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Diseases of oral cavity

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Diseases of oral cavity

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Diseases of oral cavity

  1. 1. DISEASES OF MOUTH, PALATE, LIPS & CHEEK
  2. 2. ORAL MANIFESTATIONS OF SYSTEMIC DISEASES • The oral cavity is a mirror that reflects the health of the individual.
  3. 3. 1.Systemic Infectious diseases 2.Connective tissue disorders 3.Granulomatous diseases 4.Gastrointestinal diseases 5.Respiratory diseases 6.Haematological diseases 7.Endocrine diseases 8.Neurologic diseases 9.Nutritional deficiency 10.Immunodeficiency diseases 11.Drug reactions/radiotherapy 12.Dermatological diseases 13.Metabolic disorders 14.Neoplastic diseases CLASSIFICATION
  4. 4. INFECTIVE DISEASES 1.Viral infection 2.Bacterial infection 3.Fungal infection 4.Protozoal infection
  5. 5. VIRAL INFECTIONS 1.Herpes Simplex Stomatitis 2.Herpes Zoster 3.Herpangina 4.Hand Foot Mouth Disease 5.Cytomegalovirus Infection 6.Measles 7.Infectious Mononucleosis 8.Mumps 9.HIV
  6. 6. HERPES SIMPLEX STOMATITIS • HSV-1: Primary herpetic Gingivostomatitis Recurrent herpes labialis • HSV-2: • Primary herpetic Gingivostomatitis: -most frequent cause of acute stomatitis in children -varies in severity, many infections - subclinical -misdiagnosed as “teething” -malaise, anorexia, irritability, fever, anterior cervical lymphadenopathy, diffuse, purple, boggy gingivitis -multiple vesicles scarred ulcers(1-3mm) -occasionally in adults
  7. 7.  Diagnosis: -clinically -scrapping or smears from the lesion -immunofluorescent staining -exfoliative cytology- typical multinucleated giant cells  Treatment: -symptomatic -acyclovir (systemic)-severe cases
  8. 8.  Recurrent Intraoral Herpes Simplex Infection: -may affect healthy individual -persistent lesions in immunocompromised -chronic ulcer, raised, white border -esp. at sites of trauma -acyclovir
  9. 9. HERPES ZOSTER (SHINGLES) • Reactivation of Varicella –Zoster virus • Predisposing factor: Immunocompromised status • One dermatome affected (trigeminal nerve) • Unilateral • Ulcers in the distribution of dermatome • Mandibular nerve: ulceration of one side of tongue, floor of the mouth, lower labial & buccal mucosa • Maxillary nerve: one side of palate, the upper gingiva, buccal sulcus • Lesions persists for 2-3 wks Lesions on lips and chin
  10. 10. • Herpes Zoster Oticus (Ramsay Hunt Syndrome) • Ophthalmic Herpes Zoster • Post Herpetic Neuralgia • Diagnosis: clinically • Treatment: -Analgesics -Antivirals(within 72 hrs of onset of the lesions):acyclovir, famciclovir, valacyclovir, & gabapentin
  11. 11. HERPANGINA  Common in children  Coxsackie virus group A, Enteroviruses(30 & 71)  Self limiting vesicular eruptions in the oropharynx eg. soft palate, uvula, tonsillar pillars, posterior pharyngeal wall  Similar to herpes simplex except the lesions more commonly in oropharynx rather than oral cavity  Diagnosis: Clinically  Treatment: Supportive
  12. 12. HAND, FOOT AND MOUTH DISEASE  Enterovirus 71,Coxsackie viruses, some untypeable enteroviruses  Young children  Vesicular eruption in the oral cavity & oropharynx dysphagia, dehydration  Vesicles on the hands & feet  Pyrexia, malaise, vomiting  Short lived(5-8 days)  Diagnosis: clinically  Treatment: supportive
  13. 13. INFECTIOUS MONONUCLEOSIS • Acute, self limiting, systemic viral infection • Epstein-Barr Virus • Typical presentation: acute sore throat & tender cervical lymphadenopathy • Glandular disease • Kissing disease • Children & young adults • Prodromal symptoms: 4-5 days, anorexia, malaise, fatigue, headache
  14. 14. • Clinical features:- Oral manifestations - early and common- palatal petechiae, uvular edema, tonsillar exudate, gingivitis, & rarely ulcers -Generalized lymphadenopathy, hepatosplenomegaly, maculopapular skin rash • Laboratory tests: Heterophile antibody(Paul Bunnel test, Monospot test) • Treatment: -Mild to moderate cases: Symptomatic -Severe disease: Famciclovir • Anti-EBV compounds: Maribavir • Ampicillin based antibiotics should be avoided
  15. 15. CYTOMEGALOVIRUS INFECTION • Relatively rare • Cytomegalovirus (CMV) • HIV infection and immunocompromised • Clinical features: asymptomatic Oral lesions -nonspecific painful ulcerations- gingiva & tongue -Enlargement of parotid & submandibular glands, dry mouth, fever, malaise, myalgia, headache • Laboratory tests: HPE/Immunochemistry • Treatment: -Resolve spontaneously -Ganciclovir (Persistent case)
  16. 16. MEASLES (RUBEOLA) • Paramyxovirus • Highly contagious • Coryza, conjunctivitis & generalised cutaneous erythematous rashes • Oral cavity lesions: Pharyngotonsillitis Koplik’s spot: small, spotty, exanthematous lesions on buccal mucosa • Vaccination program
  17. 17. MUMPS • Common viral illness • Incubation period: 2-3 weeks • Fever, malaise, myalgia, headache, & painful parotid gland swelling • Self limiting • Complications: SNHL • Diagnosis: Clinical • Treatment: Supportive
  18. 18. BACTERIAL INFECTIONS 1. Tuberculosis 2. Syphilis 3. Leprosy
  19. 19. TUBERCULOSIS • Chronic, granulomatous, infectious disease • Mycobacterium tuberculosis • Clinical features: Oral lesions – rare secondary to pulmonary tuberculosis • Pharynx- not common Primary infection (Tonsils, Adenoids) Secondary to coughing heavily of infected sputum • Ulcer: multiple, painful, irregular, undermined border, granulating floor, usually covered by a gray-yellowish exudate, inflamed & indurated surrounding tissue
  20. 20. • Dorsum of the tongue - most commonly affected- lip, buccal mucosa, & palate • TB Esophagitis: -swallowed sputum or direct spread from adjacent lymph nodes -stricture, fistula, mucosal irregularities • Granulomatous Cheilitis- rare • Laboratory tests: Sputum culture, HPE, CXR • Treatment: ATT
  21. 21. SYPHILIS  Treponema pallidum -Acquired -Congenital 1. Primary Syphilis 2. Secondary Syphilis 3. Tertiary Syphilis
  22. 22. PRIMARY SYPHILIS • Lips, tongue, buccal mucosa, & tonsils • Site of inoculation- 3 weeks after the infection, Papule, breaks down to form an ulcer (chancre) • Oral chancre: painless ulcer with a smooth surface, raised borders, & indurated margin • Non tender cervical lymphadenopathy • Spontaneous healing
  23. 23. SECONDARY SYPHILIS • Most infectious • Secondary stage – after 6–8 weeks & lasts for 2-10 weeks • Clinical features: Malaise, low-grade fever, headache, lacrimation, sore throat, weight loss, myalgia,arthralgia, & generalized lymphadenopathy Mucous patches
  24. 24.  Hyperemia and inflammation of pharynx & soft palate  Snail Track ulcer :- -Oral cavity & oropharnyx -Ulcerated lesion covered with grayish white membrane which when scraped has pink base with no bleeding
  25. 25. SYPHILITIC PHARYNGITIS • May be congenital or acquired by sexual intercourse • Secondary stage most likely • HIV positive patients
