Oral mucosa and histology Flashcards
Important details to get when doing a history and why
Pre-exisiting/underlying conditions, medical history, medications, family history, chronic illnesses - all can affect oral presentations and management options
Special tests/investigations for oral medicine
Biopsy Imaging Sialometry (saliva) Shirmers (eye) Blood tests Swabs/smears/oral rinses
Different types of oral samples
Biopsy
Aspirate
Plain swab
Rinse
What is an aspirate sample/how do you take it
Inject into an abscess/something similar and get some pus - better because keeps the bacteria in the natural environment.
Different types of biopsies and details
Fine needle aspirate
Core needle biopsy - similar to FNA but a bigger tissue sample
Incisional - when you don’t have clear margins, don’t know how to manage, large diffuse lesions.
Excisional - small, clear margins.
Punch biopsy - but gives you a circular sample which is hard to orientate
How to take a plain swab sample
If on dry tissue - moisten with saline solution
If on abscess/wet tissue - use dry
What kind of samples would you take of a pus lesion
Plain swab sample or fine needle aspirate
What kind of samples would you take for mucosal/skin lesions
Biopsy
Plain swab
Smear/rinse
What kind of biopsies are GDPs NOT meant to do
If malignant or pre-malignant lesion, bone biopsies
What is an abscess/how to diagnose
Pus filled cavity
Fluctuant swelling, painful.
No Xrays needed usually bc takes 7-10 days for it to show on xray. Can sometimes be shown as widening of PDL space and loss of lamina dura
Treatment of acute infections/abscesses - general/systemic
Drainage
antibiotics. IV for systemically unwell/septic patients.
Broad range -> narrow when you’ve done cultures
Usually amoxicillin/metronidazole combo
NSAIDs, analgesics
Local measures for abscesses
Drainage; - LA not into the abscess but on the mucosa overlying - horizontal incision - open and drain Warm saltwater rinses for 24h after Antibiotics to stop spread of infection Remove cause
Microbial aetiology:
Dento-alveolar abscess
Black pigmented anaerobes/ anaerobic cocci e.g. Prevotella, Pepto-streptococcus
Eurobacteria
Fusobacteria
Spirochaetes e.g. treponema/ T. denticola
Periodontal abscess and Microbial aetiology
Periodontal pockets become occluded and infected/secondary infection of lateral periodontal cyst.
Xray will show radiolucency on lateral aspect of root
Tx = Drainage and debridement
Same bacteria as chronic periodontitis + candida
Streptococcal gingivostomatitis and Microbial aetiology:
Inflammation and pain of gingiva
Can cause fasciitis, rheumatic heart failure and tissue destruction
Treat w penicillin
Bacteria = Strep. pyogenes, viral and drug causes so needs lab sampling.
Acute ulcerative gingivitis and Microbial aetiology:
Ulceration, pain and destruction of interdental papilla. Halitosis, malaise, lymphadenopathy.
Microbes:
Anaerobic cocci, black pigmented anaerobes (prevotella) spirochaetes (treponema) fusobacteria. Worsened by smoking, stress, poor OH.
Needs debridement and antibiotics
Cancrum oris/Noma and Microbial aetiology:
South african and south asian. High mortality rate.
Usually preceded by ANUG, or previous illness/parasitic infection (measles, malaria, TB), malnutrition, immuno-suppression.
Prevotella, T. denticola, fusobacterium
TB in oral cavity and Microbial aetiology and investigations
cough, lymphadenopathy, ulcers on tongue, delayed healing after XLA and can have osteomyelitis.
Investigations = Zeil Neilson stain of biopsy, Lowenstein Jenson culture, PCR/T cells serology and look at histology - giant cells, caseation, epithelioid granulomas.
Syphillis stages and effects on oral cavity
Caused by treponema pallidum spirochaetes.
Primary = ulcers, painless oedema, lymphadenopathy, lesions on lip or tongue.
Secondary = rashes on palm of hands and feet, lymphadenopathy, snail track ulcers on lip. 6 weeks after initial lesions heal
Tertiary = firm necrotic centre surrounded by inflammation on tongue, tonsils and palate. Leukoplakia on tongue which increases chance of oral cancer.
Congenital = concave incisor edge, multi-crowned molars.
Gonorrhoea in oral cavity
Neisseria gonorrhea.
Can affect any part of oral mucosa and pharynx.
Lymphadenopathy, ulcers, pseudo-membranes, pain, oedema.
Acintomycosis and Microbial aetiology:
Large lump under angle of mandible. Can be secondary to trauma e.g. broken jaw. Slow growing and walled off so needs drainage, debridement and antibiotics.
Caused by Acintomyces Oris and A. Isreali.
Acute bacterial sialadenitis - what it is, symptoms, microbial aetiology and treatment
ascending infection of parotid/Wharton’s (submandibular) duct. Can be due to blockage, or Sjogrens, drugs or infection.
