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BDS4 > Oral medicine > Flashcards

Oral medicine Flashcards

1
Q

Give a diagnosis of a middle-aged female complaining of a burning mouth with diffuse erythema.

A

Oral dysesthesia
Could be candida?

Abstract. Oral dysaesthesia is a condition characterised by persistent alteration to oral sensation, perceived by the patient to be abnormal and unpleasant, in the absence of mucosal pathology. Its aetiology remains uncertain.

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2
Q

Diagnosis for a middle aged man with dull throbbing pain in the maxillary region made worse by bending over?

A

Sinusitis

Sinusitis is a common condition in which the lining of the sinuses becomes inflamed. It’s usually caused by a viral infection and often improves within two or three weeks. The sinuses are small, air-filled cavities behind your cheekbones and forehead.

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3
Q

Diagnosis for unilateral episodic pain lasting 20mins, nose dripping and worse when shaking head?

A

Cluster headache
But think answer is Paroxysmal hemicrania

Cluster headaches are excruciating attacks of pain in one side of the head, often felt around the eye. Cluster headaches are rare. Anyone can get them, but they’re more common in men and tend to start when a person is in their 30s or 40s.

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4
Q

Diagnosis of Elderly patient with shooting pain in right cheek when bitng and lacrimination?

A

Trigeminal neuralgia or cluster headache

Trigeminal neuralgia is sudden, severe facial pain. It’s often described as a sharp shooting pain or like having an electric shock in the jaw, teeth or gums.

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5
Q

Diagnosis of temporal and weakness of shoulder muscles

A

Temporal arteritis

Temporal arteritis (giant cell arteritis) is where the arteries, particularly those at the side of the head (the temples), become inflamed. It’s serious and needs urgent treatment.

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6
Q

Mrs Patel is a 45-year-old patient who is new to your practice. She is fit and well but complains of some soreness in her right cheek which she has had for a number of years. Your examination reveals a reddened area of buccal mucosa with a white lacy edge immediately adjacent to tooth 47. This tooth is almost entirely restored with a perfectly sound amalgam and is the abutment for rest seats and claps on a cobalt chrome partial denture which Mrs Patel has worn happily for the past 5 years and has a bleeding 6mm mesio-buccal pocket with associated grade I mobility. A periapical radiograph of tooth 47 reveals some mesial bone loss but no periapical pathology. All the other teeth are sound or minimally restored with composite and the partial denture is well fitting.
1. What are your provisional diagnosises? (4)

A
  • Traumatic lesion
  • Lichenoid reaction to amalgam or CoCr
  • Chronic peridontal disease
  • Lichen planus
  • Hypersensitivity
  • Oral cancer SSC
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7
Q

Mrs Patel is a 45-year-old patient who is new to your practice. She is fit and well but complains of some soreness in her right cheek which she has had for a number of years. Your examination reveals a reddened area of buccal mucosa with a white lacy edge immediately adjacent to tooth 47. This tooth is almost entirely restored with a perfectly sound amalgam and is the abutment for rest seats and claps on a cobalt chrome partial denture which Mrs Patel has worn happily for the past 5 years and has a bleeding 6mm mesio-buccal pocket with associated grade I mobility. A periapical radiograph of tooth 47 reveals some mesial bone loss but no periapical pathology. All the other teeth are sound or minimally restored with composite and the partial denture is well fitting.

  1. What additional investigations could be undertaken and how would you arrange these? (6)
A
  • Incisional biopsy to be sent to the lab for histopathological examination and testing
  • Blood tests - FBC, haematinics, random Blood glucose test (refer to GMP for this)
  • Clinical photographs to teack the lesion
  • 6PPC and MP&BS (Chronic perio disease)
  • Patch testing - for allergy to CoCr as well as benzoate etc (refer to GMP or dermatology)
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8
Q
  1. What are Mrs Patel’s options for management of these problems? (10)
    - Traumatic lesion
    - Lichenoid reaction
    - LP
    - Chrnoic periodontal disease
A
  • If traumatic then smooth off or take off clasp in area
  • Lichenoid reaction. Replace the amalgam restoration with composite or consider crwon if restoration is extensive and little remaining tooth tissue once amalgam is completely removed
  • LP. Correct any underlyinh deficienceies, dietary avoidance (e.g benzoate, cinamon, aldehyde etc.) Switch to SLS free toothpaste, avoid foods or other triggers (e.g spicey foods(, topical steroid treatment - beclomethasone inhaler or betamethasone mouthwash (for no resolution consider tacrolimus)
  • Chronic perio disease. Start S3 guidlines from BSP guidance. Explain disease, manage risk factors, Give OH advice and encourage behavioural change and supra gingival PMPR of clinical crown.
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9
Q

Arthur is a 68-year-old retired mechanic who presents at your practice after an absence of 2 years. He is partially dentate in the upper and lower arch and wears upper and lower acrylic prosthesis. These prosthesis were well fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is uncomfortable. On examination the upper prosthesis does not seat filly in the edentulous regions. In addition, there are numerous early to moderate deep primary carious cavities. Periodontal examination revels no periodontal pockets greater than 3-4mm and minimal bleeding on probing. Radiographic examination confirms no obvious peri-radicular radiolucencies. To the contrary, there are large radiopacities in relation to the roots of several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking medication for Paget’s disease.

  1. Describe the anatomical changes, pathology and incidence behind the reason why the denture no longer fits? (4)
A
  • Pagets disease is causing increased bone turnover
  • There is abnormal bone turnover - first an osteolytic stage of. resorption followed by replacement with new form of disorganised (mixed radiolucent and radiopaque stage) which overtime will be filled in so most of the space is filled with bone
  • THis result in bone swelling and this is why dentures dont fit anymore
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10
Q

Arthur is a 68-year-old retired mechanic who presents at your practice after an absence of 2 years. He is partially dentate in the upper and lower arch and wears upper and lower acrylic prosthesis. These prosthesis were well fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is uncomfortable. On examination the upper prosthesis does not seat filly in the edentulous regions. In addition, there are numerous early to moderate deep primary carious cavities. Periodontal examination revels no periodontal pockets greater than 3-4mm and minimal bleeding on probing. Radiographic examination confirms no obvious peri-radicular radiolucencies. To the contrary, there are large radiopacities in relation to the roots of several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking medication for Paget’s disease.

Why could arthur hace developed dental caries? (2)

A
  • Polypharmacy resulting in xerostomia
  • Diet and lifestyle factor may have increased sugar intake
  • Has been absent from dentist for 2 years
  • Non-fitting denture may act as a plaque trap
  • May have decreased manual dexterity so struggles to brush and maintain as good OH
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11
Q

Arthur is a 68-year-old retired mechanic who presents at your practice after an absence of 2 years. He is partially dentate in the upper and lower arch and wears upper and lower acrylic prosthesis. These prosthesis were well fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is uncomfortable. On examination the upper prosthesis does not seat filly in the edentulous regions. In addition, there are numerous early to moderate deep primary carious cavities. Periodontal examination revels no periodontal pockets greater than 3-4mm and minimal bleeding on probing. Radiographic examination confirms no obvious peri-radicular radiolucencies. To the contrary, there are large radiopacities in relation to the roots of several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking medication for Paget’s disease.

Account for the most likely cause of the radiopacities on the radiograph? (1)

A

Paget’s disease may have caused hypercemetosis

Hypercementosis is excessive deposition of non-neoplastic cementum over normal root cementum, which alters root morphology. This cementum may be either hypocellular or cellular in nature. The aetiopathogenesis of hypercementosis is ambiguous

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12
Q

Arthur is a 68-year-old retired mechanic who presents at your practice after an absence of 2 years. He is partially dentate in the upper and lower arch and wears upper and lower acrylic prosthesis. These prosthesis were well fitting when provided by you 2 years ago. He now complains that the upper prosthesis no longer fits well and is uncomfortable. On examination the upper prosthesis does not seat filly in the edentulous regions. In addition, there are numerous early to moderate deep primary carious cavities. Periodontal examination revels no periodontal pockets greater than 3-4mm and minimal bleeding on probing. Radiographic examination confirms no obvious peri-radicular radiolucencies. To the contrary, there are large radiopacities in relation to the roots of several teeth. There is minimal periodontal bone loss. In relation to his medical history he says he is taking medication for Paget’s disease.