  26. 26. TERTIARY SYPHILIS • Tertiary syphilis - after a period of 4–7 years • Typically painless • No lymphadenopathy unless secondary infection • Gumma: -Characteristic lesion -Hard palate, Nasal septum, Tonsil, PPW, or Larynx • VDRL may be negative
  27. 27. CONGENITAL SYPHILIS Early: first 3 months of life, manifest as snuffles nasal discharge purulent Late: Manifest at puberty Gummatous lesion • Oral lesions: high-arched palate, short mandible, Hutchinson’s teeth, and Moon’s or mulberry molars
  28. 28. Diagnosis: 1.Immunoflurorescence or dark field microscopy 2. Biopsy 3.Serology Non-treponemal antibody tests: -VDRL, RPR -For screening and treatment follow up Treponema specific antibody tests: -FTA-ABS test, TPHA -For confirmation -Usually remains positive for life Treatment: Penicillin( DOC) Ceftriaxone, Erythromycin, or Doxycycline
  29. 29. LEPROSY  Mycobacterium Leprae  Optimum temperature growth-less than body temp preference for skin, mucosa & superficial nerve  Transmission- nasal discharge  Both Humoral & cellular immune response  Clinically- Chronic granulomatous disease skin, peripheral nerve & nasal mucosa
  30. 30. • Nasopharynx to oropharynx: Granulomatous lesion, ulcers, healing with fibrosis • Larynx: -Lesion like TB & Syphilis -Supraglottic- mainly epiglottis, aryepiglottic folds -Epiglottis : hollow rod, mucosa studded with tiny nodules- laryngeal stenosis & airway obstruction Diagnosis: Punch biopsy, nasal scrapings (skin lesions & ear lobules) Treatment: Dapsone, Rifampicin &/or Clofazimine
  31. 31. PROTOZOAL INFECTION 1. Toxoplasmosis 2. Leshmaniasis
  32. 32. TOXOPLASMOSIS • Toxoplasm gondii • Zoonosis • Self limiting • Immunocompetent: asymptomatic • Immunocompromised: sore throat, malaise, fever, cervical lymphadenopathy Multiple organs involvement (lungs, liver, skin, spleen, myocardium, eyes, skeletal muscles, brain
  33. 33. • Transplacental infection: about 45 % subclinical infection- intrauterine death • Diagnosis: serological • Treatment: -usually unnecessary -combination of pyrimethamine & sulphadiazine
  34. 34. Leshmaniasis involving Lips
  35. 35. FUNGAL INFECTION 1. Candidiasis 2. Histoplasmosis 3. Cryptococcosis 4. Aspergillosis 5. Mucormycosis 6. Paracoccidomycosis 7. Blastomycosis
  36. 36. SYSTEMIC MYCOSES  Chronic fungal infections  Histoplasmosis (Histoplasma capsulatum)  Blastomycosis (Blastomyces dermatitidis)  Cryptococcosis (Cryptococcus neoformans)  Paracoccidioidomycosis(Paracoccidioides brasiliensis)  Aspergillosis (Aspergillus species)  Mucormycosis (Mucor, Rhizopus)
  37. 37. • Predisposing conditions: -Immunocompromised status eg. HIV infection • Clinical features: • Oral lesions – rare • chronic, irregular ulcer • Candidiasis rarely produces ulcers • Deep mycosis: chronic lumps & ulcers
  38. 38. • Rhinocerebral Mucormycosis: -typically commences in the nasal cavity or paranasal sinuses invade the palate (black necrotic ulceration) • Laboratory tests: Smear and histopathological examination • Treatment: Amphotericin B, Itraconazole, Ketoconazole, & Fluconazole
  39. 39. COLLAGEN-VASCULAR & GRANULOMATOUS DISORDERS 1. Sjogren’s Syndrome 2. Systemic Lupus Erythematous (SLE) 3. Scleroderma 4. Dermatomyositis-Polymyositis 5. Sarcoidosis 6. Wegner’s Granulomatosis 7. Behcet’s Syndrome 8. Reiter’s Syndrome 9. Sweet Syndrome 10. Cogan’s Syndrome 11. Amyloidosis 12. Kawasaki Disease 13. Rheumatoid Arthritis (RA) 14. Polyarteritis Nodusa (PAN) 15. Sturge- Weber Syndrome 16. Ehlers-Danlos Syndrome 17. Cowden’s Disease
  40. 40. SJOGREN’S SYNDROME • Autoimmune • Female • Primary Sjogren’s Syndrome: • Secondary Sjogren’s Syndrome: associated with RA, SLE, Scleroderma, Polymyositis, Polyarteritis Nodusa • Presents with xerostomia & parotid enlargement • Oral findings: -Due to decreased salivadysphagia, disturbances in taste & speech, burning pain of mouth & tongue, increased dental caries, increased predisposition to infection (candidiasis)
  41. 41.  Mucosal changes: dry, red & wrinkled mucosa  Fissured tongue, atrophy of tongue papillae and redness of tongue, cracked & ulcerated lips Diagnosis: -Minor salivary gland biopsy (mucosa of lower lip) -Periductal lymphocytic infiltrate -Serum: Autoantibodies (ANA, antilacrimal & antithyroid antibodies, RA factor) Treatment : -Steroid & immunossuppresive drugs -Artificial saliva -Constant dental evaluation
  42. 42. SYSTEMIC LUPUS ERYTHEMATOSUS(SLE)  Approx. one quarter of SLEoral lesions  Oral lesions: superficial ulcers with surrounding erythema  Lips & all oral mucosal surfaces  Periodontal diseases, xerostomia
  43. 43. SCLERODERMA • Deposition of collagen in the tissues or around nerves & vessels • Difficulty in opening mouth(due to fibrosis of masticatory muscles), immobility of tongue, dysphagia, xerostomia • Telangiectasia: lips, oral mucosa • Association with Sjogren’s Syndrome & CREST Syndrome(Calcinosis, Raynaud’s phenomena, Esophageal hypomotility, & Sclerodactly)
  44. 44. KAWASAKI DISEASE • Mucocutaneous lymph node syndrome • Vasculitis- medium & large arteries • Children <5 yrs of age • High grade fever • Cardiovascular complications • Oral findings: swelling of papillae on the surface of tongue(strawberry tongue), erythema of the buccal mucosa & lips Lips are cracked, cherry red, swollen & hemorrhagic
  45. 45. Laboratory tests: polymorphonuclear leukocytosis, thrombocytosis, raised ESR & CRP Diagnosis: 4 out of 6 clinical features with evidence of coronary dilatation 1.Fever persisting>5 days 2.Bilateral conjunctival congestion 3.Erythema of lips, buccal mucosa & tongue 4.Acute non-purulent cervical lymphadenopathy 5.Polymorphous exanthema 6.Erythema of palms & soles (edemadesquamation) Treatment: Aspirin, IVIg Steroid avoided- risk of worsening coronary artery dilatation
  46. 46. DERMATOMYOSITIS-POLYMYOSITIS • Immunologic disease muscle • Tongue & the upper portion of the esophagus • Clinical features: -Difficulty in phonation, chewing & deglutition -Stomatitis • Difficulty in swallowingaspiration pneumonia • Xerostomia & salivary hypofunction (2* sjogren’s syndrome)
  47. 47. WEGENER’S GRANULOMATOSIS • Rare chronic granulomatous disease • Immunological • Clinical features: necrotizing granulomatous lesions of the respiratory tract, generalized focal necrotizing vasculitis, and necrotizing glomerulitis • Oral lesions: solitary or multiple irregular ulcers, surrounded by an inflammatory zone • Tongue, palate, buccal mucosa & gingiva • Laboratory tests: HPE, c-ANCA • Treatment: Steroids, Azathioprine, & Cyclophosphamide
  48. 48. SARCOIDOSIS • Systemic granulomatous disease • Any organ • Noncaseating granuloma: -characteristic lesion • Oral manifestations: multiple, nodular, painless ulceration of the gingiva, buccal mucosa, tongue, lips, & palate • Salivary gland swelling • Diagnosis: Biopsy • Treatment: Systemic steroids
  49. 49. HEERFORDT SYNDROME  Uveoparotid Fever  Rare form of Sarcoidosis  Clinical features: B/L painless, firm, parotid swelling, ocular involvement(uveitis, conjunctivitis, keratitis), facial paralysis, low grade fever, sublingual & submandibular gland may also enlarge
