aphthous ulcers

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Aphthous ulcers

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Aphthous ulcers

Aphthous ulcers

Defect in the epithelium or loss in continuity of epithelium is called as ulcer.The term aphthous was first coined by Hippocrates as far back as 460370 BC in reference to disorders of the mouth. In general usage, the word aphthae refers to the presence of an otherwise undefined ulcer.

Clinical featuresAge: second, third and fourth decades.Sex: Females>MalesA higher prevalence has been found in the higher socioeconomic groups and among individuals with stress, such as students at the time of examinations.

PresentationThe individual ulcer begins as a round or oval area of erythema which develops a pin-point central area of white ulceration. Over the next 3-7 days the ulcer enlarges laterally and becomes saucerized or cupped out.As healing commences, the red halo diminishes and small punctate red areas dot the white ulcer bed (representing blood vessels from the underlying granulation tissue which have reached the surface). Over several days the white color of the bed changes to red or pink and the area heals without scar formation in the minor type and with scar in major type.

Classification

1.Simple 2. Complex

.contdSimple aphthous is described when ulcer recurrences are few and not associated with systemic factors and occur only 24 times each year. Complex aphthous is a disorder in which patients develop recurrent oral and genital aphthous ulcers or when there is a continuous disease activity with new lesions developing as older lesions heal, or when ulcers are associated with systemic diseases.

contdThe clinical presentations of RAS include Minor, Major, Herpetiform aphthae based on severity

contdTo determine management strategies, it is classified as Type A- RAS episodes lasting for only a few days, occurring only a few times a year. Type B- Painful RAS each month, lasting between 3-10 days Type C- Painful, chronic courses of RAS in which by one ulcer heals, another develop

Minor Aphthous: Minor Aphthous MILD APTHAE, CANKER SORE & MIKULICZ APTHAE

The prodromal stage of ulceration is variable, but there is usually a sensation described as burning or prickling and white papule for a short period before the ulcers appear

Each lesion lasts 1014 days and heals without scarring .

MAJOR APTHOUS: MAJOR APTHOUS PERIADENITIS MUCOSA NECROTICA RECURRENTIS OR SUTTON DISEASE OR MIKULICZ SCARRING APTHAE

Major ulcers have an irregular border and a size exceeding 10 mm. These lesions are deeper and larger and they last longer than minor aphthae . They persist longer than minor aphthae and can last for weeks or months and often leave a scar after healing .These lesions cause substantial pain associated with fever, dysphagia , and malaise.

HERPETIFORMFirst described by Cooke in 1960 later by lehner , brooke & sapp

Herpetiform aphthae are the least common type. This variety is characterized by multiple recurrent crops of 10 or more (as many as a hundred ulcers may be present at the same time) small ulcers of 23 mm in diameter, although they may fuse producing large irregular ulcers. This tendency to coalesce is similar to what is seen in viral infections, thus, the term herpetiform and the subsequent confusion. The herpetiform type, like the other forms of RAS, occurs usually on mobile mucosa and not on attached mucosa like a true herpes infection.

They have a predilection for the posterior part of the mouth, particularly the soft palate and pharyngeal wall or tonsillar fauces

RAS Associated syndrome

Behcets Syndrome Magic Syndrome: Mouth and genital ulcers with inflamed cartilage syndrome.It is a cutaneous condition with features of bothBehet's diseaseand relapsing polychondritis.Cyclic Neutropenia

Pfapa Syndrome : Periodic fever, aphthous stomatitis, pharyngitis and adenitis orperiodic feveraphthous pharyngitis and cervical adenopathy. in which highfeveroccurs periodically at intervals of about 35 weeks, frequently accompanied by aphthous-like ulcers,pharyngitisand/or cervical adenitis (cervical lymphadenopathy).

Sweets Syndrome: acute febrile neutrophilic dermatosisAIDS

Predisposing factorsGeneticSystemic diseaseStressMechanical injuryHormonalMicroelement deficiencyBacterial

Fig.2.

recurrent aphthae appear more frequently in patients with gastro-intestinal disturbances, mainly those from the group of chronic inflammatory bowel diseases (Crohns disease, ulcerative colitis) and celiac disease

In some patients with RAS, the deficiency in hematins (iron, folic acid, vitamin B12) was revealedsome food ingredients, e.g., chocolate, gluten, cow milk, preservatives, nuts and food coloring agents may induce the pro-inflammatory cascade in RAS

There is also the correlation between the serum levels of sexual hormones and the course of RAS. Exacerbations of the condition were observed mainly in the luteal phase of the menstrual cycle and during the menopause, while the remissions seem to appear often during pregnancy and in women on contraceptives

In many RAS-predisposed patients, the lesions appear on the oral mucosa shortly after mechanical irritation of the area; however, the mechanism of this reaction remains not fully understood

Psychogeniceffects modify the immune response also in the other conditions with a suspected autoimmune background, like lichen planus and chronic inflammatory bowel diseases

bacteria (Streptococcus oralis,Helicobacter pylori) and virus (herpes simplex virus, varicella-zoster virus, cytomegalovirus, adenoviruses) antigens.

