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Oral Medicine > Systemic Disease and the Mouth > Flashcards

Systemic Disease and the Mouth Flashcards

1
Q

3 main groups of Oral manifestation of systemic disease

A
  1. Dental manifestation of systemic disease
  2. Mucosal effects of systemic disease
  3. Oral effects of tx of systemic disease
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2
Q

How does systemic disease affect teeth

A
  • disruption to tooth structure formation
  • disruption of tooth structure content
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3
Q

What are the dental manifestations of systemic disease in children?

A
  1. Usually going to be apparent in children
    - primary teeth for pre/ perinatal
    - secondary teeth for perinatal/ childhood
  2. Congenital conditions/ infections
    - syphilis, TORCH
    - ectodermal dysplasia
  3. Illness/ metabolic disorders
    - severe childhood illness
    - cancer tx
  4. Pigmentation from substances in blood
    - Bilirubin, present in high levels in jaundice cna affect teeth
    - Tetracycline, administered as an antibiotic
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4
Q

Ectodermal dysplasia

A
  • typical hypoplasia and hypodontia
  • small cone shaped teeth
  • missing teeth
  • does not have complete ectodermal dysplasia as pt has hair on upper lip
  • may have absence of sweat glands and salivary gland
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5
Q

Hutchison’s incisors

A
  • typical bulbous crown
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6
Q

Perinatal illness

A
  • show changes to the laying down of cementum and enamel
  • affect calcification of the tissues depending on the time of which the illness took place
  • same effect happening across many teeth and also affecting diff teeth at diff stages of development
  • can see upper incisors formed slightly lower than the incisors here
  • but same dark band where there is hypoplastic and hypomineralised enamel and dentine
  • extensive perinatal illness as it has gone on for some years, continue up to most of the crown
  • the upper area of crown will form at between 4-5 years of age
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7
Q

Metabolic disease - Porphyria

A
  • change in the amount of haem and haem products in blood
  • can be incorporated into dental tissues as they form
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8
Q

Tooth substance pigmentation- Bilirubin

A
  • significant perinatal jaundice with high bilirubin levels
  • leading to yellow green change within dentition
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9
Q

Tooth substance pigmentation - Tetracycline

A
  • will produce a linear band
  • affected development of all of incisor teeth
  • producing significant cosmetic deformity
  • tetracycline is not recommended to give to children due to this issue
  • may sometimes see tetracycline staining of teeth in unerupted 3rd molars due to children taking them during early teenage years when crown of tooth forming
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10
Q

Oral Mucosal effects from Systemic disease

A
  • Giant Cell Granuloma
  • Orofacial Granulomatosis
  • Recurrent Aphthous Stomatitis
  • Dermatoses, ie: Lichen Planus, Vesiculobullous
  • Immune Deficiency/ Disease
  • Drug reactions
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11
Q

Giant Cell Lesions

A
  • can be peripheral/ central
  • osteoclast related lesions
  • can also be due to local irritation, roducing multinucleate giant cells in order to remove a difficult stubborn pathogen
  • if there is central lesion extending into oral ST, usually seen on radiograph
  • consider whether they are due to hormonal changes
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12
Q

If a child had swelling, what is essential to take?

A

Radiographs

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13
Q

Hormonal changes in GCL

A
  • peripheral and central lesions
  • check parathyroid function
  • could be excess of parathyroid stimulation of osteoclasts
  1. renal failure - reactive hyperparathyroidism
  2. hypocalcaemia - reactive hyperparahtyroidism
  3. parathyroid tumour

Pt with renal failure/ on renal dialysis, will possibly have GCL appearing

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14
Q

Hyperparathyroidism

A
  • loss of cortical bone
  • densest bone and has highest calcium content
  • preferentially removed when parathyroid hormone is trying to raise plasma calcium level
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15
Q

