dental Oral Medicine Revision Tool

Summary of Cawsons, Master dentistry and Oral med cases

Oral Medicine Revision summary Andrew Pritchard

Manchester Revision toolkit

Table of Contents 1.

Salivary gland disease and Xerostemia: (dry mouth)................................................................................................ 5 1.1 Sjorgrens syndrome: ............................................................................................................................................... 5 1.2 Obstructive salivary gland disorder: ....................................................................................................................... 6 1.2.2 Sialadenosis/ sialosis (non inflammatory): .......................................................................................................... 6 1.2.3 Sialadentitis (inflammatory): ............................................................................................................................... 6 1.2.4 Sialolithiasis (calculi obstruction):........................................................................................................................ 6 1.3 Salivary gland associated swellings: ........................................................................................................................ 6 1.4 Salivary gland tumours:........................................................................................................................................... 7 14.4.2 Malignant tumours: ........................................................................................................................................... 7 1.4 Revision Questions .................................................................................................................................................. 7 Case discussion points from oral medicine seminar: .................................................................................................... 8

2.

White Patches ........................................................................................................................................................... 9 2.1 Leukoedema: ........................................................................................................................................................... 9 2.2 Frictional keratosis (linea alba) ............................................................................................................................... 9 2.3 Fordyce granules: .................................................................................................................................................... 9 2.4 Smokers Keratosis: .................................................................................................................................................. 9 2.5

Hairy tongue:..................................................................................................................................................... 9

2.6

HIV associated hairy tongue (oral hairy leukiplakia)....................................................................................... 10

2.7

White sponge naevvus: ................................................................................................................................... 10

2.8

Psoriasis........................................................................................................................................................... 10

2.9

Licken Planus ................................................................................................................................................... 10

2.10

Leukoplakia: (premalignant lesions) ............................................................................................................... 11

2.11 Mucous Membrane Pemphigoid ........................................................................................................................ 12 2.12: Pemphis Vulgaris ................................................................................................................................................ 13 2.12 3

Revision questions for White patches ............................................................................................................ 14

Fungal infections of the mouth ............................................................................................................................... 15 3.1 Pseudomembranous candidosis (thrush): ............................................................................................................ 15 3.2 Erythemateous candida ........................................................................................................................................ 16 3.3 Chronic hyperplastic candiadosis .......................................................................................................................... 16 3.4 Angular stomatitis ................................................................................................................................................. 16 3.5 Candida infections Summary ................................................................................................................................ 16

4

Viral infections of the mouth .................................................................................................................................. 18 4.1 Acute hepatic stomatitis ....................................................................................................................................... 18 4.2 Herpes zoster ........................................................................................................................................................ 18 4.3 Hand foot and mouth disease ............................................................................................................................... 18 4.4 Herpangina ............................................................................................................................................................ 18 4 .4 Human papillo virus: ............................................................................................................................................ 18

5

Oral swellings .......................................................................................................................................................... 20 5.1: types of swellings and definitions ........................................................................................................................ 20 5.2 Fibrous polyp, epulides and denture induced granuloma .................................................................................... 20 5.3 Giant cell fibroma:................................................................................................................................................. 20 5.4 Papillary hypoplasia: ............................................................................................................................................. 20 5,5 Pyogenic granuloma and pregnancy epulis .......................................................................................................... 20 5.7 giant cell epulis...................................................................................................................................................... 20 5.8 benign epithelial tumour ...................................................................................................................................... 20 5.9 Verruca vulgaris .................................................................................................................................................... 21

6

Cysts and granulomatous disorders ........................................................................................................................ 22 Cysts ............................................................................................................................................................................ 22 6.1 Radicular cysts: (swelling of the root) ................................................................................................................... 22 6.2 paradental cyst...................................................................................................................................................... 22 6.3 dentigerous cyst .................................................................................................................................................... 22 6.4 Eruption cysts ........................................................................................................................................................ 22 6.5 Odontogenic Keratocyst........................................................................................................................................ 22 6.6 residual cyst: ......................................................................................................................................................... 22 6.8 Solitary bone cyst: ................................................................................................................................................. 23 Treatment: .................................................................................................................................................................. 23 Granulomatous disorders: .......................................................................................................................................... 23

7.0 Common Oral ailments, Antibiotics and their prescription: ..................................................................................... 24 7.1 Dental abscess:...................................................................................................................................................... 24 7.2 ANUG and pericoronitis ........................................................................................................................................ 24 7.3 Fungal infections (candida) ................................................................................................................................... 24 7.4 Denture stomatitis (induced candidal infection) .................................................................................................. 24 7.5 Angular chelitis...................................................................................................................................................... 24 7.6 Herpes Simplex ..................................................................................................................................................... 24 Pharmacology: ............................................................................................................................................................ 25 9. Oral Cancer:............................................................................................................................................................. 29 Types of oral neoplasm: .......................................................................................................................................... 29 Types of squamous cell carcinoma ............................................................................................................................. 29 Referral guidelines: ................................................................................................................................................. 30 Ulcers .......................................................................................................................................................................... 32 Facial pain ....................................................................................................................................................................... 33 Trigeminal nerve info: ................................................................................................................................................. 33 Myofacial and TMJ pain .............................................................................................................................................. 34 Physcogenic:................................................................................................................................................................ 34 Atypical facial pain- ................................................................................................................................................. 34

Bells palsy: ............................................................................................................................................................... 34 Neuropathic ................................................................................................................................................................ 35 Trigeminal neuralgia: .............................................................................................................................................. 35 Burning mouth syndrome: ...................................................................................................................................... 35 Glosspharyngeal neuralgia: (tongue affected)........................................................................................................ 35 Herpatic and post herpetic neuralgia: .................................................................................................................... 35 Vascular causes of orofacial pain: ............................................................................................................................... 35 Migrainous neuralgia: (cluster headache) .............................................................................................................. 35 TMJ clinic ..................................................................................................................................................................... 36

Oral medicine Revision tool (cawsons, BDJ, oral med and pathology, master dent) 1. Salivary gland disease and Xerostemia: (dry mouth) Subjective sense of dryness due to reduced salivary flow or change in salivary composition. Patients with chronically decreased salivary flow (hyposalivation) suffer from lack of oral lubrication and more prone to candida infections and bacterial sialadentitis. Causes: Physiological: anixiety associated sympathetic activity, mouth breathers may have dry mouth. Soft tissue changes with ages – reduction of acini cells. Rarely child born without salivary gland- salivarygland aplasia. Irradiation: malignant head tumours, oral cancers treated with radiotherapy cause xerostomia. Dehydration: diabetes mellitus, chronic renal failure, hyperparathyroidism, fever causes dehydration and lack of saliva. Disease of the glands: sjogrens, sarcoidosis, HIV, hep C infection, liver disease and cystic fibrosis. Complications:  Dental caries- on smooth surfaces which would usually be unaffected, lower incisor ragion and roots.  Candidosis: causing burning sensation and mucosal erythema, lingual filiform papillae atrophy and angular stomatitis.  Halitosis  Ascending sialadentitis- presents as pain and swelling of major gland, sometimes with pirulent discharge from duct. Diagnosis: Allow patient to sit quietly and dribble into a measuring container for 15mins. Normal person, unstimulated whole salivary flow rate should be >1.5ml/ 15min or 0.1ml/ min To confirm diagnosis special investigations:  Blood tests – exclude diabetes (blood gluc ), Sjogrens (SS-A [primary], SS-B antibodies [secondary/ rheumatoid linked]), sarcoidosis, hep and HIV.  Eye tests: shirmer test to exclude Sjogrens  Imaging: sjorgrens, sarcoidosis or neoplasia.

1.1 Sjorgrens syndrome: Autoimmune disease of connective tissue in salivary glands: 10x more likely in women. Serious oral changes associated with lack of saliva (taste, eating, swallowing, caries), angular chelitis and candida. Swelling in parotid (parotius) only in 30% of patients at one point during disease. Primary (non connective tissue disease) Causes severe ocular and oral changes SS-B antibodies increased

Secondary (Linked with rheumatoid arthritis) 10-15% of rheumatic fever sufferers infected SS-A antibodies increased Also Salivary duct antibodies and rheumatoid factors increased. Diagnosis: Antibody screen, salivary flow rate below 0.5ml/min from 1-2ml/min Histologically: CD4 lymphocytes infiltrate and destroy secretory acini. Polyclonal infiltration mainly by CD4 lymphocytes Infiltrate initially periductal Progressive spread of infiltrate through the glandular tissue Progressive destruction of secretory acini Proliferation of some duct tissue as epimyoepithelial islands

Treatment: check medication for causative medicaments. Water, chewing gum and salivary substitutes (bioxtra, ophana spray) or- chlorinesterase inhibitors like Pilocarpine Caries- preventative- mouth washes Candida- if present treat with nystatin or amphoterican or Fluconazole HIV associated salivary gland disease: main difference CD8 infiltration.

Pilocarpine: parasympathetic alkaloid- non selective muscarinic actylcholine receptor agonist M3

1.2 Obstructive salivary gland disorder: Can be acute or chronic: clinical features are characteristically pain and swelling.   

Extra ductal: caused by disease outside ductal wall. Neoplasms and SSC in floor of mouth as well as salivary neoplasm. Duct wall thickening: duct wall obstruction though fibrosis leading to stricture. Orifices can become stenosed through trauma from dentures or teeth. Intraductal obstruction: most common type usually salivary calculus buildup. 80% of cases are submandibular.

1.2.2 Sialadenosis/ sialosis (non inflammatory): Non inflammatory enlargement of salivary glands (usually parotids) linked to diabetes, endocrine diseases, pregnancy, bulimia. Primarily the parotid. Histologically: hypertrophy (organ growth) of seous acini cells. Presentation: bilateral and painless. Evolving slowly.

