Trauma is the most common cause of ulceration of the oral mucous membranes. Traumatic ulceration may result from physical, chemical or thermal injury to the tissue. Diagnosis of traumatic ulceration is usually ascertained by the history alone. Acute traumatic ulceration is characterized by a break in the mucosa with a shallow base and nonraised margins. Depending on the cause, they may be diffuse or localized. These lesions are at least mildly painful.
Common physical injuries may include biting the cheek or tongue, mal-fitting denture irritation, trauma from a foreign object or even trauma from a toothbrush following over-zealous brushing. Direct mucosal contact with any number of drugs, most commonly aspirin, may cause ulceration. Chemical burns can also be seen in patients who have used phenol or silver nitrate for treating recurrent aphthous ulcers. These and other noxious chemicals cause oral ulcerations, often in the form of a generalized sloughing of the oral mucous membranes that produces a painful, raw, bleeding lesion. Hot foods or liquids may cause oral ulceration also. The classic example of this type injury is the “pizza burn” from hot melted cheese contacting the palate, tongue, or lips.
Traumatic injuries to the oral mucosa are treated by removing the responsible irritant, after which healing is usually uneventful. Healing may be expedited by cleansing the tissues with a mild saline rinse with half strength peroxide.
Chemical and thermal injuries to the oral mucosa are often more painful, requiring analgesics during the healing period. Supportive therapy, including attention to oral hygiene and the use of cleansing mouth rinses, is indicated. Although healing of thermal injuries is usually uneventful, supportive therapy, medications for pain, or topical cortcosteroids, or all, may be indicated.
Cancer chemotherapy agents are extremely powerful drugs that have as a side effect the potential for disruption or destruction of the oral tissues. Chemotherapy-induced stomatitis is a common side effect of many of the antineoplastic drugs and may present as an excruciatingly painful mucositis involving any of the oral mucous membranes either in a localized or generalized fashion. Also, the concomitant suppression of the immune system by these agents may make the patient unable to fight secondary opportunistic infections that may develop in areas in which the mucous membrane has become ulcerated. These oral manifestations of chemotherapy occur shortly after the beginning of therapy, peak within a week after its cessation, and slowly resolve unless otherwise complicated by infection, hemorrhage, or restarting therapy. These lesions are treated palliatively with cleansing mouth rinses, topical anesthetics, antimicrobial agents, or with the use of analgesics.
Infectious causes of chronic oral ulceration are rare.Viral infection will seldom lead to development of a chronic oral ulcer in an immunocompetent patient. Although secondary, nonspecific bacterial infection of chronic oral ulcer is common, specific bacterial infection is not. An example of a chronic ulcerative disease caused by specific bacterial infection would include a gumma in tertiary syphilis, a tuberculous ulcer, or actinomycosis. Deep mycotic infections, such as histoplasmosis or blastomycosis, will typically cause chronic, deep-based ulcers that may be granulomatous and friable in appearance.
Reactions that result from radiation therapy for malignancies in the oral cavity and oropharynx may be quite severe. Radiation mucositis is an early and acute reaction usually beginning during the second week of radiation. It usually presents as erythema followed by spotty mucositis. The spotty mucositis will coalesce to form areas of ulceration covered by a yellow-white pseudomembrane with a bright erythematous border.The lips are often involved, with a tenacious pseudomembrane and crusting being noted in the areas of ulceration. Exquisite pain and burning may be present even at rest and are exacerbated by spicy foods.Healing usually begins with the cessation of therapy and is usually complete within 3 to 4 weeks, though the discoloration and mucosal atrophy may be life long. This often makes dental prosthesis placement difficult. Treatment is both supportive and therapeutic and includes oxidizing mouth rinses described above to help break up the thick, ropelike saliva covering the mucous membranes. By doing so, other supportive or therapeutic medications will have a greater effect. Local anesthetic rinses described above will reduce some of the discomfort and are particularly useful before meals. Topical antibiotic solutions may aid in preventing secondary infection.
Patients with RAS will complain of recurrence of one or more painful oral ulcers at intervals ranging from days to months. RAS usually begins in childhood or adolescence and may decrease in both frequency and severity with age. Ulcers caused by RAS are confined to the soft mucosa of the mouth, or nonkeratinized mucosa that are not immediately adherent to bone. These areas include the buccal and labial mucosa, lateral and ventral tongue, floor of the mouth, soft palate, and oropharyngeal mucosa. The only areas in the mouth that are not affected by RAS are the hard palate and attached gingiva. RAS lesions are not confined to the oral cavity, they may be found elsewhere in the digestive tract, but lesions appearing outside the oral cavity are often associated with systemic disorders.
