Ulcers

Ulcers

1. Ulcerative lesions of oral cavity Presented by: ROSHNI MAURYA,2 ND YEAR PGT DEPT. OF PEDODONTICS & PREVENTIVE DENTISTRY,GNIDSR

2. INTRODUCTION Injury to the oral mucosa may result in a localized defect of the surface in which the covering epithelium is destroyed leaving an inflammed area of exposed connective tissue . Such defects are called ulcers or erosions (term commonly used for superficial ulcer) This may either follow molecular death of surface epithelium or its traumatic removal. Ulceration is the most common lesion of oral mucosa and is the manifestation for many local and genetic disorders.

3. What is an ulcer? Latin origin ULCUS means break in the skin. A mouth or oral ulcer   is an open sore in the mouth, or rarely a break in the mucous membrane or the epithelium on the lips or surrounding the mouth .

4. The surface of an ulcer is covered by mass of fibrin with intermingled, dead and dying polymorphs which would dry on the skin to form a crust or scab. A superficial ulcer with no evidence of significant fibrinous exudation on the surface of polymorph exudation suggests the possibility of bullous disorder. A heavy inflammatory infiltrate extends deep into the underlying connective tissue n blood vessels may show slight inflammatory vasculitis . Granulation tissue is formed with dilated blood vessels and heavy infiltrate of plasma cells, lymphocytes and polymorphs.

5. PARTS OF AN ULCER Ulcer consists of: Edge:- area between the margin and floor of ulcer.This is an important finding of an ulcer which by itself not only gives clue to diagnosis ulcer but also to the condition of ulcer. Floor:- this is the exposed part of an ulcer. The covering of floor is important. Base (on which the ulcer rests):- floor is the exposed surface of an ulcer whereas the base is on which the ulcer rests. Floor is seen but the base is felt. Margin:- it’s the point where the ulcer joins the normal epithelial tissue.

6. Parts of an ulcer :Davis et al. Symptom Analysis and Physical Diagnosis (2nd edn ), p. 309

7. The classic appearances of various ulcers are presented . Infective ulcers due to Mycobacterium species, and bed sores, tend to have an undermined edge while a trophic ulcer is punched out and typically round in surface shape. A raised firm ulcer edge may indicate malignancy

8. Histological examination shows an ulcer covered by thick layer of fibrous exudate with a dense, chronic inflammatory cell infiltrate in its base involving underlying damaged muscle. The deeper parts contain infiltrate rich in histiocytes and eosinophils . True granulomas are not present.

9. CLASSIFICATION OF ULCERS TWO TYPES OF CLASSIFICATON OF ULCERS IS POSSIBLE:- CLINICAL:

10. PATHOLOGIC ULCERS Ulcerations are classified on the basis of etiology. CAUSES OF ORAL ULCERATIONS:- Local Causes Aphthae Infections Drugs Systemic disease Malignant disease

11. 1) Local Causes: Trauma (physical) - Appliances. - Self-inflicted. - Sharp teeth or restorations. - Iatrogenic. Burns (chemical ant thermal ) - Chemical. - Electric. - Heat. - Radiation.

12. 2) Recurrent aphthae Minor ulcers ii) Major ulcers iii) Herpetiform type

13. 3) Infections Viral - Vesiculobullous diseases caused by viruses - Human herpesvirus 8 (HHV-8) - Human Immunodeficiency virus Bacterial - Acute Necrotizing Ulcerative Gingivitis (ANUG) - Syphilis - Tuberculusosis iii) Fungal - Chronic Mucocutaneous Candidosis (CMC)

14. 4) Drugs Drug-induced neutropenia/ anaemia ( cytotoxics ) ii) Lichenoid drug reactions (e.g. β -blockers, NSAIDs) iii) Drug-induced mucositis (cyclophosphamide)

15. 5- Malignant diseases Oral squamous cell carcinoma Kaposi’s sarcoma Non-Hodgkin’s lymphoma

16. 6 ) Systemic diseases Mucocutaneous diseases Haematological disorders Gastrointestinal disorders

17. Mucocutaneous disease - Behcet’s syndrome - Lichen planus - Vesiculobullous diseases

18. 6) Systemic diseases Haematological disorders - Anaemia - Leukemia

19. 6) Systemic diseases iii) Gastrointestinal disorders - Coeliac disease (Gluten-sensitive entropathy) - Crohn’s disease -

20. The most widely accepted form divides them into acute ulcers--sudden onset and short lasting—and chronic ulcers--insidious onset and long lasting. Commonest acute oral ulcers include traumatic ulcer, recurrent aphthous stomatitis, viral and bacterial infections and necrotizing sialometaplasia. On the other hand, oral lichen planus, oral cancer, benign mucous membrane pemphigoid, pemphigus and drug-induced ulcers belong to the group of chronic oral ulcers.

21. Epidemiology and F requency Mouth ulcer is a very common oral lesion. Epidemiological studies show an average prevalence between 15% and 30% . Mouth ulcers tend to be more common in women and those under 45.  The frequency of mouth ulcers varies from fewer than 4 episodes per year (85% of all cases) to more than one episode per month (10% of all cases) including people suffering from continuous recurrent aphthous stomatitis .

