systemic disease and the mouth Flashcards

1
Q

dental manifestations of systemic disease

A

Can be:
* Disruption to the tooth structure formation
* Disruption to the tooth structure content

Usually going to be apparent in children
* Primary teeth for pre/perinatal
* Secondary teeth for perinatal/childhood

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2
Q

ectodermal dysplasia

A

congenital condition
Hypoplasia and Hypodontia
Small cones shaped teeth and some missing

here - Not complete as hair still present on upper lip, can also have absence of sweat or salivary glands

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3
Q

what may have caused this

A

Congenital infections E.g. syphilis

Change to incisor size (termed Hutchison’s incisors – bulbous crown

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4
Q

what may have caused this

A

changes to laying down of cementum and enamel and some extent the calcification of these tissues – according to the time of which illness took place

giveaway – **same effect happening across many teeth and affecting different teeth at different stages of development

hypoplastic and hypomineralised enamel and dentine – extensive perinatal illness (gone on for years), area of crown affected forms between 4 and 5 years of age

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5
Q

what may have caused this

A

porphyria

change of haem and haem products in blood - incorporated into dental tissues as they form

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6
Q

what may have caused these appaeracnes

A

bilirubin (yellow green change)
* due to perinatal jaundice

Tetracycline
* Extent suggests administration of the drug has gone on for approx. 3 years

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7
Q

possible systemic diseases that can have oral mucosal manifestations

6

A
  • Giant Cell Granuloma
  • Orofacial Granulomatosis
  • Recurrent Aphthous Stomatitis
  • Dermatoses – lichen planus and vesiculobullous conditions
  • Immune Deficiency/Disease
  • Drug reactions
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8
Q

what could this be

A

Giant cell lesion - Peripheral’ and ‘Central’ lesions
* Most are osteoclast related lesions
* Small number due to local irritation – producing multinucleate giant cells

Central lesion extending into oral soft tissues – can be seen on radiograph
* Take for any swelling presenting in a child

Check Parathyroid function
* could be as a result of excess parathyroid stimulation of osteoclasts - Can be seen by very active parathyroid gland which is not being inhibited by normal negative feedback control
* Or reactive parathyroidsm: renal failure (on dialysis); hypocalcaemia; parathyroid tumour

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9
Q

oral manifestation of hyperparathyroidism

A

loss of cortical bone
* because it is the densest bone and has a highest amount of calcium – preferentially removed when the PTH hormone is trying to raise the plasma calcium level

Affects the lamina dura
* Loss in ongoing hyperparathyroidism
* Not mistaken for apical pathology as LD is lost around all the tooth and its neighbours
* Will reform one hyperparathryoidsm is corrected

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10
Q

what could cause this

A

Raised ACTH – Addison’s, Cushing’s (pituitary adenoma), small cell carcinoma in lung can produce ACTH

Causes pigmentation (reactive melanosis – ACTH stimulates melanocytes)
* Inc widespread oral pigmentation needs investigation by GMP

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11
Q

what could cause this

A

Raised ACTH – Addison’s, Cushing’s (pituitary adenoma), small cell carcinoma in lung can produce ACTH

Causes pigmentation (reactive melanosis – ACTH stimulates melanocytes)
* Inc widespread oral pigmentation needs investigation by GMP

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12
Q

examples of immune deficiency diseases

4

A

Orofacial Granuolomatosis
Sjogrens
Autoimmune – Addisons
Infections – fungal/viral

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13
Q

example of skin immune disease (can effect oral mucosa)

A

lichen planus
vesiculobullous disease

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14
Q

haematinic disease effect on oral mucosa

A

inc oral ulceration (esp aphthous)

caused - bleeding, diet, inc demand
effects - oral ulceration (esp aphthous), painful tongue

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15
Q

what is this

A

orofacial granulomatosis

cause unclear
similar histological features to crohns
recognised by
* Presents in head and neck in children usually, but can be adults
* Perioral swelling and erythema, lip swelling and angular cheilitis, proliferative erythematous full thickness gingivitis – no plaque responsible, FOM oedema (stag horning), linear fissured ulcer along buccal sulcus (between attached gingiva and reflected mucosa, not trauma related) - active phase - oedema and inflammation
* Can spread to any part of face

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16
Q

classical signs of OFG

5

A
  • Perioral swelling and erythema,
  • lip swelling and angular cheilitis,
  • proliferative erythematous full thickness gingivitis – no plaque responsible,
  • FOM oedema (stag horning),
  • linear fissured ulcer along buccal sulcus (between attached gingiva and reflected mucosa, not trauma related)

active phase - oedema and inflammation

17
Q

crohn’s screening

A

Parental awareness of importance of altered bowel habit or abdominal pain

Growth monitoring at each hospital visit

Faecal Calprotectin assay
* Unreliable in younger children
* Screening test for endoscopy (need GA if a child usually)
* Good predictor of Crohn’s disease activity