1.2.3 Sialadentitis (inflammatory): Inflammatory condition of salivary gland generally presenting with pain and swelling of associated gland. Caused by ductal obstructions (sialolithiasis) with secondary bacterial infection due to increased flow and stasis of secretions. Acute sialadentitis:  Viral sialendenitis: caused by mumps- acute contagious infection caused by paramyxovirus. Spread by direct contact of saliva. 2-3week incubation, fever and malaise followed by sudden painful swelling of one or both parotid glands. Orchitis occurs in 20% of affected adult males.  Bacterial sialadenitis: acute bacterial sialadenitis involves bacteria entering parotid gland ducts. Streptococcus pyogenes, staphyloccus aureus detected in clinical discharge. Accompanied by swelling, pain, fever and erythema. Treatment through antibiotic therapy, salt water washes. Chronic sialadentitis:  Bacterial sialadenitis: Chronic bacterial infection. Chronic infection usually in the submandibular region as less recognised in early stages. Presentation- duct orifice inflamedand a mucopurelent discharge on examination. Patients complain of foul taste. Gland becomes firm and fibrotic. Pathophysiology: perductal fibrosis, acinar atrophy, chronic inflammatory infiltrate. Sialograms show, atrophy, strictures, calculi buildups and abcesses. Treatment is excisional.  Relapsing parotitis: uncommon. Punctuate silaectasis peripherally.  Radiation sialadenitis: acinar damage and progressive fibrous replacement. Dose dependant.

1.2.4 Sialolithiasis (calculi obstruction): Calculi or stones develop within the salivary ducts from calcium salts and precipitate out of the saliva. Commonly occur in submandibular gland- higher viscosity of saliva and tortuous root of duct. Presentation: Patients complain of pain, severe and worsend when eating. Stone can be palpated intraorally. Xrays can assist locating the stones (lower occlusal anterior oblique). Treatment: involves massaging the stone out of the gland, sialogues (lemon juice) to promote forward secretion. Shock wave lithotripsy- has been successful. Large stones require surgical removal of the gland itself via extra oral approach.

1.3 Salivary gland associated swellings: Mucocele: Rupture of a minor salivary gland, most commonly found on the inner aspect of the lower lip. No obvious traumatic event but may have been caused by minor lib biting or catching on sharp surface. Lesion is painless, dome shaped and fluctuant. They appear blue secondary to the mucin underneath the mucosa. Can resolve spontaneously or be excised surgically.

Ranula: (large mucocele in another location) specific type of mucocele presenting in the anterolateral floor of the mouth and represent extrusion of mucus from the sublingual gland. Requires excision as Mucus retention cysts: distinguished from mucoceles by having a epithelial lining therefore becoming cysts. Often appear clinically and are painless. Come from any part of the minor/ major salivary glands and result from dental obstruction and dilation rather than trauma. Common sites- floor of mouth, buccal mucosa, upper lip. Treatment: surgical excision.

1.4 Salivary gland tumours: 3% of all tumours but maliganancy rare. Most common are in the parotid gland where 90% are benign adenomas and 10% are malignant. High relative proportion of maliganant tumours in submandibular and minor salivary glands arising in the palate. 1.4.1: Benign tumours: Pleomorphic adenoma: most common salivary adenoma- 80-90% of all salivary gland tumours. Presentation:  Major salivary glands. They present as slow growing, painless nodule, detected during routine extraoral examination. Nodule is soft but firm in texture and freely moveable.  Minor salivary glands: nodule small rubbery prinicipally in the palate and upper lip. Treatment: excisional biopsy with a margin of normal tissue. Histologically: ductal epithelia and myoepithelia show squamous differentiation. Stromal component rich in proteoglycans. Capsule of compressed fibrous tissue forms around adenoma. Warthins tumour: older men, affects parotid. 10% are bilateral, presenting as a discreet nodule, rarely exceeding 3cm in diameter. Microscopically papillary cystic structure, double layed eosinophilic ductal cells supported by lymphoid stroma.

14.4.2 Malignant tumours: Outcome depends on histological type and grade. Adenoid cystic carcinoma: arises from minor glands. Slow growing, may cause pain, palsy or paresthesia with tendency to invade and spread along nerve pathways. Shows swiss cheese appearance due to microcysts filled basement membrane. Mucoepidermoid carcinoma: most common malignant salivary gland tumour. Painless swelling in gland. Acinic cell carcinoma Polymorphous low grade adenocarcinoma

1.4 Revision Questions 1. 2. 3. 4. 5. 6. 7. 8.

Differences between type 1 and 2 Epidemiology- men or women more affected? By how much? Other predisposing conditions Antibodies checked for? What to antibodies target? Diagnosis- what to biopsies show? Sialogragh show? Treatment- what substitutes and suppressants- how do they work- cholinesterase and pilocarpine. Difference between HIV and normal sjorgrens syndrome is which t lymphocyte- CD4 or CD8 infiltration General questions: how does diabetes effect saliva, how does alcohol affect saliva, how does stress effect saliva. 9. List some drugs that affect saliva flow.

Case discussion points from oral medicine seminar: 1. Sjogrens syndrome type 2. Arthritis, gritty eyes, parotid gland removal- reduced salivary flow. Edenturelous. Discussion: Typical complaints, causes of drymouth and classifications, lymphoma history, relevant tests and results. 2. Drug induced: amitriplytine (anti depressant), fursemide (loop diuretic), captopril (ace inhibitor) vs hypertension. Denture stomatitis. 3. Radiation induced drymouth, telangietasia (redness over skin). Treatment. 4. Stressed diabetic alcohol induced: poorly controlled diabetes, smokes and drinks heavily.

2. White Patches Infalmmatory conditions cause redness (erythema) secondary to thinning of the mucosa and increased vascularity. Lesions that appear white secondary to increased thickness of the epithelium through hypertrophy/ hyperplasia/ hyperkeratosis. Thickening in the spinous or prickle layer of the epithelium is acanthosis. Mechanical friction can cause keratin production as protective response.

2.1 Leukoedema: This is a fairly common entity, generalised opacification or gray white of buccal mucosa bilaterally. Colour less evident as mucosa is stretched. Description: Diagnosis:

Bilateral, grayish thickening on buccal mucosacommon in 90% African Americans Confirm with biopsy

Histology:

Thickening of epithelium with intracellular odema at spinous level Management: Unnecessary

2.2 Frictional keratosis (linea alba) White line resulting from chronic frictional trauma of the tissues rubbing the adjacent teeth, most commonly seen as horizontal white streak along the buccal mucosa at the occlusal plane bilaterally. Description: Diagnosis: Histology: Management:

White patch caused by abrasion- biting, sharp filling Patches pale translucent can become rough Epithelium hyperplastic, thick hyperkeratosis Remove irritant

2.3 Fordyce granules: Sebaceous glands grow in size with age- appearance- creamy yellow spots

2.4 Smokers Keratosis: White thickening on palate, red centre due to pipe smoking Nicotinic stomatitis – direct irritation of the palatal mucosa from hot tobacco smoke leading to inflammatory changes initially erythemateous then become swhite secondary to progressive epithelial hyperplasia and hyperkeratosis. Crinkled, cracked appearance with red dots representing inflammation of minor salivary glands. Lesion is reversible after smoking cessation.

2.5

Hairy tongue:

Elongation of the filliform papillae secondary to decrease in the desquamation of keratin can cause a white coating on the dorsum of the tongue. Coating can become amtted and hair like with gagging/ irritation as papillae are extremely long. If burning sensation occurs then there maybe a superimposition of candida infection. Staining from dietary coffee/ tobacco can colour the area. Poor nutrition, some antibiotics certain mouth rinses and dehydration can cause. Treatment usually not needed once precipitating factor found and ceased. Description: Cause:

Alteration of microflora favouring chromogenic bacteria Smoking, antibiotics and oxygenating mouth rinses.

Histology: Hyperplasia of filiform bacteria Management: Sodium bicarbonate and treat underlying etiological factor

2.6

HIV associated hairy tongue (oral hairy leukiplakia)

Benign, well demarcated asymptomatic white lesion on lateral tongueseen in HIV or immunosuppressed patients. Differential diagnosis- pseudomembranous candidiasis. Can be associated with Epstein barr virus and a precursor to the development of AIDS. Description: diagnosis: Histology: Management:

2.7

Clinical manifestation of HIV. Soft white plaque at edges of tongue, Biopsy to confirm Kolicyte cells in prickle cell layer

White sponge naevvus:

Rare lesion inherited as an autosomal dominant trait presents in childhood or adolescence without gender predilection. Thick folded white plaque with spongy appearance on buccal mucosa bilaterally. Generally asymptomatic appearance distinctive so biopsy not always indicated. Can appear in esophagus, genitalia and rectum. Description:

Inherited autosomal dominant disease wide mucosal irregular white thickening diagnosis: Confirm by biopsy Histology: Hyperkeratosis Management: Benign so no further treatment

2.8

Psoriasis

Description: diagnosis: Histology: Management:

2.9

Licken Planus

Chronic muco curtaneous T cell mediated inflammatory condition affecting 1% of adult population. Oral lesions common and can be only manifestation. Extent of lesion may fluctuate. Occurs between 40-70yrs. Larynx and genitalia can be affected. Specific trigger can be referred to as lichnoid hypersensitivity reaction. Amalgam and cinnamon flavoured products can be associated with localised affects. Three distinct presentations- reticular erythematoeus presents as reticular lesions or wickhams striae appear as white mucosal changes. Plaque like form and erosive/ ulcerative. Buccal mucosa and tongue common sites- usually bilateral. If only gingival is affected contidiotn is desquamative gingivitis. 50% of these cases are ultimately mucous membrane pemphigoid. Treatment though corticosteroids. Desquamative can be treated with a specially constructed tray for application. Topical tacrolimus can be used in addition. High dose prednisolone used in severe cases. Most serious complication is maliganat transformation to SSC- occurs in 1% (oral pathology textbook)

Description:

Auto immune disease without specific antibody. Effects skin tongue and oral mucosa. Papular LP: White papules Reticular LP: bilateral striae and atrophic red areas that lead to desquamative gingivitis. Erosive LP: persistant painful Causes: Amalgam reaction, HCV virus, hypertension and diabetes. Histology: Hyperkeratosis Management: Remove amalgam if causative factor, change medicaments, topical corticosteroids like Tacrolimus.