How are you going to manage his clinical care? Describe the treatment you would provide and treatment you would seek to avoid? (6)

A
  • Denture hygiene instruction, oral hygiene instruction and diet advice
  • Enhanced prevention- fluoride toothpaste and fissure sealants etc.
  • HPT- OHI, supra-gingival scale, RSI as required
  • Carious management- remove caries and depending on depth of caries either restore with lining (as likely to be close to pulp) or RCT and restore
  • Replace dentures- make patient aware may need replaced or rebases more frequently that normal due to jaw enlargement
  • Regular monitoring and reassessment at regular intervals
  • Refer to specailist if complications arise if struggling to deliver denture which is appropriate or fits patient
  • As patient is on bisphosphanates. Avoid extraction and surgical treatment as if patient is taking bisphosphates as part of Paget’s treatment there is a risk of MRONJ and hypercementosis can also lead to difficulties and increased risk of extraction complications
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13
Q
  1. You decide Arthur needs to have extraction of a lower molar which does not have a radiopacity associated with its root but you are aware he is taking bisphosphonates. What precautions would you take when you extract the tooth? (7 marks)
A
  • Make patient aware of the risk of MRONJ due to medication (do this during the consent process)
  • Some clinicans conisder use of chlorohexidine 1 week prior, immediately prior and aftera XLA
  • Atruamtic technique during XLA
  • Consider suturing (and possible haemostatic agents) to encourage healing by primary intention
  • Avoid raising flaps and exposing bone
  • Stree post-op advice. To keep area super clean and avoid smoking all together as healing already impaaired
  • Review and monitor these patients
  • Warn patient to look for signs. Bad taste or smell, swelling puss, pain and seek tx if required.
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14
Q

Pemphigus Vulgaris-
A picture is shown of a direct immunofluorescence performed by the lab due to suspected pemphigus vulgaris.

  1. What are the methods of analysis shown? (2)
A
  • Direct immunofluorescence testing
  • Histopathology testing using H&E stain
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15
Q

A picture is shown of a direct immunofluorescence performed by the lab due to suspected pemphigus vulgaris.

  1. What would the pathologist report with the results of this test? (3)
A
  • Direct IF- Showing basket weave pattern-
  • Histology- Evidence of acantholysis (separation of the epithelial cells) causing a supra-basal split with tzank cells (which have dropped off from the thin superficial layer) present in the fluid of the bulla while the basal epithelial layer remains in continuity with the underlying connective tissue
  • May be evidence of fluid in the split seen as pink precipitate and underlying lamina propria contains inflammatory cells such as eosinophils and plasma cells
  • In terms of pathology report might also include type of tests performed, results are listed above, likely diagnosis, levels of circulating antibodies?, patient details, site of specimen, any other recommendations or notes
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16
Q

Pemphigus vulgaris
4. What are the reasons for this condition, why does it occur? (2)

A
  • Autoimmune condition which is characterised by a type 2 hypersensitivity reaction in which there is an intra-epithelial antibody attack on the cell-cell adhesion known as desmosomes (Which attach the epithelial cells together)
  • The target of the attach is desmoglein protein
  • This causes the cells to sperate from either other whihc results in clear fluid filled blisters which easily burst
  • Pemphigus valgaris usually gebins in the mouth by lesions are often found on the skin too and without treatment it can be fatal due to infection and histopathology
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17
Q
  1. Name one condition that would represent this lesion in the same way clinically as phemigus vulgaris but would be different histopathologically? (1)
A
  • Bullous pemphigoid or mucous membrane pemphigoid
  • Drug induced pemphigus
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18
Q
  1. What is the treatment for this phemigus valgaris disease?
A
  • Immune modulation- steroids, immune modulating drugs such as azathioprine
  • Topical steroids- betamethasone mouthwash- 0.5mg x2-3/day or beclomethasone inhaler- 50mgx2/3/day
  • Systemic steroids- prednisolone
  • May utilise biologics- monoclonal antibodies
  • Indirect IF testing can be used to determine response to treatment
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19
Q

Pemphigus & Pemphigoid-
1. What is the histological difference between pemphigus and pemphigoid?

A
  • Pemphigoid- sub-basal split, fibrin at base of vesicles, inflammation (plasma, cells, neutrophils and eosinophils) linear IF pattern (autoantibodies attack hemidesmosomes)
  • Pemphigus- supra-basal split, tzank cells (which have cropped off) found in cleft of split amongst the fluid, acantholysis (epithelial cells separate from one another), one cell thick basal layer remains under cleft, basket weave IF pattern (autoantibodies attack desmosomes)
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20
Q

Pemphigus & Pemphigoid-
2. How do they differ clinically?

A
  • Pemphigoid- thick walled blisters affecting the full epidermis usually filled with blood (but can also be filled with fluid) which will persist to be seen clinically
  • Pemphigus- thin walled intra-epithelial superficial blisters which are filled with clear fluid but which are rarely seen as the thin surface layer is easily lost

Picture of pemphigoid - see large thick blisted you can get

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21
Q
  1. How may these conditions (pemphigus and pemphigoid) be investigated?
A
  • Biopsy & traditional histological testing with H&E
  • Biopsy & direct immunofluorescent testing using fluorescent tagged IgG antibodies to demonstrate location of antigen auto-antibody reaction and either characteristic linear or basket weave pattern (NB. Biopsy always taken from unaffected area)
  • Indirect immunofluorescent testing using serum sample to test for IgG levels
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22
Q
  1. How are pemphigus and pemphigoid managed?
A
  • Immune modulation- steroids, immune modulating drugs such as azathioprine
  • Topical steroids- betamethasone mouthwash- 0.5mg x2-3/day or beclomethasone inhaler- 50mgx2/3/day
  • Systemic steroids- prednisolone
  • May utilise biologics- monoclonal antibodies
  • Indirect IF testing can be used to determine response to treatment
  • If worried about cicatricial pemphigoid then refer to ophthalmology
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23
Q

Trigeminal Neuralgia-
Patient attends with suspected trigeminal neuralgia.
1. What 2 clinical investigation would you do/what tests would you do before arriving at this diagnosis? (2)

A
  • MRI brain scan
  • Full neurological examination including terminal nerve reflex testing and cranial nerve testing
  • May perform IAN lock to rule out TMD or muscle pain
  • Baseline blood tests- full blood count (FBC), U&E’s, blood glucose and liver function tests (LFT)
  • May consider OPT to rule out dental cause
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24
Q
  1. What two neurological disorders may give rise to this type of pain? TN
A
  • MS
  • Brain tumour (pressing on trigeminal nerve)
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25
Q
  1. What is the first line drug management for trigeminal neuralgia? (1)
A
  • Carbamazepine- initially 100mg 1-2x daily then may increase gradually according to response (usual dose 200mg 3-4x daily but up to 1.6g daily)
  • Positive response to this confirms diagnosis
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26
Q
  1. What blood tests would you have done before giving the above drug?

* Carbamazepine

A
  • Full blood count
  • Liver function test & U&E’s
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27
Q
  1. What test would you carry out every 3 months? (1)

* After starting the patient on Carbamazepine

A
  • Blood tests- FBC, LFT, U&E’s
    Checking for sodium levels, liver function and risk of leukopenia
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28
Q
  1. Give two indications for surgery? (2)

TN

A
  • Maximum tolerable medical management fails to control pain- no improvement after trying for substantial period
  • Younger patients with significant drug use with good control
  • Polypharmacy which makes patient dizzy or unable to function (medical management contra-indicated as affecting quality of life from side effects
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29
Q
  1. Name one types of surgery for trigeminal neuralgia?
A
  • Microvascular decompression
  • Peripheral neuroectomy
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30
Q

A patient enters your surgery and you suspect after you initial examination that they may have trigeminal neuralgia.
1. Describe the nature of the pain from trigeminal neuralgia? (2)

A

Pain can be bilateral or unilateral. The pain is acute and severe, followed by a burning sensation. It is often assocaited with reddness and blotchy face (vasomotor component). Can be triggered by talking, eating etc and the cold.

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31
Q
  1. What are the 2 most frequent causes of trigeminal neuralgia? Name an investigation you could do into these?
A
  • Focal demyelination of the peripheral nerve
  • Trigeminal nerve compression as it exits the skull (e.g. from aberrant artery)
  • To investigate do MRI
  • Secondary to MS and trauma
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32
Q
  1. If the patient has TN due to MS or a brain tumour, what symptoms might they experience. Give one for MS and 2 for a brain tumour?
A

MS - intention tremor
Brain tumour - double vision and memory loss

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33
Q
  1. How could you manage this patient? Give 1 surgical and 1 medical treatment option? TN
A
  • Carbamazepine- initially 100mg 1-2x daily then may increase gradually according to response (usual dose 200mg 3-4x daily but up to 1.6g daily)
  • Surgical- Microvascular compression, radiosurgery with gamma knife, peripheral neurectomy
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34
Q
  1. What investigation/test would you take before giving the medical management and why? Carbamazepine
A
  • Full blood count
  • Liver function test & U&E’s
  • Drug can reduce sodium levels and liver function as well as possible resulting in leukopenia
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35
Q
  1. Give 3 side effects of this medical intervention? carbamazepine
A
  • Decrease in sodium levels, decrease in liver function and increase riskk of leukopenia.
  • Drozziness
  • Nauseau
  • Dry mouth
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36
Q

Sjogren’s Syndrome-
1. What is Sjogren’s syndrome?