Causes trismus, red painful swelling, pus released by duct. Unilateral.
Treat w antibiotics e.g. amoxicillin.
Bacteria = anaerobic strep, staph aureus.
Angular chelitis - what is it, treatment, causes
Fungal/bacterial infection at lip commissures (candida or opportunistic staph. aureus)
Caused by loss of vertical height, Vit B12/folate/iron deficiencies.
Treat using antifungals (miconazole, nystatin, fusidic acid) and treating underlying causes.
Complications of oro-facial infections - cavernous sinus thrombosis
Infection can drain into sinus surrounding pituitary gland and make the blood here thrombose.
Presents as chemosis (red eye), ptosis (dropping upper eyelid), proptosis (bulging eye) and no eye movement (opthalmoplegia)
When would orofacial infections need antibiotics
If systemic sign/spreading infection e.g. throat pain, lymphadenopathy. If chronic infection that is persistent despite drainage e.g ANUG, acintomycosis.
Why can broad spectrum antibiotics be bad
Kills all the bacteria and lets C. diff infect.
Why can antibiotics fail
- Not enough blood supply to the area/access to the area if it’s been walled off or something blocking the area
- Poor patient compliance
- Antibiotic resistance or wrong antibiotic used.
- Too low dose
- Bacteriocidal in immunosuppressed patients instead of bacteriostatic.
HHV 1
Herpes simplex virus 1
neuronal/epidermal
HHV 2
Herpes simplex virus 2
neuronal/epidermal
HHV 3
Varicella-zoster virus/chicken pox (neuronal/epidermal)
HHV 4
Epstein-Barr virus (B-cells)
Oral viral infections/viruses
Herpes virus
Paramyxovirus (measles)
HPV
Coxsakia virus
Herpes virus
Binds to cells, unsheds and inserts dsDNA and then gets translated into lots of new herpes viruses.
Paramyxovirus
Measles, mumps
Koplik’s spots - white papules on buccal and palatal mucosa, skin rashes and long term complications
HPV forms/presentations
Different forms:
- Oropharyngeal carcinogenesis
- Warts
- Focal epithelial hyperplasia
HPV related oropharyngeal carcinogenesis
Most common form is squamous cell papilloma.
Can also get genital/anal cancer
Life cycle of HPV
Infects keratinocytes so needs broken skin to get in.
When keratinocytes differentiate, it gets released from the surface (contageous).
Sometimes it get’s integrated into chromosomes of the keratinocytes and becomes carcinogenic.
Coxsackia A virus types
Herpangina form (vesicles and ulcers on soft palate of young people) and hand/foot/mouth disease form (vesicles and rash on hands, feet and mouth). Both mild illnesses and self-limiting
Types of candida infections
Acute atrophic candidosis
Acute psuedomembranous candidosis (thrush)
Chronic hyperplastic
Chronic atrophic/denture stomatitis
Risk factors for candida infection
Abnormal exfoliation
Immunosuppressed (HIV, steroids, diabetes, age)
Xerostomia
Broad range antibiotics (kill the good bacteria = commensals infect)
Poor OH
About the candida fungus
Candida albicans (yeast and hyphae forms, candidalysin punches holes in cells and cause damage) Candidia auris (systemic infections)
Investigations for candida
Swab, rinse
Biopsy
Treating fungal infections
Topical antifungals = Nystatin, miconazole gel
Systemic = fluconazole
Acute pseudomembranous candidosis
can be wiped off to leave a bleeding base.
Thick white plaques.
Acute atrophic candidosis
Red areas on dorsum of tongue.
Prolonged use of antibiotics or corticosteroids
Chronic hyperplastic candidosis
White lesions near lip connoisseurs or lateral tongue that can’t be wiped off.
Biopsy bc risk of malignant change to leukoplakia.
Chronic atrophic candidosis
/denture stomatitis
Poor denture hygiene and area isn’t kept clean e.g. wearing denture at night.
Candida associated infections/lesions
Angular chelitis
HIV-related candidosis
Median rhomboid glossitis
Angular chelitits
Immunosuppressed, reduced OVD, Vit B12/folate/iron deficiencies
HIV-related candidosis
Prolonged forms e.g. Acute pseudomembranous candidosis that doesn’t go away or erthyematous form of acute atrophic candidosis
Median rhomboid glossitis
erythematous area on dorsum of tongue.
What counts as oral cancer
Head and neck - above the clavicle and not the brain or salivary gland. Oropharynx is included
Aetiology of oral cancer
Smoking Alcohol Infections Diet and nutrition Sunlight Hereditary e.g. P53 faulty tumour suppressor gene
Infections that can contribute to oral cancer
HPV - Focal epithelial hyperplasia (benign) - Squamous cell papilloma (benign) Candida - Chronic hyperplastic candidosis
Oral lesions that predispose to cancer
Leukoplakia Erythroplakia Lichen Planus - erosive/ulcerative versions Chronic hyperplastic candidosis Actinin keratosis Oral submucous fibrosis
Leukoplakia
A white lesion that can’t be rubbed off and clinically/histologically isn’t caused by anything. No chemical or traumatic causes other than smoking. Idiopathic
Non-homogeneous = speckled, veroccous, nodules. More likely to be more dysplastic. Homogenous = smooth, even surface.
