Στοματική κοιλότητα και IBD · Metronidazole Metallic taste, glossitis,...

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Στοματική κοιλότητα και IBD Κωνσταντίνος Χ. Κατσάνος Ιωάννινα, Ιούνιος 2016

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  • Στοματική κοιλότητα και IBD

    Κωνσταντίνος Χ. Κατσάνος

    Ιωάννινα, Ιούνιος 2016

  • Στοματική κοιλότητα και IBD

    • ΚΑΛΟΗΘΕΙΣ ΕΚΔΗΛΩΣΕΙΣ

    • ΠΡΟ-ΝΕΟΠΛΑΣΜΑΤΙΚΕΣ ΕΚΔΗΛΩΣΕΙΣ

    • ΝΕΟΠΛΑΣΜΑΤΙΚΕΣ ΕΚΔΗΛΩΣΕΙΣ

  • ΚΑΛΟΗΘΕΙΣ ΕΚΔΗΛΩΣΕΙΣ

  • • A significant proportion of patients may have one or more manifestations in the oral cavity and in the perioral skin area.

    • The prevalence of oral lesions in IBD has been reported to range from 5-50%.

    • oral lesions are more common in CD as compared to UC

    • more prevalent in children as compared to adults.

    ΙBD & ΣΤΟΜΑΤΚΗ ΚΟΙΛΟΤΗΤΑ

  • • Oral manifestations may be associated with • the disease itself • with nutritional deficiencies • with complications from therapy.

    • may precede IBD diagnosis • may or not be associated with active disease • may involve any part of the oral cavity

    • They may cause significant symptoms and disability

    ΙBD & ΣΤΟΜΑΤΚΗ ΚΟΙΛΟΤΗΤΑ

  • • two common clinical scenarios:

    • 1) oral lesions associated with altered bowel habits

    • 2) established IBD but complaining of new oral lesions.

    ΙBD & ΣΤΟΜΑΤΚΗ ΚΟΙΛΟΤΗΤΑ

  • Oral lesions in CD

    • Oral lesions have a prevalence rate between 20-50%.

    • higher in proximal gastrointestinal tract and/or perianal involvement.

    • Aphthous ulcers, the most common

    • preceding GI symptoms in 5%-10% of patients.

  • Oral lesions in children with CD

    • The highest reported rate almost 50%

    • 30% may continue to manifest oral lesions despite intestinal disease control.

    • Paediatric doctors and dentists play a critical role

  • Oral manifestations in UC

    • Aphthous ulcers in 10% of UC.

    • in pediatric patients with UC in up one third and are usually non-specific.

  • DIAGNOSIS OF ORAL LESIONS IN IBD

    • Oral lesions in IBD can be

    • specific

    • non-specific

  • 1.Specific oral changes or lesions Description

    Orofacial Crohn’s disease Granular cheilitis

    Pyostomatitis vegetans

    Mostly young patients with Crohn’s

    Mostly in Crohn’s disease

    In ulcerative colitis and in Crohn’s

    2. Non-specific oral changes or lesions

    -Oral cavity changes Ulcers, cobblestonning, swelling, abscesses, tags, tongue changes, gingival changes etc.

    -Lip changes cheilitis, swelling, redness, scaling, fissures, ulcers

    -Malabsorption-related oral changes or lesions

    Folic acid deficiency Glossitis and/or cheilitis

    Iron deficiency Glossitis and/or cheilitis

    Zinc deficiency Oral candidiasis, glossitis

    Vitamin A deficiency Oral white patches/keratinization

    Vitamin B complex deficiency Stomatitis, glossitis, angular cheilitis, burning mouth syndrome, reduced or altered taste

    Vitamin C deficiency Scurvy

    Vitamin K deficiency Gum and/or oral cavity bleeding

    -Medication-related oral changes or lesions

    Adalimumab Infections, angioedema, paradoxical reactions

    Azathioprine Sicca syndrome

    Budesonide Glossitis, dry mouth

    Certolizumab pegol Angioedema, Stevens-Jonhson syndrome/toxic epidermal necrolyis, paradoxical reactions

    Cholestyramine Glossitis, altered taste,dental changes, gum bleeding

    Cyclosporin Gingivitis, gum hyperplasia

    Ciprofloxacin Angioedema,Stevens-Jonhson syndrome/ Toxic epidermal necrolyis, oral candidiasis, loss of taste

