Oral medicine Flashcards

(543 cards)

1
Q

What are the layers of normal oral tissue? (4)

A
  1. Oral epithelium
    – Keratin layer
    – Granular cell layer
    – Prickle layer
    – Basal layer
  2. Basement membrane
  3. Lamina propria
    – Papillary layer
    – Dense fibrous layer
  4. Connective tissue
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2
Q

What is stratified squamous epithelium?

A

Epithelium that consists of squamous (flattened) epithelium cells arranged in layers (stratified) upon basal membrane (basement membrane).
Only one layer is in contact with basement membrane.

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3
Q

What are the layers of the oral epithelium (4)

A
  1. Keratin layer
  2. Granular cell layer: contains granuloma cells, thin layer
  3. Prickle layer: stratum spinosum cells (in the form of star cells)
  4. Basal layer: mitosis happens here
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4
Q

What makes up the lamina propria? (2)

A
  1. Papillary layer - contains nerves, capillaries (blood vessels), lymph vessels
  2. Dense fibrous layer - fibers laid down on top of each other
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5
Q

What oral tissues have non-keratinised epithelium? (5)

A

Buccal mucosa
Labial mucosa
Ventrum of the tongue
Floor of the mouth
Soft palate

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6
Q

What oral tissues have keratinised epithelium? (3)

A

Dorsum of the tongue
Hard palate
Gingivae

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7
Q

What are the 4 different types of papillae? Appearance and function?

A
  1. Filiform papillae - NOT TASTE BUDS, small, round
  2. Fungiform papillae - taste buds present, mushroom shape
  3. Circumvallate papillae - largest, on the back 1/3 of the tongue, located in V-shape, taste buds.
  4. Foliate papillae - leaf-shaped, located on side borders of tongue, taste buds.
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8
Q

What are the tongue papillae which have NO taste buds?

A

Filiform papillae

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9
Q

What are fordyce spots?

A

Prominent intra-oral sebacous glands

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10
Q

What is a biopsy?

A

It is the sampling of tissue for histological assessment, diagnosis and therapy

e.g. incisional biopsy, excisional biopsy

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11
Q

What is an excisional biopsy?

A

Remove all clinically abnormal tissue with a margin surrounding the lesion

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12
Q

What is used immediately after an excisional biopsy?

A

Formalin

It prevents drying, autolysis and putrefaction (decay/rotting)
Aids straining and tissue preparation in the laboratory

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13
Q

What is H+E staining?

A

Haematoxylin (blue) and Eosin (red)

Haematoxylin: nuclei, ribosomes, and chromatin a deep blue-purple colour.

Eosin: cytoplasm, collagen, connective tissue, extracellular matrix, and other structures an orange-pink-red colour.

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14
Q

What are 4 types of special stains?

A

Periodic acid Schiff = mucins, glycogen and fungi

Gram stain = bacteria

Ziehl Neelsen = mycobacteria

Congo red = amyloid

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15
Q

Immunohistochemistry - what is a monoclonal antibody test?

A

Monoclonal antibodies attach to specific antigens on cells surfaces.

Wide variety of antigens can be identified.
Characterise origin of cells and formulate an antibody profile.
Panels of antibodies to create a profile of the tumour.

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16
Q

What is a frozen section?

A

Rapid freezing of samples, with immediate assessment (15-30 mins for results)

  • usually with intra-operative assessment when patient still under GA
  • Cryostat
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17
Q

What is fine needle aspiration cytology?

A

A minimally invasive procedure that involves using a thin needle to extract tissue, fluid, and cells from a suspicious mass or abnormal area of the body. This is then spread on to a slide and examined.

  • Study of cells, their structure, function, origin, and pathology
  • Not tissue architecture
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18
Q

What are the advantages and disadvantages of cytology?

A

Advantages: low cost, fast speed of diagnosis and negligible morbidity or complications.

Disadvantages: tissue architecture not represented and triage only applicable sometimes.

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19
Q

What is immunofluorescence mainly used for and what are the 2 types?

A

Mainly used for vesiculobullous disorders, uses antibodies to target antigens on cells.
Targets are visualised with fluorescence microscope.

Direct immunofluorescence
A single antibody is chemically linked to a fluorophore and used to identify antibodies bound to tissue antigens. This method is fast and has high specificity, but it’s limited in sensitivity.

Indirect immunofluorescence
A two-step process where a primary antibody binds to the target antigen, and then a secondary antibody conjugated to a fluorophore binds to the primary antibody. This method is more common than direct immunofluorescence and is highly sensitive, but secondary antibodies can bind endogenous immunoglobulin, which can introduce background noise.

Indirect immunofluorescence (IIF) is a type of immunofluorescence that uses serum to detect autoantibodies in a patient’s blood.

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20
Q

What are differences between histology and cytology?

A

Focus
Cytology examines individual cells or clusters of cells, while histology examines entire sections of tissue.

Sample size
Cytology tests require a small sample, such as a fluid specimen or vaginal or oral scraping, while histology requires a larger tissue sample.

Pain
Cytology tests are usually painless, while biopsies are generally more invasive and may require anesthesia.

Uses
Cytology is primarily used to diagnose or screen for cancer, while histology is used to diagnose diseases, analyse treatment effects, and in forensic investigations.

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21
Q

What type of test is specific to candida infections?

A

Periodic Acid Schiff Test
PASD = periodic acid schiff with digestion

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22
Q

How do you manage chronic facial pain?

A
  • Mediators of inflammatory response are closely associated with nociception
  • Peripheral nerve –> Dorsal root ganglion –> Ascending pathway –> CNS –> Pain

Antidepressant drugs, all increase levels of serotonin and noradrenaline
> Amitriptyline
> Duloxetine
> Mirtazapine
Indirect neuromodulation of the CNS opioid system with consequent effects

GABA agonists, they increase levels of GABA (inhibitory neurotransmitter in CNS)
> Gabapentin
> Pregabalin (Lyrica)

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23
Q

What are different types of immunosuppressants and what is their general aim?

A

To treat diseases with a significant auto-immune component in their pathogenesis (e.g. pemphigus vulgaris)

Glucocorticoids
> Systemic steroids such as prednisolone
> Topical steroids, via inhalers, creams and pills
> Short and long term complications of systemic steroids, such as cardiac problems, increased risk of diabetes, reduced healing, osteoporosis and weight gain

Non-glucocorticoid drugs
> calcineurin inhibitors (tacrolimus and cyclosporine), used for eczema and renal transplant immunosuppression
> pyrimidine synthesis inhibitor (Leflunomide, Teriflunomide) - block lymphocyte activation and inflammatory response
> purine synthesis inhibitor (mycophenolate mofetil and azathioprine) - prevent cell proliferation, especially leukocytes

Antibodies
> They reduce the risk of organ rejection after transplant by blocking T cell activation.
- Polyclonal antibodies (IV immunoglobulin)
- Monoclonal (Infliximab), inhibits TNFa by binding to it

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24
Q

How do calcineurin inhibitors work? what do they usually treat? examples?