Plaque like (could be leukoplakia)

reticulation, erythema and focal ulceration

Reticulation and severe erythema

reticulation, erythema, central ulceration

2.10 Leukoplakia: (premalignant lesions) White lesion that cannot be characterised as any other white lesion. Homogenous leukoplakias are plaque like lesions with uniform smooth or wrinkled surface. Less risk of malignancy. Non homogenous leukoplakias- less circumscribed, greater range of appearances- verrucous leukoplakia has wart like appearance, speckled leukoplakia has red areas indispersed. Greater risk of malignancy. 5% develop into malignancy. 25% if on floor of mouth. Sublingual keratosis: leukoplakia affecting the floor of the mouth and ventral tongue, malignant transformations in over 30%. Homogenous refers to uniform colour and texture- uniform white flat and thin. Non homogenous- irregularity in colour or texture- predominantly white or white and red (erythoropakia) irregular texture. Can be nodular. Is more malignant as further dysplasia has occurred.

Candidal leukoplakia: chronic hyperplastic candida results in firm warty specked plaque that cannot be scraped off. Occurs commonly on dorsum of the tongue and buccal mucosa behind angle of the mouth. Removal of candida should remove white plaque. Some studies say 10-40% are malignant. Histologically: nuclear hyperchromatism, large nucleus, nuclear polymorphism, aytipical mitosis, disturbance in cell arrangement and adhesion. Paradoxically the malignant change is higher in non-smokers. Description:

White patch or plaque which cannot be characterised clinically or pathologically.

diagnosis: Histology:

Can be benign to carcinoma in situ. Thick surface layer of keratin. Cellular atypia amongst epithelial cells. Management: 5% of leukoplakia progress to carcinomas. Floor of mouth – 25% can progress. Biopsy is usually indicated to check maliganacy.

A large proportion of oral cancers are associated with preceding longstanding oral leukoplakia and possibly 5% of oral leukoplakias overall become cancer. This figure is higher for the non-homogeneous form, especially the proliferative verrucous variant, which nearly always becomes cancerous. There may be no change in appearance or symptoms in the early stages of cancer development. Classic changes of cancer are ulceration, induration/hardness, bleeding and tumour outgrowth. Factors reported as associated with increased risk of SCC development: 1. Dysplasia (atypical changes) on histology is regarded as the most important factor. However it is important to note that dysplastic lesions can resolve spontaneously and nondysplastic lesions may develop into cancer. 2. Site – floor of mouth under the tongue and the sides/undersurface of tongue 3. Clinical type – speckled non-homogeneous, especially proliferative verrucous leukoplakia 4. Female sex 5. If the leukoplakia is NOT associated with tobacco use. 6. Long duration of disorder 7. Large lesion size Presence of Candida albicans – but this is most commonly found in lesions at the angles of the mouth or top surface of tongue, which are rare sites for cancer development. No molecular tumour markers have yet been found that can be used to predict cancer development in an individual or lesion. The role of human papillomaviruses (wart virus) has not yet been determined.

2.11 Mucous Membrane Pemphigoid Causes bulous and painful erosions. Uncommon for skin involvement. Desquamative gingivitis is commonly involved. Nikolskys sign (epithelium peels away during biopsy) Commonly affects oral mucosa- auto immune vesiculobulbous blistering disease characterised by auto reactive antiboidies that target hemidesmosomal complex at the basement membrane resulting in subepithelial separation. Occurs at 50-70yrs and women twice more likely to be affected. Pain and scarring can occur and blindness in ocular involved patients. Many patients present with desquamtive gingivitis- intact blisters rupture to leave irregular shaped ulcers. Diagnosis by biopsy and histologic investigation where IgG deposition is distinct in basement

membrane. Treatment: topical or systemic corticosteroids and steroid sparing agents or tacrolimus. (tacrolimus reduces interleukin -2) Always refer on for ocular change as blindness can ensue.

2.12: Pemphis Vulgaris Uncommon- causes blisters on skin. Acantholytic tzanck cells often seen histologically. Group of autoimmune vesiculobullous blistering diseases. Circulating IgG autoantibodies target desmosomal complex binding to glyvoprotiens desmoglein 1 and 3 results in intraepithelial splitting. Mediterreanen and Ashkenazi jewish descent more racially predisposed. Presents as well demarcated irregular erythemateous erosions and ulcerations that become large and painful. Buccal mucosa, palate and gingival. Intact bullae rarely observed. Biopsy to confirm for histological study- separation intraepithelial at basal cell layer and acantholysis. DIF demonstrates a classic intracellular binding pattern of IgG vs desmosomal glycoprotiens. Management requires systemic corticosteroid and steroid sparing immunomodulatory agents (azithioprine, cyclosporine, tacrolimus and mycophenolate).

Pemphis vulgaris- well defined ulceration

palatal lesion

Immunofluoresence- requires fresh sample analysed quickly. Pemphigus: fluorescence reveals IgG antibody around surface of prickle cell layer. Phempigoid: fluorescence reveals IgG concentrated in a band along basement membrane

2.12 Revision questions for White patches White patches: 1. Gray thickening on afro Americans buccal mucosa- harmless 2. Thickening and whitening of oral mucosa due to trauma 3. White creamy glands/spots 4. Thickened white patch with red centre on smoker 5. Hairytongue is caused by what two things? And how to treat: 6. Soft white plaque on sides of tongue with/out c. albicans can be what three things but importantly which major disease could it be? 7. What is prognosis of HIV over 1,2 and 2.5 years 8. 4 types of chronic mucocurtaneous candidosis- which is warty? 9. Red margins of tongue with thickend patches on arms/ legs 10. Causes of lichnoid reactions 11. White straie bilateral, white papules and desquamative gingivitis or reddened areas are clinical features of? 12. Uncharacterisable white plaque, tobacco/ paan (betel) can cause on floor of mouth under tongue can be: 13. Premaliganat in how many cases?

3

Fungal infections of the mouth

C albicans most common fungal infection in the oral cavity. Commensal organism carried by half the population and disease is caused by opportunistic overgrowth. Usually treated with antifungals- amphotericin and nystatin lozenges. Miconazole gel is better for xerostomia patients and denture stomatitis as it can be directly applied to the denture. Pharmocology: Nystatin and Amphotericin are polyene antifungal drugs. They bind to ergosterol- main component of fungal cell membranes forming transmembrane channel that leads to monovalent ion (k, Na,H and Cl) leakage. Leading to fungal death. Can cause cellular toxicity. Miconazole: ergosterol fungal cell wall inhibitor. Also works against some bacteria. Can cause burning, itching or irritation, stomach pain, nausea and fever. Daktarin (trade name). C/I in hepatic impairment (liver disease) Denture stomatitis: found exclusively around fitting surfaces of the denture, caused by poor, loose fit, inflammatory exudates enhance adherence of candida on surface but do not penetrate acrylic. Miconazole gel can be directly applied. Better denture hygiene- leave out at night and clean mechnically, soak (if acrylic) in 0.1% hypochlorite. Soak if Cobalt CR 15mins twice daily CHXD.

3.1 Pseudomembranous candidosis (thrush): Description:

Causes:

White creamy plaque, distinctive feature- can be wiped off easily. This reveals raw mucosa.

Diseases effecting oral flora conditions in mouth: Immunocomprimised are susceptible- diabetes (due to reduced function of immune cells), Aids (reduced number of CD4 cells). Anaemia and xerostomia patients Those receiving anti bacterial drugs have altered microflora sometimes favouring candida. Histology: Candidal hyphae penetrate epithelial cells, inflammatory exudate and neutrophils in area. Management: Topical antibiotics miconazole and fluconazole- or antifungals nystatin/ amphotericin lozenges. If no change suspect HIV

3.2 Erythemateous candida Description:

Red dotted and painful hard and soft palate highly suggestive of HIV sufferers Candida in HIV sufferers

Causes: Histology: Management: Itraconazole

3.3 Chronic hyperplastic candiadosis Oral and white lesions occurring from C. albicans. Presents as apersitant white plaque that cannot be scrapped off. Smoking and continous denture wear are main factors. Can be linked to reduced immunity. Can also carry increased risk of malignancy. Biopsy is essential. Systematic fluconazole can be used to treat. Clinical features: dense white nodular patch, buccal mucosa near angle of mouth. Bilateral and associated with smoking poor denture hygiene. Description:

White fixed lesion- hyphae become entrenched, at commisures of mouth Associated with chronic infection of candida

Causes: Histology: Management: Miconazole to treat

3.4 Angular stomatitis Candida alone, bacteria alone or combination of candida and staphylococcus aureus, Beta haemolytic streptococci can cause angular stomatitis. Fungal origin: Antifungals – miconazole, hydrocortisone cream (miconazole has antibacterial properties) S. aureus shown by classic yellow crusting: mupirocin or fusidic acid are appropriate. Iron deficiency is a significant aetiological factor as is loose dentures with to much free way space. Description: Cracking white patch at side of mouth Causes: Associated with leakage of saliva from candida diseased mouth. Common to denture wearers suffering from denture stomatitis. This is caused by lack of saliva contact to denture bearing surfaces. Histology: Management: Nystatin or miconazole

3.5 Candida infections Summary Pseudomembranous candidosis (thrush) cream white plaque, wiped off easily to reveal raw mucosa. Associated with immunodeficiency- diabetes/ aids, immunosuppression- steroid inhalers, Anemia, broad spectrum antibiotics disturbing normal flora, xerostomia. Common to HIV carriers immunosuppressed. Biopsy smear shows gram pos hyphae. Atropic/ erythemateous candidosis: red dotted and painful. C.albicans in HIV patients. Itraconazole is effective. Chronic hyperplastic: white lesion fixed, comissures of mouth and tongue. Associated with chronic infection with candidal species. Likely in smokers. Angular chelitis: cracking white patch at side of mouth- treat with nystatin/ miconazole cream. Chronic erythemateous (denture stomatitis): red palate and denture covered mucosa. Mucocurtaneous candidosis: initially thrush, eventually resembles hyperplastic condition. Can be familial, diffuse type (warty appearance oral and fingers) and endocrine.