22. Epidemiology of the most common oral mucosal diseases in children The lesions most frequently considered by authors and that most often appear in the different studies are: recurrent aphthous stomatitis (0.9-10.8%), labial herpes (0.78-5.2%), fissured tongue (1.49-23%), geographic tongue (0.60-9.8%), oral candidiasis (0.01-37%) and traumatic injury (0.09%-22.15%). {Med Oral Patol Oral Cir Bucal 2005 Nov-Dec;10(5): 376-87 }

23. Diagnostic Tools for Oral Mucosa Lesions Andrea Santarelli , DDS; and Lorenzo Lo Muzio , PhD, MD July 2012 Issue - Expires July 31st, 2015 Inside Dentistry - Lesions of the oral mucosa represent a diagnostic challenge for dental practitioners, because similar appearances are the final common manifestation of a wide spectrum of conditions, including autoimmune diseases; neoplastic, traumatic, or infectious lesions; nutritional deficiencies; and drug reactions, as well as oral manifestations of systemic diseases. One of the roles of dental practitioners is the identification and management of oral mucosa diseases. While the diagnosis of some oral lesions can be made on the basis of the history and/or clinical findings, for others, the definitive diagnosis requires the aid of some tools with which the general dentist should be familiar. -

24. Tools for diagnosis: History Examination Further investigation Additional diagnostic methods – biopsy

25. Further investigation – questions one should ask: How long have you had that ulcer? How many ulcers do you have? Is it painful? Can you relate them to any trauma, hot food or another factors? Is it the first time or you had them before? Where are they located in the mouth? Do they start as ulcer or as vesicle/bulla? Do you get them anywhere else on the body?

26. Things one need to look for: Site Number Size Shape Base Edge

27. Differential diagnostic, based on history How long have you had the ulcer? Long time – chronic Chronic trauma (single, can identify the cause, and should improve after removal) Malignancy (single, painless) TB (single ulcer in the tongue/palate, associated symptoms – chronic cough) Mucous membrane pemphigoid (multiple ulcers affect mainly gingiva, blood filled blisters) Primary or tetriary syphilis

28. Recent – acute Acute trauma (single, can identify the cause, and should improve after removal) Viral infection (multiple, associated symptoms – fever) Immune mediated disease (Erythema multiforme, RAS)

29. How many ulcers do you have? Single Traumatic Primary or tetriary syphilis TB Malignancy Multiple Viral infection Immune mediated disease

30. Is it painful? Yes Acute causes (trauma, viral, immune mediate) No Chronic causes (trauma, TB)

31. Can you relate them to trauma or hot food? Yes Confirm traumatic ulcer Remove the cause Review after 1 week No Look for other causes

32. Do you get them anywhere else on the body? No Think of oral conditions Yes – where? Skin – mucocutaneous disease (lichen planus, pemphigus)

33. Traumatic ulcers:

34. Traumatic ulcers : 1- Physical Trauma: - Physical traumatic ulcers are common oral lesions. - Can be caused by a sharp or broken tooth, rough fillings, dental instruments, biting, denture irritation, dental braces; sharp foreign bodies, etc. Ulcerative lesions 1) Local Causes:

35. D ental braces

36. 1- Physical Trauma: Clinical features: They are clinically diverse, but usually appear as a single, painful ulcer with a smooth red or whitish-yellow surface and a thin erythematous halo. They are usually soft on palpation, and heal without scarring within 6–10 days, spontaneously or after removal of the cause. Ulcerative lesions Traumatic ulcers 1) Local Causes:

37. 1- Physical Trauma: Clinical features: - However, chronic traumatic ulcers may clinically mimic a carcinoma. The tongue, lip, and buccal mucosa are the sites of predilection. The diagnosis is based on the history and clinical features. However, if an ulcer persists over 10–12 days a biopsy must be taken to rule out cancer. Ulcerative lesions Traumatic ulcers 1) Local Causes:

38. Physical traumatic Ulcer

39. Ulcerative lesions Traumatic ulcers 1- Physical Trauma : Differential diagnosis Squamous-cell carcinoma and other malignancies, aphthous ulcer, syphilis, tuberculosis. Treatment Removal of traumatic factors. Topical steroids may be used for a short time.

40. Ulcerative lesions Traumatic ulcers 2- Chemical trauma: Oral ulcers may arise with local application of Aspirin (Salicylic Acid), Clinical features: - It appears as a red, painful erythema that may undergo desquamation, leaving erosions. -The lesions heal spontaneously in about a week. -The diagnosis is made exclusively on clinical grounds .

41. Chemical (Aspirin burn) ulceration: - The photos show a patient who placed an aspirin on her gums.  Aspirin is an acid and burned the oral tissues (gums and cheek). - Fortunately the mouth heals quickly and within two weeks healing occurred.

42. Ulcerative lesions Traumatic ulcers 2- Chemical trauma: Differential diagnosis - Thermal burn, traumatic lesions, aphthous ulcers, drug reactions. Treatment - Discontinue the application of the causative agent.

43. RADIATION TRAUMATIC ULCERATION Oral mucosa may suffer immediate damage due to direct effects of radiation on cells or delayed effects due to epithelial atrophy and damage to underlying vascular bed during radiotherapy of head n neck cancer. The immediate effects are erythema, radiation mucositis and ulceration. Oedema due to obstruction of regional lymphatics may occur. Radiation ulcers are painful.

44. EOSINOPHILIC ULCER Its also referred to as traumatic granuloma or eosinophilic granuloma of tongue. It is particularly associated with trauma n injury although the pathogenesis is unclear.trauma may be due to missing,malposed teeth,partial denture or more commonly,erupting teeth during nursing which results in sublingual ulcerations in infants. It occurs most commonly on the tongue and presents clinically as chronic, well demarcated ulcer which may mimic a sq. Cell carcinoma.