  50. 50. BEHCET’S SYNDROME • Chronic, multisystemic inflammatory disorder • Triad of symptoms: Aphthous ulcers, Genital ulcers & Ocular lesions (uveitis, conjunctivits, keratitis) • Etiology – unclear • Immunogenetic basis • Clinical features - common in males • Onset -20–30 years age
  51. 51. Diagnostic criteria : 1. Recurrent oral ulcers (aphthae) 2. Recurrent genital ulcers 3. Ocular lesions (conjunctivitis, iritis with hypopyon, uveitis, retinal vasculitis, reduced visual acuity 4. Skin lesions (papules, pustules, folliculitis, erythema nodosum, ulcers, & rarely necrotic lesions) 5. Positive Pathergy test: The test is called positive, when the needle puncture causes a sterile red nodule or pustule that is greater than 2mm in diameter at 24 to 48 hours
  52. 52. • Diagnosis: • For accurate diagnosis, recurrent oral ulcers plus two of the four criteria must be present • Treatment: • Mild cases- Topical steroid • Severe cases- Systemic steroid, & other immunosuppressive drugs (Ciclosporin, Thalidomide, Colchicine, Dapsone)
  53. 53. RHEUMATOID ARTHRITIS • Progressive destruction of articular & periarticular structure eg. TMJ • TMJ pathology: clicking, locking, crepitus, tenderness in the preauricular area, pain during mandibular movement • Oral cavity involvement-not common • Association with secondary Sjogren’s Syndrome • Immunosuppressive drugsacute stomatitis, candidiasis, recurrent HSV infection
  54. 54. REITER’S SYNDROME • Triggered by infectious agent in genetically susceptible • Young male (20-30 yrs) • Characterized by conjunctivitis, asymmetric lower extremity arthritis, non-gonococcal urethritis, circinate balanitis, keratoderma blennorrhagia • Mnemonic : “can’t see, can’t pee, can’t climb a tree” • Oral lesions: papules & ulcerations on the buccal mucosa, gingiva, palate, & lips • Lesions on the tongue mimic geographical tongue • Diagnosis: HPE • Treatment: Systemic steroid, NSAID
  55. 55. SWEET SYNDROME • Acute febrile neutrophilic dermatosis • Etiology: unknown • Fever, leukocytosis, arthralgia, myalgia, & ocular involvement • Oral lesions: painful, aphthous like ulcer-lips, tongue, buccal mucosa, & palate • Skin lesions: nonpruritic, erythematous papules, & vesiculobullous lesions • Diagnosis: HPE • Treatment: Systemic Steroid/Dapsone
  56. 56. AMYLOIDOSIS  Deposition of amyloid protein (fibrillar protein) in tissues 1. Primary: Idiopathic or Multiple Myeloma 2. Secondary: Chronic or Inflammatory disease Oral manifestations: macroglossia, decreased mobility, yellow nodules on lateral surface  Deposition on salivary gland hyposalivation  Submandibular swelling & tongue enlargement respiratory obstruction  Diagnosis: HPE (congo red staining)  Treatment: Symptomatic
  57. 57. HEMATOLOGICAL DISEASES 1. Iron Deficiency Anaemia 2. Sickle Cell Anaemia 3. Langerhans Cell Histiocytosis 4. Osler-Weber-Rendu disease (HHT) 5. Plummer-Vinson Syndrome 6. Leukaemia 7. Agranulocytosis 8. Myelodysplastic Syndrome 9. Cyclic Neutropenia 10. Idiopathic Thrombocytopenic Purpura 11. Multiple Myeloma
  58. 58. IRON DEFICIENCY ANAEMIA  Oral manifestations: Atrophic glossitis, mucosal pallor, angular stomatitis, flattening of tongue papillae, geographic glossitis
  59. 59. LEUKAEMIA • Etiology- genetic & environmental factors (viruses, chemicals, radiation) • Clinical features: Leukaemia– acute & chronic, myeloid or lymphocytic • All forms - Oral manifestations • Oral lesions: -Ulcerations, spontaneous gingival hemorrhage, petechiae, ecchymosis, tooth loosening, & gingival hypertrophy • Laboratory tests: Peripheral blood smear, bone-marrow examination • Treatment: Chemotherapy, bone-marrow transplantation, supportive therapy
  60. 60. PLUMMER VINSON SYNDROME (PATTERSON-BROWN-KELLY SYNDROME) • Oral manifestations: Dysphagia, iron def. anaemia, atrophic glossitis, angular stomatitis, & koilonychia • Female, in fourth decade • Barium swallow: web in post-cricoid region • Pre-malignant Post-cricoid carcinoma • Treatment: -Esophageal dilatation (if symptoms from web) -Follow up-developing carcinoma
  61. 61. IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP) • Oral lesions may be the first manifestation of this condition • Petechiae, ecchymoses, & haematoma anywhere on the oral mucosa • Spontaneous bleeding from the gingiva • Treatment: -Systemic steroids, Splenectomy
  62. 62. GASTROINTESTINAL DISEASES 1.Inflammatory Bowel Disease (Crohn’s disease & Ulcerative colitis) 2.Gastro-esophageal Reflux 3.Peutz-Jegher’s Syndrome 4.Celiac disease 5.Chronic liver disease 6.Malabsorption Diseases
  63. 63. CROHN’S DISEASE  Diffuse nodular swelling in lips (painless), angular cheilitis, cobblestone appearance of buccal mucosa or mucosal tag, Aphthous ulcer  May precede intestinal symptoms or may be the only manifestations in some cases  Systemic steroids
  64. 64. ULCERATIVE COLITIS  Destructive oral ulceration due to immune mediated vasculitis  Polystomatitis Vegetans: microabscess on lips, palate, ventral tongue  May manifests as aphthous ulcers  Exacerbation & remission
  65. 65. GASTROESOPHAGEAL REFLUX DISEASE • Mucosal & gingival erosion caused by acid • Erosion of tooth enamel
  66. 66. ENDOCRINE DISEASES 1. Diabetes Mellitus 2. Thyroid Disorders 3. Cushing’s Disease 4. Addison’s Disease
  67. 67. DIABETES MELLITUS • Oral manifestations- variable & nonspecific • Fungal & bacterial infection • Gingivitis, periodontitis, xerostomia, glossodynia, taste change • Rx: Control of DM Antiobiotic/Antifungal • Oral hygiene
  68. 68. THYROID DISEASES • Hypothyroidism: Macroglossia • Congenital Hypothyroidism: Macroglossia, pronounced lips, & delayed tooth eruption with malocclusion • Hyperthyroidism: Facial & skin manifestations: upper eyelid retraction, exophthalmous, hyperpigmentation, & skin erythema Oral manifestations: early loss of primary teeth with subsequent rapid eruption of permanent teeth(young children) lymphoid tissue hyperplasia- tonsillar & oropharynx (Grave’s disease)
  69. 69. ADDISON’S DISEASE  Primary adrenal insufficiency  Destruction of adrenal cortex eg. autoimmune, metastasis, infection, haemorrhage  Oral manifestations: diffuse or patchy pigmentation of the skin & mucous membranes (due to increased ACTH-cross reacts with melanin receptors)  Buccal mucosa, palate, lips, & gingiva  Diagnosis: ACTH test  Treatment: Replace steroid (glucocorticoid/mineralocorticoid)
  70. 70. DERMATOLOGIC CONDITIONS 1. Lichen Planus 2. Pemphigus Vulgaris 3. Mucous Membrane Pemphigoid 4. Erythema Multiforme 5. Stevens-Jhonson Syndrome 6. Toxic Epidermal Necrolysis
  71. 71. LICHEN PLANUS • Chronic, mucocutaneous, autoimmune disorder • Precipitating factors: genetic predisposition, stress, drug, food • Oral manifestations: White papules -coalesce, forming a network of lines (Wickham’s striae) • Buccal mucosa, gingiva, & tongue, lips & palate