Dysplasia in the histological sample can be mild (basal third), moderate (basal and middle third) or severe (full thickness of epithelium, basically a cancer in situ that hasn’t become invasive yet)
Erythroplakia
A red oral lesion that isn’t caused by anything - no histological or clinical cause. Idiopathic
Histological features of leukoplakia/erythroplakia
Hyperkeratosis +/- dysplasia
Architectural features = loss of stratification, basal cells not aligned/polar, drop-shaped rete pegs.
Cytological features = nuclear and cellular pleomorphism, hyperchromatosis/increased DNA, more mitosis.
Actinin keratosis
Lesion on lip
Crusting, red
Easy to spot, hard to manage
Oral submucous fibrosis
Especially in people that chew tobacco products
Lots of fibrous tissue under the epithelium
Presents as fixing of tissues, white lesion
Malignant oral cancers- signs and symptoms
Fixation to underlying tissues Dysphagia Paraesthesia or numbness Bone loss and mobile teeth Swellings Non-healing lesion Systemic signs
Grading and staging of cancers
Grading = well-differentiated, moderately or poorly differentiated. Poorly differentiated is the worst.
TNM info
Determines prognosis - N is the most important. Stage 4c if any M1. T = tumour size and depth of invasion - T0 = can't detect the primary cancer - T1 = <2mm diametre, <5mm invasion - T2 = 2-4mm, <5mm or <2mm, 5-10mm - T3 = >4mm, >10mm - T4 = deep structures involved e.g. muscle, bone N = nodes involved - N0 = No local nodes involved - N1 = 1x <3cm, ipsilateral - N2a = 1x 3-6cm, ipsilateral - N2b = 1+ <6cm, ipsilateral - N2c = bilateral or contralateral - N3a = any >6cm - N3b = extracapsular spread M = metastasis - M0 = no metastasis - M1 = distant metastasis
MDT involved in the management of oral cancers
Radiologist Oncologist Max fac surgeon Restorative dentist GDP/GMP Speech and language therapist Nutritionist Pathologist
The role of the radiologist in oral cancer management
Diagnosing US-guided biopsy CT/MRI Planning for surgery or radiotherapy Monitoring after treatment
The role of the restorative dentist in oral cancer management
Pre-op assessment to determine which teeth have poor prognosis and to extract them/stabilise the mouth before any radiotherapy to the area.
Warn patient of side effects and plan for them e.g. xerostomia, trismus.
Improve OH and prevention e.g. duraphat
Radiotherapy side effects
Short term =
Long term = ORN, trismus, xerostomia, radiation-related caries (radio tx damages the ADJ), slower healing, immunosuppression, mucositis
Localised swellings of gingival tissues - differentials
Fibroepithelial polyp - mucosa coloured
Pyogenic granuloma - red and fluctuant
Peripheral giant cell granuloma - red, big, trauma
Ulcer
Pregnancy/hormone-induced epulis - plaque related
Bohn’s nodules
Gingival cyst
Generalised swellings of gingival tissues - differentials
Gingival fibromatosis Gingival hyperplasia - hormone or medication-induced Crohn's/Oro-facial granulomatosis Leukaemic infiltrate Chronic hyperplastic gingivitis
Peripheral giant cell granuloma
Vascular granulation tissue with lots of giant cells.
Can erode through cortical bone - needs debridement
Peripheral means it starts from mucosa - need Xray to determine the extent
Can be trauma related
Anterior teeth and young people = common
Gingival fibromatosis
Overgrowth of fibrous tissue - genetic and hereditary
Gingival hyperplasia
Overgrowth of gingival tissue - needs gingivectomy but can grow back.
Can be medication-related, leukaemic infiltrate (red, bleeding gums), hormone-related, or due to lack of collagen, like in Scurvy
Medication induced gingival hyperplasia
Cyclosporins - immunosuppressant
Anti-convusltant - phenytoin
Anti-hypertensive - Nifedipine
Crohn’s signs and symptoms
Swollen lips and cracking
Cobblestone mucosa, tags on mucosa
Ulcers
Gingival hyperplasia
Benign swellings affecting the oral mucosa
focal epithelial hyperplasia/Heck's disease Lipoma Neuroma Haemangioma Squamous cell papilloma Mucocele
Heck’s disease/focal epithelial hyperplasia
HPV related
lots of small flat viral warts on the lip
Can resolve on their own/excise
Traumatic neuroma
Overgrowth of nerves due to trauma
Can be painful so excise
Haemangioma
Overgrowth of blood vessels - red/purple lesion
Careful excision - don’t let it bleed out
Lipoma
Overgrowth of fat tissue - yellow/pink with a smooth surface
Taking tissue samples for testing considerations
Need to stop contamination w other organisms and use a transport medium to preserve sample until it can be processed/tested.
