recurrent disease of the oral mucosa of unknown etiology, characterized by small white ulcerative lesions lasting 7 to 14 days.
- 20% of the world population suffers from SAR at least once during life
- They occur in men and women of all ages, races and geographic regions. It is estimated that at least 1 in 5 individuals has at least once been afflicted with aphthous ulcers
- most frequently seen on women who belong to wealthy societies
- it's the most common oral ulceration of children and reaches the apex on the second decade
local burning and pain that lasts 24-48h before the clinical manifestation
The condition is classified as minor, major, and herpetiform on the basis of ulcer size and number
- minor aphtha:multilple ulceration,dm 8-10 mm.It heals in 10-14 days without leaving scars.It appears on the oral not-keratinized mucosae.80% of total aphtha.
- major aphtha:usually alone,known as recurrent necrotic mucosae periadenitis.It appears around minor salivary glands,10-15%of the total ulcerations.Syntoms are more intense.It's deeper and more than 1cm in dm.It causes disphagia.It heals slowly and leaves scars.
- herpetic aphtha:rare,5-10% of total patients,multiple,1-3mm in dm, circular,painful.They melt to form a larger ulcer.It lasts 10-14 days but it usually disappear without leaving scars.
patients with oral aphtha are frequently affected by bowel disease
"LABORATORY TEST": Laboratory investigation is indicated in patients with major RAS, when RAS is worsening, when RAS begins after age 25, or when there are associated signs and symptoms. Laboratory tests may include a complete blood count, iron/folate/Vitamin B12 levels, and an anti-nuclear antibody titer to screen for systemic illnesses.
unknown:there isn't just a single factor that causes SAR but an oral aphtha is a necrotic area with a deposit of fibrin and this description can be made for all the ulcerations of mucosae and skin. When the inflammation
starts, there is a damage of the tissue caused by a pathogenic agent or by autoimmunity; all this leads to 3 big phenomenons:
blood-interstice’s exchanges variation
blood-interstice’s cells migration.
Endothelial permeability rises because of the contraction of the cells due to factors that come from the damaged tissue or from a direct damage such as an infection or burn.
Water, electrolyte and proteins like fibrinogen and immunoglobulin flow in the damaged area and the tissue becomes edematous.
The fibrin polymerizes and the neutrophilus migrate in the area forming the inflammatory exudate.
When the inflammation gets chronic due to low self defences or to the persistence of the pathogenic agent we have: cell’s atrophy, cell’s death, granulation tissue and fibrosis.
A chronic damage of endothelium an alteration of vascular’s wall with a change in the blood flow and ipercoagulability (Virchow’s triad) thus causing thrombosis and suffering for the tissue that depended on that vessel.
The tissue becomes necrotic: no oxigen, no more ATP from mitochondrion, Na+ enters inside the cell with water, calcium rises up with membranes breaking off, cell’s content dispersion, lisosomal’s content dispersion thus starting inflammation. The necrotic tissue is rich in fibrin when there is a great deposition of fibrinogen and this is mainly seen around blood’s vessels.
There is growing evidence for an interplay between inflammatory and coagulation pathways in acute and chronic inflammatory diseases. Recent findings implicate TF in intestinal inflammation
and support an interaction between inflammation and coagulation in experimental colitis.
In chronic inflammation the levels of coagulation factors rise and this patients are highly susceptible to thrombosis
These diseases(Crohn,Coeliachiae)have an hereditary componentand and are caracterized by a high frequency of mutations of those genes which control the coagulation factors.
Cells and molecules classically implicated in the physiological process of coagulation have now been shown to behave abnormally in IBD and possibly to also play an active role in disease pathogenesis and/or disease progression. Some studies performed on the coagulation profile and risk factors for thrombosis in IBD
A peptic and an oral ulceration is characterized by necrosis and an exudates rich in fibrin.
A glomerulonefritis the same type of inflammation but here the pathogenic noxae cause damage with 2 mechanisms:
1 immunologic formation of immunocomplex
2 not-immunonologic with loss of membrane’s charges
Even here the damage is always caused by proliferation of cells like fibrocytes ,monocytes, linfocytes, polymorphousnucleatus, exudates, membrane’s thickening and fibrin’s deposition with capillary thrombosis.
Risk of Glomerular microthrombosis in lupus nephritis is attributable, at least in part, to an epistatic effect of PAI-1(plasminogen activator inhibitor 1 ) and beta-fibrinogen genes
It is caused by an immunologic disorder due to the activity of lymphocyte TCD8 that answer to an epithelial antigen causing the loss of adesion among keratinocytesand apoptosis of epithelial cells.
The course of illness, probably, starts from a not-identified antigen that stimulates keratincells and induces the secrection of cytokine by TCD8 and other chemotaxis agents by other leucocytes.
There is also a reduction of Thelper that control the activity of Tcytotoxicthanks to IL10.A genetic deficit of IL10 predispose to SAR.
- individual factors:age,sex,familiarity,heredity,hormonal alteration,hypersensitivity to foodstuff (milk,chocolate,gluten,walnut,cheese), medecins, deficit of iron, B12 ,zinc, predisposition to thrombosis
- environment factors:stress,local trauma,tobacco
- infectious factors:virus(herpes,CM, HIV ,varicella-zoster) and bacteriae
- sistemic pathology: IBD ,MC,Crohn,LES,AIDS,ematic disease
TISSUE SPECIFIC RISK FACTORS
Anatomical:oral mucosae and bowel’s show many similarities
Phisiopathological :mucosae-associated epithelial chemokine, MEC (CCL28), which is expressed by epithelia in different mucosal tissues, is selectively chemotactic for IgA Ab-secreting cells (ASC):concept of a common mucosal immune system
Oral ulceration, can be a manifestation of inflammatory bowel disease and a complication of drug therapy and in this case is highly recommended a biopsy.
Moreover oral ulceration that doesn't heal and gets easily chronic can represent an allarm of a sistemic disease such as a disorder in the coagulative factors thus leading to an accumulation of fibrin that can throttle blood vessel obstructing the flux and causing necrosis.
In the specific case of Coeliachia aphthous ulceration is related to immunologic mechanism
caused by genetic predisposure of those patients who show high frequency of HLA DRW10 and HLADQW1, while those with MC but no SAR have low frequency of the same histocompatibility complex
For those patients a treatment is possible because a gluten-free diet causes no SAR while gluten-diet increases IgA and causes SAR and often it's their dentist who is the first doctor to diagnose thier sistemic disease.