Hyperparathyroidism in dentistry

A
  • from dental perspective, this affects the lamina dura
  • with ongoing hyperthyroidism, lamina dura is often lost
  • don’t mistaken as periapical lesion when lamina dura is absent around apex of tooth but absent all around the tooth
  • once hyperparathyroidism corrected, lamina dura will form
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16
Q

Raised ACTH - Addison’s

A
  • pigmentation due to raised ACTH
  • ACTH stimulates hormone for melanocytes
  • high ACTH levels will produce a reactive melanosis of the oral mucosa
  • widespread pigmentation within mouth and also happen on skin
  • increasing of widepsread oral pigmentation should trigger investigation by referral from dentist to GMP
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17
Q

Causes of raised ACTH

A
  • Addisons
  • Cushings, where there is pituitary adenoma producing excess ACTH
  • if there is a small cell carcinoma in lung which produce ACTH inappropriately
18
Q

Systemic Illnesses

A

Immune deficiency
- Orofacial Granulomatosis
- SS
- Autoimmune- Addisons, Cushings
- Infection - fungal/ viral

Skin immune disease
- LP
- VB disease: Pemphigoid, Pemphigus

Haematinics deficinecy
- causes: bleeding, diet, increased demand
- effects; oral ulceration, painful tongue

** If pt has low iron, due to internal bleeding into gut/ poor diet/ malabsorption, will cause aphthous type ulceration

19
Q

What is Orofacial Granulomatosis

A
  • similar features to Crohns disease
  • predominately affecting H&N in children, can develop first time in adults
  • children with ginger gene and freckles
20
Q

Clinical photos of OFG

A
  • perioral erythema
  • perioral swelling
  • lip swelling
  • angular cheilitis
  • active phase of disease: oedema and inflammation going on within perioral tissues
  • can spread to any part of the face
  • causing dry and cracking surface of lower lip
  • proliferative, erythematous, full thickness gingivitis (usually in all 4 quadrant)
  • staghorning tooth appearance as they look like antlers (picture 4)
  • ## linear fissured ulcer present bottom of labial sulcus: not related to trauma
21
Q

Crohn’s screening

A
  • if pt has OFG, then one question to ask if they have Crohn’s disease
  • if they have, then normally lesions are termed oral Crohn’s rather than OFG
  • OFG normally won’t present with abdominal pain/ problems, but may develop in later time and diagnose as Crohns
22
Q

Best thing to do to determine child presenting with OFG has Crohns?

A
  • look for changes of altered bowel habit/ abdominal pain
  • any evidence of growth problems
  • if children has small bowel Crohn’s disease, they will fail to absorb nutrients properly and reduce their rate of growth
23
Q

Faecal Calprotectin assay

A
  • In young children, when they come across new pathogens for the first time, a raised calprotectin may be due to a variety of causes -> hence unreliable
  • older children above 10, calprotectin levels are more associated with gut inflammation
  • GA for screening test for endoscopy: based upon good level of suspicion
    1. growth failure
    2. abdominal pain/ symptoms
    3. raised calprotectin levels
24
Q

How to assess growth prediction?

A
  • using standardised growth charts
  • should follow their own centile group
  • blue: boys, pink: girls
25
Q

Causes of OFG without Crohns

A
  • dietary preservatives, ie: benzoic acid in fizzy drinks
  • some pts by limiting this can reduce their symptoms
  • Dietary allergens, ie: Benzoate, Sorbate, Cinnamon, Chocolate (E210-219)
  • skin testing not reliable
  • use dietary exclusion to determine trigger
  • Benzoates are in tomato and tomato products; all things with tomatoes must avoid
26
Q

Food Maestro app

A
  • parents and pt to enter substances they need to avoid
  • when buying stuff, they can scan the bar code of the food in supermarket and the app will tell them any substances they need to avoid
  • pt need to comply 100% during trial period
27
Q

