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BDS3 paeds > Paeds Oral Medicine > Flashcards

Paeds Oral Medicine Flashcards

1
Q

3 categories of oro-facial soft tissue infection

A

viral

bacterial

fungal

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2
Q

viral orofacial soft tissue infections (8, 3 key)

A
  • Primary herpes
  • Herpangina
  • Hand foot and mouth
  • Varicella Zoster
  • Epstein Barr Virus
  • Mumps
  • Measles
  • Rubella
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3
Q

5 types of bacterial orofacial soft tissue infection

A
  • Staphylococcal
  • Streptococcal
  • Syphilis
  • TB
  • Cat Scratch Disease
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4
Q

fungal orofacial soft tissue infection

A

candida

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5
Q

primary herpetic gingivostomatitis

A

Acute Infectious disease

Herpes Simplex Virus I

Primary infection common in children

  • Degree of immunity from circulating maternal ABs so infection rare in 1st year

Transmission by droplet formation with 7 day incubation period

  • Almost 100% of the adult population are carriers
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6
Q

herpes simplex virus I

primary infection

recurrent infection

A

primary herpetic gingivostomatitis

herpes labialis (coldsores)

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7
Q

primary herpetic gingivostomatitis affects

A

children (common)

but rare is 1st year of life due to immunity from circulating maternal ABs

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8
Q

transmission of primary herpetic gingivostomatitis

A

droplet formation with 7 day incubation period

almost 100% of the adult populatin are carriers

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9
Q

signs and symptoms of primary herpetic gingivostomatitis

A
  • fluid filled vesibles - rupture to painful ragged ulcers
    • gingivae, tongue, lips, buccal and palatal mucosa
  • severe oedematous marginal gingivitis
  • fever
  • headache
  • malaise
  • cervical lymphadenopathy
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10
Q

knock on effect of primary herpetic gingivostomatitis

A

the fluid filled vesicles rupture into ragged ulcers

extermely painful

child may be reluctant to eat/drink - risk dehydration

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11
Q

tx for primary herpetic gingivostomatitis

A
  • bed rest
  • soft diet/hydration
  • paracetamol
  • antimicrobial gel or mouthwash
  • acyclovir (not normally indicated but can be helpful in immunocompromised children)
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12
Q

nature of primary herpetic gingivostomatitis

A

usually self limiting - lasts 14 days

so will resolve by itself so need to manage symptoms (rest, paracetamol, soft food and fluids)

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13
Q

most common complication of primary herpetic gingivostomatitis

A

dehydration

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14
Q

resolution of primary herpetic gingivostomatitis

A

lasts 14 days

heals with no scarring

remains dormant in epithelial cells

  • recurrent disease in 50-75% = herpes labialis (cold sores)
  • triggered by: sunlight, stress, other causes of illl health
  • mananaged with topical acyclovir cream
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15
Q

prevalence of recurrence of herpes simplex I (primary herpetic gingivostomatitis)

A

herpes labialis in 50-75%

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16
Q

triggers of herpes labialis

A

sunlight

stress

other causes of ill health

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17
Q

management of herpes labialis

A

topical acyclovir cream

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18
Q

similarity between primary herpetic gingivostomatitis and coxsackie A virus

A

coxsackie A virus is a mild condition which presents with vesibles rupturing to ulceration (like primary herpetic gingivostomatitis) but presents further back in the mouth

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19
Q

coxsackie A virus

2 subtypes

A

herpangina

hand, foot and mouth

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20
Q

herpangina

A

coxsackie A virus

vesicles in the tonsillar/pharyngeal region

lasts 7-10 days

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21
Q

hand, foot and mouth

A

cozsackie A virus

ulceration on the gingivae/tongue/cheeks and palate

maculopapular rash on hands and feet

lasts 7-10 days

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22
Q

oral ulceration

A

a localised defect in the surface oral mucosa where the covering epithelium is destroyed leaving an inflamed area of exposed connective tissue

painful - hard to eat/drink

management like herpes simplex virus type 1

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23
Q

oral ulceration

history - 10 keys

A
  • Onset
  • Frequency
  • Number (how many at any one time)
  • Site
  • Size (what size? Are the all the same?)
  • Duration (how long does each episode normally last)
  • Exacerbating dietary factors
  • Lesions in other areas
  • Associated medical problems (medical history and medicines)
  • Treatment so far (helpful/unhelpful)
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24
Q

what to do if oral ulcers do not heal as expected

A

cannot be dismissed as benign

need referral to local oral cancer unit

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25
Q

causes of oral ulceration (8)

