声音简介
Recurrent aphthous ulcer (RAU), we also call it recurrent oral ulceration (ROU) or recurrent aphthous stomatitis (RAS) in clinician, is painful lesions that occur within the oral cavity, and one of the most common oral mucosa diseases seen among patients.
Its' case rate is 20% or so. Because burning pain, which can be caused on eating, swallowing and speaking, is one of the obvious symptoms of recurrent aphthous ulcer.
So the scientist name it use the term "aphthous", derived from a Greek word "aphtha", which means burning pain in Greek.
RAU presents as recurrent, multiple, small, round, or ovoid ulcers, with circumsc-ribedmargins, having yellow or gray floors and are surrounded by erythematous haloes.
Periodicity, relapse and self-limitation are three characters of recurrent aphthous ulcer.
Epidemiological research show that, RAU is inclined to afflict women more than men and people less than 40 years and present first in childhood or adolescence.
What causes recurrent aphthous ulcer?
The Predisposing factors of RAU are very complex, it may be multifactors. The genetic factors, immune system reactions, physical trauma, stress, microbiologic, nutritional and other factors have been presented by now. Individual difference is very evident. The etiopathogenesis of this disease is yet unclear. So still have no uniform point of view about the pathogeny of RAU.
Genetics
A genetic predisposition for the development of aphthous ulcer is strongly suggested as about 40% of patients have a family history and these individuals develop ulcers earlier and are of more severe nature. Various associations with HLA antigens and RAS have been reported. These associations vary with specific racial and ethnic origins.
Trauma
Trauma to the oral mucosa due to abnormal biting, sharp tooth, dental treatments, local anesthetic injections and tooth brush injury may predispose to the development of recurrent aphthous ulceration. mechanical injury may aid in identifying and studying patients prone to RAU.
Immune factors
The pathogenesis of RAU involves a predominantly cell-mediated immune response in which tumor necrosis factor, or TN, play a major role. The immunopathogenesis probably includes cell-mediated responses, involving T cells and TNF-production by these and other leukocytes. Other cytokines such as interleukin, or IL-2, IL-10, and natural killer, or NK, cells activated by IL-2 play a important role in RAU. Other studies show that abnormal humoral immunity response and abnormal autoimmunity response may be also associated with RAU.
Tobacco
Several studies reveal negative association between cigarette smoking, smokeless tobacco and RAU. Possible explanations given include increased mucosal keratinization; which serves as a mechanical and protective barrier against trauma and microbes.
Nicotine is considered to be the protective factor as it stimulates the production of adrenal steroids by its action on the hypothalamic adrenal axis and reduces production of tumor necrosis factor alpha (TNF-a) and interleukins 1 and 6 (IL-1 andIL-6).
Nicotine replacement therapy has been suggested as treatment for patients who develop
RAU on cessation of smoking.
Drugs
Certain drugs have been associated with development of RAU, these include angiotensin converting enzyme inhibitor captopril, gold salts, nicorandil, phenindione, phenobarbital, and sodium hypochloride. NSAIDS such as propionic acid, diclofenac, and piroxicam may also cause oral ulceration similar to RAU.
Hematinic deficiency.
Deficiencies of iron, vitamin B12, and folic acid predispose development of RAU. Deficiencies of these hematinics are twice more common in these individuals than controls. Contrary findings in various studies relating the association of hematinic deficiency and RAU have been explained as due to varying genetic backgrounds and dietary habits of the study population.
Stress
Stress has been emphasized as a causative factor in RAU. It has been proposed that stress may induce trauma to oral soft tissues by parafunctional habits such as lip or cheek biting and this trauma may predispose to ulceration. A more recent study shows lack of direct correlation between levels of stress and severity of RAU episodes and suggests that psychological stress may act as a triggering or modifying factor rather than etiological factor in susceptible RAU patients.
Hormonal changes
Conflicting reports exist regarding association of hormonal changes in women and
RAU. Studies state association of oral ulceration with onset of menstruation or in the luteal phase of the menstrual cycle. Mc Cartan et al. established no association between RAU and premenstrual period, pregnancy, or menopause in 1992.
Sodium lauryl sulfate - containing toothpast
An increased frequency in the occurrence of RAU has been reported on using sodium lauryl sulfate (SLS)-containing tooth paste with some reduction in ulceration on use of SLS-free tooth paste. However, because of the widespread use of SLS-containing dentifrice, it has been proposed that this may not truly predispose to RAU.
Gluten sensitive enteropathy/celiac disease, inflammatory bowel disease Gluten sensitive enteropathy (GSE) is an autoimmune inflammatory disease of small intestine that is precipitated by the ingestion of gluten, a wheat protein in susceptible individuals. It is characterized by severe malnutrition, anemia, abdominal pain, diarrhea, aphthous oral ulcers, glossitis, and stomatitis. RAU may be the sole manifestation of the disease. The use of gluten-free diet in the improvement of RAU is considered uncertain. It has been suggested that evaluation for celiac disease may be appropriate for RAU patients. Inflammatory bowel diseases such as Crohn's disease and ulcerative colitis may present with aphthous-like ulceration.
