8: Oral Ulcerative Diseases

Oral Ulcerative Diseases

Keerthilatha M Pai and Braz Campos Durso

•. Classification of Oral Ulcers

•. Traumatic Ulcers

•. Ulcers Associated with Infections

•. Herpes Simplex Infection

•. Varicella Zoster Infection

•. Coxsackie Virus Infection

Hand, Foot and Mouth Disease

•. Acute Necrotizing Ulcerative Gingivitis

•. Tuberculosis

•. Syphilis

•. Deep Fungal Infections

North American Blastomycosis

South American Blastomycosis

•. Drug-induced Oral Ulcers

Stomatitis Medicamentosa

Stomatitis Venenata

•. Erythema Multiforme

•. Blood Disorders Causing Oral Ulcers

•. Immunologic Disorders

Aphthous Ulcers

•. Dermatological Disorders

Bullous Pemphigoid

Cicatricial Pemphigoid

•. Gastrointestinal Disorders Associated with Oral Ulcers

Gastroesophageal Reflux Disease

Crohn’s Disease

Ulcerative Colitis

•. Neoplastic Ulcers

An ulcer may be described as breach in the continuity of the surface epithelium of the skin or mucous membrane to involve the underlying connective tissue as a result of micro molecular cell death of the surface epithelium or its traumatic removal.

Classification Of Oral Ulcers

Ulcerative lesions affecting the oral cavity can be categorized based on the etiology or based on the mode of onset and clinical presentation.

Classification based on etiology

Infectious (bacterial, viral and fungal infections)

Ulcers associated with blood dyscrasias

Immune mediated

Oral ulcers associated with dermatological disorders

Oral ulcers associated with GI disorders

Neoplastic oral ulcers

Ulcers of uncertain etiology.

Classification based on mode of onset and clinical presentation

– Traumatic ulcer

– Tuberculous ulcer

– Syphilitic ulcer

– Histoplasmosis

– Blastomycosis

– Mucormycosis

– Neoplastic ulcers

Multiple ulcers

– Acute multiple ulcers

• Herpes virus infections

• Primary herpes simplex virus infections

• Coxsackievirus infections

• Varicella zoster virus infection

• Erythema multiforme

• Contact allergic stomatitis

• Oral ulcers secondary to cancer chemotherapy and/or radiotherapy

• Acute necrotizing ulcerative gingivitis

– Chronic multiple ulcers

• Subepithelial bullous dermatoses

• Herpes simplex virus infection in immunosuppressed patients

Recurring oral ulcers

– Recurrent aphthous stomatitis

– Behçet’s syndrome

– Recurrent herpes simplex virus infection

– Cyclic neutropenia

– Chronic idiopathic neutropenia.

Flowcharts 1 and 2 summarize acute ulcers that are recurring in nature and those that occur as an isolated episode.

Flowchart 1 Algorithm to evaluate acute oral ulcers that are recurrent in nature. (Reprinted with minor modifications from Bruce AJ (2003), ‘Acute oral ulcers’, Dermatologic Clinics, Vol. 21, p. 2, with permission from Elsevier)

Flowchart 2 Algorithm to evaluate acute oral ulcers that occur as an isolated episode. (Reprinted with minor modifications from Bruce AJ (2003), ‘Acute oral ulcers’, Dermatologic Clinics, Vol. 21, p. 2, with permission from Elsevier)

Traumatic Ulcers

Traumatic injuries involving the oral cavity may lead to the formation of surface ulcerations. Although the exact incidence of these ulcerations is not known they are one of the most common ulcers seen affecting the oral cavity.

Types of Trauma

Mechanical (sharp tooth, overextended denture, orthodontic brackets, toothbrush, ill-fitting dental prosthesis, etc.)

Chemical (aspirin, concentrated clove oil, sodium hypochlorite, hydrogen peroxide, root canal medicaments, chemotherapy, etc.)

