Localized Acute Alveolar Osteomyelitis (Dry Socket / Alveolar Osteitis)

Definition

Pathophysiology

Incidence

• Occurs in 2-5% of routine extractions
• Rises to 20-30% after removal of impacted mandibular third molars
• More common in the lower jaw (mandible) - the maxilla is rarely affected due to its rich anastomotic blood supply from vertical arteries - Rosen's Emergency Medicine

Predisposing Factors

1. Excessive trauma during extraction
2. Inadequate blood supply to the extraction site
3. Pre-existing localized infection / pericoronitis
4. Loss of clot from sucking, straw use, rinsing, or smoking (increased negative intraoral pressure)
5. Foreign bodies remaining in the socket
6. Use of oral contraceptives or corticosteroids
7. Hormone replacement therapy
8. Periodontal disease
9. Familial tendency - Roberts & Hedges' Clinical Procedures in Emergency Medicine; Scott-Brown's Otorhinolaryngology

Clinical Features

• Onset: 2-5 days after tooth extraction (typically day 3-4)
• Pain: Moderate to severe, dull, constant, and aching - localized to the extraction site and often radiating to the ear
• Foul odor / bad taste in the mouth - in the absence of purulence or suppuration
• Duration: Can persist for 5-40 days if untreated
• Examination: Missing clot at the socket, exposed bare alveolar bone - NO significant surrounding edema, erythema, fluctuation, fever, leukocytosis, or lymphadenitis (which would suggest osteomyelitis)

Differential Diagnosis

Treatment

1. Nerve block - provides immediate pain relief; also confirms the diagnosis
2. Irrigation - gently irrigate the socket with sterile saline to remove debris; do NOT curette the socket or remove residual clot (this exposes more bone and risks osteomyelitis)
3. Socket packing - fill with medicated iodoform gauze impregnated with eugenol (oil of cloves) or a local anesthetic, packed to the level of the gingival cusps; change every 24-36 hours
4. Dry Socket Paste (e.g., Sultan Healthcare) - a commercial alternative to eugenol-soaked gauze
5. Analgesics - NSAIDs work better than narcotics for dry socket; short course of opioids (e.g., oxycodone 5 mg q4-6h) for severe pain
6. Chlorhexidine rinses - shown to prevent alveolar osteitis; role in established disease is less clear
7. Antibiotics - not routinely required once the socket is packed; prescribed at the discretion of the treating oral surgeon

Relation to Osteomyelitis of the Jaw

• (i) Acute - seen in infants post-febrile illness (measles, scarlet fever)
• (ii) Subacute - the commonest form; follows dental infection or alveolar abscess; causes endarteritis, reduced blood supply, and bone necrosis; presents with pain, swelling, numbness of chin (inferior dental nerve compression)
• (iii) Chronic - follows dental infection or fractures; X-ray shows local osteitis, localized abscess (like Brodie's abscess), or sequestrum formation - S. Das, Manual on Clinical Surgery, 13th Edition

Primary Herpetic Stomatitis (Acute Herpetic Gingivostomatitis)

Definition

Aetiology / Causative Agent

• HSV-1 - responsible for ~90% of cases
• HSV-2 - can also cause primary orofacial infection, particularly in adolescents and young adults following genital-oral contact; clinically indistinguishable from HSV-1 disease but 120 times less likely to reactivate
• Fitzpatrick's Dermatology, 9e

Mode of Transmission

• Direct contact with infectious oral secretions - the primary route; typically transmitted from caregivers (parents, relatives) who may shed virus asymptomatically or during a cold sore
• Saliva - virus is shed in saliva even during asymptomatic periods; ~12% of oral swabs are PCR-positive for HSV in seropositive individuals
• Droplet / contact with infected mucocutaneous surfaces - kissing, shared utensils, or contact with vesicle fluid
• Self-inoculation - from oral lesions to fingers (herpetic whitlow) or eyes
• Incubation period: 2-12 days (mean 4 days)
• Important: Even asymptomatic individuals can transmit the virus; >70% of transmission occurs during asymptomatic shedding
• Tintinalli's Emergency Medicine; Fitzpatrick's Dermatology

Clinical Features

Epidemiology

• Peak age: 6 months to 5 years (most common in children 2-4 years)
• Can occur in older children and adults, though primary adult infection more commonly presents as pharyngitis
• Up to 90% of the population is infected before puberty, but only ~20% develop symptomatic disease
• Robbins Pathologic Basis of Disease; Tintinalli's

Systemic / General Features

• Abrupt onset of high fever (often the presenting complaint)
• Irritability and malaise
• Decreased oral intake and drooling - due to pain on swallowing
• Myalgias and flu-like symptoms
• Tender cervical lymphadenopathy
• Symptoms typically last up to 3 weeks but commonly resolve in less than 1 week

