Oral Ulcerative Diseases
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.
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)
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.
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.
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.
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.
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).
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.
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.
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).
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.
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.
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
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.
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.
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
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 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.
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.
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).
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.
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.
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.
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
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.