A
  1. CNIs inhibit calcineurin, a protein that activates immune cells like T-cells. This prevents the transcription of IL-2 and other cytokines in T-cells, which interferes with their activation, proliferation, and differentiation
  2. Autoimmune disorders and atopic eczema.
    Organ and bone marrow transplants as well as inflammatory conditions such as ulcerative colitis, rheumatoid arthritis, and atopic dermatitis
  3. Cyclosporine and tacrolimus
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25
How do pyrimidine synthesis inhibitors work? what do they usually treat? examples?
1. Pyrimidine synthesis inhibitors work by blocking the action of dihydro-orotate dehydrogenase (DHODH), an enzyme that produces pyrimidines. This prevents lymphocytes from accumulating enough pyrimidines to support DNA synthesis, which blocks lymphocyte activation and the inflammatory response 2. Pyrimidine synthesis inhibitors are used to treat multiple sclerosis and rheumatoid arthritis. 3. Leflunomide, Teriflunomide, (Methotrexate)
26
How do purine synthesis inhibitors work? what do they usually treat? examples?
1. Suppress the immune system by preventing DNA synthesis and cell proliferation 2. Rheumatoid arthritis, Crohn's disease and ulcerative colitis, skin conditions such as lupus, and helps after an organ transplant to prevent rejection. 3. mycophenolate mofetil and azathioprine
27
How could you manage xerostomia with drugs?
Use sialagogic drugs that stimulate saliva production such as cevimeline and pilocarpine. Pilocarpine stimulates entirety of parasympathetic nervous system (PSNS), causing adverse effects.
28
What are barrier preparation used for and name 2 examples.
They produce a covering for lesions such as ulceration. Gelclair and Orabase
29
What are risks of immunsuppression? (3)
1. Increased risk of opportunistic infections such as candida and herpes 2. Increased risk of poor wound healing and subsequent infection 3. Increased risk of malignancy, lymphomas, skin and lip cancer.
30
What happens when aspirin and warfarin are taken together?
Increased risk of bleeding! do not take together
31
What happens when azole antifungals are taken with warfarin?
Decreased clearance of warfarin = increased warfarin = increased INR
32
What fungal infections can be caused by systemic disease?
Candidosis, caused by immunosuppressed and hyposalivation patients. Look for use of immunsuppresesive drugs (e.g. steroid inhalers, systemic glucocorticoids, non-glucocorticoid immunosuppressants, monoclonal antibodies...) Acute > Pseudomembranous candidosis (thrush) > Erythematous candidosis (atrophic/antibiotic sore mouth) Chronic > Hyperplastic candidosis (leukoplakia) - seen in smokers and immunocompromised. > Erythematous candidosis (denture stomatitis) Candida associated with angular cheilitis
33
What viral infections could be associated with systemic disease?
Oral warts and leukoplakia caused by HPV16. HHV-4 (EBV) can lead to oral hairy leukoplakia HIV leading to aphthous stomatitis caused ulceration through immunosuppression
34
What oral presentations can syphilis have?
Syphilis - infection via Treponema Pallidum > Primary stage - Chancre A painless, firm ulcer that can appear on the lips, tongue, gums, or soft palate during the first stage of syphilis - can then become latent in the ganglion - Secondary stage Oral lesions include white plaques, papules, or nodules, and often appear on the lips, buccal mucosa, and tongue. - Tertiary stage - gumma Leukoplakia in tertiary stage?
35
What are features of anaemia? (4)
1. Atrophic glossitis - appears as very smooth glossy tongue that is tender and painful 2. Angular cheilitis - inflammatory condition at the corners of the mouth 3. Aphthous stomatitis ulceration 4. Dysesthesis - an unpleassant sensation felt when touched due to peripheral nerve damage.
36
What symptoms can leukaemia cause?
Bleeding: Bleeding gums, spontaneous bleeding, or petechial hemorrhages on the lips, tongue, or palate Enlargement: Gingival enlargement or hyperplasia Pallor: Mucosal pallor Ulcerations: Oral ulcerations or hemorrhagic bullae on the tongue Ecchymosis: Ecchymoses, especially in areas exposed to injuries Infections: Oral infections Cracked lips: Cracked lips
37
What is Graft versus host disease?
Graft versus host disease (GvHD) is a process that can happen after a bone marrow or stem cell transplant has taken place, using cells taken from a donor. GvHD does not mean that the transplant has failed but it suggests that the immune cells from the donor (graft) are recognised by the tissues and organs of the recipient (host) as ‘foreign’, and have mounted an attack against them. Mouth symptoms can present as pain, sensitivity, reduced mouth opening and/or dry mouth. The intensity and severity of the symptoms vary from person to person. Will cause OLP to manifest in the mouth with increased risk of OSCC.
38
What are the symptoms of mouth GvHD?
Mouth symptoms can present as pain, sensitivity, reduced mouth opening and/or dry mouth. The intensity and severity of the symptoms vary from person to person.
39
What does mouth GvHD look like?
The most common appearance is of white patches which look like lacy white lines, usually on the inside of the cheeks or sides of the tongue. These are often not painful and may be present for a long time before being noticed. The other forms can look red or yellow and ulcerated. The red and ulcerative forms may be quite large and can be painful and sore when in contact with food. Other symptoms include a dry mouth as GvHD can affect the salivary glands. This can lead to difficulty in chewing and swallowing foods, and you may also notice changes in taste. Dry mouth can lead to an increased risk of developing tooth decay, especially along the gum line and between the teeth. In addition, you may notice tiny recurrent blisters called mucoceles in your lips and roof of the mouth that come and go at mealtimes. These are typically more of a nuisance than actually painful. Finally, in some patients who develop tightening of their skin due to GvHD, the same change may affect the soft tissues inside your mouth. When this happens, your mouth may be difficult, and even painful, to open normally. This may effect OH routine.
40
How is mouth GvHD diagnosed?
Usually the oncologist or the oral specialist can diagnose mouth GvHD by connecting the clinical findings with your medical history. In some circumstances a small sample from inside your mouth (a biopsy) may be necessary.
41
Can mouth GvHD be cured?
There is no cure. The condition tends to get worse if your body is stressed, both physically (such as having a cold) and emotionally. Mouth GvHD can persist for many years, although it tends to remain stable after the first couple of years.
42
Is mouth GvHD serious?
There is an increased risk of developing mouth cancer with mouth GvHD. It is important that you ensure that your mouth is checked on a regular basis by a dentist or oral specialist, so that any early changes can be spotted.
43
What treatments can I use for pain relief for GVHD?
For mild discomfort, the following topical treatments can be used to alleviate discomfort:  Anaesthetic (analgesic) mouthwashes are available and particularly helpful if used before meals. Benzydamine (eg, DifflamTM) mouthwash may be helpful.  Topical steroids which can be applied locally to your mouth are helpful for most patients. These areavailable as mouthwashes, sprays, pastes and small pellets which dissolve in your mouth.  If your gums are affected, it is important that you keep your teeth as clean as possible by regular and effective tooth brushing. If not, a build-up of debris (known as plaque) can make your gum condition worse. Your dentist/dental hygienist will be able to give oral hygiene advice and will arrange for scaling of your teeth as necessary.  An antiseptic mouthwash or gel such as Chlorhexidine mouthwash (eg, Corsodyl®) may be recommended to help with your plaque control, particularly at times when your gums are sore. If possible avoid a mouthwash containing alcohol. For moderate to severe mouth discomfort, general treatments (taken by mouth) may be required for several months or years. Your specialist will discuss with you risks and benefits of the different medication options available.
44
What treatments can I use to treat my mouth dryness?
If your mouth feels dry, avoid caffeinated or alcoholic beverages and drink plenty of water throughout the day. There are specific ‘dry mouth products’ that are available over the counter such as Biotene® and Oralieve® that may relieve dry mouth symptoms. Your dentist will advise you to use a higher strength fluoridated toothpaste such as Duraphat® 5000ppm and may suggest additional forms of fluoride application to strengthen your teeth against decay.
45
What medications can cause gingival hyperplasia?
Cyclosporine (immunosuppressant) Phenytoin (anti-convulsant) Nifedipine (calcium channel blocker) --- also amlodipine, diltiazem, felodipine, and verapamil
46
What drugs can induce OLP?
Anti-hypertensives Beta-blockers Metformin Thiazide diuretics Furosemide - loop diuretic Spironolactone - potassium-sparing diuretic NSAIDS Anti-malarials Proton pump inhibitors
47
What medications can cause MRONJ?
Bisphosphonates - Alendronic acid, Risendronate sodium, zoledronic acid, Ibandronic acid, Pamidronate disodium and Sodium clodronate Denosumab - biologic anti-resorptive. RANKL inhibitor Antiangiogenic drugs - Sunitinib, bevacizumab, aflibercept Bisphosphonate + systemic glucocorticoid
48
What are symptoms of MRONJ?
> Feeling of tingling, numbness, heaviness or other unusual sensations in your jaw > Pain in your jaw or a bad taste > Swelling of your jaw > Pus or discharge > Loose teeth > Exposed bone in your jaw
49
What medications can cause lichenoid like lesions?
- Anti-hypertensive - Beta-blockers - Metformin - Thiazide diuretics - Furosemide - Spironolactone
50
What symptoms can Addison's disease have?
Addison's disease: destruction of adrenal cortex increasing ACTH - hyperpigmentation - brown patches of gingival, vermillion border of the lips, buccal mucosa, palate, and tongue may represent the first signs of Addison's disease. - fatigue, weight loss, decreased appetite, low blood pressure and diarrhoea
51
What is hereditary haemorrhagic telangiectasia and what is its clinical presentation?
(rare autosomal dominant) genetic disorder that causes abnormal blood vessel formation, which can lead to bleeding and other complications Red or purplish spots on the lips, tongue, and inside of the mouth.
52
What are signs of IBD? (oral Chrons disease)
Swelling/oedema of the lips intermittently Mucosal tags Cobblestone mucosa Pyostomatitis vegetans (PV) ulceration - snail track ulceration Recurrent aphthous ulcerations Red and inflammed gingivae
53
What are indications of a lower GI malignancy? - referral
- Features of unexplained iron deficiency anaemia - Rectal bleeding - Older people with a sudden change in bowel habit - Fatigue, unexplained weight loss
54
What are oral symptoms of GORD?
Dental erosion - look for cupping, palatal erosion of upper anteriors, cupping lower posteriors Oral dysesthesia. Burning mouth syndrome. Soft palate erythema, wide spanning lesions. Dry mouth Impaired taste - especially in morning Bad breath Dentine hypersensitivity
55
What is Primary Biliary Cirrhosis and what oral problem can it cause?
A chronic autoimmune liver disease that causes inflammation and scarring of the bile ducts. PBC is an autoimmune disease that can be associated with Sjögren's syndrome (SS) SECONDARY SJOGRENS SYNDROME - results in xerostomia, resulting in atrophy of lingual papilla.
56
What is mucous membrane pemphigoid and what symptoms does it cause? How can you manage it?
- Mucous membrane pemphigoid, an autoimmune condition characterized by blistering lesions affecting the mucous membranes of the body - Affects mainly oral cavity, eye, nasal and pharyngeal area, genital, anus MMP is not curable, but it can be managed with topical or systemic corticosteroids, immunosuppressive therapies, and biologic agents. Treatment depends on the severity of the condition and the sites involved. For example, mild oral involvement can be treated with topical steroids, while more severe disease may require systemic corticosteroids. To help manage MMP, you can: Avoid spicy, acidic, or salty foods Have your mouth checked regularly by a dentist or oral specialist Keep your teeth clean Use a toothpaste without sodium lauryl sulfate (SLS) Stop smoking and reduce your alcohol intake Early recognition and treatment of MMP can help decrease disease-related complications.
57
What is sjogren's disease and what does it increase your risk of?
- Sjogren’s syndrome, destruction of the exocrine glands > Increases risk of lymphoma and Raynaud’s disease
58
What is pemphigus vulgaris and what are its oral manifestations?
Pemphigus vulgaris (PV) is an autoimmune disease that causes blisters to form on the skin and mucous membranes, including the mouth. Mouth, skin, nose, throat, genitals, eyes. Antibody mediated, targeting desmosome proteins (DSG1 and DSG3) Begins with oral lesions and desquamative gingivitis Painful blisters that are red and white and filled with fluid Blisters that rupture easily, leaving open sores that may ooze and become infected Difficulty swallowing and eating
59
What is wegener's granulomatosis and what are common symptoms?
Caused by autoantibodies against proteinase 3 Positive anti-neutrophil cytoplasm test (c-ANCA) Develop aphthous oral ulcers Strawberry gingivitis common symptom, labial gingiva affected much more
60
What does multiple myeloma present with?
Multiple myeloma is a type of bone marrow cancer that affects plasma cells, a type of white blood cell. In multiple myeloma, plasma cells multiply rapidly and form tumors in the bone marrow, damaging the bones and reducing the production of healthy blood cells. Mucosal and bone lesions Punched out lesions of the bone - appears like multiple small radiolucency areas in the skull. Over production of plasma cells. (For example, jaws can be affected, and patients may present with pain, bony swelling, epulis formation, or sudden tooth/teeth movement.) (swelling, mass formation paresthesia of the lower lip, pain, bleeding and fracture of the jawbone, tooth mobility and migration)
61
What is an ulcer? (definition)
A break in the epithelial continuity, usually due to lamina propria damage.
62
What is erosion? (definition)
A superficial break in epithelial continuity with lamina propria intact.
63
What is desquamation? (definition)
Used to describe thinning of the epithelium with a red appearance.
64
What features of an ulcer are features of malignancy?
If an ulcer of >3 weeks duration appears with features of malignancy such as a solitary ulcer and a proliferative appearance, then rapid referral must take place.
65
What are features that do not suggest malignancy in an ulcer?
- Trauma with an isolated ulcer - Recurrent ulceration such as recurrent aphthous ulceration - Widespread oral mucosal ulceration such as oral lichen planus.
66
What are common causes of recurrent oral mucosal ulcerations?
1. Recurrent aphthous ulceration 2. Aphthous like ulceration 3. Erythema multiforme 4. Recurrent intra-oral herpetic ulceration
67
What diseases should we consider if there is recurrent ulceration with chronic oral inflammatory disease?
1. Oral lichen planus 2. Mucous membrane pemphigoid 3. Pemphigus vulgaris
68
How doe recurrent aphthous ulceration present?
Small, round/ovoid, well defined margins, greyish or yellowish ulcer base with a fibrous membrane cap and an erythematous halo.
69
What are the characteristics of recurrent aphthous ulceration?
1. Clinically present in childhood or adolescence 2. Resolve with age 3. Family history 4. Recurrence
70
What is the aetiology of recurrent aphthous ulceration?
Immunologically mediated T cell action with humoral component (antibody dependant cytotoxicity reaction)
71
What are some predisposing factors for RAU? (7)
Trauma Stress Food allergies, to additives such as benzoates and flavouring agents such as cinnamaldehyde Chemical reactions, especially to SLS (sodium lauryl sulphate) Smoking cessation Systemic disease, such as Bechet's syndrome, SLE, GI disease, coeliac disease, HIV and anaemia Fall in progesterone (OCP/menstruation)
72
What are the classification of recurrent aphthous ulceration?
1. Minor = 2-6 per outbreak lasting up to 10 days. = involving non-keratinised mucosa = heal with no scarring 2. Herpetiform - small but >10 per outbreak, coalescing to form larger ulcers - may involve keratinised mucosa - more commonly affects women, has no link to the herpes virus 3. Major = large >1cm diameter lasting lasting >1 months = involving both keratinised and non-keratinised mucosa = heal by secondary infection often with scarring
73
What investigations should be done for RAU?
- Full blood count - Haematinic assays (check levels of ferritin, folate and B12) (- AIP (autoimmune profile)) (- TTGs (tissue transglutaminase IgA (tTg-IgA) test is used to help doctors diagnose celiac disease.)
74
What are medical management options of RAU?
- Difflam spray or mouthwash: benzydamine hydrochloride - Topical steroids: > Betnesol mouthwash (betamethasone) > Beclometasone diprioprionate aerosol inhaler > Prednisolone mouthwash > Hydrocortisone hemisuccinate buccal tablets - Systemic medication: prednisolone, azathioprine, mycophenolate mofetil, hydroxycholoquine, dapsone - Antiseptic preparations: chlorhexidine mouthwash - Doxycycline mouth wash
75
Why does HHV-3 (shingles) only present on one side of the mouth?
Shingles, also known as herpes zoster, appears on one side of the mouth because the varicella-zoster virus that causes shingles travels along specific nerves. Varicella-zoster virus lays dormant in nerve ganglion
76
What medication has side effects of oral ulceration?
Nicorandil (IHD tx) has side effects of recurrent aphthous ulceration, and can only be prevented by drug holiday
77
What disease causes strawberry gingivitis and swollen lips?
Wegener's granulomatous Granulomatosis with polyangiitis (GPA) is a rare condition where blood vessels become inflamed, mainly in the ears, nose, sinuses, kidneys and lungs.
78
How does Behcet's syndrome present?
- Triad of symptoms oral, genital and eye ulceration. - Presents with all severities of ulceration, but mainly aphthous ulceration - Compared to RAU the ulcerations are increased in frequency and involve soft palate and oropharynx. - Immune complex mediated disease - More common in eastern Mediterranean and east asian countries. The silk road disease. Symptoms include painful sores in the mouth and genitals, eye inflammation, skin rashes, and arthritis.
79
What is Behcet's syndrome triad?
1. Recurrent oral ulcers 2. Genital ulcers 3. Ocular disease, such as uveitis with hypopyon
80
How are aphthous like ulcers different to recurrent aphthous ulcers? (ALU vs RAU)
Clinically identical to RAU, treated and managed the same. The only differences are: - Doesn't begin in childhood - Does not resolve with age - Occurs in association with signs and symptoms unusual for RAU - Occurs in association with systemic disease - Occurs in association with certain drugs (NSAIDS)
81
What is pyostomatitis vegetans?
Highly specific marker for IBD Snail track ulcers typically Lots of broad based tiny abscesses develop into an area of intense erythema
82
What is recurrent erythema multiforme? Causes? Presentation? Classification? Treatment?
An immunologically mediated disease that involves multiple mucous membranes. Pathophysiology is cell mediated immunological response with destruction of epithelial cells. Causes include: - Herpes simplex virus - Medications: sulfa drugs, anticonvulsants, antibiotics, and non-steroidal anti-inflammatory drugs (NSAIDs) - Other infections: EM can be caused by mycoplasma pneumonia, fungal infections, streptococcal infection, tuberculosis (TB), Epstein-Barr virus, cytomegalovirus, hepatitis C, and influenza Presents typically with lip ulceration, crusting and desquamative gingivitis. Eye involvement Classification: - Minor (1 mucous membrane) - Major (2 or more mucous membranes) Treatment: antivirals or corticosteroids
83
What are different diagnoses to recurrent aphthous ulceration?
Oral malignancy. ALUs resemble RAUs in their physical characteristics but are associated with an underlying systemic disorder. Consider an underlying condition if the ulcers first occur later in life, affect atypical sites in the mouth (such as the palate or gums), also affect extra-oral sites (such as genitalia), or are associated with systemic features. Systemic conditions that present with aphthous-like ulcers include: > Vitamin B12 deficiency > Folate deficiency > Iron deficiency > Coeliac disease > Crohn's disease > Ulcerative colitis > Behcet's syndrome > Reiter's syndrome > Immunodeficiency, such as neutropenia and HIV > Epstein Barr virus infection (glandular fever) Other differential diagnoses include: - Primary oral herpes simplex infection - Intraoral secondary herpes simplex (cold sores) - Adverse drug reactions (for example to nonsteroidal anti-inflammatory drugs, nicorandil, or beta-blockers) - Chickenpox - Hand, foot, and mouth disease - Periodic syndrome, PFAPA (periodic fever, aphthous stomatitis, pharyngitis, and adenitis)
84
When may you be suspicious of oral malignancy for an ulcer?
A solitary ulcer or swelling of the oral mucosa persisting for more than 3 weeks. - Early lesions are often asymptomatic and appear as areas of erythroplakia (red patch) or leukoplakia (white patch) and may be ulcerated or exophytic (growing outwards). As the lesion grows it becomes more symptomatic. Cervical lymphadenopathy may be present. The level of suspicion should be increased in the presence of smoking, alcohol misuse, age over 45 years, and male sex. Other forms of tobacco use and chewing betel, gutkha, or paan, should also raise suspicion.
85
When should you consider an underlying condition when an ulcer presents?
ALUs resemble RAU in physical appearance but are associated with underlying systemic disorder. Consider an underlying condition if: - the ulcers first occur later in life - affect atypical sites in the mouth (such as the palate or gums) - also effect extra-oral sites (such as genitalia), - or are associated with systemic features.
86
Which systemic conditions present with aphthous-like ulcers?
1. Vitamin B12 deficiency 2. Folate deficiency 3. Iron deficiency 4. Coeliac disease 5. Crohn's disease 6. Ulcerative colitis 7. Behcet's syndrome 8. Reiter's syndrome (reactive arthritis) 9. Immunodeficiency, such as neutropenia, HIV infection 10. Epstein-barr virus infection (glandular fever)
87
When should you suspect if someone has Vitamin B12 deficiency?
Suspect if the person has peripheral neuropathy or posterior column degeneration (for example ataxia, gait disturbances and paraesthesia) Pallor, fatigue, weakness, decreased exercise tolerance, and shortness of breath with exercise may be caused by the resulting anaemia.
88
When should you suspect if someone has folate deficiency?
Suspect if the person has history of a diet poor in sources of folate, or of heavy alcohol use. Pallor, fatigue, weakness, decreased exercise tolerance, and shortness of breath with exercise may be caused by the resulting anaemia.
89
When should you suspect if someone has iron deficiency?
Suspect if the person has glossitis, angular stomatitis, and spooning of the nails. Pallor, fatigue, weakness, decreased exercise tolerance, and shortness of breath with exercise may result from anaemia.
90
When should you suspect if someone has coeliac disease?
Suspect if the person has unexplained gastrointestinal symptoms, chronic diarrhoea, unexplained iron deficiency anaemia, or a skin rash consistent with dermatitis herpetiformis.
91
When should you suspect if someone has Crohn's disease?
Suspect if the person has bloody diarrhoea, weight loss, labial or facial swelling, and occasionally joint manifestations. Be aware that symptoms can be highly variable.
92
When should you suspect if someone has ulcerative colitis?
Suspect if the person has left-sided abdominal pain and bloody diarrhoea.
93
When should you suspect if someone has Behcet's syndrome?
Suspect if the person has genital ulcers, uveitis, or retinal damage, skin lesions such as erythema nodosum, papulopustular lesions and acneform nodules.
94
When should you suspect if someone has reiter's syndrome (reactive arthritis)?
Suspect if the person has an asymmetrical large joint oligoarthritis with or without dactylitis, urethritis, and ocular inflammation manifesting 1-6 weeks after an acute infection.
95
When should you suspect if someone has immunodeficiency, such as neutropenia, HIV infection?
Suspect if the person has recurrent fever and recurrent infections or other clinical evidence of risk factors for HIV infection
96
When should you suspect if someone has glandular fever?
Suspect if the person has other features of glandular fever.
97
How does primary oral herpes simplex infection present?
May be asymptomatic, but may present as gingivostomatitis (inflammation of the gums and mucous membranes of the mouth) and pharyngitis.
98
How does intraoral secondary herpes simples virus present?
Cold sores. Can present as a small crop of pinhead-sized ulcers that re-occur at the same site within the mouth, often on keratinised, particularly palatal, oral mucosa.
99
What drugs can cause adverse drug reactions?
Nonsteroidal anti-inflammatory drugs, nicorandil, or beta-blockers - there may be a temporal relationship to starting or increasing the dose of the drug.
100
What is chickenpox caused by?
Chickenpox is caused by the varicella-zoster virus (VZV), a type of herpes virus. The virus is highly contagious and spreads through close contact with someone who has chickenpox. It can be spread from 1 to 2 days before blisters appear until all the blisters have crusted over. Associated skin lesions are present.