Transport medium for tissue samples
- Needs to have no growth support medium to stop the sample changing or commensals growing.
- Aerobic or anaerobic
- Reducing agent can be added to preserve anaerobes
- Charcoal/gelatin added to absorb toxic metabolic products of host microbes
Sending a sample to the lab
- Need to fill in a specimen request form
- Needs special labeling for the post (A or B if it will cause life-threatening illness if exposed e.g. hep-B, HIV)
- Leak-proof rigid container w absorbent material
Sources of pigmentation in oral mucosa pigmented lesions [4]
Intrinsic
- Melanin = is made by clear melanocytes in the basal third of the epithelium and then taken up by neighbouring basal cells
- Haemosiderin = breakdown product of RBC (iron)
Extrinsic
- Heavy metals e.g. from amalgam, lead, gold. From restorations, medications (antimalaria, amiodarone) or from occupation
- Chromogenic bacteria e.g. actinomyces in a hairy black tongue
Endogenous developmental causes of oral mucosa pigmented lesions [4]
Physiological = people with darker skin have more melanin
Peutz Jehger’s
Haemochromatosis
Melanocytic naevus
Endogenous acquired causes of oral mucosa pigmented lesions [5]
Addison’s
Melanotic macule
Post-inflammatory
Smokers melanosis
Neoplastic oral mucosa pigmented lesions [2]
Melanoma
- malignant melanocytes proliferate along epithelium/CT junction and into CT
- V aggressive
- On the palate a lot
- Can be pigmented or not. Slow growing or fast/ulcerated/painful/bony infiltration
Kaposi’s sarcoma
- HHV8/HIV
- On palate usually
- Blue/black growth due to haemosiderin.
Exogenous causes of oral mucosa pigmented lesions [2]
Chromogenic bacteria
Heavy metals
oral mucosa pigmented lesions - Addison’s
Adrenal gland disorder - autoimmune
Less adrencorticol hormone = more ACTH from pituitary = melanocytes stimulated = more melanin = pigmented areas on skin
Don’t need to treat
Melanotic macule
More melanin in the basal third
Smoker’s melanosis
Smoking stimulates melanocytes = more melanin
Melanin drops into lamina propria and gets picked up by macrophages
Post-inflammatory oral mucosa pigmented lesions
Inflammation damages or stimulates melanocytes = more melanin.
Called melanocytes incompetence.
E.g. After leukoplakia
Peutz Jehger’s
- melanin, AD
- Get little dark spots around lips and big irregular pigmented lesions on the skin
- Get GI polyps which can become malignant
- More susceptible to carcinomas
Melanocytic naevus
hamartoma/mole
regular well-defined borders that don’t grow or change but biopsy if looks suspicious
Haemochromatosis
- Autosomal recessive
- Too much iron absorbed so excessive gets stored as haemosiderin and makes skin tinted, can cause liver cirrhosis, diabetes and more susceptible to infections.
- Tx = regular partial blood draining (venesection)
Types of hypersensitive reactions
- anaphylactic
- cytotoxic (cyTWOtoxic)
- immune complex
- delayed cell-mediated
Type 1 hypersensitivity
IgE binds to free antigen and triggers Mast cells to release histamines (on 2nd exposure)
= vasodilation, vaso-permeability, bronchospasm, nose and eye secretions, rashes
- Fast reaction
Use flare and wheel skin test
Tx = adrenaline, anti-histamines, corticosteroids
Type 2 hypersensitivity
Cytotoxicity
Antigen binds to and enters cells
IgG and IgM auto-antibodies bind to the cell and trigger an immune reaction which destroys the affected cells
- macrophages
- Complement system
E.g. pemphigus/pemphigoid
Type 3 hypersensitivity
Immune complex formed
Soluble antigens and antibodies bind, accumulate and precipitate in joints, blood vessels and glomeruli
= activation of the complement system
= inflammation and tissue damage
E.g. systemic LE, erythema multiforme
Type 4 hypersensitivity
Delayed cell-mediated
An antigen binds to a cell = releases cytotoxins
T-cell (CD4) responds
- Cytotoxic cells kill basal cells so no new epithelial cells so limited healing
- Apoptosis of affected cells w the antigen (via T-cells and natural killer cells)
- Perforin (pore-forming) released by T-cells
- macrophages
E.g. contact dermatitis, lichenoid, OLP
Hypersensitivity vs allergy vs autoimmunity
Hypersensitivity = immune system reacting in an exaggerated/inappropriate way to an extrinsic non-self (allergy) or intrinsic self-antigen (autoimmunity)
Causes of Ulcers (general)
Manifestations of systemic (GI/haem/dermatological) Idiopathic (RAS) Developmental (epidermolysis bullosa) Neoplastic Iatrogenic (drugs, radiotherapy) Infective Trauma
Drug induced oral mucosa pigmented lesions
- Stimulate melanocytes = more melanin
- Or damages blood vessels = more RBC broken down and haemosiderin released.
