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FINALS - Oral Medicine > Systemic Diseases and the Mouth > Flashcards

Systemic Diseases and the Mouth Flashcards

1
Q

Which systemic disorders can affect tooth structure/development in children?

A

Congenital conditions/ infections (syphilis, TORCH infection ectodermal dysplasia)

Illness or metabolic disorder (severe illness, cancer treatments)

Pigmentation from blood substances (bilirubin, tetracycline)

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2
Q

At what point in a child’s development are the primary teeth affected by disorders which may cause developmental issues with teeth?

A

Pre/perinatal period.

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3
Q

At what point in a child’s development are the permanent teeth affected by disorders which may cause developmental issues with teeth?

A

Peri-natal/childhood period.

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4
Q

List the six oral mucosal effects from systemic disease.

A

Giant Cell Granuloma
Orofacial Granulomatosis
Recurrent Aphthous Stomatitis
Dermatoses (Lichen planus, vesicobullous)
Immune Deficiency/Disease
Drug reactions

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5
Q

What are giant cell lesions?

A

Typically osteoclast related lesions, producing multi-nucleate giant cells, in order to deal with a difficult and stubborn pathogen.

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6
Q

Which hormonal disorders can cause giant cell lesions?

A

Renal failure
Hypocalcaemia
Parathyroid tumor

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7
Q

How can hyperparathyroidism present on a dental radiograph?

A

Loss of lamina dura around multiple teeth, not due to periapical pathology. Increased osteoclastic activity leads to breakdown of cortical bone.

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8
Q

How can high ACTH cause pigmentation of the oral mucosa?

A

ACTH includes the stimulating hormone for melanocytes, leading to a reactive melanosis of the oral mucosa and skin.

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9
Q

Which conditions can lead to raised ACTH levels?

A

Addison’s/Cushing’s

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10
Q

List five effects that medical therapy can have on the oral cavity.

A

Dry mouth
Oral Ulceration
Lichenoid reaction
Angio-oedema
Osteonecrosis

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11
Q

Histologically, how can you differentiate between Lupus and Lichenoid reaction?

A

The Lymphocytic band is placed much lower in Lupus than in Lichenoid reaction.

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12
Q

What are the main causes of immune deficiency?

A

Congenital Immune Deficiency

Acquired Immune Deficiency
Diabetes
Drug therapy
Cancer therapy
HIV

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13
Q

What are the main causes of hematinic 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

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14
Q

What is orofacial granulomatosis?

A

Clinical presentation of oedema in the oral and facial soft tissues by blockage of lymphatic drainage due to immune reaction.

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15
Q

What is angio-oedema?

A

Angio-oedema is oedema of the oral and facial soft tissues due to an INCREASE in fluid exudate from the capillaries but with NO lymphatic drainage.

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16
Q

What are the 3 main groups when considering Oral manifestations of systemic disease?

A
  • Dental manifestations of systemic disease
  • Mucosal effects of systemic disease
  • Oral effects of treatment of systemic disease
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17
Q

What are the 2 broad categories that dental manifestations of systemic disease occur?

A
  • Disruption to tooth structure formation
  • Disruption to tooth structure content
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18
Q

Is dental manifestations going to be more apparent in children or adults?

A
  • Children
  • Apparent in primary teeth for pre/perinatal issues
  • Apparent in permanent teeth for perinatal/childhood issues
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19
Q

What are some congenital conditions/infections that can cause dental manifestations in children?

A
  • Syphillis
  • TORCH
  • Ectodermal dysplasia
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20
Q

What is TORCH infection?

A
  • Infection of developing fetus or newborn that can occur in utero, during delivery or after birth
  • Stands for toxoplasmosis, rubella, cytomegalovirus, herpes and other agents
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21
Q

What is ectodermal dysplasia?