  72. 72.  Skin lesions: Pruritic papules-flexor surface of extremities  Malignant transformation  Diagnosis: -Clinically -Histopathological examination  Treatment: -No treatment- asymptomatic lesions -Topical steroids & Systemic steroids
  73. 73. PEMPHIGUS VULGARIS • Autoimmune disease • Antibodies against desmoglein3 (antigen) • Disassociation of the epithelium at suprabasal layer with acantholysis • Bullous lesionsrupturespainful bleeding ulcers • Oral, ocular mucosa, & skin • Palate, gingiva, tongue • Diagnosis: -Nikolsky’s sign:(+) new lesions develops after pressure applied to asymptomatic oral mucosa -HPE -Direct immunofluorescence
  74. 74.  Treatment: Systemic steroids & immunosuppressive agents (eg. mycophenolate mofetil) Paraneoplastic Pemphigus:  Occurs in association with underlying neoplasms eg. Lymphoproliferative disease or thymoma  Often partial response to systemic steroids
  75. 75. ERYTHEMA MULTIFORME • Skin and mucous membranes • Immunologically mediated • Triggered by: infective agents (eg. HSV), drugs (sulphonamides, barbiturates), food additives or chemical, immunization ( BCG,HBV) • Oral lesions: begins as erythematous areablisterrupturesirregular painful ulcers • Lips, buccal mucosa, tongue, soft palate, & floor of mouth • Skin manifestations: erythematous, flat, round macules, papules, or plaques, usually in a symmetrical pattern- target or iris like lesions • HPE & Immunostaining • Treatment: supportive, systemic steroids
  76. 76. NUTRITIONAL DEFICIENCY • Vitamins & trace elements 1. Inadequate intake 2. Impaired digestion & absorption 3. Increased losses
  77. 77.  Vitamin A deficiency: -Dyskeratotic changes of the skin & mucous membranes -Angular cheilitis -Defects in the dentin & enamel of developing teeth  Vitamin B2 (Riboflavin) deficiency: -Angular cheilitis -Burning pain in the lips, mouth, & tongue  Vitamin B3 (Niacin) deficiency (Pellagra): -Dermatitis, dementia,& diarrhoea -Oral manifestations: glossitis (red, swollen) & stomatitis, burning tongue
  78. 78. • Vitamin B6 deficiency: -Peripheral neuropathy -Oral lesions-similar to pellagra (i.e. glossitis & stomatitis) • Vitamin C deficiency (Scurvy): -Cofactor for collagen synthesis -Weakened vessels are responsible for petechiae, ecchymoses, delayed wound healing • Deficiency of Vitamin B12 & Folic acid: -Megaloblastic anemia -Oral findings: angular cheilitis, recurrent aphthous ulcers, & glossitis
  79. 79. • Vitamin D deficiency & Calcium deficiency: -Calcium metabolism -Mandibular osteopenia/osteoporosis, enamel hypoplasia • Vitamin k deficiency: -Haemorrhagic diathesis -Oral haemorrhagic bullae • Zinc deficiency: -Taste changes -Acrodermatitis Enteropathica: angular cheilitis, ulcers, glossitis, crusting, scaling of the lips as well as ulcers, erosions & fissures
  80. 80. ORAL LESIONS ASSOCIATED WITH HIV • Early recognition, diagnosis, & treatment of HIV associated oral lesions - reduce morbidity • Oral lesions- -Early diagnostic indicator of HIV infection -Stage of HIV infection -Predictor of the progression of HIV disease
  81. 81. ORAL LESIONS ASSOCIATED WITH HIV • Fungal Infection: Bacterial Infection: -Candidiasis -Linear Gingival Erythema -Histoplasmosis -Necrotizing Ulcerative Periodontitis -Cryptococcosis -Mycobacterium Avium Complex • Viral Infection: Neoplastic: -Herpes simplex -Kaposi’s Sarcoma -Herpes zoster -Non-Hodgkin’s Lymphoma -HPV Infection Others: -CMV Infection -Recurrent Aphthous Ulcers -Hairy Leukoplakia -Salivary Gland Disease
  82. 82. HUMAN PAPILLOMA VIRUS INFECTION • Oral warts (papillomas), skin warts, & genital warts – HPV(types 7,13,& 32) Clinical Features: • Arises from Stratified squamous epithellium, painless, exophytic, numerous finger like projections- cauliflower like appearance • Tongue, gingiva, & palate • Biopsy- Histologic diagnosis • Treatment: -Surgical removal -Laser (CO2 laser)
  83. 83. HAIRY LEUKOPLAKIA  Epstein Barr virus  Common, characteristic lesion-HIV infection  White, asymptomatic, raised, corrugated, unremovable patch on lateral marigns of tongue  The surface is irregular and may have prominent folds or projections, sometimes markedly resembling hairs  Lateral margins may spread to dorsum of tongue  Diagnosis: Biopsy  Treatment: -Usually asymptomatic-Rx not required -Antiviral(Aciclovir/valaciclovir)
  84. 84. KAPOSI’S SARCOMA  Most common malignancy in HIV (+Ve)  Human Herpes Virus-8(KSHV)  Derived from capillary endothelial cells  Occur intraorally, either alone or in a/w skin & disseminated lesions (lymph nodes, salivary gland)  Intraorally- hard palate, buccal mucosa, & gingiva -bluish, purple or red patches or papulesnodular, ulcerate & bleed  Diagnosis: Biopsy  Treatment: -Low dose radiation & chemotherapy (eg.Vinblastine) -Surgical excision (eg.CO2 laser) -Immunotherapy (Interferon)
  85. 85. NON-HODGKIN’S LYMPHOMA • Etiology: Unknown, genetic & environmental factors (viruses, radiation) • Clinical features: • Both sexes - any age • Lymph nodes involved • Oral lesions - part of a disseminated disease, or the only sign • Oral Lymphoma: diffuse, painless swelling, which may or may not be ulcerated -soft palate, the posterior part of the tongue, the gingiva, & the tonsillar area • HPE & Immunohistochemical examn • Treatment: Radiotherapy & chemotherapy
  86. 86. • Junction between skin & mucosa • Pink/brown in colour • Vermilion border • Fordyce’s granules • Pits • No swellings or indurations NORMAL LIP
  87. 87. What you need to DO: • History: o Time first noticed o Any changes in size, consistency, colour,… o Any associated symptoms o Any discharge • Examination o Determine whether it is diffuse or localized o Determine it’s consistency o Determine it’s colour • Further investigations 1- SWELLINGS
  88. 88. What you need to KNOW • Differential diagnoses … • More you know a longer list of differential diagnosis and better diagnosis 1- SWELLINGS
  89. 89. INTRODUCTION • What is Cleft Lip and Palate? • Congenital abnormal space or gap in the upper lip, alveolus and palate
  90. 90. INCIDENCE • More common in south far Asians: • 1 in 500 • Less frequent in Africans: • 1 in 2000 • Prevalence in Europeans and Americans: • 1 in 750 • *Prevalence in Pakistan: • 1 in 523 *Elahi MM, Jackson IT, Elahi O, Khan AH, Mubarak F, Tariq GB, Mitra A. Epidemiology of cleft lip and cleft palate in Pakistan. Otolaryngol Clin North Am. 2007 Feb; 40(1):27-60
  91. 91. INCIDENCE • Boys are more affected than girls by 3:2 • Cleft Lip and Palate occur twice as often in boys as in girls • Isolated Clefts of Palate are more often in girls • 75% of Clefts are Unilateral, rest are Bilateral • Left side is more involved than right side
  92. 92. CLASSIFICATION • We classify as the follows: • its combined (cl+cp) or isolated cleft(cl or cp)? • is it unilateral or bilateral? • is it complete (if it cross the nasal philtrum) or incomplete ( if it doesn’t cross the nasal philtrum.