RAS is subdivided into three categories based on the size of the ulcers and the disease severity. Minor aphthae are less than 1cm in diameter and heal completely in 7 to 10 days. The minor aphthae usually involve a prodromal stage of tingling and burning for 1 to 2 days and usually occur in clusters of up to 5 ulcers. These lesions are shallow and round to oval in shape with a gray to yellow membrane. Minor aphthae are very painful for about 4 days, then heal completely without scarring after several more days. Major aphthae are uncommon and involve irregular deep ulcers of 1 to 3 cm in size. They may have a raised border and can take 4 to 6 weeks to heal. Major aphthae can leave extensive scarring and distortion with healing, and patients are rarely lesion free. The irregular and chronic nature of these lesions often necessitates a biopsy to rule out squamous cell carcinoma. Herpetiform aphthae are also uncommon, and consist of crops of up to 150 very small (1-3mm) ulcers that heal completely in 7 to 10 days. This category of RAS is unfortunately named because these ulcers, like all RAS ulcers, are completely unrelated to the herpes virus.
Many theories for the etiology of RAS have been proposed and investigated, but none has been proven. A viral association with viruses such as adenovirus, herpes, and varicella-zoster has been suggested, but is not supported by the majority of the literature. These viruses are ubiquitous and there are no reports of successful treatment of RAS with antiviral therapy. A bacterial association has also been proposed due to the fact that streptococcus species have been cultured from patients with RAS and RAS outbreaks have been associated with increased antibody titers. This has not been corroborated, however, and it is clear that antibacterial drugs do not cure RAS. Other theories for the etiology of RAS include association with estrogen and progesterone levels in women, anxiety, stress, and the "type A" personality. There is clearly a higher incidence of RAS among college, medical, and dental students, and there is a higher incidence among elementary students of higher socioeconomic status. The role of nutrition is controversial. Deficiencies in vitamins, zinc, and iron have been implicated as the occurrence of RAS improved somewhat with replacements. Some patients with gluten-sensitivities may experience outbreaks that resolve with a gluten-free diet, but lesions in the majority of patients do not respond with dietary measures. Sensitivities to foods such as nuts, chocolate, cereals, tomatoes, dairy products and citrus fruits have been implicated also, and the avoidance of such foods may decrease outbreaks. Trauma, as mentioned above, may incite outbreaks. Nicotine, interestingly, seems to have a protective effect. Studies have shown that resumption of smoking after cessation caused pre-existing ulcers to heal within a few days. Also, nicotine gum has been shown to cause ulcer healing and prevention when taken for 1 month, with relapse upon discontinuation of the gum. One hypothesis for the protective effect is the keratinizing action of nicotine on the oral mucosa. There are also numerous investigations into the possibility of an immune mechanism. When certain, yet undefined, antigens are presented to lymphocyte subpopulations, there is an autoimmune reaction against targeted epithelial cells. However, the disease is intermittent and does not always reliably respond to immunomodulating drugs. The only clear etiologic factor for RAS is that a family history may increase a person's risk for developing the disease by 20%.
The diagnosis of RAS is usually made by taking a thorough history and performing a systematic physical exam. The typical presentation and appearance are as described above. Patients may report any of the above mentioned triggering factors. The examination of the patient will show the typical shallow ulcers anywhere in the mouth except for the keratinized mucosa.