A
  • Autoimmune disorder with hypofunction of the exocrine glands (as a result of B-cell proliferation which causes exocrine gland destruction) characterised by multisystem manifestations
  • Primarily affects the mucous membrane secretion production resulting in dry mouth, reduced tear production and dryness of other bodily mucous membranes
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37
Q
  1. What other conditions can Sjogrens be associated with?
A

Lupus
Rheumatoid arthritis

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38
Q
  1. Name 6 investigation used to help diagnose Sjogrens?
A
  • (Must have 4 or more positive including 5 and 6 for modified European criteria diagnosis)
  • Subjective dry eye tests- persistent troublesome eyes >3months, recurrent sensation of san/gravel in the eye tear substitutes used >3 times a day
  • Objective dry eye tests- evidence of reduced secretion production in the eye- Schirmer test <5ml in 5 mins
  • Subjective dry mouth tests- daily feeling of dry mouth > 3months, recurrent swelling of salivary glands, frequent drinking of liquid to allow swallowing of dry food
  • Objective dry mouth tests- evidence of reduced saliva flow- unstimulated flow <1.5ml/15 minutes
  • Autoantibody findings- anti Ro and or anti La
  • Histopathology findings from labial biopsy w minimum 5 minor glands (region of (premolar inner lip)
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39
Q
  1. What are the minor histological findings for Sjogrens?
A
  • Focal lymphocytic sialadenitis- focal collections of lymphocytes (50+ lymphocytes) ≥ 1 collection/4mm2
  • Acinar loss
  • Fibrosis
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40
Q
  1. What are the major histological findings for Sjogrens?
A
  • Presence of lymphoid aggregates (clusters of immune cells) in the glandular tissue, which are characteristic of Sjogren’s syndrome. These aggregates are known as “focus scores”
  • fibrosis (scarring) of the glandular tissue, which can lead to a decrease in the function of the salivary and lacrimal glands.
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41
Q
  1. Name 4 oral complications for Sjogrens?
A
  • Oral infection e.g. candida
  • Increased caries and PD disease risk
  • Functional loss
  • Poor denture retention
  • Increased risk of salivary lymphoma (non-hodgkins)
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42
Q
  1. Give 3 other causes of xerostomia?
A
  • Medication related
  • Cancer therapies e.g. chemotherapy or radiotherapy to the head and neck
  • Dehydration
  • Smoking
  • Salivary gland tumours
  • Oral dysesthesia
  • Psychogenic
  • Sarcoidosis
  • Renal disorders
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43
Q
  1. What systemic drug may be used to manage Sjogren’s and stimulate saliva?
A

pilocarpine - salivary stimulant

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44
Q
  1. What antibodies are linked with Sjogren’s?
A

Anti-Ro
Anti-La

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45
Q
  1. What gland would be biopsied when querying Sjogren’s
A
  • Labial gland biopsy?
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46
Q
  1. What are the three broad categories of Sjogren’s syndrome?
A
  • Partial Sjogren’s= sicca syndrome- dry eyes and mouth alone (no underlying autoimmune disease)
  • Primary Sjogren’s-no associated CT disease
  • Secondary Sjogren’s= associated CT disease (SLE, rheumatoid, systemic scelrosis)
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47
Q

Fibrous Epulis-
1. What is a fibrous epulis?

A
  • Reactive localised fibrous overgrowth of the gingival tissues
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48
Q
  1. What is the aetiology? of fibrous epulis?
A
  • Low grade localised chronic trauma/irritation (e.g. chronic inflammation)
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49
Q
  1. How does fibrous epulis appear histologically?
A
  • Mass of granulation tissue
  • Lots of small capillaries
  • Covered by layer of keratinised hyperplastic stratified squamous epithelium
  • Areas of ulceration
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50
Q
  1. What is a fibrous epulis known as on sites other than the gingivae?
A
  • Fibro-epithelial polyp
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51
Q

Pyogenic Granuloma-
1. What is a pyogenic granuloma?

A
  • Mass of granulation tissue which can be found at any mucosal site and which occurs as a response to trauma or infection
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52
Q
  1. How does pyogenic granuloma appear histologically?
A
  • Mass of granulation tissue
  • Contains lots of small blood vessels which may contain visible red blood cells
  • May be covered by keratinised SS epithelium but often lost resulting in extensively ulcerated lesion
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53
Q

Hereditary White Patches?
1. Name a hereditary white patch?

A
  • White spongy naevus
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54
Q
  1. How does it appear histologically?

White spongy naevus

A
  • Thick layers of parakeratosis
  • Intra-cellular oedema in keratin layer (gives spongy feel)
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55
Q
  1. How does smoker’s keratosis appear histologically?
A

 Hyperkeratosis (usually orthokeratosis)
 Variable dysplasia
 Minimal infiltrate (inflammation underlying)

  • Hyperkeratosis (reaction to trauma) (usually orthokeratosis) and hyperplasia
  • Characteristically get wavy like appearance of keratin in smokers
  • May be areas of mild/variable dysplasia
  • Minimal infiltrate due to underlying inflammation with macrophages and melanocytes in basal layer
  • May or may not be reactive melanosis- pathological melanin pigmentation represents by foci of brown pigmentation involving the basal cell layers and the underlying LP (in epithelium it is present in keratinocytes and in LP it is present in macrophages (known as melanophages after they have phagocytosed melanin))
  • Leakage into underlying LP is known as melaning incontinence
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56
Q

OFG-
1. What is orofacial granulomatosis?

A
  • Chronic inflammatory condition characterised by lymphatic obstruction from giant cell granulomas resulting in accumulation of tissue fluids and resulting oedema
  • Chiefly associated with type IV hypersensitivity reaction but also associated with Crohn’s and sarcoidosis
  • Type 4 hypersensitivity reaction
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57
Q
  1. What condition is OFG associated with?
A

Crohns

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58
Q
  1. What is the aetiology of OFG?
A
  • Autoimmune condition
  • Hypersensitive to allergens including SLS, benzoates, cinnamon
  • Link with Crohn’s disease and sarcoidosis
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59
Q
  1. What is the histological appearance of OFG?
A
  • Giant cell formulation
  • Formation of non-caseating epithelioid granulomas- localised collection of chronic inflammatory cells (giant cells, epithelioid cells (actives macrophages), lymphocytes and fibroblasts) which lack necrosis
  • Increased tissue fluid due to inflammation
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60
Q
  1. What are the signs and symptoms of OFG?
A
  • Angular cheilitis
  • Lip swelling and crusting
  • Aphthous ulceration pattern
  • buccal cobblestoning
  • Mucosal tags
  • Tissue swelling lips cheeks and ginigvae
  • Full thickness ginigvitis
  • Staghorning
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61
Q
  1. How is OFG managed?
A
  • Dietary avoidance- diet diary used and instruction on diet of avoidance for benzoate and sorbate free. NEed to do a minimum of 3 months for complete diet exclusion. Can do a patch test also.
  • Medication management- antibiotics (macrolides- e.g. erythromycin or clarithromycin), tacrolimus ointment to lips, intra-lesion steroid injections, oral steroids, azathioprine, biologics (monoclonal antibodies)
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62
Q

What is your diagnosis?

A

Minor aphthous ulcer

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63
Q
  1. For minor aphthous ulcer what 2 investigations would you carry out? (2)
A

Haematinics
FBC

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64
Q

2 Things which cause microcytic anaemia

A
  • Thalassemia
  • Iron deficiency

In adults, microcytosis is when the MCV is less than 80 femtolitres.
…
Interpreting a full blood count
In men aged over 15 years — Hb below 130 g/L.
In non-pregnant women aged over 15 years — Hb below 120 g/L.
In children aged 12–14 years of age — Hb below 120 g/L.

