An Overview of Oral Medicine. WHAT IS ORAL MEDICINE? The specialty of dentistry concerned with the oral health care of patients with chronic, recurrent.

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!

• Idiopathic Idiopathic • Complex genetic (multifactorial) Complex genetic (multifactorial)

diseasediseaseGenetic

hypersensitivity

Stress/Smokingcessation

Hormonal

Microbial(Viral?)

Aetiology

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 3-4 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 Mucous Membrane Pemphigoid vs.vs.

Bullous PemphigoidBullous Pemphigoid• BP mainly affects skin BP mainly affects skin

with occasional with occasional mucosal involvementmucosal involvement

• Elderly (>60)Elderly (>60)

• Starts with pruritus Starts with pruritus then fluid filled bulla then fluid filled bulla developdevelop

• 20% shows oral lesions 20% shows oral lesions (desquamative (desquamative gingivitis)gingivitis)

Desquamative Gingivitis

• Hypersensitivity • Lichen planus• Pemphigoid or pemphigus

• Requires good oral hygiene!

Idiopathic oral blood blistersIdiopathic oral blood blisters(angina bullosa haemorrhagica)(angina bullosa haemorrhagica)

Clinical presentationClinical presentation

1.1. Sudden onsetSudden onset2.2. Soft palate usually Soft palate usually

involvedinvolved3.3. Unknown causeUnknown cause

1.1. EatingEating2.2. Dental treatmentDental treatment

4.4. Self limitingSelf 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

non-keratinised 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 co-

ordination 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• Oral symptoms• Ocular signs• Histopathology • Salivary gland involvement

– Salivary flow– Parotid sialography– Salivary scintigraphy

• Autoantibodies

E.g. dry eyes and mouth for 3/12

Requires a score to meet theDiagnostic 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

Dry mouth Clinical History

HxRadiotherapy

Radiation Xerostomia

YN

Reduced saliva flow

Medication Pharmacological Xerostomia

N Y

Dry Eyes

European & AmericanGuidelines for

Sjogren’s Syndrome

Connective TissueDisorder

N Y

Primary S.S

Secondary S.S

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.