Oral Manifestations

Primary herpetic gingivostomatitis with whitish ulcerations on the lip mucosa - Fitzpatrick's Dermatology

Typical vesicular/ulcerative lesions of herpetic gingivostomatitis on buccal mucosa - Tintinalli's Emergency Medicine

1. Swollen, erythematous, friable gingiva - bright red, bleeding gingiva is often the earliest sign
2. Vesicles - small fluid-filled blisters ranging from a few mm to large bullae, filled with clear serous fluid, appearing on oral mucosa
3. Painful shallow ulcerations - vesicles rapidly rupture to form red-rimmed shallow ulcers with a yellowish-grey pseudomembranous base
4. Distribution - hard and soft palate, tongue, buccal mucosa, gingiva, lips, and neighboring facial areas
5. Halitosis due to secondary bacterial colonization of lesions
6. Pain on eating/swallowing leading to dehydration in children

• Robbins Pathologic Basis of Disease; Fitzpatrick's Dermatology; Tintinalli's

Histologic Features

• Intracellular and intercellular edema (spongiosis) within the epithelium
• Acantholysis - dissolution of intercellular bridges creating clefts that become macroscopic vesicles
• Ballooning degeneration of keratinocytes
• Eosinophilic intranuclear viral inclusions (Cowdry type A bodies) - seen in individual epidermal cells at vesicle margins or free within vesicle fluid
• Multinucleated giant cells (polykaryons) - several infected cells fuse together; these are the diagnostic hallmark seen on Tzanck smear
• Vesicles are initially intraepidermal; roof may slough to leave ulcers
• Underlying lamina propria shows acute inflammatory infiltrate
• Robbins Pathologic Basis of Disease

Diagnosis

1. Clinical Diagnosis (Primary)

• Diagnosis is primarily clinical, based on the characteristic presentation of acute onset fever, irritable child with drooling, swollen red gingiva, and painful vesicles/ulcers in the oral cavity

2. Tzanck Smear

• Vesicle fluid from an unroofed lesion 24-48 hours old is smeared on a slide and stained
• Demonstrates multinucleated giant cells and eosinophilic intranuclear inclusions
• Rapid, bedside test - does not distinguish HSV-1 from HSV-2

3. Viral Culture

• The former gold standard
• Low sensitivity: only 7-25% recovery from lesions
• Swab the unroofed vesicle, place in viral transport medium
• Tintinalli's Emergency Medicine; Harriet Lane Handbook

4. PCR (Polymerase Chain Reaction)

• Most sensitive and specific - now preferred over culture
• Detects HSV DNA from vesicle fluid or lesion swab
• More accurate for lesions that have already partially healed

5. Serology

• Useful for confirming primary infection (seroconversion - rise in IgM / rising IgG titres)
• Not useful for acute diagnosis

6. Enzyme-linked immunosorbent assay (ELISA) / Direct Fluorescent Antibody (DFA)

• Additional acceptable laboratory methods
• Tintinalli's Emergency Medicine; Harriet Lane Handbook

Differential Diagnosis

Treatment

Supportive Care (All Cases)

• Antipyretics - paracetamol/ibuprofen for fever
• Topical analgesics - lidocaine gel or viscous lidocaine (used cautiously in young children)
• Oral rehydration - particularly important in children who refuse oral intake
• IV fluids if severe dehydration from inadequate oral intake
• Topical acyclovir cream is ineffective for oral HSV

Antiviral Therapy

• Children: 80 mg/kg/day in 4 divided doses for 5-7 days (max 3200 mg/day) - American Academy of Pediatrics regimen
• Alternative dosing: 600 mg/m² four times daily for 10 days in children (Goodman & Gilman)
• Shortens duration of symptoms and viral shedding

• IV acyclovir 250 mg/m² every 8 h for 7 days
• Oral acyclovir 800 mg 5 times/day or valacyclovir 1000 mg twice daily for 5-10 days

Prevention

• Diligent hand washing among children and caregivers
• Avoid sharing utensils, cups, or close oral contact during active infection
• Children with active gingivostomatitis who cannot control oral secretions should be excluded from child care settings
• Tintinalli's Emergency Medicine; Goodman & Gilman's Pharmacological Basis of Therapeutics; Harriet Lane Handbook

Latency and Recurrence

Recurrent Herpes Labialis (Cold Sore / Fever Blister)