    Infliximab Infections, angioedema, paradoxical reactions

    Loperamide Angioedema, Stevens-Jonhson syndrome/ toxic epidermal necrolyis, dry mouth

    Mesalazine Stomatitis, dry mouth, altered taste

    Methotrexate Stomatitis, gingivitis

    Metronidazole Metallic taste, glossitis, stomatitis, candidiasis, dry mouth

    (Methyl)prednisolone Oral candidiasis

    Mycophenolate mofetil Sicca syndrome

    Sulphasalazine Angioedema, stomatitis, Stevens-Jonhson syndrome/toxic epidermal necrolyis, altered taste

    Table Specific and non-specific oral changes in patients with IBD.

  • Oral involvement in IBD Clinical Signs

    Orofacial Crohn disease One or more clinical signs of spectrum: perioral erythema, metastatic Crohn’s of skin of the face with ulcers, facial swelling,

    mucosal tags, deep linear ulcers, cobblestoning, lip swelling or fissuring, granulomatous cheilitis, mucogingivitis, papules,

    nodules, plaques or persistent swelling.

    Oral mucosa

    [masticatory or lining

    (labial / buccal)]

    abscesses (mostly in buccal space)

    aphthous lesions (minor or major)

    aphthous stomatitis

    circumferential ulcers

    cobblestoning, cobblestone plaques

    diffuse oral edema

    fissures

    IgA pustulosis, leukoplakia, hairy leukoplakia

    linear ulcers ,lumps

    mucosal tags ,permanent maloformartions / scarring

    pseudopolyps

    polypoid lesions,pyostomatitis vegetans

    swelling and induration

    Lip(s) angular cheilitis

    fissuring, induration

    granulomatous cheilitis ,macrocheilia with or without fissuring

    neoformations of the genian mucosa (papilloma,fibroma) ,swelling

    Gingiva non specific gingivitis

    hyperplastic granular gingivitis

    Hard palate palatal ulcer(s)

    Teeth parodontal lesions

    paraodontosis

    reduction of the alveolar bony tissue

    Tongue erosions

    glossitis

    ulcers

    Tonsills granulomatous tonsillitis

    tonsillar granulomas

    Salivary glands Fistula,granulomatous inflammation,

    minor salivary gland enlargement reduced salivation

    sicca syndrome

    Table Clinical signs of oral involvement in IBD by oral anatomic location.

  • Dental symptoms Discomfort, pain, infections, dental caries, decay,

    periodontal involvement

    Oral symptoms dry mouth (sicca syndrome), reduced salivation,difficulty

    in speaking and/or swallowing, halitosis

    Gingiva gingival hypertrophy, swelling, pain, bleeding

    Lip changes swelling, macrocheilia, redness, scaling, fissures

    Oral mucosa changes ulcer(s), cobblestoning, polypoid tags, buccal swelling,

    leukoplakia, mucosal discoloration

    Perioral skin changes perioral erythema with scaling, erythema migrans,

    swelling, malformations, scarring

    Lymphadenopathy persistent submandibular lymphadenopathy

    Tongue changes painful tongue, glossitis in top or lateral or whole tongue,

    hairy tongue, metallic dysgeusia

    Table Oral symptoms in patients with inflammatory bowel disease.

  • Oral aphthous or ulcerous or edematous lesions Oral granulomatous lesions

    Recurrent aphthous stomatitis (RAS) Orofacial granulomatosis (OFG)

    Autoimmune rheumatic diseases

    (Reiter's syndrome, systemic lupus erythematosus,

    Adamandiadis-Behcet's syndrome)

    Melkersson-Rosenthal syndrome

    Autoimmune bullous diseases, cicatricial pemphigoid,

    pemphigus vulgaris, epidermolysis bullosa acquisita

    Cheilitis granulomatosa

    (Miescher cheilitis)

    Infections

    (mucobacterial, systemic fungal infections, parasites,

    sexually transmitted infections, herpetic gingivostomatitis,

    CMV, Coxsackie, oral histoplasmosis) Oral

    staphylococcal (S. aureus) mucositis

    Foreign body reaction-sarcoid-like

    (Polishing-paste-induced silica granuloma,

    delayed hypersensitivity to cobalt, oral cavity

    piercing)

    Lymphatic edema, lymphangioma, vascular edema, Sarcoidosis

    Neutropenias Sjögren syndrome

    Desquamative gingivitis Wegener’s granulomatosis

    Precancerous lesions (lichen planus) Tuberculosis

    Cancer (mouth T-cell lymphoma)

    Traumas and Allergies

    Tuberculoid leprosy

    Table Differential diagnosis of oral aphthous and oral granulomatous lesions in patients with inflammatory bowel disease.

