Oral medicine Flashcards
What are the layers of normal oral tissue? (4)
- Oral epithelium
– Keratin layer
– Granular cell layer
– Prickle layer
– Basal layer - Basement membrane
- Lamina propria
– Papillary layer
– Dense fibrous layer - Connective tissue
What is stratified squamous epithelium?
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.
What are the layers of the oral epithelium (4)
- Keratin layer
- Granular cell layer: contains granuloma cells, thin layer
- Prickle layer: stratum spinosum cells (in the form of star cells)
- Basal layer: mitosis happens here
What makes up the lamina propria? (2)
- Papillary layer - contains nerves, capillaries (blood vessels), lymph vessels
- Dense fibrous layer - fibers laid down on top of each other
What oral tissues have non-keratinised epithelium? (5)
Buccal mucosa
Labial mucosa
Ventrum of the tongue
Floor of the mouth
Soft palate
What oral tissues have keratinised epithelium? (3)
Dorsum of the tongue
Hard palate
Gingivae
What are the 4 different types of papillae? Appearance and function?
- Filiform papillae - NOT TASTE BUDS, small, round
- Fungiform papillae - taste buds present, mushroom shape
- Circumvallate papillae - largest, on the back 1/3 of the tongue, located in V-shape, taste buds.
- Foliate papillae - leaf-shaped, located on side borders of tongue, taste buds.
What are the tongue papillae which have NO taste buds?
Filiform papillae
What are fordyce spots?
Prominent intra-oral sebacous glands
What is a biopsy?
It is the sampling of tissue for histological assessment, diagnosis and therapy
e.g. incisional biopsy, excisional biopsy
What is an excisional biopsy?
Remove all clinically abnormal tissue with a margin surrounding the lesion
What is used immediately after an excisional biopsy?
Formalin
It prevents drying, autolysis and putrefaction (decay/rotting)
Aids straining and tissue preparation in the laboratory
What is H+E staining?
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.
What are 4 types of special stains?
Periodic acid Schiff = mucins, glycogen and fungi
Gram stain = bacteria
Ziehl Neelsen = mycobacteria
Congo red = amyloid
Immunohistochemistry - what is a monoclonal antibody test?
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.
What is a frozen section?
Rapid freezing of samples, with immediate assessment (15-30 mins for results)
- usually with intra-operative assessment when patient still under GA
- Cryostat
What is fine needle aspiration cytology?
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
What are the advantages and disadvantages of cytology?
Advantages: low cost, fast speed of diagnosis and negligible morbidity or complications.
Disadvantages: tissue architecture not represented and triage only applicable sometimes.
What is immunofluorescence mainly used for and what are the 2 types?
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.
What are differences between histology and cytology?
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.
What type of test is specific to candida infections?
Periodic Acid Schiff Test
PASD = periodic acid schiff with digestion
How do you manage chronic facial pain?
- 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)
What are different types of immunosuppressants and what is their general aim?
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
How do calcineurin inhibitors work? what do they usually treat? examples?
- 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
- Autoimmune disorders and atopic eczema.
Organ and bone marrow transplants as well as inflammatory conditions such as ulcerative colitis, rheumatoid arthritis, and atopic dermatitis - Cyclosporine and tacrolimus
How do pyrimidine synthesis inhibitors work? what do they usually treat? examples?
- 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
- Pyrimidine synthesis inhibitors are used to treat multiple sclerosis and rheumatoid arthritis.
- Leflunomide, Teriflunomide, (Methotrexate)
How do purine synthesis inhibitors work? what do they usually treat? examples?
- Suppress the immune system by preventing DNA synthesis and cell proliferation
- Rheumatoid arthritis, Crohn’s disease and ulcerative colitis, skin conditions such as lupus, and helps after an organ transplant to prevent rejection.
- mycophenolate mofetil and azathioprine
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.
What are barrier preparation used for and name 2 examples.
They produce a covering for lesions such as ulceration.
Gelclair and Orabase
What are risks of immunsuppression? (3)
- Increased risk of opportunistic infections such as candida and herpes
- Increased risk of poor wound healing and subsequent infection
- Increased risk of malignancy, lymphomas, skin and lip cancer.
What happens when aspirin and warfarin are taken together?
Increased risk of bleeding! do not take together
What happens when azole antifungals are taken with warfarin?
Decreased clearance of warfarin = increased warfarin = increased INR
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
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
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?
What are features of anaemia? (4)
- Atrophic glossitis - appears as very smooth glossy tongue that is tender and painful
- Angular cheilitis - inflammatory condition at the corners of the mouth
- Aphthous stomatitis ulceration
- Dysesthesis - an unpleassant sensation felt when touched due to peripheral nerve damage.
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
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.
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.
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.
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.
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.
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.
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.
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.
What medications can cause gingival hyperplasia?