Median rhomboid glossitis: diamond red oval behind the circumvillate papilla on tongue. Treatment: For fungal candidosis (pseudomembranous, erythemateous, chronic hyperplastic) Use amphotericin B, nystatin or miconazole systemic fluconazole or itraconazole (if immunosupressed). angular chelitis: Cream nystatin/ miconazole

4

Viral infections of the mouth

4.1 Acute hepatic stomatitis Herpes simplex virus usually contracted in many peoples lifetimes especially during teenage years. Primary HSV characterised by flu like symptoms that precede onset of oral lesions by 2-3days and severe ulceration on keratinised and non keratinised mucosa. Gingival is red and painful. Small vesicles that develop in clusters and break to reveal ulcers. Clinical course is 14 days with complete resolution of signs and symptoms. Diagnosis by hist and clinical evidence. viral culture and direct fluorescent anti body testing in the ulcers confirms. Positive serology for HSV IgM antibodies signifies primary exposure. IgG for previous exposure. Can become latent in trigeminal ganglion and be triggered y stress, sunlight, trauma. Secondary infections occur on the lips. Description:

Causes:

Type 1 : cold sores Type 2: genital manifestation Clinical features: vesicles on palate and ulcers on tongue. Fever, malaise and swollen lymph glands Vesicles dome shaped 2-3mm, rupture to leave painful ulcers Viral infection causing vesiculating stomatitis. Sometimes subclinical- herpes labialis (lip blisters/ cold sores) Diagnosis confirmed by antibody rise 2-3weeks

Histology: Management: Aciclovir is used to treat- potent anti hepatic medicine. Can be topically applied to herpes labialis

4.2 Herpes zoster Infection is primarily chicken pox then virus becomes latent in the spinal dorsal root ganglia. Reactivation by shingles can develop at any time. Significant complication is postherpatic neuralgia. Characterised by burning neuropathic pain. Description: Causes:

Chicken pox and later shingles- small red ulcers at skin level relevant to ganglions Viral infection by VZV – varicella zoster virus Causing chicken pox and can be reactivated as shingles

Histology: Management: Self managing

4.3 Hand foot and mouth disease Cocksackie A virus causing oral lesions and small red macular rash resolving in a week.

4.4 Herpangina Cocksackie virus type A with small ulcers, soft palate and tonsils affected and painful. Sore throat fever, heals after a week. Children highly affected.

4 .4 Human papillo virus: Large group of virus’s over 100 subtypes. Aosicated with benighn and malignant epithelial growths. Transmition by direct contact and prevalence in the population is estimated to be at least 50%. Common subtypes associated with benign mucosal proliferations 2, 4, 6, 11 ,13 and 32. Characterised by well defiened epithelial proliferations pink to white in colour 0.1-1cm pebbly wart like surface. Lesions need to be biopsied to rule out malignancy. Management by excision or cryogenic freezing.

Case 1: loose dentures, anaemia, GTN spray, smokes, angular chelitis and denture stomatitis. Nystatin resistant so other anti fungals needed. Anaemia, steroid spray and smoking predispose candiadosis Case 2: white patch, asthma sufferer – needs further diagnosis- biopsy and if patch rubs off. Probably thrush. Case 3: dry mouth, sore ngles, white patches at corner of mouth, hypertension, atenol (dry mouth) and warfarin (cannot use miconazoles), smoker and drinker. Wipe to see if patch stays or pathc is wiped off, biopsy shows active hyphae so rules out malignancy. Hyphenated so use systemic. Case 4: herpes labialis, transmitted by sister, bites fingers and this has transferred. Hepatic whitlo (is the transfer of HSV to finger) primary gingival herpatonemia Viral infections: 1. Difference between type 1 and type 2 HSV virus. 2. Key features of acute hepatic gingivostomatitis are: I/O and E/O and rise in serum…………. correctly diagnoses it. 3. Treatment: 1……….. or 2………… 4. How does acyclovir work 5. Herpes labialisis reactivates due to triggers: 6. More potent treatment than acyclovir 7. Herpes zoster caused by ……….. virus and causes……… 8. Can be reactivated causing ……….. 9. How does shingles manifest itself, which treatment:………….. can affect which trunks of trigeminal 10. A) Coxsackie virus key features: B) Herpangina key features 11. Differences between herpangina and HFMD 12. Which type of coxsackie virus causes which disease?

5

Oral swellings

5.1: types of swellings and definitions Developmental: Inflammatory: Traumatic: Neoplasms: Fibro osseous lesions: Hormonal: Drug induced:

Unerupted teeth, boney torus Abscess, granuloma Denture induced granuloma, irritation induced epulide Benign epulides Fibrous dysplasia Pregancy epulides phenytonin, ciclosporin, Ca channel blockers

Definitions: Hyperplastic swelling- response to a stimuli under normal regulatory mechanisms Neoplastic: response to abnormal regulatory mechanisms- leads to cancer/ malignant swellings Granuloma: inflammatory response causing a nodule

5.2 Fibrous polyp, epulides and denture induced granuloma Nodule due to irritation. Causes: hyperplastic response to chronic irriation- denture, sharp filling, fractured tooth. Clinical features of different types: 1. Leaflike fibroma: looks like a leaf and is usually found under denture bearing surface. 2. Fibrous epulide: (epulide means of gingival) found between teeth. Can ossify (bone growth) 3. Denture induced granuloma Histologically: consist of irregular connective and fibrous tissue covered by hyperplastic epithelium Treatment: excised and send for biopsy.

5.3 Giant cell fibroma: Proliferation of scar tissue, painless and contains mono nucleate and fibrous tissue bundles. Treatment- excise.

5.4 Papillary hypoplasia: Nodular overgrowth of the palate seen under dentures. Trauma and infection exacerbate. Histologically- fibrous over growth and hyperplastic epithelium Treatment: fix causative factor- treat infection and repair/ remake dentures

5,5 Pyogenic granuloma and pregnancy epulis Bright red / brown/ purple swelling containing many blood vessels on gingival. Pregnancy epulis is a similar swelling on gingival caused by hormonal imbalance of pregnant female.

5.7 giant cell epulis Purplish swelling found on gingival between teeth. May be relayed to Histology: numerous multi nucleate cells in vascular stroma covered in stratified squamous epithelium. Treatment: excised

5.8 benign epithelial tumour Squamous cell papilloma- cauliflower like appearance vascularised core, HPV associated sometimes.

5.9 Verruca vulgaris Oral warts in children similar to papilloma and seen in immunocomprimised patients. Result from auto inoculation from hands. 1. Types of developmental swellings? 2. Types of Inflammatory swellings? 3. Drugs that can induce swelling: (3)- gingival hyperplasia 4. Other types of swellings? 5. What is a granuloma? 6. Define hyperplastic and neoplastic 7. Hyperplastic hardening due to trauma- non malignant. What is it called if on the gingival? What types of things can cause the trauma? 8. Flat leaf shaped swelling is called? And found under? 9. Giant cell fibroma is caused by what? Is it painful and what is found in it histologically? 10. Bright red raspberry coloured swelling, highly vascularised and found in pregnant women? 11. Which quadrant and what colour is a gaint cell epulis? Occurs when traumatised 12. Benign epithelial cell have what type of appearance and which virus is associated? Also called papilloma. 13. Oral warts in spread from hands of child to mouth.

6

Cysts and granulomatous disorders

Cysts Most common form of swelling in the mouth. Cyst = fluid filled epithelial lined. Grow slowly displacing teeth, they are compressible and are symptomless until they become infected. Mechanisms of growth- epithelial proliferation, internal hydraulic pressure and bone resorption. Classification: location, cell type and pathogensis Show as radiolucency but can be differentially diagnosed: Anatomical structures like the antrum or foramina, pseudocysts, neoplasms, gaint cell granulomas of the jaw and hyperparathyroidism.

6.1 Radicular cysts: (swelling of the root) Radicular cyst

Dentigerous cyst

Clinical features:  Adult onset, more common in males (3:2), more common in maxilla (3x)  Centre on root of non vital teeth  Progressive pain from swelling, if infected can expand from odema and become more painful  RESIDUAL CYST- mandibular premolar region Pathogenesis. Derived from periapical granuloma containing epithelial rests of malassez. Epithelial lining becomes hyperplastic and collagenous fibrous capsule proliferates, inflammatory exudates hydrostatic pressure and bone resorbing prostaglandins E2 and E3 expand the cyst. Treatment: enucleation- dead tooth extracted, mucoperisteal flap opened, cyst carefully separated wholly and boney cavity wall smoothed off. Disadvantages of enucleation: recurrence due to incomplete enucleation, haemorrhage, damage to vital teeth, opening of antrum, fracture of jaw.

6.2 paradental cyst Results around partially erupted teeth – mandibular third molar- affects males 20-25 and causes intense inflammation.

