More than a mouth ulcer. Oral ulcer due to Wegener's granulomatosis.
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Oral ulceration has many different causes. The association between Nicorandil and oral ulceration is not a new phenomenon. There have been several previous case reports regarding a possible association although none in publications for general dental practice. In this report we have a case series of seven patients and we compared our findings with those in the current literature.
Oral ulcers represent a comprehensive group of lesions. Because they are both common and painful, the dentist and physician are frequently consulted for diagnosis and treatment. The pathogenesis, clinical appearance, and suggested treatment modalities for the most common ulcerations are presented. Knowledge of the classification of oral ulcers will aid in proper diagnosis and direct the clinician toward appropriate therapy. In many cases, only palliative care can be offered, but symptoms can often be ameliorated.
Oral ulceration is a common problem. The presentation is often very similar, irrespective of the underlying cause. This paper illustrates some of the more commonly encountered forms of oral ulceration.
Oral ulcers may be the result of allergic, infectious, metabolic, nutritional, or malignant systemic disorders or a variety of other inflammatory diseases. These range from minor irritations to signs of life-threatening illnesses. Patients with oral ulcers should adhere to a variety of general measures that are recommended plus specific treatments for specific diagnoses.
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Recurrent oral ulcer (ROU) is a common disease whose the etiologic factors have not yet been identified. Although the autoimmune mechanism due to streptococcal antigens may be involved in this disease, serum immunoglobulins are reported to be higher than normal controls in various phases of ROU. Oral ulcers are one of the criteria in the diagnosis of some systemic diseases such as Wegener's granulomatosis, Behçet's syndrome, suppurative arthritis, Reiter's syndrome and neutropenias. Any patient with recurring oral ulcers should be evaluated medically for the possible presence or future development of serious systemic diseases. In this study of the 58% of the ROU patients who had positive ASO values, only one female patient had a moderate increase: ++ASO(= 400 IU), the rest had a slight increase: +ASO(= 200 IU). In the control group only 3 female subjects had +ASO (= 200 IU). The aim of this study was to determine whether there is any relationship between ROU and rheumatoid arthritis. Patients with ROU were examined for antistreptolysin O, rheumatoid factor and C-reactive protein and compared to healthy controls.
Although oral ulcers are commonly encountered in clinical dental and medical practice, current therapeutic options with respect to pain relief are limited. This study evaluated the mucosal binding characteristics and the pain relief and protection properties of Zilactin, a hydroxypropyl cellulose film former. In 12 healthy volunteers, the mean duration of mucosal adherence of Zilactin was 3.92 hours, which was significantly longer than that of a widely available topical preparation (1.38 hours, p = 0.0001). When evaluated in 20 subjects with recurrent aphthous ulcerations, Zilactin demonstrated the ability to significantly decrease ulcer pain over a 4-hour period when compared with the subjects' individual standardized level of initial discomfort, which was used as an internal control for all subsequent steps. Challenge with an irritating citrus beverage was made before and after application of the medication. A significant difference in premedication and postmedication sensitivity was shown (p = 0.0001), indicating that the film provides protection, as well as pain relief. As a result of its unique and tenacious film-forming characteristics, this agent is exceptionally effective in the treatment of oral mucosal ulcerations. Greater awareness on the part of physicians and dentists may lead to the development of additional applications.
Ulcers commonly occur in the mouth. Their causes range from minor irritation to malignancies and systemic diseases. Innocent solitary ulcerations, which result from trauma and infections, must be distinguished from squamous cell carcinomas, which also typically present as solitary ulcers. Multiple oral ulcers may be classified as acute, recurrent and/or chronic. The most common causes of rapid-onset oral ulcers include acute necrotizing ulcerative gingivitis, allergies and erythema multiforme. The two common forms of acute (short-term) recurrent oral ulcers, "cold sores" or "fever blisters," which are caused by the herpes simplex virus, and recurrent aphthous ulcers ("canker sores"), may be distinguished largely on the basis of their location. Most types of multiple chronic oral ulcers are associated with disturbances of the immune system. They include erosive lichen planus, mucous membrane pemphigoid and pemphigus vulgaris. Clinical criteria which are most useful in identifying the cause of oral ulcers are vesicles or bullae, which may not be seen because they rupture rapidly in the oral environment; constitutional signs and symptoms; and lesions on the skin and/or other mucosa. In some cases, diagnosis depends upon culture or biopsy, particularly with the application of immunofluorescence to the surgical specimen.