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65
Q
  1. Give three topical treatments which are available for aphthous ulcers? (Not brand name) (3)
A
  • Benzydamine
  • Lidocaine
  • Betamethasone
  • Beclomethasone
  • Doxycycline
  • Hydrocortisone
  • Chlorhexidine
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66
Q
  1. What would microcytic and macrocytic blood results show?
A
  • Microcytic- small RBC’s which are paler than normal
  • Macrocytic- large RBC’s (occurs due to vitamin B12 or folic acid deficiency)
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67
Q
  1. What is an ulcer?
A
  • Full thickness epithelium loss with fibrin formation on the surface
  • Vascular underlying LP becomes exposed with yellow fibrin formation on the surface
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68
Q
  1. What is an erosion?
A
  • Partial loss of epithelium thickness
  • Appears red due to loss of layers and underlying inflammation
  • Can only be diagnosed histologically
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69
Q
  1. How can you differentiate between recurrent major and minor aphthous ulceration?
A
  • Minor- last less than 2 weeks, less than 1cm in size, 1-20 per crop, round or oval, red halo with yellow fibrin base, always affect non-keratinised mucosa, no scar on healing, multifactorial aetiology- genetic, hematinic deficiency, external sensitives, systemic diseases, drugs
  • Major- last longer than 2 weeks (6-12 weeks usually, months in some cases), more than 1cm in size, affect keratinised and non-keratinised mucosa, often single but always <5 in crop, can heal with or without scarring
  • Herpetiform- 1-200 per crop, <0.5mm ulcers, can merge into larger areas of ulceration, last up to 2 weeks, heal without scarring, only affect non-keratinised mucosa (NB. Same appearance as primary HSV infection but all mucosa will be affected)
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70
Q
  1. What are the potential problems of recurrent aphthous ulceration/stomatitis?
A
  • Can be painful and prevent eating- dehydration and malnutrition
  • Affect speech and mastication
  • Infection
  • Problems wearing dentures
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71
Q

Difference between aphthous ulcers and herpetic ulcers?

A

Age of patient
Number
Size
Location
Margins

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72
Q
  1. What are the causes of recurrent aphthous stomatitis?
A
  • Genetic- HLA gene
  • Nutritional/Haematinic deficiency- iron, folate, vitamin B12
  • Systemic disease- menorrhagia, chronic GI blood loss, dietary malabsorption (Crohn’s, coeliac, pernicious anaemia), UC, OFG
  • Endocrine factors
  • Immunity
  • Trauma
  • Allergies- e.g. SLS In toothpaste
  • Other- smoking, infection, stress
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73
Q
  1. How is RAS treated?

Recurrent aphthous ulcer

A
  • Treat the underlying cause, why important to diagnose properly
  • Give Difflam (benzydamine) spray for acute phase
  • Topical steroids betametalone MW and Beclamethasone inhlaer
  • Systemic steroids prednisolone
  • Chlorohexidine MW

patch testing for benzoate and cinnamon aldehyde sensitivity
* Treat any underlying cause- correct deficiency, correct systemic disease, remove trauma, remove allergens- change to SLS free toothpaste and consider dietary avoidance
* Give benzydamine (0.15% spray) and lidocaine topical analgesics in acute phase
* Consider giving gel clair to cover as a protective layer and allow eating
* Can also use topical steroids/immune modulator- hydrocortisone pellets (start with as least potent) then betamethasone mouthwash (0.5mg x2/3 daily) or beclomethasone inhaler (50µg puffs x2/3 daily)
* Alternatively, may use doxycycline (100mg dispersive tablets dissolve in water for use as mouthwash 2 mins 4x daily for 3 days) or CHX mouthwash (0.2% x2 daily)
* If this fails may consider systemic immune modulation- prednisolone (systemic steroids), azathioprine (immunosuppressive), adalimumab, thalidomide (immunomodulator)

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74
Q

Candidosis-
1. Give 6 types of candida infections?

A
  • Pseudomembranous candidosis
  • Erythematous candidosis
  • Hyperplastic candidosis
  • Angular cheilitis
  • Median rhomboid glossitis
  • Denture induced stomatitis
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75
Q
  1. Where does median rhomboid glossitis occur?
A
  • Dorsum of the tongue (anterior to the sulcus teminalis)
  • Characterised by central papillary atrophy of the tongue
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76
Q
  1. Give 3 histological features of it?

median rhomboid glossitis

A
  • Candida hyphae infiltration
  • Elongated, hyperplastic rete ridges
  • Numrous inflammatory cells- polymorphonuclear leukocytes (polymorphs) which migrate from the LP towards the surface of the epithelium
77
Q
  1. Give three methods of testing for candida?
A
  • Swab, foam pad or oral rinse then culture (then can perform germ tube formation, sugar assimilation, antifungal sensitivity or typing)
  • Biopsy and histological testing
  • Smear and microscopy
78
Q
  1. What are the virulence factors of candida?
A
  • Adhere to host
  • Invade host
  • compete for nutrients
  • Resist innate immune response
  • Evade adapted immune response

  • Adhesins
  • Hydrolytic enzymes- phospholipase, haemolysin, proteinase
  • Switching mechanisms
  • Germ tube formation
  • Extracellular enzymes
  • Acidic metabolites
79
Q
  1. Give 5 antifungal agents?
A
  • Miconazole
  • Fluconazole
  • Nystatin
  • Itraconazole
  • Chlorhexidine
80
Q
  1. What medication is contraindicated for use of azoles?
A
  • Warfarin
  • Statins
81
Q

Patient attends with redness at the corner of their mouth. (Candida infection).
1. What is the diagnosis of this disease? (1)

A

Angular chelitis

82
Q
  1. Name 2 micro-organisms involved in this condition? (2)

angular chelitis

A

S.aureus C.albicans

83
Q
  1. What microbiological sampling method should you ask for angular chelitis ? (1)
A

Swap and PCR or culture

84
Q
  1. Name one immune deficiency disease and one GI bleeding disease. Why are they more susceptible to this lesion? (2) candida infection
A
  • HIV- immunodeficient and so impaired immune function allows for opportunistic infections and harmless residual microflora to become pathogenic and cause infection
  • Coeliac disease- impaired nutrient absorption and malabsorption which again is linked with immunosuppression and so increased likelihood of infection
85
Q
  1. Name on intra-oral disease that would be associated with angular chelitis? (1)
A

OFG

86
Q
  1. Why is miconazole prescribed to a patient when microbiological sampling is not available? (1)
A
  • Effective against both fungal (e.g. candida albicans) and gram-positive bacteria (e.g. staphylococcus aureus) pathogens
  • NB. Don’t use In patients taking warfarin or statins)
  • Can also be given in form with hydrocortisone (steroid) which acts to help reduce inflammation
87
Q
  1. What two instruction should be given to this patient who wears a denture? (2)
A
  • Don’t wear denture overnight- take out before bed
  • Ensure good denture hygiene- clean dentures after eating, before bed and in the morning with a soft brush and soapy warm water (or non-abrasive toothpaste) and thoroughly rinse, soak dentures in cold water over night, use denture cleaners in accordance with the manufacturer’s instructions once daily (generally 10-15 minutes), don’t soak in sodium hypochlorite containing products for more than 10 minutes especially if metal base and don’t soak in hot water as can cause leaching, don’t clean in boiling water and clean over sink
  • Clean mouth with soft brush and toothpaste
    • Wear as little as possible till resolved
88
Q

Picture of generalised white plaques that scrape off easily and leave an erythematous base.
1. What is your diagnosis?

A
  • Pseudomembranous candidosis
89
Q
  1. Give two medical conditions that we might see pseudomembranous candidosis in?
A
  • Diabetes
  • HIV
  • Immunosuppressed- cancer patient
90
Q
  1. What are the advantages and disadvantages of a mouth swab and oral rinse?
A
  • Oral swab- simple, site specific but can be easily contaminated and uncomfortable for patient
  • Oral rinse- records whole mouth, is quantifiable amount and can separate healthy organisms out but not site specific, difficult to standardise and some patients find the rinse process difficult to do
91
Q
  1. What should you ask the lab for when sending the sample?
A

A culture and identification of the micro-organism

  • Ask for culture and laboratory identification either by appearance on chromogenic agar or reaction in MALDI-TOF (laser spetoscopy)
  • If rinse can doe semi-quantitative culture which shows degree of growth and therefore if commensal coverage or more or less
92
Q
  1. Fluconazole interacts with many drugs. Name 2 drugs it would interact with and the effect the interaction would have?
A
  • Warfarin (anticoagulant)- competitively binds to warfarin binding site causing release of more free warfarin into the blood and so potentiates the anti-coagulant effect (sever interaction) and increases the bleeding tendency and likelihood of a catastrophic bleed (increases INR)
  • Simvastatin- statin- increases exposure to simvastatin and so in turn can increase risk of hepatotoxicity
93
Q
  1. What information is required on a lab sheet for a sample?
A
  • GDP and GMP details- name, address and contact number
  • Overview of relevant medical, drug, dental and social history
  • Clinical description of lesion
  • Provisional diagnoses
  • Any tests previously done and the test required to be done- e.g. culture, viral, ESR
  • Any current or previous antibiotics use (any resistance)
  • Specimen site and type of sample
  • Date and time of sample
  • Referring clinical name and signature
94
Q
  1. What other local conditions might cause pseudomembranous candidosis?
A
  • Oral steroid use- inhalers containing steroids
  • Nutritional deficiencies
  • Broad spectrum antibiotic use
95
Q

A 10 year-old-boy presents your surgery with his mother. His only complaint is a bad taste in his mouth. On examination, you notice a generalised white plaque that scraped off easily and leaves an erythematous base.
1. What is your diagnosis?