101
What is hand, foot and mouth disease caused by?
Presents as blister-like lesions which may also be seen on hands or feet. Hand, foot, and mouth disease (HFMD) is caused by a virus, usually from the coxsackievirus group of enteroviruses
102
What is periodic syndrome and who does it occur in?
Periodic syndrome, PFAPA (periodic fever, aphthous stomatitis, pharyngitis, and adenitis) - although rare, this tends to occur in young children.
103
What is oral lichen planus?
It is a chronic mucocutaneous cell mediated autoimmune condition which targets oral keratinocytes. Multifactorial aetiology, mostly spontaneous with unknown cause. Mostly idiopathic however can be due to drug indications and mercury. Stress and anxiety may be a cause Demographic features: M2:F3 middle aged
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What are intraoral features of oral lichen planus?
Reticular (web-like) appearance of white lacy lesions, buccal mucosa, often bilateral and symmetrical. Papular form consisting of small white dots in the initial disease phase Annular (ring like) and plaque like hyperkeratosis may be present Erythematous type, red patch surrounded by white striae, with areas of atrophic inflamed oral mucosa. Desquamative gingivitis, which is full thickness gingivitis, has exacerbation of inflammation in areas of plaque accumulation. Erosive, ulcerative or bullous lesions that are normally white in colour.
105
What can amalgam cause intraorally?
Amalgam associated OLL due to allergy or toxic reactions. Amalgam associated lichenoid lesion can develop into plaque-like lesions that resemble leukoplakia.
106
What are complications of OLP?
pain : reduces quality of life, nutrition and oral hygiene measures, pain on eating spicy food. Periodontal attachment loss Malignant risk, OLP is a potentially malignant lesion
107
What drug interactions can cause OLL?
Drug and vaccine use: antidiabetic drugs; antirheumatic drugs (NSAIDs mainly, but also others); antihypertensive agents, such as beta-blockers, thiazides and diuretics; antimalarials, such as quinacrine; many other drugs; occasionally hepatitis B vaccine omalizumab or TNF-alpha antagonists
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What are differential diagnoses of OLP (mainly for reticular type)?
- Graft versus host disease is a differential diagnosis both histologically and clinically (GVHD) - Hepatitis C virus may be associated with OLL - SLE and DLE lesions are very similar to reticular OLP and OLL. Clinically DLE involves only skin and mucous membranes unlike SLE a. Oral lichenoid lesions b. Graft vs host disease c. HCV d. Lupus erythematosus (SLE/DLE) e. Leukoplakia f. Candida g. Chronic ulcerative stomatitis h. Keratosis i. Carcinoma
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What needs to be excluded as a cause of OLL?
- Drug-induced lesions - Dental-material-induced lesions - Diabetes mellitus - Graft-versus-host disease - Hepatitis disease or hepatitis C virus infection - HIV
110
How do you diagnose OLP?
1) Histopathological confirmation via incisional or punch biopsy > Evidence of basal membrane immune mediated damage > Sub basal lymphocyte band > Hyper/hypokeratosis * Request separate/second sample if desquamative gingivitis/suspected MMP to send for direct immunofluorescence – best results from punch biopsies of normal perilesional tissue (usually buccal mucosal). 2) Bloods * FBC, Haematinics (Vit B12/F/F), Random Glucose, AIP (autoimmune profile (SLE)), (Pemphigoid and pemphigus antibodies if desquamative gingivitis), (Hep C antibody (HCV serology) if risk factors). others: GVHD history, epidermal patch testing
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How do you manage OLP?
Primary care: start with - Predisposing factors should be corrected: - Removal of dental amalgams or other materials if the lesions are clearly closely related to these, or unilateral. - Consult with a GP if HCV infection or other systemic background, of if drugs are implicated, and relevant specialist if skin, genital or ocular involvement is possible. - Improve OH, smoking/alcohol advice, Diet advice: little acidic, spicy or citrus content - Aloe vera (if they want natural) - Topical medications: Difflam - Benzydamine hydrochloride (0.15%) spray or mouthrinse or 2% lidocaine gel applied to painful areas. - Topical corticosteroids: o Hydrocortisone o Betamethasone sodium phosphate (Betnesol MW) (0.5mg soluble tabs, 2 tabs dissolve 10-15ml water, MW 2-3mins, then spit. PRN up to bd) o Synalar gel: Fluocinonide acetonide 0.025% PRN up to bd o Beclomethasone dipropionate aerosol inhaler 100-200mcg/puff 1qds o Prednisolone sodium phosphate (MW)/Prednisolone 5mg soluble tabs, 1 in 10-15ml water for 2-3 mins used PRN up to qds. - Refer to oral med (if severe/unresponsive/unsure) Secondary care: - Removal of differential diagnoses: SLE/GVHD/HCV/SLE - Higher potency topical steroid (Clobetasol proprionate 0.0.5%) PRN up to bd. - Protopic ointment: Topical tacrolimus (0.03% or 0.1% strength) - Systemics: Prednisolone. Hydroxychloroquine, Mycophenolate mofetil, Azathioprine, Dapsone.
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What are the 2 main types of OLP and what percentage of the population does it affect?
Lichen planus — an inflammatory condition that affects 1–2% of adults. There are two main types: 1) Reticular lichen planus is characterised by bilateral, asymptomatic, white, lacy, striations (or papules) on the posterior buccal mucosa. This form is easily identifiable and does not usually require further investigation. 2) Erosive lichen planus manifests as zones of tender erythema and painful ulcers surrounded by white, radiating striae, and may require biopsy to rule out serious causes.
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What is mucous membrane pemphigoid?
A vesiculobullous disease, characterised by vesicles and blistering, fluid filled lesions on the mucosa. More protracted (prolonged) than bullous pemphigoid Affects skin and mouth, causing blistering on mucous membranes. Autoimmune condition with antibodies directed at antigens in the epithelial basement membrane (BP230, BP180 LP5 protein affected), resulting in splits and blistering forming.
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What are symptoms of mucous membrane pemphigoid?
Desquamative gingivitis Genital, mouth, skin and eye involvement Mucosal inflammation and erosion, as well as frank ulceration Scarring Bulls eye blistering
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What is the histopathology or mucous membrane pemphigoid?
Separation of the epidermal basement membrane junction Direct or indirect immunofluorescence to diagnose properly: wobbly line appearance of immunofluorescence. No result with indirect an direct IF for OLP, but result with MMP and PV
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What are complications of MMP?
Skin blistering and ulceration Genital and eye involvement Pharyngeal involvement, causing stricture formation and dysphagia Oral involvement
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How do you treat mucous membrane pemphigoid?
Treat using topical steroids and topical immunosuppressants, as well as systemic steroids. - Prednisolone, however, both long and short-term complications. - Mycophenolate Mofetil, inhibits the synthesis of purine nucleotide guanine and inhibits the proliferation of B and T cells in response to antigen stimulation.
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What is pemphigus vulgaris?
An autoimmune disease, antibody mediated. Targets desmoglobins DSG1 and DSG3, separates between epithelial cells. Acantholysis is the loss of intercellular connections, such as desmosomes, resulting in loss of cohesion between keratinocytes.
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How does pemphigus vulgaris present?
Present initially with oral lesions and blisters, with later skin involvement Positive Nikolsky sign (skin rubs off) Complications of disease and therapy. Could be caused by drug induced by Sulfhydryl group drugs. Symptoms: - desquamative gingivitis - involves genital, mouth, skin but NO EYE INVOLVEMENT - blisters that typically burst - mucosal erosion and frank ulceration even including hard and soft palate - affects lateral ventral borders of the tongue, palate, labial and buccal mucosa.
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How do you diagnose pemphigus vulgaris?
histological exam, high numbers of haemoxylin and eosin Blood sample (indirect) or Direct IF
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How does pemphigus vulgaris appear in direct immunofluorescence?
Fishnet appearance
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What are the results from a biopsy for positive PV?
rounded up separated keratinocytes
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What is the treatment of pemphigus vulgaris?
Systemic and topical steroids or immunosuppressive agents
124
What is a pyogenic granuloma? Clinical features?
A reactive proliferation of capillary blood vessels. They arise due to trauma to the mucosal tissues, causing exaggerated granulation tissue grown. - Reactive response to trauma, often caused by poor restorations. - Clinical features: > maxillary anteriors, normally due to poor oral hygiene. > most frequently develops on the buccal gingiva in the interproximal tissue between teeth. > size varies massively, exophytic pedunculated lesion, red/purple colour and painless > frequent ulceration and bleeds easily > nodular lesion on buccal mucosa > raspberry-like appearance
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What two lesions are clinically identical to pyogenic granuloma if they occur on the gingiva?
Two lesions, peripheral ossifying fibroma and peripheral giant cell granuloma, are clinically identical to the pyogenic granuloma when they occur on the gingiva.
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What does the colour or oral mucosal lesions depend on?
- Concentration and dilatation of blood vessels in connective tissue - Degree of keratinisation - Melanin in epithelium - Thickness in epithelium
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Why can lesions appear red?
Atrophic epithelium Reduction in number of epithelial cells Increased vascularity in lamina propria
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What are differential diagnoses of red lesions?
1) Vascular anomalies - lingual varices - capillary/cavernous haemangiomas and telangiectasia (hereditary haemorrhagic telangiectasia) - clinically appear like blood blisters 2) Infectious - viral - HSV and VZV - fungal - candida albicans and candidiasis - bacterial - syphilis 3) Inflammatory - oral submucous fibrosis - erythema migrans (geographic tongue) 4) Idiopathic causes - geographic tongue 5) Neoplastic casues: - erythroplakia - OSCC - kaposi sarcoma 6) Systemic/immunological/inflammatory - oral lichen planus - graft vs host disease - systemic/discoid lupus erythematosus - mucositis 7) Purpura, bleeding into connective tissues - angina bullosa haemorrhagic - trauma - platelet disorders 8) Reactive - Pyogenic granuloma 9) Erosive - burns both chemically (aspirin burn) and heat - vesiculobullous disorders such as MMP and PV - OLP both erosive and atrophic 10) Atrophic (thin red patches, can see blood vessels shining through) - Erythema migrans (geographic tongue) - Atrophic oral lichen planus - Iron deficiency, causing glossitis - Erythroplasia, is a red lesion with no surface markings. Often cancer is missed as seen as inflammatory but is much firmer than inflammation, loss of epithelial structures.
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What can cause the white appearance of a white patch?
Thickened stratum cornea keratin layer (hyperkeratosis) Hyperplasia of the epithelium layer (acanthosis) Leukoedema Necrosis of oral epithelium Fluid collection in epithelium Reduced vascularity in lamina propria.
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What are differential diagnoses of white patch lesions?
1. Variation of normal anatomy: > fordyce spots > leukoedema 2. Hereditary causes: > white sponge naevus 3. Infections causes: > fungal: candidosis > viral: oral hairy leukoplakia (EBV) > bacterial: syphilis 4. Inflammatory causes: > oral submucous fibrosis > erythema migrans (geographic tongue) 5. Idiopathic causes: > Leukoplakia 6. Systemic causes/immunological causes? > oral lichen planus > oral lichenoid lesions > graft vs host disease > systemic/discoid lupus erythematosus 7. Reactive causes > frictional keratosis > occlusal keratosis > tobacco associated lesions > chemical burns > thermal burns > actinic cheilitis
131
What can cause a pigmented appearance within the oral cavity?
- Pigmentation derived from foreign bodies (amalgam tattoos), heavy metal poisoning or drugs - Number of melanocytes increases - Increase in amount of melanin produced by melanocytes - Melanocytes present in basal layer, at a rate of 1 per 10 cells.
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What does exogenous mean and what are 5 exogenous factors causing pigmentation?
Exogenous = outside source Focal 1. Tattoo on oral mucosa 2. Foreign bodies e.g. amalgam fragments embedded in tissue = amalgam tattoos 3. Heavy metals e.g. mercury can cause pigmentation secondary to heavy metal poisoning Diffuse 4. Smoking - smokers melanosis 5. Drugs - minocycline, oral contraceptive, arsenic, heroin drug use
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What does endogenous mean and what are 5 forms of oral endogenous focal pigmentation?
Endogenous = increase in melanocytes or increase in melanin production A. Oral nevi = increase in melanocytes B. Melanotic macule = increase in melanin production C. Malignant melanoma = malignant increase in melanocytes D. Oral melanoacanthoma = increase in melanocytes (benign) E. Ecchymosis, bleeding + trauma
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What are 7 forms of oral endogenous diffuse pigmentation?
1. Oral melanotic macules (ephelis) 2. Racial pigmentation 3. Addison's disease 4. ACTH producing tumours 5. Physiological pigmentation of pregnancy (melasma) 6. Peutz Jeghers syndrome 7. Post inflammatory melanin incontinence.
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What is oral melanoma?
Melanoma is a type of skin cancer that develops from proliferation of malignant melanocytes along junction between epithelial and connective tissue. - Rare <1% of all oral malignancies - Often clinically silent, but can be confused with several benign and pigmented lesions - Largely macular but can be nodular and even pedunculated - Most commonly on the hard palate (40%) followed by gingivae - Treated by wide excision surgically
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What is Addison's disease? Clinical appearance? Tests for diagnosis? Care?
Autoimmune condition characterised by primary adrenal insufficiency and hypocortisolism, a chronic endocrine disorder in which adrenal glands do not produce enough steroid hormones. Destruction of adrenal glands causes insufficient production of cortisol and aldosterone/mineralocorticoid + glucocorticoid levels - It has 4 main causes: idiopathic, malignancy, autoimmune, TB. Excess ACTH Adrenocorticotropic hormone (ACTH) (due to negative feedback cycle as no cortisol present) stimulates melanocytes to produce more melanin pigment in OC. Diffuse endogenous hyperpigmentation on lips, buccal mucosa, hard palate + tongue. Other symptoms include always tired, oral and skin pigmentation, dizzy when standing, sudden weight loss, loss of appetite/anorexia, permanently tanned. Blood tests will show a) elevated plasma ACTH due to negative feedback. Synacthen test - synthetic ACTH given to pt, if no cortisol produced, it is Addison's disease. Histopathology - melanosis with no increase in melanocytes. - Systemic corticosteroids. (might need steroid cover for dental tx).
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What is peutz-jeghers syndrome?
Genetically inherited condition. Autosomal dominant. Endogenous diffuse pigmentation. Melanotic macules/dark blue/brown macules on lips, oral mucosa, eyes, fingers, mouth which appear like freckles. Present in most affected children by 5 years old. Tend to fade with age, might completely disappear in puberty or adulthood. Pigmented areas in oral mucosa tend to persist. Diagnosis is key as there is a genetic risk of bowel cancer so family needs to be screened.
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What is the CN1 Olfactory nerve? Problem? Test?
Smell perception Passes through the cribriform plate of ethmoid bone, continues to cerebral cortex Anosmia = loss of sense of smell. Can be due to trauma or meningitis Testing: ask if any problems with smell, using an odorous object, as well as a CT and MRI scan.
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What is the CN2 Optic nerve? Problem? Test?
Visual acuity, visual fields and pupillary reflexes. Peripheral visual field is ipsilateral, whilst your central visual field is contralateral. Homonymous hemianopia = if there is a left cerebrovascular lesion Bitemporal hemianopia if there is a chiasmal compression from pituitary gland (situated on lateral optic) Testing: visual acuity (snellen chart), visual fields and pupillary reflexes (PERLA), as well as funodscopy
140
What is the CN3,4,6 Oculomotor, Trochlear and Abducens nerves? Problem? Test?
Motor nerves which carry LMN fibres from the nuclei to the brainstem, through the cavernous sinus and superior orbital fissure, into the orbit to supply the extraocular muscles and elevators of the upper eyelid. Nystagmus = a pattern of involuntary eye movement Horner's syndrome = damage to the oculo-sympathetic pathway input to the eye
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What is the CN5 Trigeminal? Problem? Test?
V1 = ophthalmic, passes via superior orbital fissure to V ganglion, sensory innervation to the superior portion of the face. V2 = maxillary, passes via foramen rotundum to trigeminal ganglion, sensory innervation to the middle portion of the face V3 = mandibular, passes via foramen ovale, sensory innervation to the lower portion of the face (posterior division) and motor function to the muscles of mastication (anterior division) - Trigeminal neuralgia - Carcinoma - Herpes virus affecting Trigeminal nerve Testing: sensory test, corneal reflex test, motor function test via movement of the mandible.
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What is the CN7 Facial nerve? Problem? Test?
Begins in the pons, via the IAM, appears via stylomastoid foramen and branches through parotid gland. 5 branches: temporal, zygomatic, buccal, mandibular, cervical Motor supply to muscles of facial expression and stapedius, PSNS to sublingual and submandibular salivary glands via submandibular ganglion and lacrimal glands, sensory innervation to lips and tongue Schirmer's test Facial nerve pathology often caused by stroke or tumour of parotid gland. Ramsay Hunt syndrome Bell's palsy
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What is Ramsay Hunt syndrome?
Varicella Zoster virus VZV / Human herpesvirus (HHV3) (shingles) affecting the facial nerve that can result in facial palsy and loss of taste. After a primary infection of chickenpox (varicella) (usually in childhood), VZV establishes a latent infection in the trigeminal and dorsal root ganglia. After a variable latent interval the virus reactivates to produce shingles (herpes zoster). This can affect the facial nerve. Symptoms: > A rash or blisters in or around the ear, scalp or hair line. The blisters may also appear inside the mouth. > The rash/blisters are often painful with a generalised sensation of burning over the affected area. > Weakness on the affected side of your face which causes the facial muscles to droop. > Difficulty closing the eye or blinking on the affected side. > Altered taste on the affected half of the tongue. > Loss of facial expression on the affected side. > Difficulty eating, drinking and speaking as a result of weakness in the lip and cheek on the affected side. > Ear, face or head pain. Hearing loss on the affected side > Dizziness/vertigo > Tinnitis (ringing in the ear) on the affected side. ( otalgia (earache), hearing loss, vesicles in the external ear canal and palate, ipsilateral facial paralysis) - Treat with anti-viral medication (acyclovir) 800mg x5/day, can take up to several weeks to resolve. - Prompt treatment with a short-course of high dose steroids is also recommended. - Painkillers - Eye lubrication for the unblinking eye
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What is Bell's palsy?
Lesion in the parotid gland, present with LMN facial paralysis to entirety of the facee. Often due to viral inflammatory demyelination Symptoms: - unilateral LMN facial weakness - Pain behind the ear - Associated with altered taste and hyperacusis - Possible numbness of skin over EAM Usually caused by HSV but also by CMV, EBV (HHV-4), HIV, Mumps and Influenza. Usually resolves without any treatment, with 60-80% making a full recovery. Recovery usually begins within 8 weeks and complete after 6-12 months. Residual effects may be present. > Steroids Oral corticosteroids are the primary treatment for Bell's palsy, and should be started within three days of the onset of symptoms. Steroids reduce inflammation and swelling, and increase the likelihood of facial nerve function recovery. > Antivirals In severe cases, antiviral therapy may be combined with glucocorticoids to improve outcomes. > Analgesics Pain can be relieved with over-the-counter analgesics such as aspirin, acetaminophen, or ibuprofen. > Eye care To protect the affected eye, you can use lubricating eye drops during the day and eye ointment at night. You can also wear glasses or goggles during the day, and an eye patch at night. > Physical therapy Physical therapy, facial massage, or acupuncture can help improve facial nerve function and pain
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How to tell the difference between Stroke, Bells palsy and Ramsay Hunt Sydrome
If the cause is Bell's palsy, watch for symptoms such as watering from the eye on the affected side of the face, changes in the ability to taste, sound sensitivity, and ringing ears. With a stroke, watch for trouble finding words, eyes gazing in one direction, trouble walking, and vision changes. Stroke can affect arms and legs, not just face. Ramsay Hunt syndrome is characterized by a painful rash with fluid-filled blisters on the ear, ear canal, hard palate, or tongue. Bell's palsy doesn't typically cause a rash. Ramsay Hunt syndrome can cause more severe paralysis and permanent facial asymmetry than Bell's palsy. Bell's palsy symptoms usually improve within a few weeks to six months, while Ramsay Hunt syndrome can be more difficult to recover from
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What is the difference between LMN and UMN facial weakness?
LMN facial weakness Affects all facial muscles, including the frontalis muscle, and makes it difficult to close the eyes. The angle of the mouth may also fall. LMN facial weakness is often caused by Bell's palsy or Ramsay Hunt syndrome. --> All ipsilateral facial muscles affected. UMN facial weakness Spars the frontalis muscle, allowing the patient to furrow their brow normally. Eye closure and blinking are also not affected. UMN facial weakness is often caused by stroke, multiple sclerosis, subdural haemorrhage, or intracranial neoplasia. --> Lower contralateral facial muscles affected
147
What is the CN8 Vestibulocochlear nerve? Problem? Test?
Involved in balance (vestibular) and hearing (cochlear). Travels via temporal bone to auditory canal to pontine angle and then brainstem. Common disorders: - Vertigo - Tinnitus - Deafness - Nystagmus Caused by cochlear concussion, ossicles disruptions and nerve damage. Diagnose using tuning fork testing (Weber and Rinne) and vocal distraction testing
148
What is the CN9 Glossopharyngeal nerve? Problem? Test?
Emerges from medulla alongside X and XI, passing through jugular foramen, descends between jugular vein and ICA. Supplies oropharynx, posterior tongue and palate. - PSNS to parotid gland via otic ganglion - Sensation from middle ear, pharynx and posterior tongue (taste) - Oxygen and carbon dioxide monitoring in the blood.
149
What is the CN10 Vagus nerve? Problem? Test?
Sensation from larynx, pharynx, EAM and tympanic membrane. - Motor to muscles of larynx, pharynx and soft palate. - PSNS to various areas Recurrent laryngeal nerve damage, (Branch of X), left sided damaged more easily as loops under aortic arch. Pathology normally caused by IX and X damage > Uvula deviation suggests X lesion on opposite side > Assessment of coughing and dysphagia > Gag reflex failure > vocal cord weakness and aphonia
150
What is the CNXI Accessory nerve? Problem? Test?
Function is motor control of pharynx, larynx, soft palate, SCM and trapezius muscles - Lesions with cause unilateral ability to lift shoulders and rotate neck - Paralysis of SCM and Trapezius due to trauma
151
What is the CN12 Hypoglossal nerve? Problem? Test?
Function is motor control of tongue muscles. Atrophy and fasciculations of the tongue muscles, tongue bends towards the affected side. Can cause dysarthria and dysphagia.
152
What does a PET scan show?
A positron emission tomography (PET) scan is an imaging test that can help reveal the metabolic or biochemical function of your tissues and organs. A small amount of radioactive glucose is injected into the patient's vein. The tracer gets trapped in tissues, and the scanner detects gamma rays emitted by the tracer's unstable nuclei. A computer then uses this data to create a 3D image of the tracer in the body. Sugar is metabolized by cells in the body, the scan shows where the body is metabolically active, good screening method for activity, such as tumours, infections and inflammation. Used anatomically to give more info
