Definisi[sunting]

Stomatitis berasal dari Bahasa Yunani, stoma yang berarti mulut dan itis yang berarti inflamasi (radang).[1] Stomatitis adalah inflamasi lapisan mukosa dari struktur apa pun pada mulut; seperti pipi, gusi (gingivitis), lidah (glossitis),[2] bibir, dan atap atau dasar mulut. Kata stomatitis sendiri secara bahasa berarti inflamasi pada mulut. Inflamasi dapat disebabkan oleh kondisi mulut itu sendiri (seperti oral hygiene yang buruk, susunan gigi yang buruk), cedera mulut akibat makanan atau minuman panas, atau oleh kondisi yang memengaruhi seluruh tubuh (seperti obat-obatan, reaksi alergi, atau infeksi).

Deskripsi[sunting]
Stomatitis adalah inflamasi lapisan struktur jaringan lunak apa pun pada mulut. Stomatitis biasanya merupakan kondisi yang menyakitkan, yang terkait dengan kemerahan, pembengkakan, dan kadang-kadang perdarahan dari daerah yang terkena. Bau mulut (halitosis) juga mungkin menyertai keadaan ini. Stomatitis terjadi pada semua kelompok umur, dari bayi hingga dewasa tua.

Sebab dan Gejala[sunting]

Sejumlah faktor dapat menyebabkan stomatitis, masalah umum pada populasi orang dewasa di Amerika Utara. Peralatan gigi yang kurang pas, pipi tergigit, atau gigi bergerombol dapat mengiritasi struktur mulut secara terus-menerus. Pernapasan mulut kronis karena saluran hidung yang tersumbat dapat menyebabkan jaringan mulut kekeringan, yang selanjutnya akan menjadi iritasi. Minum minuman yang terlalu panas dapat membakar mulut, dan berlanjut pada iritasi dan nyeri. Penyakit-penyakit seperti infeksi herpes, gonorrhea, campak, leukemia, AIDS, dan kekurangan vitamin C dapat menimbulkan tanda-tanda oral. Penyakit sistemik lain yang berkaitan dengan stomatitis termasuk Inflammatory bowel disease (IBD) dan Sindrom Behet, suatu kelainan inflamasi multisistem dengan sebab yang tidak diketahui (idiopatik). Stomatitis aftosa, juga dikenal sebagai Stomatitis aftosa rekuren (SAR),[2][3] adalah jenis spesifik stomatitis yang muncul dengan ulkus yang dangkal dan nyeri yang biasanya ada di bibir, pipi, gusi, atap atau dasar mulut. Rentang diameter ulkus ini dari bintik kecil hingga 1 inchi (2,5 cm) atau lebih. Walaupun penyebab SAR tidak diketahui; yang diduga adalah defisiensi nutrisi, khususnya vitamin B12, folat, atau besi. Stomatitis generalisata atau stomatitis kontak dapat terjadi akibat penggunaan berlebihan dari alkohol, merica, makanan panas, atau produk tembakau. Sensitivitas terhadap obat kumur, pasta gigi, dan lipstik, dapat mengiritasi lapisan mulut. Paparan terhadap logam berat, seperti merkuri, timah, bismut, dapat menyebabkan stomatitis.[3] Stomatitis mikotik atau lebih dikenal sebagai Kandidiasis oris[4] adalah suatu jenis stomatitis yang disebabkan oleh infeksi jamur.[3] Stomatitis herpetika adalah herpes simpleks yang mengenai mukosa oral dan bibir, ditandai dengan pembentukan vesikel kekuningan yang pecah dan menghasilkan ulkus tidak rata, nyeri, yang dilapisi dengan membran abu-abu dan dikelilingi oleh halo yang eritematous. [2]

Stomatitis medikamentosa adalah stomatitis akibat reaksi alergi terhadap obat-obatan yang ditelan, diabsorbsi lewat kulit atau mukosa, atau diberikan dengan injeksi hipodermik. Gejala utama antara lain vesikel, erosi, ulkus, eritema, purpura, angioedema, rasa terbakar, dan gatal. [2]

Diagnosis[sunting]
Diagnosis stomatitis bisa saja sulit. Riwayat pasien mungkin menyingkap defisiensi nutrisi, penyakit sistemik, atau kontak dengan bahan yang menyebabkan reaksi alergi. Pemeriksaan fisik dilakukan untuk mengevaluasi lesi oral dan masalah kulit lainnya. Pemeriksaan darah dapat dilakukan untuk menentukan jika ada infeksi. Apusan mukosa mulut dapat dikirim ke laboratorium untuk evaluasi mikroskopik, atau kultur mulut juga dapat dilakukan untuk menentukan jika kemungkinan agen infeksius adalah penyebab masalahnya.

Perawatan[sunting]
Perawatan stomatitis berdasarkan pada masalah penyebabnya. Pembersihan lokal dan oral hygiene yang baik adalah hal mendasar. Makanan bertepi tajam seperti kacang, tacos, keripik kentang sebaiknya dihindari. Sikat gigi dengan buku sikat lunak sebaiknya digunakan, gigi dan gusi sebaiknya disikat dengan hati-hati; pasien sebaiknya menghindari mengetukkan sikat gigi ke gusi. Faktor lokal seperti peralatan gigi yang tidak pas atau gigi yang tajam, dapat dikoreksi oleh dokter gigi. Penyebab infeksi biasanya dapat dirawat dengan obat-obatan. Masalah sistemik seperti AIDS, leukemia, dan anemia dirawat oleh dokter spesialis yang sesuai. Cedera mulut minor akibat minuman atau makanan panas biasanya akan membaik sendiri dalam seminggu atau lebih. Masalah stomatitis aftosa yang kronis dirawat pertama kali dengan mengoreksi defisiensi vitamin B12, besi, atau folat. Jika terapi tersebut tidak berhasil, dapat diresepkan obat-obatan yang diaplikasikan pada tiap ulkus aftosa dengan aplikator kapas. Terapi ini berhasil pada sejumlah kecil pasien. Lebih terkini, perawatan laser karbon dioksida berdaya rendah telah ditemukan untuk meringankan ketidaknyamanan akibat SAR. Wabah stomatitis aftosa dapat dirawat dengan antibiotik tetrasiklin atau kortikosteroid. Valasiklovir telah terbukti efektif untuk merawat stomatitis yang disebabkan oleh virus Herpes (Stomatitis Herpetika). Pasien juga dapat diberikan anestesi topikal (biasanya gel lidokain 2%) untuk meringankan nyeri dan pasta protektif (Orabase) atau agen pelapis seperti Kaopektat untuk melindungi daerah erosi dari iritasi lanjut gigi, gigi palsu, atau kawat gigi.

Perawatan Alternatif[sunting]
Perawatan alternatif stomatitis secara garis besar melibatkan pencegahan masalah. Pasien dengan peralatan gigi seperti gigi palsu sebaiknya mengunjungi dokter giginya secara teratur. Pasien dengan penyakit sistemik atau masalah medis kronis perlu bertanya kepada penyedia pelayanan kesehatannya, jenis masalah oral apa yang dapat diperoleh akibat penyakit tertentu mereka. Pasien ini juga harus menghubungi klinik mereka saat tanda awal masalah. Sensasi umum perlu dilatih saat mengonsumsi makanan atau minuman panas. Penggunaan tembakau

sebaiknya dihindari. Alkohol sebaiknya digunakan secara moderat. Obat kumur dan pasta gigi yang diketahui pasien menyebabkan masalah sebaiknya dihindari. Kedokteran herbal dapat mendampingi dalam menyelesaikan stomatitis. Salah satu herba, kalendula (Calendula officinalis), dalam bentuk tingtur (ekstrak herbal berdasar alkohol) dan dilarutkan untuk kumurmulut, mungkin cukup efektif dalam merawat stomatitis aftosa dan manifestasi lain stomatitis. Lebih terkini, sekelompok peneliti di Brazil telah melaporkan bahwa ekstrak yang dibuat dari daun Trichilia glabra, tanaman yang ditemukan di Amerika Selatan, efektif dalam membunuh beberapa virus yang menyebabkan stomatitis.

