Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Oral disease - 4th year > Oral mucosa > Flashcards

Oral mucosa Flashcards

1
Q

What are the different parts of tissue that you can see histologically?

A

There is the epithelium which may be stratified squamous. This is divided into the basal cell layer, prickle cell layer and granular layer which produces keratin. Beneath the epithelium there is the the connective tissue consisting of the lamina propria which is the superficial part and submucosa which contains fat. Beneath this there is muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the types of keratinised epithelium?

A

There is orthokeratinised which has no nuclei and parakeratinised which has nuclei.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the types of mucosa in the mouth?

A

The gingiva and hard palate is masticatory mucosa. The uvula, soft palate, floor of mouth and buccal mucosa is lining mucosa. The tongue is gustatory mucosa or specialised mucosa. There is a junction between the lining and masticatory mucosa called the mucogingival junction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why are palatal injections more painful?

A

The palate doesn’t have a submucosa and is firmly fixed to the underlying bone and is called mucoperiosteum. It resists the stresses and strains of eating and mastication. During palatal injections there is little space for anaesthetic to diffuse anywhere. Whereas lining mucosa has a loose submucosa for movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does specialised mucosa on the tongue consist of?

A

It is found on the dorsum of the tongue. There are 4 types of papillae which are filiform, fungiform, foliate and circumvallate. Filiform is the most common papillae on the tongue. Fungiform are found all over the tongue. Circumvallate papillae are found on the posterior border of the tongue. Foliate are found on the lateral border of the tongue. They can get caught on the molars and become hyperplastic. All the papillae are for taste buds except for filiform which are for abrasion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 common variations on normal mucosa?

A
  • Leukoedema
  • Geographic tongue
  • Fordyce spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Leukoedema?

A

It is a variation on normal which is common in African-Americans. There are milky white areas often seen bilaterally on buccal mucosa. It has a classic appearance and if you stretch the cheek it will disappear.
Histologically there is oedema in the epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What might the differential diagnoses be for leukoedema?

A
  • Lichen planus (sore, lacey white lines)
  • White sponge naevus (hereditary, patches are thicker)
  • Frictional keratosis (chronic cheek biting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is geographic tongue and the treatment?

A

It is also called erythema migrans and there are islands of red erythema with white halos/borders around them which move around the tongue and varies day to day. It affects the dorsal tongue, sometimes the lingual side but this is less common. It is usually asymptomatic but can become symptomatic with mild soreness due to spicy foods or aggravating factors. It is common. Patients should avoid spicy or acidic foods e.g. tomatoes. Difflam mouthwash can be prescribed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What might the differential diagnoses be for geographic tongue?

A
  • Lichen planus

- Frictional keratosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are fordyce spots?

A

They are ectopic sebaceous glands which appear as white or yellow speckling. It is common, easily diagnosed and asymptomatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is white sponge naevus?

A

It is a hereditary condition which is autosomal dominant and a point mutation in keratin 4 or 13 genes. There will be a family history but it may skip generations. it it bilateral and seen on cheeks and the floor of the mouth. it appears as thick white folds which are wrinkled and ebbing tide. It is lifelong and may affect other mucosa sites also. The floor of mouth is a common site for dysplasia and SCC so refer if seen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does white sponge naevus appear histologically?

A

The epithelium is thickened and hyperplastic. The prickle cell layer is increased and there is lots of keratin on the surface. There is no inflammatory component or dysplasia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the differential diagnoses for white sponge naevus?

A
  • Lichen planus (burning sensation with acidic/spicy foods)
  • Lichenoid drug reactions (usually have reddening and not from childhood)
  • Frictional keratosis
  • Leukoedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can the oral mucosa change with age?

A
  • Mucosa may appear atrophic and smoother
  • Decrease in elasticity
  • Prominence of fordyce spots
  • Varicosities - ventral surface of tongue (prominent veins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the types of trauma in the oral mucosa?

A
  • Mechanical - from dentures, teeth, orthodontic appliances, surgical wounds
  • Chemical - burns e.g. aspirin, allergic response to dental materials
  • Physical - extremes of hot and cold, irradiation
    There will be epithelial changes and connective tissue changes in trauma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of traumatic ulceration?

A
  • Trauma from dentures
  • Teeth
  • Chemical burns
  • Irradiation for malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does an ulcer appear histologically?

A

It is complete loss of the epithelium. There is a pinker band on top which is fibrinopurulent slough. Underneath there is granulation tissue which is endothelial cells forming new blood vessels and fibroblasts forming collagen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can the epithelium respond to trauma?

A

It can ulcerate. It can produce more keratin to protect itself. If non-keratinised mucosa becomes keratinised this is called keratosis. If keratinised mucosa produces more keratin this is hyperkeratosis. Another change is hyperplasia of the epithelium or atrophy where it becomes thinner. Atrophy is a reduction in the thickness of the epithelium due to a loss of cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the connective tissue changes in trauma?

A

There can be hyperplasia which is overgrowth of the connective tissue and this produces a fibrous polyp. Polyps can vary in how they look. They may be seen on the anterior palate due to deep/traumatic overbite. They can be seen on the ridges due to denture trauma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some specific examples of trauma affecting the oral mucosa?

A
  • Frictional keratosis
  • Stomatitis nicotina
  • Papillary hyperplasia of the palate
  • Chemical burns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is frictional keratosis?

A

It is a white patch caused by continuous trauma and usually seen along the occlusal line or opposite sharp cusps, orthodontic wires or dentures. Histologically you would see hyperkeratosis, acanthosis and no inflammation or dysplasia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the management of frictional keratosis?

A

You must be able to demonstrate the lesion is caused by trauma. If you remove the cause then the lesion should regress. If not then consider other white lesions in differential diagnosis. Leukoplakia is a white patch of unknown cause and there is increased risk of malignant change so this is important to note. The management is incisional biopsy to establish diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is stomatitis nicotina and the treatment?

A

It is seen on the palate in pipe and cigar smokers. It is a response to chronic heat. It is not a pre-malignant condition and there is a positive correlation between intensity of smoking and severity. The treatment is to stop or reduce smoking and the lesions may disappear. It should be regularly reviewed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is papillary hyperplasia of the palate?

A

It is caused by ill-fitting dentures and is symptomless erythematous overgrowth of the mucosa. It corresponds to the outline of the denture. The management is provision of new dentures. There can be excision of papillary projections for advanced cases. It is not a pre-malignant lesion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What factors affect healing?

A
  • Primary or secondary intention (wounds closely opposed heal faster than those separated)
  • Foreign body - acts as a focus of infection and delays healing (e.g. bone, root - there will be neutrophils around it and form an abscess containing puss, there may also be osteoclasts to remove bone - open up wound and remove)
  • Vascular supply (reduced blood supply reduces healing capacity)
  • Nutritional deficiencies (vitamin C)
  • Irradiation (reduces blood supply)
  • Malignancy (failure to heal e.g. non-healing tooth socket)
  • Infection (reduces healing capacity)
  • Poor immune response (Leukaemia, diabetes, immunosuppression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is primary and secondary intention?

A

Primary intention is when the edges of a wound are brought together. It is used for incisional biopsy and a big biopsy will heal just as quickly as a small one. Secondary intention is for a gingivectomy or tooth extraction socket.
Refer ulcer on pathway after 3 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the types of localised gingival swellings?

A
  • Fibrous hyperplasia (fibroepithelial polyp)
  • Pyogenic granuloma
  • Peripheral giant cell granuloma
  • Gingival cyst
  • Bohn’s nodules (and epstein pearls - dots along midline of palate, disappear on own)
    (top three are most important)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the types of generalised gingival swellings?

A
  • Inflammatory - chronic hyperplastic gingivitis
  • Hereditary - gingival fibromatosis
  • Neoplastic -leukaemia infiltration
  • Hormonal - endocrine related (puberty, pregnancy)
  • Diet related - scurvy
  • Associated with GI tract disease - crohn’s disease
  • Drug related - drug induced hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a fibroepithelial polyp?

A

They are caused by an overgrowth of fibrous connective tissue and covered by hyperkeratinised stratified squamous epithelium. They can be pedunculated or sessile and are the same colour as the oral mucosa. It is a firm nodule which is painless unless traumatised. It is caused by trauma (dentures, teeth, orthodontic appliances). They are common on the cheeks, tongue and lip. The treatment is to excise and remove the cause, then send for histopathological examination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is a pyogenic granuloma?

A

It is a red/blue/purple vascular growth which grows rapidly. it can be sessile or pedunculated and is soft and bleeds easily. It is usually seen in age less than 40. It is common in pregnancy/puberty (pregnancy epulis). It is caused by trauma (plaque, calculus, dentures, teeth, orthodontic appliance). In pregnancy/puberty there is a hormonal induced exuberant response to the above. There is overgrowth of very vascular granulation tissue (endothelial cells and fibroblasts) which explains the red colour seen clinically. The top is always ulcerated which is why it appears red. There is fibrin on the top.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is a pyogenic granuloma managed?

