A guide to common oral lesions part 2

Aphthous stomatitis
(Canker sores, recurrent aphthous stomatitis, RAS)
DESCRIPTION: This is one of the most common oral diseases. The exact incidence is unknown, but
estimates range from 20% to 60% of the population. Lesions appear as painful ulcers ranging in size from
less than 1 mm to 2 centimeters. They may be single or multiple. Small lesions (less than 0.5 cm) have
been referred to as minor aphthae and large lesions (more than 0.5 cm) have been called major aphthae.
An uncommon presentation of this disease appears as multiple, pinpoint areas of ulceration that seldom
exceed 1 mm. This has been referred to as the herpetiform pattern, an unfortunate terms since herpes
virus is not the cause.
Each lesion begins as a red macule, less often a papule but not as a blister. It soon ulcerates and the
ulcer becomes covered by a pyogenic membrane producing the characteristic yellow-white center with
surrounding erythematous flare. The shape is usually round to oval but may be elongated in natural folds
such as the vestibule. Aphthous stomatitis occurs on freely movable mucosa that does not overlie bone.
The lips, cheeks, soft palate, floor of mouth, ventral and lateral tongue are often involved but attached
gingival, hard palate and dorsal tongue are seldom affected.
Aphthous lesions affect all age groups from young to old but young adults and females are more
affected. Elapsed time between recurrences is extremely variable; some unfortunate patients have almost
continuous disease whereas others go from months to years between episodes.
ETIOLOGY: The cause is unknown. The concept that canker sores are caused by a microbiologic agent
has been superceded by theories revolving around an immunopathogenesis. The deposition of antibodies
and complement within epithelium and basement membrane during the early stages of the disease
suggests a humoral immune response, and the influx of lymphocytes rather than neutrophils in early
lesions points to a cellular immune reaction as well. It is yet to be learned if the immune response is
directed against self (autoimmunity) or against an extrinsic antigen such as bacteria or viruses. To
further cloud the issue, a variety of other factors have been implicated. Withdrawal of certain foods such
as cheese, tomato products and gluten, as well as sodium lauryl sulfate-containing toothpastes, has
been claimed to help some patients whereas in others, correction of iron, B12 and folate deficiencies have
brought about a cure.
Improvement of aphthous lesions during the last stages of pregnancy with exacerbation after delivery
suggests that gonadal hormones may lay a role. The occurrence of canker sores during menstruation
also suggests a hormonal basis. To add a final element of mystery, aphthous stomatitis has been
reported to worsen when cigarette smoking is discontinued. There are too many theories for them all to
be correct. Aphthous stomatitis may not be a single disease with a single cause but instead a variety of
diseases all manifested by painful mouth sores.
TREATMENT: To reduce pain, patients with few lesions may be treated with topical medications such as
Orabase® with Benzocaine, Zilactin®, or Soothe-N-Seal®. Anti-inflammatory agents such as topical
steroids or Aphthasol® have also been shown to be effective. For severe or widespread disease, systemic
prednisone such as a Medrol 4 mg Dosepak® is helpful. Long-term systemic steroid therapy may be
associated with numerous adverse effects, including osteoporosis, asceptic necrosis, cataracts,
depression, fluid retention and exacerbation of diabetes.
PROGNOSIS: Cure is seldom achieved but palliation and long-term remission may be achieved by above
mentioned treatment. Without treatment, healing time varies from 4 days for a small lesion to a month or
more for major aphthae. Major aphthae may also cause scarring.
DIFFERENTIAL DIAGNOSIS: Aphthous stomatitis must be differentiated from herpetic stomatitis, the
disease with which it is most often confused. Recurrent intraoral herpes occurs almost exclusively on
mucosa overlying bone. The hard palate is the most common site. Lesions indistinguishable from
aphthous stomatitis have been reported in Behcet’s syndrome, Reiter’s syndrome, Crohn’s disease and
celiac disease.

Oral cryptococcosis:
-Cryptococcosis is a rare fungal disease, caused by cryptococcus nepformans. Two varieties of the
organism have been identified, C.Neoformans Var. Neoformans and C.Neoformans Var. Gatti.
The fungus is found all over the world in soil. It may also be associated with bird droppings, and it is
acquired through inhalation of the spores.
Sometimes the infection is asymptomatic. In immunocompromised patients, it can spread to anywhere in
the body, including the central nervous system, and it can be lethal.
-Recently, there's been large increase in the incidence of Cryptococcal infections. The main predisposing
factors are HIV Infections, Diabetis, Immunosuppresive therapy.
-Two forms of the disease have been recognized- PULMONARY which is the commonest and
Disseminated which may involve CNS, Lymph nodes, Skin, GIT and Oral mucosa.
-In Oral cavity, It presents as abnormai chronic ulcerations with vegetating surface, tender on palpation.
-Tongue, Palate, Gingiva, Tooth socket are the most common sites.
-DIAGNOSIS: Culture test, Detection of cryptococcus in the serum.
-TREATMENT: Systemic amphotericin B, Fluconazole, & Itraconazole

