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BDS4 Oral Medicine > Systemic diseases and the mouth > Flashcards

Systemic diseases and the mouth Flashcards

1
Q

What are the ways in which a dental manifestation of systemic disease can present?

A
  • Affects tooth structure formation
  • Affects Tooth structure components
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2
Q

When does disruption affecting primary teeth occur?

A

Pre-natal/Peri-natal period

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3
Q

When does disruption affecting secondary teeth occur?

A

Perinatal/early childhood

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4
Q

What are the systemic causes of dental abnormalities?

A

Congenital conditions/infections
-> Syphilis,TORCH
-> Ectodermal Dysplasia

Illness/metabolic disorder
-> Severe childhood illness
-> Cancer treatments

Pigmentation from substances in the blood
-> Bilirubin, tetracycline

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5
Q

What are some of the features of ectodermal dysplasia?

A
  • Hypoplasia- cone shaped teeth
  • Hypodontia
  • Abscess of sweat and salivary glands
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6
Q

What are the dental features of syphillis?

A

Bulbous crown- Hutchison’s teeth

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7
Q

What occurs to teeth as a result of jaundice and hyperbilirubinaemia?

A

They become green

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8
Q

What can occur if tetracycline is used during period of tooth formation?

A

Can become incorporated into tooth structure
- Linear banding
- Significant cosmetic deformity- especially if taken over years
- No longer given to children (don’t use if better drug available)
- May be seen in unerupted third molars- if patient taken tetracycline in early teens

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9
Q

What is the effect of porphyria on dental development?

A

Changes amount of haem and haem products in blood which may be incorporated into tooth structure
-> Dark pink appearance

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10
Q

What systemic issues can present as change in oral mucosa?

A

Giant Cell Granuloma

Orofacial Granulomatosis

Recurrent Aphthous Stomatitis

Dermatoses

Immune Deficiency/Disease

Drug reactions

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11
Q

What are the features of Giant cell granulomas?

A
  • Peripheral or central
  • Often osteoclast related
  • Can be due to irritation- giant cells produced to remove stubborn pathogen
  • Central lesion extending into ST- seen on radiographs (essential to take)
  • May be due to hormonal changes- PTH excess (not being inhibited by negative feedback control)
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12
Q

What are the causes of excess PTH?

A

Gland adenoma

Reactive
-> renal failure (dialysis)
-> hypocalcaemia

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13
Q

What are some of the effects of hyperparathyroidism?

A
  • Loss of cortical bone- highest calcium and highest density (preferentially removed when PTH is trying to raise Ca)
  • Can be seen as resorption at terminal flanges of the hand
  • Can affect lamina dura- lost (do not mistake for PA lesion)- this will reform after disease is corrected
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14
Q

What are the causes of raised ACTH?

A

Addison’s

Cushing’s (pituitary adenoma)

Small cell carcinoma in lung can also produce excess ACTH

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15
Q

What are the results of raised ACTH?

A

Stimulates melanocytes
-> Reactive melanosis
-> Widespread brown patches in mouth and skin

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16
Q

How does OFG present?

A
  • Perioral redness/swelling, lip swelling, angular cheilitis
  • Can spread to any part of the face
  • Fissures can occur
  • Proliferative erythematous fill thickness gingivitis in all quadrants (plaque not responsible)
  • Stag horning- oedema in floor of mouth
  • Linear fissured ulcer in sulcus- between attached gingivae and reflected mucosa
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17
Q

What phenotype of patients in Scotland commonly get OFG?

A

People with red hair and freckles

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18
Q

What is OFG called if the patient also has Crohn’s?

A

Oral Crohn’s

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19
Q

Why may children be diagnosed with OFG?

A

May be diagnosed as OFG in children as at this point they have no gut symptoms yet
-> Find out from parents about bowel habits, abdominal pain and issues with growth (related to malabsorption)

20
Q

Why is a faecal calprotectin assay useful when screening for crohns?

A

FC- suggests active IBD (also happens with adeno virus of the gut)

21
Q

Why may a FCA be less reliable in younger kids?

A

In young children the raised FC may be attributed to the fact that they are coming into contact with many new pathogens

-> when they are over 10, raised FC levels is more reliable sign of inflammation

22
Q

When would an endoscopy for Crohns’s be carried out?

A

Only if clinicians were highly suspicious the patient had Crohns after screening tests
-> requires GA

23
Q

How are growth charts utilised in Crohn’s screening?

A

Child should follow predictive centile
-> Blue chart for boys, pink for girls

If growth moves across lines it suggests a malabsorption or GH issue
-> Fairly accurate at predicting patient’s final height

24
Q

What are common triggers for OFG?