A

You should excise and remove the cause. In pregnancy give OHI and excise, however it may recur whilst the patient is pregnant. They can mature into fibroepithelial polyps.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a peripheral giant cell granuloma?

A

It is a soft red/blue sessile or pedunculated swelling consisting of vascular fibrous tissue. It usually occurs around anterior teeth and is seen more commonly in the mandible. The average age is less than 40. It is similar to a pyogenic granuloma clinically and can cause superficial bone resorption. It is only found on the gingiva. Histologically there are numerous multinucleate cells and haemorrhage. The histological diagnosis is based on a giant cell lesion but it is the same as giant cell lesions arising in bone e.g. central giant cell granuloma and hyperparathyroidism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is a peripheral giant cell granuloma managed?

A

It is important to determine whether the lesion has arisen in the gingiva or within bone and burst through the cortical plate. Take radiographs to check this. If it has arisen in bone the differential diagnoses include central giant cell granuloma and hyperparathyroidism (more common in 60+). Blood tests are used to check this.
Excise peripheral giant cell granuloma and curettage underlying bone to prevent recurrence. Send lesion for histopathological examination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are differential diagnoses for epulides?

A
  • Firm mucosa coloured - fibroepithelial polyp
  • Soft red, red/blue - pyogenic granuloma, giant cell granuloma
  • If patient pregnant/puberty - more likely to be pyogenic granuloma
  • Definitive diagnosis by excisional biopsy
  • Exclude abscesses - red/yellow/soft/fluctuant, special investigations are vitality tests, radiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is gingival fibromatosis?

A

It is hereditary (autosomal dominant) and lifelong. There is pale pink, firm overgrowth which may cover and submerge the teeth. It may regrow after removal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is chronic hyperplastic gingivitis?

A

It is associated with poor oral hygiene and there is erythematous, hyperplastic gingiva which bleed on probing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is hormonal related gingival hyperplasia?

A

It is related to puberty and pregnancy and there is an exuberant response to plaque. The gingiva are red, erythematous and bleed easily on probing. You should disclose plaque and give OHI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does diet affect the gingiva?

A

There can be gingival hyperplasia in scurvy. It is caused by a diet poor in vitamin C and therefore failure to synthesis collagen. It is an inflammatory type hyperplasia which can lead to loss of teeth. It is very rare in the UK.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is gingival hyperplasia associated with leukaemia?

A

There will be red, swollen gingivae which may exude pus and be ulcerated. It is in response to an excess amount of plaque. It may be associated with petechial haemorrhages, tiredness so look out for fatigue and easy bruising.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is drug induced gingival hyperplasia?

A

It is associated with certain drugs such as cyclosporin (immunosuppressant), nifedipine (anti-hypertensive) and phenytoin (anti-convulsant). The gingivae are pale with a lobulated surface and little inflammation. Histologically you will see dense fibrous tissue, little inflammation and long epithelial rete ridges. The management is surgical reduction, improve oral hygiene and change drug regime if possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Crohn’s related gingival hyperplasia?

A

There may be labial swelling, aphthous ulcers, mucosal tags and cobblestoning.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What may the differential diagnoses be for generalised gingival hyperplasia?

A
  • Pale, uninflamed gingivae - gingival fibromatosis or drug induced, distinguish on duration and drug history, more likely to be drug induced
  • Red, inflamed gingivae - inflammatory hyperplasia or hormonal induced, distinguish by history
  • Red, inflamed, pus, ulceration - leukaemia, further investigations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is squamous cell papilloma?

Following questions on oral mucosa swellings

A

It is a benign neoplasm which is HPV driven (6 and 11 as 16 and 18 are oncogenic). It is a white cauliflower-like growth which can be pedunculated or sessile. It is common on the palate. Histologically there is an overgrowth of epithelium which is hyperkeratinised hence the white colour. The surface is thrown into fronds (folds) and it has a vascular connective tissue core. Management is to excise with a margin and HPV 6 and 11 are not contagious.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is Heck’s disease? (focal epithelial hyperplasia)

A

It is multiple papillomas caused by HPV 13 and 32. There are multiple flat viral warts. It may resolve spontaneously or you can excise. It is rare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is fibrous hyperplasia and traumatic neuroma?

A

Fibrous hyperplasia can be called leaf fibroma and is caused by an ill-fitting denture. It is fibrous connective tissue covered by mucosa.
Traumatic neuroma is a reactive condition. It is haphazard overgrowth of nerve fibres usually caused by trauma. It is often seen in the mental foramen region. It is frequently painful. Histologically you will see scar tissue and lots of nerve fibres in a haphazard arrangement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is lipoma?

A

It is a benign neoplasm composed of fat. It is yellow/pink and has a smooth surface. It is common on the cheek and tongue and the management is to excise. They tend to be quite large and seen on the buccal mucosa. Histologically there are lots of adipocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is haemangioma?

A

It is an example of a hamartoma which is proliferation of tissue which is normal for that site. A choristoma is proliferation of tissue which is abnormal for that site for example in the middle of the tongue you can get a nodule of cartilage. There are excess blood vessels. It is localised or diffuse and may bleed excessively so take care. It will blanch under pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Sturge Weber syndrome?

A

It is present from birth (congenital) and has characteristic features:
- Port wine stain which follows the distribution of the trigeminal nerve, it is an overabundance of capillaries near the skin
- Varying degrees of mental retardation/learning difficulties
- Glaucoma
- Seizures
Intraorally you can see gingival swelling and haemangioma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is lymphangioma?

A

It is also a hamartoma. It is similar to haemangioma but is an overgrowth of lymphatic vessels. It has a paler colour clinically.
Common head and neck lymphangioma in neck and floor of mouth is cystic hygroma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a neural tumour?

A

It is a neurofibroma or neurilemmoma. It is more deep seated and relatively rare. It is firm and mucosa coloured.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is a granular cell tumour?

A

It is common on the tongue and has a neural origin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is a congenital epulis?

A

Similar to granular cell tumour histologically but it occurs in neonates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What may the differential diagnoses be for mucosal swellings?

A
  • Cauliflower like and white - squamous cell papilloma
  • Smooth, mucosa coloured, related to denture or other source of trauma - fibrous hyperplasia
  • Smooth, yellow - lipma
    Red/red-white, related to trauma - pyogenic granuloma
  • Red/blue - haemangioma, mucocele
    Deep seated/normal mucosa - neuroma, neural tumour, salivary gland tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When is FNA used?

A

When you can’t get to a lesion with a scalpel. Deeply seated lesions e.g. lymph nodes in the neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the sources of pigment?

A
  • Melanin (majority) which is endogenous so produced by the body
  • Haemosiderin (endogenous)
  • Amalgam and heavy metals (exogenous)
  • Chromogenic bacteria (exogenous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is haemosiderin?

A

It is a breakdown product of red blood cells. They are consumed by macrophages and break down. The haem which contains iron breaks down into haemosiderin which stores iron but cannot be used until it breaks down further. Haemosiderin builds up in tissues where there has been damage e.g. haemorrhage. It is brown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is melanin?

A

Melanin is produces by melanocytes (or nevus cells) which are found in the basal third of the epithelium. Melanosoma are packages of melanin found in melanocytes. Melanocytes become visible on histology when they are active or atypical. You usually see melanin pigment in the basal epithelium and it absorbs UV light so protects from the sun. Melanin is transferred to adjacent keratinocytes by membrane bound organelles called melanosomes. There can be increased melanin production without increased melanocytes but if melanocytes increase this is abnormal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the sources of occupational exposure to heavy metals?

A
  • Manufacture of ammunition, dental x-ray films, plumbing, ceramic glazes
  • Jobs - lead miners, plumbers, mechanics, glass manufacturers, construction workers, welding, processing of ore, production of paints and pigments
  • Agyria is ingesting too much silver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are chromogenic bacteria?

A

They are bacteria that produce pigment such as aspergillus and actinomyces. They are often seen in hairy tongue. Bacterial enzymes act on iron in saliva.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the types of oral pigmented lesions?

A

Look at image on lecture and learn this.

There is exogenous and endogenous which is categorised by developmental, acquired and neoplastic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What information would you need to make a differential diagnosis on a pigmented lesion?

A
  • Name, age, occupation
  • History of lesion
  • Medical history
  • Drug history
  • Dental history
  • Social history
  • Extraoral and intraoral examination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is an amalgam tattoo?

A

A pigmented lesion which tends to be very close to where the amalgam is. A radiograph is needed to confirm amalgam and will show a radiopacity in the tissues. A biopsy may not be required.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How can chewing a pencil cause a pigmented lesion?

A

Chewing a pencil can get lead into the tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do heavy metals cause pigmented lesions?

