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An Overview of Oral Medicine WHAT IS ORAL MEDICINE? “The specialty of dentistry concerned with the oral health care of patients with chronic, recurrent and medically related disorders of the oral and maxillofacial region, and with their diagnosis and non-surgical management.” • Some conditions are very common e.g. mouth ulcers, white patches and infections (usually viral and fungal) • Some conditions are very distressing e.g. orofacial granulomatosis and Sjogren’s syndrome • Some conditions are persistent and difficult to manage e.g. psychogenic facial pain The mouth - what’s it got to do with medicine? • • • • An entity in its own right – dentistry ! The upper end of the GIT- gastroenterology ! In continuity with the skin – dermatology ! Often reflects haematological problems at an early stage • Oral mucosa not dissimilar to genital mucosa – combinations of oral, genital and conjunctival problems occur • Can frequently be affected by side effects of medication – dryness, ulceration, pigmentation etc. • Has a lot of sensory cortex devoted to it - oral problems are often very distressing– psychiatry ! Which One Is Potentially Serious Three key questions • What is it ? • What is its significance ? • What should be done about it ? What is it ? • History • Examination • Investigations » » » » Biopsy Haematological Imaging Etc What is its significance ? • Is it ? – – – – – Local (single/multiple) General (systemic) Benign (nuisance) Malignant (serious) A Syndrome What should be done about it ? • Leave +/- review • Treat • Refer Surgical sieve • Congenital – developmental , hereditary/familial • Traumatic - physical/chemical/thermal • Inflammatory – acute / chronic • Neoplastic – benign / malignant • Other Oral mucosa • • • • • • Limited ways it can react to an insult It can breakdown – (ulceration) It can thicken – (white patches) It can blister – (vesiculobullous disorders) It can pigment – (eg. with melanin) Consequently many oral disorders can appear very similar ! History and investigation (eg. Biopsy) are often essential Oral Ulceration Causes of Oral Ulceration • • • • • Traumatic Recurrent aphthous stomatitis Viral disease Dermatological conditions Malignancy Traumatic • Mechanical (toothbrush, dentures) • Chemical (aspirin burn) • Thermal (pipe smoking, hot food) Traumatic • Mechanical (toothbrush, dentures) • Chemical (aspirin burn) • Thermal (pipe smoking, hot food) Traumatic • Mechanical (toothbrush, dentures) • Chemical (aspirin burn) • Thermal (pipe smoking, hot food) Management of traumatic oral ulceration • Try to identify and remove the cause • Review in 2 weeks • If not healed, reconsider diagnosis e.g. if it is a solitary ulcer, consider carcinoma and requires biopsy Recurrent Aphthous Stomatitis • Occurs in 20% of the population • Definite cause unknown, but some precipitating factors or triggers have been identified • Mainly “minor aphthous stomatitis” (80%) but also “major” & “herpetiform” (20%) stomatitis Minor RAS • < 1cm round/oval ulcers - painful • Occur in crops, variable with ulcer free periods • Last up to 10 days & heal without scarring • Never occur on keratinised mucosa (hard palate or attached gingiva) Major Aphthous Ulceration • > 1cm, irregular, deep ulcers • Heal after several weeks with scarring • Destructive • Occur anywhere on the oral mucosa • Can mimic malignancy! Aetiology • Idiopathic • Complex genetic (multifactorial) disease Genetic hypersensitivity Stress/ Smoking cessation RAS……known triggers • Haematinic deficiency in 20%, with 60% positive response following appropriate supplementation – Check Hb, ferritin, Vit.B12 & Folate • Psychological factors • Allergies (preservatives e.g. benzoic acid E210-219), fizzy drinks • Trauma (penetrating) (crisps, also preservatives!) • Cessation of smoking (reverts mucosa to normal non-keratinised state) • Drugs • Family history (not genetic) • Endocrine • Immunological factors • No microbiological association Bowel problems associated with RAS • Crohn’s disease • Ulcerative colitis • Coeliac disease Gluten Enteropathy – Coeliac Disease • Allergy to wheat products • Starts during early childhood - weaning • Lose villi • Malabsorption • Fatty stools – steatorrhoea • Failure to thrive • Aphthous ulcers • (Dermatitis herpetiformis) Systemic history for RAS • • • • • • Lassitude Weakness Breathlessness Abdominal pain Frequency and type of stool Weight loss ANAEMIA GIT problems Management of RAS • Confirm diagnosis by eliminating any systemic underlying cause – Check for haematinic deficiency – If suspect systemic involvement refer to specialist • Therapy – How severe are the symptoms – How frequent are the ulcers – Location of the ulcer