A
  • infection
  • immune mediated disorders
  • vesiculobullous disorders
  • inherited or acquired immunodeficieny disorders
  • neoplaste/heamatological
  • trauma
  • vitamin deficiencies (iron, B12, folate)
  • recurrent apthous stomatitis (no clear cause)
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26
Q

infections which can cause oral ulceration

A

Viral: Hand foot and mouth/ Coxsackie Virus/ Herpes Simplex/ Herpes Zoster, CMV, EBV, HIV

Bacterial: TB, syphilis

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27
Q

immune mediated disorders which can cause oral ulceration

A

crohns,

bechets

SLE

coeliac

periodic fever syndromes

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28
Q

vestibullous disorders which can cause oral ulceration

A

bullous or mucous membrane pemphigoid

pemphigus vulgaris

linear IgA disease

erythema multiforme

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29
Q

neoplastic/heamatological causes of oral ulceration

A

anaemia

leukaemia

agranulocytosis

cyclic neutropenia

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30
Q

trauma causes of oral ulceration

A

physical, thermal, chemical

usually a local factor can be identified

usually resolve 2 weeks after causative factor has been managed (e.g. sharp tooth)

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31
Q

most common cause of oral ulceration in children

A

recurrent apthous ulceration (RAU)

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32
Q

typical appearance of RAU

A

round or ovoid in shape

grey or yellow base

varying degree of perilesional erythema

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33
Q

RAU cause

A

no clear underlying cause

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34
Q

3 patterns of RAU

A

minor

major

herpetiform

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35
Q

minor RAU

A

<10mm

always on non-keratined mucosa

heal 10-14 days

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36
Q

major RAU

A

>10mm

non-keratinised and keratinised mucosa

can take weeks to heal, scarring possible

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37
Q

herpetiform RAU

A

1-2mm

normally present with multiple ulcers

up to 100 at a time

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38
Q

RAU and primary herpetic gingivostomatitis similarity and difference

A

similar appearance

but no clear cause, can be recurrnet and no fever

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39
Q

factors for RAU

A
  • hereditary predisposition (FH in 45%)
  • haematological and deficiency disorders
  • gastrointestinal disease (coeliac in 2-4%)
  • minor trauma in susceptible individual
  • stress or anxiety
  • allergic disorders
  • hormonal disturbance: mestruation
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40
Q

what indicates RAU not just a heriditary disorder

A

can change in pattern from genetic predisposition e.g. become more frequent

indicates other factors at play

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41
Q

iron deficiency in children

A

iron demands increase in growing child, so can be seen during periods of growth

linked to oral ulceration

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42
Q

vitamin B12 and folate deficiency in child may indicate

A

coeliac disease - refer

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43
Q

allergic disorder which could be factors for RAU

A

toothpaste containing SLE

foods with benzoate or sorbate perservatives

benzoic acid

chocolate

tomatoes

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44
Q

initial investigation for RAU consists of (4)

A
  • Diet diary
  • Full blood count
  • Haematinics (folate/B12/ferritin)
  • Coaeliac screen: anti-transglutaminase antibodies
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45
Q

low ferritin management

A
  • 3 months iron supplementation
  • Diet advice of iron rich food
    • tea can inhibit absorption of iron so do not take with meals
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46
Q

Low folate/B12 or positive Anti-transglutaminase antibodies

managment

A

referral to paediatrician for further investigation

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47
Q

diet analysis for RAU may

A

suggest exacerbating food groups

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48
Q

management of exacerbating factors in RAU (4)

A
  • Nutritional deficiencies
  • Traumatic factors
  • Avoid sharp or spicy food – uncomfortable, exacerbate ulceration
  • Allergic factors
    • Dietary exclusion
    • SLS free toothpaste
49
Q

pharmacological management of RAU in GDP

3 prong

A

Prevention of Superinfection:

  • Corsodyl 0.2% Mouthwash

Protect healing ulcers

  • Gengigel topical gel (hyaluronate)
  • Gelclair mouthwash (hyaluronate)

Symptomatic relief

  • Difflam (0.15% benzydamine hydrochloride)
  • Local anaesthetic Spray

Potential to use steroid medication but should be considered in liaison with oral medicine

50
Q

orofacial granulomatosis

A

uncommon chronic inflammatory disorder

OFG

51
Q

cause of OFG

A

idiopathic or associated with systemic granulomatous conditions (Crohn’s disease or Sarcoidosis)

52
Q

average age of onset of OFG

A

11 years

53
Q

sex prevalence of OFG

A

male>female

54
Q

characteristic pathology of OFG

A

due to a combination of an allergic component resulting in lymphoedema and swelling or the oral tissues and presence of non caseating giant cell granulomas which then result in lymphatic obstruction.