A

Heavy metals include lead, bismuth, mercury, silver, arsenic and gold. They may leach directly into the mucosa from dental restorations and crowns. They are deposited due to drugs containing heavy metals e.g. pepto-bismol. Lead in blood leaks out of gingival tissues as it is in crevicular fluid. It looks similar to an amalgam tattoo histologically.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is black hairy tongue?

A

It affects the posterior dorsal tongue and there is a decrease in the normal desquamation process. It is associated with a soft diet, smoking and antibiotic use. There are elongated filiform papillae which may be black/brown/white. Discolouration is caused by chromogenic bacteria, smoking, chlorhexidine and foods. Histologically you may see clusters of aspergillus bacteria. Difficult to treat - avoid smoking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the developmental endogenous pigmented lesions?

A
  • Physiological (melanin)
  • Peutz Jehger’s syndrome (melanin)
  • Haemochromatosis (haemosiderin)
  • Pigmented naevus (melanin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How can oral pigmented lesions be physiological?

A

We all have different coloured skin. Symmetrical pigmentation will be seen in gingivae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is Peutz Jehger’s?

A

It is a genetic disorder which is autosomal dominant. There are pigmented mucocutaneous macules, GI polyps usually in the small intestine with an increased risk of malignant change associated with the polyps. The melanotic spots are characteristically small and multiple and are very obvious around the lips. It is seen in children. Histologically there will be an increase in the amount of melanin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is haemachromatosis?

A

It is a rare genetic disorder (autosomal recessive). There is an accelerated rate of intestinal iron absorption leading to raised serum ferritin and transferrin saturation, There is accumulation of iron (as haemosiderin) in the liver and islets of langerhans. This leads to bronze skin pigmentation, liver cirrhosis and diabetes mellitus. It is treated with regular venesection. This leads to fatigue, lethargy and you are more prone to bacterial infections (some bacteria have an affinity for iron).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is a melanotic naevus?

A

It is a mole but if it is not well-defined it may be something sinister. Melanin is also produced by nevus cells which are derived from the neural crest. They are found in the skin and mucosa. There are many histological types of nevus which are junctional (epithelium), intradermal/mucosal (connective tissue) or compound (both).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the types of acquired endogenous oral pigmented lesion?

A
  • Addison’s disease (melanin)
  • Drug induced (melanin)
    Post-inflammatory (melanin)
    Smoker’s melanosis (melanin)
    Melanotic macule (melanin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is Addison’s disease?

A

Approximately 90% of cases are caused by autoimmune disease. There is destruction of the entire adrenal cortex followed by a subsequent lack of adrenocortical hormone. This leads to increased production of adrenocorticotropic hormone ACTH by the anterior pituitary gland. ACTH induces melanocyte stimulating hormone leading to increased pigmentation of the skin and oral mucosa. There are diffuse brown patches on the buccal mucosa, palate, tongue and gingivae. Extra-oral sites include palmer creases and new scars. Patients need steroid cover due to adrenal crises.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is a melanotic macule?

A

The histology appears the same as a freckle. It has different histology to a naevus as there are no nevus cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What medication can cause drug induced pigmentation?

A
  • Antimalarians - quinacrine, chloroquine, hydroxychloroquine
  • Quinidine
  • Zidovudine (AZT)
  • Tetracycline
  • Minocycline
  • Chlorpromazine
  • Oral contraceptives
  • Clofazimine
  • Ketoconazole
  • Amiodarone
  • Busulfan
  • Doxorubicin
  • Bleomycin
  • Cyclophosphamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the three ways drug induced pigmentation happens?

A
  • Increased production of melanin
  • Deposition of iron after damage to mucosal vessels
  • Deposition of heavy metals in tissues (exogenous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is post-inflammatory pigmentation?

A

Lichen planus destroys basal cells which hold melanin. The melanin is lost to the connective tissue and drops into the lamina propria so brown pigment is seen within lichen planus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is smokers melanosis?

A

There is a protective mechanism of the oral tissues to produce melanin. 21.5% of smokers will have this. It has a similar histology to lichen planus but no basal cell loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the two types of endogenous neoplastic pigmented lesion?

A
  • Malignant melanoma

- Kaposi’s sarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is malignant melanoma?

A

It makes up less than 1% of all oral malignancies. There is proliferation of malignant melanocytes along the junction between the epithelium and connective tissue as well as within the connective tissue. It is seen on the anterior palate and anterior gingivae most commonly. It is seen in men more than women and ages 30-70. It may present with typical signs and symptoms of malignancy such as rapidly enlarging mass associated with ulceration, bleeding, pain and bone destruction. Or it can be asymptomatic, slow growing, brown or black patch with asymmetric and irregular borders. Some are non-pigmented (amelanotic) which can make it difficult to diagnose. It is an aggressive and often fatal disease (worse prognosis than skin lesions). Risk factors are unknown. The treatment is radical surgical excision with clear margins. Radiation and chemotherapy are ineffective which adds to the difficulties associated with management of this malignancy. Over 5 year survival rate – 15%. Every melanoma starts at T3 – so aggressive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is Kaposi’s sarcoma?

A

It is a malignant tumour associated with immunosuppression. It is a hallmark of AIDs caused by HHV-8. There are black/purple lesions orally on the gingivae most commonly. Treatment is excision with or without chemotherapy/radiotherapy. Histologically it can appear similar to melanoma and appear as a bruise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is an ulcer?

A

It is a full thickness loss of the epithelium which exposes the underlying connective tissue. The ulcer is covered by a fibrinopurulent slough. There is underlying granulation tissue and mixed inflammatory infiltrate. They are usually painful. Erosion is partial loss of the epithelium. Histologically there is fibrinopurulent slough with granulation tissue underneath. Primary ulcers begin as ulcers and secondary ulcers begin as vesicles or blisters.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the differential diagnoses for ulcers?

A
  • Neoplastic e.g. SCC
  • Traumatic e.g. sharp tooth
  • Developmental e.g. epidermolysis bullosa
  • Manifestation of systemic disease e.g. Crohn’s
  • Manifestation of dermatological disease e.g. lichen planus
  • Idiopathic e.g. RAS
  • Iatrogenic e.g. drugs
  • Infective e.g. syphillis, TB, HSV, fungal infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Give examples of single episode and recurrent episode ulcers?

A

Take a good history:
- Single episode
Single ulcer e.g. SCC
Multiple ulcers e.g. herpes zoster
- Recurrent episode
Single ulcer e.g. mucocutaneous disorders
Multiple ulcers e.g. RAS, mucocutaneous disorders
- Some causes fit into many categories e.g. drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the causes of single episode ulcers?

A
  • Trauma - physical, chemical, thermal, factitious
  • Malignancy - SCC, salivary neoplasm, lymphoma
  • Infective - TB, syphillis, HSV
  • Drugs - methotrexate (immunosuppressive - target cells that are breaking down quickly such as epithelium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How would you treat a single episode traumatic ulcer?

A
  • Reassurance
  • Remove the cause
    Consider Difflam and Corsodyl
  • Should show signs of improvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the signs of a malignant ulcer?

A

Look out for a raised ulcer with raised borders. If there is a loss of epithelium there should be no growth. Look out for lateral border of the tongue and floor of mouth as these are common areas. Any ulcer that is over 3 weeks in duration of unexplained cause should be regarded as malignant until proven otherwise (biopsy). Don’t be afraid of being wrong.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the causes of single episode multiple ulcers?

A
  • Herpes simplex
  • Herpes zoster
  • Erythema multiforme
  • Hand, foot and mouth
  • Herpangina
  • Oral lichen planus
  • Vesticulo-bullous disorders
  • Iatrogenic e.g. drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What drugs can cause ulcers?

A
  • Allopurinol
  • Cytotoxics
  • Gold
  • Indomethacin
  • Methotrexate
  • Methyldopa
  • Nicorandil (angina)
  • Penicillamine
    Irradiation can also cause ulcers
90
Q

What is the management for drug and infective causes?

A

Liase with the GP or consultant for drug related causes. For infective causes most are self-limiting and some require anti-fungals/antibiotics/acyclovir.

91
Q

What are the causes of recurrent multiple ulcers?

A
  • RAS
  • Mucocutaneous disorders
  • Behcet’s disease
  • Recurrent erythema multiforme
  • Other systemic disorders
92
Q

What are the types of RAS?

A
  • Minor recurrent aphthous stomatitis
  • Major recurrent aphthous stomatitis
  • Herpetiform recurrent aphthous stomatitis
  • All idiopathic
93
Q

What is RAS?

A

It is common and affects 20% of the population at some time. It is painful, may affect eating, drinking and speech. Occasionally it is very disabling. There may be a familial component. When taking a history the patient may say it keeps coming and going and they feel run down. SCC is rare in young people.

94
Q

What are the features of minor RAS?