Prognosis[sunting]
Prognosis untuk kesembuhan stomatitis tergantung pada penyebab masalah. Banyak faktor lokal dapat dimodifikasi, dirawat, atau dihindari. Penyebab infeksius stomatitis biasanya dapat diatasi dengan obat-obatan, atau jika masalahnya disebabkan oleh obat-obatan tertentu, dengan mengganti agen penyebab tersebut.

Pencegahan[sunting]
Stomatitis yang disebabkan oleh iritasi lokal dapat dicegah dengan oral hygiene yang baik, pemeriksaan-gigi yang teratur, dan kebiasaan-diet yang baik. Masalah stomatitis yang disebabkan oleh penyakit sistemik dapat diminimalkan dengan oral hygiene yang baik dan secara cermat mengikuti terapi medis yang diberikan oleh penyedia pelayanan kesehatan pasien.[3]

Daftar Pustaka[sunting]
1. Jump up (en) Mosby's Medical Dictionary. 8th ed. [Place unknown]: Elsevier, Inc.; c2009. Stomatitis. 2. Jump up to:2,0 2,1 2,2 2,3 (en) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health. 7th ed. Philadelphia: W.B. Saunders; c2003. Stomatitis. 3. Jump up to:3,0 3,1 3,2 3,3 (en) Gale Encyclopedia of Medicine. [Place unknown]: The Gale Group, Inc.; c2008. Stomatitis. 4. Jump up (en) Dorland's Medical Dictionary for Health Consumers. Philadelphia: W.B. Saunders; c2007. Stomatitis.

http://id.wikibooks.org/wiki/Catatan_Dokter_Muda/Stomatitis

Stomatitis
From Wikipedia, the free encyclopedia

Stomatitis
Classification and external resources

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ICD-10

K12

ICD-9

)2*.+

DiseasesDB

2,1)*

Stomatitis is inflammation of the mouth.[1] The term refers to any inflammatory process affecting the mucous membranes of the mouth and lips, with or withoutoral ulceration.[2] In its widest meaning, stomatitis can therefore have a multitude of different causes and appearances. Common causes include infections, nutritional deficiencies, allergic reactions, radiotherapy, and many others. When there is inflammation of the gums and the mouth generally, sometimes the term gingivostomatitis is used, although this is also sometimes used as a synonym for herpetic gingivostomatitis.

Examples[edit]
Nutritional deficiency[edit]
Malnutrition (improper dietary intake) or malabsorption (poor absorption of nutrients into the body) can lead to nutritional deficiency states, several of which can lead to stomatitis. For example, deficiencies of iron, vitamin B2 (riboflavin),[3]:490vitamin B3 (niacin), vitamin B6 (pyridoxine), vitamin B9 (folic acid) or vitamin B12 (cobalamine) may all manifest as stomatitis. Iron is necessary for the upregulation of transcriptional elements for cell replication

and repair. Lack of iron can cause genetic downregulation of these elements, leading to ineffective repair and regeneration of epithelial cells, especially in the mouth and lips. Many disorders which cause malabsorption can cause deficiencies, which in turn causes stomatitis. Examples include tropical sprue.[3]:49

Aphthous stomatitis[edit]
Main article: Aphthous stomatitis Aphthous stomatitis (canker sores) is the recurrent appearance of mouth ulcers in otherwise healthy individuals. The cause is not completely understood, but it is thought that the condition represents a T cell mediated immune response which is triggered by a variety of factors. The individual ulcers (aphthae) recur periodically and heal completely, although in the more severe forms new ulcers may appear in other parts of the mouth before the old ones have finished healing. Aphthous stomatitis is one of the most common diseases of the oral mucosa, and is thought to affect about 20% of the general population to some degree.[4] The symptoms range from a minor nuisance to being disabling in their impact on eating, swallowing and talking, and the severe forms can cause people to lose weight. There is no cure for aphthous stomatitis, [5]and therapies are aimed at alleviating the pain, reducing the inflammation and promoting healing of the ulcers, but there is little evidence of efficacy for any treatment that has been used.

Angular stomatitis[edit]
Main article: Angular cheilitis Inflammation of the corners (angles) of the lips is termed angular stomatitis or angular cheilitis. In children a frequent cause is repeated lip-licking and in adults it may be a sign of underlying iron deficiency anemia, or vitamin B deficiencies (e.g. B2-riboflavin, B9-folate or B12-cobalamin, which in turn may be evidence of poor diets or malnutrition such as celiac disease). Also, angular cheilitis can be caused by a patient's jaws at rest being 'overclosed' due to edentulousness or tooth wear, causing the jaws to come to rest closer together than if the complete/unaffected dentition were present. This causes skin folds around the angle of the mouth which are kept moist by saliva which in turn favours infection; mostly by Candida albicans or similar species. Treatment usually involves the administration of topical nystatin or similar antifungal agents. Another treatment can be to correct the jaw relationship with dental treatment (e.g. dentures or occlusal adjustment).

Denture-related stomatitis[edit]
Main article: Denture-related stomatitis This is a common condition present in denture wearers. It appears as reddened but painless mucosa beneath the denture. 90% of cases are associated with Candidia species, and it is the most common form of oral candidiasis. Treatment is byantifungal medication and improved dental hygiene, such as not wearing the denture during sleep.

Allergic contact stomatitis[edit]

Patch test

Allergic contact stomatitis (also termed "allergic gingivostomatitis" or "allergic contact gingivostomatitis")[6] is a type IV (delayed) hypersensitivity reaction that occurs in susceptible atopic individuals when allergens penetrate the skin or mucosa.[7] Allergens, which may be different for different individuals, combine with epithelial-derived proteins, forming haptens which bind with Langerhans cells in the mucosa, which in turn present the antigen on their surface to T lymphocytes, sensitizing them to that antigen and causng them to produce many specific clones. The second time that specific antigen is encountered, an inflammatory reaction is triggered at the site of exposure. [7] Allergic contact stomatitis is significantly less common than allergic contact dermatitis because the mouth is coated in saliva, which washes away antigens and acts as a barrier. The oral mucosa is also more vascular than skin, meaning that any antigens are more quickly removed from the area by the circulation. Finally, there is substantially lesskeratin in oral mucosa, meaning that there is less likelihood that haptans will form.[7] Allergic contact stomatitis appears as non-specific inflammation, so it may be mistaken for chronic physical irritation.[7] There may be burning or soreness of the mouth and ulceration. [7] Chronic exposure to the allergen may result in a lichenoid lesion.[7] Plasma cell gingivitis may also occur, which may be accompanied by glossitis and cheilitis.[7] Example allergens that may cause allergic contact stomatitis in some individuals include cinnamaldehyde, Balsam of Peru,peppermint, mercury, gold, pyrophosphates, zinc citrate, free acrylic monomer, nickel and sodium lauryl sulfate.[8][9][10][7][11][12] These allergens may originate from many sources, including foods and drink, chewing gum, toothpaste, mouthwash, dental floss, dental fillings, dentures, orthodontic bands or wires, or many other sources. [7] If the substance containing the allergen comes into contact with the lips, allergic contact cheilitis can occur together with allergic contact stomatitis. The diagnosis is confirmed by patch test, and management is by avoidance of exposure to the allergen.[7]

Migratory stomatitis[edit]
Main article: Geographic tongue Migratory stomatitis (or geographic stomatitis) is an atypical presentation of a condition which normally presents on the tongue, termed geographic tongue. Geographic tongue is so named

because there are atrophic, erythematous areas ofdepapillation that migrate over time, giving a map-like appearance. In migratory stomatitis, other mucosal sites in the mouth, such as the ventral surface (undersurface) of the tongue, buccal mucosa, labial mucosa, soft palate or floor of mouth may be afflicted with identical lesions, usually in addition to the tongue. [13] Apart from not being restricted to the tongue, migratory stomatitis is an identical condition in every regard to geographic tongue. Another synonym for geographic tongue which uses the term stomatitis is "stomatitis areata migrans".

