Acute Oral Lesions Guide: Herpes, Canker Sores, Gingivitis
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This document discusses various acute oral lesions caused by viruses including herpes simplex virus, varicella zoster virus, and coxsackie virus. It describes primary and recurrent infections, complications, investigations, differential diagnoses, and management for conditions such as herpes labialis, herpes gingivostomatitis, chickenpox, hand foot and mouth disease, erythema multiforme, and stevens johnson syndrome. The document also covers plasma cell stomatitis, necrotizing ulcerative gingivitis, and hypersensitivity reactions of the oral cavity.
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Acute Oral Lesions Guide: Herpes, Canker Sores, Gingivitis
- 1. Acute Multiple Oral lesions By Amir Salaudin
- 7. Primary acute herpes simplex infection
- 10. Neonatal Herpes Simplex Virus (HSV) Infection
- 16. Recurrent HSV
- 17. Recurrent Herpes Labials (RHL)
- 18. Recurrent Intraoral Herpes (RIH)
- 21. Bell palsy
- 23. Corneal (keratitis); may cause blindness
- 24. Herpetic whitlow
- 25. Rare complications • HSV-1 appears to increase the risk of developing Alzheimer disease. • Meningitis, encephalitis and seizures specially in people with impaired immunity, such as infants whose immune responses are still developing, or immunocompromised patients. • Viremia and/or viral dissemination to any organ like skin, lung or liver.
- 26. Investigations • HSV culture or PCR. • Electron microscopy. • Confirmation serologically by the demonstration of a fourfold rise in antibody titer in acute samples. • Chair-side kits using immunofluorescence is the fastest, but its use limited by cost.
- 27. Tzanck test
- 28. Management
- 29. • A topical anesthetic agent 2 minutes before each meal. • Soft diet and adequate fluid intake. • Antipyretics/analgesics such as paracetamol relieve pain and fever. • Never ever use aspirin with children with any fever or illness suspected to be of viral origin, as this risks causing the serious and potentially fatal Reye syndrome (fatty liver plus encephalopathy).
- 30. • Acyclovir is safe and cheap antiviral agent. It is active only against virally infected cells, preventing viral dsDNA replication. • Acyclovir should be considered in severe cases, neonates and immunocompromised patients. • Acyclovir could help during itching and burning sensation stag to prevent RHL and RIH. • The standard regimen is 400 mg acyclovir 3-5 times daily for 7-10 days. The dosage should be halved in children under the age of 2 years.
- 31. HERPES VARICELLA-ZOSTER VIRUS INFECTIONS (VZV)
- 37. Diagnosis • Diagnosis is usually clinical. • Viral culture, PCR tests, immunostaining or electron microscopy are indicated mainly in immunocompromised patients.
- 38. Management • A child with chickenpox should stay home and rest until the rash is gone and all blisters have dried, usually about 1 week. • Paracetamol helps analgesia and to reduce fever. • Acyclovir may be indicated in adults, pregnant women, neonates or immunocompromised patients.
- 39. Secondary VZV infection Herpes Zoster; Shingles
- 44. Complications
- 46. Differential Diagnosis • 1. Trigeminal neuralgia. • 2. Maxillary sinusitis. • 3. Periodic migrainous neuralgia. • 4. Myocardial pain. • 5. Atypical facial pain. • 6. Munchausen’s syndrome.
- 47. Management • 1. Patient isolation • 2. Management of skin lesions • 3. Control and elimination of pain
- 48. 4. Antiviral drugs • Acyclovir 800 mg, 5 times daily, for 10 days. • Famciclovir 500 mg, 3 times daily, for 7 days. • Valacyclovir 1 gm 3, times daily, for 7 days.
- 49. 5. Management of PHN pain • The PHN pain is because of injury to the CNS and therefore is unlikely to respond to standard NSAID. • Treatment includes antidepressants, anticonvulsants (e.g. gabapentin), lidocaine patches or capsaicin lotion. Opioids may be required.
- 58. Complications • Meningoencephalitis. • Myocarditis. • thrombocytopenia.