153
What test can be used for TB and actinomycosis?
MC&S (microscopy, culture and sensitivity) for TB and actinomycosis
154
Name 5 congential cysts
Lymphangioma Dermoid cysts Thyroglossal cysts Brachial cysts Pharyngeal pouch
155
Name 7 causes of acquired cysts?
Trauma, infective, inflammatory, iatrogenic, neoplastic, metabolic, autoimmune.
156
What are 6 development causes of lumps and swelling of the oral cavity and lips?
1. Unerupted teeth 2. Odontogenic cyst 3. Developmental cyst 4. Eruption cyst 5. Haemangioma 6. Tori
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What are 8 inflammatory causes of lumps and swelling of oral cavity?
1. Abscess 2. Cellulitis 3. Cysts 4. Sialadenitis 5. Pyogenic granuloma 6. Sarcoidosis 7. Granulomatosis 8. Crohn's disease
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What are 4 traumatic causes of lumps and swellings in the OC and lips?
1. Denture stomatitis 2. Epulis 3. Mucocele 4. Fibro-epithelial polyp
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What are 4 neoplasm causes of lumps and swelling of the oral cavity and lips?
1. Carcinoma 2. Lymphoma 3. Odontogenic tumour 4. Salivary gland tumour
160
What are 3 fibro-osseous causes of lumps and swelling of the oral cavity and lips?
1. Cherubism 2. Fibrous dysplasia 3. Pagets disease
161
Characteristics of reactive lesions, usually caused by trauma?
Fibrous overgrowths > sessile or pedunculated > appear on the mucosa > chronic irritation due to calculus, fractured/rough restorations and prosthesis > often ulceration, characterised by hyperplastic epithelium with bundles of interlacing fibroblasts
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What are common types of localised hyperplasia?
1. Epulis 2. Pyogenic granuloma 3. Fibroepithelial poly 4. Denture induced hyperplasia 5. Palatal papillary hyperplasia often complicated by candida.
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What is an epulis?
Any tumour like enlargement (lump) situated on the gingivae. — Normally situated on gingival margin, term only describes the mass location not the type
164
What are histological features of fibrous overgrowths?
> Hyperplastic epithelium and ulceration > Has bundles of interlacing fibrous tissue (fibroblasts) > Osseous metaplasia as located next to periosteum > Dystrophic calcification
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What is a vascular epulis?
Pyogenic granuloma - exuberant granulation tissue associated with growth factors sourced from macrophages. Also called a pregnancy epulis Histologically there is vascular proliferation and sheets of endothelial cells Peripheral fibroma
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What is a giant cell epulis? Characteristics? Histology?
= peripheral giant cell reparative granuloma Normally present in the anterior mouth, very vascular and usually purple in colour The aetiology is thought to be epithelial hyperplasia in reaction to irritant factors such as trauma or calculus. Clinically, the characteristic appearance is a red to blue mass that is variably ulcerated occurring anterior to the first molars. Histologically, peripheral giant cell granuloma displays an unencapsulated proliferation of mononuclear and multinucleated giant cells in a vascular stroma.
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Polp
A tumour present in the mucous membrane, term describing the mass location not the type
168
Squamous cell papilloma (SCP) - histology? - cause?
> Normally a hyperplastic, hyper keratinized lesion with papillomatosis surface > Normally associated with virus such as HPV
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What are odontogenic cysts and how are they categorised?
Odontogenic cysts are described as an epithelial lined fluid filled cavity, with the epithelial lining arising from the odontogenic epithelium. They are generally categorised by origin; this is either developmental or inflammatory.
170
What type of cyst is a radicular cyst and what is it's origin? appearance? Radiographic appearance? Treatment?
Radicular cysts are odontogenic cysts of inflammatory origin. They arise from the cell rests of malassez in the PDL. They develop at the apex of a non-vital tooth. Occurrence: Most common odontogenic cyst. 52% of cystic jaw lesions Why: Bacteria from a carious lesion travels down the root canal to the periapical region. The inflammatory response leads to the destruction of bone and the formation of granulation tissue. Eventually, this results in cyst formation Appearance: There may be a small swelling present intraorally. The patient may report pain if the lesion has become infected Radiographically: Unilocular radiolucent lesion with a well-defined border at the root of a tooth Treatment: Root canal treatment and a review radiographically in one year to see if the lesion resolves. In addition, apicectomy and removal of cyst, extraction of the tooth and removal of the cyst.
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Residual cyst. Origin? Where? Why? Appearance? Radiographic appearance? Treatment?
Origin: Inflammatory – epithelial rests of Malassez Occurrence: 8% Where: At an area where previously a tooth has been extracted Why: Remaining tissue following inadequate removal of a periapical cyst Appearance: Possibly visible intraorally as it’s an area of bony expansion. It may become symptomatic if it gets infected Radiographically: Unilocular radiolucent lesion in a tooth bearing area but not associated with a tooth Treatment: Surgical enucleation of the cyst. May require referral to Oral and Maxillofacial Surgery (OMFS) for this procedure depending on confidence and skill level.
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Paradental cyst. Origin? Where? Why? Appearance? Radiographic appearance? Treatment?
Occurrence: 3-5% Origin: Inflammatory – odontogenic epithelium Where: At the crown or root of a partially erupted tooth. It can occur on the buccal, distal or (rarely) mesial aspects of the tooth. It only occurs in the mandible and most commonly occurs in partially erupted mandibular third molars Why: A response to chronic inflammation. In the majority of cases there is a history of recurrent episodes of pericoronitis Appearance: Not visible intraorally Radiographically: Unilocular radiolucent lesion attached to the cementoenamel junction (CEJ) and the coronal of a third of the roots. Lesions may vary between 1-2cm in size Treatment: Removal of the tooth and enucleation of the cyst. In addition, it may require referral to OMFS for this procedure
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Dentigerous cyst. Origin? Where? Why? Appearance? Radiographic appearance? Treatment?
Occurrence: Second most common odontogenic cyst at 20% Origin: Developmental – reduced enamel epithelium Where: Unerupted teeth, occurring in the mandible 70% of the time. It most commonly affects mandibular third molars, then maxillary canines Why: The accumulation of fluid between the crown of the tooth and the reduced enamel epithelium pf the dental follicle. Resulting in dilation of the tooth follicle and prevention of the tooth from erupting Appearance: Can result in delayed eruption of a tooth or, if it’s large enough, may cause bony expansion Radiographically: Unilocular radiolucent lesion around the crown of the tooth starting at the CEJ Treatment: For mandibular third molars treatment it’s likely removal of the tooth and enucleation of the cyst is needed. But depending on treatment planning, maxillary canines may be planned for extraction and cyst enucleation, or exposure and bonding to bring the canine into the arch.
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Eruption cyst. Origin? Where? Why? Appearance? Radiographic appearance? Treatment?
Occurrence: 1-10% Origin: Developmental – reduced enamel epithelium Where: On the mucosa overlying an erupting tooth, appearing shortly before the tooth is visible in the oral cavity. They most commonly occur in children aged from 6-9 years and in the molar or incisor regions Why: Accumulation of fluid or blood between the crown of the tooth and the reduced enamel epithelium of the dental follicle Appearance: Well circumscribed fluctuant swelling overlying an erupting tooth. In a cystic lesion containing blood there will likely be a blueish hue to the swelling. A lesion filled with fluid will be the same colour as the mucosa. Usually less than 1.5cm in size Radiographically: It may be hard to identify as the lesion is in the oral cavity rather than within the bone Treatment: The majority resolve on their own without requiring any intervention. If the eruption is impeded or the lesion become painful or infected, surgical exposure and drainage of the cyst may be required.
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Odontogenic keratocyst. Origin? Where? Why? Appearance? Radiographic appearance? Treatment?
Occurrence: 10% of odontogenic cysts Origin: Developmental – dental lamina Where: Twice as common in the mandible as in the maxilla. Large lesions are most likely to occur at the angle of the mandible or in the ramus. Benign but locally invasive and aggressive with a high recurrence rate Why: Multiple keratocysts are present in people with Gorlin-Goltz syndrome Appearance: Often asymptomatic and identified on routine radiographs Radiographically: If small, lesions are usually a unilocular radiolucency with a sclerotic margin. If lesions are larger they are often multilocular radiolucencies with scalloped margins Treatment: Referral to OMFS for assessment and treatment planning. Treatment options include enucleation, marsupialisation, chemical cauterisation and surgical resection. Each technique has their individual pros and cons.
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What are the 2 types of mucoceles?
Extravasation mucocele A broken salivary gland duct causes mucus to spill into the soft tissue around the gland. This is often the result of trauma, such as biting your lip. Retention mucocele A blockage in the salivary gland ducts causes a decrease or absence of glandular secretion, which leads to a buildup of mucus. This is also known as a salivary duct cyst or sialocyst
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What is a haemangioma?
Vascular cause of a swelling — Present like a purple blood blister — Epithelium lining with large vessels present in the connective tissue, filled with blood
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What are torus palatinus and torus mandibularis?
Bony exostoses/ outgrowths that are non-neoplastic, developmental but sometimes reactive. Flat, lobulated or bosselated clinical appearance. Normal lamellar bone. Dense cortical bone
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What are the 3 major paired salivary glands?
1. Parotid 2. Submandibular 3. Sublingual
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What are components of salivary gland anatomy?
1. Ducts 2. Acini cells = both serous and mucous, they appear purple on a histology slide. 3. Myoepithelial cell, they appear brown on a histology slide 4. Variable levels of fat, they appear white
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Salivary gland disease - Non-neoplastic pathology types: Developmental? (3), Inflammatory (3), Sialosis, Systemic (2), Obstructive/traumatic (3)
Developmental A. Aplasia - the failure of an organ or tissue to develop or to function normally B. Heterotopic - abnormal location of tissue growth, normally acini cells with no duct system C. Stafne bone cavity = unilateral lingual mandibular depression with no anatomical and histology abnormality. Sits below IAN, submandibular benign tissue not in correct position. Inflammatory A. Bacterial (acute or chronic) B. Viral, such as mumps which present with bilateral salivary gland swelling C. Therapeutic - radiography Sialosis - diffused, non-inflammatory, non-neoplastic. Recurrent enlargement of the major salivary glands - bilateral welling of glands. Systemic A. Sarcoidosis, granulomatous (increased macrophages) condition which affects the whole body B. Sjogren syndrome (autoimmune condition that affects exocrine glands) Obstructive/traumatic A. Sialolithiasis (salivary stones) caused by sialolith (calcified mass), obstructing ducts (usually the submandibular duct (Wharton's duct) B. Mucoceles C Necrotising sialometaplasia
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What is sialosis?
Diffused, non-inflammatory, non-neoplastic recurrent enlargement of the major salivary glands leading to bilateral swelling of glands. Due to > hormonal disturbances (pregnancy, diabetic hypothyroidism) > malnutrition (alcohol, bulimia, protein deficiency) > drugs (iodine, isoprenaline, antihypertensives) Clinical appearance like a hamster
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What is a mucous extravasation cyst?
A pseudo-cyst (no epithelial lining) Seen in younger patients Almost always on lower lip Due to ruptured duct (trauma) Results in mucous spilling via surface epithelium into the mucosa Granulation tissue histopathology Clinical features: painless, smooth surface, variation in size, soft consistency, rarely firm
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What is a mucous retention cyst?
older patients due to obstruction of the duct (complete or partial) cyst lined by epithelial tissue (no granulation tissue) common in submandibular salivary gland clinical features: recurrent swelling, painful, worsens during mastication, bluish colour true cyst, mucin surrounded by epithelium foamy macrophages pool to form the mucin pool pseudo-stratified or stratified squamous epithelium surrounding the cyst minimal inflammation in stroma
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What is a ranula?
Mucocele found on the floor of the mouth (sublingual gland affecting) Translucent blue, dome shaped, fluctuant swelling of the floor of the mouth (Frog's belly) Mucous extravasation cyst (mucocele) Larger than other mucocele They elevate the tongue Appear lateral to the midline Mucin may herniate to the submental and submandibular space.
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What is superficial mucocele?
Subepithelial and intraepithelial blister Ruptures to leave a shallow ulcer Small, multiple and recurrent can be mistaken for RAU Clinically/microscopically mistaken for MMP or PV
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What is necrotising sialometaplasia?
Benign inflammatory disease of glands of the palate Clinically/microscopically resembles malignancy Mimics SCC and mucoepidermoid carcinoma Cause unknown, thought to be due to minor gland trauma Initially tender, often entirely painless Deep ulcer, slow healing and erythematous nodule Requires a biopsy Heals spontaneously 4-10 weeks M>F 3:1 mean age 50 yo
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what does necrotising sialometaplasia mimic?
SCC and mucoepidermoid carcinoma
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When faced with a patient who presents with bilateral parotid swellings, differential diagnosis should include?
1. Mumps 2. Sjogren's syndrome 3. Salivary gland tumours (benign and malignant) 4. Sarcoidosis 5. Sialadenosis/ 6. Sialosis due to diabetes mellitus, alcoholism, hypothyroidism, malnutrition, medications and bulimia nervosa
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What is a neoplasm?
An abnormal growth of cells. Neoplastic disease refers to conditions that cause tumour growths (benign or malignant).
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What is the difference between benign and malignant tumours?
Benign tumours - non cancerous growths. They usually grow slowly and can't spread to other tissues Malignant tumours - cancerous and can grow slowly or quickly and spread to other parts of the body in a process called metastases.
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What are features of malignant tumours?
Irregular shaped lesion with poorly defined margins Induration, an increase in fibrous elements in tissue with deep thickening of the skin Necrosis Poor circumscription Assortments of colours Rapid infiltrating growth
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Percentages of neoplasm signs glands? % of which are malignant?
Parotid glands (73%) --> 15% malignant Minor salivary glands (14%) --> 46% malignant Submandibular (11%) --> 37% malignant Sublingual (0.3%) --> 85% malignant
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Name 10 types of benign epithelial tumours of the salivary glands
1. Pleomorphic adenoma 2. Myoepithelioma 3. Basal cell adenoma 4. Warthin tumour 5. Oncocytoma 6. Canalicular adenoma 7. Sebaceous adenoma 8. Lymphadenoma (sebaceous or non-sebaceous) 9. Ductal papillomas (inverted ductal papilloma, intraductal papilloma, sialadenoma papilliferum) 10. cystadenoma
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What is the most common benign salivary gland epithelial neoplasms?
Pleomorphic salivary adenoma - most common Warthin tumour - second most common benign neoplasm; associated with tobacco smoking; often multiple, sometimes bilateral; frequency increasing. Myoepithelioma - rare Basal cell adenoma - older pts affected Oncocytoma - older pts affected. may follow irradiation, may be bilateral Canalicular adenoma - most common in upper lip, and in older patients
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The 'rule of nines' is an approximation that states that 9 out or 10 salivary gland tumours:
- affect the parotid gland - are benign - are pleomorphic salivary adenomas (PSAs)
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What is a pleomorphic adenoma?
Arise from myoepithelial cells Well circumscribed benign tumour with a pleomorphic or mixed appearance Commonest salivary tumour, affecting mainly parotid (65%) Slow growing, painless, usually well demarcated, mobile and smooth Macroscopic features: fibrous capsule and bosselated surface Microscopic features: > epithelium forms sheets and duct-like structures > connective tissue appears chondroid and fibrous Complications > recurrent that can result in malignant progression, as its capsule may be not properly formed, allowing intracapsular invasion and bulge through capsule. - originate from ductal epithelium, which proliferates to contribute to duct-like spaces, sheets of epithelial cells and sometimes areas of squamous metaplasia. There are also areas reminiscent of connective tissue, such as cartilage. The admixture of epithelial elements with what resembles fibrous, myxoid or cartilage tissue, leads to the name 'mixed tumour'. These lesions usually have a thin fibrous capsule, but this is not complete and neoplastic cells may be seen in or outside the capsule. - usually a slow-growing, lobulated, rubbery swelling with normal overlying skin, but a bluish appearance if intraoral. - usually benign. however, if recurs if excision is inadequate (around 3% recur in 5 years). The neoplasm is poorly encapsulated and parotid adenomas are in intimate relationship with the facial nerve, both of which make complete excision difficult to guarantee. (carcinoma ex-pleomorphic adenoma) - rapid growth, pain, fixation to deep tissues, facial palsy.
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What is Warthin's tumour?
Papillary cystadenoma lymphomatosum Benign tumour composed of glandular and often cystic structures, with a papillary cystic arrangement lined by eosinophilic epithelium - stroma contains a variable amount of lymphoid tissue with follicles - parotid gland specific (14%) - M>F 50-70 yo - Relationship with smoking - Impaired hearing, earaches, facial paralysis, tinnitus - Well circumscribed, mobile, painless, slow growing - Histology > double-layered, oncocytic columnar epithelium lining > lymphoid stroma with germinal follicles > capsules - mimics malignancy Warthin tumour is found virtually only in the parotid, and: - is found mainly in smokers, in people with autoimmune disease, or those exposed to radiation - accounts for about 1:10 parotid neoplasms - is benign - is multiple in about 20% and bilateral in 5% - may rarely be associated with other salivary neoplasms such as Pleomorphic salivary adenoma or other malignant disease. > Columnar cells surround lymphocytes in a folded (papillary) lining to cystic spaces.
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What is a canalicular adenoma?
Benign salivary gland tumour on the upper lip (90%) and buccal mucosa (10%) - develop next to a minor gland forms a large cyst - histology: capsule and multi focal
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Name 24 malignant epithelial tumours of the salivary gland
1. Acinic cell carcinoma 2. Mucoepidermoid carcinoma 3. Adenoid cystic carcinoma 4. Polymorphous low-grade adenocarcinoma 5. Epithelial-myoepithelial carcinoma 6. Clear cell carcinoma, not otherwise specified 7. Basal cell adenocarcinoma 8. Sebaceous carcinoma 9. Sebaceous lymphadenocarcinoma 10. Cystadenocarcinoma 11. Low-grade cribriform cystadenocarcinoma 12. Mucinous adenocarcinoma 13. Oncocytic carcinoma 14. Salivary duct carcinoma 15. Adenocarcinoma, not otherwise specialised 16. Myoepithelial carcinoma 17. Carcinoma ex pleomorphic adenoma 18. Carcinosarcoma 19. Metastasizing pleomorphic adenoma 20. Squamous cell carcinoma 21. Small cell carcinoma 22. Large cell carcinoma 23. Lymphoepithelial carcinoma 24. Sialoblastoma
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What are the more common malignant salivary gland epithelial neoplasms?
Carcinoma ex pleomorphic adenoma = variable prognosis Acinic cell carcinoma = mainly in parotid. Poor prognosis Mucoepidermoid carcinoma = most common malignancy Adenoid cystic carcinoma = poor prognosis Polymorphous low grade adenocarcinoma = most are seen in palate, good prognosis Epithelial-myoepithelial carcinoma = most in major glands, variable prognosis
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What is a mucoepidermoid carcinoma?
- common in children - malignant tumour of glandular neoplastic epithelium characterised by presence of 3 cell types 1. squamous cells 2. mucus secreting cells 3. cells of intermediate type - low grade - appear like pleomorphic adenoma - high grade - > rapid growth, pain, ulceration, fixation, nerve involvement, metastasis (invades surrounding tissues) - clinical features: swelling (can be painful), common in posterior mandible - F>M - The mucoepidermoid tumour consists of large pale mucous-secreting cells ('muco) surrounded by squamous epithelial cells ('epidermoid'). - mucoepidermoid tumour accounts for up to 10% of salivary gland neoplasms, but is the most common childhood salivary neoplasm.
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What is adenoid cystic carcinoma?
Infiltrative malignant tumour with cribriform appearance Tumour cells either two types: > duct lining cells > myoepithelium cells Microscopically is non-encapsulated, infiltrative with perineural involvement and variable morphology Appears histologically like swiss cheese - minor salivary gland (palate ~10-15%) - major salivary glands (parotid ~3%) - Wraps around nerves in the parotid gland, causes facial palsy clinically - Bone destruction and local invasion (lymphonodes) - Distant spread to lungs, bone, brain - Mid. aged or elderly - survival rate - 75% (5 years), 13% (15 years) Adenoid cystic carcinoma is rare, and: - slow growing - malignant, with a tendancy to infiltrate, spread perineurally and metastasize. Rounded islands of small darkly staining cells surrounding multiple clear areas of varying size (swiss-cheese appearance) are characteristic. Adenoid cystic carcinomas are graded based on pattern, with solid areas corrrelating with a worse prognosis. They occasionally transform to highly aggressive pleomorphic high-grade carcinomas with frequent nodal metastases,.
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What is acini cell carcinoma?
- Rare ~2% of parotid tumours - consists of cells like serous cells - can recur and metastasise - unilateral Acinic cell tumour is very rare, and: - is found virtually only in the parotid - is usually malignant, although all grades of malignancy have been reported and, although generally considered of low grade malignancy, they can recur, metastasize, or even prove lethal. Acinic cell tumours comprise large cells with a granular basophilic cytoplasm with spaces between some cells. The cells resemble serous cells of normal salivary glands. Aggressive histopathological parameters (anaplasia, necrosis and mitoses) are predictive of poor outcome.
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What is hyposalivation vs xerostomia?
Hyposalivation = an objective decrease in salivary flow Xerostomia = the subjective sensation of having a dry mouth, it is not a disease but rather a symptom.
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What is the percentage of saliva secreted from each major salivary gland?
1. Parotid (60%) 2. Submandibular (30%) 3. Sublingual (5%)
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What are the functions of saliva?
Lubrication of oral tissues Mastication, swallowing, speech Taste Enzymatic action Digestion Mineral action: pH and buffering Antimicrobial action and immune function
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What are the effects of hyposalivation?
Dry mouth Difficulty eating and swallowing dry foods Dry lobulated tongue Candida --> Candidosis and angular cheilitis Increase plaque and caries Increase chance in salivary gland swelling and infection
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What are causes of xerostomia? (6)