Thermal (extremely hot or cold insults such as hot cheese, hot beverages, popsicle) (Figure 1)

Figure 1 A thermal burn on the hard palate secondary to intake of a hot bread sandwich. Courtesy: Department of Oral Medicine and Radiology, MCODS, Mangalore

Radiation (used in treatment of head and neck cancer)

Self-inflicted (self-harm)

Iatrogenic (injuries caused by high speed rotary instruments, cotton rolls, etc.)

The oral cavity is prone to injuries from events such as accidentally biting oneself while talking, sleeping, mastication or as a result of an epileptic seizure. Fractured, malposed, or malformed teeth, as well as the premature eruption of teeth, can contribute to the formation of surface ulceration.

Nocturnal parafunctional habits, such as bruxism may be associated with the development of traumatic ulcers of the buccal mucosa, the labial mucosa and the lateral borders of the tongue. Ulcerations may be the result of voluntary, selfinduced, and deliberate acts by patients with physical or psychological symptoms who suffer from attention seeking behavior. These ulcers are characteristically present over visible surfaces such as the lips, corner of mouth and facial aspects of gingiva (ulcers caused by gingival picking). Bulimic individuals may present with nail marks or minute pinpoint red spots and/or ulcerations over the palate which is brought about by the frequent efforts to vomit.

Newborns and infants may present with sublingual ulcerations (Riga-Fede disease). These ulcers may occur as a result of chronic mucosal trauma due to adjacent anterior natal or neonatal teeth. The trauma is often associated with breast feeding. The lingual frenum may be ulcerated by repeated trauma because of the frenum rubbing against the mandibular incisors teeth in cunnilingus and in recurrent coughing episodes.

Young children are commonly susceptible to electrical and/or thermal burns of the lips and commissure areas. Extensive ulcerations with necrosis may develop. Children in this age group have a tendency to chew their lips immediately after surgical removal of teeth under the influence of local anesthesia.

Clinical features

In most cases, the source of the injury is identified. The patient’s usual complaint is pain or a painful ulceration. Individual lesions usually appear as shallow or deep ulcers associated with areas of erythema. The ulcer may reveal the presence of a central yellowish purulent exudate. Occasionally the border of the ulcer is indurated.

Ulcerations can occur throughout the oral cavity. Ulcers associated with mechanical trauma are often found on the buccal mucosa, the labial mucosa of the upper and lower lips, and the lateral border of the tongue (Figure 2). The mucobuccal folds, gingiva, and palatal mucosa may also be involved. Most lesions associated with electrical burns occur in children and involve the lips and commissural areas. Ulcers formed due to thermal injuries are generally seen to occur on the posterior regions of the buccal mucosa and the palate.

Figure 2 A traumatic ulcer on the left lateral aspect of the tongue due to sharp teeth. Courtesy: Department of Oral Medicine and Radiology, KLEDC, Bangalore

Caustic chemical agents can damage any area of the oral mucous membrane. However, they are commonly seen on the gingival margins and buccal vestibular regions of the oral cavity. Very frequently these ulcers are covered by a whitish pseudomembrane which when peeled leaves behind a raw ulcerated surface (Figure 3). Some patients in the Indian subcontinent use cloves and topical pain balms meant for extraoral application over the gingiva to relieve tooth pain. Hence, most of the chemical burns are generally seen adjacent to carious teeth.

Figure 3 A chemical burn on the right buccal mucosa extending into the vestibule in patient who had the habit of applying pain balm in the vestibule to manage periodontal pain. Courtesy: Department of Oral Medicine and Radiology, MCODS, Mangalore

Diagnosis

The diagnosis of traumatic ulcerations is based on the history of trauma or insult (hot/cold or radiation therapy) prior to onset of ulcer. Mechanical trauma induced ulcers often have linear configuration. The depth of ulcer depends on nature of trauma. Generally the area surrounding the ulcer is inflamed. A traumatic factor will often be evident in the vicinity of the ulcer (e.g. sharp edge of tooth).