Goals in the management of RAS reflect that it is generally mild and self-limiting, and that, currently, there is no treatment widely believed to be curative. Therefore, treatments that reduce pain and maintain function during attacks, or that reduce the severity and frequency of recurrent attacks, are considered successful. Treatments used for this generally benign disease should not be associated with more morbidity that the disease itself. Treatment options are those that either provide palliation or those that truly alter the course of the disease. Palliative medications are generally applied topically and are available over the counter. Preparations of benzocaine, diclonine, or benzydamine can be effective. Also, as described above, mixtures of lidocaine, diphenhydramine, and Kaopectate may provide some relief. Other therapies that have been reported include hydrogen peroxide, phenol, silver nitrate, topical antimicrobials, antivirals, and antiseptic mouthwashes. These treatments are generally not very effective. The mainstay of treatment of RAS is topical steroid application. Triamcinolone 0.1% in a cream, paste or an aqueous base is the most commonly used. If applied in the prodromal stage, outbreaks can be prevented or even aborted. Beclomethasone spray has also been shown to be of benefit in treating RAS. If patients have a large number of lesions or long duration of attacks, a "burst regimen" of systemic steroid treatment may be used in addition to topical therapy. For RAS major that is difficult to control, intralesional triamcinolone injection will often promote ulcer healing. Because oral candidiasis has been reported in patients using steroid sprays and solutions, prophylaxis with antifungal agents should be considered in these patients.
Squamous cell carcinoma (SCC) is the most common malignancy of the oral cavity. These lesions often begin as mixed white or red lesions and occur most often on the tongue, floor of mouth, or soft palate. Later lesions will often involve irregular ulcers with indurated or heaped margins. These lesions are chronic and do not heal with time or immunosuppressants. Oral SCC most often presents as an ulcerative lesion but can also be exophytic, infiltrative, or verrucoid. Histologically, these lesions show typical malignant epithelioid cells with intracellular bridging and possible keratin production. Treatment of oral SCC generally involves wide local resection, radiation therapy, or both. Clinically apparent metastases to cervical nodes will be found on presentation in about 30% of patients; the presence of occult nodes must be considered and addressed as well. Decision making in the workup of early SCC involves correlating the history and physical examination. Worrisome historical factors are the presence of risk factors of tobacco and alcohol use and lesions that have not healed for several weeks to months. Factors on examination are irregular ulcers with indurated or heaped margins and of course enlarged cervical nodes. Areas of leukoplakia in the oral cavity should generally be biopsied or carefully followed. Areas of long term erythroplakia, induration, or exophytic growth in the oral cavity should generally be biopsied immediately. A high degree of suspicion must be maintained to allow early diagnosis, as these malignant lesions may mimic lesions of lichen planus, pemphigus or pemphigoid, sialometaplasia, or even major aphthae.
Lichen planus is a chronic disease of the skin and mucous membranes which is felt to be due to basal cell layer destruction by activated lymphocytes. Characteristic skin lesions include violaceous, pruritic papules over the flexor surfaces of the extremities and several types of oral lesions have been described, including reticular, papular, plaque, and atrophic (erosive), ulcerative, and bullous variations. Desquamative gingivitis can also frequently present as a manifestation of Oral Lichen Planus. Reticular lichen planus shows fine, slightly raised, white or violaceous threadlike lesions in a ring like, lacy pattern (Wickman’s striae). These lesions are often located on the buccal mucosa. The hypertrophic form resembles leukoplakia as homogenous white plaques. Atrophic or erosive lichen planus present as erythematous shallow ulcers that, in contrast to most forms of lichen planus, may be painful. Histologically, lichen planus shows hyperkaratosis, “saw-tooth” rete ridges, liquefactive degeneration of the basal cell layer, and a band-like subepithelial inflammatory infiltrate. Discrete eosinophilic ovoid bodies (Civatte bodies) are occasionally seen in the basal cell layer. Treatment is symptomatic, the mainstay of therapy involves the use of either topical or systemic steroids. The use of other immunomodulatory agents is often necessary, these include Dapsone, Azathioprine, Cyclosporin and Tacrolimus. Mild cases usually do not require therapy. Topical steroids may be useful in controlling local symptoms and topical retinoids, with antikeratinizing effects, can be used for the plaque form. Dapsone has also been used for severe forms with some success.
Aetiology
The aetiology of OLP is unclear, though there is clear evidence of a T lymphocyte attack on the stratified squamous epithelia. Usually no aetiological factor is identifiable but a minority of cases are related to:
Clinical Features
The oral lesions of OLP are usually:
Lesions are usually white and may be asymptomatic or may cause soreness, especially if erosive. Presentations include:
Lichen Planus may also affect
Management
The history and clinical appearance are usually highly indicative of the diagnosis but lesional biopsy is often indicated, particularly to exclude lupus erythematosus, leukoplakia (keratosis), or malignancy.
OLP is often persistent but is usually benign. Atrophic LP clinically closely resembles erythroplasia – a premalignant condition – but there is about a 1 to 3% chance of malignant transformation over 5 years, predominantly in those with long-standing erosive LP.