A

Benzoic acid (found in fizzy drinks)
-> Limiting intake of these beverages can limit symptoms

Sorbic acid

cinnamon derivatives

chocolate

E numbers

25
Q

What is the best way of determining the trigger for OFG?

A

Carrying out dietary exclusions is best way of determining dietary trigger
-> must have 100% compliance- difficult as some natural products contain benzoate

Slowly reintroducing food stuffs one at a time after exclusion can help patient single out which ones they must avoid

26
Q

How is OFG managed?

A

Topical treatment to angular chelitis/fissure
-> Miconazole/hydrocortisone cream

Topical treatment to lip swelling or facial erythema
-> Tacrolimus ointment 0.03%
-> Intralesional steroids to lip
-> Systemic immune modulation

27
Q

Why are intrapersonal steroids helpful to treat OFG?

A

Applying these to oedematous lips may allow drainage if they can break up giant cell lesions in lymphatic system

28
Q

What does an exclusion diet not prevent?

A

Children developing Crohn’s in the future

29
Q

What are the different autoimmune connective tissue diseases?

A

Systemic lupus erythematosis (SLE)

Systemic sclerosis (Scleroderma)

Sjogrens syndrome

Mixed connective tissue disease (MCTD)

30
Q

How is SLE distinguished from LP?

A
  • Different results in immunology assays
  • SLE lesions can occur in palate
  • Histologically- the lymphocytic band is occurring lower down in connective tissue
31
Q

How does systemic sclerosis present?

A
  • Crest syndrome- BV form haemangiomas on surface of skin (can occur in oral mucosa)
  • Ischaemic necrosis of digits
  • Oesophagus can lose elasticity- swallowing issues
  • Calcinosis- calcification of soft tissue
  • Loss of elasticity around mouth (peri-oral fibrosis)- difficulty opening, facial tissues cannot stretch to move bone
32
Q

What are the dental implications of Systemic Sclerosis?

A

 Dental treatment is difficult- may need to plan 10 years ahead (aim to reduce amount of treatment required)
 Dentures are difficult to insert and remove
 Posterior extractions are difficult/impossible
 Aim for low maintenance dentition, seek advice from restorative consultant

33
Q

What are the different types of Vasculitic diseases?

A

Large vessel Disease
-> Giant cell (temporal) arteritis

Medium Vessel Disease
-> Polyarteritis nodosa
-> Kawasaki disease

Small vessel Disease
-> Wegener’s Granulomatosis

34
Q

Which vasculitic disease is most likely to affect oral cavity and present to dentist?

A

Wegners- seen on gingivae and palate
-> Ischaemia and necrosis of tissues that can spread throughout upper airway
-> Refer urgently to rheumatologist- will require systemic immunosuppression to control potentially fatal condition

35
Q

What are the causes of immune deficiencies with oral implications?

A

Congenital Immune Deficiency- failure of T/B cell development

Acquired Immune Deficiency:
Diabetes
Drug therapy
Cancer therapy
HIV- ulceration/perio

36
Q

What systemic diseases can be related to candidiasis?

A

Sjogren’s

HIV related salivary disease

-> both cause dry mouth creating conditions for candida infection

37
Q

What is a purple change in mucosa caused by?

A

Kaposi sarcoma (HIV)
-> Unusual to see now due to development of HHART therapy

38
Q

How does hairy leukoplakia present?

A

Ridged white lesion on posterior/lateral aspect of tongue
- Can be manifestation of HIV

39
Q

What is the likely cause of a cluster of blisters appearing on tongue?

A

Reactivation of HSV

40
Q

What are the causes of haematinic deficiencies?

A

Poor intake – dietary analysis/reinforcement

Malabsorbtion
-> GI diseases – Coeliac Disease, Crohn’s Disease

Blood loss
-> Crohn’s Disease, Ulcerative Colitis, Peptic ulcer disease, Bowel Cancer, Liver Disease

Increased Demand
-> Childhood growth spurts

41
Q

What are the oral effects of haematinic deficiency?

A

Painful tongue

Ulcers

Oral dysaesthesia

LP

42
Q

How is ulceration due to increased demand in growth spurt managed?

A

Iron supplementation- even if iron levels are not low

43
Q

What are the oral effects of medical therapy?

A

Dry mouth

Oral Ulceration- Nicorandl

Lichenoid reaction- BB, ACE Inhibitors

Angio-oedema- ace inhibitors

Osteonecrosis- bisphosphonates

44
Q

What occurs in angio-oedema?

A
  • Rapid swelling of face within an hour, subsides within an hour/day
  • Inhibition of complement cascade controlling enzymes
45
Q

What is nicorandl used for? What are its side-effects

A

Angina
 Shallow painful ulcers with no erythematous halo
 Only treatment is to stop drug but this may not be safe systemically

BDS4 Oral Medicine (28 decks)

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