Differential diagnosis

Carcinomatous ulcer, recurrent aphthous ulcerations, ulcers associated with deep fungal infections can be considered in the differential diagnosis of traumatic ulcers.

Histologic features

Histopathologically an area of surface ulceration covered by a fibrinopurulent membrane consisting of acute inflammatory cells intermixed with fibrin is seen. The stratified squamous epithelium from the adjacent surface may be hyperplastic and exhibit areas of reactive squamous atypia. The ulcer bed is composed of a proliferation of granulation tissue with areas of edema and an infiltrate of acute and chronic inflammatory cells.

Management

Consumption of a soft and bland diet.

Removal of traumatic factor (extraction of root stumps, supraerupted teeth and malposed third molars, sharp cuspal edges of teeth may be grounded, irritating dentures may be corrected, restoration of fractured teeth and orthodontic correction of malposed teeth) will cause the resolution of the ulcer in 10–14 days.

Patient may be advised to rinse his/her mouth with warm saline.

Topical application of antiseptic and analgesic/anesthetic medication (choline salicylate 8.7%, benzylkonium 0.01% and lignocaine hydrochloride 2%—patient can be asked to apply the agent over the ulcers 10 minutes prior to food intake, 3–4 times a day).

In case of multiple ulcers—analgesic/antiseptic mouth-wash (chlorhexidine gluconate 0.2% or benzydamine hydrochloride 0.15% mouthrinse—one teaspoon of the agent can be dissolved into 50 ml of water. This prepared solution is swished in the mouth for 1 minute. The patient is advised to rinse the mouth 3 times a day, 30 minutes after food intake).

Application of topical corticosteroids (triamcinolone acetonide oral paste 0.1%). Patient can be advised to apply the paste 30 minutes prior to food intake, 3 times a day for 2 weeks.

For extremely large and deep seated ulcers, penicillin may be administered (Capsule Amoxicillin, 500 mg, 3 times a day for 5 days) to prevent secondary infections.

Patients presenting with ulcers secondary to self-inflicted injuries may be referred to a psychiatrist or psychologist after symptomatically managing the ulcer.

Complications

Most traumatic ulcers resolve with the removal of the etiological agent. However, some ulcers may be secondarily infected and subsequently heal with extensive scar formation.

Prognosis

The outcome of traumatic ulcerations is excellent, provided the etiological factor is eliminated. Healing of the ulcerated mucosa is usually delayed when the lesions overlie the maxillary or mandibular alveolar process, hard palate and tip of the tongue.

If the ulcer does not resolve within 2 weeks of removal of the etiological agent, biopsy of the ulcer may be considered to rule out malignancy.

Ulcers associated with infections (bacterial, viral and fungal infections)

Table 1 summarizes ulcers associated with infections.

Table 1

Ulcers associated with infections

Primary Herpetic Gingivostomatitis

Primary herpetic gingivostomatitis is caused by herpes simplex virus (double-stranded DNA virus which is a member of the human herpes virus family). Most orofacial and ocular infections are caused by HSV-1. Infections involving the genitalia and the skin surface of the lower part of the body are caused by HSV-2. It has been reported that HSV-2 has a greater virulence. Almost 95% of the cases have a subclinical infection, only about 5% manifest symptoms. The infection confers resistance against another primary infection for lifetime.

Clinical features

Primary herpetic gingivostomatitis has an acute onset.

Typically affects children (generally below 6 years of age), but this infection also occurs in adults (immunocompromised).

Males and females are equally affected.

Prodromal systemic symptoms (fever, malaise, myalgia) precede oral lesions by 2–3 days.

The skin, mucous membranes, eyes and central nervous system are the most commonly affected sites.

Multiple oral ulcers affecting all parts of the mouth.

Generalized erythema of gingiva usually associated with multiple vesicles or ulcers (Figure 4).