Treatment options • No treatment • Prevention/treatment of/for possible causes – Sodium Lauryl Sulfate-Free Toothpastes – Sharp edges, ill fitting prosthesis, calculus • Topical therapy • Systemic therapy • Referral for severe disease RAS management • Pain relief – lignocaine lollipops, Gengigel, Aloclair, Difflam • Address precipitating factors e.g. replacement therapy & investigation of underlying cause. Often asking children to eliminate (individually) fizzy drinks, crisps & chocolate helps • Treatment can include Corlan pellets, steroid in orobase (protects and a small amount of steroid) Tetracycline mouthwash in adults (not pregnant) • Gengigel (Hyaluronic acid) gives good pain relief and accelerates healing – useful in children as non-irritant • More severe cases require a steroid inhaler or betnesol mouthwashes (occasional use) • Systemic steroids on rare occasions (short course) Systemic therapy • Prednisolone – Burst therapy (5-30mg once in morning for 5 days) • Immunomodulator – Azathioprine – Colchicine – Thalidomide (TNF- inhibitor) Guidelines for prescribing topical steroids for oral lesions • Topical medications are effective on contact therefore anything by mouth should be avoided for ½ -1 hr • Gel applied directly on lesion after meals & at bedtime 34 times daily • Could apply it on gauze for large lesions for 15-30 min Guidelines for prescribing systemic steroids for oral lesions • Tapering of prednisolone is not necessary with 5-7 days burst therapy • Tapering of prednisone is not necessary with alternate day therapy if dose did not exceed 20 mg • 30-60 mg AM X 5 days followed by 5-20 mg AM every other day Behcet’s Syndrome • RAS • Ocular – uveitis,optic atrophy,retinal vasculitis • Genital ulceration • Dermatological eg. Pustules • Neurological – symptoms like MS • Joint disease – recurrent arthralgia • Others – eg.depression • Strong association with HLA B5 Epidemiology • The usual onset of the disease is in the third and fourth decade of life. • Male to female ratio is approximately equal. Epidemiology • Prevalence in Turkey 80-370:100,000 • Prevalence in UK (0.3-0.5):100,000 Behcet’s • Affects persons of Mediterranean, Middle Eastern, or Japanese decent • Easily confused with Stevens-Johnson syndrome or Reiter’s disease • Need referral for systemic treatment Treatment • Multidisciplinary approach • Systemic therapy – – – – Corticosteroid Azathioprine Colchicine Thalidomide (TNF- inhibitor) Viral Oral Ulceration • Tends to be all over the mouth, including keratinised epithelium • Usually extensive ulceration • If primary HSV, may be preceded by flu-like illness and no previous history of cold sores • If secondary HSV, should be history of cold sores Dermatological causes of oral ulceration • Lichen planus • Lupus • Vesiculobullous disorders • Erythema multiforme Oral Lichen Planus • A common chronic inflammatory mucocutaneous disorder which affects the skin and mucous membranes (mainly mouth) • Occurs in approximately 1% of the population, usually in middle age and is slightly more common in females Clinical presentation • Reticular – often symptoms of roughness rather than pain • Papular – raised white areas of 1-2mm in diameter • Plaques – homogeneous leukoplakia, more usual in smokers • Atrophic – thin mucosa, red but not ulcerated and often painful • Erosive – frank painful ulcers • Bullous – vesicles or small blisters within white patches Ulcerative Lichen Planus • Erosive or desquamative types • Intermittent ulcers for up to 20 years • If unilateral may be lichenoid - ? Related to old amalgam or other contact allergy • Can be drug related • Usually striae present • If lichenoid try to eliminate allergen, whereas treat LP symptomatically & attempt to eliminate ulceration • Attempt to maintain intact mucosa i.e. revert to white patch or striae • Use potent steroids with caution in case of potential risk of malignant change OLP – malignant transformation risk • Erosive & plaque variants • ~ 1% over 5-10 year period • Dysplastic lichen planus Lupus • • • • • • • Discoid (DLE) Systemic (SLE) “Butterfly” rash on face Oral red/white patches Sunray appearance Oral ulceration Sjogren’s & TMJ disease - autoimmune • Oral malignancies Vesiculobullous disorders • Pemphigus • Pemphigoid • Erythema multiforme (also under allergy) Pemphigus • An autoimmune disorder characterised by widespread bullous or blistering eruptions of skin and mucous membranes • Potentially fatal as there is gross loss of fluids and electrolytes as well as wound infections • 70% present in mouth first (50% in mouth only) • Usually the elderly • Rarely see blisters – usually irregular ulcers and skin tags • Usually on areas of pressure (e.g. denture) • May present as a