  • Non-specific oral lesions

    In IBD and non-IBD patients

    -Malabsorption related

    -Medication related

    -Other

    Highly specific

    -“Metastatic”

    -Orofacial

    -Granulomatous

    cheilitis

    Highly specific

    -pyostomatitis

    vegetans

    Highly suspicious

    -Tag-like lesions

    -Cobblestoning

    -Mucogingivitis

    -Lip swelling &

    vertical fissuring

    -Deep linear oral

    ulcers (buccal sulci)

    Spectrum of oral manifestations and lesions in inflammatory bowel disease

    Crohn’s disease

    Ulcerative colitis

  • a. Highly specific oral lesions

    • Highly specific oral lesions are almost pathognomonic for IBD diagnosis

    • orofacial and granulomatous cheilitis in CD

    • pyostomatitis vegetans in UC and CD

  • Orofacial Crohn’s disease

    • oral ulcers and cobblestoning appearance in the mouth of patients with CD

    • “CD of the mouth”.

    • Orofacial CD is a specific manifestation of CD (5-15% )

    • relapsing aphthous ulceration with coexisting edema of the oral

    cavity and of the lips

    • Usually the bowel disease develops within a few months of the orofacial condition, but delays of up to nine years have also been reported.

  • Orofacial Crohn’s disease

    • Orofacial CD is clinically and histologically indistinguishable from orofacial granulomatosis (OFG), which occurs in the absence of any bowel disease.

    • OFG encompasses two conditions:

    • Granulomatous cheilitis (or Miescher cheilitis or cheilitis granulomatosa)

    • Melkersson-Rosenthal syndrome

  • Granulomatous cheilitis

    Melkerson-Rosenthal syndrome Orofacial

    Crohn’s

    (preceeding

    bowel

    symptoms) Other causes (i.e sarcoidosis, allergy)

    Orofacial

    Crohn’s

    (extraintestinal

    manifestation)

    Orofacial granulomatosis

    Absence of bowel disease Bowel disease

  • Granulomatous cheilitis

    • Granulomatous cheilitis (or cheilitis granulomatosa or Miescher cheilitis)

    • Changes are restricted to the lip, mostly focal granulomatous inflammation of the lower lip.

  • Pyostomatitis vegetans

    • Pyostomatitis vegetans (PV) is a rare condition characterized by erythematous and thickened oral mucosa with multiple pustules and superficial erosions.

    • PV is associated with IBD in 75% of cases

    • Other differential diagnoses include autoimmune

    pemphigoid diseases and sometimes infections. •

  • b. Highly suspicious oral lesions for IBD

    • are highly suggestive of underlying IBD, especially CD

    • The most common affected portions are the buccal mucosa, gingiva, lips

  • c. Non-specific lesions in IBD

  • Recurrent aphthous stomatitis

    • Any patient with recurring or insisting oral ulcers should be evaluated medically for the possible presence of a more serious systemic disease.

    • Aphthous-like lesions may be seen in 4-5% of patients with IBD.

    • Colonic, rather than small intestinal, CD is more often associated with oral

    • The list of differential diagnosis is long

  • Salivary duct and saliva in IBD

    • Patients with IBD may complain of dry mouth, similar to the sicca syndrome observed in transplanted patients under immunosuppressive therapy.

    • Granulomatous inflammation of minor salivary gland ducts has been suggested as another oral manifestation of active intestinal CD.

  • Tongue involvement in IBD

    • Rare cases of non-neoplastic tongue involvement in IBD have been described

    • Alterations of taste (metallic dysgeusia) may be related with

    • disease activity,

    • nutritional habits

    • therapy with metronidazole.

  • Dental and gingival manifestations in IBD

    • dental infections and dental alterations related to malabsorption and to disease activity of IBD.

    • Gingival involvement in CD is infrequent.

    • Gingival biopsy may be helpful for early diagnosis of an underlying CD.