Figure 4 Gingival erythema, multiple small ulcers and vesicles in the attached gingiva in a 36-year-old man suffering from acute herpetic gingivostomatitis. Reproduced with permission from editor, JCDA. Ajar AH and Chauvin PJ. Acute herpetic gingivostomatitis in adults: a review of 13 cases, including diagnosis and management. J Can Dent Assoc 2002;68(4):247–51

Cervical lymphadenopathy occurs as a rule.

Food intake becomes difficult and dehydration may ensue.

Self-limiting condition in normal children. However, it may become disseminated in immunocompromised children or adults.

Diagnosis

Primary herpetic gingivostomatitis can be identified based on history and clinical findings. Cytological (PAP/Tzanck) smears of intact or recently broken vesicles may demonstrate epithelial giant cells containing intranuclear eosinophilic viral inclusions, that are typical of herpes viral infections.

Differential diagnosis

Leukemia, erythema multiforme and stomatitis medicamentosa can cause lesions that resemble primary herpetic gingivostomatitis.

Treatment

Symptomatic management

Ensure that the patient is adequately hydrated and electrolyte balance is maintained.

Antipyretic and analgesic medication like acetaminophen, 500 mg given thrice daily is effective (3 times a day).

Soothening oral rinses (anesthetic mouthwashes like dyclonine hydrochloride 0.5%, about 10 ml can be used 4 times a day as an oral rinse).

Specific management

Antiviral therapy can be instituted in children and adults. These medications will decrease the fever, pain, severity of the lesions and minimize viral shedding.

In children antiviral medications like acyclovir can be given within first 72 hours in a dosage of 200 mg 5 times a day for 10 days. Acyclovir helps to decrease fever, pain, lesions and viral shedding.

Newer drugs like valacyclovir (1 g orally times a day for 7 days) and famciclovir (500 mg times a day for 7 days) are more effective.

Prognosis

The outcome of primary herpetic gingivostomatitis is good in otherwise healthy individuals. Complications may occur in immunocompromised individuals. The virus remains dormant in nerve ganglion and may get reactivated later in life causing secondary infection.

Recurrent Herpes Infection

Recurrent infections of herpes can manifest in two forms:

1. Intraoral herpes (occurs on highly keratinized mucosa of hard palate/gingiva)

2. Herpes labialis (occurs along external vermillion border of lips).

Precipitating Factors

Exposure to UV light (sunlight)

Decreased immunity

Traveling and change in climatic conditions.

Clinical presentation

Patients present with cluster of tiny fluid filled vesicles (Figure 5A–C) which rupture to form pinpoint ulcers. These ulcers may coalesce to form larger areas of ulceration.

Figure 5 (A) Vesicles on the upper lip in a patient with recurrent herpes labialis. (B) Ulcers formed subsequent to vesicle rupture in a patient with recurrent herpes labialis. Courtesy: Department of Oral Medicine and Radiology, MCODS, Mangalore. (C) Healing lesions of herpes labialis. Courtesy: Department of Oral Medicine and Radiology, KLEDC, Bangalore

Lesions may be preceded by burning, itching, tingling sensation or pain in the region.

The lesions last for 5–7 days and subside and subsequently recur. Now the frequency of recurrence may be varied.

Occasionally associated with fever and pharyngitis.

As a consequence to healing an area of pigmentation is noticed at the site of the lesion (however this pigmented area is readily visualized only in fair skinned individuals).

Diagnosis

Recurrent herpes infection can be identified by their typical location and clinical presentation. In addition, biopsy and Tzanck smear can be performed.

Treatment

The management of recurrent lesions is generally symptomatic. Patients can be advised to stay indoors to minimize exposure to sunlight. Sunscreen lotion can be used when venturing out. However in individuals where there is an increased frequency of recurrence, acyclovir therapy can be instituted as a prophylactic measure (400 mg twice a day for 10 days).

Varicella Zoster Infection

Varicella zoster virus causes two distinct clinical entities. The primary infection by varicella zoster causes chicken pox, while the reactivated virus causes a secondary infection termed herpes zoster or shingles.