6.3 dentigerous cyst Attached to neck of a tooth and usually engulfing the tooth prevents eruption and displaces tooth. Results from a dilation of dental follicle- cyctic change in the enamel organ after enamel formation is complete, it also retains enamel epithelial lining. Twice as common in males and arises from cystic change in enamel organ after enamel formation. Frquently found around the mandibular third molar.

6.4 Eruption cysts Form over erupting teeth, soft tissue cyst arising from enamel organ epithelium. Treatment – remove cyst roof to allow eruption.

6.5 Odontogenic Keratocyst Frequently symptomless, discovered on dental examination or radiography. Tooth displacement and occasional paresthesia of lower lip. Found in the angle of the mandible. Daughter cysts can be found within the main cyst capsule is a well recognised finding. High recurrence rate- enucleation must be thorough. Marsupialisation wont help.

6.6 residual cyst: Well defined similar to radicular cyst but occurs on lower mandible, premolar region. Doesn’t have characteristic strands of epithelium extending into the capsule.

6.8 Solitary bone cyst: well defined but non corticated radiolucency. Little affect on adjacent structures and arches up between roots of teeth. Cyst lined with fibrovascular tissue, includes haemosiderm and multinucleate giant cells. Anuerysmal bone cyst benefits from curettage. However it may be associated with second pathological lesion such as vascular malformation.- needs to be managed in hospital due to the risk of complication. Radiographically: cysts have well defined margins peripheral cortication (radioopaque margin, infection causes loss of this margin. Shape- most grow due to hydrostatic mechanism so therefore grow in a circular shape.

Treatment: Enucleation: removal of whole cysts surgically and capsular layers from bony walls of the cavity. Large mucopersteal flap is raised (usually buccal). Primary closure undertaken unless heavily infected in which case Bismuth Iodoform Parrifin paste is applied on ribbon gauze. Enucleation of nasopalatine cyst requires raising a palatal flap. This damages the nasopalatine nerves and vessels and results in small area of paresthesia. Marsupliasation: simple operation performed under LA in which a window is cut into the cyst allowing decompression which slowly heals by bone deposition in the base of the cavity. Oral mucosa is suture to the cyst to keep open. The cavity must be filled with BIPP and frequently replaced to prevent debris trapping. This is indicated when cyst is so large its enucleation could cause a jaw fracture or if it is in close proximity to ID canals, sinus’s.

Granulomatous disorders: Investigation- deep mucosal biopsy needed for diagnosis because granulomas may be seen in the underlying muscle. Granulomas are non-caseating, consist of mononuclear macrophages, epitheloid macrophages and langhans giant cells. Lympoedema, dilated lymphatic channels and scattered chronic cells found in the lamina propria often in small channels. Causes: Foreign body: found around implanted materials such as retained sutures, restorative materials and vegetable pulses causing proliferative periostitis. Orofacial granulomatosis: Crohns disease: oral manifestations are diffuse swelling of top lip, cobblestone mucosa, mucosal tags resembling irritation hyperplasia, angular chelitis, aphthous or deep slit like non healing ulcers, granular gingivitis. Glossitis related to maematinic deficiency. Sarcoidosis: multisystem chronic granulomatous disorder affecting predominantly young adults. Pulmonary lymph node, skin, salivary and eye lesions are most common. Oral lesions present as submucosal nodules erythema or granular gingival patches. Wegeners granulomatosis: autoimmune vascilitic disorder. Strawberry hyperplastic gingival lesions, palatal ulceration and delayed healing may be presenting signs antineutrophil cytoplasmic antibodies ANCA can be detected in the circulation. Histopathologically, fibrinoid necorsis of vessels, dense chronic inflammation of infiltrate and multi nucleated giant cells may be found.

7.0 Common Oral ailments, Antibiotics and their prescription: 7.1 Dental abscess: Use anti bacterials 5 day treatment: 1. Amoxillin 250 mg TDSx 5-7 days (C/I- penecillinin allergy/warfarin/ contraceptive) 2. Penecilin 250mg QDS x 5-7 days (C/I if allergic) 3. Metronizadole 200mg TDS x 5 days (C/I warfarin and alcoholics) 4. Erythroycin 250mg QDS x 5 days (C/I warfarin) Contains bacteria- viridans, streptococucuss and gram negative bacteria. Indications- major pain, LA doesn’t affect, spread to lymph nodes or systemic spread- fever. Symptoms: Severe pain, disturbs teeth, TTP. Signs: Tooth extruded, mobile TTP,. Localised or diffuse swelling. Widening of PDL apparent on xray. RX: drain pus and relieve area from pressure. Either enter pulp if periapical pathology or drain via incision. When systemic involvement- lymphadenopathy or pyrexia/ fever use antibiotics. Diagnosis between perio

7.2 ANUG and pericoronitis Use anti bacterials 3 day treatment 1. Amoxillin 250 mg TDSx 3 days (C/I- penecillinin allergy/warfarin/ contraceptive) 2. Penecilin 250mg QDS x 3 days (C/I if allergic) 3. Metronizadole 200mg TDS x 3 days (C/I warfarin and alcoholics) 4. Erythroycin 250mg QDS x 3 days (C/I warfarin) ANUG- soft tissue necrosis, ulcers on interdental papilla, lymphodenitis and pain. Gingival connective tissue invaded by spirochetes, p.intermedia, fusobacterium nucleatum- stress, environmental and systematic stressorsimmunocomprimised (HIV/ AIDS). Mechanical debridemnet and OHI. Pericoronitis- when 8s impacted and cause plaque and bacteria traps. Can result in spontaneous pain, localized swelling, purulence/drainage, foul taste in mouth and major problems associated with bacterial infection. Treat via debridement, irrigation and antibacterials.

7.3 Fungal infections (candida) Use anti fungals 7 days: 1. Fluconazole 50mg od x 7 days (C/I warfarin/ statin users) 2. Miconazole 10ml topical QDS x 7 days (C/I warfarin and statin users) OR 3. Amphotericin 10mg lozenge OD x 7 days 4. Nystatin oral suspension 1ml QDS x 7 days Pseudomembranous candidosis and erythemateous candida- cause- opportunistic candida albicans infection patients using corticosteroids, cytotoxics, broad spectrum anti biiotics, diabetics nutritional deficiencies and sustemic diseases/ immunocomprimised.

7.4 Denture stomatitis (induced candidal infection)   

Use anti fungals as above. Clean dentures with chlorahexedrine or sodium hypochlorite (C/I cobalt chrome) Leave dentures out at night.

7.5 Angular chelitis   

Candida infection at side of lips causes pain, redness and cracking Miconazole used vs candida and gram positive cocci. Miconazole 25 cream BD x 10 days

7.6 Herpes Simplex Aciclovir 200mg x5 x 5 days (double for immunocomprimised) Aciclovir cream 5% (type 1) QDS x 5 days Sympotamtic releief: bed rest, nutriotional guidance, bed rest, analgesics

Pharmacology: Classification: bacteriostatic (arrest bacterial multiplication sulphonamides, tetracyclines and chloamphenicol), bacteriocidal (kill bacteria- penicillins, cephalosporins, aminoglycosides, isoniazid and rifampicin) ImportantMIC minimum inhibitory concentration – amount it takes to inhibit growth at site of infection. PAE post antibiotic effect- suppresses growth until next dose Mechanism of action:  Cell wall: B lactams-contain B lactam ringo Penicllins: inhibits enzymes (penicillin binding proteins) involved in crosslinkingof peptidoglycan layer of cell wall which protects bacterium. Benzylpenicillin is destroyed by gastric acid, half life of 2hrs, secreted in kidneys. o Clavulanic acid- mechanism based B-lactamase inhibitor which when combined with penicillin over comes antibiotic resistance. Works by suicide inhibition- helps to inactivate the enzyme responsible for making B lacatamase resistant to antibiotics. o Cephalosporin  Cytoplasmic membrane: o Aminoglycosides- end in mycin- bind to ribosomes and cause incorrect sequencing of peptide chains causing deadly microbes that kill the bacteria. Poor absorption requires IV, eliminated by kidney with 2.5hr half life. Good vs- gram negative- staphylococci. o Tetracyclines-bind to ribosomes interfering with protein synthesis and are bacteriostatic. Partially absorbed through GI tract, active against gram pos and neg bacteria. Can cause hypoplasiaof enamel in developing teeth as has chelating properties to calcium.  Protein synthesis o Sulphonamideso Quinolones: inhibit DNA gyrase preventing supercoiling of DNA- bactericidal. Active against E. coli, salmonella, shigella. o Azoles  Metronidazole: activated theough reduction of nitro group. Binds with nucleic acid acting bacteriostatically. Well absorbed orally. Half life is 8h and excreted through kidneys. Side effects- nausea, vomiting, diarrhoea, headaches, dizziness and ataxia. Disulfram like effect occurs with alcohol- inhibiting aldehyde dehydrogenase.  Nucleic acid metabolism

BNF pharmaceutical guide: Mouthwashes CHXD Hydrogen peroxide

Antibacterials Penicillin based - Amoxillin 250mg every 8hrs, doubled in severe infections, halved for children- 125mg. o C/I- penicillin hypersensitivity, warfarin, contraceptives o Side affects: nausea, vomiting, daihorrea rarely antibiotic colitis - Co amoxyclav- (trade name augmentin) amoxicillin as trihydrate and clavulanic acid. o C/I- penicillin hypersensitivity o Side effects: 1 in 10- diahorrea, 1 in 100- nausea and vomiting reduced if eaten with meals, skin nails and mucous membrane infection.

Tetracyclines: (broad spectrum antibiotic)- deoxycilin better than tetra cycline as longer action and better use against refractory anaerobes involved in destructive perio. Use in RAS, oral herpes and adjunct in perio scaling - Tetracycline: and doxycline o Cautions: hepatically impaired, increase muscle weakness in myathis gravis. Poor absorption with people treated for stomach ulcers- antacids. o C/I- can deposit in bones and growing teeth. – should not be given to children under 12, or pregnant women or breast feeding women. Do not give to patients with renal disease or acute porphyria o Side affects- nausea, vomiting, diarrhoea, dysphagia. Rarer side affects- hepatotoxicity, pancreatitis, blood disorder.