A
  • Dsiorders that affect skin, sweat glands, hair, teeth and nails
  • Can also cause immune system problems like hearing and vision
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22
Q

What are some illness’ or metabolic disorders that can cause dental manifestations in children?

A
  • Severe childhood illness
  • Cancer txt (the earlier the txt starts the more dental development issues can be seen)
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23
Q

What are some pigmentations from substances in the blood which can cause dental manifestations in children?

A
  • Bilirubin (found in high levels in pt with jaundice can affect the teeth)
  • Tetracycline (administered within antibiotic can then be incorporated iinto tooth substance)
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24
Q

What systemic disease can manifest as this picture?
- Describe what you see

A
  • Ectodermal dysplasia
  • Shows hypodontia and hypoplasia
  • Small cone shaped teeth and missing teeth
  • This pt does not have full ectodermal dysplasia as has hair on upper lip
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25
Q

What is a common finding of pt with ectodermal dysplasia?

A
  • Absence of sweat glands or salivary glands
  • Can cause issue with xerostomia - caries - perio - etc
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26
Q

What systemic infection can cause this manifestation?
- Describe what you see

A
  • Syphilis
  • Show changes to incisors in particular termed Hutchinson’s incisor with a bulbous crown
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27
Q

What systemic disease can cause this dental manifestation?
- Describe what you see

A
  • Perinatal illness
  • Shows chnages to the laying down to dentine and enamel
  • Shows some changes to the calcification of these tissues according to the time at which the illness happened
  • Give away is the Clearly same effect through different teeth
  • Upper incisors formed slightly more than lower incisors but both show the hypoplastic and hypomineralised enamel and dentine
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28
Q

What systemic disease can cause this dental manifestation?
- Describe what you see

A
  • Metabolic disease called Porphyria
  • Produce a change in the amount of hem in the blood and can induce this into the teeth
  • Can see the dark pigmentation in the tooth tissues
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29
Q

What systemic disease can cause this dental manifestation?
- Describe what you see

A
  • Sever jaundice as a child
  • Increase the bilirubin in the blood which manifests into the tooth tissues
  • Leads to yellow green change in dentition
  • This case the jaundice went on for some years as all of the crown is affected with the colouring
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30
Q

What tooth substance pigmentation can cause this dental manifestation?
- Describe what you see

A
  • Tetracycline from drug prescription
  • Produce a linear band
  • Tetracycline are not recommended for children anymore for this problem
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31
Q

What are the oral mucosal effects from systemic disease we need to consider?

A
  • Giant cell granuloma
  • Orofacial granulomatosis
  • Recurrent Aphthous stomatitis
  • Dermatoses
  • Immune deficiency/disease
  • Lichen planus (drug reactions)
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32
Q

What is this a picture of?

A
  • Giant cell Lesion
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33
Q

What are giant cell lesions?

A
  • Type of noncancerous tumour
  • Can be central or peripheral lesions
  • Most are osteoclast related lesions but some can be due to local irritation producing multinucleated giant cells to remove stubborn pathogen
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34
Q

If a giant cell lesion is due to hormonal changes what can this be due to?

A
  • Parathyroid hormone excess
  • Shows active parathyroid gland not being inhibited by normal negative feedback control
35
Q

When can reactive hyperparathyroid occur and what can they cause?

A
  • Can occur due to renal failure or hypocalcaemia
  • Can cause giant cell lesions as a result of excess parathyroid stimulation of osteoclasts
36
Q

What radiographic changes are being seen here and what can it be a result of and why?

A
  • Loss of cortical bone
  • Cortical bone is the densest and has highest calcium content therefore it is preferentially removed when parathyroid hormone is trying to raise the plasma calcium level during Hyperparathyroidism
37
Q

What condition is showing these radiographic changes?

A
  • Hyperparathyroidism
  • Lamina dura often lost around all teeth and along the whole root (don’t mistake for pathology)
38
Q

What hormone is causing this mucosal change?