Etiopathogenesis-AutoimmuneThere is an increased secretion of Th1 which causes increased cytokine releaseThis observation confirms that the imbalance in pro- and anti-inflammatory cytokines production may contribute to the development of autoimmunisation and RAS in predisposed subjects.decreased expression of heat shock protein 27 was observed in the oral mucosa of the RAS patients

lower incidence of aphthae in smokers compared to non-smokers due to increased hsp

HistopathologyAnitshkow cells: Pathognomic for rheumatic heart disease. The cells are also calledcaterpillar cells, as they have a large amount of clear cytoplasmsurrounding a rod-shapednucleusthat to some resembles a caterpillar.Squamous epithelial cellswith nuclear changes resembling Anitschkow cells have also been observed inrecurrent aphthous stomatitis,iron deficiency anemia, children receivingchemotherapy, as well as in healthy individuals

.contd.A central ulcer with a thick fibrin bed containing numerous neutrophilsA lichenoid infiltrate consisting of histiocytes, lymphocytes, neutrophils and a few eosinophilsWidely dilated capillaries in the lamina propriaSlight hyperplasia of the surrounding epithelium

D/DTraumatic ulcerSquamous cell carcinomaTB ulcerHerpetic ulcerPemphigus, pemphigoid.ANUG

TreatmentCauterizing drugs Azathioprine, Vitamins, Dapsone, Milk of Magnesia, Levamisole, NSAIDS, Pentoxifylline Topical Steroid, Thalidomide, Systemic Steroid.

Bechets syndrome

Behet's syndrome is diagnosed based on the finding of recurrent mouth ulcerations combined with any two of the following: Uveitis; eye inflammation, Genital ulcerations, or Skin abnormalities

EtiologySame as RASAutoimmune with trigger e may be either HSV or Strep, staph or E coli.GeneticHsp

Aphthous and genital ulcers:Aphthous ulcers are usually the first sign of Behet disease. These sores occur on the lips and tongue and buccal mucosa. The ulcers look like common canker sores, and they typically heal within one to two weeks.About 75 percent of all people with Behet disease develop similar ulcers on the genitals.These ulcers occur most frequently on the scrotum in men and on the labia in women.

Skin lesionsRashes and vesciculobullous lesions(resembling acne) on the face, neck, and arms

Uveitis:An inflammation of the eye is found in more than half of people with Behet disease. Eye problems are more common in younger people with the disease and affect men more often than women. Uveitis can result in blurry vision and an extreme sensitivity to light (photophobia). If untreated, the eye problems associated with Behet disease can lead to blindness.

Behet disease can also affect the joints, gastrointestinal tract, large blood vessels, and brain and spinal cord (central nervous system).

Treatment To manage symptoms so that there are no complicationsTetracyclineSteroidsAnaesthetics

Reiters syndrome

The classic triad of ReA symptoms (found in only one third of patients) consists of the following: Arthritis, urethritis and conjunctivitisReactive arthritis, after a GI or GU infection genitourinary tract symptoms foll sexual transmission of chlamydia andconjunctivitis. Lesions of the skin resembling psoriasis and mucous membranes also develop in some patients. Pus-filled sores on soles, palms, and penis. May also include mouth sores.

Common in AIDS patients

TreatmentAntibiotics to eliminate original bacterial infection, especially if genitourinaryNonsteroidal anti-inflammatory drugs (NSAIDs) to reduce joint inflammation and painDrainage of swollen joints then corticosteroid injections into painful joints

Sarcoidosis

Unknown etiology that manifests as non caseating granulomas,predominantly affects the lungs and intrathoracic lymph nodes.

Etiologyit's due to an overactive immune system that responds too strongly to an invading organism. Other researchers think sarcoidosis may be inherited, caused by an infection, or caused by allergens that are breathed in or toxins found in the environment.

Age: People in their 30s or 40sSex: F>M

Common symptoms, which tend to bevague, includefatigue(unrelieved by sleep; occurs in 66% of cases),lack of energy,weight loss, joint aches and pains (which occur in about 70% of cases),arthritis(1438% of persons), swelling of the kneesdry eyes, blurry vision,shortness of breath, a dry, hacking cough. Less commonly, people may cough up blood.or skin lesions.

Nearly all organs like skin, eyes, nervous system, joints are affected.

PathologyA noncaseating granuloma

Lab diagnosis

Increased ESRNeg Mantoux test.Kveim's test (intradermal injection of splenic material from a confirmed case of sarcoidosis, and histological examination of any nodule formed) has fallen out of favour due to the risk of transmission of new-variant Creutzfeldt-Jakob disease (nvCJD), and the several weeks it takes to get a diagnosis.

TreatmentAbout half of all people with sarcoidosis get better without needing treatment. For others, medications such as corticosteroids may help reduce lesions