- 63. Differential diagnosis • Single ulcers of acute onset present for weeks or months should be evaluated for squamous cell carcinoma or other malignancies. • In patients with human immunodeficiency virus (HIV)/AIDS, infections with mycobacteria, fungi, and other organisms must be ruled out. • Single ulcers on the tongue may also represent traumatic ulcerative granuloma.
- 65. Management
- 66. • No standard antiviral agent is available against this virus. Only palliative treatment with analgesics, antipyretics and antibiotics are given. • Immunocompromised and HIV patients : • Ganciclovir. • Valganciclovir. • Cidofovir. • Foscarnet.
- 70. Herpangina
- 75. HAND, FOOT AND MOUTH DISEASE
- 81. Necrotizing Ulcerative Gingivitis and Periodontitis (Vincent's angina) (trench mouth)
- 84. Complications
- 87. Differential diagnosis • Primary herpetic gingivostomatitis. • Desquamative gingivitides e.g; • Mucous membrane (cicatricial) pemphigoid. • pemphigus vulgaris. • Erosive Lichen planus. • Hypersensitivity reaction. • All may present primarily on the gingiva, with no skin findings. However, these conditions are not of acute onset but chronic and/or progressive, characterized by inflammation rather than necrosis.
- 88. Treatment • Oral debridement and hygiene instruction. • Hydrogen peroxide mouthwashes. • Metronidazole (penicillin in pregnant or lactating females). • Periodontal assessment.
- 96. Differential diagnosis • Toxic epidermal Necrolysis. • Viral stomatitis. • Pemphigus. • Subepithelial immune blistering disorders.
- 97. Management • Spontaneous healing can be slow, taking up to 2–3 weeks. • supportive care • Oral hygiene should be improved with 0.2% aqueous chlorhexidine mouth baths. • EM may respond to topical corticosteroids, although systemic corticosteroids may still be required. • Acyclovir or valacyclovir is used in herpes-associated EM. • Tetracycline is used in EM related to Mycoplasma pneumonia.
- 98. Stevens Johnson Syndrome and Toxic Epidermal Necrolysis (Lyell Disease)
- 105. Management • Withdrawal of causative drugs. • Urgent specialist referral to a burns or intensive care unit for treatment (with intravenous immunoglobulins. • High doses of systemic corticosteroids. • Supportive management.
- 106. Plasma cell stomatitis and Oral Hypersensitivity Reactions (contact stomatitis)
- 110. Differential diagnosis • Desquamative gingivitis; • erythematous/erosive lichen planus, and the autoimmune vesiculobullous disorders, such as MMP and PV. • The biggest difference is the rapid onset of PCS and the presence of generalized gingival inflammation without desquamation or blistering
- 111. • Pubertal or pregnancy-induced gingivitis and Mouth-breathers gingivitis; • The difference in the histopathology is in the density of plasma cells since nonspecific gingivitis generally is associated with a plasma cell infiltrate. • The history of a topical irritant helps make the diagnosis. • Erythematous candidiasis with marked gingival erythema without the usual white “thrush” or pseudomembranous candidiasis. • Candida may also secondarily infect an area of PCS.
- 112. Diagnosis • Patch testing can identify suspected allergen. • The biopsy reveal the most significant finding is a dense infiltrate of plasma cells in the lamina propria with dilated surface blood capillaries.
- 113. Management • Removal of the causative agent. • Systemic steroids are rarely required for contact stomatitis. Intraoral topical steroids are prescribed in severe cases of contact stomatitis. • Sucking on ice cubes provides temporary relief from contact stomatitis. • Pain control and anti-inflammatory agents may be helpful.
- 114. Thank youReference; Burket's Oral Medicine
Editor's Notes
- -Herpes viruses are widely distributed in nature, and most animals are infected with one or more of the 100 types discovered.
- -The herpes viruses are relatively large, very complex, enveloped viruses with linear double stranded DNA (dsDNA).
- -At least, seven distinct human herpes viruses have been described each causing a characteristic disease. -An important feature common to all the human herpes viruses is their ability to establish latency in the host. -In general, infections above the waist are caused by HSV-1 and those below the waist by HSV-2, it is not uncommon to culture HSV-2 from oral lesions and vice versa.