Systemic disease, drugs, or local possible predisposing factors (such as amalgam restorations) should be excluded. If drugs are implicated, a physician should be consulted as to possible changes in therapy. If amalgam restorations might be implicated, it may be worth considering replacing amalgams adjacent to lesions by an alternative restorative material. Unfortunately, skin patch testing for mercury hypersensitivity is not reliable in suggesting patients who might benefit from replacement of restorations. However, if lesions are in close relationship to a restoration, or are unilateral, or if an associated amalgam restoration is in need of repair, a replacement trial may be indicated.
Symptomatic OLP may respond to topical corticosteroids, and patients should be informed about the condition. Recalcitrant lesions can be managed with intralesional corticosteroids or topical cyclosporin. Systemic immunosuppressive agents, including corticosteroids, azathioprine, cyclosporin or dapsone – or, rarely, vitamin A derivatives such as etretinate – may be required but should be given only by a specialist in view of the serious adverse effects possible. If the GP is in any doubt about the diagnosis or management of OLP, then specialist referral is indicated
In 1937, Behçet described a symptom complex consisting of recurrent aphthous ulcers of the mouth, as well as recurrent painful ulcers of the eyes and genitals. Behçet's disease is a multisystem disorder that tends to affect persons of Mediterranean, Middle Eastern, or Japanese descent. Most of these patients present with the classic triad of aphthous ulcers, genital ulcers and uveitis or conjunctivitis. Other systemic manifestations may include arthritis of the rheumatoid type, neurological, vascular, and gastrointestinal involvement, as well as malaise and fever with ulcer eruptions, papulopustular truncal lesions, or development of a pustule at any site of minor skin trauma. The diagnosis of Behçet's disease is made on the basis of the clinicopathologic findings, which may be confused clinically with Stevens-Johnson syndrome and Reiter's disease. The oral manifestations of Behçet's disease may be treated in the same manner as those not associated with the disease, but these patients need referral for systemic treatment as well.
Pemphigoid is characterized by the formation of tense, subepithelial bullae of the skin and mucous membranes. Two separate entities, benign mucous membrane pemphigoid and bullous pemphigoid, are often described but they represent variants of the same disease. BMMP occurs in the 40 to 50 year old age group and affects women twice as often as men. Tense oral bullae form and may persist for days before rupturing, forming large erosions that usually scar with healing. Involvement of the conjunctivae is relatively common and may lead to blindness. Bullous pemphigoid affects older patients and cutaneous lesions are more common than mucosal lesions. This condition is often associated with the prescribing of various medications. The lesions are similar but may heal with less scarring. Both lesions are histologically similar and show direct immunofluorescence to IgG in the basement membrane, supporting an autoimmune etiology. Biopsy shows subepithelial clefting with dissolution of the basement membrane but no degenerative intraepithelial changes. Treatment is often difficult and multiple sites are involved but potent topical steroids or intralesional steroids can be effective. Systemic steroids may be required for severe cases for ocular involvement. Steroids combined with immunosuppressants maybe needed in refractory cases.
Pemphigus vulgaris is a more severe, potentially fatal form characterized by intraepithelial bullae and acantholysis. The disease is more common in Jewish and Italian people and males are more often affected than females. The lesions almost invariably initially involve the oral mucosa and the bullae are so easily ruptured that painful irregular ulcers are often the presenting lesions. The most common sites include the buccal mucosa, palate and gingiva. Microscopically, the lesions show early intercellular edema and loss of intercellular bridges. The lack of cohesion allows cell separation and rounding (acantholysis). Intraepithelial clefting (as opposed to subepithelial clefting in bullous pemphigoid) occurs, and a gentle rubbing of adjacent uninvolved skin may denude the epithelium, producing an ulcer or vesicle (positive Nikolsky’s sign). As this causes a lesion, this test is no longer considered appropriate. The basal cells remain attached to the lamina propria creating a “tombstone” affect and free acantholytic cells assume a spherical form (Tzanck cells) which are considered pathognomonic for pemphigus vulgaris. Direct immunofluorescence shows antibodies against intercellular bridges, more specifically against the desmoglein 3 protein in the desmosomes. Serum levels of intercellular antibodies have been shown to correlate with the severity of the disease. Treatment with high dose steroids has greatly reduced the mortality and morbidity of pemphigus but significant morbidity from steroids has been reported as doses of 100 mg/day are often required for initial control. The dose can be tapered down to 20 mg/day over three months. Intramuscular gold has been used with some success and plasmaphoresis is currently under investigation.