Cyclosporine (immunosuppressant)
Phenytoin (anti-convulsant)
Nifedipine (calcium channel blocker)
— also amlodipine, diltiazem, felodipine, and verapamil
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
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
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
What medications can cause lichenoid like lesions?
- Anti-hypertensive
- Beta-blockers
- Metformin
- Thiazide diuretics
- Furosemide
- Spironolactone
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
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.
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
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
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
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.
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.
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
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
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
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)
What is an ulcer? (definition)
A break in the epithelial continuity, usually due to lamina propria damage.
What is erosion? (definition)
A superficial break in epithelial continuity with lamina propria intact.
What is desquamation? (definition)
Used to describe thinning of the epithelium with a red appearance.
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.
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.
What are common causes of recurrent oral mucosal ulcerations?
- Recurrent aphthous ulceration
- Aphthous like ulceration
- Erythema multiforme
- Recurrent intra-oral herpetic ulceration
What diseases should we consider if there is recurrent ulceration with chronic oral inflammatory disease?
- Oral lichen planus
- Mucous membrane pemphigoid
- Pemphigus vulgaris
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.
What are the characteristics of recurrent aphthous ulceration?
- Clinically present in childhood or adolescence
- Resolve with age
- Family history
- Recurrence
What is the aetiology of recurrent aphthous ulceration?
Immunologically mediated T cell action with humoral component (antibody dependant cytotoxicity reaction)
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)
What are the classification of recurrent aphthous ulceration?
- Minor
= 2-6 per outbreak lasting up to 10 days.
= involving non-keratinised mucosa
= heal with no scarring - 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 - Major
= large >1cm diameter lasting lasting >1 months
= involving both keratinised and non-keratinised mucosa
= heal by secondary infection often with scarring
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.)
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
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
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
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.
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.
What is Behcet’s syndrome triad?
- Recurrent oral ulcers
- Genital ulcers
- Ocular disease, such as uveitis with hypopyon
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)
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
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
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)
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.
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.
Which systemic conditions present with aphthous-like ulcers?
- Vitamin B12 deficiency
- Folate deficiency
- Iron deficiency
- Coeliac disease
- Crohn’s disease
- Ulcerative colitis
- Behcet’s syndrome
- Reiter’s syndrome (reactive arthritis)
- Immunodeficiency, such as neutropenia, HIV infection
- Epstein-barr virus infection (glandular fever)
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.
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.
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.
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.
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.
When should you suspect if someone has ulcerative colitis?
Suspect if the person has left-sided abdominal pain and bloody diarrhoea.
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.
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.
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
When should you suspect if someone has glandular fever?
Suspect if the person has other features of glandular fever.
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.
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.
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.
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.
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
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.
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
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.
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.
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
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
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
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
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
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.
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.
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.
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
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
What are complications of MMP?
Skin blistering and ulceration
Genital and eye involvement
Pharyngeal involvement, causing stricture formation and dysphagia
Oral involvement
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.
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.
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.
How do you diagnose pemphigus vulgaris?
histological exam, high numbers of haemoxylin and eosin
Blood sample (indirect) or Direct IF
How does pemphigus vulgaris appear in direct immunofluorescence?
Fishnet appearance
What are the results from a biopsy for positive PV?
rounded up separated keratinocytes
What is the treatment of pemphigus vulgaris?
Systemic and topical steroids or immunosuppressive agents
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
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.
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
Why can lesions appear red?
Atrophic epithelium
Reduction in number of epithelial cells
Increased vascularity in lamina propria
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.
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.
What are differential diagnoses of white patch lesions?
- Variation of normal anatomy:
> fordyce spots
> leukoedema - Hereditary causes:
> white sponge naevus - Infections causes:
> fungal: candidosis
> viral: oral hairy leukoplakia (EBV)
> bacterial: syphilis - Inflammatory causes:
> oral submucous fibrosis
> erythema migrans (geographic tongue) - Idiopathic causes:
> Leukoplakia - Systemic causes/immunological causes?
> oral lichen planus
> oral lichenoid lesions
> graft vs host disease
> systemic/discoid lupus erythematosus - Reactive causes
> frictional keratosis
> occlusal keratosis
> tobacco associated lesions
> chemical burns
> thermal burns
> actinic cheilitis
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.
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
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
What are 7 forms of oral endogenous diffuse pigmentation?
- Oral melanotic macules (ephelis)
- Racial pigmentation
- Addison’s disease
- ACTH producing tumours
- Physiological pigmentation of pregnancy (melasma)
- Peutz Jeghers syndrome
- Post inflammatory melanin incontinence.
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
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).
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.
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.
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
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
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.
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
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
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
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
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
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
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.
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
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
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.
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
What test can be used for TB and actinomycosis?
MC&S (microscopy, culture and sensitivity) for TB and actinomycosis
Name 5 congential cysts
Lymphangioma
Dermoid cysts
Thyroglossal cysts
Brachial cysts
Pharyngeal pouch
Name 7 causes of acquired cysts?