  • Biopsy of infected tissue has histology of non-caseating granulomas and lymphoedema

May be a predictor of future Crohn’s disease

55
Q

clinical features of OFG

A
  • Lip Swelling – most common
  • Full thickness gingival swelling
  • Swelling of the non labial facial tissues
  • Peri-oral erythema
  • Cobblestone appearance of the buccal mucosa
  • Linear oral ulceration
  • Mucosal tags
  • Lip/ tongue fissuring
  • Angular cheilitis
56
Q

similarities between OFG and oral crohns

A

have the same clinical features, but these features vary between pts

57
Q

OFG aetiology

A

Largely unknown

  • Limited evidence of genetic factors
  • Numerous associated allergens reported:
    • Cinnamon Compounds
    • Benzoates
    • Much higher IgE mediated atopy rates compared to the general popn
58
Q

OFG diagnosis

A

clinical (oft made solely on - lip biopsy can be uncomfortable and distressing, may cause additional post-operative swelling)

59
Q

investigations for OFG

A

considered to rule out any underlying conditions

  • Measure growth – paediatric growth charts growth failure/delay is seen in Crohn’s
  • Full Blood Count
  • Haematinics
    • iron deficiencies can cause oral ulceration over and above OFG
  • Patch testing – ID triggers
  • Diet diary to ID any triggers
  • Faecal Calprotectin
  • Endoscopy risky in childhood
  • Serum Angiotensin Converting Enzyme (raised in sarcoidosis)
60
Q

OFG management

A
  • Can be difficult and sore
  • Oral hygiene support
  • Symptomatic relief as per oral ulceration
  • Dietary exclusion (does not cure just reduces orofacial inflammation)
  • Manage nutritional deficiencies which may contribute to oral ulceration

medicaments can be considered with careful consideration with specialist

  • Topical steroids
  • Topical tacrolimus
  • Short courses of oral steroids (severe or unresponsive to topical)
  • Intralesional corticosteroids
  • Surgical intervention – unresponsive long standing disfiguremen

t

61
Q

most common mucosal lesion of tongue in children

A

georgraphic tongue

62
Q

geographic tongue presentation

A

Idiopathic and non contagious, benign

  • May be seen at a young age

Shiny red areas on the tongue with loss of filiform papillae are surrounded by white margins

63
Q

appearance of geographic tongue

A

Shiny red areas on the tongue with loss of filiform papillae are surrounded by white margins

64
Q

impact of geographic tongue in children

A

intense discomfort (spicy food/ tomato or citrus fruit/juice)

more sensitive than adult presenation as have a thinner oral mucosa and more sensitive to taste

65
Q

management of geographic tongue in children

A

bland diet during flare ups

if tongue sensitivity present - rule out haematinic deficiencies of iron, folic acid and vitamin B12

  • Likely to become less troublesome with age
    • So dietary restrictions can gradually decrease
66
Q

solid swellings in children oral cavity (5)

A
  • fibroepithelial polyp
  • epulides
  • congential epulis
  • HPV associated mucosal swelling
  • neurofibromas
67
Q

fibroepithelial polyp

A

common, benign

firm pink lump (pedunculated or sessile)

68
Q

sites of fibroepithelial polyp

A

mainly

  • cheeks (along occlusal line)
  • lips
  • gingiva
  • tongue
69
Q

size of fibroepithelial polyps

A

once established remains constant in size

70
Q

cause and effect of fibroepithelial polyp

A

thought to be intiated by minor trauma - accidental biting or sharp tooth edges

generally cause no discomfor unless subject to repeated trauma

71
Q

tx of fibroepithelial polyp

A

surgical excision is curative

may need to be delayed untile the child can co-operate for it - as since benign difficult to justify GA

72
Q

epulides

A

common solid swelling on oral mucosa

bening, hyperplatic lesion

73
Q

epulides presentation and common cause

A

localised gingival enlargements, most arise from interproximal dental tissues

related to chronic irritation - particularly presence of plaque or calculus

74
Q

3 main types of epulides

A

fibrous epulis

pyogenic granuloma

peripheral giant cell granuloma

75
Q

common clinical features of 3 types of epulides

A
  • Majority occurring anterior to the molar teeth and being more common in the maxilla
    • interproximal areas of gingival enlargements
  • Management is surgical removal and identification and management of exacerbating factors
    • plaque, calculus