The aim of this study was to test the potential of liposomes as drug carriers to the ulcerated oral mucosa. Radioactive triamcinolone acetonide palmitate (3H-TRMAp) was encapsulated in large multilamellar lipid vesicles and served as the test lotion. 3H-TRMAp in solution served as control. Forty-six hamsters were divided into three groups. In group I, multiple confluent ulcers in both cheek pouches were treated by topical application. In group II, single ulcers on the cheeks were treated by intramucosal injection. In group III, multiple confluent ulcers were produced in the cheek pouch on one side, with a single ulcer in the contralateral cheek pouch; no drug was applied, and the tissues were prepared for histology. Hamsters were killed at three and 24 hours, respectively, after treatment. Pouches were divided into ulcerated and intact adjacent mucosa. Cheeks were divided into ulcerated mucosa and distant mucosa. Drug levels in the four mucosal portions as well as in the blood, liver, spleen, brain, and thalamic region were determined by radioactive tracer technique. At three hours, liposomal drug concentrations were lower than in control animals in the brain and the thalamic region. At 24 hours, liposomal drug values were higher than in control animals in the ulcerated mucosa and lower than in control animals in the thalamic region. Mean drug concentrations in the ulcerated mucosa were higher in group II than group I. The results parallel those of Mezei and Gulasekharam (1980, 1982); liposomes increase local and decrease systemic drug concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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In this study we used the polymerase chain reaction (PCR), slot blot and Southern blot hybridization, direct sequencing and in situ hybridization (ISH) to show the possible presence of EBV-DNA in pre-ulcerative oral aphthous lesions of patients with recurrent aphthous ulcers (RAU) or Behçet's disease (BD). For this purpose, formalin-fixed biopsy specimens were obtained from 13 pre-ulcerative oral aphthous lesions of nine RAU and four BD patients. Five specimens of normal oral mucosa (NOM) from five normal control subjects and 10 specimens of oral erosive or ulcerative lesions from 10 patients with erosive lichen planus (ELP) were also included. EBV-DNA was detected by PCR in 5 of the 13 (38.5%) pre-ulcerative oral aphthous lesions, two from RAU patients and three from BD patients. However, no EBV-DNA was demonstrated in five NOM specimens from normal control subjects and in 10 specimens of oral lesions from ELP patients. EBV-DNA was also demonstrated in patients' peripheral blood lymphocytes and/or plasma, suggesting that the lymphocytes may be the reservoir of latent EBV infection and there is EBV shedding in the plasma. EBV-DNA was detected by ISH in only one PCR-positive case; the reaction product was found to deposit on the nuclei of some of the epithelial cells and lymphocytes. By immunohistochemistry, expression of Epstein-Barr nuclear antigen and EBV/C3d receptors was also noted in some of the epithelial cells and lymphocytes in this ISH-positive case. Therefore, we suggest that the epithelial cells of pre-ulcerative oral aphthous lesions may be infected by EBV through EBV-infected lymphocytes; also, the cytotoxic T lymphocyte-induced lysis of the EBV-infected epithelial cells, but not the virus-induced cytolysis, may be the main mechanism causing oral ulcer formation. Our data provide preliminary evidence for an association of EBV with pre-ulcerative oral aphthous lesions in RAU and BD patients.
