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What do you know about Aphthous Ulcer??

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What do you know about Aphthous Ulcer?? Empty What do you know about Aphthous Ulcer??

مُساهمة من طرف Optimistic Doctor 06/05/11, 10:07 am



What do you know about Aphthous Ulcer?? 221914_199314933439521_185665968137751_460312_8381319_n




Background

Recurrent
aphthous stomatitis (RAS) is a common condition, restricted to the
mouth, that typically starts in childhood or adolescence as recurrent
small, round, or ovoid ulcers with circumscribed margins, erythematous
haloes, and yellow or gray floors. A positive family history of similar
ulcers is common, and the natural history is typically of resolution in
the third decade of life.

Ulcers with similar clinical features
but rarely resolving spontaneously with age may be termed "aphthous-like
ulcers," and may then be associated with systemic conditions such as
Behçet syndrome, auto-inflammatory syndromes, gastrointestinal disease,
or immune defects such as HIV/AIDS.

Pathophysiology

The
etiology of recurrent aphthous stomatitis (RAS) is not entirely clear,
and aphthae are therefore termed idiopathic. RAS may be the
manifestation of a group of disorders of quite different etiology,
rather than a single entity.

Despite many studies trying to
identify a causal microorganism, RAS does not appear to be infectious,
contagious, or sexually transmitted. Immune mechanisms appear at play in
persons with a genetic predisposition to oral ulceration.

A
genetic basis exists for some RAS. This is shown by a positive family
history in about one third of patients with RAS, an increased frequency
of HLA types A2, A11, B12, and DR2, and susceptibility to RAS which
segregates in families in association with HLA haplotypes. RAS probably
involves cell-mediated mechanisms, but the precise immunopathogenesis
remains unclear. Phagocytic and cytotoxic T cells probably aid in
destruction of oral epithelium that is directed and sustained by local
cytokine release.

Patients with active RAS have an increased
proportion of gamma-delta T cells compared with control subjects and
patients with inactive RAS. Gamma-delta T cells may be involved in
antibody-dependent cell-mediated cytotoxicity (ADCC). Compared with
control subjects, individuals with RAS have raised serum levels of
cytokines such as interleukin (IL)–6 and IL-2R, soluble intercellular
adhesion modules (ICAM), vascular cell adhesion modules (VCAM), and
E-selectin; however, some of these do not correlate with disease
activity.

Cross-reactivity between a streptococcal 60- to 65-kd
heat shock protein (hsp) and the oral mucosa has been demonstrated, and
significantly elevated levels of serum antibodies to hsp are found in
patients with RAS. Lymphocytes of patients with RAS have reactivity to a
peptide of Mycobacterium tuberculosis. Some cross-reactivity exists
between the 65-kd hsp and the 60-kd human mitochondrial hsp. Monoclonal
antibodies to part of the 65-kd hsp of M tuberculosis react with
Streptococcus sanguis. RAS thus may be a T cell–mediated response to
antigens of S sanguis, which cross-react with the mitochondrial hsp and
induce oral mucosal damage. RAS patients have an anomalous activity of
the toll-like receptor TLR2 pathway that probably influences the
stimulation of an abnormal Th1 immune response.

Predisposing factors found may include any of the following:

*
Hematinic deficiency: Up to 20% of patients are deficient of iron, folic acid (folate), or vitamin B.
*
Malabsorption in gastrointestinal disorders: About 3% of patients
experience these disorders, particularly celiac disease
(gluten-sensitive enteropathy) but, occasionally, Crohn disease,
pernicious anemia, and dermatitis herpetiformis. HLA DRW10 and DQW1 may
predispose patients with celiac disease to RAS.
*
Cessation of smoking: This may precipitate or exacerbate RAS in some cases.
*
Stress: This underlies RAS in some cases; ulcers appear to exacerbate during school or university examination times.
*
Trauma: Biting of the mucosa and wearing of dental appliances may
lead to some ulcers; RAS is uncommon on keratinized mucosae.
*
Endocrine factors in some women:
RAS is clearly related to the
progestogen level fall in the luteal phase of the menstrual cycle, and
ulcers may then temporarily regress in pregnancy.
*

Allergies to food: Food allergies occasionally underlie RAS; the
prevalence of atopy is high. Patients with aphthae may occasionally have
a reaction to cow's milk, and may have been weaned at an early age.
*
Sodium lauryl sulphate (SLS): This is a detergent in some oral
healthcare products that may aggravate or produce oral ulceration.
*
Immune deficiencies: Ulcers similar to RAS may be seen in patients with HIV, neutropenias and some other immune defects.


Optimistic Doctor
Optimistic Doctor
 
 

ذكر
عدد الرسائل : 1354
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المزاج : OpT!M!St!C
كيف تعرفت علينا ؟ : Ahlamontada
تاريخ التسجيل : 25/08/2008

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مُساهمة من طرف mona 27/05/11, 12:25 pm

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انثى
عدد الرسائل : 95
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تاريخ التسجيل : 11/09/2008

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