A

It makes up 80% of RAS ulcers and the peak age range is 10-30. There are usually 1-5 ulcers approximately 3-8mm in diameter. Minor RAS must be less than 1cm. They last 7-10 days with a variable ulcer free period. They are usually seen on non-keratinised mucosa towards the front of the mouth and heal without scarring.

95
Q

What are the features of major RAS?

A

It makes up 10% of RAS ulcers and the ulcers may be larger up to 1.5-2cm. They must be greater than 1cm to be major RAS. They last longer and can last from 3 weeks to 3 months. There can be single or multiple ulcers which often affect the back of the mouth. They often affect non-keratinised mucosa but can affect masticatory mucosa and may heal with scarring.

96
Q

What is herpetiform RAS?

A

It makes up <5% of ulcers and there are dozens of small (1-2mm) ulcers which may coalesce to form large, irregular ulcers. It mainly affects the floor of the mouth, margins and the ventral surface of the tongue. They last 7-10 days. Treat with doxycycline mouthwash.

97
Q

What is the difference between contributory and predisposing factors?

A

A predisposing factor makes an individual vulnerable to disease/disorder. A contributing factor increases the effect or the speed.

98
Q

What are the aphthous ulcer contributory factors?

A
  • Stress
  • Trauma
  • Hormones
  • Smoking has a negative relationship
99
Q

What are the aphthous ulcer predisposing/underlying factors?

A
  • Haematological deficiencies (B12, folate, iron)
  • Neutropenia
  • Immune deficiency (HIV)
  • GI tract disease (coeliac, Crohn’s, ulcerative colitis)
  • Vitamin deficiency (B1, B2, B6)
  • Food intolerance e.g. chocolate, benzoates, cinammon
100
Q

What investigations can be done for ulcers?

A
  • FBC, ferritin, B12, folate
  • Coeliac screen
  • Other tests according to history e.g. for food allergens
101
Q

What are the types of treatment for ulcers?

A
  • Preventative
  • Symptomatic
  • Suppressive
102
Q

What is the preventative treatment for ulcers?

A
  • Correct haematological deficiencies
  • Treat underlying systemic disease
  • Remove trauma
  • Dietary elimination
  • OHI/diet advice
103
Q

What is the symptomatic treatment for ulcers?

A

(local)
- Corsodyl mouthwash (chlorhexidine)
- Difflam mouthwash (Benzydomine hydrochloride)
- Covering agents e.g. Genigigel, orobase paste

104
Q

What are the local suppressive treatments?

A

Topical steroids:

  • Hydrocortisone pellets (Corlan)
  • Beclomethasone spray (clenil modulite inhaler)
  • Betamethasone mouthwash (Betnesol) - most commonly prescribed
  • Flixonase nasules
105
Q

What are the systemic suppressive treatments?

A

(if local doesn’t work)

  • Prednisolone (immunosuppressed so more at risk of candidosis etc)
  • Thalidomide
  • Azathioprine (cytotoxic, affects bone marrow, regular blood tests)
106
Q

What is Behcet’s disease?

A

It is named after a Turkish physician and is a type of vasculitis. It is a serious systemic disease which can involve blindness, neurological damage, severe oro-genital ulceration, vasculitis and death. It is mainly in young adult males, approximately 30 years old. The male: female ratio is 2:3:1. There is increased incidence in Japan and Turkey.

107
Q

What is the international study group criteria for Behcet’s disease?

A

Recurrent oral aphthous ulceration plus two of the following:
- Recurrent genital ulcers
- Uveitis, cells in the vitreous or retinal vasculitis
- Skin lesions: erythema nodosum, acne like papulopustular lesions
- Positive pathergy test: pin prick the skin and there will be an exaggerated response after a week (crusting lesions)
Other common features are arthritis, GI lesions, CNS involvement, vascular lesions etc.

108
Q

What multi-disciplinary groups will be involved in the management of Behcet’s disease?

A
  • Dermatology
  • Rheumatology
  • Oral medicine
  • Ophthalmology
109
Q

What ask when taking a history of an ulcer and look for during an examination?

A

History:

  • Size
  • Shape
  • Number
  • Location
  • Duration
  • Periodicity
  • Pain
  • Precipitating factors
  • Relieving factors

Examination:

  • Size
  • Shape
  • Number
  • Site
  • Base
  • Edge
  • Discharge
  • Consistency
  • Nodes - if malignant they may be enlarged, hard, not moveable, attached to underlying tissue
110
Q

What are the different terms for mucocutaneous disease features?

A
  • Macule - flat, circumscribed lesion which is not elevated or palpable
  • Papule - raised, circumscribed lesion which is palpable
  • Blisters - fluid filled sacs within or below the epithelium
  • Vesicle - small blister less than 5mm diameter e.g. herpes simplex vesicles
  • Bulla - large blister greater than 5mm in diameter e.g. pemphigoid/pemphigus
  • Erosion - marked thinning/partial loss of the epithelium but with a thin epithelial covering of the connective tissue, it usually looks red and sensitive
  • Ulcer - localised loss of entire thickness of epithelium which exposes underlying connective tissue, usually painful
111
Q

What are the types of mucocutaneous disease?

A
  • Autoimmune bullous diseases (type II hypersensitivity - antibody mediated, organ specific):
    - Pemphigus
    - Pemphigoid
    - Dermatitis herpetiformis
  • Epidermolysis bullosa congenita (congenital abnormality)
  • Erythema multiforme (type III/IV)
  • Oral lichen planus and lichenoid reactions (type IV)
112
Q

What is the epidemiology of pemphigus?

A
  • The incidence is 0.5-3.2 per 100000
  • The main age group is 40-60
  • Female to male ratio is 1:1
  • It is an organ specific autoimmune disease which targets the skin and oral mucosa
113
Q

What are the oral features of pemphigus?

A

The mouth is involved in most cases and is the only site involved in over 50% of cases. It affects the palate, buccal mucosa and gingiva most commonly. There are bulla which are short lived on the mouth and skin and large shallow non-healing ulcers. It can be life threatening if not treated due to protein, fluid and electrolyte loss and an increased risk of secondary infection, therefore it is important to recognise. OHI must be maintained in these patients. Nikolsky’s sign is when you rub the mucosa/skin and it causes bulla to appear.

114
Q

What is the pathogenesis of pemphigus?

A

There are circulating autoantibodies (IgG) against binding proteins which keep epithelial cells (keratinocytes) together (desmosomes). It targets part of the desmosomal complex (desmoglein 3 usually and sometimes desmoglein 1). It binds and causes acantholysis where the cells break apart causing the formation of an intra-epithelial bulla. Under the microscope there are Tzank cells in the intraepithelial bulla.

115
Q

What investigations are required for pemphigus?

A
  • Biopsy of paralesional and/or normal tissue and send tissue to lab fresh (do not fix)
  • Routine histology (separate or part of fresh specimen - bulla) and this can be fixed in formalin
  • Direct immunofluorescence staining on fresh tissue, used to detect whether autoantibodies are present in patient tissue
116
Q

What is direct immunofluorescence?

A

The fresh sample is processed and placed on a glass slide. The patient’s autoantibodies will be present in the section if the patient has pemphigus. Add fluorescent labelled anti-human IgG which identifies tail portion on autoantibodies which causes fluorescence. A positive direct immunofluorescent staining in epithelial cells appears as a fish net pattern.

117
Q

What is indirect immunofluorescence?

A

A sample is taken of the patients blood and a normal tissue sample (human or pig) is placed on a glass slide. The blood is spun and we collect the serum containing autoantibodies which are added to the slide. We add fluorescent labelled anti-human IgG which will bind, fluoresce and give a positive result.

118
Q

Why may we need a blood sample?

A
  • Circulating desmoglein levels
    For indirect immunofluorescence
  • Used to detect circulating autoantibodies
  • Not used routinely anymore
119
Q

What are the subtypes of pemphigus?

A
  • Pemphigus vulgaris (most common, autoantibodies to DSG3)
  • Pemphigus foliaceous (lesions more superficial, usually to DSG1)
  • Paraneoplastic pemphigus (associated with a neoplasm, usually lymphoma or chronic lymphocytic leukaemia, extremely serious with a high morbidity and mortality)
120
Q

What is the management of pemphigus?

A
  • Exclude cancer
  • Immunosuppression
  • Prednisolone alone or in combination with azathioprine
  • Occasionally other immunosuppressants or plasmapheresis
121
Q

What are the differences between intra and sub epithelial bulla?

A

Sub epithelial bulla are partial thickness and very fragile so burst easily. On rupturing, basal epithelial cells remain and as there isn’t full thickness loss there is no stimulus to heal. However the epithelial permeability barrier is lost so infection can get in and there is loss of tissue fluids. Together these are life threatening.

Sub-epithelial bulla are full thickness loss as the bulla form between the epithelium and connective tissue. They are less fragile so you are more likely to see the bulla clinically. On rupturing there is exposure of the underlying connective tissue so the body has a stimulus to heal. There is healing by secondary intention as there is epithelial migration from the edges and wound contraction e.g. scarring.