Trauma, infective, inflammatory, iatrogenic, neoplastic, metabolic, autoimmune.
What are 6 development causes of lumps and swelling of the oral cavity and lips?
- Unerupted teeth
- Odontogenic cyst
- Developmental cyst
- Eruption cyst
- Haemangioma
- Tori
What are 8 inflammatory causes of lumps and swelling of oral cavity?
- Abscess
- Cellulitis
- Cysts
- Sialadenitis
- Pyogenic granuloma
- Sarcoidosis
- Granulomatosis
- Crohn’s disease
What are 4 traumatic causes of lumps and swellings in the OC and lips?
- Denture stomatitis
- Epulis
- Mucocele
- Fibro-epithelial polyp
What are 4 neoplasm causes of lumps and swelling of the oral cavity and lips?
- Carcinoma
- Lymphoma
- Odontogenic tumour
- Salivary gland tumour
What are 3 fibro-osseous causes of lumps and swelling of the oral cavity and lips?
- Cherubism
- Fibrous dysplasia
- Pagets disease
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
What are common types of localised hyperplasia?
- Epulis
- Pyogenic granuloma
- Fibroepithelial poly
- Denture induced hyperplasia
- Palatal papillary hyperplasia often complicated by candida.
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
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
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
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.
Polp
A tumour present in the mucous membrane, term describing the mass location not the type
Squamous cell papilloma (SCP)
- histology?
- cause?
> Normally a hyperplastic, hyper keratinized lesion with papillomatosis surface
Normally associated with virus such as HPV
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.
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.
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.
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
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.
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.
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.
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
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
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
What are the 3 major paired salivary glands?
- Parotid
- Submandibular
- Sublingual
What are components of salivary gland anatomy?
- Ducts
- Acini cells = both serous and mucous, they appear purple on a histology slide.
- Myoepithelial cell, they appear brown on a histology slide
- Variable levels of fat, they appear white
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
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
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
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
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.
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
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
what does necrotising sialometaplasia mimic?
SCC and mucoepidermoid carcinoma
When faced with a patient who presents with bilateral parotid swellings, differential diagnosis should include?
- Mumps
- Sjogren’s syndrome
- Salivary gland tumours (benign and malignant)
- Sarcoidosis
- Sialadenosis/
- Sialosis due to diabetes mellitus, alcoholism, hypothyroidism, malnutrition, medications and bulimia nervosa
What is a neoplasm?
An abnormal growth of cells. Neoplastic disease refers to conditions that cause tumour growths (benign or malignant).
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.
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
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
Name 10 types of benign epithelial tumours of the salivary glands
- Pleomorphic adenoma
- Myoepithelioma
- Basal cell adenoma
- Warthin tumour
- Oncocytoma
- Canalicular adenoma
- Sebaceous adenoma
- Lymphadenoma (sebaceous or non-sebaceous)
- Ductal papillomas (inverted ductal papilloma, intraductal papilloma, sialadenoma papilliferum)
- cystadenoma
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
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)
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.
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.
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
Name 24 malignant epithelial tumours of the salivary gland
- Acinic cell carcinoma
- Mucoepidermoid carcinoma
- Adenoid cystic carcinoma
- Polymorphous low-grade adenocarcinoma
- Epithelial-myoepithelial carcinoma
- Clear cell carcinoma, not otherwise specified
- Basal cell adenocarcinoma
- Sebaceous carcinoma
- Sebaceous lymphadenocarcinoma
- Cystadenocarcinoma
- Low-grade cribriform cystadenocarcinoma
- Mucinous adenocarcinoma
- Oncocytic carcinoma
- Salivary duct carcinoma
- Adenocarcinoma, not otherwise specialised
- Myoepithelial carcinoma
- Carcinoma ex pleomorphic adenoma
- Carcinosarcoma
- Metastasizing pleomorphic adenoma
- Squamous cell carcinoma
- Small cell carcinoma
- Large cell carcinoma
- Lymphoepithelial carcinoma
- Sialoblastoma
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
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.
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,.
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.
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.
What is the percentage of saliva secreted from each major salivary gland?
- Parotid (60%)
- Submandibular (30%)
- Sublingual (5%)
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
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
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
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
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
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
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.
What is the difference between primary and secondary sjogren’s syndrome?
- Primary Sjogren’s syndrome: only Sjogrens disease and no other associated condition - dry mouth and eyes only.
- Secondary Sjogren’s syndrome: secondary presentation to a pre-existing autoimmune condition, most commonly associated with Rheumatoid arthritis, lupus or systemic sclerosis.
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
- Bloods - FBC, Haematinics, AIP incl Ro/LA, ESR, Random glucose, (consider ACE/HIV in sialosis)
- Salivary flow rates over 10 min
- USS
- Sialography
- 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
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)
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