  93. 93. PRENATAL DIAGNOSIS • Cleft lip can be easily diagnosed by performing ultrasonography in the second trimester • Diagnosing a cleft palate with ultrasonography is very difficult • Three-dimensional imaging has been introduced to prenatal ultrasonography diagnostics of cleft anomalies
  94. 94. DIAGNOSIS • Advantages of Prenatal Diagnosis: 1. Time for parental education 2. Time for parental psychological preparation 3. Opportunity to investigate other associated anomalies 4. Gives parents the choice of continuing the pregnancy 5. Opportunity for fetal surgery
  95. 95. ETIOLOGY • “Actually no one knows exactly what causes clefts” • Multiple factors may be involved, like: • Genetics (inherited characteristic) from one or both parents . • Environmental factors • Drugs: corticosteroids (anti-inflammatory), phenytoin (anticonvulsant), retinoid. • Infections: like rubella during pregnancy. • Alcohol consumption, smoking, hypoxia during pregnancy, some of dietary and vitamins deficiencies (like folic acid and vitamin A deficiency) • Maternal Age
  96. 96. PROBLEMS ASSOCIATED WITH CLEFT LIP AND PALATE • Feeding • Dental problems • Nasal Deformity and Esthetic Problems • Ear Problems • Speech Difficulties • Associated Anomalies
  97. 97. FEEDING DIFFICULTIES • Cleft lip= makes it more difficult for an infant to suck on a nipple • Cleft Palate= may cause formula or breast milk to be accidently taken up into the nasal cavity • Inability to create negative pressure inside oral cavity • Frequent regurgitations • Upper respiratory tract infections
  98. 98. NASAL DEFORMITY AND ESTHETIC PROBLEMS • Facial Disfigurements • Poor nasal shape • Scar marks of surgeries • Poor lip function during speech • Poor dental alignment and smile
  99. 99. MANAGEMENT OF CLEFT LIP AND PALATE
  100. 100. SCHEDULE OF TREATMENT Birth:  Initial Assessment  Pre-surgical assessment 3 Month:  Primary Lip repair 9-18 month:  Palate Repair 2 Year:  Speech assessment 3-5 Year:  Lip Revision Surgery 8-9 Year:  Initial interventional Orthodontics  Preparation for alveolar bone grafting 10 Year:  Alveolar Bone Grafts 12-14 Year:  Definite Orthodontics 16 Year:  Nasal Revision Surgery 17-20 Year:  Orthognathic Surgery
  101. 101. MULTIDISCIPLINARY CLEFT LIP AND PALATE TEAM • Genetic Scientist • Pediatrician • Pedodontist • Orthodontist • Oral and Maxillofacial Surgeon • Prosthodontist • ENT Surgeon • Plastic Surgeon • Psychiatrist • Speech Therapist • Social Worker
  102. 102. FEEDING • Cleft lip= makes it more difficult for an infant to suck on a nipple • use special nipples to allow the baby to latch properly (either pump or use formula) • Cleft Palate= may cause formula or breast milk to be accidentally taken up into the nasal cavity • don’t feed baby without palatal obturator (prosthetic palate) • feed in an upright position to keep milk from coming out of the nose
  103. 103. Mead Johnson/Enfamil Cleft Feeder Special Needs Feeder / Haberman Feeder Pigeon Feeder Dr. Brown’s Natural Flow to relieve gas
  104. 104. • Latham Appliance
  105. 105. RULE OF TEN  Primary repair- repaired at approximately 10 weeks • The surgeon usually uses the “Rule of Ten” • The child weighs 10 pounds • The child has a hemoglobin of at least 10 grams • The child has a white count of no higher than 10,000 • The child is at least 10 weeks of age
  106. 106. SURGICAL TECHNIQUES • Cleft Lip Repair • unilateral • rotation-advancement flap developed by Millard • complications • dehiscence • infection • excess tension
  107. 107. CLEFT PALATE REPAIR FURLOW PALATOPLASTY • Lengthens the soft palate • Reconstructs the muscle sling. • Also commonly used to correct velopharyngeal insufficiency in patients with submucous cleft palate • Speech outcomes are improved compared with other palatoplasty techniques.
  108. 108. Angioedema (allergic / non-allergic) DIFFUSE LIP SWELLING
  109. 109. Oedema caused by infection / trauma DIFFUSE LIP SWELLING
  110. 110. DIFFUSE LIP SWELLING • Healthy young girl • Swelling notices 6 years ago, increasing gradually • Previous treatment with steroid inj. unsuccessful
  111. 111. DIFFUSE LIP SWELLING • Orofacial granulomatosis • Oral Crohn’s disease • Monosymptomatic Melkerson-Rosenthal syndrome
  112. 112. Haemangioma Vs Haematoma LIP SWELLING
  113. 113. Adenoma LOCALIZED LIP SWELLINGS
  114. 114. Mucocele LOCALIZED LIP SWELLINGS
  115. 115. Keratoacanthoma LOCALIZED LIP SWELLINGS
  116. 116. WHITE LESIONS OF THE LIP Actinic Cheilitis High risk High risk
  117. 117. Exfoliative chelitis WHITE LESIONS OF THE LIP • Excessive production of keratin • More common in females • Associated with stress & anxiety • Some improve by antidepressant/tranquilizers • Spontaneous remission
  118. 118. Allergic chelitis Perioral dermatitis LESIONS OF THE LIP
  119. 119. Causes: • Allergic reaction to topical ointments/creams or lipstick • Tooth paste • Food • Medication Management: • Detailed history to identify allergen confirmed by patch testing eliminate • Topical steroid (short course) ALLERGIC CHEILITIS
  120. 120. • Is a clinical entity with many etiological factors • Most common in females • Could be allergic / idiopathic • Some cases respond to long term tetracycline others to topical steroid (1% hydrocortisone) *DO NOT USE MORE POTENT STEROID ON FACE PERIORAL DERMATITIS
  121. 121. • Mainly children are affected • Might not be aware of the habit • Heals by stopping the licking Management: • Appliance can be used to interfere with tongue LESIONS OF THE LIP LICK ECZEMA
  122. 122. • Less common than angular cheilitis • Common in OFG and Down’s patients • Usually persist due to secondary infection (s.aurius or candida) • Management: o Remove pathogen by topical antibacterial / antifungal o Steroid ointment • Usually it recure LESIONS OF THE LIP LIP FISSURES
  123. 123. Cheilocandidosis LESIONS OF THE LIP Causes: 1.Candidal infection affecting unstable epithelium (Solar irritation) in healthy individual 1.Associated with IO candida Treatment: Early treatment by antifungal might lead to resolution
  124. 124. Angular chelitis Inflammation of the corners of the mouth LESIONS OF THE LIP ANGLES
  125. 125. • History: o Generalized ill health o Xerogenic medication o Antibiotics / steroid therapy o Ill fitting denture / night wearing • Examination o Signs of anemia o Salivary gland swelling (xerostomia / diabetes) o Intraoral candidosis o Oral dryness o Signs of OFG o Lymphadinopathy o Ill fitting denture / reduced vertical dimension HOW TO DETERMINE CAUSING FACTOR?
  126. 126. • Special investigations o Swab & smear o Blood test (CBC, B12, ferritin, folate) o Blood glucose • when blood testing should by performed? o If suspecting an underlying systemic factor o If local therapeutic measures fail HOW TO DETERMINE CAUSING FACTOR?
  127. 127. 1.Eliminate predisposing factor 2.Correct deficiencies 3.Antifungal / anti bacterial MANAGEMENT OF ANGULAR CHELITIS
  128. 128. TONGUE LESIONS
  129. 129. • Only will consider lesions specific to the tongue NOT ones which are presentation of systemic conditions • Mobile organ • Specialized epithelial lining • Rich in sensory nerve endings THE TONGUE
  130. 130. DEVELOPMENTAL ABNORMALITIES OF THE TONGUE Ankyloglossia – Tongue tie
  131. 131. Fissured tongue (scrotal tongue) LESIONS OF THE TONGUE
  132. 132. GLOSSITIS • Glossitis is inflammation of the tongue. It causes the tongue to swell and change color. Finger-like projections on the surface of the tongue (papillae) may be lost, causing the tongue to appear smooth.
  133. 133. CAUSES • Bacterial or viral infections (including oral herpes simplex). • Poor hydration and low saliva in the mouth may allow bacteria to grow more readily. • Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma • Tongue piercing. Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament. • Exposure to irritants such as tobacco, alcohol, hot foods, or spices. • Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors). • Administration of ganglion blockers (e.g. Tubocurarine, Mecamylamine). • Disorders such as iron deficiency anemia, pernicious anemia and other B- vitamin deficiencies, oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris,syphilis, and others. • Occasionally, glossitis can be inherited. • Albuterol (bronchodilator medicine)
  134. 134. SYMPTOMS • Tongue swelling. • Smooth appearance to the tongue due to pernicious anemia (vitamin B12 deficiency). • Tongue color changes (usually dark "beefy" red). • Sore and tender tongue. • Difficulty with chewing, swallowing, or speaking.
  135. 135. TREATMENT • Treatment usually does not require hospitalization unless tongue swelling is severe. Good oral hygiene is necessary, including thorough tooth brushing at least twice a day, and flossing at least daily. • Corticosteroids such as prednisone may be given to reduce the inflammation of glossitis. • For mild cases, topical applications (such as a prednisone mouth rinse that is not swallowed) may be recommended to avoid the side effects of swallowed or injected corticosteroids. • Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of glossitis is an infection. • Anemia and nutritional deficiencies (such as deficiencies in niacin, riboflavin, iron, or vitamin E) must be treated, often by dietary changes or other supplements. • Avoid irritants (such as hot or spicy foods, alcohol, and tobacco) to minimize the discomfort.
  136. 136. LEUKOPLAKIA • Leukoplakia are patches on the tongue, in the mouth, or on the inside of the cheek that occur in response to long-term irritation. Leukoplakia patches may also develop on the outer female genitals.