122
Q

What are the sub-epithelial autoimmune bullous diseases?

A
  • Bullous pemphigoid
  • Mucous membrane pemphigoid
  • Dermatitis herpetiformis
123
Q

What is the pathogenesis of pemphigoid?

A

There are autoantibodies targeted against components of hemidesmosomes which are structures attaching epithelial cells to the basement membrane. The targeted part of hemidesmosomes varies between different types of pemphigoid. BP targets BP230 and BP180 and MMP targets alpha6beta4, laminin and BP230. Histologically they will both appear as the epithelium separating from the connective tissue at the level of the basement membrane.

124
Q

What are the features of bullous pemphigoid?

A

The skin is usually involved and there are bulla and large shallow ulcers or erosions. The mouth and other mucous membranes are frequently involved. There are autoantibodies against BP180 (BPAG1) and BP230 (BPAG2) antigens in hemidesmosomes.

125
Q

What are the features of mucous membrane pemphigoid?

A

It is a chronic disease of the elderly. There is desquamative gingivitis in 90% with very erythematous, tender, friable gingiva and plaque. There is other mucosal involvement (82.5% other oral mucosa, 48.3% conjunctiva, 8.3% skin, 7.5% nasal). Skin lesions are rare in MMP. The buccal mucosa and palate are often involved. The eyes may be severely damaged by scarring (cicatricial pemphigoid) so ask about dry eyes. There are well marginated ulcers and healing in 3-4 weeks. There is a risk of scarring of eyes and the larynx and oesophagus can be involved. It is Nikolsky’s sign positive. Conjunctival lesions are common (up to 80%) such as symblepharon, ankyloblepharon, lid inversion/entropion.

126
Q

What eye lesions are seen in MMP?

A
  • Blisters and ulcers (conjunctivitis)
  • Trichiasis, fibrosis and scarring
  • Entropion plus adhesions - symblepharon
127
Q

What is the treatment of MMP?

A
  • Steroids (topical if mild such as mouthwash or systemic if severe such as prednisolone
  • Plaque reduction (OHI, chlorhexidine)
  • Tetracycline/nicatinamide (B3)
  • Other immunosuppressive agents such as azathioprine, cyclophosphamide, dapson, mucophenolate
  • Steroids and immunosuppressive agents have bad side effects so we try stay away from them where we can
  • Immediate referral by telephone, needs ophthalmology opinion
128
Q

What are the investigations and what will they show?

A

Same investigations as pemphigoid. Immunofluorescence will show linear IgG or IgM immunofluorescence at the basement membrane. Standard indirect immunofluorescence studies are usually negative as circulating antibody levels tend to be lower.

129
Q

What is the management of bullous pemphigoid (and MMP)?

A
  • Systemic or topical steroids are the mainstay of treatment
  • Sulphonamides or dapsone may be an effective alternative to systemic steroids
  • Mycophenolate mofetil - additional systemic agent
  • Ocular examination is essential
130
Q

What is dermatitis herpetiformis?

A

It is similar to BP but it may affect a younger age group including children. There are smaller bullae and vesicles hence herpetiform appearance of lesions. There is an association with coeliac disease (gluten enteropathy). If you see a child with ulcers always ask if they have stomach problems. The management is a gluten free diet, may respond well to dapsone or sulphonamides. Good OH is also important.

131
Q

What does the histology and immunofluorescence show for dermatitis herpetiformis?

A

The histology shows small regions of epithelial separation at the level of the basement membrane. There are neutrophil/eosinophil abscesses under the epithelium and mixed inflammation in the connective tissue.

In the immunofluorescence there is a speckled/granular pattern with IgA immunofluorescence - basement membrane and adjacent connective tissue.

132
Q

What is epidermolysis bullosa congenita?

A

This is not autoimmune, it is an inherited group of conditions. There are genetic effects in key proteins associated with epithelial integrity or anchoring to the connective tissue. There is a variable clinical presentation depending upon which protein is defective. It mainly affects children and is often present at birth. Some forms are severe mutilating or fatal.

133
Q

What are the three types of epidermolysis bullosa congenita?

A
  • EB simples EBS - abnormality within keratin, blisters, ulceration on rubbing surfaces (hands and feat) (within epithelium)
  • EB junctional EBJ - most severe and life threatening
  • EB dystrophica EBD - type 7 collagen defect
134
Q

What is erythema multiforme?

A

It has an acute onset and short duration (2-3 weeks). It is a mucocutaneous blistering disorder and the peak age range is 20-30. It has a complex pathogenesis as it can be type III or IV hypersensitivity. Some cases are immune complex mediated (III) where immune complexes are deposited in tissues. There are some recurrent cases (type IV hypersensitivity to herpes antigens).

135
Q

What are the clinical features of erythema multiforme?

A
  • Oral (haemorrhagic crusting of lips, extensive irregular mucosal ulceration, erythema and blistering)
  • Ocular (conjunctivitis)
  • Skin (target lesions)
  • Severe cases (Steven Johnson syndrome - acute response to drug or medication)
136
Q

What are the causes of erythema multiforme?

A

The single episode causes are drugs, mycoplasma pneumonia (bacteria), radiotherapy and idiopathic. The recurrent causes are recurrent herpes simplex (cold sores). Infections are the most common cause. Drugs are more likely to cause erythema multiforme major which is more serious. Drugs:

  • Antibiotics e.g. tetracycline, amoxicillin
  • Anticonvulsants e.g. phenytoin
  • Proton pump inhibitors
  • H2 receptor antagonists
  • NSAIDs
  • Biologics e.g. infliximab, etanercept, adalimumab
137
Q

What is the management of erythema multiforme?

A
  • Remove/avoid trigger
  • Short, reducing dose course of steroids
  • Chlorhexidine/benzydamine mouthwash
  • Gengigel/gelclair
  • Analgesics
  • Soft diet
  • May require admission for parenteral nutrition and more intensive therapy
  • For recurrent prevention with Acyclovir
138
Q

What is oral lichen planus?

A

It is common and seen in 1.5% of the population. The onset is mainly age 30-50. It is a cell mediated auto-immune condition and stress may exacerbate it. It is chronic and difficult to treat. It is cyclical so will flare up and then go away. There are different clinical presentations such as reticular, plaque like, erosive (red atrophic mucosa), desquamative gingivitis and bullous. There can be skin involvement but less than 10% of patients presenting with oral lesions have skin lesions and approximately 50% of patients with skin lesions have oral lesions. There are purple, itchy papules and Wickham’s striae. Lesions particularly occur on the flexor surface of wrists and on the shins. It is pre-malignant and there is a 1-3% risk of change (alongside drinking and smoking etc).

139
Q

What is the epidemiology of skin/cutaneous lichen planus?

A

It affects 0.9-1.2% of the population worldwide. It is seen in middle to late life, both genders and is rare in childhood.

140
Q

What should you ask a patient with oral lichen planus?

A

If they have it anywhere else such as oesophageal, genital, anal or other.

141
Q

What is the histology of lichen planus?

A

It is a type IV hypersensitivity reaction so cell mediated autoimmune process. There is band like accumulation of T cell lymphocytes along the basement membrane. They start to attach and disrupt the basement membrane. There is cell mediated autoimmune damage to the basal cells and the T cells invade the epithelium. This is called lymphocyte epithelial tropism. The basement membrane appears pinked which is called hyalinisation of the BM. The basal cell layer is lost. There are apoptotic bodies (epithelial cells) and these are pink. Damage to the basal cells stimulates an attempt to repair. If the rate of repair exceeds the rate of damage then epithelial thickening and marked keratinisation will occur (reticular and plaque like lesions). If the rate of damage exceeds the rate of repair then epithelial thinning will occur (atrophic/erosive lesions or ulceration).
Sometimes see plasma cells with lichenoid reactions to amalgam.

142
Q

Why are basal keratinocytes targeted for cell mediated autoimmune damage?

A

Probably as keratinocytes start to express altered self-antigen or because cytotoxic T cells fail to recognise the keratinocytes as self.

143
Q

What are lichenoid lesions and the causes?

A

They look like oral lichen planus clinically and histologically but there is a known antigen cause. The causes are:

  • Graft vs host disease
  • Contact sensitivity to dental materials e.g. amalgam
  • Reactions to systemic drugs
  • SLE/DLE
144
Q

How can graft vs host disease cause lichenoid lesions?

A

It is the result of a bone marrow transplant usually used to treatm haematological malignancies e.g. leukaemia. The patients bone marrow is ablated with chemo and/or radiotherapy and reconstituted with bone marrow from a healthy patient. However the patients T cells are now someone elses. If there is the slightest mismatch (HLA markers), the new T cells may regard the patients keratinocytes as foreign in which case they will accumulate and damage the basal keratinocytes.