Herpetic gingivostomatitis[edit]

Herpetic stomatitis (herpetic gingivostomatitis)

Main article: Herpetic gingivostomatitis This is inflammation of the mouth caused by herpes simplex virus.

Irradiation and chemotherapy[edit]

Stomatitis may also be caused by chemotherapy, or radiation therapy of the oropharyngeal area.
[14]

The term mucositis is sometimes used synonymously with stomatitis, however the former refers to mucosal reactions to radiotherapy orchemotherapy, and may occur anywhere in the gastrointestinal tract and not just in the mouth.[15]

Necrotizing ulcerative gingivostomatitis[edit]

See Necrotizing periodontal diseases The term necrotizing ulcerative gingivostomatitis is sometimes used as a synonym of the necrotizing periodontal disease more commonly termed necrotizing ulcerative gingivitis, or a more severe form (also termed necrotizing stomatitis). The termnecrotizing gingivostomatitis is also sometimes used.[16]

Stomatitis nicotina[edit]
Main article: Stomatitis nicotina Also called smoker's palatal keratosis,[17]:176 this condition may occur in smokers, especially pipe smokers. The palate appears dry and cracked, and white from keratosis. The minor salivary glands appear as small, red and swollen bumps. It is not a premalignant condition and the appearance reverses if the smoking is stopped.[17]:176

Chronic ulcerative stomatitis[edit]

Chronic ulcerative stomatitis is a recently discovered condition with specific immunopathologic features.[18] It is characterized by erosions and ulcerations which relapse and remit. Lesions are located on the buccal mucosa (inside of the cheeks) or on the gingiva (gums).[19][20] It is characterized by painful erosions and ulcerations which relapse and remit. Th condition resembles Oral lichen planus when biopsied. The diagnosis is made with Immunofluorescence techniques, which shows circulating and tissuebound autoantibodies (particulate stratified squamous-epithelium-specific antinuclear antibody) to DeltaNp63alpha protein, a normal component of the epithelium. Treatment is with hydroxychloroquine.[18]

Plasma cell gingivostomatitis[edit]

Main article: plasma cell gingivitis Terms such as plasma cell gingivostomatitis,[21] atypical gingivostomatitis and idiopathic gingivostomatitis[22][23] are sometimes a synonym for plasma cell gingivitis, or specifically to refer to a severe form of plasma cell gingivitis.

Other forms of stomatitis[edit]

Periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA) syndromeoccurs in children. Uremic stomatitisa rare form of stomatitis that occurs with renal failure.[24] Neutropenia.[citation needed] Pyostomatitis vegetans Bovine papular stomatitis

http://en.wikipedia.org/wiki/Stomatitis

Aphthous stomatitis
From Wikipedia, the free encyclopedia

Aphthous stomatitis
Classification and external resources

Canker sore on the #ower #ip

ICD-10

K12.+

ICD-9

)2*.2

MedlinePlus

+++--*

eMedicine

ent/,++ derm/4*.ped/2.,2

MeSH

D+132*1

Aphthous stomatitis (also termed canker sores,[1] recurrent aphthous stomatitis, RAS, recurring oral aphthae and recurrent aphthous ulceration) is a common cause of benign and non-contagious mouth ulcers, (also called canker sores or aphthae). This condition is characterized by the repeated formation of ulcers in the mouth, in otherwise healthy individuals.[2]These ulcers occur periodically and heal completely between attacks. Symptoms range from a minor nuisance to interfering with eating and drinking, and more severe forms may be debilitating. The cause is not completely understood, but the condition involves a T cell-mediated immune response which is triggered by a variety of factors. Individuals vary in their observed triggers, which may include nutritional deficiencies, local trauma, stress, hormonal influences, allergies, a genetic predisposition and other factors. The condition is very common, affecting about 20% of the general population to some degree.
[3]

Most aphthae appear on the non-keratinizing epithelial surfaces in the mouth (i.e. anywhere

except the attached gingiva, the hard palate and the dorsum of the tongue), although the more severe forms may also involve keratinizing epithelial surfaces. In the majority of cases, the

individual ulcers last about 710 days,[2] and ulceration episodes occur about 3-6 times per year.
[4]

Aphthous stomatitis often starts during childhood or adolescence, and the condition usually

lasts for several years before gradually disappearing. [5] There is no cure, and treatments aim to manage pain, promote healing and reduce the frequency of episodes of ulceration. [2]

Signs and symptoms[edit]

Aphthous ulcers on the labial mucosa (lower lip is retracted). Note erythematous "halo" surrounding ulcer.

Persons with aphthous stomatitis have no detectable systemic symptoms or signs (i.e. outside the mouth).[5] Generally, symptoms may include prodromal sensations such as burning, itching or stinging, which may precede the appearance of any lesion by some hours; and pain, which is often out of proportion to the extent of the ulceration and is worsened by physical contact, especially with certain foods and drinks (e.g. acidic). Pain is worst in the days immediately following the initial formation of the ulcer, and then recedes as healing progresses. [6] If there are lesions on the tongue, speaking and chewing can be uncomfortable, and ulcers on the soft palate, oropharynx or esophagus can cause odynophagia (painful swallowing).[6] Severe disease, characterized by virtually constant ulceration (new lesions developing before old ones have healed), may cause debilitating chronic pain, weight loss and malnutrition.[6] Signs are limited to the lesions themselves. Aphthous ulcers typically begin as erythematous macules (reddened, flat area of mucosa) which develop into ulcers that are covered with a yellowgrey fibrinous membrane that can be scraped away. An erythematous "halo" surrounds the ulcer.
[3]

The size, number, location, healing time and periodicity between episodes of ulcer formation are all dependent upon the subtype of aphthous stomatitis.

Causes[edit]
The cause is not entirely clear,[5] but is thought to be multifactorial.[2] It has even been suggested that aphthous stomatitis is not a single entity but rather a group of conditions with different causes.[5] Multiple research studies have attempted to identify a causative organism, but aphthous stomatitis appears to be non-contagious, non-infectious and not sexually transmissible. [5] The mucosal destruction is thought to be the result of a T cell (T lymphocyte) mediated immune response which involves the generation of interleukins and tumor necrosis factor alpha (TNF-).[2] Mast cells and macrophages are also involved, secreting TNF- along with the T cells. When early aphthous ulcers are biopsied, the histologic appearance shows a dense

inflammatory infiltrate, 80% of which is made up of T cells. [3] Persons with aphthous stomatitis have circulating lymphocytes which react with peptides 91-105 of heat shock protein 65-60. [5] Furthermore, the ratio of CD4+ T cells to CD8+ T cells in the peripheral blood of individuals with aphthous stomatitis is decreased.[3] Despite this preferred theory of immuno-dysregulation held by most researchers, [1] aphthous stomatitis behaves dis-similarly to autoimmune diseases in many regards. There is no association between aphthous stomatitis and other autoimmune diseases, which often accompany each other; common autoantibodies are not detected, the condition tends to resolve spontaneously with advancing age rather than worsen,[5] and usually serum immunoglobulins are at normal levels.[5] Evidence for the T cell-mediated mechanism of mucosal destruction is strong, but the exact triggers for this process are unknown and are thought to be multiple and varied from one person to the next. This suggests that there are a number of possible triggers, each of which is capable of producing the disease in different subgroups. In other words, different subgroups of individuals with aphthous stomatitis appear to have different causes for the condition. These sub-groups have been considered to be in three general groups, namely primary immuno-dysregulation, decrease of the mucosal barrier and states of heightened antigenic sensitivity. [1][3]