  • Oral lesions secondary to nutritional deficiencies

    • Nutritional deficiencies may cause oral lesions, the most common being angular cheilitis associated with iron deficiency.

    • deficiencies in iron, folic acid, vitamin B12, potassium, calcium, magnesium, vitamin A, vitamin C, vitamin D, zinc and selenium.

  • Therapy-related oral lesions

    • All medications may cause oral lesions or symptoms

    • Oral paradoxical reactions to biologicals include oral lichenoid reaction to infliximab and new onset of oral lichen planus during certolizumab pegol use.

  • MEDICAL TREATMENT OF ORAL MANIFESTATIONS IN IBD

    • topical and/or systemic therapies combined

    with dietary instructions

    • In refractory or intractable cases the algorithms of management may also include surgical treatment

  • Medical treatment of oral IBD Surgical treatment of oral IBD

    Effective treatment of intestinal IBD

    Standard treatment (reported)

    -Corticosteroids (methlyprednisolone)

    -Azathioprine

    -Infliximab

    -Thalidomide (refractory cases)

    -isotretinoin, dapsone (pyostomatitis)

    -Long-term p.os antibiotics (tetracycline, erythromycin, penicillin,

    metronidazole)

    Other possible options (unreported)

    -Methotrexate

    -Adalimumab

    -Certolizumab

    Nutrition

    -Total enteral nutrition (selected cases)

    -Elemental diet (selected cases)

    -Elimination diets (special dietary restrictions i.e cinnamate- and benzoate-

    free diet)

    -Supplementation formulas, vitamins (A,B,C) and trace elements (zinc)

    Major surgery

    Oral and oropharyngeal surgery

    -Oral surgery

    -Orthognathic surgery

    -Maxillofacial surgery

    Plastic facial and lip surgery

    -Reconstructive

    -Elimination

    Colectomy in intractable oral IBD

    Minimal or Elective surgery

    -small lesion removal

    -small fistula repair

    -abcess drainage

    - oral biopsies (multiple)

    Topical treatement

    Local intralesional injections

    -corticosteroids

    - triamcinolone 0.1%

    -Infliximab

    -analgesics

    -lidocaine 2%,

    Local ointments

    -corticosteroids(1% hydrocortisone)

    -tacrolimus

    -non-steroidal anti-inflammatory pastes

    Mouthwash

    -5-aminosalicylic,-corticosteroids,-antiseptic,Elixirs (dexamethasone)

    Local dental surgery

    (functional repair and cosmetic)

    -Dental surgery

    -Biopsy of small oral lesion

    -Laser for gingival Crohn's disease

    Table Treatment of the oral manifestations in inflammatory bowel diseases.

  • Treatments of oral IBD Type of oral IBD Author/Year Number

    of all

    patients

    Type of trial

    (controlled/C

    Uncontrolled/U)

    Response rates

    Oral Crohn’s Plauth et al,30 1991 12 Topical steroids/ U 7 of 12 (58%) patients

    Oral Crohn’s Casson et al,142

    2000

    3 Topical tacrolimus ointment /U Marked improvement in 1-6 months

    Orofacial

    franulomatosis/ora

    l Crohn’s

    Mignogna et al,139

    2004

    7 Triamcinolone injections

    / U

    Response (2 or 3 injection

    sessions over 14 or 21

    days)

    Oral Crohn’s Plauth et al,30 1991 26 Azathioprine and/or systemic

    steroids / U

    13 of 26 (50%) patients

    Oral Crohn’s Williams J et al,145

    1991

    12 Systemic steroids / U Improvement in all, 3

    steroid-dependent

    Oral Crohn’s Litsas140 ,

    2011

    1 Systemic prednisone / U Response after 6 months

    Resistant oral

    Crohn’s

    Hegarty et al,153

    2003

    5 Thalidomide/ U Response

    Oral Crohn’s Campbell et al,163

    2013

    10 Phenolic acid exclusion diet

    with micronutrient

    supplementation/ U

    7 responded

    Oral Crohn’s White et al,161 2006 32 Elimination diets

    cinnamon- and benzoate-free

    diet (CB-free diet) / U

    Response after 8 weeks

    Oral Crohn’s Cameron et al,159

    2003

    1 Elemental diet/ U Response but 2 relapses

    Granulomatous

    cheilitis

    Kano et al,70 1992 1 Metronidazole / U Response

    Oral Crohn’s Sánchez et al,147 2005

    1 Adalimumab+dapsone/ U Response after 5 months

    Oral Crohn’s Cardoso et al,149

    2006

    1 Infliximab/ U Successful treatment

    Fistulizing oral

    Crohn’s

    Staines et al,151

    2007

    1 Infliximab/ U Successful treatment

  • Management of oral aphthous ulcers in IBD (Target in parallel bowel disease remission)