45. 2-Recurrent Aphthous Stomatitis Ulcerative lesions Recurrent aphthous ulcers are among the most common oral mucosal lesions, with a prevalence of 10–30% in the general population. -The cause remains unclear. Recent evidence supports the concept that cell-mediated immune responses play a primary role in the pathogenesis. - Several predisposing factors have been reported, such as trauma, allergy, genetic predisposition, endocrine disturbances, emotional stress, hematological ,nutritional deficiencies, and AIDS. -Three clinical variations have been recognized: minor , major and herpetiform ulcers . -They are very painful and cause the patient a lot of discomfort.

46. Herpetiform recurrent Aphthous Stomatitis The herpetiform variation is characterized by small, painful, shallow ulcers, 1–2 mm in diameter, with a tendency to coalesce into larger irregular ulcers. Characteristically, the lesions are multiple (10–100), persist for one or two weeks, and heal without scarring. usually in old age group, common in females. Ulcerative lesions 2-Recurrent Aphthous Stomatitis

47. Herpetiform aphthae                                      

48. Minor recurrent Aphthous Stomatitis Minor aphthae are the most common form, and they present clinically as small, painful, round ulcers 3–6 mm in diameter, covered by a whitish-yellow membrane and surrounded by a thin red halo. The lesions may be single or multiple (two to six), and they heal without scarring in 7–14 days. Mainly found in on the non-keratinized mobile mucosa, lips, cheeks, floor of the mouth. Ulcerative lesions 2-Recurrent Aphthous Stomatitis

49. Minor aphthous ulcer

50. Major recurrent Aphthous Stomatitis The major form is characterized by deep painful ulcers, 1–2 cm in diameter, that persist for 3–6 weeks and may cause scarring. The number of lesions varies from one to ten. Found in any area of the mucosa, including keratinized dorsum of the tongue, palate. Ulcerative lesions 2-Recurrent Aphthous Stomatitis

51. Major aphthous ulcer

52. Aphthous Lesions Clinical Types Minor (Lip) Minor (Tongue) Major

53. CLINICAL FEATUERS OF RECURRENT APHTHOUS STOMATITIS

54. Oral Aphthous Lesions Treatment Options Topical Therapy - Topical Corticosteroids Intralesional - Triamcinolone: 40 mg /ml (0.5 ml-1.0 ml injected bid) Systemic Therapy - Prednisone: - Diet supplementation: Vit.B12,FOLIC ACID,IRON,ZINC SULFATE

55. Ulcerative lesions 3) Infections Viral - Herpetic gingivostomatitis , herpangia , hand-foot and mouth disease, varicella ,EBV - Human herpesvirus 8 (HHV-8) - Human Immunodeficiency virus - Vesiculobullous diseases caused by viruses Bacterial - Acute Necrotizing Ulcerative Gingivitis ( ANUG) - Syphilis - Tuberculosis, leprosy iii) Fungal - Chronic Mucocutaneous Candidosis ( CMC)

56. Primary herpetic gingivostomatitis Most common cause of severe oral ulceration in children. Caused by simplex type 1 virus Usually occurs after 6 months of age. Peak incidence: b/w 12 & 18 months of age Incubation time:3-5 days with a prodromal 48 hour history of irritability, pyrexia and malaise Child is often unwell , has difficulty in eating and drinking and typically drools.

57. Clinical features Stomatitis is present Gingival tissues becoming red & oedematous Intra-epithelial vesicles appear; rapidly breakdown to form painful ulcers. Vesicles may form on any part of the oral mucosa, including the skin around the lips Solitary ulcers are usually small (3mm);painful with an erythematous margin, but larger ulcers with irregular margins often result from the coalescence of individual lesions. Disease is self –limiting and the ulcers heal spontaneously without scarring within 10-14 days.

58. Diagnosis: History & clinical features Exfoliative cytology Viral antigen can be detected by PCR amplification. Viral culture Viral antibody detection in blood samples

59. Management Symptomatic care Encourage oral fluids Analgesics Mouthwashes for older children : CHX gluconate ,0.2%, 10 ml 4- hourly. Topical anaesthetics: lidocaine viscous 2% or lidocaine (xylocaine) spray Antiviral chemotherapy

60. Herpangina By coxsackievirus A4 Affect children from 3-10 years ,peak from June to October

61. Clinical features - prodrome ,milder than herpes simplex (fever ,anorexia ,malaise) - sore throat ,dysphagia - ulcers mainly at post .area of oral cavity (soft palate ,fauces ,tonsils ,posterior pharynx) - ulcers smaller than herpes -at post area and more painful. - no marginal gingivitis -mainly in epidemics

62. - Hand- foot and mouth disease Caused by coxsackie virus A16,from 8 months to 33 years ,75%under 4 years.

63. Clinical features - low grade fever - oral vesicles and ulcers more extensive than herpes(mainly palate ,buccal mucosa) - macules and papules on extensor surface of hand and feet. - examine hands and feet for maculopapular lesions and vesicles if there is acute stomatitis and fever

64. Infectious mononucleosis Caused by Epstein –Barr virus (EBV) Mainly affects older adolescents and young adults. Disease is highly infective and is characterized by malaise, fever and acute pharyngitis. In young children, ulcers and petechiae are often found in posterior pharynx and soft palate. Disease is self limiting

65. Diagnosis History & clinical features Paul –Bunnell agglutination test and atypical monocytes on blood film

66. Varicella A highly contagious virus causing chickenpox in younger subjects and shingles in older individuals. There is prodromal phase of malaise and fever for 24 hours followed by macular eruptions and vesicles. In chickenpox, oral lesions occur in around 50% of cases but only a small number of vesicles occur in the mouth These lesions may be found anywhere in the mouth in addition to other mucosal sites such as conjunctivae, nose or anus . Healing of oral lesions is uneventful

67. Diagnosis Clinical appearance and history

68. Human Herpes virus-8 (HHV-8) The causative microbe for Kaposi’s sarcoma (KS). Kaposi sarcoma is a malignant neoplasm of endothelial cell origin. -Four forms of KS are recognized: Classic , African (endemic) , Immunosuppression-associated (iatrogenic) and AIDS-related (epidemic) : This has a high incidence among AIDS patients, primarily involves the skin, lymph nodes, viscera, and frequently the oral mucosa.