Metronizadole: high activity vs anaerobic bacteria, good for ANUG, pericorontis, suitable alternative in other infections when penicillin/ erythromycin are c/i. o Cautions: disulfiram reaction with alcohol, pregnancy, hepatic impairment, breast feeding, acute porphoria. Warfarin users- increases effects. o Side affects: GI disturbances, furred tongue, oral mucocitis, anorexia, o Dose: ANUG and oral infections- 200mg TDS 3/7,

Options for when first line amoxicillin and metronizadole are contra indicated (erythromycin) or resistant (clinda) Erythromycin indicated for those with penicillin hypersensitivity o Cautions: neonatal, pregnant or breast feeding, acute porphyria, hepatic and renal impairment, warfarin users- increases effects. o Side affects: nausea, vomiting, discomfort, diarrhea, urticia rashes. Rarer- steven Johnson syndrome, o Dose: Clindamycin: active vs gram pos cocci, streptococci and penicillin resistant staphylococci- only used dentally for abscesses non respondant to penecillins or metronizadole. o Cautions: discontinue immediately if diarrheo or coilitis occur o C/I: diarrohea states o Side aeffects: diarrheoa (discontinue use), abdominal discomfort, ulcers, taste disturbances, nausea vomiting, jaundice, leukopenia, o Dose: 150-300mg every 6hrs.

Antifungals miconazole fluconazole o o o o

Cautions: pregnancy, breast feeding, hepatic and renal impairment, acute poryphria C/I: acute porphria Side affects: nausea, vomiting, diarrheao, flatulence, rash

Nystatin Side affects: steven Johnson syndrome, diarrheao, oral irritation, sensitisation amphotericin o Cautions: hepatic and renal impairment, corticosteroids, pregnancy and breast feeding, warfarin. o Side affects: anorexia, nausea, vomiting, epigastric pain, febrile reactions, headache muscle and joint pain,

Antivirals Acyclovir - Caution- maintain hydration, elderly (risk neurological reactions), pregnant and breast feeding - Side affects- nausea, vominting, head aches, photosensitivity

-

Aciclovir: Acts by inhibiting viral DNA synthesis after phosphorylation by virus specific thymidine kinase. It can then inhibit DNA polymerase preventing viral DNA synthesis

Interactions:

9. Oral Cancer: Types of oral neoplasm:  Basal cell carcinoma: locally invasive tumour of epidermal cells affecting skin and face. Causes local tissue destruction but doesn’t spread. 3% of all cancers, male to female ratio 2.5:1, 5 year survival rate 50%  Squamous cell carcinoma: malignant tumour of squamous epithelial origin. In situ (confined not metastatic) and invasive. CF- highly variable, ulcers, reddish swellings, bleeding, raised edged ulcers, on lip it fails to heal/ bleeds, more risk of metaststes (unlike basal cell carcinoma). HPV can cause.  Karposis sarcoma: human herpes virus 8 causes. Curtaneous lesions in oral cav, lymph nodes and viscera. Tissue biopsy to diagnose.  Salivary gland tumours  Lymphoma  Maliganant melanoma:  Metastatic neoplasms from other organs  Odontogenic tumours

Oral cancer book: Malignancies involving the minor salivary glands:  Mucoepidermal carcinoma: most common minor salivary gland malignancy, average age- 43, generally in fifth and sixth decasdes and also most common in children aged 11-16. o Females> males o Asymptomatic, painless, slow growing mass with very little complaint and usually seen on intraoral examination. Usually discovered for 1.5yrs o Can be pigmented- blue, red, purple or magenta resembling vascular proliferations. o Palate most common site o Soft, smooth fluctuant appearance. o Can have a mucous draining site – sinus  Polymorphous low grade adenocarcinoma o Females 2x higher than males, presents at age 58, never seen in first or second decade o Palate most affected site o Can cause dentures to become loose o Non aggressive good prognosis  Adenoid cyctic carcinoma: third most common  Mucosal melanoma:

Types of squamous cell carcinoma Lip Squamous cell carcinoma: etiology- occurs in 25-30% of all carcinoma cases, male females ratio 6:1, age of onset usually 50 and above, caused by carcinogens- UV light, smoking alcohol and immunosuprression. High survival rate90% as quickly diagnosed. Oral Squamous cell carcinoma: caused by smoking, alcohol, Paan/ betel/ areca chewing, viruses. Etiology- 75% of all SCC are located on floor of mouth.  Premaliganant leukoplakia: usually keratosis to irritation (metaplasia), however 20% are premaliganantdysplasia or carcinoma. Different anatomical sites confer different risks- Floor of mouth and side of tongue are 45% premaliganant.  Oral submucosa fibrosis: chronic, complex, irreversible pre cancerous condition. Inflammatory reaction and progressive fibrosis of submucosal tissue. Jaw becomes rigid. Associated with areca nut chewing- main component of betel quid. Mucosa becomes palpable and fibrotic, stiff.  Phenotypical progression of carcinogenesis: epithelium> hypoplasia, mild dysplasia, severe dysplasia, iinvasive carcinoma. (hypoplasia= incomplete/decreased / arrested cell growth, dysplasia= abnormal growth of cells hyperplasia=increased number of cells).

Symptoms: pain, halitosis, paresthesis, anaesthesia, mobility and tooth loss, trismus, restricted tongue movement, weight loss. Referral guidelines:  Undiagnosed lump- recent onset or changed over 3-6 weeks  Unexplained swelling in parotid or submandibuilar gland  Unexplained persistant sore or painful throat  Unilateral eunexplained pain in head/ neck with pain for more than 4 weeks  Unexplained unhealed red/ white patch/oral ulceration 3 weeks. Painful swollen or bleeding. Unexplained tooth mobility- refer to dentist Non urgent: unexplained red/ white patches not painful/swollen or bleeding review in 6 weeks- if still presenturgent referral. Oral SCC- lymphnode involvement: palpable, firm, non tender, fixed. Biopsy: SCC- always refer to specialist unit and perform incisional biopsy Histology: featuresNuclear polymorphism, cellular polymorphism, nuclear hyperchromatism, prominent nucleoli, increased nuclear cytoplasmic ratio and abnormal mitotic figures. Carcinoma in situ: dysplasia in epithelium (abnormal cell growth), aytipical cells present, no invasion. Histological grading: pattern of invasion, perineural invasion, peri vascular invasion, degree of differentiation. More tumour closely resembles normal Tumour staging: TNM- tumour, Node involvement and metastasis: T- tumour size: TX, Tis (in situ), T1 <2cm, T2= 2-4cm, T3= >4cm N- Lymph node involvement: M- distant metastasis- M0 (none), M1 (pesent) TNM stage I: 85% 5 year survival rate, TNM stage II 65%, TNM stage III 40%, TNM stage IV 10%

Radiation therapy and dental disease: causes radiation induced hyposalivation: causing rampant caries, buffering rate is far reduced as less HCO3, favours survival of cariogenic S.mutans and lactobacilli, which are aciduric and acidogenic, undersaturation of teeth with hydroxyapaptite and mechanical cleansing affects of saliva.

Specific destruction to dentin affects at the dentino enamel junction leaving the CEJ blackened and soft. Requires remineralisation using fluoride trays, fluoride mousses, but do not use alcoholic based mouth washes as will cause burning sensation in mouth.

characteristic radiation caries- black rings around CEJ Xerostomia and Mucositis following radiation therapy.

Manifestation of radiation toxicity on rapidly proliferating cells in the basal regions of the epithelium. Decreased cell regeneration leads to epithelial atrohyand mucosal thinning. Erythema and desquamative patches occur which are extremely painful.

Ulcers Recurrent aphthous stomatitis: common disease affecting 10-25% of the population Aetiology: unknown- certain factors are thoerised to be the cause:  Genetic factors: family history can be strong factor  Trauma: patients may think trauma but it actually occurs in more protected areas of the oral cavity.  Infections: no evidence that apthae are directly due to microbes or herpes  Immunological abnormalities: Many theories but not an autoimmune condition. Also fail to respond to immunosuppressants and become more severe in immuno defficent state in HIV sufferers  GI disease: rarely associated with GI disease. Association only by dietary deificency Haematological deficiency: in vit B12, folate and iron reported in 20% of patients. Deficiency is latent, haemoglobin within normal limits and the main sign is micro and macrocytic anemia. Remedying the deficiency remedies the ulcers.  Hormonal factors: associated with stressful luteal phase of menstruation  Stress: can relate exacerbations to periods of heightened stress.  HIV infection: aphthous stomatitis a recognised feature of HIV infection.  Non smoking: exclusive disease to non smokers. Smoking has a systemic protective action against the disease. Clinical features: frequency of ulceration peeks in mid life, rare in the elderly. Great majority of patients clerical, professional. Painful ulcers recurring at intervals of approximately 3-4 weeks. Individual minor apthae persist for 7-10days. Typically affect only non keratinsed mucosa such as buccal mucosa, sulces, lateral border of tongue, major aphthae can effect masticatory muscle. Pathology: initial lymphocytic infiltration followed by destruction of the epithelium and infiltration into tissues by neutrophils. Consistent with type III or IV reactions.   

Minor- most common type, non keratinised mucosa affected, ulcers shallow, 5-7mm one or several present. Major- uncommon, several cm across, persist for months, masticatory mucosa, dorsum of tongue affected. Herpitiforme- uncommon, non keratinised, ulcers 1-2mm, dozens- hundreds present, may coalesce, bright erythema around ulcers.