Immunity[edit]
At least 40% of people with aphthous stomatitis have a positive family history, suggesting that some people are genetically predisposed to suffering with oral ulceration. [2] HLA-B12, HLAB51, HLA-Cw7, HLA-A2, HLA-A11, and HLA-DR2 are examples of human leukocyte antigen types associated with aphthous stomatitis.[3][5] However, these HLA types are inconsistently associated with the condition, and also vary according to ethnicity. [7] People who have a positive family history of aphthous stomatitis tend to develop a more severe form of the condition, and at an earlier age than is typical.[7] Stress has effects on the immune system,[1] which may explain why some cases directly correlate with stress. It is often stated that ulceration is exacerbated during examination periods and lessened during periods of vacation.[3][5] Alternatively, it has been suggested that oral parafunctional activities such as lip or cheek chewing become more pronounced during periods of stress, and hence the mucosa is subjected to more minor trauma. [7] Aphthous-like ulceration also occurs in conditions involving systemic immuno-dysregulation, e.g. cyclic neutropenia andhuman immunodeficiency virus infection. In cyclic neutropenia, more severe oral ulceration occurs during periods of severe immuno-dysregulation, and resolution of the underlying neutropenia prevents the cycle of ulceration. The relative increase in percentage of CD8+ T cells, caused by a reduction in numbers of CD4+ T cells may be implicated in RAStype ulceration in HIV infection.[3]

Mucosal barrier[edit]
The thickness of the mucosa may be an important factor in aphthous stomatitis. Usually, ulcers form on non keratinizing mucosal surfaces in the mouth. Factors which decrease the thickness of mucosa increase the frequency of occurrence, and factors which increase the thickness of the mucosa correlate with decreased ulceration.[3]

The nutritional deficiencies associated with aphthous stomatitis (B12, folate, and iron) can all cause a decrease in the thickness of the oral mucosa (atrophy).[3] Local trauma is also associated with aphthous stomatitis, and it is known that trauma can decrease the mucosal barrier. Trauma could occur during injections of local anesthetic in the mouth, or otherwise during dental treatments, frictional trauma from a sharp surface in the mouth such as broken tooth, or from tooth brushing.[7] Hormonal factors are capable of altering the mucosal barrier. In one study, a small group of females with apthous stomatitis had fewer occurrences of aphthous ulcers during the luteal phase of the menstrual cycle or with use of the contraceptive pill.[3][5] This phase is associated with a fall in progestogen levels, mucosal proliferation and keratinization. This subgroup often experiences remission during pregnancy. However, other studies report no correlation between aphthous stomatitis and menstrual period, pregnancy or menopause. [7] Aphthous stomatitis is uncommon in people who smoke.[2] Tobacco use is associated with an increase in keratinization of the oral mucosa.[3] In extreme forms, this may be diagnosed as leukoplakia or stomatitis nicotina (smoker's keratosis). This increased keratinization may mechanically reinforce the mucosa and reduce the tendency of ulcers to form after minor trauma, or present a more substantial barrier to microbes and antigens, but this is unclear. Nicotine is also known to stimulate production of adrenal steroids and reduce production of TNF- , interleukin-1 and interleukin-6.[7] Cessation of smoking is known to sometimes precede the onset of aphthous stomatitis in people previously unaffected, or exacerbate the condition in those who were already experiencing aphthous ulceration.[5] Despite this correlation, starting smoking again does not usually lessen the condition.[8]

Antigenic sensitivity[edit]
It has been hypothesized that the condition represents a state of heightened sensitivity to antigenic stimuli, with cross-reactivity of the resulting cell-mediated immune response with cells of the epithelium. Some hypothesize that aphthous stomatitis is caused by expression of HLA class II antigens along with the normally found HLA class I antigens in epithelial cells, which results in them being recognized by the immune system as foreign cells rather than self.
[1]

Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster virus,adenovirus, and cytomegalovirus.
[3]

Others argue that there is no available evidence that demonstrates that any of these organisms are capable of causing aphthous stomatitis by themselves.[1] Some people with aphthous stomatitis may show herpes virus within the epithelium of the mucosa, but without any productive infection. In some persons, attacks of ulceration occur at the same time as asymptomatic viral shedding and elevated viral titres. [3] However, antiviral medication has no effect on aphthous stomatitis.[1] In some subgroups, food allergy may be involved, and some may respond to strict elimination diets based on the results ofpatch testing.[3][5] Sodium lauryl sulphate (SLS), a detergent present in some brands of toothpaste and oral healthcare products, may produce oral ulceration. [5] It has been shown that aphthous stomatitis is more common in people using toothpastes containing SLS, and that some reduction in ulceration occurs when a SLS-free toothpaste is used.

[7]

However, others have argued that since SLS is almost ubiquitously used in oral hygiene

products, there is unlikely to be a true predisposition for aphthous stomatitis caused by SLS. [7]

Systemic disease[edit]
Systemic disorders associated with aphthousli e ulceration/30 (eh1et2s disease Ce#ia% disease C&%#i% neutropenia 3utritiona# de i%ien%ies 4g5 de i%ien%& 4mmuno%ompromised states! e.g. 64' 4n #ammator& bowe# disease M574C s&ndrome 89585 s&ndrome :eiter2s disease Sweet2s s&ndrome ;#%us <u#<ae a%utum Main article: Oral ulceration Aphthous-like ulceration may occur in association with several systemic disorders (see table). These ulcers are clinically and histopathologically identical to the lesions of aphthous stomatitis, but this type of oral ulceration is not considered to be true aphthous stomatitis by some sources.
[2][9]

Some of these conditions may cause ulceration on other mucosal surfaces in addition to the mouth such as the conjunctiva or the genital mucous membranes. Resolution of the systemic condition often leads to decreased frequency and severity of the oral ulceration. [3] The main feature of Behet's disease is aphthous-like ulceration, but this is usually more severe than seen in aphthous stomatitis without a systemic cause, and typically resembles major or herpetiforme ulceration or both.[2][10]Aphthous-like ulceration is the first sign of the disease in 2575% of cases.[3]Behet's is more common in individuals whose ethnic origin is from regions along the Silk Road (between the Mediterranean and the Far East).[11] MAGIC syndrome is a possible variant of Behet disease, and is associated with aphthous-like ulceration. The name stands for "mouth and genital ulcers with inflamed cartilage" (relapsing polychondritis).[7] PFAPA syndrome is a rare condition that tends to occur in children.[7] The name stands for "periodic fever, aphthae, pharyngitis (sore throat) and cervical adenitis" (inflammation of the lymph nodes in the neck). The fevers occur periodically about every 35 weeks. The condition appears to improve with tonsillectomy or immunosuppression, suggesting an immunologic cause.[10]

In cyclic neutropenia, there is a reduction in the level of circulating neutrophils in the blood that occurs about every 21 days.Opportunistic infections commonly occur and aphthous-like ulceration is worst during this time.[10] Nutritional deficiencies may occur without any underlying gastrointestinal disease. Hematinic deficiencies (vitamin B12, folic acid and iron) may be twice as common in people with RAS, but iron and vitamin supplements only infrequently improve the ulceration. [10] The relationship to vitamin B12 deficiency has been the subject of many studies. Although these studies found that 0-42% of those with recurrent ulcers suffer from vitamin B12 deficiency, an association with deficiency is rare. Even in the absence of deficiency, vitamin B12 supplementation may be helpful due to unclear mechanisms. [12] Hematinic deficiencies can cause anemia, which is also associated with aphthous-like ulceration. [2] Gastrointestinal disorders are sometimes associated with aphthous-like stomatitis, e.g. most commonly Celiac disease, but also inflammatory bowel disease such as Crohn's disease or ulcerative colitis.[2] The link between gastrointestinal disorders and aphthous stomatitis is probably related to nutritional deficiencies caused by malabsorption.[10] Less than 5% of people with RAS have Celiac disease, which usually presents with severe malnutrition, anemia, abdominal pain, diarrhea andglossitis (inflammation of the tongue).[7] Sometimes aphthous-like ulcerations can be the only sign of celiac disease.[7]Despite this association, a gluten-free diet does not usually improve the oral ulceration.[10] Other examples of systemic conditions associated with aphthous-like ulceration include Reiter's syndrome,[2] and recurrenterythema multiforme.[2]

Diagnosis[edit]

Patch test. Areas of the skin on the back are stimulated with various common allergens. The ones which cause an inflammatory reaction may also be involved in recurrent oral ulceration