69. Human Immunodeficiency Virus (HIV) A minority of patients with severe HIV disease will develop deep, necrotic ulcers of unknown aetiology . These ulcers are painful, cause profound dysphagia and can arise on any oral mucosal surface, although the buccal and pharyngeal mucosa are the more commonly affected sites.

70. Human Immunodeficiency Virus (HIV) The ulcers typically resolve with systemic thalidomide (e.g. 200 mg daily) Small number of patients with HIV disease may have ulcers similar to that of recurrent aphthous stomatitis (RAS), although whether the frequency of RAS in HIV is truly increased remains unclear.

71. HIV-associated ulceration

72. 2- Bacterial i) Acute Necrotizing Ulcerative Gingivitis ( ANUG) ii) Syphilis iii) Tuberculusosis iv) Leprosy

73. i ) Acute Necrotizing Ulcerative Gingivitis (ANUG) This entity used to be called "Trench Mouth" because of its prevalence in soldiers fighting in the trenches during world war I.  Etiology : Fusobacterium nucleatum , Treponema vincentii , and probably other bacteria play an important role. - Predisposing factors are emotional stress, smoking, poor oral hygiene, local trauma, and mainly HIV infection.

74. Clinical features The characteristic clinical feature is painful necrosis of the interdental papillae and the gingival margins, and the formation of craters covered with a gray pseudomembrane . Spontaneous gingival bleeding, halitosis, and intense salivation are common. Fever, malaise , and lymphadenopathy are less common . -Rarely, the lesions may extend beyond the gingiva ( necrotizing ulcerative stomatitis ). -The diagnosis is made at the clinical level.

75. ِ Acute Necrotizing Ulcerative Gingivitis

76. Differential diagnosis Herpetic gingivitis, Desquamative gingivitis,Agranulocytosis , leukemia. - Treatment Systemic metronidazole and oxygen-releasing agents topically are the best therapy in the acute phase, followed by a mechanical gingival treatment.

77. ii ) Syphilis Syphilis is a relatively common sexually transmitted disease. - Etiology Treponema pallidum . Clinical features: Syphilis may be acquired (common) or congenital (rare). Acquired syphilis is classified as primary , secondary and tertiary.

78. Clinical features: - The characteristic lesion in the primary stage is the chancre that appears at the site of inoculation, usually three weeks after the infection. Oral chancre appears in about 5–10% of cases, and clinically presents as a painless ulcer with a smooth surface, raised borders, and an indurated base. Regional lymphadenopathy is a constant finding.

79. Solitary chancre on the ventral surface of the tongue Two chancres on the tongue

80. - Differential diagnosis Traumatic ulcer, aphthous ulcer, tuberculosis, herpes simplex, candidiasis, erythema multiforme, lichen planus. - Treatment Penicillin is the antibiotic of choice. Erythromycin or Cephalosporins are good alternatives.

81. iii ) Tuberculosis -Tuberculosis is a chronic, granulomatous, infectious disease that primarily affects the lungs . Etiology Mycobacterium tuberculosis .

82. Clinical features The oral lesions are rare, and usually secondary to pulmonary tuberculosis. The tuberculosis ulcer is the most common feature. Clinically, the ulcer is painless and irregular, with a thin undermined border and a vegetating surface, usually covered by a gray-yellowish exudate. The dorsum of the tongue is the most commonly affected site, followed by the lip, buccal mucosa, and palate.

83. - Differential diagnosis: carcinomas , syphilis, eosinophilic ulcer , necrotizing sialadenometaplasia , malignant granuloma, major aphthous ulcer . Treatment Antituberculous drugs.

84. Tuberculosis: typical ulcer on the dorsal surface of the tongue

85. Leprosy Children are deemed more susceptible to leprosy because of their immature immune systems. Mycobacterium leprae is a member of the same family of organisms found to cause tuberculosis . The disease affects multiple systems and organs of the body such as the nerves leading to muscle weakness, the liver, kidneys, eyes resulting in blindness, lymph nodes, bones, and joints. The bones are resorbed and deformity occurs.

86. Oral Manifestations The oral manifestations of leprosy may be present in 19% to 60% of patients. Shambulingappa , et al. (2012) states that the oral examination is neglected in most leprosy clinics today. When oral lesions appear, they usually occur in the LL form (disseminative and progressive lepromatous form). This form presents with the most severe effects on the body. The second form is the tuberculoid form (TT), and this form is less contagious. Combinations of both types may also occur. Oral lesions occur in the palate intraorally, but may manifest as skin lesions periorally affecting the lips. The lips present as macrocheilia and exhibit flat-topped nodules .

87. Other oral lesions may occur causing superficial ulcers, candidiasis, fissured tongue, and loss of papillae, glossitis , and swellings . Treatments for leprosy include antibiotics, anti-inflammatory medications, steroids, thalidomide, or combinations of MRD therapy, depending upon the type and extent of the leprosy. Often, pain and ulceration are treated as other complications would be treated to relieve discomfort.

88. The World Health Organization estimates approximately 182,000 cases world wide in 2012, with elimination of the disease in 119 countries out of 122 since 1985. However, new cases have recently been reported to have increased in India.

