teeth.

Chemical or thermal damage to pulp.

Entry of micro-organism in peri apical tissues


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is usually through;

Apical foramina.

Bacteria or bacterial by products or toxins from necrotic pulp.

Endodontic perforation.

Chemical Irritation.

Accessory canals.

Root fracture.

Clinical features: History of previous pulpitis.

Carious or heavily filled tooth.


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Tooth is tender and felt extruded in the tooth socket.

When pus has formed there is severe throbbing painin the affected tooth.

Tooth is sensitive to percussion. Over lying gum may or may not be swollen

Mobility may or may not be present.

Radiographic presentation:

Little informative in initial stages.


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Treatment :

Antibiotics ,Analgesics & Drainage throughpulp chamber.

Extraction or endodontic treatment.


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Acute Dento Alveolar Abscess1

This is continuation of peri apical abscess.

When pus does not remain confined to intrabony or in the peri apical region.

It perforates the cortex and comes to lie underperiosteum--- SUB PERIOSTEAL ABSCESS.

The perforating the abscess come into the

soft tissues then called as Acute DentoAlveolar Abscess.


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Clinical features:

Pain depend on the stage of disease.

Sub mucosal swelling in the sulcus,usually on outer aspect of alveolarprocess.

Fluctuation may come after few days. If untreated may point or burst producing a

discharging sinus.


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Radiographic features:

Little informative in acute phase exceptlittle widening of periodontal ligament.

But previous pathology if present will beseen.

Treatment: Same i.e. endo or ext.

Plus intra or extra oral drainage.


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Acute Periodontal Abscess

Arise in periodontal membrane fromadjacent periodontal pocket.

Dull pain, rarely severe.

Pus discharge via gingival pocket.

May produce a sinus on alveolar process.

Historically it was called PAROLIS.


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CHRONIC PERI APICALPERIODONTITIS1

When the irritation in the peri apicaltissues persists either due incompleteresolution or treatment of acute

periodontitis or pulpitis leading to necroticpulp or a forgotten blow or massive fillingsor unsuccessful R.C.T lead to chronic

periodontitis. This goes on painlessly and chronic


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periodontitis converts in to granulationtissue, which grows and causes theresorption of surrounding bone by the

initiation of osteoclastosis and becomeseparated from the surrounding bone by alayer of collagen. This lesion is called the

DENTAL GRANULOMA.


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SIGNS AND SYMPTOMS

Usually no symptoms and it is chancefinding on routine X-rays.

Involved tooth is discolored and non-vital.

Some times there is mild discomfort or

intermittent pain, tooth may be slightlytender to percussion and over lying gumtissues opposite tooth apex may also


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tender to touch.

If pus has formed in side the granuloma(Central Abscess) there will be local tissueswelling and pus may penetrate thetissues forming chronic discharging sinus.

In long standing cases pus may track tothe skin forming extra-oral skin sinus.


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PATHOLOGY

It is the typical chronic inflammatoryreaction that is infiltration of Lymphocytes,Plasma cells and Macrophages.


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RADIOGRAPHY

There is well circumscribed radiolucentarea around the apex and is due to theresorption of bone around the granuloma.

This is usually with in the limits of 5mm.More than 5mm and if out line is sharplydefined than cyst is forming but is alwaysconfirmed by histopathology.


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CHRONIC PERI APICALPERIODONTITIS


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BACTERIOLOGY

Some granulomas are sterile but bacteriacan be cultured from many and mixedinfection is the rule.


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Dental granuloma grows symptomlesslycausing resorption of bone or the rootapex

Central abscess formation chronicsinus or track to the skin to form the Skinsinus.

Acute exacerbation


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Skin Sinus Due Chronic infectionfrom deciduous molar


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Spreading type of infection

Into soft tissueintra oral or extra oralswelling or abscess depending on muscleattachments.

Spread into adjacent surgical spacesalong facial planes cellulitis.

More dangerous distant spread


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Maxillary teeth

Molars

PALATAL ABSCESS

BUCCAL VESTIBULAR/ SULCULAR ABSCESS

FACIAL SWELLING OR ABSESS which maylead to cellilitis.


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Anterior & Premolars.

Palatal abscess.

Labial abscess.

Cellulitis from maxillary teeth cause swelling ofupper half of face direction towards eye maycause dangerous complicationCAVERNOUS SINUS THROMBOSIS.


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Mandibular premolars and molars.

Labial or buccal vestibular / sulcular abscess.

Lingual palate perforation depending on

mylohyoid muscle infection or pus orexudation may involve submandibular/sublingual spacesLUDWIGS ANGINA.


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Mandibular anterior teeth.

Incisors or canines.

If pus perforate above mentalis labial abscess.

Below insertion of mentalis cause subcutaneousabscess. Most often between two mentalismuscles.


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Usually odontogenic infection remainedconfined in the peri apical area orperiodontal pockets.

Peri apical infections may perforate cortexand form local abscess or spread intramedullary chronic infection or focal

osteomyelitis.


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But depending on;

The number and virulence of microorganisms, type and severity of mechanical or

chemical irritant and defense of the host; Or initial PAI is not completely or adequately

treated.

It may lead to spreading type of infectionCellulitis.

Or may spread to adjacent facial and cervical ordistant spaces


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FACIAL SPACES

Fascialined areas-- potential spaces thatdo not exist in healthy persons.

They become filled by pus or exudationduring infection.

Some contain neurovascular structurecompartments.

Others filled with loose areolar CT-- Clefts


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Primary facial spaces

Primary spaces are adjacent to tooth bearingarea & are directly involved by infection.

Primary maxillary spaces.

Canine

Buccal

Infratemporal.

Primary mandibular spaces.

Submental.

Buccal.

Submandibular.

Sublingual.


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Secondary Facial Spaces

Secondary spaces are away or lie moreposteriorly tooth bearing area and arelined with a CT fascia which has poor

blood supply.

Involvement of these spaces producemore complicated infective conditions.

They are;


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Masseteric.

Pterygomandibular.

Superficial & deep temporal.This group is also known as the

MASTICATOR SPACE because muscle &fascia of mastication bound them.


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Cervical Facial Spaces

Uncommon occurrence.

But spread to deep cervical spaces may have

life threatening sequelae. Lateral pharyngeal.

Retropharyngeal.

Prevertebral.


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PRIMARY MAXILLARY SPACES


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Primary mandibular spaces 1


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When bilateralsubmandibular,sublingual & submentalspaces become involved

--- Ludwig's angina. It is a rapidly spreading

cellulitis and commonlyspread to secondary

mandibular spaces. This usually produce life

threatening condition.


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Cervical Facial Spaces


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Principles of management

Determine the severity of infection

Evaluate the state of patients host defensemechanism

Determine , whether treated by GDP or refer tospecialist Appropriate antibiotic & their proper

administration

Treat infection surgically

Diet & i-v fluids

Evaluate pts frequently


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MANAGEMENT

Proper diagnosis.

Antibiotics.

Other Adjuncts.

I & D


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infections of oro facial & neck region a

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