Orofacial Infections In Paediatric Dentistry

Course Information¹

Course Code: DENT 5312
Module: Paediatric Dentistry Module
Focus: Diagnosis and management of common orofacial infections, with a primary emphasis on viral conditions.

Presenter Details

Dr Jilen Patel
- Specialist Paediatric Dentist
- Senior Lecturer, Clinical Dentistry
- UWA Dental School

Introduction and Recommended Resources

Required Reading² readings

Handbook of Pediatric Dentistry
- Authors: Cameron and Widmer (4th Edition)
- Access: Ebook available through UWA Onesearch
  - Chapter 10 is considered a "must-read" resource as it provides concise snippets of conditions with extensive clinical imagery.

Specific Study Areas

Chapter 10: Paediatric oral medicine, oral pathology and radiology

Learning Objectives

Understanding the scope of practice regarding pharmacological management.

Knowledge of drug dosages based on pediatric age and weight.

Triaging: Determining if a case requires immediate Emergency Department (ED) referral or specialist consultation.

Diagnostic Framework

The Diagnostic Sieve (VITAMIND IC)³

The diagnostic sieve is a structured framework used to categorize potential causes of a clinical presentation.

Letter	Category
V	VASCULAR
I	INFLAMMATORY
T	TRAUMATIC
A	AUTOIMMUNE
M	METABOLIC
I	INFECTION
N	NEOPLASTIC
D	DEGENERATIVE
I	IDIOPATHIC
C	CONGENITAL

- ==Vascular: Red/purple hue, blanches under pressure (e.g., venous malformations).==
- ==Inflammatory: Cardinal signs of inflammation (e.g., gingivitis).==
- ==Traumatic: Requires history of injury (e.g., cheek biting post-local anesthetic).==
- ==Autoimmune: Oral manifestations of systemic disease (e.g., Sjogren’s syndrome, Lupus).==
- ==Metabolic: (e.g., Diabetes-related oral changes).==
- ==Neoplastic: Assessing changes in size, shape, and displacement of structures (e.g., Squamous cell carcinoma).==
- ==Degenerative: Rare in children (e.g., TMJ osteoarthritis).==
- ==Idiopathic: Unknown etiology (e.g., idiopathic root resorption).==    - ==Congenital: Present from birth (e.g., Port-wine stain/Sturge-Weber syndrome).==

Differential Diagnosis of Orofacial Infections⁴

Orofacial infections in paediatric dentistry are generally categorized into three primary types:

Bacterial
Viral
Fungal

Bacterial Infections

Odontogenic Infections
- Dental caries
- Periodontal disease
Systemic and Localized Bacterial Infections
- Scarlet fever
- Tuberculosis
- Atypical mycobacterial infection
- Actinomycosis
- Syphilis
- Impetigo
- Osteomyelitis

Fungal Infections⁵

Candidosis

Bacterial and Viral Differential List⁶

Bacterial
- Odontogenic (dental caries, periodontal disease)
- Scarlet fever
- Tuberculosis
- Atypical mycobacterial infection
- Actinomycosis
- Syphilis
- Impetigo
- Osteomyelitis

Management of Bacterial Infections

First-line treatment for localized infection is source removal (extraction/pulpotomy). Antibiotics are reserved for systemic involvement.

Viral
- Primary herpetic gingiva-stomatitis
- Herpes labialis
- Herpangina
- Hand, foot and mouth disease
- Infectious mononucleosis
- Varicella

Fungal

Candidosis

Viral Infections Overview⁷⁸

Virus	Disease
Herpes Simplex Virus Type 1 (HSV)	• Primary herpetic gingivostomatitis • Herpes labialis
Epstein Barr virus (EBV)	Infectious mononucleosis
Coxsackie A, B, enterovirus 71	Hand foot and mouth disease
Coxsackie A	Herpangina
Varicella Zoster Virus (VZV)	Chickenpox

Visual clinical markers of viral orofacial infections often include redness, blisters, and ulcerations on the lips and tongue, characteristic of the Herpes Simplex Virus family.

Viral Diagnosis

Ulceration is the most common manifestation of herpes simplex . Diagnosis relies on background history, systemic signs, and the specific location/pattern of oral ulcers.

Primary Herpetic Gingivostomatitis

Etiology and Epidemiology

Viral Agents⁹

Herpes simplex type 1 virus
Herpes simplex type 2 virus (occasional cases related to genital herpes or sexual abuse)

Demographics

Age: Primary infection usually occurs after 6 months of age, with peak incidence between 12 and 18 months.
- Approximately 60% of the population is infected with the virus, though only about 1% of those infected will manifest acute primary symptoms.
- The peak incidence around 6 months of age often coincides with the eruption of the lower incisors.
Gender: No gender predilection.