Diagnosis is mostly based on the clinical appearance and the medical history. [5] The most important diagnostic feature is a history of recurrent, self healing ulcers at fairly regular intervals.
[13]

Although there are many causes of oral ulceration, recurrentoral ulceration has relatively few causes, most commonly aphthous stomatitis, but rarely Behet's disease, erythema multiforme, ulceration associated with gastrointestinal disease, [8][13] and recurrent intra-oral herpes simplex infection. A systemic cause is more likely in adults who suddenly develop recurrent oral ulceration with no prior history.[10]

Special investigations may be indicated to rule out other causes of oral ulceration. These include blood tests to exclude anemia, deficiencies of iron, folate or vitamin B12 or celiac disease. Some suggest that screening for celiac disease should form part of the routine work up for individuals complaining of recurrent oral ulceration.[7]Many of the systemic diseases cause other symptoms apart from oral ulceration, which is in contrast to aphthous stomatitis where there is isolated oral ulceration. Patch testing may be indicated if allergies are suspected (e.g. a strong relationship between certain foods and episodes of ulceration). Several drugs can cause oral ulceration (e.g. nicorandil), and a trial substitution to another drug may highlight a causal relationship.[5] Tissue biopsy is not usually required, unless to rule out other suspected conditions such as oral squamous cell carcinoma.[13] The histopathologic appearance is not pathognomonic (the microscopic appearance is not specific to the condition). Early lesions have a central zone of ulceration covered by a fibrinous membrane. In the connective tissue deep to the ulcer there is increased vascularity and a mixed inflammatory infiltrate composed of lymphocytes, histiocytes andpolymorphonuclear leukocytes. The epithelium on the margins of the ulcer shows spongiosis and there are many mononuclear cells in the basal third. There are also lymphocytes and histiocytes in the connective tissue surrounding deeper blood vessels near to the ulcer ("perivascular cuffing").[3][13]

Classification[edit]
Aphthous stomatitis has been classified as a type of non-infectious stomatitis (inflammation of the mouth).[13] One classification distinguishes "common simple aphthae", accounting for 95% of cases, with 3-6 attacks per year, rapid healing, minimal pain and restriction of ulceration to the mouth; and "complex aphthae", accounting for 5% of cases, where ulcers may be present on the genital mucosa in addition to mouth, healing is slower and pain is more severe. [4] A more common method of classifying aphthous stomatitis is into three variants, distinguished by the size, number and location of the lesions, the healing time of individual ulcers and whether a scar is left after healing (see below). Minor aphthous ulceration[edit] This is the most common type of aphthous stomatitis, accounting for about 80% of all cases. This subtype is termed minor aphthous ulceration (MiAU),[5] or minor recurrent aphthous stomatitis (MiRAS). The lesions themselves may be referred to as minor aphthae or minor aphthous ulcers. These lesions are generally less than 10 mm in diameter and affect non-keratinized mucosal surfaces (i.e. the labial and buccal mucosa, lateral borders of the tongue and the floor of the mouth). Usually several ulcers appear at the same time, but single ulcers are possible. Healing usually takes seven to ten days and leaves no scar. Between episodes of ulceration, there is usually an ulcer-free period of variable length.[2] Major aphthous ulceration[edit] This subtype makes up about 10% of all cases of aphthous stomatitis. [3] It is termed major aphthous ulceration (MaAU) or major recurrent aphthous stomatitis (MaRAS). Major aphthous ulcers (major aphthae) are similar to minor aphthous ulcers, but are more than 10 mm in diameter and the ulceration is deeper.[2][3] Because the lesions are larger, healing takes longer

(about twenty to thirty days), and may leave scars. Each episode of ulceration usually produces a greater number of ulcers, and the time between attacks is less than seen in minor aphthous stomatitis.[3] Major aphthous ulceration usually affects non keratinized mucosal surfaces, but less commonly keratinized mucosa may also be involved, such as the dorsum (top surface) of the tongue or the gingiva (gums).[7] The soft palate or the fauces (back of the throat) may also be involved,[7]the latter being part of the oropharynx rather than the oral cavity. Herpetiform ulceration[edit] Herpetiform ulcers,[2] (also termed stomatitis herpetiformis,[14] or herpes-like ulcerations) is a subtype of aphthous stomatitis so named because the lesions resemble a primary infection with herpes simplex virus (primary herpetic gingivostomatitis).[3]However, herpetiform ulceration is not caused by herpes viruses. As with all types of aphthous stomatitis, it is not contagious. Unlike true herpetic ulcers, herpetiforme ulcers are not preceded by vesicles (small, fluid filled blisters).[7]Herpetiforme ulcers are less than 1 mm in diameter and occur in variably sized crops up to one hundred at a time. Adjacent ulcers may merge to form larger, continuous areas of ulceration. Healing occurs within fifteen days. The ulceration may affect keratinized mucosal surfaces in addition to non keratinized. Herpetiform ulceration is often extremely painful, and the lesions recur more frequently than minor or major aphthous ulcers. Recurrence may be so frequent that ulceration is virtually continuous. It generally occurs in a slightly older age group than the other subtypes,[7] and females are affected slightly more frequently than males.[5] RAS type ulceration[edit] Recurrent oral ulceration associated with systemic conditions is termed "RAS type ulceration", "RAS like ulceration" or "aphthous-like ulcers".[5] Aphthous stomatitis occurs in individuals with no associated systemic disease.[2] Persons with certain systemic diseases may be prone to oral ulceration, but this is secondary to the underlying medical condition (see thesystemic disease section).[2] This kind of ulceration is considered by some to be separate from true aphthous stomatitis.[2][9]However, this definition is not strictly applied. For example, many sources refer to oral ulceration caused by anemia and/or nutritional deficiencies as aphthous stomatitis, some also consider Behet's disease to be a variant.[3]

Treatment[edit]
The vast majority of people with aphthous stomatitis have minor symptoms and do not require any specific therapy. The pain is often tolerable with simple dietary modification during an episode of ulceration such as avoiding spicy or acidic foods and beverages. [6] Many different topical and systemic medications have been proposed (see table), sometimes showing little or no evidence of efficacy when formally investigated.[2] Some of the results of interventions for RAS may in truth represent aplacebo effect.[10] No therapy is curative, with treatment aiming to relieve pain, promote healing and reduce the frequency of episodes of ulceration. [2] Pharmacotherapies used in aphthous stomatitis Dru! type Intende d action "#ample$s%

$opi%a# %o<ering agents / barriers

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$opi%a# antisepti%s

:edu%e $opi%a# mi#d in #amm 6&dro%ortisone sodium su%%inate./)0 poten%&%orti%osteroids ation :edu%e (e%#omethasone dipropionate aeroso#!/)0 #uo%inonide! $opi%a# moderate in #amm /1+0 %#obetaso#!/)0betamethasone sodium phosphate! poten%&%orti%osteroids /)0 ation deBamethasone./1)0 'arious! most#& 8redniso#one!/20 %o#%hi%ine!/20 pentoBi &##ine!/20 aAathioprine! tha#i modu#ati domide!/20dapsone!/20 m&%opheno#ate mo eti#!/20 ada#imumab! ng /1+0 <itamin (12!/20C#o aAimine!/20 Ce<amiso#e!/20 Monte#ukast! immune /20 Su#odeBide!/20 #e<amiso#e./1+0 respons e