- Or have heavy metals in them
E.g. antimalaria, amiodarone
Black hairy tongue
Overgrowth of filiform papillae which get stained by bacteria (e.g. acintomyces) or smoking
Can be caused by soft diet, PEG, smoking, antibiotics
HIV opportunistic infections
Bacterial = TB, strep, s. pyogenes, salmonella
Viral = EBV, HSV, HHV8
Fungal = candida
Other e.g. toxoplasma
HIV medications
Meds that stop DNA from being transcribed properly e.g. Fusion-inhibitors, integrase-inhibitors, protease-inhibitors (fat loss from legs, fat gain in belly) and reverse transcriptase inhibitors (SE = nausea, headache, anaemia, rash, lactic acid)
Anti-retroviral drugs ART = good at stopping the progression to AIDS and reducing opportunistic infections
Preventing and treating opportunistic infections
How to diagnose HIV
Bloods - CD4 levels
ELISA test for HIV antigens
HIV associated oral manifestations
Group 1 /v HIV = Kaposi sarcoma, Non-Hodgkin lymphoma, candidiasis (thrush, erythematous candidosis), hairy leukoplakia, periodontitis/ANUG
2 = ulcers, viral infections, low platelets
3 = other candida/fungal infections
Normal histological structure of different types of oral mucosa [4]
Attached gingival mucosa = keratinised SSE, less submucosa, just attached straight onto the bone
Palate = Keratinised SSE, less submucosa, minor salivary glands
Normal mucosa = non-keratinised SSE, lamina propria, submucosa, muscle/fat
Specialised mucosa e.g. tongue = keratinised SSE + papilla - filiform (keratin extensions, abrasion), foliate/fungiform (taste), circumvalate
Variations of normal mucosa [4]
White spongey naevus
Fordyce spots - ectopic sebaceous glands
Geographic tongue
Leukoedema
Age-related changes to oral mucosa [3]
Less elastic
Thinner/atrophic
Smoother
Mucosal changes with trauma
Ulcer Atrophic - erosive OLP Hyperplastic - Increased CT/collagen = fibroepithelial polyp, papillary hyperplasia, Keratosis Hyperkeratosis - Stomatitis nicotina - Frictional keratosis
Factors that affect the healing of oral mucosa [8]
Blood supply Radiotherapy Immunity/immunocompromised Foreign body (neutrophils and lympcytes surround it and cause an abscess) Primary or secondary healing intention Nutritional deficiencies (e.g. VitC) Infection Malignancy Age of patient, hormones, risk factors, smoking
White sponge naevus
Inherited, AD
Keratinocyte mutation = Keratinised hyperplastic epithelium
Shows as thick white plaques that can’t be wiped off/don’t disappear on stretching, bilateral and symmetrical and usually on FOM, buccal mucosa
Don’t need to treat
Differentials = OLP, frictional keratosis, leukodaema
Leukodaema
+/- smoking
Diffuse milky areas that disappear on stretching
Bilateral/symmetrical
Doesn’t need treatment
histology = larger clear epithelial cells
Differentials = OLP, leukoplakia, white sponge naevus, frictional keratosis
Geographic tongue
Red areas with white halos on dorsum of tongue
Can be sore to food + have aggrevating factors
Lesions can move around tongue
Doesn’t need treatment or biopsy
Frictional keratosis and how to diagnose
Needs to have a continuous traumatic cause that when removed, makes the lesion heal.
Normal healing response of the mucosa
I it doesn’t heal, may need to reconsider diagnosis e.g. leukoplakia, OLP
Stomatitis nicotina
Hyperkeratosis of palate with red spots where minor salivary glands have been traumatised
Response to smoke/thermal trauma
Improves with smoking cessation
Not premalignant
Papillary hyperplasia
Ill-fitting denture
Causes hyperplasia and nodules, erythema
Need to improve denture fit and hygiene (can get superimposed w candida)
What is an ulcer - histology, different types
Loss of the full thickness of the epithelium, revealing the underlying CT
Fibrin/neutrophil slough covers it, with granulation tissue under to allow healing + inflammatory cells
- Primary
- Secondary - bulla/vesicle that bursts and becomes an ulcer
Questions / examinations when a patient presents with an ulcer
SH - smoking, alcohol, diet MH - new drugs FH Ulcer pain history How many do you have, where, for how long Ulcer free period Oral, genital, skin lesions Any other symptoms Aggravating/alleviating factors
E/O = lymph nodes (fixation = SCC?), skin and eye lesions
I/O
- how many ulcers, where, describe them (shape, size, raised, rolled margins?