Denture sore mouth (DSM) and Papillary hyperplasia (PH)
DESCRIPTION: Long treated as separate entities, there is evidence that PH and DSM may be different
expressions of the same disease. Both are related to the wearing of dentures. The mildest form of denture
sore mouth appears as small, localized and asymptomatic red spots on the posterior palatal mucosa. As
the condition worsens, large confluent areas turn crimson red. This is the classic form of DSM. In later
stages, hyperplasia of palatal mucosa occurs and produces the red, pebbly appearances of papillary
hyperplasia. In some cases of PH, the mucosa has a more mossy than mulberry appearance and the
hyperplasia is not apparent until a gentle blast of air opens the crevices revealing the papillary nature of
the lesion. Whether or not DSM.
ETIOLOGY: The cause is unknown but there is evidence that Candida albicans is at least contributory.
DSM has been called chronic atrophic candidiasis. Organisms are found more often in PH and DSM than
in normal controls. Treatment with the antifungal drugs such as nystatin, clotrimazole and fluconazole
have been reported to bring about remission in most cases, especially in DSM. Since organisms have
been shown to colonize the tissue surface of the denture, sterilization of the denture with fungicide is
indicated. Factors other than Candida albicans seem to be involved, but it is difficult to assess the role of
denture trauma and bacterial pathogens. Because the disease is limited to the area covered by the
denture, it is often assumed that the patient is allergic to denture base material.. There is little evidence to
support his view. Patients with palatal lesions ordinarily do not have lesions under the lower denture as
would be expected if the patient were truly allergic.
TREATMENT: We know of no effective therapy other than fungicides such as nystatin, clotrimazole,
ketoconazole or fluconazole in the usual doses for oral candidiasis. Good oral and denture hygiene may
help. The denture should fit well and not be worn at night. In cases of excessively redundant papillary
hyperplasia, surgical reduction may provide a better denture base.
PROGNOSIS: The condition is benign. For many years, papillary hyperplasia had the undeserved
reputation of being premalignant. It is not.
DIFFERENTIAL DIAGNOSIS: The disease has such a characteristic appearance that diagnosis is seldom a
problem.

Epulis fissuratum (Inflammatory fibrous hyperplasia)
DESCRIPTION: This lesion occurs in those who wear prosthetic appliances. The lesion consists of two or
more folds of soft tissue separated by a central groove into which fits the appliance border. It most often
is found in the buccal vestibule of the anterior maxilla, but any mucosal area touched by a denture border
is vulnerable including the lingual aspect of the mandible. In a study of 583 cases, 64% were found in
females.
Those in the fifth and sixth decade are most often affected. Duration ranged from one week to 10 years,
40% of the patients reported a duration of 6 months to two years. Symptoms are absent except in
ulcerated lesions which may be painful. Histologically, the excessive tissue is composed of cellular,
inflamed fibrous connective tissue.
ETIOLOGY: This is an inflammatory fibrous hyperplasia or oral mucosa caused by ill-fitting or over-
extended denture borders.
TREATMENT: Surgical excision of the lesion and reduction of the denture border.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The lesion has such a characteristic clinical appearance that differential
diagnosis is not a problem. Persistent ulcerated areas in epulis fissuratum should be biopsied to rule out
squamous carcinoma. Folds similar to epulis fissuratum may be seen in Crohn’s disease

Plaque induced gingivitis
DESCRIPTION: Inflammation of the gingiva is among the mildest but most common human ailments. The
gingival that envelops the neck of the teeth is swollen, red and bleeds easily. It is not painful. It may show
patchy involvement with skip areas or it may involve virtually the entire marginal gingiva. If untreated,
some patients show progression to bulky enlargement of the gingiva called hyperplastic gingivitis.
Gingivitis is stated to be enhanced by pregnancy and puberty.
ETIOLOGY: The gingival inflammation is the response to bacterial plaque on the adjacent tooth surface.
TREATMENT: Treatment consists of regular dental prophylaxis and the good oral hygiene.
PROGNOSIS: The disease is easily treated and the prognosis is good. If ignored, inflammation may
spread to deeper periodontal tissues in which case the patient is said to have periodontitis.
DIFFERENTIAL DIAGNOSIS: Mucosal pemphigoid, lichen planus, dilantin hyperplasia, and leukemic
infiltrate.

Angular cheilosis
DESCRIPTION: This lesion appears as fissuring and maceration at the labial commissures. The term
cheilitis and cheilosis have both been used to describe the same disease.
ETIOLOGY: It is doubtful that this condition is caused by vitamin deficiency in the United States. Studies
have shown that the two most common organisms responsible for this condition are Candida albicans
and Staphylococcus aureus. This condition is commonly seen in older patients having loss of vertical
dimension, in younger patients with orthodontic appliances, and those with a lip licking habit.
TREATMENT: In those patients who have obvious overclosure, restoration of vertical dimension is of
benefit. Application of antifungal ointment to eliminate Candida organisms is indicated.
PROGNOSIS: Good
DIFFERENTIAL DIAGNOSIS: The disease is so characteristic that it cannot be confused with any other
lesion.