145
Q

How do contact sensitivity reactions cause lichenoid lesions?

A

The oral cavity was not thought capable of displaying hypersensitivity until the 1980’s. Mucosal lesions associated with amalgam fillings were thought to be due to ‘galvanism’. Reactions occur most frequently with amalgam but can also occur with other dental materials. Lesions are closely associated with the filling material and the patient is often patch test positive to the filling material. Removing or replacing the restoration results in the lesion resolving in 3-6 months.

146
Q

How do lichenoid reactions happen to systemic drugs?

A

Medication in the blood stream can be deposited in the tissues and then T cells attack this. Examples of drugs are anti-hypertensives e.g. propranolol, anti-coagulants, antimalarials e.g. quinine, anti-inflammatorys e.g. dapsone, NSAIDs, antimicrobials e.g. metronidazole, tetracycline, streptomycin, diabetes treatments e.g. metformin and psychiatric drugs. Look at lecture for more.

147
Q

How do you distinguish between oral lichen planus and lichenoid reactions?

A

Oral lichen planus lesions are generally bilateral, symmetrical, may involve gingivae or skin and no strong relationship to fillings or drugs.
Oral lichenoid reactions are generally unilateral, asymmetrical, don’t involve gingiva or skin and are closely related to the cause e.g. amalgam or drugs.

148
Q

What is the treatment for oral lichen planus?

A
  • Symptomatic relief
  • Dietary advice
  • Oral hygiene improvement
  • Discussion of premalignant potential
    Less common:
  • Topical analgesics
  • Topical corticosteroids
  • Topical immunosuppressants
  • Systemic immunosuppressants
149
Q

What topical analgesics can be used for oral lichen planus?

A
  • Benzydamine hydrochloride 0.15% mouthwash (difflam)
150
Q

What topical corticosteroids can be used for oral lichen planus?

A
  • Prednisolone mouthwash
  • Betamethasone mouthwash
  • Fluticasone spray/inhaler
  • Beclomethasone inhaler
  • Clobetasol preparations
  • Triamcinolone acetonide in orabase (don’t have anymore)
151
Q

What are the topical immunosuppressants used for oral lichen planus?

A
  • Topical tacrolimus 0.1% ointment
  • Cyclosporin mouthrinse 100mg/ml
  • Retinoids
    (don’t use these much)
152
Q

What systemic immunosuppressants can be used for oral lichen planus?

A
  • Prednisolone
  • Azathioprine
  • Mycophenolate
  • Dapsone
  • Hydroxychloroquine
  • Retinoids
153
Q

What are the complications of oral lichen planus?

A

It is typically lifelong and has a 1-3% risk of malignant change. There is a higher rate in lichenoid reactions, smokers, erosive lesions and viral infection (hep C, HPV).

154
Q

How do you treat lichenoid reactions?

A
  • Remove or treat the underlying cause (replace filling material, change medication)
  • Lesions will usually resolve
  • If not treat as for oral lichen planus
155
Q

What are the definitions for allergy, autoimmunity and hypersensitivity?

A

Allergy is when the immune system responds in an exaggerated or inappropriate way to an extrinsic (non-self) antigen.
Autoimmunity is when the immune system responds in an exaggerated or inappropriate way to an intrinsic (self) antigen.
Hypersensitivity is when the immune system responds in an exaggerated or inappropriate way resulting in harm. It occurs on second exposure to the antigen. Allergy and autoimmunity are forms of hypersensitivity.

156
Q

What are the types of hypersensitivity?

A
  • Type I - immediate/anaphylaxis
  • Type II - cytotoxic
  • Type III - immune complex
  • Type IV - delayed (cell mediated)
    The top three are antibody mediated.
157
Q

What is type I hypersensitivity?

A

It is acute and called anaphylaxis. There is a rapid onset and it is IgE mediated. It is normally in low amounts in the body, however these people have high levels of IgE. There is a response to an allergen (antigen) and most are small (10-40kDa).

158
Q

Give examples of antigens causing type I hypersensitivity?

A
  • Der P1/2 - dust mite faeces
  • Fel d1 - cats
  • Rat N1 - rats
  • Pollen - grass
159
Q

How does the immune system react in type I hypersensitivity?

A

On the first exposure to the antigen, B cells (APC) bind to the antigen and there is antigen recognition. The B cell becomes a plasma cell which produces IgE. The IgE binds to FC receptors on mast cells which contain histamine. On second exposure to the antigen it binds to the antibodies on the surface of the mast cell. The antigen cross links the Fc receptors and this causes degranulation of the mast cell and release of histamine.

160
Q

What does histamine cause?

A
  • Vascular dilation (vasodilation)
  • Increased vascular permeability i.e. oedema
  • Bronchospasm
  • Urticarial rash
  • Increased nasal and lacrimal secretions

These responses commonly present as:

  • Hay fever
  • Asthma
  • Acute allergic responses (angio-oedema/anaphylaxis - penicillin, latex, LA allergy)
161
Q

How do you diagnose type I hypersensitivity?

A

The wheel and flare skin test:

  • Apply a small amount of the allergen just under the skin using the prick test
  • The skin response is fast - 5 mins
  • The wheel is caused by extravasation of serum into skin due to histamine (angio-oedema)
  • The flare is caused by erythematous red patch due to axon reflex
  • The late phase happens at 6 hours + and is due to leukocyte infiltrate and further oedema
162
Q

How do you manage type I hypersensitivity?

A
  • Adrenaline (epinephrine)
  • Anti-histamines
  • Corticosteroids e.g. dexamethasone
  • Avoidance of allergen
163
Q

What is type II hypersensitivity?

A

It is called cytotoxic and is antibody mediated. There are antibodies which target self antigens called autoantibodies. The antibodies induce cell damage and inflammation. Type II hypersensitivity responses are important in acute transplant rejection (host vs graft) and autoimmune diseases such as pemphigus and pemphigoid.

164
Q

In type II hypersensitivity what do the autoantibodies activate?

A

ADCC (antibody dependent cell cytotoxicity:
- T cells, neutrophils and macrophages secrete lots of factors to kill the cell and there will be inflammation and cell death.
Complement:
- Series of 20 proteins which are normally inactive in the blood
- When activated they can activate the membrane attack complex
- Results in inflammation, attracts white blood cells to the area
- Results in cell death

165
Q

What is type III hypersensitivity?

A

It is immune complex mediated and immune complex form between antibodies and antigens. They may deposit in the lining of blood vessels, glomeruli or the lung. They sit in between endothelial cells in blood vessels. They induce complement activation and neutrophil binding. This leads to inflammation and vascular permeability. Type III hypersensitivity is important in erythema multiforme and systemic lupus erythematosus.

166
Q

What is type IV hypersensitivity?

A

It is cell mediated/delayed hypersensitivity. It is mediated by T cells. As the response is cellular it is slow to develop, slow to resolve and localised. It is important in:

  • Delayed type hypersensitivity responses
  • Contact dermatitis
  • Lichenoid reactions to amalgam fillings and other materials
  • Oral lichen planus
167
Q

How do cells cause type IV hypersensitivity?

A

Within the oral mucosa there are immune cells which are dendritic cells called Langerhans cells. They are surveillance cells and form a network in the epithelium. They have the protein CD1+ which is specific to Langerhans cells. Langerhans cells intercept and process extrinsic antigens entering the mucosa. The antigen also stimulates keratinocytes to release TNF which tells dendritic cells to go to the lymph nodes. The antigens are processed by Langerhans cells in the lymph nodes and present parts to circulating T cells. The antigen specific T cells become activated and proliferate (clonal expansion). They preferentially re-circulate to the oral mucosa where the antigen is.
TNF also induces endothelial cells in blood vessels to express VCAM-1. It selectively binds and allows T cells to stick to the endothelium underneath the tissue where they need to be. The TNF also causes epithelial cells to release a chemokine called CCL5. This attracts T cells into the site of infection as they pass down the chemokine gradient and into the tissue. There will be lots of T cells in the tissue. Epithelial cells express ICAM1 as it is a pro-inflammatory environment and this allows the T cells to squeeze between the cells and into the epithelium from the connective tissue. ICAM-1 and HLA II enable the keratinocytes to also present the antigen to the T cells. This results in local activation of the antigen specific T cells and they proliferate. This can be seen histologically. Cytotoxic T cells (CD8) kill basal keratinocytes (apoptosis) so there is tissue damage. They secrete tissue damaging cytokines. Tissue damage is seen at post 12 hours (delayed) and it is resolved if antigen is removed.

168
Q

What are the two mechanisms by which T cells induce apoptosis?