There are a number of variants of pemphigoid, with autoantibodies directed against different basement membrane proteins. Oral involvement is also probably more common in bullous pemphigoid than was formerly supposed: bullae and/or other erosions are found in up to 50% of patients.
Linear IgA disease is a rare disorder, the lesional IgA deposits are linear at the epithelial basement membrane zone.
Linear IgA disease is usually idiopathic i.e. it arises spontaneously. However, it sometimes follows infection and is rarely caused by drug allergy. Vancomycin is the most frequently associated drug, although diclofenac, cotrimoxazole, cyclosporin, lithium, penicillin, phenytoin, and sodium hypochlorite have been implicated in case reports. Drug-induced disease resolves with withdrawal of the offending agent. Linear IgA disease has also been rarely associated with lymphoma, haematological conditions, rheumatological conditions, ulcerative colitis and solid tumours.
As Linear IgA disease is a subepidermal blistering disorder, skin biopsy reports blistering just under the epidermis as opposed to some blistering disorders that result in blistering within the epidermis e.g. pemphigus.
A special skin biopsy antibody test, direct immunofluorescence, reveals the immunoglobulin IgA along the basement membrane of the epidermis in a linear pattern. Sometimes these IgA antibodies can be detected by a blood test (indirect immunofluorescence). Research indicates the antibodies are directed against various basement membrane components (target antigens).
Most patients with Linear IgA disease improve or clear with Dapsone 50: 100mg daily. Although the condition may eventually be cured, many patients require long-term treatment as a reduction in dose of medication results in further blistering.
Erythema multiforme is an uncommon, often recurrent, immune-mediated vesiculo-bullous eruption, seen especially in younger men. It is characterized by serosanguinous exudates on the lips, and often target-like lesions on the skin.
Aetiology
Although the aetiology is unclear in most patients, in some it is precipitated by infections (such as herpes simplex or mycoplasma), drugs (sulphonamides, barbiturates, hydantoins and others) or a range of other triggers such as hormonal changes.
Clinical features
The oral lesions often recur but the condition usually resolves after six or seven episodes. Usually attacks occur for 10 to 14 days once or twice a year but the periodicity can vary from weeks to years. Erythema multiforme may affect the mouth alone, or skin and/or other mucosa.
The major form (Stevens-Johnson syndrome) causes widespread lesions affecting mouth, eyes, skin and genitals, with fever and toxicity, bullous and other rashes, pneumonia, arthritis, nephritis or myocarditis. Toxic epidermal necrolysis (TEN) presents similarly but is usually drug-related.
The minor form of erythema multiforme is much more common and affects only one site.
Oral lesions include:
Other lesions:
Management
Specialist referral is indicated, particularly in patients with major forms such as Steven-Johnson syndrome, who may need hospital care.
Biopsy may well be indicated but pathology can be variable because there may be subepithelial or intra-epithelial vesiculation, and immunostaining is not specific – showing fibrin and C3 at the basement membrane zone, and perivascular IgM, C3 and fibrin. Differentiation from acute herpetic stomatitis can be difficult; virolological studies may thus be indicated.
Precipitating factors, when identified, should be treated. Aciclovir or periciclover may be indicated in erythema multiforme related to herpes simplex infection.
Oral hygiene should be improved with 0.2% aqueous chlorhexidine mouthbaths. In addition, major erythema multiforme should be treated with systemic corticosteroids and/or azathioprine or other immunomodulatory drugs. Specialist care is indicated and some patients need hospitalization. Levamisole and thalidomide have been used to some effect on occasion. Minor erythema multiforme may respond to symptomatic treatment and topical corticosteroids, but systemic steroids may still be required.
Candidiasis is the most common type of fungal infection involving the oral mucous membranes. The causative organism, Candida albicans , is a common normal inhabitant of the mouth and is nonpathogenic under normal conditions. Oral candidiasis usually occurs only when there has been a reduction in the competitive oral microflora, as seen following long-term broad-spectrum antibiotic therapy, or when there is a decrease in the resistance of the host tissue to infection. When there is a decrease in the host resistance to infection, some predisposing factor is usually present and should be sought out. Possibilities include infancy, pregnancy, decreased salivary flow, denture, poorly controlled diabetes, hypoparathyroidism, hypoadrenocorticism, malnutrition, immunosuppression including AIDS, underlying malignancy, and lymphoreticular disorders such as agranulocytosis, leukemia, lymphoma, etc.