    Topical treatment Antibiotics, tacrolimus ointment, corticosteroids (elixirs, ointments, mouthwashes, intralesional injections), analgesics (lidocaine 2%), antiseptic mouthwashes, NSAID pastes

    Elimination diets (Cinnamon, benzoate, glutaminate, cocoa) Vitamin and trace element supplementation

    Systemic treatment Corticosteroids, azathioprine, methotrexate, tacrolimus

    Systemic treatment for refractory cases Biological therapy, thalidomide, long-term antibiotics

    Figure . Algorithm for management for oral aphthous ulcers in IBD.

  • Management of oral Crohn’s disease (Target in parallel bowel disease remission)

    Topical treatment Antibiotics, tacrolimus ointment, corticosteroids (elixirs, ointments, mouthwashes, intralesional injections), analgesics (lidocaine 2%), antiseptic mouthwashes, NSAID pastes

    Food restriction, Enteral / Parenteral nutrition

    Elimination diets (Cinnamon, benzoate, glutaminate, cocoa) Vitamin and trace element supplementation

    Surgical treatment Head-neck surgery, oral surgery (for local repair and cosmesis) Dental surgery

    Systemic treatment Corticosteroids, azathioprine, methotrexate, tacrolimus, biological therapies

    Systemic treatment for refractory cases Switch to a 2nd biological therapy, thalidomide, long-term antibiotics, dapsone, Cyclosporin A (for pyostomatitis)

    Figure. Algorithm for recommended management for oral Crohn’s disease.

  • SURGICAL TREATMENT OF ORAL MANIFESTATIONS IN IBD

    • for severe complications refractory to medical therapy. • Minimal or elective surgery • Local dental surgery

    • Major surgical interventions include

    • oral and oropharyngeal surgery, (orthognathic and/or maxillofacial

    surgery) • plastic surgery (reconstructive, elimination i.e for hyperplastic

    gingiva). • Colectomy is reserved as an ultimate option for patients with UC

    and intractable or highly resistant oral lesions that significantly affect oral feeding and overall quality of life.

  • ΠΡΟ-ΝΕΟΠΛΑΣΜΑΤΙΚΕΣ ΕΚΔΗΛΩΣΕΙΣ

  • Environmental factors Sun exposure (UV light), passive smoking(?)

    Infections (HPV E6 and E7 oncogenes, HIV, syphilis DNA detected from CMV and EBV in oral cancerous lesions, chronic candidiasis)

    Life style (smoking , smokeless tobacco use, pipe smoking, marijuana use, heavy alcohol use, access to medical care or dental care, low consumption of fruits and vegetables)

    Drugs (immunosuppressants, anti-TNFa ?, others?)

    Alterations in oral homeostasis (xerostomia, reduced salivary flow, candida colonization)

    Demographics (age>40, males, African-American (oral cavity cancer), fair skin (lip cancer)

    Education level (Absence of oral screening, no annual oral exam, poor oral hygiene)

    Precancerous oral lesions unrecognized and untreated

    (leukoplakia, erythroplakia, leukoerythroplakia, chronic candidiasis (?)

    Chronic irritation in oral cavity (traumatic ulcers, poor fitting denture, broken or sharp-edged teeth or fillings)

    Underlying conditions (immunodeficiency, transplantation, Plummer-Vinson)

    Nutrition deficiencies (low vitamin A, B12, folic acid levels, iron deficiency)

    p53 gene alterations-dysplasia-cancer in situ-invasive cancer

    Figure. The puzzle of mechanisms and conditions leading to the development of oral precancerous lesions

    and oral cancer in inflammatory bowel diseases.

  • Author Drug Patient Disease Type of

    oral lesion

    Outcome

    Mocciaro et al.54 Certolizumab

    pegol

    1 Crohn’s Oral lichen

    planus

    Non evolution

    to Ca

    Fluckiger et al.55 Azathioprine 1 Ulcerative

    colitis

    Oral hairy

    leukoplakia

    Non evolution

    to Ca, HIV(-)

    Worsnop et al.52 Infliximab 1 Crohn’s Oral lichen

    planus

    (probable)

    Non evolution

    to Ca

    (Paradoxical

    reaction to IFX)

    Moss et al.53 Infliximab 1 Crohn’s Oral

    lichenoid

    reaction to

    IFX

    Non evolution

    to Ca

    (Paradoxical

    reaction to IFX)

    Table. Oral precancerous lesions reported in the form of case reports in patients with inflammatory bowel disease.

  • a. Typical oral lichen planus (OLP) of the tongue’s right side. (AB)

    b. Diffuse OLP, plaque form, of the entire oral mucosa. Note the leukokeratotic aspect to be distinguished from a leukokeratosis. (AB)

    c. Cheek’s OL erosive and planus. (AB & ED)

    d. Tongue’s atrophic OLP after a long time evolution. Note the typical network of overlapping white striae of the point. (AB)

  • ΝΕΟΠΛΑΣΜΑΤΙΚΕΣ ΕΚΔΗΛΩΣΕΙΣ

    • The incidence and prevalence of oral cancerous and pre-cancerous lesions in IBD is currently unknown.

    • No routine oral screening is performed or is advised so far.

    • HPV infection!

  • a.Squamous cell carcinoma (SCC) of the tongue’s point arising on an atrophic oral lichen planus. (ED)

    b.SCC of the tongue in a 19-year-old smoker female. The question of the responsability of HPV as cofactors is raised in such a

    case. (AB & ED)

    c.Typical SCC of the lower lip in a smoker patient arising on a leukokeratosis. (ED)

    d.SCC of the lower lip in a young male, rapidly appeared after a kidney transplantation. (ED)

  • Melanoma of the soft palate in non-IBD non-HIV patient

  • Kaposi sarcoma of the hard palate in non-IBD non-HIV patient

  • Author Drug Patient(s) with oral

    Ca

    Disease Location / Type of

    oral cancer

    Details

    Vilas-Boas et al.61

    (case report)

    AZA

    (9 years)

    1 CD Right superior retromollar trigone, SCC /

    HPV (-)

    Surgery

    Li et al.60

    (case report)

    AZA

    (3 years)

    1 CD Tongue

    SCC (ulcerous in situ)

    Surgery

    Dulai et al.39

    (case report)

    IFX+AZA 1 IBD Parotid

    Non-Hodgkin lymphoma

    Unknown

    Biancone et al.26

    (multicenter study)

    non-biological therapies 1 CD Oropharyngeal

    (larynx)

    Death

    Lichtenstein et al.42

    (TREAT cohort registry n=6,773)

    IFX

    or

    Any other therapy

    6 CD Oral cavity

    (3 patients on IFX)

    SIR (95%(CI)

    IFX-treated

    1.77 (0.37, 5.17)

    Any other therapy

    1.78 (0.37, 5.21)

    Cottone et al.43

    (cohort study)

    IFX=2,475

    ADA=604

    1

    0

    CD Pharyngeal 18 months after IFX

    (died)

    Pasternak et al.62

    (Danish IBD cohort database

    n=45,986)

    AZA= 5,197 69 IBD Lip/oral cavity/pharynx non-AZA=60

    former AZA=4

    current AZA=5

    RR 95%(CI)

    Non-users (referrent)

    Former users

    1.70 (0.63-4.60)

    Users

    1.69 (0.57-5.00)

    Nyboe- Andersen et al.50

    (Danish IBD cohort database)

    antiTNF=4,553

    non -antiTNF

    =51,593

    3 IBD Lip/oral cavity/pharynx Crude

    1.24 (0.39-3.93)

    Adjusted

    1.47 (0.43-5.00)

    Adjusted for use of azathioprine

    1.08 (0.31-3.70)

    Colombel et al.44

    (Adalimumab cohort trials)

    ADA=3,160 1 CD Oral cavity

    SCC

    1 of total 35 Ca on ADA

  • CONCLUSIONS

    • The list of oral lesions is extensive.

    • may have devastating consequences

    • most lesions are easily handled and respond to the treatment of intestinal IBD

    • A multidisciplinary approach is essential for the correct diagnosis and management.

  • The Henry D. Janowitz Division of Gastroenterology at Mt Sinai, NY, USA

    + JAN 12th, 2016