Management of OFG

A
  1. 3 month empirical dietary exclusion
    - Benzoate/ cinnamon, unless clear of other dietary triggers
  2. Topical tx for angular chelitis/ fissure
    - Miconazole
    - Hydrocortisone cream
  3. Topical tx to lip swelling/ facial erythema
    - Tacrolimus ointment 0.03%
    - Intralesional steroids to lip
    ** lip swelling is oedema, problem is within lymphatics deep inside lip tissues, medicaments are required to be absorbed and soak into tissues and be carried to lymphatics, drain out
  • some cases, need systemic immune modulation
28
Q

CT disease/ autoimmune disease

A
  1. Systemic lupus erythematosis (SLE)
  2. Systemic sclerosis (Scleroderma)
  3. SS
  4. Mixed CT disease (MCTD)
29
Q

Lupus

A
  • similar to LP
  • histologically also similar to LP
  • changes in mucosa with white striae on erythematous background
  • gingival lesions
  • difference is found by immunology assays of blood and also unusual pattern
  • in histological exam, lymphocytic band is much lower placed within CT in lupus than in LP
30
Q

Systemic sclerosis

A

Crest syndrome (picture 1)
- telangiectasia/ little BV forming haemangiomas on surface of skin
- may continue through mucosa and cause oral bleeding problems
- problems with oesophagus, no longer has elasticity to stretch and allow bolus to pass
- perioral fibrosis means that mouth cannot be opened as facial tissues will not stretch to move bones
- denture and extraction will be difficult due to limited mouth opening

31
Q

Vasculitic diseases

A

Large vessel disease
- Giant Cell (temporal) Arthritis

Medium vessel disease
- Polyarteritis nodosa
- Kawasaki disease

Small vessel disease (picture bottom)
- Wegener’s Granulomatosis ** most frequently reported
- vasculitic change on gingiva/ palate often cause ischaemia and necrosis of tissue and spread throughout upper airway
- pt must be referred urgently to rheumatologist
- require systemic immunosuppression to control as may become fatal

32
Q

Immune deficiency

A

Congenital Immune Deficiency
- failure of either B/ T cell development

Acquired Immune deficiency
- diabetes
- drug therapy: immunosuppresive medicines
- cancer therapy
- HIV

33
Q

What is most commonly associated with opportunistic infections?

A

Immune deficiency

34
Q
A

This case of SS, may have left pt with a very dry mouth and led to candida infection

  • HIV may also produce similar effect and hence more susceptible to candidiasis
  • Purple change in mucosa (picture beside), commonly associated with HIV and termed Kaposi sarcoma
35
Q

Hairy Leukoplakia

A
  • ridged white lesion on posterior laterla aspect of the tongue
  • uncommonly seen as a manifestation of HIV
36
Q

Herpes simplex reactivating

A
  • viral reactivation on tongue dorsum
  • if significant, should be accompanied by immune deficiency investigations
37
Q

What causes haematinic deficencies?

A
  1. Poor intake of diet
  2. Malabsorption
    - GI disease: Coeliac, Crohns
  3. Blood loss
    - Crohns disease, Ulcerative colitis, Peptic ulcer disease, Bowel cancer, Liver disease
  4. Increased demand
    - childhood growth spurts
38
Q

Oral effects of medical therapy

A
  • dry mouth
  • oral ulceration
  • lichenoid reaction to ACE inhibitors, beta blockers and other drugs
  • angio-oedema- ACE inhibitors
  • osteonecrosis: bisphosphonates
39
Q

Oral ulceration

A
  • ulcer related to Nicorandil
  • although it may look like a major aphthous ulcer, there is no erythematous halo around ulcer
  • responds poorly to topical steroids
  • only tx is to remove drug causing the problem

Nicorandil- used to treat angina, usually concern to stop the drug as it is for poorly- controlled angina

40
Q

Angio-oedema

A
  • due to por regulation of complement cascade
  • caused by inhibition of controlling enzymes as side effect of ACE inhibitor use
41
Q
A

Oral Medicine (24 decks)

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