- -Transmission occurs via direct contact with contaminated secretions from an infected individual. -The virus then travels along the sensory nerve axons and establishes chronic, latent infection the sensory ganglion such as the trigeminal ganglion.
- - HSV initially infects epithelial cells of the oral mucosa to produce intraepithelial blisters.
- -Neonatal Herpes Simplex Virus (HSV) Infection is usually transmitted during delivery and has high mortality and significant morbidity. -HSV type 2 causes more cases than HSV type 1.
- -A typical sign is vesicular eruption, which may be accompanied by or progress to disseminated disease. -Diagnosis is by viral culture, PCR, immunofluorescence, or electron microscopy. -Treatment is with high-dose parenteral acyclovir and supportive care.
- -Most often, exposure to HSV infection in children results in a subclinical infection and the child may complain of mild flulike symptoms (as fever, malaise, irritability, headache, and cervical lymphadenopathy) -Approximately 1% of patients develop primary herpetic gingivostomatitis; fiery red inflammation of gingiva and other intraoral mucosal surfaces.
- -The prodromal signs and symptoms are followed by eruption of clusters of vesicles that affect any intraoral mucosal surface. -The vesicles rupture within a few days to produce clusters of painful, small, round, shallow ulcers that may coalesce to form larger irregular-shaped ulcerations. -Gradual healing, without scarring, occurs within 1 to 2 weeks. -The virus remain latent at sensory ganglion until triggered for reactivation while extra neuronal latency HSV in cells other than neurons such as the epithelium may play a role in recurrent lesions.
- -While latent, the virus exists in a non-replicating immunologically shielded state. -triggering factors like; Sunlight, trauma, menstruation, fever, immunosuppression, decompression of the trigeminal nerve, and irritation by dental instruments. -burning, tingling, itching, soreness at the site where the lesions will develop. Within hours, small vesicles develop along the vermilion border of the lips and other perioral sites such as the skin or ala of the nose.
- -less common than RHL and mostly involve the keratinized mucosa.
- -An infection of the fingers when virus is inoculated into the fingers through a break in the skin This was a common occupational hazard before the widespread use of gloves.
- Tzanck test of the lesion base may show characteristic multinucleated giant cells and intranuclear inclusions, but this test is less sensitive than culture, and false-positives can occur.
- Acyclovir is a synthetic analogue of purine guanosine that inhibits viral DNA polymerase. Acyclovir is active only in virally infected cells because only viral-encoded enzyme thymidine kinase converts acyclovir to acyclovir monophosphate. Cellular enzymes (cellular kinase) then phosphorylate acyclovir monophosphate to acyclovir triphosphate, which is the active form of the drug. Failure of acyclovir therapy is usually associated with HSV infections caused by thymidine kinase-deficient strains of HSV. Foscarnet; causes renal failure.
- - Alpha herpes virus.
- The primary infection with VZV is through direct contact and/or inhalation of airborne respiratory secretions. Used to be a childhood illness especially in kids under age 12 but It's much rarer now, due to the varicella vaccines. After the incubation period, primary infection may be subclinical or present with chickenpox. Chickenpox often starts with a fever, headache, sore throat, stomachache, malaise, irritability, anorexia, cervical lymphadenitis. These symptoms may last for a few days.
- A centripetal itchy rash crops in waves all over the body and flu-like symptoms. The rash begins as many small red bumps that look like insect bites. They appear in waves over 2 to 4 days, then develop into thin-walled blisters filled with clear fluid. Fluid become turbid or pus. The blister walls break, leaving open sores, which finally crust over to become dry, brown scabs.
- All three stages of the chickenpox rash (red bumps, blisters, and scabs) macular, papular, vesicular and pustular stages appear on the body at the same time. Intraoral Vesicles, especially in the palate, rupture to produce painful, round or ovoid ulcers, with inflammatory haloes.
- A painful unilateral rash in a dermatome (distribution of a sensory nerve) due to reactivation of VZV latent in the associated sensory ganglion. The reactivation; neonates, nonimmune persons, pregnant women, and immunocompromised patients. 75% of cases affect people over 50 years. Children may suffer if they are immunocompromised, or if their mother had varicella during pregnancy. Shingles of the trigeminal nerve is a disease that falls within the diagnostic field of all dentists. Prodromal signs may be Odontalgia. 30% affects the trigeminal nerve to cause ipsilateral pain, rash and mouth ulceration in a dermatome.