A
  • Fas/Fas-ligand mediated apoptosis. All cells express Fas and only T cells and natural killer cells express Fas-ligand. The T cell can only bind to the cell with the antigen that the T cell recognises. This allows Fas and Fas-L to engage and induce apoptosis. The target cell is instructed to kill itself.
  • Perforin/Granzyme B. T cells secrete perforin which is a series of molecules which punch a hole in the cell. Granzyme B is then secreted which passes into the cell through the channel and kills the cell by toxicity. Keratinocytes are the target cell.
169
Q

Why is allergy a growing problem.

A

There is a large increase in children suffering from asthma and in allergic diseases among adults. It is also a growing problem in the dental surgery as dentists and nurses are becoming increasingly sensitised to latex and dental materials. Patients are also increasingly sensitised to latex, materials and drugs (main allergies in dentistry).

170
Q

What hypersensitivity reaction is the main concern?

A

Type I hypersensitivity such as penicillin and other antibiotics, local anaesthetics and NSAIDs. Reactions can range from a rash to angioedema. A true allergy to LA is rare since preservatives have been removed from dental cartridges. Most reactions are vasovagal and due to IV injection. Latex allergy can occur.

171
Q

What are some common orthodontic and restorative dental materials that can cause allergy?

A 
Orthodontic:
- Nickel containing wires
- Bracket adhesives - BisGMA
- Acrylic materials 
Restorative:
- Amaglam (lichenoid reaction to mercury)
- Composite filling materials - BisGMA
- Denture bases - acrylics 
- Rarely metals in crowns and denture bases

Dental materials can be grouped into plastics (denture bases and composites) and metals.

172
Q

What do dental material allergies usually present as and how can you test for one?

A

They usually present as Type IV hypersensitivity. They are usually chronic and localised and skin patch testing can be very helpful. It tests for type IV cell mediated delayed hypersensitivity responses. Samples are applied to the skin on the back or arm for 72-96 hours.

173
Q

What parts of denture acrylic can cause hypersensitivity?

A
  • Polymethylmethacrylate (mainly) - inert
  • Methylmethacrylate monomer
  • Stabiliser e.g. hydroquinone
  • Initiator e.g. benzoyl peroxide
  • Chemicals released during polymerisation e.g. formaldehyde
174
Q

How are cold cure acrylics different?

A
  • Less polymerisation
  • More free monomer, stabiliser, initiator
  • Activator e.g. tertiary amine
175
Q

What do composites contain (which may cause allergy)?

A
  • Quartz or borosilicate fillers - inert
  • BisGMA
  • Low MW monomers e.g. TEGDMA, EGDMA
  • Coupling agents
  • Stabilisers, activators, initiators
    Bonding agents contain more resin and less filler than composite materials so are more likely to cause problems.
176
Q

What are the causes of latex allergy and what products contain latex?

A
  • Latex protein allergy (mainly patients)
  • Chemical allergy
  • Powder irritancy
  • Last two are mainly occupational

Latex can be found in gloves, rubber dam and rubber cups.

177
Q

What is a latex protein allergy?

A

It is a type I reaction:

  • Skin contact (urticaria, angioedema, rarely anaphylaxis)
  • Air dispersal on glove powder particles (asthma, wheeze, cough, rhinitis, conjunctivitis, rarely anaphylaxis)
178
Q

What is a chemical allergy to latex?

A
  • Accelerators and antioxidants used during manufacture
  • Chemicals produced during manufacture
  • Allergic contact dermatitis
  • 75% of work related glove allergies
179
Q

What is powder irritancy to latex?

A
  • Continual rubbing and contact with glove powder

- Irritant contact dermatitis (enhances skin penetration of allergens, increases chance of sensitisation)

180
Q

How can you avoid occupational glove allergy problems?

A
  • Use powder free gloves
  • Use hypoallergenic latex gloves
  • Use latex free gloves
  • Gloves provided here are powder and latex free
  • Using latex free also protect patients
181
Q

What are the types of oral manifestations of GI disorders?

A
  • Primary effects which are part of the disease process e.g. Crohn’s
  • Secondary effects which occur due to malabsorption, blood loss etc. Most oral effects are in this category.
182
Q

What GI conditions can cause oral problems?

A
  • GORD
  • Coeliac disease
  • Idiopathic inflammatory bowel disease (Crohn’s, OFG and ulcerative colitis)
  • Intestinal polyposis syndromes (inherited syndromes where there are polyps in bowel)
183
Q

What is GORD, the oral effects and treatment?

A

The symptoms are dyspepsia (heart burn). The risk factors are obesity, smoking and alcohol. There is a risk of Barrett’s oesophagus which is pre-malignant so there is a risk of oesophageal cancer. Oral effects are halitosis and erosion but there may be none. Treatment is with proton pump inhibitors such as omeprazole.

184
Q

What is coeliac disease and the pathogenesis?

A

It is intolerance to alpha-gliadin peptides found in gluten in wheat, rye and barley. It can affect any age and there are genetically susceptible individuals and families. The prevalence is 0.5-1% of the population. It is probably underdiagnosed. The pathogenesis:

  • Exposure to gluten
  • Proliferation of lymphocytes
  • Oedema
  • Crypt hyperplasia and sub-total villous atrophy
  • Mostly affects jejunum and duodenum
185
Q

What are the clinical features of coeliac disease?

A 
The effects are due to malabsorption of iron (anaemia), calcium and vitamin D. When it is more advanced it is also due to folic acid, vitamin C and B12. 
Clinical features:
- Diarrhoea and steatorrhoea
- Wasting (failure to thrive)
- Loss of appetite 
- Abdominal discomfort/pain
- Tiredness and weakness
- Peripheral neuropathy and CNS disturbances
- Tetany and osteomalacia
- Dermatitis herpetiformis
- Oral ulceration
- Increased risk of intestinal neoplasms (lymphoma)
186
Q

What are the oral manifestations of coeliac disease?

A
  • Oral ulceration
  • Glossitis
  • Candidiasis
  • Angular cheilitis
  • Hypoplasia of enamel of permanent teeth (often generalised and symmetrical, secondary to malabsorption)
187
Q

How is coeliac disease diagnosed?

A
  • History and clinical signs
  • Blood tests (FBC, haematinics which are nutrients required for formation of blood cells including iron, B12, folate and other tests include anti-endomysial antibodies, tissue transglutaminase antibodies, antigliadin antibodies and andti-reticulin.
  • Endoscopy and jejunal mucosal biopsy
188
Q

What is the treatment for coeliac disease?

A
  • Exclusion diet to remove gluten
  • Replacement of haematinics (iron and folate)
  • Increased risk of T-cell lymphoma and other bowel malignancies
189
Q

What is Crohn’s disease?

A

It is seen in many young adults in the western world and affects any part of the GIT. It may affect several separate areas (skip lesions) and mostly the terminal ileum and ascending colon. It can also affect extra-gastrointestinal sites such as the skin. There is transmural inflammation (through entire wall) and granuloma formation which gives a cobblestone appearance. The wall is thickened and the lumen narrowed and there is aphthous like ulceration and fissuring. There can be fistulae and abscesses. In addition there is chronic inflammation and lymphoid hyperplasia.

190
Q

What are the clinical features?

A

(They are relapsing and remitting)

  • Abdominal pain
  • Diarrhoea
  • Weight loss
  • Malabsorption - B12, bile salts
  • Variable presentation, depends on severity and sites and often intermittent
191
Q

What are the oral manifestations?

A
  • Ulceration (may be RAS like)
  • Glossitis
  • Lip swelling
  • Cobblestone mucosa
  • Tissue tags
  • Fissures and ulcers
  • Angular cheilitis
  • Mucosal inflammation especially the attached gingiva
    Biopsy of these show granulomatous inflammation.
192
Q

What investigations should be done for Crohn’s?

A
  • History
  • Oral biopsy - include muscle as granulomas tend to be deep down
  • Blood tests (FBC, haematinics, gut antibodies, ACE (to include sarcoid))
  • Onward referral
193
Q

What is the treatment for Crohn’s?

A
  • Symptomatic relief
  • Topical measures first for oral manifestations
  • Immunosuppressives e.g. methotrexate or azathioprine
  • Replacement therapy
  • Anti-TNF antibodies, infliximab etc
  • Elemental diet
  • Surgery
194
Q

What is oro-facial granulomatosis (OFG)?

A

It has oral features of Crohn’s with no clinical features of gut involvement. It may have an allergic aetiology. It responds to exclusion diet but not in all cases.

195
Q

What are other causes of lip swelling?

A

These need excluding:

  • Crohn’s
  • Sarcoidosis
  • Foreign body reactions
  • Melkerson-Rosenthal syndrome e.g. triad of lip swelling, fissured tongue and facial palsy
  • Infections (rare) e.g. syphilis, TB, leprosy
196
Q

What is the management of orofacial granulomatosis?

A
  • Surgery in severe cases
  • Topical and intralesional steroids (temporary relief)
  • Systemic drugs e.g. azathioprine
  • Exclusion diet (chocolate, crisps, carbonated drinks, carvone, cinnamon, benzoates e.g. E210-E219) NB tomatoes, fruit juices, carbonated drinks, pickles
197
Q

What is ulcerative colitis and the symptoms?