Clinical Presentation¹⁰

General Systemic Features¹¹

Febrile illness (37.8-38.9 °C / 100-102 °F)
Headaches, malaise, and irritability
Cervical lymphadenopathy
- Difficulty eating and drinking due to pain, which presents a significant risk of dehydration.

Oral Manifestations

Oral pain and mild dysphagia
Stomatitis
Vesicles: Characteristic intraepithelial fluid-filled vesicles appearing on the tongue, lips, buccal, and palatal mucosa.
Ulcerations:
- Solitary ulcers: Small (3 mm), painful, with erythematous margins.
- Larger ulcers: Irregular margins resulting from the coalescence of individual lesions. - Ulcers are typically well-demarcated, featuring a characteristic red halo and a yellow or grey central slough.

Clinical presentation of Primary Herpetic Gingivostomatitis typically involves widespread oral lesions and significant gingival inflammation.

Gingival Involvement¹²

Painful, enlarged, and erythematous palatal gingiva.
Painful, enlarged, and erythematous facial gingiva.
Notable erosions of the free gingival margin.
- Gingiva appears diffuse, erythematous, and shiny.
- Significant edema and friable tissues often lead to spontaneous bleeding.

Transmission and Disease Course

Incubation and Transmission¹³

Incubation Time: 3–5 days, often preceded by a 48-hour prodromal history of irritability, pyrexia, and malaise.
Transmission:
- Direct contact with active lesions.
- Contact with infected oral secretions (droplet infection).

Prevention of Autoinoculation

Children should be closely monitored and discouraged from touching their mouths and subsequently touching their eyes to prevent the spread of the infection (herpetic keratoconjunctivitis).

Disease Course

The disease is self-limiting.
Ulcers typically heal spontaneously without scarring within 10–14 days.
- Following the primary infection, the virus travels to the neuronal ganglia (typically the trigeminal ganglion) where it remains in a latent state.

Histology and Diagnosis

Histopathological Features¹⁴

Tzanck Cells: Multinucleated giant cells with a “jig-saw” nucleus.
Viral Inclusion Bodies: Present within affected tissues.

Diagnostic Methods

Clinical Assessment: Based on history, clinical features, and the age group of the child.
Exfoliative Cytology: Rapid diagnosis via identification of multinucleated giant cells.
Laboratory Testing:
- Viral antigen testing
- Viral culture
- Viral antibody detection in blood samples - Diagnosis can be confirmed via a viral swab of the lesions if the clinical presentation is unclear.

Differential Diagnosis and Complications

Differential Diagnosis¹⁵

Necrotizing ulcerative gingivitis
Erythema multiforme
Herpangina

Complications¹⁶

While rare, severe complications can include:

Aseptic meningitis
Encephalitis

Management and Pharmacotherapy

Symptomatic Care¹⁷

Encourage high fluid intake.
Recommend bed rest and a soft diet.

Analgesics and Pain Control

Paracetamol: 15 mg/kg, every 4-6 hours.
Topical Therapy Precautions:
- 2% viscous lidocaine is not recommended due to systemic overdose risks and the child’s inability to spit.
- Topical benzocaine gel should be avoided in children under 6 years old to prevent methaemoglobinaemia.

Mouthwashes¹⁸

Young Children (Severe Ulceration): 0.2% chlorhexidine may be swabbed over affected areas using cotton wool.
Older Children: Chlorhexidine gluconate 0.2%, 10 mL every 4 hours.
Children Over 12 Years: Tetracycline or minocycline mouthwashes may be beneficial.
Combination Therapy: Benzadamine hydrochloride 0.15% & chlorhexidine 0.12% (Difflam C™) may offer advantages over chlorhexidine alone.

Antiviral Chemotherapy¹⁹

Aciclovir: Approved for use in children for managing primary herpetic gingivostomatitis.
Timing: Administration within the first 72–96 hours of infection provides the most benefit.
- Aciclovir is most effective when administered during the prodromal phase; its efficacy during the eruptive phase is currently a subject of clinical debate.
Dosage:
- Oral (PO): 20 mg/kg body weight, 5 times daily (or TDS depending on clinical guidance).
- Intravenous (IV): 10 mg/kg body weight.
Note: Evidence for oral use in children under two years of age is limited.