=ra##& administered drugs

The first line therapy for aphthous stomatitis is topical agents rather than systemic medication. [2] Topical corticosteroids are the mainstay treatment for aphthous stomatitis. [5][10] Systemic treatment is usually reserved for severe disease due to the risk of adverse side effects associated with many of these agents. A systematic review found that no single systemic intervention was found to be effective.[2] Good oral hygiene is also important to prevent secondary infection of the ulcers.[5] Amlexanox applied topically is highly-studied and effective in healing; less conclusive research suggests that vitamin B12 supplementation and the avoidance of sodium lauryl sulfate in toothpaste may prevent recurrence.[16] Occasionally, in females where ulceration is correlated to the menstrual cycle or to an oral contraceptive, progestogen or a change in oral contraceptive may be beneficial. [5] Use of nicotine replacement therapy for people who have developed oral ulceration after stopping smoking has also been reported.[7] Starting smoking again does not usually lessen the condition.[8]Trauma can be reduced by avoiding rough or sharp foodstuffs and by brushing teeth with care. If sodium lauryl sulfate is suspected to be the cause, avoidance of products containing this chemical may

be useful. If investigations reveal deficiency states, correction of the deficiency may result in resolution of the ulceration. Similarly patch testing may indicate that food allergy is responsible, and the diet modified accordingly.[5] Surgical excision of aphthous ulcers has been described, but it is an ineffective and inappropriate treatment.[3] Silver nitratehas also been used as a chemical cauterant.[10] Apart from the mainstream approaches detailed above, there are numerous treatments of unproven effectiveness, ranging from herbal remedies to otherwise alternative treatments, including aloe vera,myrtus communis, Rosa damascena, zinc sulfate, nicotine, polio virus vaccine and prostaglandin E2.[5]

Prognosis[edit]
By definition, there is no serious underlying medical condition, and importantly the ulcers do not represent oral cancer and they are not infectious. However, aphthae are capable of causing significant discomfort. There is a spectrum of severity, with symptoms ranging from a minor nuisance to disabling.[6] Due to pain during eating, weight loss may develop as a result of severe aphthous stomatitis. Usually, the condition lasts for several years before spontaneously disappearing in later life.[5]

Epidemiology[edit]
Reported prevalence ranges from 5 to 66%, but is probably about 20% for most populations, [3] making it the most common disease of the oral mucosa.[13] Aphthous stomatitis occurs worldwide, but is more common in developed countries.[5] There is a slightly higher prevalence in higher socioeconomic groups. There is no gender predilection, and the peak age of onset between ten and nineteen years.[2] About 80% of people with aphthous stomatitis first developed the condition before the age of 30.[3] There have been reports of ethnic variation. In the United States of America, aphthous stomatitis may be three times more common in white-skinned people than black-skinned people.[10]

History[edit]
"Aphthous affectations" and "aphthous ulcerations" of the mouth are mentioned several times in the treatise "Of the Epidemics" (part of the Hippocratic corpus, in the 4th century B.C), [17] although it seems likely that this was oral ulceration as a manifestation of some infectious disease, since they are described as occurring in epidemic-like patterns, with concurrent symptoms such as fever. Aphthous stomatitis was once thought to be a form of recurrent herpes simplex virus infection, and some clinicians still refer to the condition as "herpes" despite this etiology having been disproven.[18] The current most widely used medical term is "recurrent aphthous stomatitis" or simply "aphthous stomatitis", and colloquially, "canker sores".[6] The origin of the word "canker" is thought to have been influenced by Latin, Old English, Middle English and Old North French. [19] In Latin, cancertranslates to "malignant tumor" or literally "crab". The closely related word in Middle English and Old North French, chancre, now more usually applied to syphilis, is also

thought to be involved.[19] Despite these terms, aphthous stomatitis is not a form of cancer but rather entirely benign. An aphtha (plural aphthae) is a non specific term that refers to an ulcer of the mouth. The word is derived from the Greek word aphtha meaning "eruption" or "ulcer".[7] The lesions of several other oral conditions are sometimes described as aphthae, including Bednar's aphthae (infected, traumatic ulcers on the hard palate in infants),[20] oral candidiasis, and foot-and-mouth disease. When used without qualification, aphthae commonly refers to lesions of recurrent aphthous stomatitis. Since the word aphtha is often taken to be synonymous with ulcer, it has been suggested that the term "aphthous ulcer" is redundant, but it remains in common use. [1]
[21]

Stomatitis is also a non-specific term referring to any inflammatory process in the mouth, with or without oral ulceration.[22] It may describe many different conditions apart from aphthous stomatitis such as angular stomatitis. Historically, many different terms have been used to refer to recurrent aphthous stomatitis or its sub-types, and some are still in use. Mikulicz' aphthae is a synonym of minor RAS, [7] named after Jan Mikulicz-Radecki. Synonyms for major RAS include Sutton's ulcers (named after Richard Lightburn Sutton), Suttons disease,[23] Sutton's syndrome and pariadenitis mucosa necrotica recurrens.[5][7] Synonyms for aphthous stomatitis as a whole include (recurrent) oral aphthae, (recurrent) aphthous ulceration and (oral) aphthosis. [3][9]

http://en.wikipedia.org/wiki/5phthous_stomatitis

Herpetic gingivostomatitis
From Wikipedia, the free encyclopedia

&in!i'ostomatitis
Classification and external resources

ICD-10

5.-.1! (++.2!

ICD-9

+)4.2! )23.1+

MedlinePlus

++1+)2

Gingivostomatitis (also known as primary herpetic gingivostomatitis or orolabial herpes) is a combination of gingivitis and stomatitis, or an inflammation of the oral mucosa and gingiva.
[1]

Herpetic gingivostomatitis is often the initial presentation during the first ("primary") herpes

simplexinfection. It is of greater severity than herpes labialis (cold sores) which is often the subsequent presentations. Primary herpetic gingivostomatitis is the most common viral infection of the mouth.[2] Primary herpetic gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes simplex virus (HSV) infection, since the vast majority of other primary infections are symptomless. PHGS is caused predominantly by HSV-1 and affects mainly children. Prodromal symptoms, such as fever,anorexia, irritability, malaise and headache, may occur in advance of disease. The disease presents as numerous pin-head vesicles, which rupture rapidly to form painful irregular ulcerations covered by yellowgrey membranes. Sub-mandibular lymphadenitis, halitosis and refusal to drink are usual concomitant findings.[3]

Symptoms[edit]

Herpes lesions on the gingiva.[4]

The symptoms can be mild or severe and may include:

Not able to chew or swallow Sores on the inside of the cheeks or gums Fever General discomfort, uneasiness, or ill feeling Very sore mouth with no desire to eat Halitosis (bad breath)

Differential Diagnosis[edit]
Gingivostomatitis symptoms in infants may wrongly be dismissed as teething. "Coincidentally, primary tooth eruption begins at about the time that infants are losing maternal antibody protection against the herpes virus. Also, reports on teething difficulties have recorded symptoms which are remarkably consistent with primary oral herpetic infection such as fever, irritability, sleeplessness, and difficulty with eating."[5] "Younger infants with higher residual levels of antibodies would experience milder infections and these would be more likely to go unrecognized or be dismissed as teething difficulty."[6] Gingivostomatitis must also be differentiated from herpangina, another disease that also commonly causes ulcers in the oral cavity of children, but is caused by the Coxsackie A virus rather than a herpes virus.[7] In herpangina, ulcers are usually isolated to the soft palate and anterior pillar of the mouth.[7] In herpetic gingivostomatitis, lesions can be found in these locations, but they are almost always accompanied by ulcerations on the gums, lips, tongue or buccal mucosa and/or by hyperemia, hypertrophy or hemorrhage of the gums. [7]

Causes[edit]
Herpes Stomatitis is caused by Herpes hominis virus, type I and II infect oral mucosa but type I is more common. Gingivostomatitis generally affects children under the age of three and young adults. There are prodromal symptoms (fever, malaise, irritability, headache, vomiting, lymphadenopathy) 12 days prior to local lesions. Then small, yellowish vesicles form, which rupture quickly, resulting in shallow, round, discrete ulcers with erythematous halo. It affects both the free and attached mucosa. A generalized marginal gingivitis may precede the ulcers. In addition, chronic elemental mercury poisoning can manifest with gingivostomatitis, in addition to neurologic (tremor,paresthesias) and psychiatric (forgetfulness, mood disturbances) symptoms.