Diagnosis and treatment: Blood tests to look for MCV- macro/ microcytosis present. Vit B12, folate def Corticosteroids: corlan, hydrocortisone hemisuccinate- hasten healing of ulcers. Triamcinolone dental paste: orticosteroid with anti inflammatory action slowly released, gel adheres to ulcers and protects for several hours. Tetracycline mouth rinse: reduces severity and frequency of aphthae. 250mg stirred in water and swirled for 2-3mins three times daily. CHXD: 0.2% solution used three times daily after meals reduces duration and discomfort of aphthaes stomatitis. Topical salicylate preparations: have an anti inflammatory action and local affects. For major aphthae: aziathoprine, cyclosporine, colchicine and dapsone, thalidomide is most effective. Points to consider: Infections that cause ulcers:- HSV, Coxsackie, HIV. Bacterial- ANUG. Drugs that cause ulceration: cytotoxic drugs- methotrexate, NSAIDS, alendronate (bisphosphonate), nicorandil (cardiac- vasodilator for angina). Behcets disease: Ulcerative stomatitis

Facial pain Local disorders Odontogenic Jaw Max antrum Salivary gland pharynx

neurological physcogenic vascular Referred Idiopathic trigeminal Atypical facial pain Migraine Nasopharyngeal neuralgia Burning mouth Migraine neuralgia Ocular Neoplasms on syndrome Giant cell arteritis Aural trigeminal nerve TMJ pain dysfunction cardiorespiratory Glossopharyngeal neuralgia Herpes zoster Multiple scelerosis Nocieptive pain caused by actual tissue trauma and inflammation, neuropathic pain caused by dysfunction of the central/ peripheral nervous system in the absence of injury/ inflammation. Two types of pain: 1. Fast pain: nerve impulses- A-delta fibres myelinated- acute, sharp prickling 2. Slow pain: increases proportionally to stimul in intensity. Conducted along unmyelinated C fibres. Chronic, burning, aching or throbbing. C fibres in the pulp terminate beneath odontoblasts, A fibres traverse odontoblastic layer terminating in dentinal tubules. Classify as dental pain:  Dentine hypersensitivity  Pulpal pain  Periapical pain  Other pains of periodontal origin

Trigeminal nerve info: Three branches: 1. Ophthalmic (leaves skull superior orbital fissue) 2. Maxillary (foramen rotunde) 3. Mandibulary (motor visceral) (foramen ovale) Somatosensory system: touch. Position and pain/ temp 

Touch/ position, fast twitch fibres, sensory receptors (meissners corpuscules, merkels receptors, pacinian corpuscules, ruffinis corpuscules). Pain and temp are bare nerve endings requiring tissue destruction which leads to release of material causing synapse.

Sensory receptor---neurone 1--- sensory nucleus----neurone 2---- thalamus---neurone 3---- cortex    

Each sensory pathway decussates at the secondary neurone. Pain/ temp third neurone is the spinothalamic tract, from the face it is carried by the trigeminothalamic tract. Trigeminal nucleus runs throughout brain stem split into three parts spinal trigeminal nucleus (pain/ temp), main trigeminal nucleus (touch/ position), mesenphalic trigeminal nucleus (proprioceptor and mechanoreceptor from jaw) Spinal trigeminal nucleus: represents pain and temp sensation from peripheral nociceptors carried from CN V, VII, IX and X. it carries this up the trigeminothalamic tract to the contralateral thalamus.

Pain from extra oral diseases Maxiallary antrum disease Acute sinusitis Neoplasms in the ear

Acute parotitis Malignant neoplasms MI radiating pain to jaw

Salivary calculi Diseases of the ear Mumps

Sjogens syndrome Ottit media

Myofacial and TMJ pain Pain can come from dysfunction, trauma, inflammation and tumours. Over use and bruxing can cause pain in the muscles (myofacial pain) with or without joint arthralgia. Pain is dull and aching, radiating down jaw and can be bilateral. If joint and ear pain then arthralgia is suspected. Pain exacerbated by chewing, talking, made worse by osteoarthritis and rheumatoid causing joint inflammation. Masseteric hypertrophy is common and all muscles of mastication should be checked with patient noting tenderness and trigger points for pain. Joint palplated for pain, tenderness, clicking or crepitis. Trismus can be a complication. Treatment: NSAIDS and joint limitation. Avoid eating foods requiring forceful biting and chewing and keep teeth apart whilst chewing. Topical NSAIDS (ketoprofen) and for severe attacks – corticosteroids maybe helpful. Marked arthralgia – intralesional corticosteroid therapy can be effective- triamcinolone acetonide 40mg/mL can be used. Parafunctional activity can be reduced through clonazepa,or lorazepam.

TMJ pain dysfunction: Common problem characterised by pain, clicking and jaw lock or limitation of opening of the jaw. Afflicting young women mainly. Factors implicating – overactivity (bruxism, clenching) TMJ disruption and psychiatric history. Management: spontaneous recovery, reassurance and conservative measures are main management.

Physcogenic: Atypical facial painDiagnosis by exclusion Common features:  Women of middle age  Absence of organic signs  Pain poorly localised  Pain may be bizarre  Delusional symptoms occasionally associated  Lack of response to analgesics  Unchanging pain persistant for years  Sometimes responds to anti depressive treatment Common site is maxillary region or in relation to upper teeth. Localisation may be difficult and unprecise. Pain not usually provoked by any recognisable symptoms. Analgesics completely ineffective. Treatment of diseased teeth doesn’t relieve symptoms. Some patients are depressed, complain of bizarre and delusion type symptoms Treatment: may respond to low dose tricyclic antidepressants, clonozepam, gabapentin. Bells palsy: Common facial paralysis. Results from compression of the facial nerve and its canal as a result of inflammation and swelling. Viral infection, particularly herpes simplex can be suspected as the cause. Either sex affected between ages of 20-50. Though this disease is uncommon in dental practice its recognition is important early diagnosis prevents permanent disability and disfigurement. Function of facial nerve is tested by asking the patient to perform facial movements. Telling features: When asked to close the eyes, lids on affected side cannot be brought together. Eyeball motor rolls up normally- ocularmotor unaffected. When asked to smile lip on affected side is not pulled upwards. (shows lower motor lesion)

Majority of patients recover without treatment. 10% have permament disfiguration. Prednisolone 20mg orally 4x daily can be effective. Acyclovir works better if role of herpes virus is apparent.

Neuropathic Trigeminal neuralgia: characterised by severe unilateral paraoxysmal electric shock like/ short sharp severe stabbing pain. Typically down one division of the trigeminal pain- either second or third division first, but then pain affects both. Pain stimulated by touch of the trigger zone.pain does not transmit to other side. Prognosis: disease goes into spontaneous remission, can go away for weeks or months. Pathophysiology: Vascular compression of trigeminal ganglion thought to be main cause. Osteomyelitis or neoplasm can result in secondary trigeminal neuralgia. Can be a feature of MS- differential diagnosis. Treatment: carbazepine (treats 80%), gabapentin and baclofen. Sometimes combination with phenytonin. Surgical therapies include radiofrequency ablation of the ganglion, nerve blocks and microvascular decompression. Burning mouth syndrome: Characterised by burning dysesthesia commonly affecting the tongue. Also affects inner aspect of lips and anterior hard palate. Majority of patients are peri- and post menopausal women. Some young men affected. Most patients anxiety, depression, panic attacks. Onset of symptoms correlates with major life event inducing stress. Intense severe pain elliviated by drinking/ eating. Pain begins after waking continues through the day and gets more severe in the evening. Altered taste- bitter and metallic often used to describe. Also describe lump in back of throat. Sleeping disturbances are quite common. Diagnosis by exclusion: Oral burning differential diagnosis: - Infection, mucosal disease, uncontrolled diabetes, thyroid disease and haematological disease. First line of treatment especially when sleep disturbances reported- clonazepam (0.5mg) just before bed. Topical clonazepam can be effective as a tablet or gel. All patients should be re- evaluated after one month. Second line agents- gabapentin and tricylcic depressants. Glosspharyngeal neuralgia: (tongue affected) Rare condition characterised by pain similar to trigeminal neuralgia, but felt in the base of the tongue and fauces on one side. Can radiate to ear. Pain is sharp lancinating and transient. Can respond to carbamazipine but not as much and surgical treatment usually needed. Herpatic and post herpetic neuralgia: Herpes zoster (shingles) the recrudescence of Herpes varicella zoster virus latent in sensory ganglia after chicken pox. Presents as neuralgia, unilateral rash and ulceration. Can cause continous burning pain after rash subsides. Different to lancinating (shooting/ stabbing) pain of trigeminal neuralgia. Posthepatic neuralgia: 10% who have trigeminal herpes zoster may get persistant neuralgia. Diagnosis straightforward if history of facial zoster. Unfortunately it is resistant to treatment. Response to nerve root sections and carbamazipine are poor. Large doses of analgesia and transcurtaneous electrical stimulation are sometimes affected. Instrument applied hourly for 5-10mins every day. Multiple scelrosis: minority of patients develop pain indistinguishable from trigeminal neuralgia. 2-3% of those presenting with classical trigeminal neuralgia have MS. Disturbances of sensation linked to sites of lesions in the brain. Lip may be affected and symptoms range from paresthesia to extreme hypersensitivity. Diagnosis rests on presence of MS especially with vision disturbances, muscle weakness and sensory loss. Carbamazipine sometimes effective. Sometimes surgical intervention required.

Vascular causes of orofacial pain: Migraine, migrainous neuralgia, giant cell arteritis. Migrainous neuralgia: (cluster headache) Caused by vascular changes at the base of the skull and may occasionally be mistaken for trigeminal neuralgia. Due to odema and dilation of the wall of internal carotid and probably external carotid arteries. Attacks 3 times a day.