PISSDD Psychogenic - anxiety, exam stress Irradiation - damage via radiotherapy to head and neck region Systemic disease Salivary gland disease Drugs - most common Dehydration - avoid alcohol, caffeine, smoking
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List some medications which cause dry mouth:
a. Anti-anxiety = diazepam b. Anti-asthma = salbulamol c. Anti-cholinergic = atropine d. Anti-depressant = amitriptyline e. Anti-histamine = certirizine f. Anti-nausea = metoclopramide g. Anti-parkinsons = procyclidine h. Anti-psychotic = chlorpromazine i. Diuretic = furosemide j. Neuroleptic = haloperidol
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What 3 consequences may there be from radiotherapy of malignant tumours in the head and neck region? (e.g. SCC of mouth & jaws, larynx or SCC/BCC of skin)
a. Damage to the salivary tissues b. Damage to the bony structures promotes poor healing and reduced blood supply – this means osteoradionecrosis may occur if there is significant bone damage (extraction) c. Trismus if the MOM are involved
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What are 6 examples of salivary gland disease? WHAT IS THE ACRONYM?
PISSSSC Primary biliary cirrhosis Infections - HIV, Hep C, EBV Sjogren syndrome Sarcoidosis Salivary aplasia Systemic - diabetes mellitus, COPD, chronic renal disease Cystic fibrosis
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What is Sjogren's syndrome
Autoimmune condition causing xerostomia, affects the exocrine glands and most commonly middle-aged women. It causes dry eyes and mouth.
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What is the difference between primary and secondary sjogren's syndrome?
1. Primary Sjogren's syndrome: only Sjogrens disease and no other associated condition - dry mouth and eyes only. 2. Secondary Sjogren's syndrome: secondary presentation to a pre-existing autoimmune condition, most commonly associated with Rheumatoid arthritis, lupus or systemic sclerosis.
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How do you diagnose sjogren's?
Symptoms of xerostomia, objective evidence of hyposalivation and dry eyes on examination. Positive labial gland biopsy, presence of +ve antibodies (anti SSA and anti SSB, RHF and ANA) Positive imaging investigations (+ve parotid sialogram), with a leafless fruit laden tree of cherry-blossom appearance on the sialogram 1. Bloods - FBC, Haematinics, AIP incl Ro/LA, ESR, Random glucose, (consider ACE/HIV in sialosis) 2. Salivary flow rates over 10 min 3. USS 4. Sialography 5. Labial gland biopsy Challacombe dry mouth scale Haematological - use blood tests to rule out SS (SS with be positive for SS-A proteins) Schirmeer test - used for dry eyes (piece of paper placed in corner of eye) Salivary flow rate (sialometry) - unstimulated salivary flow less than 0.1mL/min Imaging (sialography/ultrasound/MRI) if there is a swelling Labial gland biopsy
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What is normal and abnormal unstimulated salivary flow rate?
Normal is 0.3-0.4ml/min Abnormal is <0.1ml/min (<1ml in 10 mins)
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What eye symptoms are present for Sjogren's?
Persistence of eye dryness and burning sensations Itching of eyes and sensation of foreign body Schirmer Test: filter paper under eye lid, examine after 5 mins. <10mm=xeropthalmia
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What is involved in the labial gland biopsy?
5-10 minor salivary glands removed from lower lip for histopathological analysis to assess presence of lymphocyte infiltrate around the salivary ducts.
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What is the most severe complication of sjogrens syndrome and what does it present as?
a. Most severe complication is lymphoma. 10% of Sjogren’s patients. b. This commonly presents as B-cell non-hodgkins lymphoma, with parotid gland being a common site. Patients with primary SS have a 33x risk of lymphoma (B cell non- Hodgkin’s lymphoma), with painless swelling of lymph nodes, axilla and groin all symptoms
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What are tx options for sjogrens?
Saliva orthana: artificial saliva Biotene oralbalance gel PRN Glandosane spray PRN Salivix pastilles 1 PRN (Give 100) SST tablets 1 PRN (Give 100) Xerontin oral spray PRN Pilocarpine 1% eye drops onto tongue, 2 tds Systemic pilocarpine hydrochloride 5mg po qds
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Why can pilocarpine be prescribed for sjogrens?
Pilocarpine: PSNS stimulator (cholinergic drug) that increases saliva but has adverse side effects linked with parasympathetic system Cannot be used by asthmatics and COPD patients
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What are complications of xerostomia?
Ascending infection (bacterial sialadenitis) Pain and swelling of salivary glands Purulent discharge from salivary duct Streptococci, anaerobes and amoxicillin
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How can you manage dry mouth? (4)
a. Dental advice (Caries, perio, diet, fluoride) b. Saliva stimulants – sugar free gum/sweets c. Saliva substitutes – gel sprays or pastels but may have acidic PHs d. Cholinergic antagonists – pilocarpine – parasympathomimetic would stimulate saliva glands = 5mg TDS (contraindicated in asthma/copd)
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What are 3 examples of common saliva substitutes?
a. Saliva Orthana b. Glandosane c. Oral balance gel
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What saliva artificial salivas can be prescribed?
a. Artificial Saliva Gel – apply to mucosa as required. b. Artificial Saliva Oral spray – spray as required. c. Artificial Saliva Pastilles – suck 1 as required. d. AS Saliva Orthana Oral Spray – Spray 3x as required. e. * BioXtra Gel – apply to mucosa as required. f. * Glandosane Aerosol spray – spray as required g. * Saliveze Oral spray – 1 spray as required. h. ! Saliva-stimulating tablets – such one as required. * = only prescribed for dry mouth associated with radiotherapy or primary Sjogren’s syndrome. ! = only prescribe for dry mouth associated w salivary gland function and patent salivary ducts.
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What is bacterial sialadenitis? How does it present (3)
a. It is the bacterial infection of a salivary gland and can be a result of xerostomia b. Presents as pain, swelling and pus discharge from the duct Swab pus sample, see what antibiotics are needed.
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What is sialolithiasis?
Salivary gland stones - Tiny Ca rick stones form in the salivary glands - Linked to dehydration which thickens the saliva and decreased food intake which lowers demand for saliva - Linked to drugs that cause xerostomia: antihistamines, blood pressure drugs and psychiatric medications - Symptom is a painful lump, usually in the FOM - Most commonly in submandibular gland
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How does mumps present?
It is a viral infection that causes bilateral facial swelling near sites of parotid gland Pain and eating difficulties Orchitis v common (testicular swelling) Increased meningitis and infertility risk Pyrexia, headache, muscle ache, joint pain and malaise
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What is sialodenosis?
Non-inflammatory salivary gland enlargement. - Salivary glands become enlarged without evidence of infection, inflammations or tumour - Condition typically causes painless bilateral swelling of the parotid glands
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What is sialadenitis (sialoadenitis)?
Inflammation of salivary gland (most common parotid) Causes: > bacterial - staphylococcus aureus > viral - mumps > autoimmune condition - Sjogren's syndrome Common in elderly and infant patients Clinical features: unilateral tender swelling at angle of the mandible, decreased salivary flow due to fibrosis Acute sialadenitis: > painful swelling > red > tender on touch > purulent discharge from a duct > can be secondary to obstruction (sialolithiasis) Chronic: > less painful > recurrent swelling, especially after meal > no redness
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What questions in MH can be useful for diagnosis of salivary gland disease?
- Decreased intake of food and liquids after surgery can increase the risk of sialolithiasis - Have ever received radiation treatments for cancer of the head or neck? - Were ever diagnosed with mumps or immunised against mumps? - Have recently been exposed to anyone with the flu or another viral illness? - Have any autoimmune conditions, such as rheumatoid arthritis or sjogren's syndrome?
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What is sialography?
Dye is injected into the glands duct so that the pathways of saliva flow can be seen
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What is acute suppurative sialadentitis?
Obstruction or stenosis of the parotid gland duct Ascending bacterial infection (staphylococcus aureus) Clinical features: acute inflammatory response, diffuse, tender, red, hot, pain on eating, toxic and upper deep cervical lymphadenopathy. Treat with anti-staphylococcal IV antibiotics and urea and electrolytes Investigate with a bacterial culture, FBC and CRP
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What is acute submandibular sialadenitis?
Secondary to a calculus Plain intra oral x-ray, when infection settled = sialography Proximal stones - remove submandibular gland Distal stones = incision of duct in floor of mouth
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What are some complications of parotidectomy?
Nerve injury haematoma temporary facial weakness Frey's syndrome - due to damage of parotid gland normally from surgery, causes gustatory sweating and facial flushing numbness of the ear salivary fistula wound dimple
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How is pain detected in acute orofacial pain? (nerves)
Nociceptors with sensory nerve transmission via spinal cord - ascending to cerebral cortex via thalamus
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What is paraesthesia?
Abnormal sensation whether spontaneous or evoked
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What is dysaesthesia?
Unpleasant abnormal sensation whether spontaneous or evoked
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What is neuralgia?
paroxysmal (sudden increase in symptoms) and often severe pain in the distribution of a sensory nerve or nerves.
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What is neuropathic pain?
Pain caused by a lesion or disease of the somatosensory nervous system
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What is neuropathy?
Disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy
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How do you take a history for acute orofacial pain?
C/O HPC (SOCRATES) SH, MH, DH Exam > E/O: trigger spots, cranial nerve exam, TMJ, facial expression > I/O: hard tissue, soft tissue, sinus and muscle > special tests: TTP, X-ray, EPT, PE > examination of teeth and gingiva
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What are the 3 main groups for pain classification?
1. Dental disease 2. Musculoskeletal (TMD) 3. Neurovascular
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What is acute necrotising ulcerative gingivitis? (ANUG)
Rapid onset and very painful Poly-microbial infection + predisposing factors Punched out ulceration of interdental papilla, presenting with white necrotic slouth Severe halitosis, submandibular lymphadenopathy, necrosis of interdental papillae Caused by gram -ve spirochetes and fusobacterium species, anaerobes Treatment: metronidazole and amoxicillin, hydrogen peroxide-based/chlorhexidine mouth rinses
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Where do viruses lie dormant?
Nerve ganglion - dorsal root gangion, trigeminal nerve ganglion. e.g. viral infection can lie dormant in ganglion after initial infection, then sporadically replicate if triggered and are released and infect epithelial cells along the innervation pathways of the trigeminal nerve (ipsilateral unilateral apparent)
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What can HSV1 cause?
Primary herpetic gingivo-stomatitis > primary exposure to HSV, usually in young people > oral vesicles filled with fluid that break down to produce irregular painful ulcers > if severe or pt immunocompromised then acyclovir 200mg 5x/day? HSV-1 is latent in the trigeminal ganglion after primary infection. The virus can be reactivated, is shed into saliva, and there may be clinical recrudescence, recurrently to produce herpes labialis or, occasionally, intraoral ulceration. Herpes labialis (cold sores) - Secondary infection, lesion initiates a vesicle, which erupts to leave an erosion after 48 hours, recurrent episodes and healing after 7-10 days both very common features. - transmits through skin touch and saliva - triggers: > sunlight, cold weather, stress, immune deficiency, change in hormone levels e.g. menstrual cycle. - 5 stages of presence > initial tingling - best time to apply anti-viral > blister formation > burst of blister - the most contagious stage > scab formation > healing - topical treatment: acyclovir 5% cream, will not prevent lesion but will reduce duration Recurrent intraoral herpetic ulceration - multiple red small ulcers - prodromal burning - present on any site, especially palate (unlike RAU, which is just mucosal tissue)
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What does herpes zoster (HHV-3) cause?
Primary infection with varicella zoster virus in childhood --> VZV latent within dorsal root ganglia. Reactivation of VZV latent in sensory ganglia --> shingles - Macular rash 24-48 hours following fever and malaise, develop into a red popular rash - Burning pain and allodynia - Oral manifestation; small vesicles, well defined ragged ulceration confined to a sensory nerve distribution, doesn't cross midline - Management with antiviral - complications of HHV-3: > post herpetic neuralgia and Ramsay-Hunt syndrome (unilateral vesicle formation)
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What does Epstein Barr virus (HHV-4) cause?
1) Infectious mononucleosis (glandular fever) - Subclinical infection with generalised malaise, pyrexia, sore throat - Bilateral lymphadenopathy - Virus replicated in mucosa cells and salivary glands and spreads to B lymphocytes and blood stream - No specific oral manifestations - Paul Bunnell test diagnostic 2) Oral hairy leukoplakia - Disease affecting oral mucosa associated with EBV and immunosuppression (HIV) - Benign painless white patch with vertical folds or ridges involving the lateral aspect of the tongue - Management: valacyclovir for 4 weeks? has no long-term complications or malignancy
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What does HHV-8 cause?
Kaposi sarcoma - Oral manifestation of HIV or immunosuppression - Diagnosis based upon clinical appearance - Initial stages it appears like an amalgam tattoo - Management: intralesional injections or injected chemotherapy.
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What type of human papilloma virus causes? 1) verruca vulgaris? 2) genital lesions? 3) focal epithelial hyperplasia? 4) Squamous cell papilloma? 5) verruca vulgaris?
Verruca vulgaris: HPV2 and HPV4 Genital lesions: HPV6, HPV11 and HPV 16 Focal epithelial hyperplasia (Heck's disease): HPV 13 and HPV32, they are benign conditions with clustered papules in buccal, labial, tongue and gingivae Squamous cell papilloma: HPV6 and HPV11 Verruca vulgaris: HPV 2 and HPV4
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Oral SCC and premalignant lesions, mainly oropharyngeal, base of tongue and tonsillar cancers are associated with which type of HPV in particular?
HPV 16
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Squamous cell papilloma
Any location in the oral cavity White exophytic lesion that looks like a cauliflower, can be sessile or pedunculated Warts may be observed on digits or patients with the same oral infection
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What is verruca vulgaris?
Oral warts Caused by HPV2 and HPV4 Involves oral mucosa, white sessile and verrucous usually labial or lingua
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What is hand, foot and mouth disease caused by?
Coxsackie virus Groups of 5-10 vesicles that rupture resulting in shallow ulcerations surrounded by erythema in oral cavity
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What is herpangina caused by?
Coxsackie virus - Non-specific symptoms, with vesicular lesions on posterior aspect of pharynx - Macules evolve into erythematous papules which evolve into vesicles that vesicles that ulcerate
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What are 7 oral problems associated with immunosuppression, often the earliest indicators of HIV infection?
1. Oral candidosis 2. Oral hairy leukoplakia (HHV4) 3. Kaposi Sarcoma (HHV8) 4. Linear gingival erythema 5. HIV periodontitis 6. Necrotising ulcerative gingivitis 7. Non-Hodgkin's lymphoma
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What percentage of the population harbour candida as a commensal organism?
40-70%, most common species if C. albicans.
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What are risk factors predisposing to oral candidosis?
- Trauma - Antibiotic use - Corticosteroids - Xerostomia (dry mouth) - Malnutrition, high carbohydrate diet, or smoking - Physiological: age and pregnancy - Endocrine disorders (hormonal imbalances), especially Diabetes mellitus - Malignancy: SCC or leukaemia - Immunodeficiency
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What are the 4 main types of oral candidosis?
1. Acute pseudomembranous (thrush) 2. Acute erythematous (antibiotic sore mouth) 3. Chronic hyperplastic (candida leukoplakia) 4. Chronic erythematous (denture stomatitis)
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What is pseudomembranous candidosis?
Thrush - Creamy non-adherent (scrapable) white plaque lesions found on any oral site, clinical diagnosis - Seen in inhaler users - Soft palate of long-term steroid inhaler users - Pt often anaemic, diabetic, immunosuppressed - If no local cause (antibiotics use etc.), investigate for anaemia, diabetes, HIV screening - Tx local factors, if not --> systemic antifungal (Fluconazole, 50mg/day)
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What is acute erythematous candidosis?
Antibiotic sore mouth Erythematous areas (superficial abnormal redness of mucosa) In difference to other conditions, this tends to be very painful = acute. Typically, dorsum of tongue and palate. Usually cause by local inhalers and antibiotics Tx causing factors, if not --> systemic antifungal (fluconazole, 50mg/day)
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What is chronic hyperplastic candidiosis?
Candida leukoplakia Normally seen in elderly male smoker and alcohol drinker. Relatively rare, appears as white adherent plaques or can be nodular/speckled; can't be wiped off. Described as homogenous or heterogenous lesions Typically, bilateral commissure regions and dorsum of tongue Invasion of epithelium by candida hyphae Linked with dysplasia/malignancy (biopsy), if present called Candida Leukoplakia; 15% risk of dysplasia Tx with systemic fluconazole and smoking cessation.
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What is chronic erythematous candidosis?
Denture stomatitis Most common oral candidosis; 65% in denture wearers. Appears as an erythematous painless lesion on denture bearing zone Local cause (poor oral hygiene) Can be due to immunosuppression Usually, non-painful unless severe. Tx local factors + topical antifungal (miconazole gel) applied to fitting surface of dentures.
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What is angular cheilitis?
Erythematous areas at bilateral angles of mouth Painful Accompanies any form of oral candidosis, sometimes combined with Staphylococcus aureus and MRSA. Swab to screen for bacterial infection in addition to fungal infection. Treat underlying cause --> topical antimicrobial (miconazole gel) Cannot use miconazole if pt taking warfarin.
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What is median rhomboid glossitis?
Atrophy of filiform papillae on the rhomboid area of tongue (junction between anterior and posterior) Chronic and asymptomatic, possible kissing lesion on palate Associated with immunodeficiency, smoking, denture and inhaler use Investigate for anaemia, deficiency, swab for C. albicans, diabetes controlled? Correct local cause + treat with topical antifungals (fluconazole)
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What is chronic mucocutaneous candidosis (CMC)?
Range of candida infections grouped into different syndromes Genetic link, it can be present in families Chronic recurrent infection occurring > infection of skin, mucous membrane, nails - impaired cellular immunity/deficiency against Candida - often patients on long-term prophylactic anti-fungal treatment. - patients more prone to fungal and viral pneumonia. Investigations: > swab, oral rinse, biopsy to rule out any dysplasia or malignant change. Management: - correct local factors (OH e.g. rinse after inhaler use, chlorhexidine, denture) - correct systemic factors (diabetes, anaemia etc) - antimicrobial agents - topical (miconazole gel 5-10ml); systemic (fluconazole caps 50mg or 100mg od 2/52). If azoles contraindicated use Nystatin drugs e.g. patient on warfarin. - Follow up to ensure resolution of infection and to identify/manage risk factors.
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What acute or chronic infections can be caused by untreated infections?
Periapical abscess Periodontal abscess Pericoronitis Infected cysts Osteomyelitis ANUG
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What is a dentoalveolar abscess?
Localised collection of bacteria, preceded by chronic infection, break out, subsequent spread of infection to outlying tissues. Collection of pus Generally, polymicrobial (3-8 species), anaerobes predominate (facultative and obligate) Highly proteolytic (parvinomas and porphyromonas) Acute apical abscess most common (endodontic infection) Tissue destruction Perforation of bone can lead to cellulitis
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What is a periodontal abscess?
Endogenous, subgingival bacteria implicated in periodontitis Anaerobic gram -ve rods Haeomlytic and anaerobic streptococci Spirochetes and actinomycoses
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What is cellulitis?
Bacterial infection of the skin and soft tissues, normally happens after trauma. Swelling of tissues, no suppuration. Often due to dentoalveolar abscesses spreading infection. Usually confined to area round jaw. Severe systemic reaction, body failing to respond to the organism. Spreads to adjacent tissue spaces, crossing the midline and down the neck and lead to difficulty swallowing. Rapid spread through fascial planes. If severe can lead to septicaemia (enters into the blood stream). If body responds get suppuration. Mixed infection, mainly ora anaerobes.
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What is osteomyelitis?
Infection and inflammation of the medullary bone within mandible or maxilla (acute or chronic) due to bacterial/fungal infection entering the bone tissue from blood stream (injury/surgery). - Seen in patients on bisphosphonates/radiotherapy/post XLA of wisdom tooth, Pedget's - Clinical features: pain, swelling, lymphadenopathy, TTP, mobile, suppuration, trismus, paraesthesia, feer and malaise. - Local debridement, topical antiseptic to exposed bone + antibiotics (clindamycin/metronidazole)
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What are clinical features of osteomyelitis?
Pain, swelling, lymphadenopathy, TTP, mobile, suppuration, trismus, paraesthesia, fever malaise.
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How do you treat osteomyelitis?
Local debridement Topical antiseptic to exposed bone Antibiotics (clindamycin/metronidazole)
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How can TB present orally? How do you diagnose it? What is the treatment?
Chronic oral ulceration due to tubercle bacilli in sputum coughed into mouth --> oral lesion Clinical features: single chronic ulcer (dorsum of tongue), cervical lymphadenopathy, property of latency. Diagnosis: > mucosal biopsy that will show caseating granulomas > skin test > sputum culture > CXRay Treatment: - TB antimicrobial therapy - oral lesions resolve with successful treatment of the pulmonary condition.
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What do you know about syphilis? What are the 4 principle stages? Treatment?
- Increased number of new cases due to man-man sex ~73% - Co-infection with HIV or congenital syphilis - Remains latent in nerve ganglion - Caused by Treponema Pallidum (spirochete): detected by blood test or biopsy samples. 4 principle stages: 1. Primary > chancre - following oro-genital transmission > painless/non-healing ulcer > regional lymphadenopathy 2. Secondary: - snail track ulceration, heals within 2-6 weeks and mucous patch 3. Latent phase 4. Tertiary > gumma of palate - ulcer on palate which extends into bone > leukoplakia - affects dorsum of tongue (potentially malignant) Treatment: - I.M benzthine penicillin for 1 months - Referral to GUM - Contact tracing + screening of partners
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What are the four principal stages of syphilis?
1. Primary: > Chancre- following oro-genital transmition > painless/ non-healing ulcer > regional lymphadenopathy 2. Secondary: snail track ulceration, heals within 2-6 weeks and Mucous patch 3. Latent phase - remains latent in nerve ganglion 4. Tertiary > Gumma of palate- ulcer on palate which extends into bone > Leukoplakia- affects dorsum of tongue (potentially malignant)