Treatment[edit]
Treatment includes fluid intake, good oral hygiene and gentle debridement of the mouth. In healthy individuals the lesions heal spontaneously in 714 days without scarring.

http://en.wikipedia.org/wiki/6erpeti%_gingi<ostomatitis

Angular cheilitis
From Wikipedia, the free encyclopedia

An!ular cheilitis
Classification and external resources

5ngu#ar %hei#itis @ a issure running in the %orner o the mouth with reddened! irritated a%ia# skin adDa%ent.

ICD-10

K13.+

ICD-9

)2*.)! .*..*

MeSH

D++2.13

Angular cheilitis, (pronounced /kalats/, sometimes abbreviated to AC,[1]and also called perlche,[2] cheilosis,[3] angular cheilosis,[4] commissural cheilitis,[4] or angular stomatitis),[5] is inflammation of one, or more commonly both,[6] of the corners of the mouth. It is a type of cheilitis(inflammation of the lips). Angular cheilitis often represents an opportunistic infection of fungi and/or bacteria, with multiple local and systemic predisposing factors being involved in the initiation and persistence of the lesion. [3][7] Such factors include nutritional deficiencies,[1] overclosure of the mouth,[8] dry mouth,[1] a lip-licking habit,[8] drooling,
[6]

immunosuppression,[9] and others. Treatment for angular cheilitis varies based on the exact

causes of the condition in each case, but often an antifungal cream is used among other measures. It is a fairly common problem,[3] and is more prevalent in people without any natural teeth who wear dentures,[8] and in elderly people, although it may also occur in children.[4]

Classification[edit]

Angular cheilitis could be considered to be a type of cheilitis or stomatitis. Where Candida species are involved, angular cheilitis is classed as a type of oral candidiasis, specifically a primary (group I) Candida-associated lesion.[3] This form angular cheilitis which is caused by Candida is sometimes termed "Candida-associated angular cheilitis", [3] or less commonly, "monilial perlche".[4] Angular cheilitis can also be classified as acute or chronic and refractory to attempts to treat it.[4]

Signs and symptoms[edit]

A fairly mild case of angular cheilitis extending onto the facial skin in a young person (affected area within the black oval).

A mild case of angular cheilitis, confined to a small split in the labial mucosa, in a young person.

Angular cheilitis is a fairly non specific term which describes the presence of an inflammatory lesion in a particular anatomic site (i.e. the corner of the mouth). As there are different possible causes and contributing factors from one person to the next, the appearance of the lesion is somewhat variable. The lesions are more commonly symmetrically present on both sides of the mouth,[6] but sometimes only one side may be affected. In some cases, the lesion may be confined to the mucosa of the lips, and in other cases the lesion may extend past the vermilion border (the edge where the lining on the lips becomes the skin on the face) onto the facial skin. Initially, the corners of the mouth develop a gray-white thickening and adjacenterythema (redness).[4] Later, the usual appearance is a roughly triangular area of erythema, edema (swelling) and maceration at either corner of the mouth.[4][6] The mucosa of the lip may become fissured (cracked), crusted, ulcerated oratrophied.[4][6] There is not usually any bleeding.[10] Where the skin is involved, there may be radiating rhagades (linear fissures) from the corner of the mouth. Infrequently, the dermatitis (which may resemble eczema) can extend from the corner of the mouth to the skin of the cheek or chin. [6] If Staphylococcus aureus is involved, the lesion may show golden yellow crusts.[5] In chronic angular cheilitis, there may be suppuration (pus formation), exfoliation (scaling) and formation ofgranulation tissue.[4][6] Sometimes contributing factors can be readily seen, such as loss of lower face height from poorly made or worn dentures, which results in mandibular overclosure ("collapse of jaws"). [8] If there is a nutritional deficiency underlying the condition, various other signs and symptoms such as glossitis (swollen tongue) may be present. In people with angular cheilitis who wear dentures, often there may be erythematous mucosa underneath the denture (normally the upper denture), an appearance consistent with denture-related stomatitis.[6] Typically the lesions give symptoms of soreness, pain, pruritus (itching) or burning or a raw feeling.[4][8]

Causes[edit]
Angular cheilitis is thought to be multifactorial disorder of infectious origin, [7] with many local and systemic predisposing factors are known to be involved. [3] The sores in angular cheilitis are often infected with fungi (yeasts), or sometimes bacteria, or a combination.[5] This may represent a secondary, opportunistic infection by thesepathogens, and some studies have linked the initial onset of angular cheilitis with nutritional deficiencies, especially of the B vitamins and iron (which causes iron deficiency anemia).[11] which in turn may be evidence of malnutrition or malabsorption. Angular cheilitis can be a manifestation of contact dermatitis,[12] which is considered in two groups; irritational and allergic.

Infection[edit]
The involved organisms are:

Candida species alone (usually Candida albicans), which accounts for about 20% of cases,[9] Bacterial species, either: Staphylococcus aureus alone, which accounts for about 20% of cases,[9]

-hemolytic streptococci alone. These types of bacteria have been detected in between 8-15% of cases of angular cheilitis,[4] but less commonly are they present in isolation,[7]

Or a combination of the above organisms, (a polymicrobial infection)[5] with about 60% of cases involving both C. albicans and S. aureus.[9][13]

Candida can be detected in 93% of angular cheilitis lesions.[4] This organism is found in the mouths of about 40% of healthy individuals, and it is considered by some to be normal commensal component of the oral microbiota.[4] However, Candida shows dimorphism, namely a yeast form which is thought to be relatively harmless and a pathogenic hyphal form which is associated with invasion of host tissues. Potassium hydroxide preparation is recommended by some to help distinguish between the harmless and the pathogenic forms, and thereby highlight which cases of angular cheilitis are truly caused by Candida.[4] The mouth may act as a reservoir of Candida that reinfects the sores at the corners of the mouth and prevents the sores from healing. A lesion caused by recurrence of a latent herpes simplex infection can occur in the corner of the mouth. Really this is herpes labialis (a cold sore), and is sometimes termed "angular herpes simplex".[4] A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips, and follows a pattern of vesicle (blister) formation followed by rupture leaving a crusted sore which resolves in about 710 days, and recurs in the same spot periodically, especially during periods of stress. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugssuch as aciclovir.

Irritation contact dermatitis[edit]

A famous sketch by Leonardo da Vinci in preparation to depict the face ofJudas Iscariot in The Last supper. The subject shows overclosure of the jaws and loss of facial support around the mouth.

Pronounced skin folds extending from the corner of the mouth.

Main article: Irritant contact dermatitis 22% of cases of angular cheilitis are due to irritants.[4] Saliva contains digestive enzymes, which may have a degree of digestive action on tissues if they are left in contact. [4] The corner of the mouth is normally exposed to saliva more than any other part of the lips. Reduced lower facial height (vertical dimension or facial support) is usually caused by edentulism (tooth loss), or wearing worn down, old dentures or ones which are not designed optimally. This results in overclosure of the mandible (collapse of the jaws),[8] which extenuates the angular skin folds at the corners of the mouth,[9] in effect creating an intertriginous skin crease. The tendency of saliva to pool in these areas is increased, constantly wetting the area,[7]which may cause tissue maceration and favors the development of a yeast infection.[9] As such, angular cheilitis is more commonly seen in edentulous people (people without any teeth).[8] It is by contrast uncommon in persons who retain their natural teeth.[14] Angular cheilitis is also commonly seen in denture wearers.[12]Angular cheilitis is present in about 30% of people with denture-related stomatitis. [7]It is thought that reduced vertical dimension of the lower face may be a contributing factor in up to 11% of elderly persons with angular cheilitis and in up to 18% of denture wearers who have angular cheilitis.[4] Reduced vertical dimension can also be caused by tooth migration, wearing orthodontic appliances, and elastic tissue damage caused by ultraviolet light exposure and smoking.[4] Habits or conditions that keep the corners of the mouth moist might include chronic lip licking, thumb sucking (or sucking on other objects such as pens, pipes, lollipops), dental cleaning (e.g. flossing), chewing gum, hypersalivation, drooling andmouth breathing.[4][6][9] Some consider habitual lip licking or picking to be a form of nervous tic, and do not consider this to be true angular cheilitis,[6] instead calling itperlche (derived from the French word pourlcher meaning "to lick ones lips"),[4] or "factitious cheilitis" is applied to this habit.[4] The term "cheilocandidiasis" describes exfoliative (flaking) lesions of the lips and the skin around the lips, and is caused by a superficial candidal infection due to chronic lip licking.[9] Less severe cases occur during cold, dry weather, and is a form of chapped lips. Individuals may lick their lips in an attempt to provide a temporary moment of relief, only serving to worsen the condition.[15]