Definition

Aetiology and Pathogenesis

• Robbins & Kumar Basic Pathology; Goldman-Cecil Medicine

Triggers for Reactivation

• Fitzpatrick's Dermatology; Robbins & Kumar

Clinical Features

Site

• Vermilion border of the lips - two-thirds of labial lesions involve this border
• Lower lip (outer one-third) is the most commonly affected area
• Less common: nose, chin, cheek (<10% of cases), nasal orifices
• Immunocompetent patients rarely get recurrent intraoral lesions; when present, they appear on the anterior hard palate or attached gingiva (keratinized mucosa only)

Stages of Classical Lesion Progression

Erythema and early vesicles of recurrent herpes labialis - Fitzpatrick's Dermatology

Grouped vesicles with overlying crust in established recurrent herpes labialis - Fitzpatrick's Dermatology

1. Prodrome - pain, burning, tingling, or itching at the site of impending eruption; precedes lesions in 45-60% of episodes
2. Erythema - localized redness appears at the site
3. Papule - small raised firm lesion

1. Vesicle - small (1-3 mm) fluid-filled blisters in clusters; tense, clear, on an erythematous base
2. Ulcer - vesicles rupture to form shallow, painful, red-rimmed ulcerations
3. Hard crust - ulcers dry and crust over with a honey-colored scab

1. Dry flaking - crust detaches
2. Residual swelling - mild erythema and swelling may persist briefly

• Lesions resolve in 5-15 days without treatment
• Severity is highly variable - may range from prodromal symptoms alone (aborted episode) to extensive disease from severe sunburn
• In patients with frequent recurrences, lesion location may shift slightly with each episode
• Fitzpatrick's Dermatology

Histologic Features

• Ballooning degeneration of keratinocytes with large eosinophilic intranuclear inclusions (Cowdry type A bodies)
• Multinucleated polykaryons (giant cells) - adjacent infected cells fuse together
• Intraepidermal vesicle formation from acantholysis and intercellular edema
• Inflammatory infiltrate in the underlying dermis/lamina propria
• Robbins & Kumar Basic Pathology

Comparison: Recurrent vs. Primary Infection

Diagnosis

• Primarily clinical - characteristic prodrome followed by grouped vesicles at the vermilion border in a known HSV-positive individual
• Tzanck smear - multinucleated giant cells from unroofed vesicle (does not distinguish HSV-1 from HSV-2)
• PCR - most sensitive; useful when diagnosis is in doubt
• Viral culture - from vesicle fluid (low sensitivity 7-25%)
• Serology - not useful for acute diagnosis in recurrent disease (IgG already positive)

Treatment

Topical Agents

Systemic (Episodic) Agents

Suppressive Therapy (for frequent recurrences)

• Oral acyclovir 400 mg twice daily - reduces recurrences; controversial benefit
• Valacyclovir suppressive therapy - more effective than episodic therapy for herpes labialis
• Perioperative prophylaxis (before facial laser resurfacing): famciclovir 125-250 mg twice daily or valacyclovir 500 mg twice daily starting 1-2 days before procedure

Adjunct Measures

• Sunscreen - shown to prevent sun-triggered recurrences in some trials
• No evidence for lysine supplementation or gammaglobulin
• A "holiday" from suppressive therapy every year or so to reassess the continuing need
• Fitzpatrick's Dermatology; Goodman & Gilman's Pharmacological Basis of Therapeutics

Complications

• Eczema herpeticum - widespread HSV superimposed on eczematous skin
• Herpetic whitlow - autoinoculation to fingers (especially in thumb-sucking children)
• Herpetic keratoconjunctivitis - corneal involvement; may cause dendritic ulcers and vision loss; requires ophthalmology referral and topical antivirals
• Erythema multiforme - HSV-triggered immune reaction
• Disseminated disease - in immunocompromised patients; may require IV acyclovir

Human Immunodeficiency Virus (HIV) - with Oral Manifestations

Definition and Aetiology

• HIV-1 - the predominant global cause; more virulent
• HIV-2 - mainly in West Africa; slower progression

Transmission

Pathogenesis

1. HIV binds gp120 to the CD4 receptor and co-receptors (CCR5 or CXCR4) on T helper cells and macrophages
2. Viral RNA is reverse-transcribed into DNA by reverse transcriptase
3. Viral DNA integrates into the host genome as a provirus via integrase
4. Progressive CD4+ T cell depletion leads to immune failure
5. The virus replicates continuously throughout infection; even during the clinically asymptomatic phase, active viral replication occurs in lymphoid tissue
6. When CD4 count falls below 200 cells/µL, opportunistic infections and AIDS-defining malignancies emerge

Clinical Stages

Oral Manifestations of HIV/AIDS

EC-Clearinghouse / WHO Classification of HIV-Associated Oral Lesions

• Oral candidiasis (pseudomembranous, erythematous, angular cheilitis)
• Oral hairy leukoplakia
• HIV-associated periodontal disease (linear gingival erythema, necrotizing ulcerative gingivitis/periodontitis)
• Kaposi sarcoma
• Non-Hodgkin lymphoma