- The vesicles progress to pustules within 1 to 7 days. The pustules begin to dry and form crusts. These crusts fall off within 14 to 21 days, leaving erythematous macular lesions, which result in hyperpigmented or hypopigmented scarring. The active stage is characterized by rash, may be accompanied by generalized malaise, headache, low-grade fever, and nausea. The rash progresses from erythematous papules to vesicles in 12 to 24 hours.
- Pain is minimal when the rash is active. the pain returns during crust formationthen subsides as the crusts clear off. Intraoral lesions usually appear after the cutaneous rash.
- - Herpes zoster oticus (Ramsay-Hunt syndrome type 2) is caused by VZV reactivation in the geniculate ganglion. The syndrome refers to the combination of facial nerve weakness with rash in the ear and external auditory meatus, impaired taste and moisturization of eyes and mouth
- PHN is pain lasting for 1 to 3 months after the skin lesions disappear but may in fact last for years and decades. PHN; Constant, deep pain, Brief recurrent shooting or shocking tic-like pain Sharp radiating dysaesthetic sensation evoked by very light touching of the skin
- - The diagnosis is usually clinical. - misdiagnosis of toothache is possible. - Cytology, viral culture, DNA sequentiation, immunostaining or electron microscopy are indicated mainly in immunocompromised patients.
- Patients with shingles remain contagious until crusting phase has taken place. soaking of gauze is in cool water and applying to the rash area for 30 minutes 3 to 6 times a day. Creams and lotions may be used after the acute phase to soften and remove adherent crusts. corticosteroids are not recommended. Mild to moderately strong analgesics.
- Acyclovir is less toxic than other antiviral drugs. On the other hand they are more effective and used in resistant VZV.
- CMV is a β-herpesvirus, herpes virus 5, the largest virus at herpes family.
- Primarily affects the salivary gland tissue. Affect infants, Children who are livening in poverty and immunocompromised patients. Primary infection may be asymptomatic or cause an infectious mononucleosis–like disease.
- Vaccines still not available.
- 60 to 70% of the adult population has been exposed.
- Once exposed to CMV, this virus establishes latency within the connective tissue cells, such as the endothelium of blood vessels, mononuclear cells, white blood cells, and epithelial cells. CMV mononucleosis syndrome.
- CMV within endothelial cells may contribute to vascular inflammation, vascular occlusion, and end-organ damage.
- Trans-placental CMV infection may cause abortion. In severe cases the disease may produce hepatosplenomegaly, jaundice, pneumonia, purpura, microcephaly, cerebral calcification and dental or neurological abnormalities, etc.
- Perinatal Cytomegalovirus-Associated Bullae in an Immunocompetent Infant. Accompanied by CMV hepatitis.
- cytomegalovirus retinitis.
- CMV infection in the mouth in the immunocompromised patient tends to present as a single large necrotic ulcer and less often as multiple ulcers.
- Esophageal Ulcers in AIDS. Ulcers due to vascular inflammation, vascular occlusion. Reports about Mandibular osteomyelitis and tooth exfoliation associated with CMV and VZV infection. Both viruses are associated with vasculopathy and thrombosis.
- CMV is fairly difficult to grow in culture. Biopsy for microscopic examination and/or to obtain tissue for culture is the test of choice for identification of CMV in such ulcers. It is important to make sure that the biopsy includes normal epithelium because if the ulcer is co-infected with HSV or VZV, these would be identified on the biopsy in the intact epithelium adjacent to the ulcer. Infected cells are dramatically swollen (cytomegaly) contain large intra-nuclear inclusion bodies giving ‘owl-eye’ appearance.
- Caused by Coxsackie virus type A and the disease occurs more commonly among children.
- - Spreads via saliva or by inhalation of air-borne droplets.
- Clinical appearance is usually diagnostic because the Culture for Coxsackie viruses is not widely available. Only palliative treatment is done.
- highly contagious systemic infection commonly occurs among children. Caused by Coxsackie virus (A-16 and A-9) type.