sore throat • Ulcers differ from RAS as bigger, present in older people and are persistent. • Most common type of oral presentation is P. vulgaris • Need to treat for life as potentially fatal and autoimmune. Pemphigus • Not easily distinguished from pemphigoid, which is not fatal, but can cause blindness as can involve eyes and scarring causes opacity (symblepharon) Mucous Membrane Pemphigoid vs. Bullous Pemphigoid • BP mainly affects skin with occasional mucosal involvement • Elderly (>60) • Starts with pruritus then fluid filled bulla develop • 20% shows oral lesions (desquamative gingivitis) Desquamative Gingivitis • Hypersensitivity • Lichen planus • Pemphigoid or pemphigus • Requires good oral hygiene! Idiopathic oral blood blisters (angina bullosa haemorrhagica) Clinical presentation 1. Sudden onset 2. Soft palate usually involved 3. Unknown cause 1. Eating 2. Dental treatment 4. Self limiting Erythema Multiforme • An acute, self limiting eruption of the skin and mucous membranes • Antigen can be HSV, EBV, Mycoplasma, sulphonamides, phenytoin, other drugs (including alcohol) • May be prodromal flu-like symptoms followed by widespread vesiculobullous eruptions of skin, oral, genital & ocular mucosa • Ulcers all over mouth and lips (crusting) • Skin lesions are either bullous or “target” lesions • Usually resolves in 10-14 days • Management is supportive – no particular diagnostic test or treatment (topical anaesthetic & betnesol mouthwash). Ensure fluid intake is adequate • Recurs, but each episode is less severe • Severe form is Stevens – Johnson Syndrome Importance of History in Oral Ulceration • Have the patients had previous ulcers and are they cyclical or persistent • Age of patient • Site of ulcers - ? On keratinised or nonkeratinised mucosa • Has the patient had herpes in the past? • Has the patient any known allergies? • Does it involve any other mucosal sites? • Has the patient started new drugs that preceded onset of ulcers • Has the patient stopped smoking • Is the patient in generally good health Diffuse Lip Swelling • Orofacial Granulomatosis • Allergic angioedema • Hereditary angioedema Orofacial Granulomatosis • • • • • • Lip swelling Oral ulceration Mucosal tags Angular cheilitis Cobblestone mucosa Full-width gingivitis Causes of OFG • Allergy • Crohn’s disease – may not manifest itself until 10 years after onset of OFG! • Others – foreign bodies, sarcoidosis Investigations of OFG • FBC, B12, Red cell folate, ferritin, LFT’s, CRP • Buccal mucosal biopsy down to muscle • Patch testing (Type 4 hypersensitivity) • GIT investigations (?Crohn’s) • Most common allergens identified on patch testing in OFG are benzoic acid (E210-219) found in fizzy drinks and tomatoes & cinammonaldehyde • Chocolate is commonly a cause • Negative patch tests do not confirm absence of allergy Allergic Angioedema Type 1 Hypersensitivity • Speed of onset • Swelling of lips, cheeks, tongue, throat, itch within minutes • Oedema of larynx, GIT involvement (vomiting & diarrhoea), urticaria, vasodilatation & bronchospasm • Adrenaline (followed by hydrocortisone) is required for bronchospasm & acute drop in BP Management • Tests: Skin prick tests & RAST (Radioallergosorbent test) • Control by: – Avoidance of allergen – Antihistamines in mild cases and adrenaline/steroids in severe cases Hereditary Angioedema • Hereditary (more common) or acquired (usually in middle age) angioedema • Genetic defect of inhibitor of first component of C1 (C1 esterase inhibitor) • Repeated episodes of swelling of deep dermis, subcutaneous tissues and mucous membranes • Uncontrolled activation of classical complement pathway & excess release of vasoactive agents Clinical manifestations • Swelling poorly circumscribed, no-pitting and not associated with urticaria or pruritis • Precipitated by trauma (including dentistry) anxiety, emotional upset, physical exertion and sometimes spontaneously • Develops over 12-18 hours with tingling and tightness and usually over 48-72 hours • Involves the extremities, face, oropharynx and can compromise the airway • Treatment: stanazol (androgenic steroid) or antifibrinolytics 1 week before planned dentistry • Emergency dental treatment may require fresh frozen plasma • Rarely responds to antihistamines or steroids Intraoral White Patches Leukoplakia • Clinical term for persistent adherent white patch (histology unknown and no attributable diagnosis) • Prevalence of keratosis is 3-4% • 15% of leukoplakias regress and 3-6% undergo malignant transformation over 10 years Leukoplakia • Homogenous leukoplakias are prevalent in the buccal mucosa and have a low pre-malignant potential • Nodular or speckled leukoplakias are more serious • Leukoplakias in the floor of mouth