Effect mainly men, up to 50 yrs. Precipitated by alcohol and vasodilators, can recur at night. Duration 0.5-2hrs. vascular changes in the face- suffused eye, blocked nostrils, sweating. Can spontaneously remission and patient fine for months and years. Differential diagnosis- trigeminal neuralgia, migraine (should have vomiting and nausea) Responds to simple analgesics- ergotamine 2-3 times daily.

TMJ clinic Masticatory system is a trio of tooth tissue, perio and articulatory system. Articulatory system- muscles TMj and occlusion Hinges, motors and contacts Exam: 1. Check TMJ: finger on joint- lateral aspect of condyl and check tenderness to palpitation 2. Little finger interauricularly- (into earole) check TTP 3. Listen for click or crepitus 9ontinuous crackling). Qualify which side click is on, whether soft loud, multiple clicks or whether on opening/ closing 4. Measure incisive edge to edge when mouth fully open 5. Opening pathway- straight, deviated.  Lasting devisiation (manible in left or right of midline at full opening) suggestive of a permanent obstruction in TMJ could be displacement without reduction  transient deviation (mandible deviates but returns to midline) both condyls finish in same place but take different paths. Disc reduction with reduction 6. muscles:  role massetter using two digits in and out of mouth, role muscle in and out of muscles for tenderness.  Check temporalis anterior and posterior fibres on side of head  Resisted movement test- check lat slide of jaw teeth apart and resist by pushing mandible back to middle- should hurt on opposite side 7. Check centric occlusion, lift chin fingers on lat aspect, fall open jaw relax muscles and find premature contact in premolar region.  Centric occlusion: or ICP describes how teeth fit together  Centric relation: RCP, jaw relationship, relation between maxilla and mandible. 8. Check anterior guidance, articulation paper one colour in ICP and another in RCP 9. Check centric relation and centric occlusion relationship – get patient into RCP Reduction means back into original placeDisc displacement without reduction: disc out of normal range of motion and doesn’t fit into proper place/ original position. Patients have a lot of muscle spasm causing disc not to return to normal position. To get back, muscle relaxants temazepam at night can unlock the disc displacement this is a lot less painful and can be treated with physio Disc displacement with reduction: (moves back to original position) patient has click and undergoing physio. Click becomes intermittent and displacement disappears. TMj information from occlusion manual: Signs and symptoms of TMJ:

    

Pain and tenderness in and around the TMJs and muscles of mastication. Limitation and incoordination of jaw movement Joint sounds – clicking and crepitus Headaches Tinnitus

Function makes symptoms worse- patients have difficulty eating or simply talking. A common misconception is that problems with the occlusion are a principle cause of TMD- this is only the case in some patients. 20% of population experience clicking but only a few have problems Multifactorial: Predispose: genetic, hormonal, anatomical Precipitate: trauma, occlusal changes and parafunction Prolong TMDs- parafunction and physcological stress Systemic: fibromyalgia (generalised muscle pain), systemic joint laxity (collagen defect straining ligaments) and rheumatoid arthritis- around half of patients experience pain in their jaws. Three diagnosis need to be made:  Group I: muscle (myofascial pain)- muscle tenderness on palpation  Group II: disc displacement with/out reduction with clicking or locking  Group III: TMJ pain and degenration o Arthralgia (joint pain): characterised by local TMJ tenderness o Arthrosis(degeneration of bone surfaces): characterised by crepitis o Arthritis: characterised crepitis and TMj tenderness

Treatment of TMDs: Counselling, self help, physiotherapy and jaw exercises, analgesics, occlusal splints Occlusal splints: Made using acrylic fitted to teeth in either jaw  Partial coverage splints: not recommended as they produce unwanted tooth movement and occlusal changes.  Soft splints: produced from heat or vacuum formed vinyl.mechanism of action unclear. Can make discomfort worse, esp if deflective contacts or interference.  Stabilisation splint: cover the cusps and provide a flat surface allowing the mandible to find a comfortable position without deflective contacts. Allows condyls to rest fully in the glenoid fossae in the hinge axis. Splint provides canine guidance and posterior disclosure on lateral excursion. Stabilastion splint- 2week review appointment check even occlusion and smooth but shallow anterior guidance with articulation paper. Encourage as much use as possible, continue with two week adjustments.

Anterior positioning splint: recaptures an anteriorly placed disc

Systemic diseases and oral implications Aneamia:  Glossitis: sore tongue- inflammation and atrophy of filiform papillae. Any sore tongue should be investigated with hemotynics, FBC and deficiencies should be followed up.  Angular stomatitis  Recurrent apthathae: particularly B12 and folate  Infection: candidiasis and angular stomatitis are classic signs of iron deficiency. Carry a risk in GA as sortage of oxygen can be dangerous. Patients also carry a risk of infection. Iron deficiency (microcytic hypochromic) Pernicious (vit b12 def) anemia (macro) Folate deficiency (macro) Leukaemia:- overproduction of white cells, suppress erythrocyte production, raise susceptibility to infection due to leukocyte abnormality/ deficiency, bleeding tendency (papura) due to suppression of platelet production. Dental affects:  Gingival swelling: resulting from lack of mature white blood cells to counter gingival infection. Gingivae can become purplish and gingival hyperplasia can occur.  Mucosal ulceration: combination of immunodefiency and cytotoxic drugs like methotrexate. Herpatic infections and thrush are common.  Leukaemic deposits: tumour like deposits of leukaemic cells form in the mouth.  Purpura - bleeding: can appear as excessive gingival bleeding purplish mucosal patches, blood blisters or bleeding after surgery.  Cervical lymphadenopathy Sickle cell: Thalessaemia AIDs: 75% of patients with HIV have orofacial diseases. – frequently hairy leukoplakia, erythemateous candida, karposis sarcoma and oral ulcers.

Lips and FOM

history: PCO- aesthetic swelling no pain comes and goes- mucele

ranula

Palate:

massive pain, fluctuant, not solid periapical abscess

MH: no pain, hard boney s swelling been there for long time, boney torus

lymphoma palate, soft painless swelling hard/soft palate junction brought on by Epstein bar/ HIV usually older patient rx- radiatiotherapy

basal cell adenoma

pleomorphic adenoma

muco epidermoid carcinoma

adenoid cystic carcinoma

79yr cuacasian, poor OH, new growth

lesion doesn’t rub off, sexually active young male, doesn’t rub off with no fever

Lesions based on colour change

many, painless, small yellow, Fordyce

white line, keratosis, occlusal/ linea alba

new white lesion since filling/ associated with bitingtraumatic keratosis

smoker, prominent patch top of mouth smokers keratosis

verrucus carcinoma

red blood like colouration, no blanching, occurs after trauma, red, purple then yellow brown. (purpura, hematoma – large bruise)

erythroplakia

erytholeukoplaia

SSC

speckled erythroplakia

SSC

Lreticular LP

erosive LP

Atrophic LP

plaque form LP

LP extra oral- skin, nails, genitalia

lupus discoid and

steroid user candida

denture wearer

papillary hyperplasia

amalgam tattoo

melanoplakia

melanoma

Swellings

tori

extoses

osteoma Osteomas- benign neoplastic growth distinct from developmental lesions (tori) due to size, rapidity of growth. Can be periosteal osteoma from the outersurface of the bone (periosteam), or from the inside of the bone- medullary tissue- endosteal osteomas. Well defined smooth hard, radiodense structures, well defined smooth borders. Multiple osteomas suggests presence of gardners syndrome – large chromosome 5 – osteomas, dermal cycts multiple impacted supernumary teeth and odontomas. Bowel polyps with high propensity for malignant change.

irritation fibroma- common benign swelling in the mouth. Reactive hyperplasia to chronic irritant. Well defined pale pink nodule, smooth symmetric round and firm and painless. If repeatly traumatised it could be ulcerated and have white keratosis. Contains bundles of collagenous material covered by thin epithelium. Treatment through biopsy and surgical excision.

Giant cell fibroma- similar signs to irritation fibroma but without irritant and contain polynucleated stellate shaped fibroblasts.

human papilloma: Most common benign epithelial neoplasm, small pink-white, painless mass <1cm. Smooth pink surface or may have fingerlike projections. Intra-oral lesions soft but keratin producing lesions are rough and scaly. HPV virus found in 50% of papillomas. Verruca vulgaris

wart like seen on fingers and then spread to oral cavity through contamination. Up to page 162 colour atlas of disease

Xerostomia Physiological Irradiation Diseases effecting glands Complications ofxerostomia Diagnosis Why blood test Eye test called Imaging to detect? Sjorgrens more likely in By how much Oral changes Parotid swelling in how many Primary- associated with Secondary associated with, incidence in this group Difference in anti bodies and factors Diagnosis by... measurement.... Histologically what causes what and how does it progress Treatment primary xerostomia problems and secondary problems HIV associated gland disease – difference in what 3 types of obstructive gland disorder Sialadenosis/ sialisis systemic causes Classic presentation Which gland histologically Sialadenitis presents as Acute sialenditis has two causes Signs and symps of first Signs symps and treatment of the second Chronic sialendenitis bacterial Radiation sialendenitis Sialothiasis is what Which gland most likely and why Sialothiasis Presentation Treatment Mucocele usually found.... caused by...., lasts for....., colouration due to What happens to it? Ranula presents where How to treat ranula Mucus retention cyst difference to mucocele caused by treatment common sites salivary gland tumours common site? Benign/ malignant ratio Pleomorphic adenoma Clinical presentation Treatment

Warthins tumour Adenoic cystic carcinoma Mucoepidermal carcinoma Polymorphous low grade adenocarcinoma Leukodema common in what population and what percentage Frictional keratosis (linea alba) caused by? Smokers keratosis looks like Hairy tonguecaused by If burning what does this show HIV associated hairy tongue presents where on the tongue, differential diagnosis is