A
  • Pseudomembranous candidosis
96
Q
  1. Name 4 pre-disposing factors for Pseudomembranous candidosis condition- 2 local and 2 medicals?
A
  • Local- oral steroid use (e.g. steroid inhaler for asthma), nutritional deficiencies, broad spectrum antibiotic use
  • Medical- diabetes, HIV, immunocompromisation
97
Q
  1. Give an advantage and disadvantage of oral swab and oral rinse?
A
  • Oral swab- site specific but can be easily contaminated and uncomfortable
  • Oral rinse- records whole mouth, can separate health organism and is a quantifiable amount // difficult to standardise, some patient find it difficult to do, not site specific
98
Q
  1. What is your first-line medication for this condition? State two drugs that it interacts with and the nature of this interaction. Candida infection
A
  • First line topical= miconazole oromucosal gel (20mg/g) apply 4x daily after food for 7 days send 80mg tube
  • First line systemic= Fluconazole capsule 50mg x1 daily for 7 days send 7 tablets
  • Azoles interact with warfarin and statins (e.g. simvastatin) and act to displace them and therefore potentiate their effects
  • This results in increased bleeding in warfarin patients and hepatotoxicity in statin patient
99
Q

Denture Induced Hyperplasia-
Patient presents with denture induced hyperplasia.
1. Give two differential diagnosis?

A

SSC
Fibroepithelial polyp

  • (Leaf fibroma)
  • Giant cell granuloma
  • Pyogenic granuloma
  • SSC
  • Drug induced hyperplasia (phenytoin, calcium channel blockers (nifedipine), cyclosporin)
  • Papilloma
  • Fibroepithelial polyp
100
Q
  1. What factors have resulted in denture induced hyperplasia?
A
  • Ill fitting denture causing chronic trauma (may be ill fitting due to initial overextension or due to bone resorption which has resulted in flanges starting to dig into the area
  • This in turn results in fibrous reaction of the gingivae characterised by reactive hyperplasia and hyperkeratosis
101
Q
  1. How would you manage denture induced hyperplasia?
A
  • Trim existing denture
  • LA then surgical excision of the fibrous tissue overgrowth
  • Allow area to heal (may place tissue conditioner in interim to allow area to heal) before taking impression for a new denture (must address causative factor to prevent recurrence)
102
Q
  1. Name 2 histological features of denture induced hyperplasia?
A
  • Papillary hyperplasia of the palate (pseudo-epihtliomatous hyperplasia)
  • Extensive hyperplasia of the epithelial cells with cells extending into CT (hyperplastic rete ridges) (similar to invasive SSC due to invasion of epithelium into CT but no signs of cellular atypia)
  • Hyperkeratosis
  • Chronic inflammatory cells
  • Often candidal involvement
103
Q

This is what normal mucosa should look like under H&E staining

A

!

104
Q

A 48-year-old male patient presents for the first time in your practice. He is otherwise fit and healthy and takes no medications. He also wears a complete upper denture which is 9 years old.
1. What do you notice about the patient’s palatal tissue? (2)
2. Diagnosis

A
  • Erythematous(fiery red) and oedematous, inflamed denture bearing areas
  • (May be papillary hyperplasia (pseudo-epitheliomatous hyperplasia))
  • Patient may also complain of discomfort from the area, burning sensation, bad taste and halitosis
  • Denture induced stomatitis
105
Q
  1. What would be your first line treatment for denture induced stomatitis?
A
  • Clean palate daily
  • Give denture hygiene advice including cleaning (clean with soft brush and warm soapy water or non-abrasive water and leave to soak in denture solution as per manufacturer instruction (usually 10-15 minutes twice daily)) and leaving out at night
  • Improve fitting surface of the denture- may consider providing new denture or rebasing denture in the long run but initial use of a tissue conditioner on the denture will help to reduce inflammation of the tissue in order to take accurate impression for new denture or denture rebase
  • Encouraged patient to leave dentures out as often as possible till inflammation resolved
106
Q
  1. If this condition persisted, what would be the second line of treatment? (after denture hygiene)
    Denture stomatitis
A
  • Appropriate antifungal treatment- miconazole oromucosal gel (20mg/g- apply pea sized amount to fitting surface 4x daily after food for 7 days to lesions have healed (80g tube))- first line as both anti-bacterial and anti-fungal activity (some avalibel with hydrocortisone
  • Other options= fluconazole (50mg capsule x1 daily (send 7 capsules (may increase to 14 day course if no resolution) OR nystatin oral suspension (100,000 units/ml- 1ml after food 4x daily for 7 days and continue for 48hrs after the lesions have healed)
  • If doesn’t resolve after 7 days of antifungals consider switching to nystatin (if miconazole used first line) or extending the course by a further 7 days or switching to systemic treatment with fluconazole
107
Q
  1. You decide to make a new denture. What instructions would you give to the lab technician regarding the construction of the upper special tray?
A
  • ‘Please pour impressions in 50/50 dental stone/plaster’
  • Please construct upper non-perforated special tray in light cure PMMA with a 2mm wax space, intra-oral handles and finger rests
108
Q
  1. Erythematous candidosis can be classified using Newton’s classification- what are the classifications?
A

1- Pinpoint hyperaemia (localised inflammation with hyperaemic foci)
2- Diffuse erythema (diffuse inflammation and erythema confined to mucosa contacting denture without hyperplasia)
3- Granular erythema (papillary hyperplasia) (granular inflammation with inflammation, erythema and papillary hyperplasia)

109
Q
  1. What are the most likely causative agent(s)?

Denture induced stomatitis (micro-organisms which cause)

A
  • Candida albicans
  • S. aureus (may be mixed)
110
Q

Photograph of a slide prepared from a biopsy taken from a 58-year old man (smoker’s keratosis).
1. What is layer A formed from? (1)

Top layer

A

Keratin

111
Q
  1. What type of epithelium can you see in the picture? (1)
  2. What is the brown pigment at the bottom
A
  • Keratinised stratified squamous epithelium
  • Melanin
112
Q
  1. Describe smokers keratosis clinically, based on what you can identify in the slide?
A
  • Thickened white patch with some areas of brown/grey colouration
  • Likely painless
  • May be other lesions elsewhere in the mouth if smoking related
113
Q
  1. Name two possible aetiological factors for the development of this lesion? (smokers keratosis)
A
  • Smoking (tobacco or pipe smoking)
  • Chronic inflammation
  • Drugs- hydroxychloroquine
114
Q
  1. Using the photograph, how would you assess if the lesion was potentially malignant?
A
  • Look for signs of cellular atypia (epithelial dysplasia is the most important type)- the more severe the more likely the lesion is to become malignant
  • Examples include pleomorphism, hyperchromatism, abnormal and increased mitosis, loss of basal cell polarity, basal cell hyperplasia
115
Q
  1. What features in the clinical appearance would make you highly suspicious that the lesion was potentially malignant?
A
  • Exophytic growth, raised rolled margins, indurated, mixed red and white colouration, erythematous, non-homogenous, bleeding, pain
116
Q

A patient attends with inflamed gingiva extending beyond the mucogingival junction.
1. Give a clinical description (diagnosis)?
2. Give one term to describe its appearance? (1)

A
  • Desquamative gingivitis
  • Erythematous
  • Ulcerated
117
Q
  1. Name three oral conditions associated with disquamative gingivitis/ three differential diagnosis? (3)
A
  • Lichen planus
  • Pemphigoid
  • Pemphigus
118
Q
  1. What 2 local factors may exacerbate Desquamative gingivitis? (2)
A
  • Smoking
  • Plaque
  • SLS toothpaste
  • Other traumatic source like denture and restoration overhangs
119
Q
  1. What 2 local factors may exacerbate Desquamative gingivitis? (2)
A
  • Smoking
  • Plaque
  • SLS toothpaste
  • Other traumatic source like denture and restoration overhangs
120
Q
  1. Give 2 topical treatments for desquamative gingivitis? (2)
A
  • Betamethasone mouthwash (topical steroid)
  • Beclomethasone inhaler (topical steroid)
  • Tacrolimus ointment (immune modulator)
121
Q

A patient arrives at the oral med clinical complaining of pain and on examination, the consultant diagnoses desquamative gingivitis. (cannot diagnose as it is a clinically descriptive term)
1. Describe desquamative gingivitis?

A

Red inflamed and ulcerated gingivae which extends across the mucoginigval junction.