- Tongue movement or fixation
- Any dysesthesia/nerve issues
Further investigations for non-healing ulcer
Biopsy
Blood tests - FBC, VitB, folate, iron,
Viral/fungal/bacteria
Ulcer biopsies
Only to rule out malignancy or dysplasia
Otherwise, it will be a non-specific ulcer
Can test for candida?
Differential diagnosis/causes for ulcers
MMIDNIIT (MIDNIGHT) Manifestations of systemic disease (haem, GI) Manifestations of dermatological disease - OLP, pemphigus/pemphigoid Infection Developmental - epidermolysis bullosa Neoplastic Idiopathic - RAS Iatrogenic - drugs, radiotherapy Trauma
Traumatic ulcers
Can be due to mechanical, physical, thermal, chemical or self-inflicted trauma
Remove the cause of trauma and see if the ulcer resolves
+ Symptomatic relief
If it doesn’t resolve, may need to reconsider the diagnosis
Malignant ulcers
SCC
Salivary gland tumour
Lymphoma
- raised rolled margins on a suspicious site e.g. FOM, lateral borders of the tongue, posterior mouth. 3+ weeks
- Biopsy to diagnose + need more imaging e.g. chest x-ray, CT
Ulcers caused by infection
Viral - herpes, coxsackie, HIV
Bacterial - TB, syphilis, gonorrhoea, ANUG bacteria
Fungal - candida
Erythema multiforme is triggered by bacteria and viruses too
Drugs that cause ulcers
Methotrexate
Cytotoxins
Nicorandil
Radiotherapy
RAS (diagnosis, risk factors, causes)
Recurrent aphthous stomatitis
Risk factors = familial, smoking, stress, hormones, poor OH.
Causes = low Vit B12, folate, iron levels, immunocompromised, GI tract disease, food intolerances
Blood tests and clinical form to diagnose (+/- biopsy to rule out cancer) - FBC, folate, iron levels, B12
Minor RAS
1-5 ulcers, <10mm
Front of mouth, non-keratinised tissues
Heal after 7-10 days, without scarring
Young patients 10-30yrs
Major RAS
5+ ulcers, 1.5-2mm All over mouth inc posterior and keratinised tissues Heal w scarring Take 3 weeks-months to heal Older patients
Herpetiform RAS + Tx
Lots of little pinprick ulcers, that can merge together
FOM, tongue, lips
7-10 days to heal
- Treat w doxycycline MW
Management of RAS
Prevent
- Correct any underlying conditions e.g. B12, iron
- Improve OH
- Reduce RF e.g. smoking
Symptoms
- benzydamine mouthwash (Difflam)
- Corsodyl/chlorhexadine
- Covering gel
Suppress
- Topical steroids e.g. hydrocortisone pellets, betamethasone MW, beclomethasone spray
- Systemic steroids e.g. prednisolone,
Behcet’s disease
- Affects the whole body, high mortality
- RAS and recurrent oro-genital ulcers
GI, joints, skin lesions, neuropathy, retinal vasculitis = blindness - Diagnose using clinical signs
Different types of mucocutaneous diseases
Pemphigus - Vulgaris - Foliaceous - Paraneoplastic Pemphigoid - Bullous - Mucous membrane Dermatitis herpetiform Epidermolysis bullosa Erythema multiforme Lichen planus Lichenoid reactions
Define: Macule Papule Blister [2] Erosion Ulcer
Macule = flat, not palpable, circumscribed/well-defined
Papule = palpable, raised circumscribed/well-defined lesion
Blister - fluid-filled sub or intra-epithelial area
Erosion = partial-thickness loss of epithelium
Ulcer = Full-thickness loss of epithelium
Pemphigus
Autoimmune, type 2 hypersensitivity
Autoantibodies attack desmosomes (releasing desmoglein) and cause intra-epithelial separation.
Blisters can burst but because it’s only a partial loss of epithelium, the body doesn’t heal. Loss of permeability membrane = loss of tissue fluid and infection gets in.
Variable sized, short-lived ulcers on the palate, gingiva, buccal and can get skin lesions
Pemphigus vulgaris = desmoglein 3
Pemphigus foliaceous = desmoglein 1
Pemphigus paraneoplastic
Histology = intraepithelial separation, Tsank cells (floating epithelial cells)
How to diagnose pemphigus/pemphigoid
Para-lesional biopsy to see intra or subepithelial separation
Direct immunofluorescence of fresh sample = IgG w immunofluorescence, specific to human autoantibody added to sample. Binds to autoantibodies.
- Pemphigus = fishnet appearance
- Pemphigoid = thick line at the basement membrane
- Dermatitis herpetiform = speckled granular line at the basement membrane.