Have tendency to recur

76
Q

similarlity between fibroepithelial polyp and epulides

A

similar in appearance but epulides on gingiva only

whereas FEP - cheeks, lips, tongue, gingiva

77
Q

fibrous epulis

A
  • Pedunculated or sessile mass
  • Firm consistency
  • Similar color to surrounding gingivae
  • inflammatory cell infiltrate and fibrous tissue
78
Q

pyogenic gramuloma

A
  • Soft, deep red/purple swelling
    • Often ulcerated
  • haemorrhage spontaneousl or with mild trauma
  • vascular proliferation supported by delicate fibrous stroma
  • probably reaction to chronic trauam (calculus)
  • tend to recur after removal
79
Q

pyogenic epulis and preganncy epulis

A

Both types of vascular epulis

Clinically and histologically identical with distinction purely based on whether they are found on a pt who is pregnant or not

  • In pregnancy tend to regress spontaneously or decrease in size and assume features of a fibrous epulis after a child is born*
  • delay excision until this time
80
Q

peripheral giant cell granuloma appearance

A

Pedunculated or sessile swelling

  • Typically dark red and ulcerated

Usually arises inter-proximally and has an hour-glass shape

  • Buccal and lingual swellings with narrow middle section joined between the teeth

May recur after surgical excision

81
Q

peripheral giant cell granuloma radiographic change

A

Radiographs may reveal superficial erosion of the interdental bone

  • Need to rule out central giant cell lesion – perforate the cortex and presented similarly as peripheral swelling
82
Q

peripheral giant cell granuloma histology

A

Multinucleate giant cells in a vascular stroma (so histological distinct from other epulis)

83
Q

congenital epulis (congential gingival granular cell tumour)

A

Rare lesion

Occurs in neonates

  • Most commonly affect the anterior maxilla (incisor region)
  • F>M

Granular cells covered with epithelium (histological)

  • Benign
  • Simple excision is curative
84
Q

congenital epulis effects

A

Occurs in neonates (rare)

Most commonly affect the anterior maxilla (incisor region)

F>M

85
Q

congenital epulis

histological

A

granular cells covered with epithelium

86
Q

2 types of HPV associated swellings

A

both benign

  • verruca vulgaris
  • squamous cell papilloma

associated with different types of HPV but are clinically similar - pedunculated cauliflower like growths

87
Q

verruca vulgaris

appearance

A
  • Solitary or multiple intra-oral lesions
  • Most commonly on keratinized tissue – gingivae and palate

pedunculated cauliflower like growths

88
Q

verruca vulgrais

association

A

caused by HPV 2 and 4

May be associated with skin warts

  • May transfer to mouth by autoinoculation from lesions on the finger
89
Q

verucca vulgaris resolution

A

most resolve spontaneously

can be removed surgically - if required

90
Q

squamous cell papilloma

cause

A

HPV 6 and 11

91
Q

squamous cell papilloma

appearance

A
  • Small pedunculated cauliflower like growths
  • Benign
  • vary in colour - pink to white
  • usually solitary
92
Q

tx of squamous cell papilloma

A

surgical excision

93
Q

6 types of fluid swellings

A
  • Mucoceles
  • Ranula
  • Bohn’s nodules
  • Epstein pearls
  • Haemangioma’s
  • Vesiculobullous lesions
    • Primary herpes
    • Epidermolysis bullosa
    • Erythema multiforme
94
Q

mucoceles

A

cyst arising in connection with minor salivary gland

95
Q

2 variants of mucoceles

A

mucous extravastation cycst

mucous retention cyst

96
Q

mucous extravastation cyst

A

normal secretions rupture into adjacent tissue

97
Q

mucous retention cysts

A
  • secretions retained in an expanded duct
98
Q

mucocele appearance

A
  • Bluish, soft, transparent cystic swelling, with a history of rupture, collapse and reswelling
99
Q

mucoceles occur

A

Can affect minor or major salivary glands

  • Most = minor glands of the lower lip, extravasation cysts
    • Related to minor trauma e.g. biting lip

Peak incidence = 2nd decade

100
Q

mucoceles peak incidence

A

2nd decade

101
Q

resolution of mucoceles

A

Most will rupture spontaneously

  • Surgery only if lesion fixed in size as will likely damage adjacent glands leading to recurrence or causing distress to the child or inhibiting daily function

Surgical excision involves removal of the cyst and the adjacent damaged minor salivary gland