  • Inflamed gingiva extending beyond the mucogingival margin with erythematous shedding and ulceration which involves the full width of the gingivae
  • Clinical descriptive term of non-specific clinical expression in the gingivae (redness, burning, erosion, pain and plaque) or several disorders
122
Q
  1. Describe how you would manage desquamative gingivitis? (4)
A
  • Confirm diagnosis- histological testing, blood tests and possible immunofluorescent testing- and deal with diagnosis appropriately
  • Control local irritating factors- traumatic overhangs or areas on dentures (also can consider replacement with fixed pros)
  • Consider plaque control- improve OH
  • Modify OH if patient cannot manage regular toothbrushing due to pain; topical antiseptic mouthwash e.g. difflam 0.15% benzydamine hydrocortisone (analgesic and anti-inflammatory)
  • Change to SLS free toothpaste
  • Topical steroids- betamethasone or beclomethasone (rinse, metered dose inhaler or steroid cream in gum shield) (NB. Can’t give in general practice but could give dissolved hydrocortisone while waiting for referral)
  • If no resolution consider use of topical tacrolimus immunomodulator (mouthwash, rinse or cream) or systemic immunosuppressants
123
Q
  1. Name another gingival disease that is typically painful on presentation?
A
  • Erythema multiforme- characterised by crops of oral ulcers which are very painful, usually found in the anterior part of the mouth and associated with crusting and cracking of the lips
  • Can render patient unable to eat or drink and may require admission for IV fluids
  • Seems to be linked to immune complex and herpes simplex so treatment with steroids and anti-viral
  • Major form also known as Steven’s Johnson syndrome where there is severe multi system involvement- skin, conjunctiva, nose, pharynx and resulting in patient not only not only unable to intake fluids but also losing lots of fluids resulting in severe dehydration (and immune suppression due to high dose steroids used)
124
Q

Pigmentation & Haemangiomas-
A patient presents to your practice with a large brown/grey discoloured swelling.
1. Name 3 local causes of pigmentation?

A
  • Vascular malformations (haemangioma’s, Sturge Webber syndrome)
  • Amalgam tattoo (macrophages surround amalgam)
  • Mucosal melanoma
125
Q
  1. Name 3 generalised caused of pigmentation?
A
  • Smoking (leakage of melanocytes and sub-mucosal fibrosis)
  • Racial/familial pigmentation
  • Hyperparathyroidism (primary Addison’s disease, secondary cushing disease, lung tumour producing ACTH)
  • Medication related pigmentation- contraceptive pill, antimalarial (hydroxychloroquine)
126
Q
  1. Name two types of haemangioma?
A
  • Capillary
  • Cavernous
127
Q
  1. What is the histological difference between a cavernous and capillary haemagioma?
A
  • Capillary- groups of smaller vessels, most of which are capillaries (spaces filled with red blood cells)
  • Cavernous- larger dilated vascular spaces
  • NB. Blood is present within the vessel in continuation with the circulation unlike in a hamartoma when blood is present outside the vessels
128
Q
  1. What is a haemangioma?
A

A haemangioma is a collection of small blood vessels that form a lump under the skin.

  • Type of hamartoma characterised by a collection of normal blood vessels with normal regular structure but either greatly increased in number or in an abnormal location
  • They rapidly grow in the first few weeks of like then regress over the next 10 years leaving birth mark (in vascular malformations they persist during life)
129
Q

Intra-Oral Manifestations of Viral Infection-
1. What are the intra-oral manifestations of herpes simplex virus?

A
  • Gingiva stomatitis- vesicles that burst to form blisters, 1-3mm in size
  • Herpes labialis- cold sores affecting the lips
  • Oral ulceration
130
Q
  1. Name 2 other types of human herpes virus?
A
  • Epstein Barr virus (EBV)
  • Varicella zoster virus
  • Cytomegalovirus
  • HHV-8 (Kaposi’s Sarcoma Associated Virus)
131
Q
  1. Which cranial nerves does herpes become associated with/ resident to?
A
  • Trigeminal nerve
132
Q
  1. Name the common triggers for reactivation of herpes simplex lesions?
A
  • Stress
  • Infection
  • Exposure to UV light, excessive heat or cold
  • Hormonal changes during menstruation
  • Fatigue
  • Immunosuppression
133
Q
  1. How does herpes labial forms?
A
  • Primary infection with herpes simples (replication of virus in epithelium, uptake by sensory nerves, transport to sensory ganglia)
  • Period of latency (Productive viral replication in neurons and establishment of latent infection
  • Reactivation (causes transport to mucosal and cutaneous sites, release from nerve ending, viral replication and lesion formation)
  • Secondary infection causing herpes labial lesion
134
Q
  1. Name 2 groups of virus that cause oral ulceration?
A

Herpes simplex
HIV

  • Herpes simplex
  • Cytomegalovirus
  • Varicella zoster
  • EBV?
135
Q
  1. What is coxscakie virus?
A
  • RNA virus

Coxsackieviruses are part of the enterovirus family of viruses (which also includes polioviruses and hepatitis A virus) that can live in the human digestive tract.

136
Q
  1. Name 2 oral mucosa disease caused by Coxsackie virus?
A
  • Hand, foot and mouth disease
  • Herpangina
  • (Non-oral- aseptic meningitis, haemorrhagic conjunctivitis)
137
Q
  1. What is Epstein Barr Virus?
A
  • Human herpes virus 4
    Also known as mono the kissing disease
138
Q
  1. Name 3 diseases caused by EBV?
A
  • Oral hairy leucoplakia
  • Infectious mononucleosis (glandular fever)
  • Burkitt’s lymphoma
139
Q
  1. What are three diseases which cause vesicles?(Vesicles are small fluid-filled sacs covered by epithelium)
A
  • Erythema multiforme
  • Pemphigoid
  • Pemphigus

Vesicles are small fluid filled sacs covered by epithelium

140
Q
  1. What is kaposi’s sarcoma
A
  • Vascular tumour with different clinical manifestations caused by mass proliferation of blood vessels throughout the body
141
Q

Pigmented Tongue-
1. What are the local causes of a pigmented tongue?

A
  • Smoking
  • Bacteria (chromogenic)
  • Debris from food

  • Smoking
  • Food colourings
  • Chromogenic bacteria causing black hair tongue
  • Medication- hydroxychloroquine
  • Melanoma
  • Melanotic macule
142
Q
  1. What are the general causes of a pigmented tongue?
A
  • Smoking
  • Racial (genetic)

  • Racial/familial
  • Hyperparathyroidism (primary Addison’s disease, secondary Cushing’s disease, lung tumour secreting ACTH)
  • Kaposi’s sarcoma
  • Lead positioning
  • Hemochromatosis
  • Smoking
143
Q

Burning Mouth-
1. What is the proper name for burning mouth syndrome?

A
  • Oral dysesthesia
144
Q
  1. Who is most likely affected by oral dysesthesia?
A
  • More common in women and peak age of 40-60
  • Generally menopausal women
145
Q
  1. What are your differential diagnosis or oral dysesthesia?
A
  • Dry mouth
  • Other oral conditions
  • Not enough nutrients
  • Allergies
  • Medications (high BP meds)
  • Oral parafunctional habits like bitng tongue etc things irritating the tongue
  • Psychological issues

  • Lichen planus
  • Median rhomboid glossitis
  • Hematinic or nutritional deficiency- iron, folate, vitamin B12
  • Geographic tongue
  • Diabetes (or other endocrine disorders)
  • Gonorrhoea
  • Recurrent oral ulceration
  • Poorly fitting denture problems
  • Xerostomia
  • Psychological factors- stress, anxiety and depression
146
Q
  1. What investigation might you carry out for burning mouth syndrome?
A

As it could be secondary to something else, would try to diagnose to find out what the problem was.
* Full blood count
* Other blood tests- Haematinics, Blood glucose (HbA1c), liver function test, thyroid function test, U’s & E’s
* Salivary flow rate for xerostomia assessment
* Denture assessment
* Psychiatric assessment
* Parafunctional habit assessment- intra and extra-oral assessment

147
Q
  1. How is burning mouth syndrome managed?
A
  • Reassurance
  • Correct any underlying causes- nutritional deficiencies, blood sugar (diagnose and treat diabetes), manage parafunctional habits or correct denture faults
  • Conservative advice- keep fluids up and use of difflam 0.15% benzydamine mouthwash. Avoid smoking, limiting acidic or spicey foods and not drinking carbonated beverages. Stress management methods.
  • Pharmacotherapy- gabapentin, antidepressant therapy- tricyclics, CBT (cognitive behavioural therapy)
148
Q
  1. What symptoms might the patient with burning mouth syndrome complain of?
A
  • Sever burning of tingling sensation in the mouth, commonly affecting the tongue
  • Sensation of dry mouth with increased thirst
  • Taste changes or paraesthesia such as bitter or metallic taste or loss of taste
  • Mucosa clinically normal
149
Q

Geographic Tongue-
1. What is geographic tongue?