  137. 137. CAUSES • Irritation in the mouth may be caused by: • Rough teeth • Rough places on dentures, fillings, and crowns • Smoking or other tobacco use (smoker's keratosis), especially pipes • Holding chewing tobacco or snuff in your mouth for a long period of time. • HPV, Candida albicans and possibly alcohol SYMPTOMS • Usually white or gray • Sometimes red (called erythroplakia, a condition that can lead to cancer) • Thick and slightly raised with a hard surface that can't be easily scraped off
  138. 138. TREATMENT • Treat dental causes such as rough teeth, irregular denture surface, or fillings as soon as possible. • Stop smoking or using other tobacco products. • Do not drink alcohol.
  139. 139. CARCINOMA ORAL TONGUE • Involving 2/3rd of tongue • Age of 50-70 years. • SITE • Middle of the lateral border or ventral aspect • CAUSE • Pre-existing leukoplakia • Longstanding dental ulcer or syphilitic glossitis
  140. 140. CLINICAL PRESENTATION • An exophytic lesion like a papilloma • Non healing ulcer with rolled edges, greyish white shaggy base and induration • SYMPTOMATOLOGY • Early lesion are painless and asymptomatic for a longer time • Pain at the site of ulcer • Pain in ipsilateral ear due to common nerve supply of tongue(lingual nerve) and ear (auriculo temporal) from the mandibular division of trigeminal nerve. • Lump in mouth. • Enlarge lymph node mass in the neck • Dysphagia, difficulty to protrude the tongue, slurred speech and bleeding from the mouth are late features
  141. 141. TREATMENT • Aim of treatment is to treat primary tumour in the tongue, control neck disease(nodal metastasis) and preserve function of the tongue.
  142. 142. HYPOGLOSSIA • It is a short, incompletely developed tongue. • CAUSES - malformation, other deformities, such as Hypodactylia, Peromelia, micrognathia. • SYMPTOMS – underdeveloped tongue, feeding problems, breathing problems, speech problems, swallowing problems, missing teeth, tooth enemel defects. • TREATMENT – speech therapy , orthodontic treatment
  143. 143. FISSURED TONGUE • Also known as "scrotal tongue," "lingua plicata," "Plicated tongue” "furrowed tongue. • Is a benign condition characterized by deep grooves (fissures) in the dorsum of the tongue. The condition is painless and individuals experience no physical discomfort. • Fissured tongue is seen in Melkersson- Rosenthal syndrome, in most patients with Down syndrome, in association with geographic tongue, and in healthy, normal individuals.
  144. 144. GLOSSODYNIA • Glossodynia refers to a painful or burning feeling of the tongue. • CAUSES • Long-term irritations in the mouth • Nerve damage from tooth extractions • Trauma (injury) • Dry mouth (xerostomia) • Vitamin or mineral deficiencies (such as vitamin B, iron or zinc) • Allergies • Changes in hormones or the immune system • Tobacco use • Psychological conditions such as anxiety or depression • Infections of the mouth, caused by bacteria or fungus (thrush) • Anemia
  145. 145. TREATMENT Treatment depends upon the cause. Treatments may include: 1. Removal of irritants (rough edges on fillings, crowns or dentures) 2. Construction of a soft plastic tray to correct or cover irregular areas of the teeth 3. Pain relievers applied to the area 4. Microsurgery to repair the lingual nerve, if nerve damage is a cause 5. Low doses of benzodiazepine, antidepressant or anticonvulsant drugs 6. Changes in current medicines, which may be causing the pain 7. Supplements or diet changes for nutritional deficiencies 8. Antifungal medicines
  146. 146. MACROGLOSSIA • Macroglossia is the medical term for unusual enlargement (hypertrophy) of the tongue. Severe enlargement of the tongue can cause cosmetic and functional difficulties including in speaking, eating, swallowing and sleeping.
  147. 147. • CAUSE • Amyloid Disorders • Amyloidosis is an accumulation of insoluble proteins in tissues that impedes normal function • Hypothyroid Macroglossia • Macroglossia is also a clinical feature in Hypothyroid disorders which include • Overgrowth Disorders • Acromegaly • Chromosomal disorders • Downs Syndrome
  148. 148. TONGUE- TIE (ANKYLOGLOSSIA) • Ankyloglossia, commonly known as tongue tie, is a congenital oral anomaly which may decrease mobility of the tongue tip and is caused by an unusually short, thick lingual frenulum. • there may be a V shaped notch at the tip.
  149. 149. • CAUSE • congenital oral anomaly • SYMPTOMS/EFFECT • can affect feeding, • speech, and • oral hygiene • as well as have mechanical/social effects. • TREATMENT • Physician education • Parental education and reassurance • Monitor for appropriate weight gain if exclusively breastfeeding • Complete fusion requires surgery
  150. 150. HYPERKERATOSIS OF THE TONGUE • Hyperkeratosis is a thickening of the outer layer of the skin. This outer layer contains a tough, protective protein called keratin
  151. 151. • CAUSE • Chronic (long-lasting) inflammation • Infection (HPV) • Radiation • Irritating chemicals • SYMPTOMS • Painless • TREATMENT • The treatment of hyperkeratosis depends on the type and possible cause. • corticosteroid ointment or cream • cryosurgery to remove a single actinic keratosis. Multiple keratoses can be treated with skin peels, laser therapy or dermabrasion.
  152. 152. FIBROMA OF TONGUE • Fibromas are over growths of soft tissue. They appear as raised, relatively small areas. • SITE- the lips, inside the cheeks and on the tongue. • Fibromas are usually pink. They also can be whitish or light-colored. If injured, fibromas may be reddish or bluish
  153. 153. • CAUSE • A habit of biting these areas • Tooth grinding (bruxism) • Rubbing from poorly fitting dentures or sharp areas on a tooth • SYMPTOMS • They are usually no symptoms. Fibromas may get bigger over time • TREATMENT • Surgery
  154. 154. TONGUE WARTS (PAPILLOMA) • A Squamous cell papilloma is a generally benign papilloma that arises from the stratified squamous epithelium of the skin, lip, oral cavity, tongue, pharynx, larynx, esophagus, cervi x, vagina or anal canal.
  155. 155. • CAUSE • Squamous cell papillomas are a result of infection with human papillomavirus (HPV) • SYMPTOMS • Oral papillomas are usually painless, and not treated unless they interfere with eating or are causing pain. They do not generally mutate to cancerous growths, nor do they normally grow or spread. Oral papillomas are most usually a result of the infection with types HPV-6 and HPV-11 • TREATMENT • cryotherapy, • application of a topical salicylic acid compound, • surgical excision and • laser ablation
  156. 156. RANULA • A ranula is a type of mucocele found on the floor of the mouth. • Ranulas present as a swelling of connective tissue consisting of collected mucin from a ruptured salivary gland duct. • A large mucocele in the floor of the oral cavity. It usually results from obstruction of the ducts of the sublingual salivary glands. Less often, it results from obstruction of the ducts of the submandibular salivary glands.
  157. 157. • CAUSE • local trauma. • SYMPTOMS • Asymptomatic • can fluctuate rapidly in size, shrinking and swelling • interfere with swallowing • swelling is not fixed and is non-painful unless it becomes secondarily infected. • TREATMENT • excision of both the gland and lesion • Marsupialization in which the cyst is opened to create a pocket. The pocket will lie flat and be unable to fill with fluid again. However, sometimes the opening of the pocket heals over, allowing the cyst to develop again. In this case, the growth must be removed along with the attached blocked gland to prevent reformation of the ranula.
  158. 158. LINGUAL THYROID • In the first trimester of embryonic development, the thyroid gland originates in the back of the tongue and migrates to the front of the neck. If it fails to migrate properly, it can remain high in the neck or even in back of the tongue. In rare instances, the thyroid gland can also migrate too far into the mediastinum; it is then called a substernal thyroid. • When migration fails and the gland remains in the base of the tongue, it is called lingual thyroid or ectopic lingual thyroid
  159. 159. PATHOLOGY • A lingual thyroid results from failure of the normal caudal migration of the thyroid from foramen caecum down to its normal location anterior to the larynx and upper trachea. Thyroid tissue may be found anywhere along the course of the thyroglossal duct, however complete arrest with thyroid tissue located at the base of tongue is most common, and represents 90% of all cases of ectopic thyroid 1-2. Microscopic deposits of thyroid tissue along its route of descent have been identified in up to 10% of the population, representing small amounts of tissue being 'left behind' during normal development 2. • The thyroid tissue is normal histologically and functionally. • Carcinoma of a lingual thyroid has been reported but is very rare, presumably no higher than normal thyroid.