Oral candidiasis usually presents with profuse creamy white plaques, which cover any portion of the mouth, rub off easily, leaving a bright red, raw, bleeding surface. In some cases it may present as a brightly erythematous mucosa with only scattered white plaques. Chronic hyperplastic cadidiasis is the form of the disease that presents clinically as a leukoplakic lesion that does not rub off the underlying mucosa. A biopsy is necessary to differentiate this form of candidiasis from other forms of leukoplakia. Although the diagnosis may be made primarily on the clinical features alone, cytologic smears are helpful in confirming it. This may easily be done by making a smear of the suspected lesion on a glass slide, adding a drop of 20% potassium hydroxide, and examining the slide for the typical hyphae. Oral Candida infection is usually treated with various topical antifungal preparations. The use of systemic antifungal therapy such as Fluconazole or Itraconazole may be initiated under specialist supervision.
Gluten-sensitive enteropathy or coeliac disease, is an autoimmune inflammatory disease of the small intestine that is caused by the interaction of gluten, a component of wheat protein, with the small intestinal mucosa in genetically susceptible persons. Gluten causes the intestinal mucosa to lose its villous structure and absorptive capacity.
Gluten, a prolamine, is the primary protein in wheat. Barley and rye contain similar proteins. Hence, these grains and their products must be avoided. Oats are a subject of controversy.Although oats themselves may be nontoxic in limited quantities, commercial oat products are measurably contaminated with wheat. Rice, corn, maize, are safe as are grain substitutes such as tapioca, potato, nuts and beans.
Until recently, coeliac disease was considered to be relatively uncommon. However, studies conducted in Europe estimate the seroprevalence of coeliac disease to be one case per 130 to 300 persons.
Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serum IgA antiendomysial and tissue transglutaminase are found in up to 95% of patients with gluten sensitivity. Anti-gliadin levels are less specific for sprue.
Intestinal biopsy is the most sensitive means of making the diagnosis.
To make the diagnosis unequivocal, the patient’s symptoms must be relieved with an adequate trial (a few weeks) of a gluten-free diet. An objective means of demonstrating improvement may be to repeat the intestinal biopsy and evaluate for histological improvement or repeat the serum titres for anti-endomysial antibodies which should decrease in the absence of gluten exposure.
Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e. family history of coeliac disease or personal history of type I diabetes) and in patients who have chronic diarrhoea, unexplained anaemia, chronic fatigue, or unexplained weight loss. The likelihood of having gluten-sensitive enteropathy increases to 10 to 20 percent in persons who have a first-degree relative with coeliac disease.
Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of coeliac disease. The primary treatment for coeliac disease is the removal of gluten and related proteins from the diet. Complete exclusion of dietary gluten generally results in rapid and complete healing of small-bowel inflammation.
Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anaemia. Patients with coeliac sprue are also at increased risk for both intestinal and extra intestinal lymphomas, oesophageal squamous cell carcinomas, and small intestinal adenocarcinomas. If symptoms so indicate, a search for these malignancies should be performed.
Blood blisters in the mouth are not uncommon in elderly people.
Aetiology
Unclear. No bleeding tendency appears to underlie this condition. Corticosteroid inhalers may sometimes predispose.
Clinical features
Blood blisters are seen in the mouth or pharynx, mainly on the soft palate (sometimes termed angina bullosa haemorrhagica) and occasionally on the lateral border of the tongue in elderly people. There is rapid onset, with breakdown in a day or two to a large round ulcer.
Diagnosis and management
It is necessary to differentiate this condition from pemphigoid and other vesiculobullous disorders, trauma, and purpura. Confirm that haemostasis is normal first and then perform biopsy to exclude pemphigoid if that is likely.
There is no specific treatment other than reassurance. The blisters should be carefully burst. Topical analgesics may provide symptomatic relief.
Trauma and suction
Platelet disorders:
Infections
Localized oral purpura (ABH)
Vascular disorders
Amyloidosis
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Updated 12.08.2007 |
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