A
  • Normal process characterised by areas of red, smooth depapillation (loss of lingual papilla) which migrate over time
150
Q
  1. How is geographic tongue managed?
A
  • reassure the patient that this is normal and monitor
151
Q

Salivary Gland Tumors-
1. Order the salivary gland tumours by incidence?

A
  • Pleomorphic adenoma (75%)
  • Warthin tumour (15%)
  • Adenoid cystic carcinoma (5%)
  • Mucoepidermal carcinoma (3%)
  • Acini cell carcinoma (<1%)
152
Q
  1. What are the histological features of a pleomorphic adenoma?
A
  • Variable fibrous CT capsule which may be incomplete (breaks in capsule allow continued outgrowth of the tumor)
  • Presence of epithelial duct-like structure or epithelial sheets
  • Areas of myoepithelial cells, myxoid tissue and chorndroid tissue
153
Q
  1. What histological feature of pleomorphic adenoma is related to recurrence?
A
  • Incomplete CT capsule and presence of outgrowths can result in multifocal types and difficulty removing
154
Q
  1. What are the histological features of Warthin’s tumour?
A
  • Distinctive histology
  • Contain cystic cavities or spaces lined by 2 layers of oncoytic epithelial
  • Lots of lymphoid tissue sometimes with germination centres
  • Covered by fibrous CT capsule
155
Q
  1. What is are the histological features of adenoid cystic carcinoma?
A
  • Varying pattern possible possible
  • Cribriform pattern shows collections of spaces which contain ground substance
  • Small cuboidal malignant cells present
  • Connective tissue stroma found between cells
  • May show signs of perineural infiltration
  • No capsule present and may be tubular or solid in nature
156
Q
  1. What features of a parotid swelling would make you suspicious of malignancy?
A
  • Firm
  • Attached to underlying structures/tissue
  • Fast growing
  • (Asymmetry or obstruction of the gland)
  • (Late stage will have pain and possible facial palsy)
157
Q
  1. How are salivary gland neoplasm diagnosed?
A
  • Fine needle aspiration (FNA)- doesn’t give a lot of tissue
  • Core biopsy- much more invasive but get more information
  • Incisional biopsy
  • Excisional biopsy
158
Q
  1. Where are you most likely to get a salivary neoplasm?
A
  • Parotid- 80% (15% malignant)
  • Submandibular- 10% (30% malignant)
  • Sublingual- 0.5% (80% malignant)
  • Minor 10% (45% malignant)
159
Q
  1. What are the causes of xerostomia?
A
  • Local- Cancer therapies- chemotherapy and radiotherapy to head and neck
  • Smoking
  • Steroid inhalers
  • Mouth breathing
  • Systemic- Medication (e.g. amitriptyline, diuretics, antihistamines)
  • Sjogren’s syndrome
  • Psychogenic factors
  • Dehydration
  • Viral causes- HIV, Hep C, EBV
  • Chronic syndromes- dry mouth, Addison’s, sarcoidosis, renal disorders
160
Q
  1. How can you assess xerostomia intra-orally?
A
  • Measure unstimulated saliva flow over 15 minutes- <1.5ml/15 mins is abnormal
  • Palpate and assess ducts of salivary glands for secretion
  • Check for saliva pooling
  • Check if mirror sticks to cheek and tongue
  • Challacombe scale- additive score of 1 to 10

(1 least dry and 10 most severe oral dryness) to determine degree of oral dryness- mirror stick to buccal mucosa, mirror stick to tongue, frothy saliva, no saliva pooling in floor of mouth, tongue shows generalised shortened papillae, altered gingival architecture (smooth), glossy appearance of oral mucosa especially the palate, tongue lobulated or fissured, cervical caries affecting more than 2 teeth, debris on palate or sticking to teeth

161
Q
  1. What are the oral signs and symptoms of xerostomia?
A
  • Swallowing difficulties
  • Clicking speech
  • Oral soreness and discomfort
  • Struggles with denture control and retention
  • Altered taste
  • Food debris lying around the mouth
  • Increased caries and peridootnal disease (especially in uncommon areas such as cervical)
  • Oral candidosis infection increased
  • Depapillation and lobulation of the tongue dorsum
  • Oral malodour- halitosis
  • Ascending infection of the major salivary gland
  • Loss of gingival architecture and glossy appearance
162
Q
  1. How can xerostomia be managed?
A
  • Remove/manage causative agent-
  • Discuss and consider alternative medications/drugs
  • Identify and control diet, blood sugar and other systemic medical issues
  • Moderate alcohol use (including in mouthwash) and smoking cessation
  • Change to SLS free toothpaste
  • Assess mouth breathing including consider referral for sleep apnoea
  • Moderate caffeine intake and encourage fluid and water intake
  • Encourage use of chewing gum
  • Consider salivary substitutes for symptomatic relief- sprays (glandone, saliva orthana), lozenges (saliva orthana, salvix), stimulants (pilocarpine), oral care system (biotine)
  • Give high fluoride concentration toothpaste (+/- mouthwash)
  • Monitor bacterial and fungal load
  • Pilocarpine medication may be considered to increase salvia production
163
Q

What types of LP are each of these photos

A

 Reticular (1L)
- Most commonly be seen
 Papular (1R)
 Plaque (2L)
 Atrophic* (2R &3L)
 Erosive* (3L & 3R)
- *These types tend to be more tender and hence that patient may be aware of the lesions while the other types tend to be an incidental finding of your investigation
- 3L shows an ulcerated erosive patch with reticular involvement
- This ulcerated and erosive lichen planus lesion has the possible for malignant transformation and so specialist input and review is important to determine if static or transformative
 Bullous (4L)
 Desquamative gingivitis (4R)
- This is a clinically descriptive term and has no histological connotation

  • Papular- white plaques
  • Plaque- white plaques arranged in lines
  • Bullous- fluid filled vesicles and bullae
  • Reticular- white striae lacy pattern
  • Erosive- ulcerated areas with yellow fibrinous covering
  • Atrophic- central red lesion due to thinning of the surface epithelium surrounded by white-blueish colour
  • Desquamative gingivitis
  • NB. May be asked to comment on the type/appearance of a given lesion
164
Q
  1. What is lichen planus?
A
  • Chronic mucocutaneous autoimmune issue whereby autoantibodies are formed against body’s own tissue resulting in range of intra-oral as well as cutaneous presentations
  • Involves cell mediated reaction involving T4 (early) and T8 (late) cells
165
Q
  1. What are the histological features of lichen planus?
A
  • Keratinisation- will give white clinical appearance
  • May be hyperplasia or atrophy of the epithelium
  • Hugging band of chronic inflammatory cells (lymphocytes and macrophages- blue) beneath the epithelium
  • Possible epitheliotropism- movement of lymphocytes into the epithelium
  • Basal cell layer destruction which occurs as a result of apoptosis
  • Acantholysis- loss of inter-cellular attachment
  • Saw tooth rete pegs
166
Q
  1. What are the types of lichen planus?
A
  • Papular- white plaques
  • Plaque- white plaques arranged in lines
  • Bullous- fluid filled vesicles and bullae
  • Reticular- white striae lacy pattern
  • Erosive- ulcerated areas with yellow fibrinous covering
  • Atrophic- central red lesion due to thinning of the surface epithelium surrounded by white-blueish colour
  • Desquamative gingivitis
  • NB. May be asked to comment on the type/appearance of a given lesion
167
Q
  1. What is the aetiology of lichen planus?
A
  • Autoimmune
  • Idiopathic
  • Hepatitis C related
  • May also be- drug related (NSAIDs, anti-hypertensives, antimalarial, anti-diabetics), contact sensitivity- amalgam, SLS toothpaste, plaque related; technically lichenoid tissue reaction as cause can be identified
168
Q
  1. How is lichen planus managed?
A
  • If asymptomatic- once identifies and rules out other more sinister cause then clinical photograph and observe for any changes or transformation (biopsy may be indicated if transforms or becomes symptomatic)
  • If symptomatic- identify and remove cause or triggers (switch to SLS free toothpaste, avoid spicy food, diet of avoidance (e.g. cinnamon and benzoate free)
  • Symptomatic management- topical antiseptic 0.15% benzydamine hydrochloride, topical steroid or inhaler either dissolved hydrocortisone or betamethasone mouthwash or beclomethasone inhaler
  • Topical steroids- betamethasone mouthwash (500µg tablets dissolved in 2ml water and swirled round mouth)
  • If no resolution, consider systemic steroids (prednisolone) or systemic immunomodulation (azathioprine)
169
Q
  1. Outline some other key features of LP?
A
  • Affects 1% of the population
  • Mainly affects females 30-50-year-olds
  • Can also affect the genitals and skin as small papules with a shiny surface and white lines known as Whickham’s striae
  • Typically, asymptomatic and painless but can give burning sensation
  • Normally bilateral and symmetrical and affecting the buccal mucosa as a white lesion but multiple presentations
170
Q