Indirect immunofluorescence (patient’s blood sample used on tissue) = negative for pemphigoid
Blood tests = autoantibodies and free desmoglein (pemphigus)
Blunt probe on healthy mucosa - pemphigus will develop a blister
Different types of pemphigus
Pemphigus vulgaris = desmoglein 3. Most common
Pemphigus foliaceous = desmoglein 1. Surface and skin lesions (less oral)
Pemphigus paraneoplastic = can lead to lymphoma and chronic lymphocytic leukaemia
Bullous pemphigoid
Autoimmune Type 2 hypersensitivity
Against hemidesmosomes that connect epithelium to basement membrane = subepithelial separation
- Proteins BP180 and BP230 affected
Bullae are less fragile bc full thickness, and if they rupture they become an ulcer and get normal healing
Skin usually involved + oral mucosa - large, shallow ulcers
Mucus membrane pemphigoid
Hemidesmosomes, subepithelial separation
- Hemidesmosome protein BP230, lamina and Alpha4Beta6 affected
Chronic disease of the elderly
Affects mucous membrane e.g. mouth, genital, anal, larynx, pharynx, nasal
Desquamative gingivitis
Get blisters and vesicles which rupture and cause scarring
In the eyes, this can lead to conjunctive scarring, eyes sticking to eyelids and inverted lashes/inverted eyelids
These patients need referrals.
Dermatitis herpetiform
In kids
Like bullous pemphigoid but lots of small vesicles and ulcers on the palate and buccal mucosa which can merge
+ Desquamtive gingivitis
Can be linked with Coeliacs so patients need to be gluten-free
Epidermolysis bullosa congenita
Inherited AS - not autoimmune, from birth
Problems with epithelium connecting to CT
- EB Simplex = intraepithelial separation
- EB junctional = above basement membrane
- EB dystrophic = basement membrane separated from CT
V bad :(
Erythema multiforme
Type 3 or 4 hypersensitivity
Acute, young patients, resolves in 2-3 weeks
Single episode = drugs, radiotherapy
Recurrent episodes = HSV antigen (type 4 hypersensitivity) - give acyclovir
Bleeding, haemorrhage crusting on lips
Eye problems
Bullseye ulcer lesions on skin
Lots of irregular mucosal ulcers and bulla
General management of muco-cutaneous diseases
Prevention
- Diet
- OH
- Risk factors e.g. stress. smoking, trauma
Symptoms
- Difflam
- Corsodyl (alcohol-free?)
Steroids
- Topical or systemic
Immunosuppression
- Cyclosporin MW
Lichen planus - mucosal presentations [6]
Radicular interconnecting striations Ulcers Desquamative gingivitis Erosive Plaque-like Bullous form
Lichen planus - skin presentations
Purple itchy papules and striations, especially on wrists and shins.
Itch them = more papules
Lichen planus vs lichenoid reactions
Lichenoid
- Closely related to a cause
- Type 4 hypersensitivity
- Unilateral, asymmetrical
- No skin lesions
Lichen planus
- Idiopathic
- Type 4 hypersensitivity
- Skin and gingiva signs
- Bilateral, symmetrical
Cause of lichen planus
Smoking Stress OH Trauma Infections
T-cell mediated - Basal cells destroyed by lymphocytes so epithelium can’t heal = erosive lesions
Or responds by overproduction of epithelial cells and keratin = plaque-like lesions
Rate of destruction: rate of new cells determines if it’s plaque-like or erosive
Management of lichen planus
Prevention
- Reduce risk factors
- Avoid food triggers
- OH improvement
Symptomatic relief
- Topical steroids - beclomethasone spray, betamethasone MW, hydrocortisone pellets
- Benzodyamine MW
- Cyclosporin (MW)
Systemic immunosuppression
- Prednisolone
Warn patient that 1-3% become malignant
Lichenoid reactions - causes
Metal from restorations, instruments
Diet
Medications
Graft vs host disease
Histological signs of OLP
Loss of basal cells
Lots of blue lymphocytes under the basal layer
Can be erosive, ulcerated, bullous or hyperplastic depending on the presentation
GORD
Gastric-oesophageal reflux disease
RF = obesity, smoking, alcohol
Symptoms = dyspepsia (indigestion e.g. heartburn, acid reflux, abdo pain, nausea, vomiting) and oral symptoms (tooth erosion, ulcers, halitosis)
Can lead to Barrett’s oesophagus (squamous cells metaplasia to cuboidal cells, premalignant)
Tx = reduce risk factors, PPI e.g. omeprazole
SE of PPI = interacts w warfarin, the pill and can cause erythema multiforme, taste disturbances, dry mouth.