89. OTHER INFEC-TIONS CLINICAL FEATURE CAUSE SIGNIFICANCE GONORRHEA GENITAL LESIONS WITH RARE ORAL MANIFESTATIONS; ERYTHEMA OR ULCERS N.gonorrhea MAY BE CONFUSED WITH OTHER ULCERATIVE DISEASES TUBERCULOSIS INDURATED, CHRONIC ULCER THAT MAY BEPAINFUL- ON ANY MUCOSAL SURFACE M.tuberculosis INFECTIOUS ORAL LESIONS ARE ALWAYS RESULT OF LUNG LESIONS LEPROSY SKIN DISEASE WITH RARE NODULES OR ULCERS M.leprae COMMON IN SOUTHEAST ASIA, INDIA, SOUTHAMERICA ACTINOMYCOSIS TYPICALLY SEEN IN MANDINLE, WOOD HARD NODULE WITH SULFUR GRANULES A.israelii INFECTION FOLLOWS ENTRY THROUGH SURGICAL SITE, PERIODONTAL DISEASE OR OPEN ROOT CANAL NOMA NECROTIC, NONHEALING ULCER OF GINGIVA OR BUCCAL MUCOSA; RARE; AFFECTS CHILDREN ANAEROBES IN PATIENT WHOSE SYSTEMIC HEALTH IS COMPROMISED OFTEN ASSOCIATED WITH MALNUTRITION; MAY RESULT IN TISSUE DESTRUCTION

90. 3- Fungal Chronic Mucocutaneous Candidosis (CMC) Chronic mucocutaneous candidiasis (CMC) is the label given to a group of overlapping syndromes that have in common a clinical pattern of persistent, severe, and diffuse cutaneous candidal infections. These infections affect the skin, nails and mucous membranes Chronic oral candidiasis -Related to denture stomatitis - HIV-associated candidiasis - Related to inhaled corticosteroid use

91. CMC

92. DRUG-INDUCED LESIONS A wide spectrum of drugs can occasionally cause mouth lesions, by various mechanisms. Ulcers are common in those treated with cytotoxic drugs . The more common examples of drug reactions include: Cytotoxic agents, particularly methotrexate,producing ulcers. Agents producing lichen-planus-like ( lichenoid ) lesions , such as non-steroidal anti-inflammatory agents , some antihypertensives , antidiabetics , gold salts, antimalarials and other drugs .

93. Agents causing local chemical burns (especially aspirin held in the mouth). Agents causing erythema multiforme (especially sulphonamides and barbiturates). Other drug reactions are uncommon or rare . Cytotoxic induced ulcers: these have a nonspecific appearance , but are widespread and very painful. Lichenoid lesions: resemble lichen planus clinically and histologically

94. Management Diagnosis of a drug reaction is made from the drug history and sometimes by testing the effect of withdrawal. Skin patch tests are, unfortunately, rarely of real practical value. Treatment is to stop the causative drug and treat the ulceration symptomatically with topical benzydamine and, possibly, aqueous chlorhexidine .

95. Management Diagnosis of a drug reaction is made from the drug history and sometimes by testing the effect of withdrawal. Skin patch tests are, unfortunately, rarely of real practical value. Treatment is to stop the causative drug and treat the ulceration symptomatically with topical benzydamine and, possibly, aqueous chlorhexidine .

96. Ulcerative Lichen Planus in Childhood Lichen planus (LP) is an autoimmune, chronic, inflammatory disease that affects mucosal and cutaneous tissues . The exact etiology is unknown, but it is believed to result from an abnormal T cell-mediated immune response in which basal epithelial cells are recognized as foreign because of changes in the antigenicity of their cell surface Oral lichen planus (OLP ) is a common disease in the middle aged and elderly population and has a prevalence of about 0.5% to 2%. By contrast , oral lichen planus in childhood (OLP) is rare and it was first reported in the 1920s. Oral mucosal involvement in adults itself accounts for 0.5% to 19%, while in children, it is very uncommon

97. The oral lesions are more pleomorphic than those of their cutaneous forms and subtypes are categorized as reticular, papular , plaque-like, atrophic, erosive, and bullous . The erosive form is extremely rare in children and few reports on this subject have been published in the literature.

98. OLP in childhood was first described in 1920 and since then only few articles have been published and most of the studies have suggested that childhood LP is more common in tropical countries like India( A. J. Kanwar andD.De , “Lichen planus in childhood: report of 100 cases,” Clinical and Experimental Dermatology , vol. 33, pp.423–427 , 2008 .) Sharma and Maheshwari reported 50 children with LP and with concomitant oral lesions in 15 of them and they stated that the oral mucosa seems to be less commonly involved in children with LP than in adults.( R. Sharma and V. Maheshwari , “Childhood lichen planus: a report of fifty cases,” Pediatric Dermatology , vol. 16, no. 5, pp. 345–348 , 1999 .)

99. Kanwar and Kumar reported only one case having oral ulcerative lichen planus out of 25 patients with cutaneous lichen planus [ A. J. Kanwar andD.De , “Lichen planus in childhood: report of 100 cases,” Clinical and Experimental Dermatology , vol. 35, no.3 , pp. 257–262, 2010 .]