A

It involves the large intestine and rectum and tends to be a continuous region of variable extent. Inflammation extends no further than the lamina propria. It is inflamed, bleeds easily and later ulceration develops. There is chronic inflammatory infiltrate. It results in:

  • Bloody diarrhoea
  • Pain
  • Weight loss
  • Tiredness
  • Iritis, ankylosing spondylitis etc
  • Oral manifestations: oral ulceration, pyostomatitis vegetans (pustular, yellow papules on gingiva)
198
Q

What are the oral effects of drugs used to treat GIT disorders?

A
  • Steroids - candida infections
  • Immunosuppressants e.g. azathioprine, methotrexate - ulceration and infection
  • Antispasmodics - dry mouth
  • H2 receptor antagonists e.g. ranitidine - erythema multiforme, discolouration of tongue, dry mouth
  • Proton pump inhibitors e.g. omeprazole - taste disturbance, dry mouth, erythema multiforme, angio-oedema
  • Cytokines inhibitor e.g. infliximab - oral ulceration, taste disturbance
199
Q

Name two intestinal polyposis syndromes (inherited syndromes where there are polyps in bowel)?

A
  • Gardner’s syndrome

- Peutz Jeghers syndrome

200
Q

What is Gardner’s syndrome and the oral manifestations?

A

It is an autosomal dominant condition and caused by an APC gene mutation leading to multiple colon polyps (premalignant), epidermoid cysts, osteomas of jaw, thyroid cancer, fibromas. There is risk of colon cancer and the risk is 10% at 21 and 95% at 50. Oral manifestations:

  • Osteomas
  • Odontomes
  • Supernumerary teeth
  • Osteomas develop first, often 10-30 years so early referral
201
Q

What is Peutz Jeghers and the oral manifestations?

A

It is autosomal dominant. There are hamartomatous polyps and only a small risk of developing cancer. There is an increased risk of cancer in the ovaries, pancreas and liver. There are pigmented macules on the lips and oral cavity (develop in childhood before anything else).

202
Q

What haematological disorders can cause oral manifestations?

A
  • Anaemias (iron deficiency anaemia and macrocytic anaemia)
  • Leukaemias
  • Multiple myeloma
  • Neutropenia/agranulocytosis
  • Stem cell transplants/GVHD
  • Angina bullosa haemorrhagica
203
Q

What is anaemia?

A

It is a decreased ability of the blood to carry oxygen. Haemoglobin concentration is below the normal range which is 13.5g/dl for males and 11.5g/dl for females. It is due to decreased numbers of RBC:
- Loss/destruction (injury, chronic diseases, infections, sickle cell anaemia, haemolytic anaemias e.g. spherocytosis, red cell auto-antibodies)
- Failure of production (low Fe, folate, B12, aplastic anaemia, leukaemia, thalassemia, renal failure, gives decreased erythropoetin)
It is also due to a reduction of concentration of haemoglobin e.g. blood loss or hypervolaemia and reduced ability of red blood cells to carry oxygen e.g. sickle cell anaemia and thalassemias.

204
Q

How is anaemia categorised by the morphology of red blood cells?

A
  • Normocytic anaemia e.g. blood loss
  • Macrocytic anaemia (overly large RBCs and not enough normal) e.g. B12 or folate deficiency
  • Microcytic anaemia (smaller RBCs) e.g. iron deficiency
205
Q

What can iron deficiency anaemia be caused by?

A
  • Inadequate intake (diet/malabsorption e.g. coeliac)
  • Increased loss e.g. GI bleed
  • Increased demand e.g. pregnancy
    It leads to hypochromic (less Hb) microcytic anaemia (small).
206
Q

What is macrocytic anaemia?

A

It is a rise in mean cell volume above the normal range of 80-95fl in adults - lower in children. The causes are:

  • Dietary deficiency of B12/folate
  • Alcohol
  • Malabsorption
  • Liver disease
  • Hypothyroidism
  • Increased demand e.g. pregnancy
  • Drugs e.g. azathioprine
207
Q

How does a vitamin B12 deficiency occur?

A

It is absorbed in the ileum and there can be dietary insufficiency or affected by GI disease e.g. Crohns. Pernicious anaemia is auto-immune gastritis and parietal cells are damaged which affects intrinsic factor usually secreted by parietal cells. B12 is therefore not absorbed in the small intestine. Achlorhydria and absent intrinsic factor are signs.

208
Q

How does a folate deficiency occur?

A

It is absorbed in the upper intestine 100-200ug daily. There may be a dietary insufficiency, malabsorption (especially in coeliac disease), excessive drug use e.g. anticonvulsants, sulphasalazine.

209
Q

What are the systemic features of iron deficiency anaemia?

A
  • Lethargy
  • Dyspnoea
  • Skin and nail changes
  • Mucosal changes
  • Oesophageal webbing
  • Tachycardia/palpitations
  • Cardiac failure/exacerbation of cardiac diseases
210
Q

What are the systemic features of macrocytic/megaloblastic anaemia?

A
  • Pallor
  • Jaundice
  • Neurological changes
  • Neural tube defects
  • Gonadal dysfunction
  • Mucosal changes
  • Cardiovascular disease
  • Risks with GA
211
Q

What are the oral manifestations of anaemia?

A
  • None
  • Pallor - Hb<8g/dl
  • Oral ulceration and exacerbation of RAS
  • Mucosal atrophy/stomatitis/glossitis
  • Depapillated, smooth tongue
  • Altered taste
  • Oral candidosis
  • Worsening of existing mucosal pathology
  • Burning mouth syndrome
  • Dysphagia (oesophageal web) Plummer vinson syndrome (rare disease characterised by difficulty swallowing, iron deficiency anaemia, cheilitis, glossitis and oesophageal web.
212
Q

What is leukaemia and the types?

A

These are malignant diseases of blood forming cells in bone marrow. One type of white blood cell is produced in excess at the detriment of others. It can be acute:
- Lymphoblastic (children 85% and late middle age)
- Myeloid (adults)
It can be chronic:
- Lymphocytic (adults)
- Myeloid (adults)

213
Q

What are the clinical features of acute leukaemia?

A

The features are due to bone marrow failure or organ infiltration:

  • Symptoms and signs of anaemia
  • Bacterial infections (mouth, throat, chest, skin, peri-anal)
  • Delayed healing
  • Bruising and bleeding (including gingival)
  • Bone pain
  • Lymphadenopathy
  • Hepetosplenomegaly
214
Q

What are the clinical features of chronic leukaemia?

A
  • Anaemia
  • Bleeding
  • Infection
  • Splenomegaly
  • Weight loss
  • Fatigue
  • Sweating
215
Q

What are the oral manifestations of leukaemia?

A
  • Gingival inflammation, swelling and bleeding
  • Ulceration (cytotoxic drugs/infection)
  • Increased susceptibility to oral infections
216
Q

How can GVHD have oral manifestations?

A

GVHS is when someone receives a stem cell transplant and the graft attacks the host. In someone who has chemotherapy or chemo-radiotherapy, they may have a transplant of own or donor stem cells. This can lead to GVHD. In the oral cavity it presents as lichen planus and Sjogren’s like syndrome. The management would be steroids.

217
Q

What is multiple myeloma?

A

It is a tumour of monoclonal plasma cells (B cell origin) and they produce and secrete monoclonal protein (Ig). You can look for Bence-Jones protein in the urine. As plasma cells are produced in the bone marrow you can get bone pain, osteoporosis, osteolytic lesions. There can be recurrent infections as plasma cells are produced in favour of other cells. You can get anaemia, renal failure (proteins get clogged in kidneys) and amyloidosis. Amyloid is an abnormal protein which can get deposited in organs. The tongue may appear swollen due to amyloid.

218
Q

What is leucopenia?

A

There is a reduction in white cell population. It may be primary (reduction in haemopoesis) or secondary (autoimmune disease, infection, drug therapy e.g. carbamazepine, HIV). Cyclic neutropenia is an example.

219
Q

What is cyclic neutropenia and the oral manifestations and management?

A

It is rare, has unknown aetiology and is most common in childhood. There is neutropenia, average cycles of 21 days then recovers and drops again and infections. Oral manifestations:
- Ulceration (irregular, any surface, may heal with scarring within 2 weeks)
- Gingivitis
- Periodontitis
- Susceptibility to infection e.g. candidosis
The management is supportive as it is self-limiting.

220
Q

What is angina bullosa haemorrhagica?

A

It is idiopathic and can occur is thrombocytopenia. The diagnosis is from history and clinical signs. Do FBC and clotting screen and reassure the patient. There are large blood blisters in the mouth which burst and ulcerate. Risk of bleeding and infection.

Oral disease - 4th year (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions