systemic disease and the mouth Flashcards
dental manifestations of systemic disease
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
ectodermal dysplasia
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
what may have caused this
Congenital infections E.g. syphilis
Change to incisor size (termed Hutchison’s incisors – bulbous crown
what may have caused this
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
what may have caused this
porphyria
change of haem and haem products in blood - incorporated into dental tissues as they form
what may have caused these appaeracnes
bilirubin (yellow green change)
* due to perinatal jaundice
Tetracycline
* Extent suggests administration of the drug has gone on for approx. 3 years
possible systemic diseases that can have oral mucosal manifestations
6
- Giant Cell Granuloma
- Orofacial Granulomatosis
- Recurrent Aphthous Stomatitis
- Dermatoses – lichen planus and vesiculobullous conditions
- Immune Deficiency/Disease
- Drug reactions
what could this be
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
oral manifestation of hyperparathyroidism
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
what could cause this
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
what could cause this
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
examples of immune deficiency diseases
4
Orofacial Granuolomatosis
Sjogrens
Autoimmune – Addisons
Infections – fungal/viral
example of skin immune disease (can effect oral mucosa)
lichen planus
vesiculobullous disease
haematinic disease effect on oral mucosa
inc oral ulceration (esp aphthous)
caused - bleeding, diet, inc demand
effects - oral ulceration (esp aphthous), painful tongue
what is this
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
classical signs of OFG
5
- 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
crohn’s screening
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
management of OFG
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?
autoimmune connective tissue dieases
4
- Systemic lupus erythematosis (SLE)
- Systemic sclerosis (Scleroderma)
- Sjogrens syndrome
- Mixed connective tissue disease (MCTD)
systemic lupus erythematous
clinical appearance
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
systemic sclerosis signs
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
types of vasculitis diseases
3
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
types of immune deficiency
2
Congenital Immune Deficiency
* Failure of B or T cell development
Acquired Immune Deficiency
* Diabetes
* Drug therapy
* Cancer therapy
* HIV
immune deficiency presentations in oral mucosa
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
causes of haematinic deficiencies
4
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
5 oral effects of systemic medications
Dry mouth
Oral Ulceration
Lichenoid reaction (ACE inhibitors, beta blockers)
Angio-oedema (ACE inhibitors)
Osteonecrosis (bisphosphonates etc)
what caused this
describe
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)
what caused this
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