100. The difference in the prevalence of OLP in children (0.03 %) versus that of OLP in adults (0.5%–2%) is understood by less number of associated systemic diseases in children, autoimmune diseases, infections, drug usage, and dental restorations in childhood; this may reduce the risk for developing OLP in childhood [ M. Rybojad, I. Moraillon, S. Laglenne et al., “Lichen plan del’enfant ,” Annales de Dermatologie et de Venereologie , vol. 125, no . 10, pp. 679–681, 1998. ]. Moreover , the diagnosis of OLP may be missed due to irregular dental checkups, lack of symptoms, and ignorance by clinicians in diagnosing the condition.[ A. Pakfetrat , A. Javadzadeh - Bolouri , S. Basir-Shabestari , and F. Falaki , “Oral lichen planus: a retrospective study of 420 Iranian patients ,” Medicina Oral, Patologia Oral y Cirugia Bucal , vol. 14, no . 7, pp. E315–E318, 2009 .]

101. Dorsum of tongue showing ulcerative lesion.

102. BEHÇET’S SYNDROME ( Behçet’s Disease) Aphthae of any of the RAS types described earlier may rarely be a manifestation of Behçet’s syndrome where they are associated with systemic disease, manifesting usually with genital ulcers and uveitis. This rare condition affects mainly young adult males and is most common in people from the Middle East, Japan , China and Korea, along the ancient silk route from Europe to the Far East.

103. Aetiology Behçet’s syndrome appears to have an immunogenetic basis , with a specific association with HLA genetic type HLA-B5101. Immuno -logical changes are like those in aphthae . The precipitating factor is unknown but may be Streptococcus sanguis . There appears to be a subset of T cells which react to an immunostimulatory human heat shock protein with cross-reactivity to streptococci, and produce tumour necrosis factor (TNF) and interleukin 8 (IL-8). The interleukin leads to the chemo-attraction of neutrophils, which are also hyperactive and release superoxide, leading to vasculitis .

104. Clinical Features Behçet’s syndrome is a multisystem disease affecting the mouth in most cases and many other sites including, commonly: Genitals : ulcers resembling oral aphthae Eyes : uveitis is one of the more important ocular lesions and visual acuity is often impaired . Skin : erythema nodosum (painful red lumps on the shins), various rashes may develop as well as pustules at the site of venepuncture ( pathergy ). Joints : large joint arthropathy is not uncommon. Neurological system : headache, psychiatric, motor or sensory manifestations. Vascular system : thrombosis of large veins may be life-threatening.

105. Diagnosis Behçet’s syndrome is a clinical diagnosis, the cardinal features being oral and genital ulceration, uveitis and erythema nodosum . Other causes of this constellation of lesions, such as ulcerative colitis , Crohn’s disease, mixed connective tissue disease , lupus erythematosus and Reiter’s syndrome , must be excluded. Diagnostic criteria for Behçet’s syndrome are not completely agreed but include: recurrent oral ulceration plus two or more of the following: recurrent genital ulceration; eye lesions; skin lesions; pathergy .

106. Management No test of reliable value, except HLA typing Oral ulcers : treat as for aphthae Systemic manifestations : immunosuppression using, typically, corticosteroids, colchicines or thalidomide. Behçet's syndrome, oral ulceration.

107. Erythema multiforme, Stevens-Johnson syndrome and Toxic epidermal necrolysis These conditions exist that present with similar clinical signs & histological appearances. There is a now view that these are distinct pathological entities and might be intiated by quite distinct aetiological agents. Ailternative view: these disorders represent different presentations of the same basic disorder,distinguished by the severity and extent of the lesions.

108. Erythema multiforme Original description of it was that of a self-limiting but often recurrent and seasonal skin disease with mucosal involvement limited to oral cavity. Lips are typically ulcerarted with blood staining and crusting. Characteristics macules (‘target lesions’) occur on the Limbs but with less involvement of the trunk or head and neck. Lesions are concentric with a erythematous halo and a central blister.

109. Although lesions are extremely painful, th course of illness is benign and healing uneventful .

110. S tevens-Johnson syndrome The condition presents with acute febrile illness,generalized exanthema, lesions involvement the oral cavity and a severe purulent conjunctivitis. Skin lesions are more extensive than those of erythema multiforme. It is characterised by Vesiculobullous eruptions over the body, in particular the trunk and severe involvement of multiple mucuous membranes including the vulva, penis and conjunctivia . Course of condition is longer and scarring may occur.

111. Toxic epidermal necrolysis (TEN) TEN or Lyell’s syndrome is a severe, sometimes fatal, bullous drug –induced eruption where sheets of skin are lost. It resembles third-degree burns or staphylococcal scalded skin syndrome. Oral involvement is similar to SJS

112. AETIOLOGY Erythema multiforme is often initiated by herpes simplex reactivation. there is some evidence that Stevens-Johnson syndrome is initated by a mycoplasma pneumonia infection or drug reaction. TEN is drug-induced.

113. Management If there is a known precipating factor such as herpes simplex infection then antivirals such as topical acyclovir can be used as a form of prophylaxis. Management is generally symptomatic and supportive. Debridement of oral cavity with 0.2% CHX gluconate or benzydamine hydrochloride and CHX ( Difflam C) is effective in removing much of the necrotic debris from the mouth.

114. Extensive areas of ulceration tend to be less responsive to CHX and a minocycline mouthwash may prove more effective.The role of systemic steroids is controversial but they may be necessary in severe cases requiring hospital admission. It also includes: Adequate fluid replacement and total parentral nutrition if required. Pain control which may necessitate the use of narcotics and sedation.

115. Oral manifestations of gastrointestinal diseases Lesions within the jaws, oral mucosa or perioral tissues may sometimes be seen as manifestations of gastrointestinal ( GI) diseases . The oral lesions may occasionally occur before the onset of GI disease, be present during the disease process or persist even after the disease has resolved. Sometimes the oral lesions are similar to GI lesions, while at other times, the oral changes are caused by systemic alterations secondary to GI disease, such as those related to malabsorption.