A
  • Raised ACTH - Addisons or cushings (pituatory adenoma producing Excess ACHT) or small tumour in lung producing ACHT
  • High ACTH produces reactive melanosis of oral muscosa
  • Widespread mucosal change and can happen on the
39
Q

What is Orofacial granulomatosis?

A
  • Clinical presentation of oedema in the oral and facial soft tissues by blockage of lymphatic drianage due to immune reaction
40
Q

What is angio-oedema?

A
  • Oedema of the oral and facial soft tissues due to increase in fluid exudate from capillaries but with no lymphatic drainage
41
Q

What is the difference between angio-oedema and OFG?

A
  • OFG blockage of lymphatic drainage
  • OFG swelling comes up quick and settles slow (over weeks or months if at all)
  • Angio swelling comes up quick and settles quickly usually in 24-48hrs
42
Q

What are some diseases other than OFG than can be responsible for swelling in facial or oral areas?

A
  • Produce giant cells responsible for the granulomatosis
  • Sarcoidosis (rare)
  • Tuberculosis (rare)
  • Crohns disease
43
Q

What is this picture showing us?

A
  • Angio-oedema
  • Can see lots of fluid present within the tissue leading to facial swelling
44
Q

What disease is this picture presenting as?

A
  • Orofacial granulomatosis
  • Giant cells forming within the tissues preventing lymphatic drainage
  • Can see the multinucleated cells within the membrane
45
Q

What is going on during OFG histologically and immunologically speaking?

A
  • Type IV ( Cell mediated) hypersensivity
  • Bacteria or antigen trigger an immune response
  • Antigen presenting cells activate the T helper cells (TH1)
  • T helper cells bind to macrophages to produce activated machrophages which will try and phagocytose the antigen.
  • Macrphages fusion induced by IL-4 occurs to produce multinucleated giant cell which also try to phagocytose the antigen
46
Q

What age does OFG present?

A
  • Can present any age
  • Common in later childhood and adolescent
  • Most are mild and controlled with simple measures and pt unaware
47
Q

What clinical findings can be seen with OFG?

A
  • Perioral erythema
  • Swelling of lips
  • Angular chelillits
  • Fissuring of lips
  • Full thickness gingivitis (not plaque related initially)
  • Swelling of intra oral tissues
  • Ulceration (usually filled with granulomas histologically)
48
Q

What should the parents be warned about if the child has OFG?

A
  • Should undergo a Chrohns screening
  • Parents be aware of altered bowel habit or abdominal pain
  • Growth monitoring at each hospital visit
49
Q

What is the best way to measure Chrohsns in child if diagnosed with OFG?

A
  • Faecal Calprotectin assay
  • Good predictor of Crohns disease activity
  • Screening test for endoscopy
  • Unreliable in children
50
Q

When initially manging diagnosis of OFG for a child what is the first port of call?

A
  • Consider whether this if OFG or part of Crohns disease
  • Check GI symptoms
  • Faecal calprotectin
  • Start sequential growth monitoring
  • Take diet history and identify overuse of dietary allergen
51
Q

What does the Exclusion Diet trail entail?

A
  • Avoid all food containing
  • Benzoic acid
  • Sorbic acid
  • Cinnamon products
  • Chocolate
  • E210-219
  • Compliance needs to be 100% for 3 months
52
Q

What medical therapy can be used when diet testing is not useful? (Specialist only)

A

Topical txt
- Miconazole to angular chelitis
- Tacrolimus ointment to areas of lip swelling and facial erythema

Intralesional steroid injection
- Triamcinolone injected into area of swelling - often weekly for 3 weeks

Systemic txt to help immune modulation
- Pulse azithromycin for 3 months 3 days in every week
- Prednisolone pulps for short term issues
- Azathioprine/mycophenolate Mofetil for longer term

53
Q

What are the key features of viruses?