Oral streptococci
Oral streptococci have been considered as microbial agents in the pathogenesis of RAS. They have been implicated as microorganisms directly involved in the pathogenesis of these lesions or as agents which serve as antigenic stimuli, which in turn provoke antibody production that cross-react with oral mucosa. It has been suggested that L form of a-hemolytic streptococci, Streptococcus sanguis, later identified as Streptococcus mitis was the causative agent of this disease.
What are symptoms of recurrent aphthous ulcer?
RAU is characterized by recurrent bouts of solitary or multiple shallow painful ulcers, at intervals of few months to few days in patients. RAU has been described under three different clinical variants as classified by Stanley in 1972.
• Minor Aphthous Ulcer (MiAU). MiAU is the most common variant, constituting 80% of RAU. The ulcers are small and scarce in number to 5 everytime. Every ulcer is isolated, round or oval, clearly defined. Ulcers vary from 2 to 4 mm millimetres in size. It is most commonly seen in the nonkeratinized mucosal surfaces like labial mucosa, buccal mucosa, and floor of the mouth. When MiAU in active stage, red, yellow, sunken and pain are four characters of it.
The center of it is sunken, its' basement is soft. A 1mm wide red hematodes circle around them. Accidental membrane cover the surface of every ulcer.
Burning pain is obvious, and disturbs the speaking, biting and mood of patients.
Ulcers heal within 10-14 days without scarring.
* ��Major aphthous ulcer (MjAU). MjAU is also known as periadenitis mucosa necrotica recurrens or Sutton's disease. It affects about 10% -15% of patients.�Appearing after puberty, the prodrome is more intense and the ulcers are deeper, exceed 1 cm in diameter, and longer lasting (weeks to months) than minor aphthous ulcer. Most common sites of involvement are lips, soft palate, and throat. Fever, dysphagia, malaise, and scarring may occur.
* ��Herpetiform ulcer (HU). Herpetiform ulceration is characterized by recurrent crops of multiple ulcers. It accounts for 5% of cases. may be up to 100 in number. These are small in size, measure 2-3 mm in diameter. Lesions may coalesce to form large irregular ulcers. These ulcers last for about 10-14 days.�Unlike herpetic ulcers, these are not preceded by vesicles and do not contain viral infected cells. These are more common in women and have a later age of onset than other clinical variants of RAU.
How is recurrent aphthous ulcer diagnosed?
The diagnosis must be based on the periodicity, relapse and self-limitation history, symptoms and careful clinical examination. Possible systemic association with RAU must be ruled out, especially in cases where there is sudden development of ulceration in adulthood. Large, deep and long history ulcer, we should make a biopsy to nail down it's RAU or oral cancer.
How is recurrent aphthous ulcer treated?
There is no enough evidence about the etiopathogenesis of RAU by now, so all treatment can only attempt to restrain symptoms. Aims of treatment are easing the pain when ulcers happen, and to help them to heal as soon as possible. Any treatment can't prevent RAU from recurring. Treatment is symptomatic, the goal being to decrease symptoms, reduce ulcer number and size, and increase disease-free periods. The best treatment is that which will control ulcers for the longest period with minimal adverse side effects. The treatment method should be determined by disease severity, the medical history of patient, the frequency of flare-ups and the patient's ability to tolerate the medication. In all predisposing factors and treat any such factors, where possible, before introducing more specific therapy.
Topical Treatment
In patients with poor oral hygiene, professional help from a dental hygienist should be considered once ulcers heal.
A number of different treatments exist for aphthous ulcers including:anesthetics agents, antiseptics, anti-inflammatory agents, steroids.
Topical steroids, when used for a short period, have a very safe profile and should be the first line of treatment for recurrent oral stomatitis. In addition, oral medicine specialists may administer intralesional injections of a corticosteroid such as betamethasone, dexamethasone or triamcinolone to enhance or boost the local reponce, thus allowing for shorter systemic treatment.
Topical application of 5% amlexanox oral paste has been also shown to increase the healing rate and provide greater pain relief.
Those that exist showed that chlorhexidine gluconate mouthwashes and topical corticosteroids both can reduce the severity and duration of RAU.
Systemic Treatment
Patients with systemic diseases and nutritional deficiencies should be referred to appreciate health-care specialists.
In the majority of patients, symptomatic relief of RAU can be achieved with topical corticosteroids alone, with other immunomodulatory topical agents or by combination therapy. For those patients who present with major and herpetiform RAU, local and /or systemic corticosteroids, antibiotics, antiviral, and oral suspensions of tetracycline or nystatin have been recommended. In patients with recalcitrant RAU, a short course fo systemic corticosteroid therapy may be required, never exceeding more than 50mg per day for five days. This course of treatment is best left to a physician or oral medicine specialist. If corticosteroids are used, patients should be monitored for yeast superinfection.
Its pathogenesis remains unknown, and there are no diagnostic tests available.
Diagnosis, therefore, is made on clinical ground alone. several factors-such as trauma, diet and stress are known to trigger the disease. The most important role of the HCP is to identify underlying precipitating factors and try to eliminate them. Furthermore, it is essential to educate the patient regarding the nature of this condition, especially the fact that RAU is not a contagious condition, as often is thought, and that it is not caused by the herpes simplex virus.
Given its painful presentation and inflammatory nature. RAU responds quite well to the use of topical or systemic anti-inflammatory drugs, particularly corticosteroids.
Since the advent of high-potency topical steroids, most patients with RAU can be managed this way. However, early intervention is the key.
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