116. Crohn’s disease Dupuy et al (3) found that only 0.5% of their patients with Crohn’s disease developed oral lesions, and these patients were more likely to also have anal and esophageal lesions. There is a predilection for males and onset in youth. Occasionally, the oral manifestations may be the first indication that a patient has Crohn’s disease, but the oral lesions usually develop in patients with known bowel disease. The oral lesions are multifocal, linear, nodular, polypoid or diffuse mucosal thickenings, with a predilection for occurring in the labial and buccal mucosa, and the mucobuccal folds (Figure 1). They are characteristically firm, pink and painless to palpation unless there are ulcerations that may cause pain on touch, or when eating acidic, spicy or hot foods.

117. These ulcers, which are typically persistent , linear and deep (3), should not be confused with aphthous ulcers, which are shallow, round to oval shaped lesions that heal spontaneously in approximately seven to 14 days (4). On palpation , the lesions may feel granular below the epithelium, reflecting the histological findings . Microscopically, the lesions exhibit subepithelial , noncaseating granulomatous inflammation characterized by epithelioid histiocytes , giant cells and lymphocytes (Figure 2), identical to those seen in the bowel. There is great variability in the severity of the inflammation, which is worse if ulcers are present.

118. Oral lesions are routinely subjected to special histochemical stains to rule out infectious agents such as deep fungal infections or tuberculosis, and polarized to rule out foreign body reactions. Because granulomatous microscopic lesions are seen in other diseases, including orofacial granulomatosis and sarcoid (4), the definitive diagnosis of Crohn’s disease cannot be made on oral biopsy alone. However, the biopsy may direct the clinician to investigate the GI tract for Crohn’s disease lesions.

119. Oral lesions of Crohn’s disease are typically persistent, and remit and relapse over the years (3). Their response to systemic therapy is highly variable and unpredictable, and they do not necessarily parallel the activity of gut disease. Some oral ulcerating lesions may require topical corticosteroid therapy or even intralesional corticosteroid injections.

120. Ulcerative colitis Oral lesions of ulcerative colitis – termed pyostomatitis vegetans (5,6 ) – are rare, and are far less common than oral manifestations of Crohn’s disease. There is a male predilection (5), and oral outbreaks may occur at any age (6). The oral lesions may precede GI lesions but are generally present synchronously. Clinically, the lesions consist of scattered, clumped or linearly oriented pustules on an erythematous mucosa at multiple oral sites, with variable severity (Figure 3), but usually sparing the dorsum of the tongue.

121. Patient discomfort is proportional to the degree of ulceration of the lesions , many of which remain epithelialized. Long-standing lesions may become granular, polypoid or fissured (6), clinically mimicking Crohn’s disease. Some patients exhibit oral aphthous-like lesions (6 ) in addition to the pustular lesions, an approximately 10% of patients develop inflammatory bowel disease-associated arthritis of the temporomandibular joints (6).

122. Microscopically, the lesions mimic the crypt abscesses of colonic lesions, without evidence of granulomatous inflammation. The oral submucosa shows edema with neutrophils, eosinophils and lymphocytes, while the epithelium shows spongiosis with neutrophilic and eosinophilic abscesses (5) (Figure 4). The microscopic appearance in itself is not diagnostic, because neutrophilic or eosinophilic intraepithelial abscesses may be seen in other conditions such as candidiasis, benign migratory glossitis , or stomatitis areata migrans and pemphigus vegetans (

123. The clinical appearance and historical information must be correlated with the microscopic findings; otherwise, asymptomatic patients who receive an oral diagnosis of pyostomatitis vegetans should be investigated by a gastroenterologist for bowel disease The oral lesions usually respond to colonic disease treatment (6 ). Topical or systemic corticosteroids (5) and dapsone (6) have been used for recalcitrant oral lesions with variable effectiveness. Because the severity of oral disease usually reflects the severity of the bowel disease, the gasteroenterologist may use oral manifestations , when present, as an additional gauge to determine the severity of the bowel disease and/or the response to therapy.

124. MALABSORPTION CONDITIONS AFFECTING HEMATOPOIESIS GI diseases related to protein-caloric malnutrition (10) or micronutrient malabsorption (11) may have an effect on the oral tissues. The classical examples are iron malabsorption inducing iron deficiency anemia and vitamin B12 malabsorption in pernicious anemia [ Field EA, Speechley JA, Rugman FR, Varga E, Tyldesley WR. Oral signs and symptoms in patients with undiagnosed B12 deficiency. J Oral Pathol Med 1995;24:468-70 .] When the malabsorption is sufficiently severe, the first oral manifestation is atrophic glossitis (Figure 6), in which the filiform papilla and sometimes the fungiform papilla of the dorsumof the tongue undergo atrophy, leaving a bald, red tongue (

125. In milder cases, the atrophy is patchy, but more severe cases show involvement of the entire dorsum. In very severe cases, there may be shallow, round to oval-shaped, persistent ulcers with bright red borders , clinically resembling aphthous ulcers but often responsive to appropriate replacement therapy. Overt tongue lesions are usually sore, but a more common complaint is a burning sensation ( glossopyrosis ) that may precede clinically detectable oral lesions

126. Other oral mucosa may also become involved with atrophic zones , with or without aphthous-like ulcers and the burning sensation, but these lesions are not as dramatic as the bald tongue and often go unnoticed. Affected patients are predisposed to developing angular cheilitis , which is a candidal infection that can be treated with antifungal medication. The gastroenterologist may use atrophic glossitis as an indicator of moderate to severe nutrient malabsorption.