A
  • Incredibly small size
  • Human herpes virus is 0.1-0.2um
  • Simple chemical composition (phospholipid envelope, nucleic acid genome, protein capsid, spike projections)
  • No intracellular organelles meaning they are obligate intracellular parasites
  • Genetic info is either DNA or RNA
54
Q

Give an example of viral replication for a DNA virus? Give the 8 key stages

A
  • Herpes Simplex
    1. Binding to receptor molecules in host cell membrane
    2a/2b. Entry of envelope fusing to host membrane
    3. Release capsid into cytoplasm and Nuclear transport (whilst VHS virion host shutoff degrades host cells mRNA)
    4. Nuclear entry of herpes chromosome through nuclear pore
    5. VP16 causes Gene expression of immediate early mRNA and LAT mRNA
    6. DNA replication by DNA polymerase
    7. Packaging of DNA into capsids and envelopes
    8. Egress of completed virion in epithelial cells
55
Q

What are the two types of infections associated with herpes simplex and what type of mRNA creates them?

A
  • Lytic infection created by immediate early mRNA
  • Latent infection created by LAT mRNAs (stay dormant in nerve cells and can later cause lytic infection)
56
Q

What are the principles of Laboratory diagnosis?

A
  • History and examination
  • Provisional diagnosis
  • Diagnosis
  • Take appropriate specimen if needed
  • Detection of viral nucleic acid (detecting nucleic acid amplification)
  • Or serology (detecting nucleic acid amplification or antibody levels)
57
Q

How would you take a viral swab?

A
  • Use flocked swab
  • Place in molecular sample solution (MSS)
  • After immersion remove swab
  • Label correctly and send to lab
58
Q

How would you take a blood sample? What can they be used for?

A
  • EDTA (purple top)
  • Serology or molecular
59
Q

For maculo papular / erythematous lesions what are the common pathogens found , what specimen would you take and what is the lab testing for?

A
  • Enterovirus, HHV6, HHV7, Measles, Rubella
  • Mouth swab
  • DNA/RNA detection
60
Q

For vesicular lesions what common pathogens are found in the lesion, what specimen would you take and what is the lab testing for?

A
  • HSV1, HSV2, VZV, Enterovirus
  • Mouth swab
  • DNA/RNA detection
61
Q

For ulcers what common pathogens are present, what specimen would you take and what test would you do?

A
  • HSV, Enterovirus
  • Mouth swab
  • DNA/RNA detection
62
Q

For maculo papular/ erythematous lesions when using serology what is the common pathogens found, what specimen would you take and what is the lab testing for?

A
  • B19, CMV, EBV
  • EDTA blood
  • DNA/RNA detection or serology
63
Q

What virus are included in the Human Herpes Virus infections?

A
  • Herpes simplex type 1
  • Herpes simplex type 2
  • Varicella zoster
  • Epstein Barr
  • Cytomegalovirus
  • HHV-6
  • HHV-7
  • HHV-8 (Kaposi’s Sarcoma Associated virus)
64
Q

What are 3 common features of Human herpes Virus’?

A
  • Primary infection
  • Period of latency
  • Recurrent infection

All have slightly diff clinical features of these stages

65
Q

What are the clinical features of Herpes simplex types 1 & 2?

A
  • Gigivo stomatitis
  • Herpes labialis
  • Keratoconjuctivitis
  • Herpetic whitlow
  • Bell’s palsy
  • Genital herpes
66
Q

What is the pathogenesis of HSV-1?

A
  • HSV-1 enters mucosal surface or through damaged epithelium (is a mucocutaneous disease)
  • Replicates in the epithelial cells which give the classic cold sore characteristic
  • HSV is taken up by sensory neurones undergoing retrograde transport back to sensory ganglia
  • Latent infection is established in the sensory ganglia
  • Latent virus lies dormant until reactivation of the virus occurs in the neuron (most likely the trigeminal ganglion)
  • Virions then transported back down the neuron in anterograde fashion to the epithelial cells (recurrent infection) where viral shedding, epithelial shedding and cold sores appear
  • Can feel tingling or pain before recurrent lesions occur (Aciclovir can be used to reduce the mitigation)
67
Q

What is the epidemiology of Herpes simplex virus?