A sensitive radio-assay for ferritin was developed and used to examine serum ferritin levels in 105 patients with recurrent oral ulceration (ROU), 41 patients with Behçet's syndrome (BS), 42 with other ulcerative oral lesions, 35 patients with non-ulcerative oral lesions and in 78 controls. Ferritin levels increased with age and were significantly higher in males than females. The mean ferritin concentrations in male patients with ROU, BS or with other oral ulcers were significantly reduced in comparison with controls, and in female patients were significantly reduced in those with major aphthous ulcers. The prevalence of low serum ferritin levels was about 8% in patients with ROU, 15% in BS and 9.5% in patients with other ulcerative oral lesions, compared with less than 3% in patients with non-ulcerative oral disorders and in controls. Most of the iron-deficient patients were female. Serum ferritin levels did not directly correlate with serum iron levels and may be a more accurate indicator of iron deficiency. Furthermore, serum ferritin can distinguish between patients with true iron deficiency and those with secondary sideropenia. It is suggested that in a small number of patients, oral ulceration may be a presenting sign of iron deficiency, and that in a further small proportion of patients, ROU already present will be exacerbated by concurrent iron deficiency. Both groups will show a therapeutic response to correction of the iron deficiency. The results suggest that serum ferritin levels are a useful part of the haematological investigations in patients with ROU.
Oral ulceration in HIV infection may be due to: (1) mycotic; (2) bacterial, protozoan; (3) and viral infections; (4) oral neoplasia; (5) aphthous ulceration/ulceration not otherwise specified (NOS); or (6) ulceration of iatrogenic origin. Of particular significance are oral ulcerations caused by viruses of the herpes virus group (HSV 1/2, CMV, VZV) and ulcerations of the aphthous type. It was shown recently that coinfection of viral ulcers occurs. The aetiopathogenesis of the aphthous type of ulcerations including the still debated ulceration NOS is not clear. Further basic and clinical research is necessary in order to better understand ulceration particularly in relation to immunoregulation, tissue breakdown and repair.
Different side effects of drugs have been described in the oral cavity, including oral ulcerations. Direct contact between drugs and oral mucosa may induce chemical burn or local hypersensitivity. Less frequently, these drug-induced oral ulcerations are part of a complex reaction with cutaneous or systemic manifestations. Sometimes, one or more oral ulcerations appear as the main side-effect of a drug, or exceptionally as solitary lesions. Solitary oral ulcerations usually appear after few weeks of treatment. In most of cases, these lesions resist to conventional treatments, with a rapid healing following the suppression of the responsible drug. This diagnosis is usually difficult, particularly with patients receiving multiple drug therapy. Besides, special attention must be paid to new drugs. Oral ulcerations following symptoms of burning mouth, metallic taste, dysgueusia or agueusia are strongly suggestive of a pharmacological origin. Most of the molecules able to induce solitary oral ulcerations are commonly prescribed in a) rheumatology: NSAI (diclofenac, flurbiprofen, indomethacin, naproxen), long-term rheumatoid arthritis therapy (azathioprine, methotrexate, penicillamine, gold compounds, tiopronin); b) cardiology: angiotensin-converting-enzyme inhibitors (captopril, enalapril), angiotensin 2-receptor antagonist (losartan), anti-angorous (nicorandil), c) psychiatry: antidepressants (fluoxetine, lithium), d) AIDS therapy (foscarnet, zalcitabine).
Behçet oral ulceration (BOU) is described as being indistinguishable from conventional recurrent oral ulceration (ROU). A clinical comparison between 38 Behçet patients and 38 control ROU cases was effected by completion of a standard questionnaire. Behçet patients reported an increased number of concurrent ulcers and involvement of the soft palate and oropharynx. No differences were detected with respect to duration, frequency, age of onset or family history. In addition, photographs of BOU in 15 patients revealed the concurrence of atypical aphthous and herpetiform varieties. Number, site and appearance of oral ulceration may therefore provide diagnostic features for the development of Behçet's disease.
Ulcers commonly occur in the oral cavity, their main symptom being pain. There are different ways to classify oral ulcers. The most widely accepted form divides them into acute ulcers--sudden onset and short lasting--and chronic ulcers--insidious onset and long lasting. Commonest acute oral ulcers include traumatic ulcer, recurrent aphthous stomatitis, viral and bacterial infections and necrotizing sialometaplasia. On the other hand, oral lichen planus, oral cancer, benign mucous membrane pemphigoid, pemphigus and drug-induced ulcers belong to the group of chronic oral ulcers. It is very important to make a proper differential diagnosis in order to establish the appropriate treatment for each pathology.