  160. 160. • CAUSE • SYMPTOMS • interfere with swallowing and breathing • INVESTIGATION • MRI • Ultrasound • absent thyroid tissue in the normal location thyroid tissue both at the tongue base and elsewhere in the neck • CT • hyperdense soft tissue mass due to accumulation of iodine within the gland. • TREATMENT • surgical excision
  161. 161. • Differential diagnosis • The differential of a posterior midline mass includes 3: • lingual tonsil • thyroglossal duct cyst • malignancy • haemangioma • dermoid
  162. 162. PRE-MALIGNANT LESIONS • Leukoplakia - chronic, white, verrucous plaque with histologic atypia • Severity linked to the duration and quantity of tobacco and alcohol use • Occur anywhere in the oral cavity • Lip, tongue, or floor of the mouth lesions are prone for progression to SCC • Erythroplakia - non-inflammatory erythematous plaque • Analagous to intra-oral erythroplasia of Queyrat or SCC in situ • Biopsies - severe dysplasia and areas of frank invasion
  163. 163. LEUKOPLAKIA
  164. 164. ERYTHROPLAKIA
  165. 165. PRE-MALIGNANT LESIONS… • Submucous fibrosis • generalized white discoloration of oral mucosa with progressive fibrosis, painful mucosal atrophy and restrictive fibrotic bands • individuals who chew betel quid, a concoction of tobacco, lime, areca nut and betel leaves • Ultimately leads to trismus, dysphagia and severe xerostomia • 5 - 10 % progress to SCC
  166. 166. CANCEROUS LESION OF LIPS& ORAL CAVITY • Lips –SCC, Melanoma, BCC(rare) • Oral cavity: -- scc: 9/10 incidence --verrucous ca: <5% low grade, slow growing rarely metastasizes with tendency to invade deep tissue.
  167. 167. CANCEROUS LESION OF LIPS& ORAL CAVITY • Minor salivary gland tumor: -in the glands lining the oral cavity -adenoidcystic ca, mucoepidermoid ca, adenocarcinoma. -Sarcoma
  168. 168. INCIDENCE • Globally >300,000 people diagnosed/year • Eighth most common malignancy • India –upto 40% of all malignancies • M>F • Raising trend • 6-7th decade • Most of the people are dying because of ignorance
  169. 169. INCIDENCE • Demographic and clinical profile of oral squamous cell carcinoma patients: a retrospective study ( Shenoi R, Sharma BK, et.al, Indian J Cancer. 2012 Jan;49(1):21-6: Most common site: mandibular alveolus Major cause: tobacco chewing Majority of patients presented in stage III Majority presented within 6 months of onset
  170. 170. RISK FACTORS  Tobacco: About 90% of people with oral cavity and oropharyngeal cancer use tobacco  Alcohol: Drinking alcohol strongly increases a smoker's risk of developing oral cavity and oropharyngeal cancer.  Ultraviolet light: More than 30% of patients with cancers of the lip have outdoor occupations associated with prolonged exposure to sunlight.  Irritation: Long-term irritation to the lining of the mouth caused by poorly fitting dentures
  171. 171. RISK FACTORS CONT… • Poor nutrition: A diet low in fruits and vegetables is associated with an increased risk • Mouthwash: Some studies have suggested that mouthwash with a high alcohol content • Human papillomavirus (HPV) infection: • Immune system suppression: • Age: The likelihood of developing oral and oropharyngeal cancer increases with age, especially after age 35. • Gender: Oral and oropharyngeal cancer is twice as common in men as in women
  172. 172. HOW TOBACCO AFFECTS • Tobacco smoke contains >4000 chemicals, at least 60 shown to be carcinogens. • Smoke less tobacco: main form: chewing, snuff at least 28 carcinogens found in smokeless form
  173. 173. Habit • None • Betel nut Chewing • Smoking only • Betel chewing + Tobacco chewing • Betel chewing + Smoking • Betel+Tobacco+smoking • 1% • 4% • 3-6% • 8-15% • 4-25% • 20% RELATIVE RISK FACTORS FOR ORAL CANCERS Relative Risk %
  174. 174. HOW ALCOHOL AFFECTS • Chronic alcohol exposure results in increased cancer incidence in animal model. • Acetaldehyde , reactive oxygen species- main mutagen • Acetaldehyde: directly binds to DNA, alters methyl transfer leading to hypomethylation leading to alerted gene products • Alcohol promotes cytochrome P450- which increases activation of procarcinogens( tobacco, alcohol). • Alcohol can act as solvent facilitating entry of carcinogens into cells
  175. 175. ROLE OF HPV IN ORAL SCC • Role of human papilloma virus in the oral carcinogenesis: an Indian perspective (Chocolatewala NM, et.al. J Cancer R Ther. 2009 Apr-Jun;5(2):7-17). • Association strongest for Oropharynx, specially cancer of tonsils followed by base of tongue. • High risk HPV-16 predominate type. • Commonly affects younger age groups , male, non smokers. • Better outcomes, more responsive to RT, higher survival rate.
  176. 176. MOLECULAR BIOLOGY • Cytogenetic : chromosomes 3,5,8,11,17,18. • Tumor suppressor genes inactivation: p16,p21,p53,RB gene. • Proto-oncogene activation: cyclinD1/PRADD1. • Growth factors /receptors overexpression: EGF,EGF-R,TGF-ɑ,HER- 2/neu,FGF,FGF-R,PDGF).
  177. 177. MOLECULAR BIOLOGY • RAS family oncogene. • Telomeres, telomerase, cell senescence • Tumor immunology(role of TIL, CTL, IL-2/4/6) • Tumor invasion and metastasis:(endothelial proliferation:PGE2,TGFβ,FGF,VEGF),MMP
  178. 178. CARCINOGENESIS Normal squamous mucosa EGF, EGFR Overexpression Squamous hyperplasia Telomerase activation p16 inactivation Dysplasia PRAD-1 amplification 3p deletion p53 inactivation Carcinoma in-situ 4q, 5q, 8p, 13q deletion Invasive carcinoma Matrix metalloproteinase Over-expression Metastasis
  179. 179. SITE OF ORAL CAVITY  Tongue : 35%  Floor of mouth: 30%  Lower alveolus: 15%  Buccal mucosa: 10%  Upper alveolus/hard palate: 8%  RMT: 2%  Lips: lower-93%, upper-5%, commissure- 2%
  180. 180. SYMPTOMS  a sore in the mouth that does not heal (most common symptom)  pain in the mouth that doesn't go away (also very common)  a persistent lump or thickening in the cheek  a persistent white or red patch on the gums, tongue, tonsil, or lining of the mouth  a sore throat or a feeling that something is caught in the throat that doesn't go away  Increased salivation
  181. 181. MORE SYMPTOMS  difficulty chewing or swallowing  difficulty moving the jaw or tongue  swelling of the jaw that causes dentures to fit poorly or become uncomfortable  loosening of the teeth or pain around the teeth or jaw  voice changes  a lump or mass in the neck  weight loss  persistent bad breath
  182. 182. PATIENT WORKUP  History  Clinical examination  Investigations
  183. 183. PATIENT WORKUP • Investigations : Primary: photographs incisional biopsy FNAC Orthopantogram CXR ECG Routin blood investigations
  184. 184. PATIENT WORKUP Investigations: for staging - CT face + neck ± CT chest - MRI - USG of neck or primary ± USG guided FNAC of suspicious lymphadenopathy - PET
  185. 185. STAGING OF THE DISEASE American joint committee on cancer: T , N , M Tx- primary tumour cannot be assessed T0- No evidence of primary tumour T1- ≤ 2cm in greatest dimension T2- 4cm < 2cm> in greatest dimension T3- > 4cm in greatest dimension
  186. 186. STAGING OF THE DISEASE T4a- Oral cavity: tumour invades through cortical bone, into deep(extrinsic) muscle of tongue, maxillary sinus or skin. Lips: cortical bone, inferior alveolar nerve, floor of mouth, skin i.e. chin or nose. T4b- involves masticator space, pterygoid plates, skull base and/or encases internal carotid artery
  187. 187. STAGING OF THE DISEASE N stage: Nx- regional lymph nodes can not be assessed. N0- no regional lymph node metastasis. N1- metastasis in a single ipsilateral lymph node ≤ 3cm in greatest dimension. N2a- metastasis in a single ipsilateral LN > 3cm but < 6cm in greatest dimension.
