DMD 19. Dentoalveolar infections

Dentoalveolar Infection

• Definition: Refers to pyogenic (pus-forming) conditions affecting teeth and

• supporting structures.

• polymicrobial infection

  • Examples include:

    • Periodontal abscess (lateral periodontal abscess)

    • Acute dentoalveolar abscess (acute periapical abscess)

• Differentiation between them

  • Periodontal abscess is associated with a vital pulp.

  • Acute dentoalveolar abscess indicates necrotic pulp at root apex.

• Pathogenesis:

  • Majority are preceded by chronic infection.

  • Bacterial access to apical tissue through:

    • Direct spread from the pulp chamber

    • Periodontal membrane on root surface

    • Local blood vessels

Microbiology of Dentoalveolar Infections

• Role of bacteria in infections is well-established.

• Currently, no single causative pathogen is identified, classifying these infections as polymicrobial infections.

Types of Dentoalveolar Infections

• Includes:

  • Dentoalveolar abscess

  • Periodontal abscess

  • Ludwig's angina

  • Osteomyelitis

  • Actinomycosis

Periodontal Abscess

• Caused by blockage in established periodontal pockets, sometimes due to foreign body impaction (e.g., toothbrush bristle).

• Leads to infection extension into supporting tissues, evidenced by pus exudate after probing.

Bacteria Associated with Periodontal Abscess

• Obligate Anaerobes ( gram -ve)

  • Porphyromonas spp.; Porphyromonas gingivalis

  • Prevotella spp.; Prevotella intermedia

  • Fusobacterium spp.; Fusobacterium nucleatum

  • others - spirochaete - Treponema denticola

• faculatative anaerobes

  Streptococci -Alpha-haemolytic - Streptococcus mutans

Dentoalveolar Abscess

• Arises typically due to:

  1. Caries extending into dentine and reaching pulp via dentinal tubules

  2. Pulpal exposure from trauma/fracture

  3. Infections spreading from periodontium (gingiva, alveolar bone, etc.

  4. via circulation (anachoresis, bacteria seeding from bloodstream)

Bacteria Associated with dentoalveolar Abscess

Obligate anaerobes

 Peptostreptococcus spp.

 Porphyromonas gingivalis

 Prevotella intermedia

 Prevotella melaninogenica

 Fusobacterium nucleatum

Facultative anaerobes

 Streptococcus milleri

 Streptococcus sanguinis

 Actinomyces spp.

samples can be collected from dentoalveolar abscess by direct aspiration of pus into sterile syringe or aper points

microscopy, culture sensitivity of samples - directing antomicrobial therapy (for sever case)

Spread of Infection

• Risks if dental abscesses are untreated:

  • Can progress into fascial spaces beyond the oral cavity leading to serious conditions like Ludwig's angina. - life threating

• Direct Spread:

  • Into superficial soft tissues, adjacent fascial spaces (e.g., Ludwig’s angina), alveolar bone (osteomyelitis), maxillary sinus

• Indirect Spread:

  • Through lymphatic or hematogenous routes

• infection in the anterior mandible spreads to the sublingual space

• infection in the posterior mandible spreads to the submandibular space

• *infection in 3rd molar wisdom tooth - which is located at the junction of varies facial space. easily spread along fascial planes and compromise the airway

Ludwig’s Angina

• Description: A rapidly spreading cellulitis (subcutanous ) in the floor of the mouth. Submandibular space infection

• Characteristics:

  • Potential for airway obstruction. - angina - strangling and choking feeling

  • Swelling of anterior tissue can lead to a ‘bull's neck’ appearance.

  • Urgent hospitalization required for management.

Bacteriology of Ludwig’s Angina

• Majority caused by dental infections; cultures show oral cavity flora.

• Common Organisms:

  • Anaerobic Gram-negative bacilli, alpha-haemolytic streptococci, Staphylococci, Enterobacteria.

• Treatment: Urgent hospitalization for tracheostomy and drainage due to combination of aerobic and anerobic organism - syneregistic effect - producing protease (collagenase, hyaluronidase), rapidly spreading cellulitis.

Sialadenitis

• Definition: Inflammation of salivary glands from bacterial or viral infections.

• Mechanism: In health, saliva prevents bacterial ascension through ascending parotid duct and invading the salivary gland tissue by the natural flushing activity of saliva

• infections occur with reduced salivary flow (xerostomia) or abnormal gland architecture.

Predisposing Factors for Bacterial Sialadenitis

• Factors include:

  • Oral microorganisms

  • reduced salivary flow by drugs (e.g., opiates), irradiation, Sjogren’s syndrome, dehydration

  • salivary gland infection

  • abnormal gland architecture, sialoliths (stones), strictures (narrowing of duct), sialectasis dilation of duct)

Management of Bacterial Sialadenitis

• Conditions leading to bacterial sialadenitis include calculi, duct stricture, dehydration, and poor oral hygiene.

  • Particularly common in hospitalized patients receiving multiple medications affecting oral flora.

  • if patient is not eating - > salivary flow further reduce

• Results in ascending infections potentially leading to suppuration within the gland.

• Treatment - anti-staphyloccal antibiotics - dicloxacillin, amoxillin, cephalosporin, clindamycin

Bacteria Associated with Bacterial Sialadenitis

• Main pathogens include:

  • Alpha-haemolytic streptococci, Staphylococcus aureus, and occasionally: Haemophilus spp., Eikenella corrodens, Bacteroides spp., facultative anaerobic streptococci, Mycobacterium tuberculosis, Actinomyces.

Viral Sialadenitis

• More common in children.

• Common Viruses:

  • Paramyxoviridae (mumps), Epstein-Barr virus, Coxsackie A, Cytomegalovirus, influenza.

• Characteristic of mumps: viral infection of the parotid glands, Bilateral parotid swelling resembling “hamster cheeks.”in children