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What are the two types of anti-fungals? + example
Polyene (nystatin) Azole (miconazole, fluconazole)
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How do polyene antifungals work?
Disrupt fungal cell membrane Fungicidal Used topically as poorly absorbed through GIT Broad spectrum of activity
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How do azole antifungals work?
Inhibit ergosterol synthesis Fungistatic, hence address local factors Fluconazole is well absorbed in the GIT and secreted in saliva Candid may be resistant to azoles Interaction with warfarin
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What is a dentoalveolar abscess?
Localised collection of bacteria, preceded by chronic infection, break of our subequent spread of infection outlying tissues. Collection of pus Generally, polymicrobial (3-8 species), anaerobes predominate (facultative and obligate) Higly proteolytic (parvinomas and porphyromonas) Acute apical abscess most common (endodontic infection) Tissue descruction Perforation of bone can lead to cellulitis
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What bacteria can invade dentinal tubules?
- S.gordonii can invade dentinal tubules when a functioning Antigen 1 or 2 molecule present. - P. gingivalis can only invade when S.gordonii expresses antigens - S.mutans restores ability of S.gordonii to invade but doesn't allow P.gingivalis to co-invade. - Ala-risk repeat region mediates attachment to Collagen Type 1 S.Gordonii + Antigen 1 or 2 = invasion of dentinal tubules P.gingivalis + S.Gordonii expressing P.G. antigens 1 or 2 = invasion of dentinal tubules S.mutan + antigen 1 or 2 = restore ability to invade dentine for S.gordonii but not for co-invasion with P.gingivalis
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What is actinomycosis?
Rare chronic and progressive suppuration infection. - soft tissue swelling - angle of mandible, upper neck - multiple sinuses - fibrosis - trismus - gram +ve anaerobe (actinomycoses israelli causative agent) - becomes pathogenic whenever there is devitalisation of the tissues and the oxygen tension is reduced. A rare infection with Actinomyces israelii, below the mandibular angle (not lymph nodes) that may follow jaw fracture or tooth extraction. Prolonged therapy, usually with penicillin is indicated.
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What are tissue spaces?
They are potential spaces that exist between the fascia and underlying organs and other tissues. They are only created by pathology, via the spread of suppuration or cellulitis in an infection.
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What dictates the direction of spread from the apex of a tooth?
The relationship of the apex to the cortical plate and the bones thickness. Suppuration tracks into tissue spaces via muscles and fascial attachments.
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Where does upper central incisor infection tend to spread?
Thin labial cortical plate, means pus can travel to labial sulcus.
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Where does upper later incisor infection tend to spread?
Apices close to palate, results in palatal swelling
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Where does upper canine infection tend to spread?
Pus into labial sulcus or infraorbital
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Where does maxillary posterior teeth infections spread to?
Buccal sulcus. > due to thin buccal cortical plate > high attachment buccinator
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Where do mandibular molar infections spread?
Spread is dictated by mylohyoid attachment!!! > above mylohyoid line = sublingual > below mylohyoid line = submandibular space
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Where do mandibular incisor infections spread?
Submental space due to: - thin cortical plate - mentalis attached above apices - chin point
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What are the fascial systems of the neck?
Deep cervical fascia = wraps around the SCM Carotid sheath = sits around the carotid vessels Prevertebral fascia = contains the vertebra and vetebral muscles Pretracheal fascia = contains the thyroid gland
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What are the potential tissues in the neck?
Retropharyngeal Lateral pharyngeal
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What is the submandibular space?
Lies between anterior and posterior belly of digastric muscle - can spread across the midline into the contralateral space The submandibular triangle is bounded anteriorly by the anterior belly of the digastric muscle and posteriorly by the posterior belly of the digastric muscle. The superior border of the triangle is the inferior border of the mandible. The triangle's floor is formed by the mylohyoid muscle.
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What is the sublingual space?
Lies above the mylohyoid muscle - Aetiology, infection can spread from mandibular first molars and premolars.
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What is Ludwig's angina?
Bilateral swelling of the sublingual and submandibular spaces. Communicate around posterior margin of mylohyoid. - presents as a swelling or the floor of the mouth, forces tongue against palate. - risks obstruction of pharyngeal airway - management: > airway opening > drainage of infection > antibiotics (IV) - Can spread to mediastinum
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What is acute cellulitis?
Swelling of tissues with no suppuration, usually confined to the jaw. - Severe systemic reaction, body fails to respond to organism. - Rapid spread via fascial planes - Mixed infection, normally oral anaerobes
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What is erysipelas?
Acute streptococcal infection of the deep dermis with lymphatic spread. - usually streptococcus pyogenes - produces exotoxin, which appears clinically as a rash
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What is carcrum oris (ANUG spread)
Appears in immunocompromised, malnourished and poor oral hygiene. Necrotizing gingivitis Gross oedema - 2 gangernous slouth of soft tissue and bone Anaerobes: bacterioides, termponema vincenti, fusobacterium necrophorum
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What are 2 characteristic of patients with chronic pain disorders?
1. Somatisation > presentation of physical symptoms due to psychological distress > symptoms medically unexplained or disproportionate to tissue damage Somatization is the expression of psychological or emotional factors as physical (somatic) symptoms. e.g. headache, back ache, nausea, fatigue, chest pain. 2. Pain catastrophizing
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How can you measure pain?
1. McGill Pain questionnaire 2. HAD scale 3. Pain rating scale
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What is trigeminal neuralgia?
Sudden, unilateral severe brief recurrent pains in trigeminal nerve branches. Either idiopathic or secondary to another condition. Involves the peripheral trigeminal (primary afferent) neurone. May have lesion compressing the V nerve Demyelination and hypermyelination on electron microscopy Triggered by light pressure
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Trigeminal nerve summary
V1 (Ophthalmic nerve), with branches of nasociliary, lacrimal and frontal nerve V2 (Maxillary nerve) with cranium, pterygopalatine fossa, infraorbital and facial branches V3 (Mandibular nerve) with anterior (motor control of muscles of mastication) and posterior (sensory innervation of mandible and tongue) divisions - Treated with either drugs (carbamazepine, gabapentin, lamotrigine or phenytoin) - Or surgical treatment, via a peripheral neurectomy or microvascular decompression (MVD)
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How does trigeminal neuralgia present?
Sudden, unilateral severe brief recurrent pains in trigeminal nerve branches Triggered by light pressure
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What is the treatment for trigeminal neuralgia?
- Treated with either drugs (carbamazepine, gabapentin, lamotrigine or phenytoin) - Or surgical treatment, via a peripheral neurectomy or microvascular decompression (MVD)
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What is glossopharyngeal neuralgia?
Paroxysmal bursts of sharp, lancinating pain felt in the distribution of ninth nerve. - Particularly the throat, tonsillar fossa and adjacent area of fauces. - Spontaneous or evoked by mechanical stimulation - Pain radiated to external ear or to angle of jaw and adjacent neck - LA injected to tonsil alleviates pain - Managed the same as TN
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What is post-herpetic neuralgia?
Chronic pain with skin changes after acute herpes zoster - Clinical features: chronic burning, dysesthesia, paraesthesia, intractable cutaneous pain - usually V1 (ophthalmic) division of trigeminal nerve involved - pain usually moderate intensity but constant and intractable - may be cutaneous scarring, loss of pigmentation in area of herpetic lesion - prevent with acyclovir during shingles episodes.
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What is burning mouth syndrome?
Burning sensation affecting tongue or oral mucosa. - associated with: xerostomia, dysgeusia, thirst, intolerant to dentures. - Pain must be in absence of other causes such as anaemia, candida, Sjogren's and diabetes. - Normally follows a significant life event. - Oral mucosa appears normal and bloods and swabs are normal. - management: rule out other pathology and tx with antidepressants.
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What is temporal arteritis?
Continuous throbbing headache, normally systemically unwell and with muscular pains. - unilateral or bilateral - swollen tender scalp near temporal artery - vision loss due to involvement of central retinal artery - vasculitis affecting branches of ECA can result in ischaemia of blood vessel Clinical features: temporal artery pulseless, tender to palpation, bulging and irregular in its appearance - Ischaemia and gangrene of the tongue - Treatment: high dose corticosteroids or immunosuppression (azathioprine).
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What is trigeminal autonomic cephalgia?
rare causes of facial pain short lasting severe unilateral headache attacks with autonomic symptoms cluster headaches paroxysmal hericrania
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What are 2 unexplained chronic facial pains? AFP, AO
Atypical facial pain: chronic with unknown aetiology, associated anxiety and depression. With constant dull pain, usually unilaterally, midline often crossed. Atypical odontalgia: persistent chronic pain in region where tooth has been surgically or endodontically treated. No dental pathology, associated with TMD and oral dysaesthesia. Antidepressants used for tx: amitriptyline and nortriptyline
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What is atypical facial pain?
chronic with unknown aetiology, associated anxiety and depression. With constant dull pain, usually unilaterally, midline often crossed
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What is atypical odontalgia?
persistent chronic pain in region where tooth has been surgically or endodontically treated. No dental pathology, associated with TMD and oral dysesthesia
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What is Tempo Mandibular Joint Disorder (TMJD)?
TMJ disorder is an umbrella term covering pain and dysfunction of the muscles of mastication and the TMJ itself, it is several associated disorders with similar symptoms. > Limitation in jaw movements. > painful clicking and locking > joint noises MRI increasingly used to study TMD
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What anatomical structures may TMJD arise from?
Joint capsule, retrodiscal tissues or associated muscles of mastication.
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What is the normal painless maximal opening of the jaw?
40-55mm
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What are differential diagnoses to TMJD?
Dental pain Disorders of the ears, nose and sinuses Neuralgias Headaches Diseases of the major salivary glands.
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What can osteoarthritis of the TMJ present like?
Degenerative arthritis of the TMJ - Crepitus - Difficulty masticating - Trismus - Chronic pain
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What are symptoms of infective arthritis?
Pyrexia and systemic illness Trismus Throbbing pain Swelling and erythema Suppuration
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What is ankylosis?
Abnormal union across the joint space. Fibrous or bony, intra or extracapsular Ankylosis caused by trauma, infection next to joint, tumours and periarticular fibrosis. Intracapsular ankylosis can be caused by systemic disease (various arthritis conditions)
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What is TMJ surgery?
Arthrocentesis: placement of two hyperdermic needles into the joint Eminectomy and subsequent prosthesis placement
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What should you be careful not to confuse with TMJD?
Condylar fracture
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What is a cyst?
A pathological cavity with fluid, semi-fluid or gaseous contents. All cysts have a wall, an epithelial lining and a lumen of some kind. Note: an abscess is due to accumulation of pus.
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How can you classify cysts?
Odontogenic cysts of inflammatory origin Odontogenic cysts of developmental origin Bone cysts
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Radicular cyst: - age? origin? site? shape? effect? epithelium? differential?
Age: 20-50 years M>F Origin: Inflammatory - from rests of malassez Site: apex of non-vital teeth. Common in maxillary incisors. Shape: unilocular, round/oval 1.5-3cm Effect: displace teeth, antral floor, IDN canal. Buccal expansion. Rarely resorb teeth. Epithelium: hyperplastic non-keratinised. Differential: Rushden bodies. Foamy macrophages.
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Residual cyst: - age? origin? site? shape? effect? epithelium? differential?
Age: >20 years Origin: Inflammatory from rests of malassez Site: area of extracted tooth Shape: unilocular, round 1.5-3mm Effect: displace teeth, antral floor, IDN canal. Buccal expansion. Rarely resorb teeth. Epithelium: hyperplastic non-keratinized
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Dentigerous cyst: - age? origin? site? shape? effect? epithelium? differential?
Age: young adults Origin: Developmental remnant of REE Site: envelops crown of un-erupted and displaced tooth. Attachment at ACJ. Shape: unilocular, round >3-4cm Effect: displace teeth and resorb in 50%. May cause bony expansion. Epithelium: Non-keratinised Differential: 3s and 8s. Bluish cyst
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Lateral periodontal cyst: - age? origin? site? shape? effect? epithelium? differential?
Age: >30 years Origin: Developmental rests of malassez Site: lateral root of vital teeth; mandible Shape: unilocular, round <1cm Effect: displace teeth, rarely resorb, may cause buccal expansion. Epithelium: non-keratinised.
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Odontogenic keratocyst cyst: - age? origin? site? shape? effect? epithelium? differential?
Origin: developmental rests of serres Site: posterior mandible Shape: unilocular, multilocular Effect: Displace teeth or orbit Epithelium: corrugated parakeratinized. Differential: gorlin goltz, high recurrence
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Eruption cyst: - age? origin? site? shape? effect? epithelium? differential?
Site: deciduous molars Epithelium: non keratinized. Differential: bluish cyst young pt
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Gingival cyst: - age? origin? site? shape? effect? epithelium? differential?
Age: new borns Origin: rests of serres Site: vital teeth and new-borns Epithelium: stratified squamous epithelium Differential: Epstein pearls, Bohns nodules.
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What is a residual cyst?
Inflammatory origin associated with erupted non-vital teeth - 55% of odontogenic cysts are radicular - Residual cysts are a radicular cyst that remains after XLA - Very rare in deciduous teeth, common in maxillary incisors - Arises from epithelial rests of malassez in PDL, after pulp death from periapical granuloma - Formation of cyst cavity which enlarges due to hydrostatic pressure and bone resorption - Clinical features: asymptomatic, round corticated demarcated radiolucency at tooth apex - Can resorb teeth and expand bone Histology of radicular cysts: mainly due to periapical granuloma - Wall composed of granulation tissue/ inflamed fibrous tissue - With lining of hyperplastic non-keratinised squamous epithelium - Foamy macrophages Rushden bodies, formed in lining of the cyst
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What do radicular cysts arise from?
Arise from epithelial rests of malassez in PDL after pulp death from periapical granuloma. Formation of cyst cavity which enlarges due to hydrostatic pressure and bone resorption.
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What is the radiographic appearance of a radicular cyst?
Unilocular, round corticated, well demarcated radiolucency at tooth apex. Can displace and resorb (rarely) teeth and expand bone.
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What is the histology of radicular cysts?
Mainly due to periapical granuloma. - wall composed of granulation tissue/inflamed fibrous tissue. - with lining of hyperplastic non-keratinised squamous epithelium - foamy macrophages present and Rushden bodies formed in lining of the cyst.
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What is an inflammatory collateral cyst (ICC)?
Buccal aspect of the roots of PE or recently erupted teeth because of inflammation in pericoronal tissue - 2 main types: Paradental and Mandibular buccal bifurcation cysts - Cyst formation exacerbated by a down growth of enamel Possible proliferation of the reduced enamel epithelium or origin from JE - Clinical features: vital teeth, radiologically well demarcated and corticated - Tooth usually tilted buccally with deep periodontal pockets Histology: not specific, appears like radicular cyst
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What are 2 types of inflammatory collateral cysts?
Paradental and Mandibular buccal bifurcation cyst
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What is a dentigerous cyst?
Odontogenic cyst attached to the cervical region of an unerupted tooth, envelops the crown. - Developmental odontogenic cyst - Attached to the cemento-enamel junction - 20% of odontogenic cysts. - Normally of unerupted 8s and ectopic 3s. - Clinical features: painless enlargement, tilting of teeth and root resorption. - Aetiology: accumulation of fluid between REE of the dental follicle and the crown of unerupted tooth. - Radiology: round, unilocular, well defined, corticated radiolucency. Histology: > lining of hyperplastic non-keratinised squamous epithelium > continuous with REE (reduced enamel epithelium)
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Which teeth most commonly have dentigerous cysts?
Unerupted 8s and ectopic 3s
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How do dentigerous cysts appear radiographically?
Round, unilocular, well defined corticated radiolucency of an unerupted tooth which is attached to the cemento-enamel junction and envelops the crown.
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What is the histology of dentigerous cyst?
> Lining of hyperplastic non-keratinised squamous epithelium > Continuous with REE (reduced enamel epithelium)
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What is an eruption cyst?
It is a variant of a dentigerous cyst, usually in younger patients, with deciduous or permanent molars. - Fluctuant bluish cysts, with haemorrhage into cyst very common. - Lining of hyperplastic non-keratinised squamous epithelium - Spontaneously resolve.
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What is an odontogenic keratocyst? (OKC)
Development cyst that arises from odontogenic epithelium. - Young patients in the posterior mandible (8s), high reoccurrence (25%) - Arises from remnants of the dental lamina (rests of serres) - Association with mutation or inactivation of the PTCH1 gene (patched) and p53. Can cause Gorlin Goltz syndrome. - Clinical features: v large, painless unilocular or multilocular radiolucency. - Displace teeth or orbit. - Primordial cyst = found in area where a tooth should have formed (mandibular 8s) - High recurrence rate due to daughter cysts (satellite cysts). Tx: peripheral ostectomy with chemical cauterisation. Histology: - Lining of stratified parakeratinised squamous epithelium (appears corrugated) - Basal palisade layer (picket fence appearance) - Has lots of mini daughter cysts and cholesterol crystals
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What syndrome is associated with odontogenic keratocysts?
Gorlin Goltz
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Where does odontogenic keratocysts arise from?
Arise from remnants of the dental lamina (rests of serres)
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Why do odontogenic keratocysts have high recurrence rate?
Daughter/satellite cysts missed on removal
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What is the histology of odontogenic keratocysts?
Lining of stratified parakeratined squamous epithelium (appears corrugated) Basal palaside layer (picket fence appearance) Has lots of mini daughter cysts and cholesterol crystals.
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What is gorlin goltz syndrome?
Basal cell nevus syndrome Clinically appear with skeletal abnormalities Multiple odontogenic keratocysts Multiple basal cell nevi, high chance of carcinoma development. Frontal bossing and hypertelorism Calcification of the falx cerebral Bifid ribs
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What is a lateral periodontal (botryoid) cyst?
Developmental, lateral cysts between roots of erupted vital teeth - Botryoid is a multicystic variant - Usually mandible, anterior to the molar in vital teeth - Cyst forms between the roots of the teeth. - Lining of non-keratinised stratified squamous epithelium
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What is a gingival cyst?
Cysts found in the oral mucosa, next to vital teeth commonly the free or attached gingiva or interdental papilla. - Lining of 2-3 mm stratified squamous epithelium - Clinical features: Bohn's nodules and Epstein's perals types of gingival cysts - Spontaneously resolve via rupture of involution - Arise from Rests of Serre's thin 1 to 2 cell layer thickness of stratified squamous epithelium that tends to most often be parakeratinized. The lumen of the cyst will contain proteinaceous debris or keratin and the basal epithelial layer of the lining epithelium will be quite flattened. Gingival cysts of the newborn typically involute or rupture by three months of age, rarely if ever requiring excision.
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What are differential diagnoses of odontogenic keratocysts?
Differential Diagnosis From a clinical differential diagnostic standpoint, an OKC that is radiographically unilocular can resemble a dentigerous cyst, if it is identified in association with the crown of a tooth, or OKC can mimic a residual cyst, if it presents as a radiolucency in a site where a tooth has been previously extracted. In the pediatric age group, OKCs can also present in a manner that is radiographically identical to unicystic ameloblastoma, especially if the lesion surrounds the crown of an impacted tooth. OKCs that are multilocular radiographically can resemble ameloblastoma, odontogenic myxoma, central giant cell tumor (granuloma), ameloblastic fibroma or a central hemangioma of bone
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What is a glandular odontogenic cyst?
Developmental cyst, with features that stimulate salivary gland differentiation - Well corticated, can be either unilocular or multilocular radiographically - Associated with roots of multiple teeth, can cross midline Glandular components of the epithelium lining
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What is a calcifying odontogenic cyst?
- Unilocular radiolucency - Lined by ameloblastoma-like epithelium with ghost cells - Gorlin Cyst
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What is a nasopalatine duct cyst? (incisive canal cyst). Arise from: Type: Site: Effects: Radiographically: Histology:
From the remnants of the nasopalatine duct Non-odontogenic cyst that appears in midline of anterior maxilla in vital teeth Can cause divergence of roots and E/O swelling - Radiologically: corticated radiolucency between roots of central incisors Histology: respiratory type epithelium with stratified squamous epithelium
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What is an aneurysmal bone cyst? (fibro-osseous lesion)
False cyst as no epithelial lining Mandible region most common (ramus area) Radiolucent area rapidly growing bulge into adjacent soft tissue Histology: giant cells, haemorrhage and osteoid, and no epithelial lining, but haemosiderin. Blood filled spaced. Big ballooning locules, corticated and well-defined radiolucency. Displaces and resorbs teeth.