  188. 188. STAGING OF THE DISEASE N2b- metastasis in multiple ipsilateral LNs, none > 6cm in greatest dimension. N2c- metastasis in B/L or C/L LNs, none > 6 cm. N3- metastasis in a LN > 6 cm in greatest dimension M stage: Mx- cannot be assessed, M0- no distant metastasis, M1- distant metastasisi.
  189. 189. Stage Grouping Stage 0 Tis N0 M0 Stage I T1 N0 M0 Stage II T2 N0 M0 Stage III T1, T2 N1 M0 T3 N0, N1 M0 Stage IV A T1, T2, T3 N2 M0 T4a N0, N1, N2 M0 Stage IV B Any T N3 M0 T4b Any N M0 Stage IV C Any T Any N M1
  190. 190. TREATMENT • Treatment goals: to eradicate primary tumor and LN metastasis, to maintain function, cosmetic reconstruction • Factors affecting choice of treatment: tumor factor patient factor resource factor
  191. 191. TREATMENT GOALS FOR CANCER OF THE ORAL CAVITY • • Cure of cancer • • Preservation or restoration of form and function • • Avoid or minimize sequelae of treatment • • Prevent second primary cancers
  192. 192. TUMOR FACTORS AFFECTING TREATMENT • • Site • • Size (T stage) • • Location • • Multiplicity • • Proximity to bone • • Pathological features • • Histology, grade, depth of invasion, tumor • type • • Status of cervical lymph nodes • • Previous treatment
  193. 193. TREATMENT • Patient factors: age, general medical condition, performance status, occupation, lifestyle(smoking/drinking) socioeconomic considerations previous treatment
  194. 194. TREATMENT • Physician factors: surgery, radiotherapy, chemotherapy nursing & rehabilitation services, dental, prosthetics, support services
  195. 195. TREATMENT • Surgery • Radiotherapy • Chemotherapy • Immunotherapy • Targeted therapy • Gene therapy
  196. 196. TREATMENT OF CHOICE  Stage I , II: single modality treatment is effective and preferable.  Stage III , IV: multimodal therapy is essential
  197. 197. TREATMENT • SURGERY: Early stage T1/2No tumor: Wide excision +/ - ND High risk of locoregional recurrent (40%) • Management of No Neck: High incidence of occult metastasis in the clinically No Neck (15-43%) Controversy : Observation or Surgery/Radiation Depend on primary site. Should be have minimal morbidity ELND if risk of occult meta >20%. (SND/SOHND). • Locally advanced tumor: Combined modality treatment
  198. 198. CLASSIFICATION OF ND 1991 Classification: • RND • Modified RND • Selective ND: Supraomohyoid Lateral Posterolateral Anterior • Extended ND 2001 Classification: • RND • Modified RND • Selective ND (SND): SND (L.I-III/IV) SND (L.II-IV) SND (L.II-V) SND (L.VI) • Extended ND Proposed by American HN Society and AAOHNS
  199. 199. Selective neck dissection Modified RND type 1,2,3.
  200. 200. Standard treatment options for management of lymph node: Radiation therapy alone or neck dissection: N1 (0–2 cm). N2b or N3; all nodes smaller than 2 cm. (A combined surgical and radiation therapy approach should also be considered.) Radiation therapy and neck dissection: N1 (2–3 cm), N2a, N3. Surgery followed by radiation therapy, indications for which are as follows: Multiple positive nodes. Contralateral subclinical metastases. Invasion of tumor through the capsule of the lymph node. N2b or N3 (one or more nodes in each side of the neck, as appropriate, >2 cm). Radiation therapy prior to surgery: Large fixed nodes.
  201. 201. SURGICAL APPROACHES  Trans-oral approach  Lower cheek approach  Upper cheek approach  mandibulotomy  Visor flap
  202. 202. SURGICAL APPROACH DEPENDS ON • • Tumor size • • Tumor site • • Tumor location • • Proximity to mandible or maxilla • • Need for neck dissection • • Need for reconstructive surgery
  203. 203. SURGICAL MARGINS  UK Royal college of pathologist guidelines:  Clear margin: histological clearance >5mm  Close margins: 1-5mm  Positive margin: <1mm  Incidence higher in oral cavity cancer than other HN sites.  Potentially due to complex anatomy and 3D shape.
  204. 204. FACTORS PREDICTING POSITIVE MARGIN • Large tumour. • Perineural spread. • Vascular permeation. • Noncohesive invasive front • Cervical metastasis
  205. 205. RADIOTHERAPY • Applications: - Radical : early tongue, fom cancer - palliative : advanced total control not possible: 20Gy x5 daily fractions x 1 week. -combined therapy. -preoperative. -postoperative.
  206. 206. RADIOTHERAPY • Small (T1/T2), superficial (<5mm thickness) lesions of tongue & FOM: interstitial brachytherapy. • Dose: 60 Gy/6days with iridium-192
  207. 207. POST-OP RT Indications: -presence of nodal disease with exptracapsular spread. -presence of involved surgical margin -excision margin less than 5mm. -stage III/IV. -perineural or vascular invasion. -poor differentiation. -oral cavity primary. -multicentric primary. ->4 nodes positive. -soft tissue invasion. -dysplasia or carcinoma insitu at resection margin.
  208. 208. IMMUNOTHERAPY  Based on two principles: -immune system should recognise and destroy abnormal cells. - tumor cells are poorly immunogenic and strongly immunosuppressive. . Tumors downregulate antigen presenting molecule . PGE2 produced by tumors inhibit lymphocyte proliferation. . Cytokines produced by tumors inhibit lymphocytes function.
  209. 209. IMMUNOTHERAPY  IL-2 : stimulate growth, diffrentiation and survival of cytotoxic T cells. -systemic injection associated with sever reaction. - Local injection in tumour: short half life requiring frequent injections. -IRX2 human cytokine mixture injected perilymphatically near tumour: in clinical trial
  210. 210. IMMUNOTHERAPY • A trial of IRX-2 in patients with squamous cell carcinomas of the head and neck(Hadden J, et. al. Int Immunopharmacology. 2003 Aug;3(8):1073- 81: using immunotherapy with 10-20 days of perilymphatic injections of a natural cytokines mixture (NCM:IRX2;200 units IL2 equivalence) Found - significant reduction in tumour mass. -increased area of leukocyte infiltration
  211. 211. IMMUNOTHERAPY  Non-Specific Active Immunomodulation  BCG vaccine  Used to induce active, non specific stimulation of the immune system  Reports of increased tumor free survival which could not be substantiated  Trials with other vaccines (strep pyogenes, trypanosoma cruzi, levamisole) show no benefits in long term survival
  212. 212. IMMUNOTHERAPY  HPV Vaccines  Estimated that 25% of HNSCC are HPV associated  Tend to arise in younger patients  Lingual and palatine tonsils  Occur predominantly in non smoker/drinker  Associated with a more favorable prognosis  HPV viral oncogenes E6 and E7 are consistently expressed in HPV associated cancers  Thought to integrate into the host DNA, and when expressed, bypass the regulation of cell proliferation  Both protein and DNA vaccines targeting HPV DNA are currently in phase I and phase II trials
  213. 213. TARGETED THERAPY  Targeted therapy in head and neck cancer: state of the art 2007 and review of clinical applications( Langer CJ. Cancer 2008 Jun 15;112(12):2635-45: -anti-EGFR monoclonal antibody(MoAb) cetuximab first targeted therapy to be developed -single agent cetuximab confer clinical benefits in patient with cisplatin refractory metastatic disease.
  214. 214. WHAT HAPPENS AFTER TREATMENT? • Speech and Swallowing Therapy • Follow-up tests • Chemoprevention • Watch for new symptoms • General health considerations
  215. 215. SUMMARY  The main problem of oral cancer is early detection  Surgery is still the most important modality in management of oral cancer.  Better understanding of molecular biology of HNSCC.  Bio-molecular markers can be used in the management of SCC oral cancer.  High risk of second primary cancer, Chemoprevention?
  216. 216. THANK YOU

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