Chicken Pox

The primary infection by varicella zoster virus usually affects children. It is characterized by the sudden onset of generalized pruritic vesicular rashes affecting the skin. The incubation period of the virus varies from 10 to 21 days. Approximately 50% of the affected children present with prodromal symptoms of fever, malaise, headache, and abdominal pain, which last for about 1–2 days before the appearance of the dermal lesions.

Dermal lesions

Typical lesions of chicken pox, clinically exhibit four phases. The maculopapular phase (erythematous macules are evident), vesicular phase (minute fluid filled vesicles are seen), ulcerative phase (commonly seen on mucous membranes of oropharynx, vagina and conjunctiva) and the phase of healing (Figure 6).

Figure 6 Vesicular lesions involving the face and neck in chicken pox. Courtesy: Dr Ceena Denny

In the maculopapular phase erythematous macules are seen. In some patients, vesicles develop within the maculopapular rash giving rise to ‘dewdrop on a rose petal’ appearance.

The commonly involved sites are the scalp, face and trunk.

The lesions are often pruritic.

On an average 100–300 new lesions are found at any given point of time. Lesions heal generally without scarring. Occasionally crusting of the lesions may be seen. However, an area of hypopigmentation may be appreciated at the site of the healed lesion. These hypopigmented areas fade away with time.

Oral lesions

The common intraoral sites affected are the hard and soft palate, labial and buccal mucosa. Oral lesions of chicken pox are seen as small vesicles that subsequently rupture to form shallow round ulcers surrounded by an erythematous halo.

Management

Vaccination against varicella zoster should be given to infants between 12th and 18th months of life. The management of the disease is mainly symptomatic. Acyclovir can be administered in the early phases of the disease.

Herpes Zoster

Herpes zoster is caused by reactivation of varicella zoster virus that is inactive in dorsal root or cranial nerve ganglion, after primary infection.

It is estimated that only in about 0.3–0.5% of the population, the virus is reactivated after the primary infection.

Clinical features

The clinical features depend on the dermatome involved.

The nerves that are commonly affected are C-3, T-5, L-1 and L-2.

Manifests in middle age.

When the trigeminal nerve is involved, the ophthalmic division of the nerve is most commonly involved. About 15–20% of the affected individuals show involvement of the maxillary or mandibular division.

Painful vesicles and/or ulcers seen both inside and outside the oral cavity, which stop abruptly at the midline (i.e. lesions do not cross midline) (Figure 7).

Figure 7 Healed lesions of herpes zoster with scab formation. Characteristically, the lesions do not cross the midline and this patient had involvement of the ophthalmic, maxillary and mandibular divisions of the trigeminal nerve. Courtesy: Dr Sumanth

Bilateral lesions may indicate severely immunocompromised state. Literature review reveals reports of necrosis of alveolar bone exfoliation of teeth in immunocompromised individuals.

Occasionally pain may be present along the course of the affected nerve in the absence of vesicles. Such a manifestation is termed zoster sine herpete or zoster sine eruption.

Ramsay Hunt syndrome is a symptom complex associated with herpes zoster. It is characterized by varicella zoster infection affecting the geniculate ganglion of the facial nerve, unilateral facial paralysis and unilateral vesicular eruptions involving the oral mucosa and external ear.

Post-herpetic neuralgia is one of the relatively common sequelae of varicella zoster infection that results from scarring of the involved nerve.

Management

Antiviral drugs like acyclovir, valacyclovir and famciclovir have been used successfully in shortening the course and healing time of the infection and reducing the pain associated with the disease.

Acyclovir (800 mg) is given 5 times a day for a week or valacyclovir (1,000 mg) or famciclovir (500 mg) can be given 3 times a day for a week.

Herpangina

Herpangina is caused by coxsackie virus (A 1–0, 16, or 22). It occurs generally in epidemics. It predominantly affects posterior parts of oral cavity.

Clinical findings

In the early stages erythematous macules are seen. As the disease progresses, vesicles with a central ulceration develop, which exhibit an/>

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