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What is a simple bone cyst?
- solitary, haemorrhagic and traumatic. - Histology: no epithelium lining, thin layer of fibrous tissue, lumen filled with blood. - Radiologically: radiolucent area extending between roots without expansion.
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What is a central giant cell granuloma?
- Benign condition of the jaws. - Most common in the anterior maxilla and mandible, often cross the midline. - Large multilocular lesions that expand cortical plate and resorb roots and teeth. Scalloped appearance radiographically.
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Nasolabial cyst can be confused with what?
odontogenic cyst
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What is a carcinoma?
Malignancy of epithelial tissue, such as enamel organ, remnants of dental lamina (rests of serres) and hertwigs root sheath (malassez)
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What is a sarcoma?
A sarcoma is a type of cancer that forms in connective tissues, such as bones, muscles, fat, blood vessels, nerves, and cartilage.
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What is an ameloblastoma?
Benign epithelial odontogenic tumour. Epithelial tumour, usually benign intraosseous tumour characterised by expansion. - Benign, slow growing and locally invasive. - Arise from Rests of Serres - Local recurrence common - 80% in posterior mandible (ramus area) - Increased size: mobile teeth, paraesthesia, trismus and soft tissue invasion. Can displace teeth apically. - Radiography: multilocular, with expansion and root resorption. - Very similar to dentigerous cysts, require biopsy to give differential diagnosis. Tumour resembles epithelial component of the stellate reticulum with ameloblastoma epithelium lining the periphery of the tumour cell islands. > Unicystic ameloblastoma - unilocular. - Peripheral palisading cellular strand with central loose stellate reticulum. - Differential diagnosis between ameloblastoma and odontogenic cysts is that the teeth are vital in ameloblastoma. Likewise, dentigerous cysts occur in unerupted tooth, if erupted then likely to be an ameloblastoma. Tx: enucleation and curettage tradition, but high recurrence rate. - En block resection more commonly used now.
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What is an odontoma?
Benign mixed epithelial and mesenchymal odontogenic tumour, composed of dental hard and soft tissues. 2 main types: compound and complex. Unknown aetiology, probably genetic mutation in tooth germ. Associated with unerupted tooth. Asymptomatic
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What is a compound odontoma?
Benign mixed epithelial and mesenchymal odontogenic tumour. Collection of denticles (multiple tooth like structures) Intercanine region, especially maxilla. Radiologically: collection of opaque denticles. Histology: dentine, cementum, enamel matrix, pulp and dental follice.
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What is a complex odontoma?
Benign mixed epithelial and mesenchymal odontogenic tumour. Irregular mass of dental tissue, dentine, cementum and connective tissue. Encapsulated. Clinical complications: can displace and replace normal teeth, impede eruption and expand bone.
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Name 4 benign epithelial odontogenic tumours
1. Ameloblastoma and its variants 2. Calcifying epithelial odontogenic tumour 3. Adenomatoid odontogenic tumor (cyst) 4. Squamous odontogenic tumour
364
Name 3 benign mesenchymal odontogenic tumours
1. Odontogenic fibroma and its central osseous and soft tissue variants 2. Odontogenic myxoma 3. Cementoblastoma
365
Name 4 benign mixed epithelial and mesenchymal odontogenic tumours.
1. Ameloblastic fibroma 2. Ameloblastic fibro-odontoma 3. Odontoameloblastoma 4. Odontoma and its variants
366
What is an odontogenic myxoma?
Benign mesenchymal odontogenic tumour, characterised by stellate and spindle cells. - painless swelling of maxilla or mandible, most common in molar region. - Early expansion in an early and consistent feature, - Histology: resembles dental papilla of developing tooth. - Locally aggressive, elevated risk of recurrence. - Tennis racket appearance on a radiograph.
367
What is a cementoblastoma?
A benign mesenchymal odontogenic tumour associated with roots of the teeth. - characterised by formation of calcified cementum like material. - mandibular molars and pre-molars are most common sites. - clinical features: buccal and lingual expansion, with pain and toothache. - radiographically: circumscribed mass, obliterates tooth root, thin radiolucent zone. - histology: calcified cementum like material deposited, causing partially resorbed root.
368
What is an adenomatoid odontogenic tumour?
A benign epithelial odontogenic tumour. Arise from lining of organs Attaches apical to the CEJ on unerupted teeth Common in anterior maxilla. Unilocular radiolucency that surrounds crown of unerupted teeth (snowflake appearance)
369
Name 7 malignant odontogenic tumours of epithelial and mesenchymal origin
1. Odontogenic carcinoma 2. Malignant ameloblastoma 3. Ameloblastic carcinoma 4. Primary intraosseous squamous cell carcinoma 5. Clear cell odontogenic carcinoma 6. Odontogenic sarcoma 7. Ameloblastic fibrosarcoma
370
What does the intrinsic and extrinsic pathway of the clotting cascade rely on?
Clotting factors made by liver
371
What is Haemophilia A?
Factor VIII deficiency
372
What is Haemophilia B?
Factor IX deficiency
373
What is Haemophilia C?
Factor XI deficiency
374
How can you treat haemophilia pts?
Fresh frozen plasma (FFP), as well as Factor factor and tranexamic acid given for prophylaxis?
375
What is von willbrand disease?
Defective vWF which is a clotting protein. VWF binds to factor VIII and platelets. Treatment like mild haemophilia, with factor VIII infusion, tranexamic acid and DDAVP for minor procedures. Factor VIII supplement must be given if there is any likelihood of oral trauma
376
What types of infections just you be careful of for pts with genetic coagulation defects?
Regional blocks or injections into floor of mouth may cause haemorrhage to spread via tissue spaces, causing potential airway obstruction. Therefore, must administer Factor VIII supplement and avoid intramuscular injections if invasive treatment essential.
377
Whats heparin and enoxaparin used for and their mechanism of action?
Prophylaxis for DVT and PE Inhibit factor Xa and thrombin?
378
How does warfarin work?
Impairs synthesis of vitamin K dependent coagulation factors (II, VII, XI, X). Requires active and regular monitoring via INR. INR must be tested 24-36 hours before tx, with local measures regarding suturing and haemostatic agents administered.
379
What medications should not be given to pts taking warfarin?
Aspirin, amoxicillin, metronidazole, erythromycin, NSAIDs, fluconazole (Daktarin) and miconazole.
380
Vitamin K deficiency
Acquired coagulation defect
381
What type of drugs are dabigatran, apixaban and rivaroxaban?
DOACs Dabigatran (thrombin inhibitor) Apixaban and Rivaroxaban (Factor Xa inhibitors)
382
Name 4 types of antiplatelet medication
Low dose aspirin Clopidogrel: treats IHD, lasts 7-10 days Ticlopidine: treats IHD, lasts 7-10 days Dipyridamole: reversible effect, acts directly on enzyme in platelets and vessel walls
383
What is thrombocytopenia?
Thrombocytopenia is a condition where your platelet count is lower than normal, which is defined as less than 150,000 platelets per microliter of blood in adults.
384
What are clinical implications for thrombocytopenia?
Oral petechia, purpura and extensive bruising. Abnormally low platelet count but 20-100 increase in bleeding time. Transfusion may be required for surgery. Tx: platelet transfusion, tranexamic acid and local measure, FBC VITAL - 80 can do XLA in practice, if less than 50 send to hospital
385
What is infective endocarditis?
Inflammation of the endocardium, affecting the heart valves, caused mainly by bacteria - Bacteraemia in bloodstream. - Predisposing abnormality of the endocardium. Procedures that involve dento-gingival manipulation enable the oral flora to enter the bloodstream, inducing such bacteraemia. Check guidelines for antibiotic prophylaxis and liaise with cardiologist. Need good OH to prevent IE Symptoms that indicate IE: flu like symptoms, fever, chills, fatigue, aching, night sweats
386
What are dental implications for diabetes mellitus?
Periodontal disease Candidosis Lichenoid like lesions with oral hypoglycaemics Sialosis and xerostomia - hypoglycaemia Delayed healing Increased risk of dental caries due to salivary hypofunction * Accelerated tooth eruption with increasing age * Gingivitis with high risk of periodontal disease (poor control increases risk) * Salivary gland dysfunction leading to xerostomia * Impaired or delayed wound healing * Taste dysfunction * Oral candidiasis * Higher incidence of lichen planus Ensure glycemic control at appointment time. Review recent diabetes control with patient, Hemoglobin A1c (HbA1c) <7 indicates good control in previous 3 months, >8 indicates poor control.
387
What is hepatitis and the different causes?
Hepatitis = inflammation of the liver, most commonly caused by excessive alcohol consumption, NSAIDS, herpes virus and the hepatitis virus (A, B, C, D, E) Causes complications of liver disease, clotting defects, chronic glomerulonephritis, hepatocellular carcinoma, cirrhosis.
388
What are the different types of hepatitis?
Hep A - faecal-oral spread - no tx needed - vaccine available Hep B - prevented by vaccine, incurable - spread via unsafe infections, sex, drug use and vertical transmission - antigen means infected, antibody means cleared or vaccinated Hep C - blood-borne RNA virus, very serious - spread by IV drug use, unsafe health care and sex, and vertical transmission - Anti-HCV antibody detection = infected - Antiviral medicine cure, but no vaccine Hep D - RNA virus that can only replicated in presence of HBV - HBV + HDV = severe symptoms - HBV vaccine protects against HDV
389
What is the management of hepatitis?
Liver support via bleeding risk and metabolism of drugs. Associated diseases HIV Current medication Liver transplant
390
What is an acquired prion disease?
Infectious transmissible proteinaceous particles that lack nucleic acid - Also known as Transmissible spongiform encephalopathies (TSE) - Incurable neurodegenerative condition, characterised by vacuolisation of grey matter - Creutzfeldt Jakob Disease (CJD) > Dementia, blindness, loss of speech and death > Has an incubation period of 40 years but symptoms can present within 4 months > Variant CJD associated with intake of BSE contaminated beef > Amyloid plaques in lymphatic tissue - Documented transmissions > Dural and corneal grafts > Blood products (from infected pool) > Inadequate sterilisation of surgical instruments > Human growth hormone & gonadotrophins (cannibalism)
391
What is radiotherapy and its effects on the oral cavity?
Use of high energy radiation from x-rays, gamma rays, neutrons and protons to kill cancer cells Intensity modulated radiation therapy (IMRT) Effects on the oral cavity - Damage not limited to cancerous cells - Mucositis, causing erythema, atrophy, ulceration and impaired healing - Dysguesia - a condition in which a foul, salty, rancid, or metallic taste sensation persists in the mouth - Trismus, due to damage to RMJ - Xerostomia, due to damage to salivary glands (acini cells specifically) > caries due to xerostomia, prevent via Duraphat and mouthwash - Osteoradionecrosis of the jaw (ORN) > Exposed bone in a patient with no history of bisphosphonate use > End arteritis obliterans, inflammation of the blood vessels.
392
What is MRONJ?
Medication Related Osteo Necrosis of the Jaw > Bisphosphonates > RANKL inhibitors > Anti-resorptives > Anti-angiogenics - Cancer treatments - Osteoporosis
393
What are signs and symptoms of MRONJ?
Pain Swelling Numbness and paraesthesia Delayed healing Exposed bone infection
394
What are the risks to immunocompromised patients?
Mucositis Systemic aspergillosis (deep mycosis), causes soft tissue necrosis Neutropenic ulcerations Oral candidosis (opportunistic infection), pseudomembranous candidiasis (thrush) Varicella zoster virus (one sided infection) Herpes Simplex Virus (herpes labialis), can be recurrent
395
What are the side effects of steroids?
Predisposition to diabetes mellitus Cushing appearance Increased risk of fungal infections (Candida) Hypertension Osteoporosis Adrenal suppression (Hypothalamic-pituitary-adrenocortical axis suppressed) Gastric and oral ulceration (omeprazole protection) Steroid crisis
396
When do you need to be careful of steroid crisis?
If pt takes <10mgs prednisolone then no cover is needed for dental tx, otherwise increase the steroid dose preoperatively. Addison's disease sufferers require steroid cover (hydrocortisone hemisuccinate) for invasive and stressful procedures.
397
How do cytotoxic agents in chemotherapy affect bone marrow?
Leukopenia Neutropenia Thrombocytopenia Anaemia Needs to repeat blood transfusions as chemotherapy affects stem cells and bone marrow FBC needed regularly Timing of pt vital as patient may need platelet support. Prophylactic ABx cover recommended before invasive treatment (amoxicillin and clindamycin) Dental infections can be fatal to a patient on high dose chemotherapy
398
How do stem cells in the bone marrow differentiate?
1) Haematopoietic stem cells in bone marrow 2. A.) Lymphoid progenitor cells 2. A. I) T cell 2. A. II) Natural Killer cell 2. A. III) B cell 2. A. III. a) plasma cell 2. B.) Myeloid progenitor cells 2. B. I.) Neutrophil 2. B. II.) Basophil 2. B. III.) Eosinophil 2. B. IV.) Red blood cell (erythrocyte) 2. B. V.) Megakaryocyte 2. B. V. a) Platelet 2. B. VI.) Monocyte 2. B. VI. a) Macrophage 2. B. VI. b) Dendritic cell
399
What are oral implications for transplant patients?
Most transplant patients will initially be on a combination of anti-rejection drugs - Cyclosporine: anti-rejection drug, with severe side effect of gingival hyperplasia. - GVHD can happen in bone marrow transplant patients, causing rejection of transplant. > Differential diagnosis with OLP, have similar erosive lesions > Palatal involvement which is extremely rare for OLP > Lichenoid like plaque lesions (keratinized) present on the tongue
400
What is HIV?
Human immunodeficiency virus (HIV) is a virus that attacks the body's immune system. Acquired immunodeficiency syndrome (AIDS) occurs at the most advanced stage of infection. HIV targets the body's white blood cells, weakening the immune system. Progressive disease in regulation and function of the immune system is impaired. Decrease in CD4 helper cells (AIDS <200) Classic sero-conversion illness Prognosis much improved due to antiretroviral medication, triple therapy <350 > nucleoside analogues > protease inhibitors
401
What are extraoral and intraoral symptoms of HIV?
Extra-oral: - cervical lymph node enlargement (painless) - sialosis (swelling of salivary glands) - skin disorders (dermatitis, molluscum contagiosum and HPV) Intra-oral: (NALPCOK) - Candidosis - HIV periodontal disease - Non-hodgkin lymphoma - Oral hairy leukoplakia - Kaposi sarcoma (HHV8 responsible), proliferation of epithelial cells - ANUG - Linear gingival erythema - Aphthous ulcerations (multiple major aphthous ulcers)
402
What is a syndrome?
A collection of signs and symptoms that indicate a disease or disorder
403
What is a congenital abnormality?
A condition that is present at birth or develops in the first month of life
404
What can foetal alcohol syndrome cause?
Caused by consumption of alcohol during pregnancy - small head - epicanthal folds - low nasal bridge - thin upper lip - underdevelop lips - flat midface - smooth philtrum Multiple problems of this, especially feeding, failure to thrive and speech problems, multiple hospital admissions and surgeries, multiple psychosocial issues. Relevance to dentistry: dietary restrictions and medications may increase caries risk, oral care may be neglected, may be unable to co-operate with a dental exam and treatment. Hypodontia, microdontia, supernumeraries, delayed eruption all much more common.
405
What dental symptoms can occur with Trisomy 21 (Down syndrome)?
Meiotic non-disjunction resulting in an extra copy of chromosome 21 - Mental impairment and stunted growth are present in all patients with Down's - Brachycephaly - Microdontia - Macroglossia - Hypodontia - Cleft palate - Tendency to have periodontal disease
406
What is Klinefelter syndrome?
XXY syndrome, causes hypogonadism and infertility. - small rounded shoulders - less facial and body hair - gynecomastia - reduced muscle mass
407
What is osteogenesis imperfecta?
Abnormality in type 1 collagen synthesis, resulting in brittle fragile bones. Types 1 to 4 exist. - Deafness (distortion of the ossicles) - Blue sclera - Skin translucent - Incompetent heart valves Type I Dentinogenesis imperfecta occurs in people who also have osteogenesis imperfecta
408
What is achondroplasia?
Dwarfism, a hereditary condition or acquired via sporadic defects. - failure of normal endochondral ossification and growth plates - Spine and skull has normal growth, but limbs shortened length
409
What is osteopetrosis?
Defect in osteoclast activity due to defective carbonic anhydrase. - Excessive formation and density of bone - Sclerosis of the skeleton - Susceptible to fracture, delayed dental dentition, causes very difficult extractions - Haematological abnormalities - Albers-Schonberg disease
410
What is Cleidocranial dysplasia?
An AD defect that affects skull, jaws and clavicles. - Partial or complete absence of clavicle - Underdeveloped maxilla, a narrow high arched palate - Supernumeraries - Skull suture and fontanelles remain open for longer than normal - Hypertelorism Delayed eruption of permanent teeth: Permanent teeth may erupt late or not at all Retention of primary teeth: Baby teeth may not fall out on their own Supernumerary teeth: There may be extra permanent teeth Impacted teeth: Adult teeth may be impacted in bone and unable to grow in Crowded teeth: Teeth may be crowded together Malocclusion: Teeth may not meet properly when biting, or may be under or open bitten Thin tooth enamel: Teeth may be more prone to cavities Abnormal dental roots or crowns: Dental roots or crowns may be abnormal Highly arched palate or cleft palate: The palate may be highly arched or cleft Dentigerous cysts
411
What is Marfan syndrome?
An AD connective tissue disease, causes reduced recoil of connective tissue. Connective tissue stretches and remains stretches. Tear in lining of blood vessels causing blood build ups. Lens dislocates and joint hypermobility Skeletal features (arms longer than height) High arched palate
412
What is McCune-Albright syndrome?
Polyostotic fibrous dysplasia > Café au lait demarcations on the skin - Precocious puberty, girls <10 - Associated endocrinopathies (hyperactivity -3’ Cushing, hyperthyroidism)
413
What is craniosynostosis syndromes?
Facial bones fuse prematurely, results in severe under development of the mid face and mandibular prognathism - Apert Syndrome - Crouzon Syndrome - Learning difficulties due to high volume of pressure placed on the brain - Narrow high-arched palate, hypodontia, posterior bilateral crossbite - Hearing loss and recurrent ear infections
414
What is cowden syndrome?
An overgrowth of benign mature tissue, resulting in multiple hamartomas. - Mutation of a tumour suppressor gene - Facial trichilemmomas, acral and palmoplantar keratosis - Oral papillomatosis - Increased risk of malignant neoplasms
415
What is Gardner syndrome?
AD condition which is a variant of familial adenomatous polyposis. - Multiple polyps of the colon, with very high malignant potential. - Multiple benign bone osteomas - supernumerary teeth, compound odontomas, hypodontia, abnormal tooth morphology and impacted or unerupted teeth
416
What is gorlin goltz syndrome?
Naevoid basal cell carcinoma syndrome, and AD defect on Ch9q. - Multiple odontogenic keratocytes - Frontal temporal bossing, multiple BCC.
417
What is Sturge-Weber syndrome?
- Encephalotrigeminal angiomatosis, causing abnormal proliferation of blood vessels - Port wine stain on the face - Glaucoma, ipsilateral haemangiomas, hemiplegia and learning difficulties
418
What can Pierre-robin syndrome cause?
- Micrognathia - Cleft palate - Glossoptosis
419
What can Riley Day syndrome cause?
Insensitivity to pain, causing burning, biting and blistering of the body.
420
What is Peutz-Jeghers Syndrome?
Genetically inherited condition - Perioral pigmentation presents via multiple benign freckles. - Intra-oral pigmentation, with multiple blood listers on lips and oral cavity. - Genetic risk of bowel cancer
421
What is Tuberous sclerosis?
AD resulting in a loss of control of cell growth and division - Patients have increased benign tumour formation - Results in patches of fibromas on the skin, with multiple small raised lobules
422
What is Ehlers Danlos syndrome?
Mutations in genes responsible for collagen production - Hyperplastic skin and hypermobile joints - Aneurysm, GI bleeds and easy bruising - Mitral valve prolapses and incompetence - Dental features: recurrent TMJ dislocation, deep fissures premolars, short deformed roots and multiple large pulp stones, early onset periodontal disease.
423
What is hereditary haemorrhagic telangiectasia?
Rare autosomal dominant genetic disorder that leads to abnormal blood vessel formation. - presence of multiple telangiectasia of the skin and mucous membranes.
424
What is Treacher Collins Syndrome?
- Rare AD mandibulofacial dysostosis due to mutation in the TCOF1 gene > Underdeveloped zygoma > Micrognathia > Malformed or absent ears
425
What is Melkerson Rosenthal Syndrome?
Recurring facial palsy Facial swelling (granulomatous cheilitis) Fissured tongue
426
What is Heerfordt syndrome?
Rare syndrome seen with sarcoidosis, causes parotid and lacrimal gland swellings.
427
What does ABCDE stand for?
Airway: look for signs of airway obstruction, give 02 at high concentration (15 I/min), use airway adjuncts appropriately Breathing: assess the breathing (look, listen, feel), record the SaO2 reading of pulse oximeter and inspired oxygen concentration (%). If breathing reduced, then use bag-valve-mask ventilation Circulation: assess for pulse, blood pressure and capillary refill time, if no pulse start CPR Disability: blood glucose, consciousness and gross neurological exam Exposure: rashes, blood loss, comfort, dignity and check patients’ medication and allergies
428
Asthma: Assessment + management
A: noisy laboured breathing, classic wheeze, unable to communicate, using accessory muscles for respiration B: RR usually increased, SpO2 may be reduced, cyanosis if very serious - C: HR usually increased Assess if acute severe asthma or life-threating asthma Management > Give Oxygen to maintain SpO2 > 94% > B2 agonist bronchodilators: Salbutamol
429
Anaphylaxis: Assessment + management
A: airway obstruction due to swelling, may have a stridor or wheeze and breathing issues B: increased RR, reduced SpO2 - C: tachycardia, hypotension, pale and clammy Management > Give Oxygen to maintain SpO2 > 94% IM adrenaline 0.5mg (0.5mI) of 1:1000 Adrenaline Advanced: IV antihistamine, corticosteroid, tracheal intubation and ventilator
430
Acute coronary syndrome: Assessment + management
Unstable Angina, NSTEMI, STEMI Management (MONA) Morphine Oxygen (15 I/min) Nitrates (GTN spray given sublingually) Aspirin
431
Epilepsy: Assessment + management
- Oxygen 15 I/min to maintain SpO2 > 94% Protect patient from injury during the tonic-clonic fit, place in recovery position - Do not attempt to place anything in mouth - Check capillary glucose and treat if hypoglycaemia Buccal Midazolam 10mg
432
Hypoglycaemia: Assessment + management
Blood glucose < 3mmol/I - History of diabetes Management > Oral glucose (Lucozade) > Buccal glucose gel (Hypostop) or 1mg Glucagon IM > Follow up with high carbohydrate meal
433
Name some potentially malignant lesions (6)
Leukoplakia Proliferative verrucous leukoplakia (PVL) Erythroplakia Oral lichen planus Actinic cheilitis (lip only) Oral submucous fibrosis
434
What is hyperplasia?
Increased number of cells in an organ/tissue that appear normal under a microscope
435
What is dysplasia?
Cells look abnormal under microscope but are not cancer
436
What changes in structure can be seen in histology?
1. Disruption and merging of layers 2. Basal cell hyperplasia, replacing prickle cell layer and drop shaped rete ridges
437
What changes in cytological features can be seen in histology?
1. Pleomorphic cells 2. Increase in cell size (hypertrophy) 3. Loss of polarity and intercellular adhesion 4. Nuclear pleomorphism, hyperchromatic-' more prominent
438
What changes to functional aspects be seen in histology?
1. Mitotic figures, mitoses in suprabasal area and abnormal forms 2. Aberrant and hyperkeratinisation
439
What are the grades of dsyplasia?
1. Mild - just lower third 2. Moderate - middle and lower third > clinically monitored and risk factors removed 3. Severe - top to bottom dysplasia, indicative of progression to malignancy normally > excision should be completed 4. Dysplastic cells invade through the basement membrane, causing cancer
440
What is the management of dysplasia?
No evidence to suggest any medical treatment has any effect on outcome. Small evidence for Vit A, retinoid, Beta carotene and lycopene may resolve dysplasia Evidence for surgical excision of high grade dysplastic lesions Removal of predisposing factors (cessation of smoking and alcoholism)
441
What is leukoplakia?
Any white lesion that cannot be identified pathologically or clinically and is not related to physical or chemical causes other than smoking
442
What are the features of leukoplakia?