• Recurrent aphthous stomatitis
• Herpes simplex / zoster reactivation
• Oral warts (HPV)
• Salivary gland disease

• Bacterial infections (Actinomyces, Klebsiella, Cat-scratch disease)
• Fungal infections (Cryptococcus, Histoplasma, Aspergillus)
• CMV oral ulceration
• Cummings Otolaryngology; K.J. Lee's Essential Otolaryngology

Detailed Oral Lesions

1. Oral Candidiasis (Most Common - ~90% of HIV/AIDS patients)

• CD4 >200: Topical antifungals (nystatin mouthwash, clotrimazole troches)
• CD4 <200: Systemic fluconazole
• Note: Prolonged/repeated fluconazole use risks azole-resistant candidiasis
• K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology

2. Oral Hairy Leukoplakia (OHL)

Oral hairy leukoplakia: corrugated white plaques on the lateral surface of the tongue - Harrison's Principles of Internal Medicine

• Cause: Reactivation of Epstein-Barr virus (EBV) in HIV-infected individuals
• Appearance: White, corrugated (hair-like), hyperkeratotic plaques on the lateral aspects of the tongue (bilateral); cannot be scraped off
• Symptoms: Usually asymptomatic - an incidental finding
• Significance: Strongly associated with HIV; its presence in a previously healthy individual should prompt HIV workup; correlates with degree of immune suppression
• Differential diagnosis: Leukoplakia, lichen planus, carcinoma in situ, oral thrush
• No malignant potential
• Diagnosis: Biopsy confirming EBV presence
• Treatment: No specific treatment required if asymptomatic; resolves with ART; local options include podophyllin, gentian violet, cryotherapy
• Fitzpatrick's Dermatology; K.J. Lee's Essential Otolaryngology; Harrison's

3. HIV-Associated Periodontal Disease

• Fiery red band of marginal gingiva, out of proportion with the degree of dental plaque
• Prone to spontaneous hemorrhage
• Persists despite conventional plaque removal
• Closely associated with oral candidiasis

• Ulceration of the interdental papillae with gingival bleeding, pain, rapid tissue sloughing, and halitosis
• Progressive recession; may invade the alveolar bone
• Strongly associated with CD4 count below 200 cells/µL
• Its presence in an otherwise healthy individual should prompt HIV testing

• Extension of necrotizing process into the mandibular or maxillary bone; the most severe form

• Topical chlorhexidine (0.1-0.2%) and povidone-iodine rinses
• Antifungals (co-existing candidiasis is common)
• Debridement of necrotic tissue and dental scaling
• Systemic clindamycin or metronidazole if no response
• Cummings Otolaryngology; K.J. Lee's Essential Otolaryngology

4. Kaposi Sarcoma (KS)

• Associated with HHV-8 (Human Herpesvirus 8)
• Typically affects the hard and soft palate; occasionally gingiva and buccal mucosa
• Appears as flat or raised, violaceous/purple, non-tender lesions
• May become nodular and ulcerate in advanced disease
• Diagnosis: Biopsy confirms spindle-cell vascular proliferation
• Treatment: Symptomatic; low-dose radiotherapy, intralesional vinblastine, or systemic chemotherapy when functionally problematic
• Cummings Otolaryngology; Scott-Brown's Otorhinolaryngology

5. Recurrent Aphthous Stomatitis (RAS) in HIV

• HIV patients develop unusually large, deep, and recalcitrant aphthous ulcers
• Very painful; cause severe odynophagia and substantial morbidity
• Treatment: Topical steroids, intralesional/systemic steroids, thalidomide, ART
• Biopsy confirms non-neoplastic, non-viral aetiology
• Scott-Brown's Otorhinolaryngology

6. Herpes Simplex Reactivation

• Presents as clusters of painful ulcers in the oral cavity
• In HIV/AIDS, lesions may be more extensive, persistent, and resistant to standard antiviral therapy
• Requires systemic acyclovir or valacyclovir; IV acyclovir for severe or refractory cases

7. CMV Oral Ulcers

• CMV co-infection occurs in ~90% of HIV cases
• Can cause painful oral ulcerations, often requiring biopsy to distinguish from other causes
• Also causes esophagitis and retinitis

8. Salivary Gland Disease

• Bilateral parotid swelling and xerostomia (dry mouth) can occur
• Dry mouth worsens dental caries and increases susceptibility to oral infections

Relationship Between Oral Lesions and CD4 Count

Treatment Overview

• K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology; Scott-Brown's; Fitzpatrick's Dermatology