The sunscreen in some types of lip balm degrades over time into an irritant. Using expired lipbalm can initiate mild angular cheilitis, and when the person applies more lipbalm to alleviate the cracking, it only aggravates it. Because of the delayed onset of contact dermatitis and the recovery period lasting days to weeks, people typically do not make the connection between the causative agent and the symptoms.[medical citation needed]

Nutritional deficiencies[edit]
Several different nutritional deficiency states of vitamins or minerals have been linked to AC.[1] It is thought that in about 25% of people with AC, iron deficiency or deficiency of B vitamins are involved.[1] Nutritional deficiencies may be a more common cause of AC in third world countries. [1] Chronic iron deficiency may also cause koilonychia (spoon shaped deformity of the fingernails) and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida. [1] Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue). [1] Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitis around the eyes, nose and mouth.[1] Vitamin B12 deficiency is sometimes responsible for AC, and commonly occurs together with folate deficiency (a lack of folic acid), which also causes glossitis and megaloblastic anemia.[1] Vitamin B3 deficiency (pellagra) is another possible cause, and in which other association conditions such as dermatitis, diarrhea, dementia and glossitis can occur.[1] Biotin (vitamin B7) deficiency has also been reported to cause AC, along with alopecia (hair loss) and dry eyes.[1]Zinc deficiency is known to cause AC.[16] Other symptoms may include diarrhea, alopecia and dermatitis.[1] Acrodermatitis enteropathica is an autosomal recessive genetic disorder causing impaired absorption of zinc, and is associated with AC. [1] In general, these nutritional disorders may be caused by malnutrition, such as may occur in alcoholism or in strict vegan diets, or by malabsorption secondary to gastrointestinal disorders (e.g. Celiac disease or chronic pancreatitis) or gastrointestinal surgeries (e.g. pernicious anemia caused by ileal resection in crohn's disease).[1]

Systemic disorders[edit]
Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa.[1] Other disorders may cause lip enlargement (e.g. orofacial granulomatosis),[1] which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC. [1] Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications, or conditions such as Sjgren's syndrome. Conversely, conditions which cause drooling or sialorrhoea(excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC.[1] Other possible oral manifestations of down syndrome includemacroglossia (a large tongue), which may protrude from the mouth

constantly. Inflammatory bowel diseases (such asCrohn's disease or ulcerative colitis) can be associated with angular cheilitis.[6] In Crohn's it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth.
[8]

Glucagonomasare rare pancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome.[17] Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis,[9] and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis.[4] Angular cheilitis may be present in human immunodeficiency virus infection,[3] neutropenia,[14] or diabetes.[6] Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants.[4] Other conditions possibly associated include plasma cell gingivitis,[10] Melkersson-Rosenthal syndrome,
[1]

or sideropenic dysphagia (also called Plummer-Vinson syndrome or Paterson-Brown-Kelly syndrome).[1]

Drugs[edit]
Several drugs may cause AC as a side effect, by various mechanisms, such as creating druginduced xerostomia. Various examples include isotretinoin, indinavir, and sorafenib.[1] Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primary hypervitaminosis A,[18] which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine,methamphetamines, heroin, and hallucinogens.[1]

Allergic contact dermatitis[edit]

See also: Allergic contact cheilitis, Allergic contact dermatitis, and Allergic contact stomatitis Allergic reactions may account for about 25-34% of cases of generalized cheilitis (i.e., inflammation not confined to the angles of the mouth). It is unknown how frequently allergic reactions are responsible for cases of angular cheilitis, but any substance capable of causing generalized allergic cheilitis may present involving the corners of the mouth alone.

Patch test

Examples of potential allergens include substances that may be present in some types of lipstick, toothpaste, acne products, cosmetics, chewing gum, mouthwash, foods, dental appliances, and materials from dentures or mercury containing amalgam fillings. [4] It is usually impossible to tell

the difference between irritant contact dermatitis and allergic contact dermatitis without a patch test.

Diagnosis[edit]
Angular chielitis is normally a diagnosis made clinically. If the sore is unilateral rather than bilateral, this suggests a local factor (e.g. trauma) or a split syphilitic papule. [6]Angular cheilitis caused by mandibular overclosure, drooling and other irritants is usually bilateral. [4] The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate. [6]

Management[edit]
There are 4 aspects to the treatment of angular chieltis.[19] Firstly, potential reservoirs of infection inside the mouth are identified and treated.[19] Oral candidiasis, especially denture-related stomatitis is often found to be present where there is angular cheilitis, and if it is not treated, the sores at the corners of the mouth may often recur.[5][12] This involves having dentures properly fitted and disinfected. Commercial preparations are marketed for this purpose, or simply the dentures are left in dilute (1:10 concentration) household bleach overnight, but only if they are plastic and do not contain any metal parts, and with rinsing under clean water before use. [8] Improved denture hygiene is often required thereafter, including not wearing the denture during sleep and cleaning it daily.[6] For more information, see Denture-related stomatitis#Treatment. Secondly, there may be a need to increase the vertical dimension of the lower face to prevent overclosure of the mouth and formation of deep skin folds.[19] This may require the construction of a new denture with an adjusted bite.[6] Rarely, in cases resistant to normal treatments, surgical procedures such as collagen injections (or other facial fillers such as autologous fat or crosslinked hyaluronic acid) are used in an attempt to restore the normal facial contour. [4][6] Other measures which seek to reverse the local factors that may be contributing to the condition include improving oral hygiene, stopping smoking or other tobacco habits and use of a barrier cream (e.g. zinc oxide paste) at night.[4] Thirdly, treatment of the infection and inflammation of the lesion themselves is addressed. This is usually with topicalantifungal medication,[5] such as clotrimazole,[9] amphotericin B, [19] ketoconazole,[14] or nystatin cream.[8] Some antifungal creams are combined with corticosteroids such as hydrocortisone[5] or triamcinolone[8] to reduce inflammation, and some antifungals such as miconazole cream also have some antibacterial action.
[5]

Diiodohydroxyquinoline is another topical therapy for angular cheilitis.[9] If Staphylococcus aureus infection is demonstrated by microbiological culture to be responsible (or suspected), the treatment may be changed to fusidic acid cream,[5] an antibiotic which is effective against this type of bacteria. Aside from fusidic acid, neomycin,[19] mupirocin,[4] metronidazole,
[10]

and chlorhexidine,[19] are alternative options for this scenario.

Finally, if the condition appears resistant to treatment, investigations for underlying causes such as anemia or nutrient deficiencies or HIV infection.[19] Identification of the underlying cause is

essential for treating chronic cases. The lesions may resolve when the underlying disease is treated, e.g. with a course of oral iron or B vitamin supplements. [6] Patch testing is recommended by some in cases which are resistant to treatment and where allergic contact dermatitis is suspected.[4]

Prognosis[edit]
Most cases of angular cheilitis respond quickly when antifungal treatment is used. [14] In more long standing cases, the severity of the condition often follows a relapsing and remitting course over time.[9] The condition can be difficult to treat and can be prolonged.[6]

Epidemiology[edit]
AC is a relatively common condition,[3] accounting for between 0.7 - 3.8% of oral mucosal lesions in adults and between 0.2 - 15.1% in children, although overall it occurs most commonly in adults in the third to sixth decades of life.[4][6] It occurs worldwide and both males and females are affected.[6] Angular cheilitis is the most common presentation of fungal and bacterial infections of the lips.[9]

http://en.wikipedia.org/wiki/5ngu#ar_%hei#itis