> diagnosis of exclusion: non-scrapable, unilateral > homogenous or non-homogenous - homogenous = generally uniform white appearance - non-homogenous = mixed colour that is predominantly white -- much higher transformation rate to OSCC -- less well circumscribed lesion > hyperkeratinisation and epithelial hyperplasia > 1% transformation rate to malignancy > buccal mucosa, lateral and ventral tongue, floor of mouth, retromolar pad and soft palate higher malignancy risk sites Clinical features: thin, flat grey/white fissure lesion, may progress to become thicker white plaques.
443
What is the risk of transformation of leukoplakia to OSCC and which are the higher malignancy risk sites?
1% transformation rate to OSCC Buccal mucosa, dorsal and ventral surface of the tongue, floor of mouth, retromolar pad area and soft palate.
444
What is the definition of erythroplakia?
Refers to any red lesions that cannot be identified pathologically or clinically - very rare but associated with a high rate of malignancy - link with smoking - biopsy is mandatory-field mapping, often reveals carcinomas
445
What is proliferative verrucous leukoplakia?
A variant of leukoplakia, presenting are white, rough irregular surface which slowly expands. - Other similar lesions may occur simultaneously and coalesce - Normally appears on the gingiva - Very high risk of progression to malignancy - Slow persistent growing lesion with high recurrence rate
446
What is oral submucous fibrosis?
Palate and buccal mucosa appear very white and fibrotic - Tissues immobile and begin to contract due to the tissue becoming fibrotic - Often trismus and extensive scarring - Leather like feel due to fibrotic scar tissue - Malignant transformation very high - Normally due to betel and areca nut chewing, lime and tobacco.
447
What is discoid lupus erythematosus?
Autoimmune condition that presents like lichen planus
448
What is the presence of OC in UK and 2 year mortality rate?
9000 cases per year in UK 2-year mortality rate of 35%
449
What are some risk factors of oral cancer? (9)
1. smoking 2. alcohol 3. diet 4. UV sunlight 5. HPV infection 6. Betel quid 7. Preserved and salted foods 8. Poor oral hygiene 9. Occuspation exposure
450
What are 7 premalignant diseases?
1. Chronic hyperplastic candidosis 2. Leukoplakia/erythroleukoplakia 3. Erythroplakia 4. Oral lichen planus 5. Submucous fibrosis 6. Actinic cheilitis 7. Discoid lupus erythematosus
451
What are 5 clinical features of oral cancer?
1. Ulcers that do not heal after 3 weeks 2. White or red patches in the mouth or throat 3. Induration (hardening) or the lesion 4. Mimicking of other benign lesions may lead to delayed diagnosis 5. Non-homogenous lesion
452
What are red flag symptoms for oral cancer? (6)
1. >3 weeks duration 2. Dysphagia and dysarthria (difficulty swallowing and speaking) 3. Lumps and tumours in the neck 4. Sudden unexplained weight loss 5. Halitosis 6. Persistent unilateral ulcers, pain and discomfort in the mouth
453
How do you diagnose mouth cancer?
Biopsy with histopathological examination Nasoendoscopy Fine needle aspiration Panendoscopy
454
What is oral squamous cell carcinoma?
Carcinoma with malignant neoplasm of stratified squamous epithelium.
455
What % of oral cavity cancers are SCC?
90% - Most oral cancers occur in patients 50-70 years old, more common in males - Very high incidence in south east asia
456
What is the 5 year survival rates of OSCC dependent on TNM?
Stage 1 TMN = 50% Stage 2 TMN = 50% Stage 3 TMN = 26.3% Stage 4 TMN = 20%
457
What is the spread of oral cancer?
Commonly involved lateral border of the tongue Common site of bone invasion is lingual aspect of mandible Lymphatic system Distant metastasis to bone, lung and liver Invasion of soft tissues and muscles, bone, veins and perineural system
458
What are prognostic indicators of OC?
Site: prognosis worse towards back of mouth Size: the larger the tumour the worse the prognosis Nodal involvement: presence makes prognosis worse, extracapsular spread = Level IV Distant metastasis to lung, liver or brain provides worse prognosis.
459
What are bad prognosis pathological indicators?
More differentiation Pattern of invasive edges Perineural invasion (PNI) Lymph vascular invasion (LV) If thickness >4mm adequacy of surgical excision (clearance >5mm around the margin) Any dysplasia at margin
460
What is the histology of oral cancer?
Adenosquamous provides very poor prognosis for patient Histology of SCC = invasion through basement membrane Dysplastic epithelium (cellular pleomorphism), especially in the epithelium. Tumour cells invade through the basement membrane and then invade connective tissue Do not see perineural invasion and lymph vascular invasion in dysplasia, only cancer
461
What are treatment options to OC?
1. Surgery > Very successful for early stage mouth cancer > Depends on size, depth and metastatic level (lymph node spreading) > Potential neck dissection if the cancer has spread to lymph nodes 2. Radiotherapy 3. Chemotherapy > If cancer has returned after surgery and radiotherapy > Treat locally advanced cancer 4. Chemoradiation (chemo with radiotherapy) > used for locally advanced cancer
462
What are problems with oral cancer?
Late presentation Morbidity and mortality Second primary tumours
463
What is the maximum time from urgent GP referral or suspected cancer to treatment if necessary?
GP referral --> Specialist (14 days max) --> Decision to treat --> First treatment (31 days max)
464
What is the epidemiology of oral cancer?
- Incidence of head and neck cancer has increased by 50% since 1989 even though alcohol and smoking levels have fallen. - % of men aged 40-64 the rates have doubled in last 30 years. Oropharynx cancer rates have increased massively - HPV 16 and 18 levels have increased > HPV cancers have favourable prognosis, with longer, stage specific survival > Sexually transmitted disease > Predicted responses to chemotherapy and chemoradiation in later stage tumours > Due to viral integration invading the nuclei of the mucosa - G1 arrest due to P53, as well as managing apoptosis > however, E6 down regulated P53, stopping G1 stage arrest and apoptosis = unregulated cell growth - HPV viral proteins (E7) interacts with pRb, causing increased expression of p16 protein > P16 over expression can be detected histologically, allowing diagnosis of malignancy > P16 positive results result in brown staining
465
What are the borders of the maxillary sinus?
Superior = floor of orbit Inferior = hard palate and roots of posterior maxillary teeth Medial = Lateral wall of the nose
466
What type of epithelium lines the maxillary sinus?
Ciliated columnar epithelium
467
What is sinusitis?
inflammation of the lining epithelium of the maxillary sinus
468
What can cause sinusitis? (3)
1. Spread of nasal infection 2. Nasal allergies 3. Infections from root and OAF/OAC
469
What is the pathology of sinusitis?
- Increase secreting from lining epithelium - Increase in ciliary activity, eventually cilia are destroyed - Thickening of mucous membrane - Fibrosis
470
What are signs and symptoms of sinusitis? (4)
Acute pain in upper teeth Beating sensation in cheek Nasal discharge Chronic --> thickened polypoid mucous membrane, purulent nasal discharge and oro-antralfistula (OAF)
471
What investigations can you do for sinusitis? (3)
Fluid levels in the maxillary antrum Mucosal thickening Radiopaque sinus
472
What is the management for sinusitis? (3)
Analgesics Antibiotics Nasal decongestants
473
What is an oro-antral fistula (OAF)?
An abnormal opening between the oral cavity and the maxillary sinus antrus, happens after XLA of upper posterior teeth if roots extend into sinus. Is lined by epithelium.
474
What is the tx of oro-antral fistula? (3)
1. Suture across the socket, either horizontal mattress or construct splint. 2. Close fistula via buccal flap with bilateral relieving incisions then buccal fat pad sutured into cavity walls, then trim buccal plate. 3. Scar tissue excision if necessary and mucosal wound closed.
475
What is frontal sinus sinusitis?
- Frontal sinus has great variation in size and shape. Lined by columnar epithelium. - Sinusitis of frontal sinus normally accompanies acute ethmoiditis. Symptoms: vacuum frontal headache, with pain above the eyes and vision problems. - Clinical features: oedema of brow and upper eyelid area, v swollen. - Complications: infection can spread to cranium and orbit
476
What is ethmoidal sinusitis?
Ethmoid has small air spaces, in the upper part of the lateral wall of the nose. Borders > Lateral = orbit > Inferior = maxillary sinus - Lined by ciliated columnar epithelium. - Symptoms: pain behind the eyes, tender medial canthus - Clinical features: complete eyelid closure and subperiosteal swelling
477
What is sphenoid sinusitis?
Occupies the body of the sphenoid. Bodies > Lateral = cavernous sinus > Superior = pituitary > Floor = nerve of the pterygoid canal - Usually part of generalised sinusitis - Symptoms: pain in middle part of the skull, temporal region and down the neck Suppuration present in phenoethmoidal recess
478
What are the paranasal sinuses?
Consist of the ethmoid, sphenoid, frontal sinuses and maxillary antrum
479
What is the pterygopalatine fossa?
Posterior wall of maxillary antrum Communicates with foramen rotundum, masticator, infra-orbital fissure and vidian canal
480
What is the drainage of the paranasal sinuses?
Sphenoid = spenoethmoidal recess Posterior ethmoid = superior concha Frontal, maxillary antrum and middle ethmoid = middle concha Nasolacrimal duct = inferior concha
481
How can you image the maxillary anturm?
Plain film: DPT or Intra-oral Cross sectional imaging: CT or MRI
482
What abnormalities can occur with the maxillary antrum?
Developmental Acquired > Inflammatory sinus disease, thickening of mucosa at base of sinus. Complete opacification, may also have sclerosis of surrounding bone. > Traumatic > Cystic > Neoplasms Fibrous dysplasia Paget's disease Osteopetrosis Thalassemia
483
How can a mucus retention cyst affect the maxillary antrum?
Mucus retention cyst will cause a changing of antrum shape, a benign tumour. Will formulate from base of the antrum, affecting the well corticated margin of the antrum.
484
What things do you need to describe for a radiolucency of the jaw?
Site and anatomical position Size Shape Outline and edge of the periphery (Corticated) Relative radiodensity Effects on adjacent structures (root resorption, expansions and displacement, closer relationship with ID canal) Time present
485
What are differentials for a unilocular radiolucency?
1. Radicular cyst 2. Periapical granuloma 3. Residual cyst 4. Lateral periodontal cyst 5. Dentigerous cyst 6. Stafne idiopathic bone cavity 7. Nasopalatine duct cyst 8. Solitary bone cyst 9. Unicystic ameloblasoma
486
What are differentials for multilocular radiolucencies?
Odontogenic tumours Odontogenic keratocyst Ameloblastoma Ameloblastic fibro-odontoma Central Giant Cell Granuloma Odontogenic Myxoma
487
What is a radicular cyst? most common site? description?
- UR2 most common, palatal swelling - Apex of a non-vital tooth - Uniform radiolucency >1.5cm, can displace teeth and press on IDN canal - Buccal expansion seen on upper occlusal - Round/oval shape, well corticated that envelopes the apices - Root resorption, bone expansion - Cyst may displace the IDB in an inferior direction if large enough
488
How can you distinguish a periapical granuloma from a radicular cyst?
Periapical granuloma and radicular cyst cannot be distinguished radiographically alone, differential is well defined corticated border more than 2cm in diameter (cyst)
489
What is a residual cyst?
Post XLA cyst Radicular cyst but in the presence of a previously pathological extracted tooth. Round or oval shaped, well corticated, uniformly radiolucent >1.5 cm.
490
What is a lateral periodontal cyst?
Developmental cyst present between roots of vital teeth. - Small <1cm, unilocular uniform radiolucency that is smooth, well defined and corticated. - Can cause buccal expansion and root resorption - Botryoid cyst = lateral periodontal cyst that is multilocular.
491
What is a dentigerous cyst?
Developmental cysts normally of the 3s and 8s. Cyst that forms around coronal aspects of unerupted teeth Remnants of the reduced enamel epithelium after tooth formation. Unilocular well defined, corticated radiolucency, oval or round shape, size >3-4mm Can displace teeth and resorb roots Expand outer cortex of jaw bone Can displace the maxillary antrum and ID canal
492
What is significant about cysts below the IDN canal?
They are NON-ODONTOGENIC
493
What is a stafne idiopathic bone cavity?
Radiographically appears like a cyst Always present below the IDN canal Unilateral Lingual surface/angle of mandible/around area of submandibular fossa
494
What is a nasopalatine duct cyst?
Epithelial remnants of the nasopalatine duct or incisive canal. A round or oval shaped, smooth, well defined, corticated unilocular uniform radiolucency. Midline anterior maxilla located, >6cm in size Can displace teeth distally, palatal expansion, rarely resorb teeth Cyst appears in palate as hard mass
495
What is a solitary bone cyst?
Seen in young people, normally due to trauma. Unilocular, corticated, well defined They appear between roots of teeth, but don't cause
496
What are characteristics of an odontogenic tumour?
Can displace or resorb teeth Halo effect around the tumour Extrinsic to antrum but can invade sinus and/or expand and destroy its margins Opacify air spaced.
497
What is an odontogenic keratocyst?
An odontogenic tumour originating from dental lamina epithelium. Most common site is posterior angle of mandible and anterior maxilla canine regions. Variable size. Oval, multilocular, smooth, scalloped, well defined corticated uniform radiolucency. Tooth displacement, but rarely resorb. Extensive expansion within cancellous bone. Considerable risk of recurrence due to daughter/satellite cells/cysts.
498
What is an ameloblastoma?
A true neoplasm of odontogenic epithelium of enamel organ. Most common in posterior mandible. Persistent. locally invasive tumour. Infiltrates connective tissue wall of the cyst, invading medullary bone spaces. Variable size, can be v large and disfiguring. Multilocular, smooth, scalloped, corticated radiolucency with raiopaque septa. Resorb and displace teeth and IDN canal, enormous rapid expansion potential. Honey comb or soap bubble appearance. Children: ameloblastomafibroma is more aggressive, but causes rapid resorption and displacement of teeth alongside rapid and extensive expansion.
499
What is a unicystic ameloblastoma?
This is unilocular. May be difficult to differentiate radiographically from a dentigerous cyst. However, it causes apical displacement of unerupted teeth, unlike dentigerous cyst. associated with impacted, displaced teeth showing incomplete root formation. Present as painless swelling Most common in posterior mandible (ramus region)
500
What is an ameloblastic fibro-odontoma?
Ameloblast with denticles present, resorption, displacement and extensive expansion. Benign true mixed odontogenic tumours. Painless, slow growing expansion, involves displacement of involved teeth. Very rare.
501
What is a central giant cell granuloma?
Benign Anterior to molars common in the mandible More granular and ill-defined septae than OKC Expansion of bone Central = bone Peripheral = gingival tissue
502
What is an odontogenic myxoma?
A benign intraosseous neoplasm that arise from ectomesenchyme. - Premolar and molar region of mandible. - Straight, thin septa - Grow in length of bone, no root resorption. - Slow growing, painless lesion, may invade maxillary sinus. - High recurrence rate (not encapsulated) - No expansion of bone, grows along the length of the bone. - Tennis racket appearance due to straight and thin septa.
503
What are general differences between cysts and tumours?
Cysts more commonly expand buccally first, however tumours will have irregular expansion. Cysts tend to not involve dental roots, whilst tumours will affect roots of multiple teeth.
504
Name 4 giant cell lesions
1. Aneurysmal bone cyst 2. Cherubism 3. Browns tumour 4. Central giant cell granuloma
505
What does hyperparathyroidism cause? (3)
Generalised demineralisation Brown tumours Cystic changes
506
What is cherubism and what does it cause?
It is a familial fibrous dysplasia Rare inherited developmental abnormality causing bilateral enlargement of jaws. Painless, firm, bilateral mandibular enlargement. Slow growing and expansive growth of lesion Submandibular lymphadenopathy Soap bubble appearance of lesions
507
What do different periosteal reactions indicate?
Onion skin = benign lesion Codman's triangle or Sunburst = malignant
508
Which unilocular radiolucency may be found in this location: a) midline of maxilla b) apex of non-vital teeth c) apex of vital teeth d) crown of impacted teeth e) inferior to IDB canal f) apex of extraction site g) between roots of teeth
a) midline of maxilla = nasopalatine cyst b) apex of non-vital teeth = radicular cyst or periapical granuloma c) apex of vital teeth = cementoma d) crown of impacted teeth = dentigerous cyst e) inferior to IDB canal = stafne bone cyst f) apex of extraction site = residual cyst g) between roots of teeth = lateral periodontal cyst
509
Which multilocular radiolucency may be found here: a) peri coronal unerupted/impacted teeth b) posterior body of mandible c) balloon lobules mandibular d) honeycomb mandibular e) soap bubble posterior mandible f) tennis racket ramus mandible g) bilateral expansive soap bubble h) soap bubble brown tumour
a) peri coronal unerupted/impacted teeth = calcified epithelial odontogenic tumour b) posterior body of mandible = keratocyst c) balloon lobules mandibular = aneurysmal bone cyst d) honeycomb mandibular = central giant cell granuloma e) soap bubble posterior mandible = ameloblastoma f) tennis racket ramus mandible = odontogenic myxoma g) bilateral expansive soap bubble = cherubism h) soap bubble brown tumour = hyperparathyroidism
510
What radiopacity abnormality can be found in the jaw?
1) unerupted teeth 2) supernumeraries or mesio-dens 3) Misplaced teeth (ectopic canines) 4) Odontomes (complex and compound) 5) Retained roots 6) Hypercementosis 7) Exostoses 8) Sclerosing osteitis 9) Periapical idiopathic osteosclerosis
511
What are the 2 types of odontomas?
1) Complex = unorganised mass of dental tissue in the posterior mandible, can cause tooth and IDN canal displacement. 2) Compound = multiple denticles present in the anterior maxilla
512
What is hypercementosis and what may it be caused by?
Formation of excessive amounts of cementum, usually around the apical area. > Paget's disease, acromegaly, gigantism. > Completely asymptomatic, with premolars and molars affected > Teeth vital and not TTP > Normal bone replaced via cellular remodelling to disorganised bone
513
What are exostoses?
- Mandibular tori can undergo increased density and volume of bone deposited. - situated in periphery of jaws, vary in size, shape and location. - Slow growing benign bony protuberances - torus palatinus and torus mandibularis
514
What is sclerosing osteitis?
Periapical inflammation of bone due to dental infection, not necessarily malignant
515
What is periapical idiopathic osteosclerosis?
Affect 6s, 4s and 3s. Teeth normally healthy with vital pulp and asymptomatic Mucosa appears normal Candy floss appearance at apex of affected tooth, shape and density may vary.
516
What radiographic feature may be present with hyperparathyroidism?
Hypercementosis, has cotton wool appearance
517
What is osteomyelitis?
Infection and inflammation of the bone marrow occurring in the jaw, very common complication of odontogenic infection (mandibular area normally) . Polymicrobial opportunistic infection (streptococci and anaerobes) - Pain, severe, throbbing and deep - Trismus - Swelling - Fibromyalgia - Virus like symptoms of malaise and fever Acute: ragged, patchy, moth eaten appearance of radiolucency to the bone with radiopaque sequestrate of dead bone. Present <1 month Chronic: localised patchy areas of destruction, with sclerosis of surrounding bone and radiopaque sequestrate
518
How does the radiographic appearance of acute and chronic osteomyelitis differ?
Acute: ragged, moth eaten appearance of radiolucency to the bone with radiopaque sequestrate of dead bone. Present <1 month. Chronic: localised patchy areas of destruction, with sclerosis of surrounding bone and radiopaque sequestrate. Acute: - mixed radiolucent and radiopaque appearance - trabeculae has lost sharpness - moth eaten appearance on radiograph - sequestra may be present - suppuration and sinus present Chronic: - mixed radiolucent and radiopaque appearance - sequestra more common in chronic - sclerosis of surrounding bone - granulation tissue and new blood vessels
519
What is sclerosing osteitis?
Sclerosis of bone induced by inflammation or infection occurring in a pulpal-apical lesion. - Proliferation of bone tissue - Has an acute and chronic variation of the disease - Acute = patchy and moth eaten radiolucent appearance of bone. - Chronic = patchy and moth eaten with radiopaque sequestra - Asymptomatic, no cortex expansion with mucosa normal appearance - Non-vital teeth - Tx: XLA or RCT
520
What are calcifying epithelial odontogenic tumours? (CEOT)
- Very rare, in posterior mandible - Unilocular/multilocular, round often associated with un-erupted or impacted tooth - Patchy radiopacities in a radiolucent lesion - Driven snow appearance - Rapid expansion with teeth resorption and displacement - Pindborg tumour
521
What is an Adenomatoid odontogenic tumour (AOT)?
Epithelium embedded in a connective tissue stroma, with slow and progressive growth - 90% before age of 30 - Anterior maxilla (canine region) in unerupted impacted teeth - Unilocular, well defined and corticated often surround entirety of un-erupted teeth - snow flake appearance - buccal and palatal expansion with teeth displacement
522
What is a calcifying cystic odontogenic tumour? (CCOT)
- gorlin cysts - locally invasive epithelial odontogenic neoplasm - maxilla or mandible in anterior or premolar regions often of impacted tooth - unilocular round, well defined and corticated - scattered radiopacities within the lesion - Driven snow appearance - Variable amount of calcified internal material - Bone expansion, teeth displacement and root divergence.
523
What is a cementoblastoma?
Apex of mandibular first molars Attached to tooth root with a round golf ball appearance Well defined, round and irregular shaped Radiopaque with thin radiolucent line of outer zone osteoid Attached to obscured roots
524
What are 2 types of osteomas?
Compact (dense lamellae bone) Cancellous (trabeculae bone) - asymptomatic and uncommon (young adults mainly), radiolucent lesions - Gardner's syndrome: autosomal dominant disorder characterised by multiple osteomas
525
What is a key characteristic of Gardner's syndrome?
Multiple osteomas
526
What is an osteosarcoma?
Primary malignant tumour of bone, with poorly defined and variable radiopacity appearance.
527
What are the 3 types of osseous dysplasia and what are their site, size, shape, outline, effects and appearance?
Peripheral osseous - apices of multiple lower anterior teeth - small 5-6mm - round unilocular - corticated - no expansion, displacement or resorption - radiopaque with peripheral radiolucency Focal osseous - posterior mandibule solitary - small - round unilocular - corticated - no expansion, displacement or resorption - radiopaque with peripheral radiolucency Florid osseous - multiple quadrants - large >2cm - round unilocular - variable - expansion, no teeth affect - Radiopaque with peripheral radiolucency
528
What is familial gigantiform osseous dysplasia?
Rare, autosomal dominant 10-20 year old white females Rapid growth with marked facial deformity
529
What is ossifying fibroma?
affects mandible variable size, can cause deformity round unilocular, smooth, well defined lesion that's encapsulated teeth displaced, with downward bowing of mandible
530
What are the dental risks in pregnacy?
Fungal infections - oral candidosis Gingivitis Foetal alcohol syndrome Blue baby syndrome
531
What is pregnancy epulis?
Pregnancy gingivitis is caused by hormonal changes during pregnancy and causes increased inflammatory response to plaque and other irritants which in turn causes pregnancy epulis. Commonly occur in 3rd trimester
532
How do you treat pregnancy epulis?
OHI, lesion resolves spontaneously after giving birth, if not --> excision, cryotherapy. Don't excise during pregnancy as it tends to reoccur
533
Do you treat pregnant women?
Treat only in emergencies, if not, 6 weeks after delivery
534
Pregnancy: What antibiotics are safe? Contraindicated?
Safe: 1) amoxicillin 2) erythromycin Contraindicated: 1) tetracyclines - ingredient in ledermix
535
Pregnancy: which analgesics are safe? contraindicated?
Safe: 1) paracetamol 2) codeine Contraindicated: 1) NSAID - aspirin, ibuprofen
536
Pregnancy: which LA is safe? Contraindicated?
LA crosses placenta in varying degree Safe: 1) lidocaine - considered safe due to the low (adrenaline) and the unlikely of affect of affecting uterine blood flow Unsafe: 1) Articaine - can cause methomoglobinemia --> blue-baby syndrome 2) Prilocaine - contains felypressin which can induce labour
537
Why is articaine unsafe to use in pregnant women?
Can cause blue baby syndrome due to causing methemoglobinemia.
538
Why is prilocaine contraindicated in pregnant women?
Prilocaine contains Felypressin which can induce labour
539
Pregnancy: which RCT medicaments are safe? contraindicated?
Safe: 1) Hypocal (CaOH) Contraindicated: 1) Ledermix - contains Demeclocycline (tetracycline) 2) Odontopaste - containe triamcinolone acetonide (corticosteroid)
540
Can benzodiazepines sedation be used in pregnant women?
NO! Benzodiazepines are contraindicated in pregnant women
541
Can inhalation sedation be performed in pregnant women?
NO! NO2 is contraindicated in pregnant women
542