Herpes Labialis

Etiology and Triggers

Etiology and Site²⁰

Agent: Herpes simplex type 1 virus
Recurrent/secondary activation of latent HSV
Occurs at the mucocutaneous junction of the lip.
Common Names: Cold sore, fever blister.
Site: Vermilion border and adjacent skin of the lips.

Triggering Factors

Ultraviolet (UV) light
Physical trauma
Stress
Fever
Seasonal changes

Clinical Signs and Symptoms

Prodromal Phase²¹

Symptoms are most severe in the first 8 hours.
Sensations: Pain, burning, itching, tingling, and localized warmth.
Erythema appears 6–24 hours before lesions develop.

Lesion Development

Multiple small, erythematous papules develop.
These form clusters of fluid-filled vesicles.
Vesicles typically rupture and crust within 2 days.

Course of Disease

Self-limiting; healing usually occurs within 7 to 10 days.

Clinical Progression Summary²²

Initial 8 Hours: Peak prodromal symptoms (tingling, itching).
6–24 Hours: Erythema of the involved epithelium.
Vesicular Stage: Formation of fluid-filled clusters.
Crusting Stage: Rupture and crusting within 48 hours.
Resolution: Spontaneous healing in 7–10 days.

Infectious Mononucleosis

Etiology and Transmission

Etiology²³

Agent: Epstein-Barr virus (EBV or HHV-4).
Terminology: Mono, Glandular Fever, Kissing Disease.

Transmission

Occurs via intimate contact, primarily through blood or saliva.
Children: Often infected via contaminated saliva on fingers, toys, or objects.
Adults: Direct salivary transfer (e.g., shared straws, kissing).
Persistence: Once exposed, EBV remains in the host for life.

Demographics

Common in children aged 1 to 5 (often asymptomatic).
No specific gender predilection noted.

Clinical Presentation and Oral Lesions²⁴


	Hyperplastic Pharyngeal tonsils with yellowish crypt exudates
Numerous Petechiae of the soft palate

Systemic Symptoms²⁵

Low-grade fever
Hepatosplenomegaly
Rhinitis or cough
Malaise and headache
Cervical lymphadenopathy and tenderness
- Posterior cervical chain involvement is particularly characteristic

Oral Lesions

Oral ulcers
Palatal petechiae
- Pinpoint hemorrhages typically located on the soft palate
Gingival ulcerations (Necrotizing Ulcerative Gingivitis)
Tonsillitis with or without pharyngitis

Disease Course

Self-limiting; typically resolves within one to two weeks. Young adults are at the highest risk for symptomatic disease.

Histopathology and Differential Diagnosis

Histopathology²⁶

Downey Cells: Atypical lymphocytes; considered a diagnostic feature.

Differential Diagnosis

Trauma
Reactive gingival lesions
Hematologic Disorders:
- Thrombocytopenia
- Platelet disorders
- Hereditary hemorrhagic telangiectasia

Diagnosis and Treatment

Diagnostic Criteria²⁷

Clinical history and presentation.
Identification of atypical lymphocytes on a blood film.
Heterophile Antibody Tests:
- Monospot test
- Paul–Bunnell agglutination test
Advanced Testing:
- Indirect immunofluorescent assays
- Real-time PCR

Treatment Protocol²⁸

Most cases resolve spontaneously within 4 to 6 weeks.
Supportive Care:
- Bed rest
- Maintenance of fluid intake and adequate nutrition
- Analgesia and antipyretics

Complications of EBV

Significant Complications²⁹

Splenic rupture
Thrombocytopenia
Autoimmune hemolytic anemia
Aplastic anemia
Neurologic problems
Myocarditis
Hemophagocytic lymphohistiocytosis
Chronic fatigue (lasting weeks to months in <10% of cases)
Increased risk for developing multiple sclerosis later in life

Discovery of Epstein Barr Virus

Historical Context³⁰

Discovered by M.A. Epstein, B.G. Achong, and Y.S. Barr in 1964.

Connection to Burkitt Lymphoma

In 1958, Dr. Burkitt identified aggressive jaw tumors in African children (Burkitt Lymphoma). By 1964, Anthony Epstein and Yvonne Barr identified viral particles in these B-cell lymphocytes using electron microscopy.

Virology

Electron microscopy reveals immature virions and mature enveloped particles.
Identified as a member of the herpesvirus family based on structural characteristics.
EBV specifically infects B-cells, causing rapid division
Genetic "mistakes" during this rapid division, combined with the virus, can lead to the development of Burkitt Lymphoma