- Fever, sore throat, dysphagia, malaise, cough, rhinorrhea, diarrhea, nausea, vomiting, anorexia and lymphadenopathy, etc.
- Vesicular eruptions occur on the palm of the hand, sole of the foot and mucosa of the anterior part of mouth. Oral vesicles then ulcerations on the hard palate, tongue, labial mucosa and buccal mucosa.
- Unlike Herpangina, these lesions are uncommon in the oropharyngeal area.
- Infection with anaerobic fusiform bacteria and spirochetes (variously Borrelia vincentii, Prevotella intermedia, Fusobacterum nucleatum, Porphyromonas gingivalis as well as Treponema, etc. Was among soldiers in WWI…. So called Great war periodontitis Antibiotics, which did not become available until WW2, were not an option in the trenches.
- Painful ulceration starting on interdental papillae, pronounced gingival bleeding, halitosis, sialorrhea, fever and cervical lymphadenopathy. children in developing countries, specially who live in extreme poverty and HIV infected patients. Predisposing factors: poor oral hygiene, smoking, poor nutrition, psychological stress and immune defects.
- Untreated patient may develop Noma (cancrum oris).
- Is a devastating infectious disease which destroys the soft and hard tissues of the oral and para-oral structures.
- Erythema multiforme (EM) is a mucocutaneous condition mediated by antigen-antibody (immune complex – mainly IgM) deposition in the superficial microvasculature of skin and mucous membranes. Younger adults. 20-30 yrs. immune complexes and the ingress of cytotoxic CD8 T lymphocytes, inducing keratinocyte apoptosis and satellite cell necrosis.
- EM minor (accounts for 80%) is a mild, self-limiting rash usually affecting one mucosa. Prodromal symptoms are usually absent or mild nonspecific flue like symptoms.
- The abrupt onset of a rash usually occurs within 3 days, starting on the extremities symmetrically, with centripetal spreading.
- Typically target, or iris-like.
- Oral: Often recurrent attacks of erythematous macules that blister that break down to irregular, extensive, painful erosions with extensive surrounding erythema. typically most pronounced in the anterior mouth; labial mucosa is, and the exudate leads to crusting of the swollen lips.
- Ocular changes: Resemble those of pemphigoid; dry eyes and symblepharon may result. Genital changes: Include balanitis, urethritis and vulval ulcers.
- There are no specific diagnostic tests. The diagnosis is mainly clinical; the Nikolsky sign is negative.
- SJS is a less severe life threating variant of TEN and separate clinically and etiopathogenetically from EM. Although all three are hypersensitivity reactions and give rise to oral bullae, erosions, ulcers, and crusted lips, the skin lesions of SJS and TEN are different from EM. They are more severe and tend to arise on the chest rather than the extremities on erythematous and purpuric macules; these lesions are called (atypical targets). Plus the triggering factors in EM is infection mainly HSV or drugs, while SJS and TEN is mainly drugs.
- Most cases occur within the first four weeks of drug exposure.
- Toxic epidermal necrolysis (TEN) is a rare, potentially lethal mucocutaneous condition in which the skin peels off in swaths, with 30% or more epithelial detachment. The primary cytokine involved is tumor necrosis factor (TNF)-α.
- Fever is common. They involve two or more mucosal surfaces and present with blisters that arise on erythematous or purpuric macules. Mucous membrane involvement can result in gastrointestinal hemorrhage, respiratory failure, and ocular and genitourinary complications.
- The typical oral manifestation is extensive oral ulceration with hemorrhagic crusts on the vermilion.
- Plasma cell Stomatitis and gingivitis. Erythema multiform. Lichenoid reactions. Angioedema Fixed drug eruption.
- inflammatory reaction of the oral mucosa by contact with irritants or allergens. intense plasma cell infiltration R; herbal gel. L; erythema and erosion unknown cause.
- Ulcers, epithelial sloughing and desquamation. The gingiva may also be swollen and edematous. pain and sensitivity and bleeding of the gingiva on brushing. Angular cheilitis with fissuring and dry, atrophic lips have been reported.
- - PCS should not be confused with a direct toxic irritation of the tissues such as from strongly flavored foods.