127. CYCLIC NEUTROPENIA THE CLINICAL FEATURES INCLUDE ORAL ULCERS WITH PERIODICITY; INFECTIONS, ADENOPATHY; PERIODONTAL DISEASE. THIS IS CAUSED BY MUTATIONS IN NEUTROPHIL ELASTASE GENE. CYCLIC NEUTROPENIA RESULTS IN RARE BLOOD DYSCRASIA. FEVER, MALAISE, ORAL ULCERS, CERVICAL LYMPHADENOPATHY AND INFECTIONS CAN OCCUR.

128. THE NEOPLASMS INCLUDE SQUAMOUS CELL CARCINOMA CARCINOMA OF MAXILLARY SINUS OTHER CARCINOMAS NEOPLASMS

129. ORAL AND OROPHARYNGEAL SQUAMOUS CELL CARCINOMAS REPRESENT ABOUT 3% OF CANCERS IN MEN AND 2% IN WOMEN. OF ALL THE FACTORS, TOBACCO IS REGARDED AS THE MOST IMPORTANT ESP THE CIGAR, PIPE AND REVERSE SMOKING. THE TIME-DOSE RELATIONSHIP OF CARCINOGENS FOUND IN TOBACCO IS OF MUCH IMPORTANCE IN THE CAUSE OF ORAL CANCER. MICRO ORGANISMS SUCH AS CANDIDA ALBICANS PRODUCES N-NITROSOBENZYLMETHYLAMINE CARCINOGEN AND HPV SUBTYPES 16 AND 18 PRODUCES ORAL SQUAMOUS CELL CARCINOMAS. SQUAMOUS CELL CARCINOMA

130. CARCINOMAS OF LOWER LIPS ARE MORE COMMON THAN UPPER LIP LESIONS BUT THE GROWTH RATE IS SLOWER. THEY APPEAR COMMONLY IN ELDERLY PATIENTS MOSTLY AFFECTING MEN THE SQUAMOUS CELL CARCINOMA CLINICALLY PRESENTS AS CARCINOMA OF LIPS AND TONGUE

131. SQUAMOUS CELL CARCINOMA OF TONGUE IS THE MOST COMMON INTRAORAL MALIGNANCY THESE PRESENT AS AN INDURATED, NON HEALING ULCER, AS A RED LESION, AS A WHITE LESION OR AS A RED-WHITE LESION.

132. Ischaemic ulcers: necrotising sialometaplasia This is an uncommon disorder that gives rise to large areas of deep ulcers on one side of the hard and sometimes the soft palate. This condition is probably associated with an ischaemic event and is associated with factors such as smoking, alcohol use, denture wearing, recent surgery and systemic disease. It can also be a feature of bulimia nervosa. The clinical and histopathological features may mimic those of SCC.

133. MALIGNANCIES OF PARANASAL SINUSES OCCUR MOST COMMONLY IN MAXILLARY SINUS. THIS AFFECTS ELDER PEOPLE AND GENERALLY MEN. PAST HISTORY FREQUENTLY INCLUDES SINUSITIS. AS THE NEOPLASM EXTENDS TOWARDS APICES OF MAXILLARY POSTERIOR TEETH, REFERRED PAIN MAY OCCUR. TOOTHACHE WHICH ACTUALLY REPRESENTS NEOPLASTIC MOVEMENT OF SUPERIOR ALVEOLAR NERVE IS THE COMMON SYMPTOM OF MAXILLARY SINUS MALIGNANCIES. OCCASIONALLY IT MAY PRESENT AS PALATAL ULCER AND MASS REPRESENTING EXTENSION THROUGH THE BONE AND SOFT TISSUE OF PALATE. CARCINOMA OF MAXILLARY SINUS

134. Pemphigus It is an important vesiculo -bullous disease mainly affecting adults; however,children can also be affected. Lesions are intra-epithelial ,rapidly break down so that affected individuals are often unaware of blistering, complaining instead of ulceration,mainly affecting the buccal mucosa,palate and lips.

135. Diagnosis There may be positive Nikolsky’s sign and cytological examination can reveal the presence of Tzanck’s cells. Direct immunofluorescence usingfrozen sections from an oral biopsy will reveal intracellular immunoglobulin(igg)deposits in the epithelium, which are diagnostic for this disease. Indirect immunofluorescence on blood samples is sometimes used to monitor patients.

136. Management Systemic corticosteroid therapy Antiseptic or minocycline mouthwashes and analgesia as necessary.

137. Epidermolysis bullosa It is aterm used to describe several hereditary vesiculo -bullous disorders of the skin and mucosa. Blisters may form from birth or appear in the first few weeks of life depending on the form of the disease. Corneal ulceration may also may be present and pitting enamel hypoplasia has been reported,mainly in the junctional forms of the disease.

138. Management Mangement is extremely difficult because of the fragility of the skin and oral mucosa.intensive preventive dental care is essential to prevent dental caries,combined with treatment of early decay. Supportive care is required with the use of CHX gluconate mouthwashes and possibly topical anaesthetics such as lidocaine(Xylocaine viscous)

139. Systemic lupus erythematous It is a chronic inflammatory multisystem disease occurring predominantly in young women.The hallmark of SLE is the presence of antinuclear antibodies which form circulating immune complexes with DNA. Oral ulceration often occurs in SLE and treatment of the condition usually involves systemic steroids.

140. leukemia The most frequently reported oral abnormalities attributed to the leukemic process include regional lymphadenopathy,mucous membrane petechiae and ecchymoses , gingival bleeding,gingival hypertrophy , pallor and nonspecific ulceration. Oral changes can be attributed to anemia,granulocytopenia,and thrombocytopenia