A
  • Very common infection >90%
  • It’s reservoir is Saliva
  • Approx 30% asymptomatic shedding (infection control vital)
  • Route of transmission is direct by close person to person contact
  • Occurrence is common in childhood
68
Q

When might a lab diagnosis be needed for cases of HSV ? What swab would you use?

A
  • Atypical cases usually HSV reactivation in immunocomprimsed host
  • Vesicle/ulcer fluid swab and molecular sample media for PCR
69
Q

What is the treatment according to SCDEP for Herpes simplex virus in non-immunocompromised pts?

A
  • Local measures of avoid dehydration and alter diet to include soft foods and adequate fluids
  • Use analgesics and antimicrobial mouthwash
  • Chlorhexidine mouthwash 0.2% 300ml rinse mouth 1 min with 10ml twice daily
  • Aciclovir cream 5% , send 2g , label apply to lesion every 4 hrs (five times daily) for 5 days
70
Q

What is the txt of herpes labialis in immunocompromised pts and sever infections in non-immunocompromised pts according to SDCEP?

A
  • Aciclovir tablets 200mg, Send 25 tablets, label 1 tablet five times daily
71
Q

What is the varicella infection?

A
  • Chicken pox
  • Primary infection varicella
  • Vesicles all along the epithelium
72
Q

What is the incubation period for varicella?

A
  • 10-21 days
73
Q

What are some complications of varicella?

A
  • Secondary bacterial infections
  • Pneumonia
  • Congenital, perinatal/neonatal
74
Q

What are the signs and symptoms of Zoster(Shingles) virus?

A
  • Vesicles appear in dermatome, representing cranial or spinal ganglia where virus has been dormant
  • Affected area intensely painful with associated paraesthesia
  • Not crossing mindline
75
Q

What are some complications of Zoster virus?

A
  • Post herpetic neuralgia
  • Secondary bacterial infections
  • Ophthalmic zoster
  • Ramsay Hunt syndrome (signs and symptoms link to paralysis of facial nerve)
76
Q

What is the Varicella-Zoster pathogenesis?

A
  • Primary infection with varicella zoster virus appears on epithelium as chickenpox lesions
  • Virus travels down by retrograde transport in a period of latency in the trigeminal ganglion where it remains dormant
  • Reactivation of latent virus from trigeminal ganglion transport to epithelium again as zoster lesions
77
Q

What is the epidemiology of Varicella?

A
  • Very common >90%
  • Source is contact with varicella and zoster
  • Highly infectious esp respiratory secretions (48hrs pre symptoms) , or vesicle fluid infections
78
Q

What is the epidemiology of the zoster part of VZV?

A
  • Latent virus remains in sensory ganglion (trigeminal)
  • Low rate of transmission from vesicle fluid
79
Q

What is the route of transmission of VZV?

A
  • Direct contact, droplet or airborne spread
80
Q

What is the occurence of VZV?

A
  • Varicella - highest in children
  • Zoster - highest in elderly and immunocompromised
81
Q

When might a lab diagnosis be needed for VZV? What swab would you use?

A
  • Can be useful for atypical cases
  • Vesicle/ulcer fluid swam and molecular sample media for PCR
82
Q

Who is the varicella vaccination given to?

A
  • Only offered on NHS yo people in close contact with someone’s who’s vulnerable to chicken pox and its complications
83
Q

What can the pain from shingles mimic?

A
  • Pain from toothache
84
Q

What is the prevention of Zoster and who is it offered to?

A
  • Zostavax vaccine
  • Live attenuated virus
  • Offered to all people aged 70+

FINALS - Oral Medicine (13 decks)

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