Associated with Dietary Allergens?
* Benzoate, Sorbate, Cinnamon, Chocolate (E210-219)
* Use dietary exclusion to determine trigger (if any)
* Benzoates found in tomato and tomato products, so All things with tomato sauces must be avoided
Skin testing not reliable

if pt has crohns then OFG=oral crohns. Can have OFG with no gut symptoms

18
Q

management of OFG

A

3 month empirical dietary exclusion
* Benzoate/cinnamon – unless clear other dietary triggers
* Can reintroduce one at a time to see which foodstuffs are actually needing to be avoided and others which can be tolerated
* Food maestro app useful; Need absolute compliance

Topical treatment to angular chelitis/fissure
* hydrocortisone cream
* Miconazole – when fungal superinfection

Topical treatment to lip swelling or facial erythema
* Tacrolimus ointment 0.03%
* Intralesional steroids to lip – as deep lymph systems are blocked so need to infiltrate them to clear the giant cell lesions so oedema receeds
* Systemic immune modulation?

19
Q

autoimmune connective tissue dieases

4

A
  • Systemic lupus erythematosis (SLE)
  • Systemic sclerosis (Scleroderma)
  • Sjogrens syndrome
  • Mixed connective tissue disease (MCTD)
20
Q

systemic lupus erythematous
clinical appearance

A

Clinically and histologically similar to lichen planus
* White striae with erythematous background
* Gingival lesions – desquamative gingivitis

Differentiate
* Immunology assays
* Pattern – LP not usually on palate
* Histologically – lymphatic band will be lower placed within the connective tissue

21
Q

systemic sclerosis signs

A

Crest syndrome – telangiectasia – haemangiomas on the skin and mucosa – oral bleeding problems

Ischaemic necrosis of digits

Opening and Swallowing issues – oesophagus and oral tissues no longer has elasticity to stretch to allow bolus to pass
* Perioral fibrosis – complicates dental tx
* Tx plan well in advance – restorative, dentures (hard to insert)

Calcinosis - calcifications in soft tissues

22
Q

types of vasculitis diseases

3

A

Large vessel Disease
* Giant cell (temporal) arteritis

Medium Vessel Disease
* Polyarteritis nodosa
* Kawasaki disease

Small vessel Disease
Wegener’s Granulomatosis
* Vasculitis change on the gingiva/palate causes ischaemia and necrosis of the tissue, spread to upper airway
* Refer urgently to rheumatology – needs systemic immunosuppression (can be fatal

23
Q

types of immune deficiency

2

A

Congenital Immune Deficiency
* Failure of B or T cell development

Acquired Immune Deficiency
* Diabetes
* Drug therapy
* Cancer therapy
* HIV

24
Q

immune deficiency presentations in oral mucosa

A

commonly associated with oral opportunistic infections
E.g. candidiasis

Purple change in mucosa – associated with HIV – Kaposi sarcoma

Hairy leukoplakia – ridge, white lesion on the posterior lateral aspect of tonge – manifestation of HIV

Cluster of ulcers on tongue dorsum – keratinised tissue so not aphthous ulcer
* Viral reactivation – Herpes Simplex Virus

If significant or persisting intraoral immune reactivation – investigate for immune def

25
Q

causes of haematinic deficiencies

4

A

Poor intake – dietary analysis/reinforcement

Malabsorbtion
* GI diseases – Coeliac Disease, Crohn’s Disease
* Infections of gut

Blood loss
* Crohn’s Disease, Ulcerative Colitis, Peptic ulcer disease, Bowel Cancer, Liver Disease, drug use
* Pt may be unaware if a low rate of loss over long time

Increased Demand
* Childhood growth spurts (8-10y) – respond well supplementation – may be better to just prescribe then trauma of blood tests

Refer to GMP for ferritin, vit B12, and folic acid assays
* if see changes in recurrent oral aphthous ulceration, lichen planus or oral dyseasthesia

26
Q

5 oral effects of systemic medications

A

Dry mouth
Oral Ulceration
Lichenoid reaction (ACE inhibitors, beta blockers)
Angio-oedema (ACE inhibitors)
Osteonecrosis (bisphosphonates etc)

27
Q

what caused this
describe

A

Shallow ulcer on lateral tongue (painful) is Fixed drug eruption

No erythematous halo – so not aphthous (has yellow slough base)

Lesion happens when drug present, will stop when drug goes away and will reoccur if drug is reintroduced

Doesn’t respond to topical tx
* Need to remove drug that caused it
* Related to Nicorandil (tx angina)

28
Q

what caused this

A

Drug related angio-oedema

Rapid swelling of the face (1hr) due to poor regulation of the complement cascade caused by inhibition of the controlling enzymes as a side effect of ACE inhibitor use
* Subside in 1hr, gone within 24hr

Unlike OFG where it will persist for days/weeks