  • GA not indicated – benign, tendency to recur
102
Q

rannula

appearance

A

Mucocele in the FOM resembles a frog’s belly (most are extravasation cysts)

103
Q

rannula arise from

A

minor salivary glands or ducts of sublingual/submandibular gland

104
Q

assessment of rannula

A

Ultrasound or MRI needed asses the extent of lesion

  • exclude plunging ranula (extend through the FOM into the submental or submandibular space – need specialist management).
105
Q

rannula can sometimes be

A

Occasionally found to be lymphangioma – benign tumour of the lymphatics

106
Q

Bohn’s nodules

A
  • Gingival cysts, benign
  • Occur on the alveolar ridge
  • Found in neonates (1st 28 days)
    • Remnants of the dental lamina
  • Filled with keratin
  • Usually disappear in the early months of life (3 months)
107
Q

Epstein pearls

A
  • Small cystic lesions
  • Found along the palatal mid-line
  • Thought to be trapped epithelium in the palatal raphe

In ~ 80% neonates (common)

  • Disappear in the first few weeks after birth
108
Q

temporomandibular joint dysfunction syndrome

A

TMJDS

The most common condition affecting the temporomandibular region

Characterised by:

  • Pain
  • Masticatory muscle spasm
  • Limited jaw opening
109
Q

history for TMJDS

A
  • A description of presenting symptoms
    • pain, swelling, clicking, cracking, limitation jaw opening, locked jaw, generalised facial discomfort, earache, numbness over masseter muscles (cheeks)
  • When did the discomfort begin? Any predisposing factors (e.g. traumatic injury)?
  • Is the pain worse at any time during the day?
    • Morning – may indicate nocturnal clenching or grindinghabit
  • Exacerbating factors – chewing, yawning
  • Habits – chew on pens/chewing gum, lean on jaw when studying, grinding teeth at night
  • Stress – sensitive – exams, traumatic life events (bereavement, divorce)
110
Q

EO for TMJDS

A
  • Palpation of the muscles of mastication both at rest and when the teeth are clenched to assess tenderness and/or hypertrophy
  • Palpation of the TMJ at rest and when opening and closing to assess tenderness and click/crepitus
  • Assessment of opening
    • Check for any deviation of the jaw
    • Assess extent of opening (normal = 40-50mm)
111
Q

IO exam for TMJDS

A
  • Assessment of any dental wear facets
  • Signs of clenching/grinding:
    • Scalloped lateral tongue surface
    • Buccal mucosa ridges
112
Q

management of TMJDS

A
  • explain condition in way pt understands
  • reduction of exacerbating factors
  • allow over worked muscles to rest
  • symptomatic relief
113
Q

how to explain TMJDS

A

TMJDs and muscle discomfort is normally due to the overworking and misuse of the muscles – like completing exercise each evening on the legs would expect leg pain, may lead to alteration in how you walk to keep more comfortable

Same with jaws – if overworked (e.g. grinding overnight), muscles will be sore and not able to function correctly, this can lead to an alteration in how we use the jaw which can worsen the problem

  • Needs rest and management of exacerbating
    • Most resolve spontaneously over a few months but can put measures in place to help this – note and explain clearly to pt and record in notes so they have realistic expectations
114
Q

reduction of exacerbating factors for TMJDS (3)

A
  • Management of stress – mindfulness/yoga
  • Avoid habits such as clenching, grinding, chewing gum, nail biting or leaning on the jaw
  • A bite raising appliance may be considered if there is nocturnal grinding/clenching
115
Q

how to allow overworked muscles to rest in TMJDS

A
  • Avoid wide opening – stifle yawns with a closed fist
  • Soft diet which required little chewing
    • Food cut small, avoid opening wide when food consumed, eaten on both sides of mouth and avoid incising food which involves anterior movement of the mandible and stretching of muscles
  • Pt must always ensure a small gap remains between the teeth and teeth only come into contact when food is being swallowed or chewed
116
Q

symtomatic relief for TMJDS

A
  • Use of ibuprofen which has anti-inflammatory action
  • Alternating use of hot and cold packs
117
Q

TMJDS improvement

A

need to be persisting with management measures for several months to see improvement

if these measures are unsuccessful referral for specialist care is indicated.

118
Q

TMJDS recurrence

A

Pts often prone to TMJDS recurrence and exacerbation throughout life during certain periods (e.g. stress)

may need to adopt some prevention measures to avoid exacerbating this when it tends to occur

BDS3 paeds (15 decks)

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