or undersurface of tongue have a high risk of malignant change Risk factors • • • • • Smoking Alcohol Diet Immunosuppression Presence of Candida Local Causes • • • • • • • Frictional keratosis Smokers keratosis Idiopathic keratosis Papillomas Carcinomas Burns Skin grafts Systemic causes • • • • • White sponge naevus Geographic tongue Lichen planus / lupus erythematosis Candidosis / candidal leukoplakia Hairy leukoplakia Biopsy of lesions • To confirm diagnosis • Essential in non-healing ulcerated areas, nodular areas, areas with red flecks, if there are associated lymph nodes, in “at risk” sites or at risk patients or if the white patch is fixed and indurated Mucosal Biopsy • Should it be undertaken in general dental practice? • Yes it could be with: – – – – Being interested in minor OS procedures Adequate training Good links with a pathology service Good resource to feed back results ( & implications) to patient • But no if any suspicion of oral cancer Management of Leukoplakia • Biopsy and other investigations • Reduction of pre-disposing factors • Definitive management e.g. excision, laser or regular review with records and re-biopsy Papillomas • Keratinised papillomas appear as white nodules • Commonly appear like cauliflowers, frequently on soft palate • Diagnosis is obvious, but biopsy is recommended in case they are the more rare venereal wart intraorally White Sponge Naevus • Benign, hereditary mucosal condition of no consequence • Very roughened “shaggy Carpet” appearance • Some reports of improvement with antibiotics Geographic Tongue • Also known as benign migratory glossitis & erythema migrans • Red and white patches that change position from time to time • White patches are hyperkeratinised areas and red the atrophic areas • Often associated with fissures and can be painful • Treat symptomatically (? Use of zinc) Oral Candidosis • Clinical types that are white are pseudomembranous, occasionally midline glossitis and candidal leukoplakia (premalignant) • Management by addressing underlying cause such as dietary deficiency, excess sugar in diet, denture hygiene, use of steroid inhalers or identification of underlying cause Oral Candidosis • Management: – address underlying cause e.g. dietary deficiency, excess sugar in diet, denture hygiene, use of steroid inhalers or identification of underlying cause Oral Hairy Leukoplakia • EBV – has been implicated in the aetiology of hairy leukoplakia • OHL is useful prognostic indicator in HIV and can also be seen in immunosuppressed transplant patients Salivary Problems • Saliva plays an essential role in numerous functions of the mouth. • Usual complaint is of dryness • Can c/o too much – sialorrhoea – Sore mouth – Neurological – poor neuromuscular coordination etc. – Medication – Psychogenic Sjögren’s syndrome • A common autoimmune “rheumatic” disease. • Women >40 yo • Can occur on its own (primary) or as a complication of other connective tissue diseases (secondary Sjögren’s syndrome). • The most common symptoms are extreme tiredness, along with dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). • Up to 90% of individuals with Sjögren’s syndrome have antibodies targeting the Ro and La autoantigens • Can have other systemic symptoms – GIT, vulval etc. Diagnostic criteria for S.S (European/American & Japanese) • • • • • Ocular symptoms E.g. dry eyes and mouth for 3/12 Oral symptoms Ocular signs Histopathology Salivary gland involvement – Salivary flow – Parotid sialography – Salivary scintigraphy • Autoantibodies Requires a score to meet the Diagnostic criteria – see Ann Rheum Dis 2002;61:54-558 General complications • • • • • Caries (often rampant) Periodontal disease Candidosis – should be checked ! Bacterial sialadenitis ulceration Non-Hodgkin’s B-cell lymphoma • Occurs in ~1% of patients with Sjögren’s syndrome. Usually, this is a slow growing, low-grade malignancy • Pseudolymphoma in ~10% Xerostomia Clinical History Dry mouth Primary S.S N Secondary S.S Y Connective Tissue Disorder Hx Radiotherapy N Y Reduced saliva flow Medication N European & American Guidelines for Sjogren’s Syndrome Radiation Xerostomia Y Dry Eyes Pharmacological Xerostomia Management • Identify a likely cause! • Referral – Oral medicine – Sjogren’s syndrome? • Rheumatology • Ophthalmology • Artificial saliva • Salivary stimulating agents (gum, pilocarpine) • Meticulous oral hygiene management • Regular dental care Summary • The mouth can be a useful site for early diagnosis of systemic disease • Painful conditions of the orofacial region can be debilitating and lead to nutritional and fluid intake problems • Because of its constant use the mouth is exposed to trauma, allergens and carcinogens and must be checked routinely.