A patient presents for a regular check-up when you notice a lesion that is white and lacey in appearance in the left buccal mucosa next to 2 old amalgams.
1. What is your diagnosis? (2)

A

lichenoid tissue reaction

171
Q
  1. What made you arrive at this diagnosis and hoe does this condition occur? (2) (lichenoid tissue reaction)
A
  • Adjacent to two amalgam restorations which can be a trigger for this type of reaction
  • Whiteness of the lesion likely to be due to increased keratinisation in response to chronic irritation from the restorations
  • This is a Type IV hypersensitivity reaction to amalgam
172
Q
  1. Name two types of biopsy you could carry out the further investigate this lesion?
A
  • Incisional biopsy (punch)
  • Fine needle aspiration biopsy
173
Q
  1. Name four histological features of this condition LTR?
A
  • Keratinisation- will give white clinical appearance (less than in LP)
  • May be hyperplasia or atrophy of the epithelium
  • Hugging band of chronic inflammatory cells (lymphocytes and macrophages- blue) beneath the epithelium
  • Basal cell layer destruction which occurs as a result of apoptosis
  • Thicker rete pegs than in LP

  • Evidence of perivascular cupping/infiltration (blood vessels surrounded by chronic inflammatory cells) sign of cell mediated immune reaction (type 4 hypersensitivity)
  • Keratinisation- will give white clinical appearance (less than in LP)
  • May be hyperplasia or atrophy of the epithelium
  • Hugging band of chronic inflammatory cells (lymphocytes and macrophages- blue) beneath the epithelium
  • Possible epitheliotropism- movement of lymphocytes into the epithelium but greater presence of macrophages (compared to LP)
  • Basal cell layer destruction which occurs as a result of apoptosis
  • Acantholysis- loss of inter-cellular attachment
  • Thicker rete pegs than in LP
174
Q
  1. What might a patient complain of if they have a sialolith?
A
  • Fluctuant swelling and pain associated with mealtimes (or thought of food) (prandial swelling and pain)
  • Rush of saliva into the mouth when eating
  • Xerostomia (Dry Mouth) or thick saliva
  • Bad taste
175
Q
  1. What gland is most commonly affected by sialolith and why?
A
  • Submandibular most commonly affected due to uphill (against gravity) and tortuous path (twisted and curvy- ideal for saliva stagnation )
176
Q
  1. What investigations can be done for sialolith?
A
  • Low dose plain radiographs- lower true occlusal
  • Sialography
  • Ultrasonography (ultrasound)

  • Isotope scan/scintiscan (if gland function uncertain)
  • (Palpation of gland and duct both intra and extra-orally)
177
Q
  1. How can you manage a Sialolith?
A
  • Surgical sialolith removal if practical- LA, secure gland and stone, make incision, remove stone, suture, give post-op instruction
  • Sialoendoscopic removal via basket retrieval
  • Sialography can be used in ‘no stone cases’ for washing affected
  • Balloon dilation
  • Shock wave lithotripsy
  • Consider gland removal if fixed swelling
  • Ultrasound? to break up the calcium stone
178
Q

Prescriptions-
1. What information should be on a prescription?

A
  • Patient details- name, address, Chi, age if under 12
  • Date of prescription (valid for 6 months)
  • Number of days treatment
  • Generic drug name
  • Form and strength of preparation
  • Dose and dose frequency
  • Duration of treatment
  • Total quantity of drug to send
  • Instruction for how and when to take (label)
  • Score out extra space
  • GDP (prescriber) name in capitals
  • GDP (prescriber) signature
  • GDP (prescriber) stamp or address details
179
Q
  1. What are the common dosages for 2 antibiotics given for dental infection, as written on prescription?
A
  • Amoxicillin capsules- 500mg for 5 days // send- 15 capsules // Label- 1 capsule three times daily
  • Metronidazole tablets- 200mg for 5 days // send 15 capsules // Label- 1 tablet three times daily

Phenyxomethylpenicillin 250mg for 5 days // send 40 capsules // label 2 capsules 4 times daily

180
Q
  1. What are the symptoms of ectodermal dysplasia?
A
  • Hypodontia and peg shaped teeth
  • Poor functioning sweat glands
  • Abnormal nails
  • Cleft lip +/- palate
  • Decreased skin pigmentation
  • Large forehead
  • Low nasal bridge
  • Thin, sparse hair
  • Learning disabilities
181
Q

Bone Diseases-
1. What are the clinical and radiographic signs of Paget’s disease?

A
  • Clinical- Localised painful/tender (feels big and tight) bone swelling, focal temperature increase due to hyperaemia and hypervascularity, may cause nerve compression- if affects trigeminal can get numbness visual issues and deafness , may affect 1 bone (monostatic) or multiple bones (polystatic), dentures become ill fitting, may be decreased range of function depending on bone affected
  • Radiographic- Variable osteoporosis and sclerosis, in immature stages presents as a radiolucent (osteolytic) area, laterally presents as an irregular shaped radiopacity with cotton wool appearance (mixture or radiopaque and lucent- lytic and sclerotic), may get hypercementosis (intact PDL surrounding)
182
Q
  1. What are the clinical and radiographic signs of Albright’s disease?
A
  • Type of fibrous dysplasia which is associated with endocrine disturbances
  • Clinical- Polycystic fibrous dysplasia (multiple slow growing, asymptomatic bony swelling which usually stop growing after the patients active growth phase; can result in facial asymmetry and possible OB and unbalanced occlusion depending on where is affected), melanin skin pigmentation (tea or coffee (stain) or early puberty as a result of endocrine disturbances
  • Radiographic- varies with stage of disease, lesion with well-defined margin, internally may have ground glass or orange-peel appearance (due to mix of radiolucent and radiopaque appearance), starts off quite radiolucent then becomes more radiopaque as there is more calcification and bucco-lingual expansion (Inc./ thickness of bone so less less x-ray beams through)
183
Q
  1. What are the clinical and radiographic signs of cherubim?
A
  • Clinical- Painless bilateral, usually symmetrical, expansion of the maxilla and mandible, rounded face and swollen cheeks, dental malocclusion, teeth in affected region may be loose or tooth eruption delayed,
  • Radiographic- Multiloculated radiolucent lesions with soap bubble appearance (due to fibrous replacement of bone) with corticated margin, as lesion progresses may become more sclerotic
184
Q
  1. Name and describe the type of dental orofacial pain syndromes?
A
  • Better or worse over time
  • Usually acute or sub-acute not chronic
  • Musculoskeletal- TMJD pain (and periodontal)
  • Visceral- abscess, pulpal pain, caries
  • Atypical odontalgia- dental pain without detected pathology which follows distinct pattern of pain (pain free episodes with immense pain which then settles quickly)
185
Q
  1. Name and describe the types of non-dental orofacial pain syndromes?
A
  • Generally acute infective non-dental pain that gets worse of chronic pain usually caused by a non-dental condition
  • Neuropathic- constant burning/aching pain with a fixed location and intensity, generally occurs after injury (e.g. trauma from LA, herpes zoster or shingle, destructive treatment or routing treatment), examples- trigeminal neuralgia, chronic region pain syndrome (CRPS), traumatic injury to facial nerve, surgical injury to H&N nerves
  • Psychogenic- persistent idiopathic facial pain which poor fits into standard chronic pain syndromes and responds poorly to treatment
186
Q

Plasma Cell Gingivitis-
1. What is the clinical appearance of plasm cell gingivitis?

A
  • Generalised erythema and oedema which can extend from the free marginal gingiva onto the attached gingivae
  • Gingiva is red, friable, bleeds easily and normal gingival stippling is list
  • May be accompanied by cheilitis (lip swelling) or glossitis
187
Q
  1. What is the aetiology of plasma cell ginigvitis?
A
  • Hypersensitivity reaction- SLS< cinnamon etc/
  • Idiopathic
188
Q
  1. What may worsen the condition of plasma cell gingivitis?
A
  • Not removing the causative agent from the oral cavity
  • Poor OH
  • Plaque retentive factors
189
Q
  1. How is plasma cell gingivitis managed?
A
  • Histological sampling to diagnose the condition
  • Preventing exposure to the causative antigen
  • Tacrolimus mouthwash

BDS4 (24 decks)

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