Coeliac’s
Type 4 hypersensitivity to a-gliadin peptides in gluten
Inflammatory bowel disease
Histology:
- The surface layer of bowels
- Crypt hyperplasia
- Villous atrophy
Clinical signs - full body - Abdo pain - Fatty stool - Diarrhoea - Malabsorption - Iron, folate, Vit B12, D, C, calcium - Tired \+ Osteomalacia (less VitD/calcium) \+ Peripheral neuropathy (less B12/folate)
Oral signs - ulcers - opportunistic infections e.g. candida - angular cheilitis - glossitis \+ dermatitis herpetiform \+ enamel hypoplasia (less calcium/VitD)
Treatment = No gluten, immunosuppression if needed/manage symptoms with topical stuff
Risk of bowel malignancy/lymphoma so monitor patient
Crohn’s
Idiopathic inflammatory bowel disease
Affects the elderly more
Histology - Affects full thickness and length of GI tract - Granulomatous inflammation \+ non-caseating granulomas \+ Tags
Clinical signs (general) - Abdo pain - Diarrhoea - Weight loss - Tired - Malabsorption \+ Blood in poo
Oral signs - Ulcers - Glossitis - Angular cheilitis - Opportunistic infections \+ Cobblestone appearance \+ Lip swelling and fissures \+ Mucosal tags
Treatment
- Prevent
- Replacement therapy/food already broken down
- Symptomatic relief
- Topical and systemic steroids and immunosuppression
+ Anti-TNF
Need to rule out other granulomatous inflammation and other inflammatory bowel diseases
OFG
Idiopathic but possibly linked to food allergies
Oral signs of Crohn’s - granulomatous inflammation
Oral signs
- Ulcers
- Angular cheilitis
- Cobblestone appearance
- Lip swelling and fissures
Treatment
= prevent (diet, exclude chocolate, cinnamon, benzos, etc), symptomatic relief, topical and systemic immunosuppression if needed
Need to rule out other granulomatous inflammation and Crohn’s (endoscopy, bowel signs/symptoms)
Ulcerative colitits
Idiopathic inflammatory bowel disease
Affects younger people more (10-30yrs)
Histology
- Surface mucosa/epithelium
- Bleeding and ulceration
- Large intestines and rectum affecting
Clinical signs (general) - Abdo pain - Diarrhoea - Malabsorption - Weight loss - Tired \+ Bleeding in poo \+ ankylosing spondylitis (fused back) \+ iritis (iris inflammation)
Oral signs
- Ulcers
- Furred tongue (not eating enough)
- Pyostomatitis vegetans (pus and inflamed gums)
+ Vit B12/folate/iron deficiencies from malabsorption
Inflammatory bowel diseases
Crohn’s
Coeliac
Ulcerative Colitis
Tests to diagnose inflammatory bowel diseases
Clinical
Blood tests - FBC, inflammatory markers (ESR, CRP), Vit/iron/folate levels, antibodies (for A-gliadin = Coeliac’s)
Endoscopy
Biopsy - non-caseating granulomatous inflammation = OFG/Crohn’s, histological signs of Coeliac’s, surface or full mucosa involved?)
Exclusion diet - does it work
Granulomatous inflammation differentials and differentiating between them
Crohn’s - full thickness and length of GI + oral
OFG - only in mouth
TB - caseating granulomas (others are non-caseating) + lungs
Sarcoidosis - in lungs (take X-ray)
Causes of lip swelling
Crohn’s
OFG
TB (rare)
Sarcoidosis
Similarities/differences in presentation between Coeliac’s, OFG, UC, Crohn’s - how to spot each one
Coeliac’s
- Specific histology: crypt hyperplasia, villous atrophy
- Caused by antibodies to a-gliadin
- genetic so in kids
+ specific signs e.g. hypoplastic enamel, osteomalacia, fatty stool
Crohn’s
- Blood in stool
- granulomatous inflammation = tissue tags, cobblestone, lip swelling and fissure
- Full-thickness and length of GI + oral
- Only one that is treated w anti-TNF
OFG - only in mouth
Ulcerative Colitits
- Blood in stool
- Large intestines and rectum, surface of mucosa only
+ Specific signs e.g. iritis, ankylosing spondylitis
- No granulomatous inflammation
Treatment for inflammatory bowel disease (+ Coeliacs)
Prevention Replacement therapy if malabsorption Symptomatic relief Steroids - topical and systemic Immunosuppression Monitor GI for malignancy (esp Coeliacs)
Intestinal polyposis syndromes
Peutz Jehgers
- Genetic
- Small pigmented lesions in the mouth and around the lips
- Risk of malignancy in ovaries, liver, pancreas
Gardner’s syndrome
- Osteomas, odontomas, supernumerary teeth
- GI polyps, cysts,
- Risk of GI malignancy
Different types of anaemia and causes
Normocytic
- Leukaemia/not enough RBC made
- Bleeding, period, need more
Microcytic
- Low iron
- Due to diet, malabsorption, increased demand e.g. pregnancy, period,
Macrocytic
- Low B12/folate
- Due to malabsorption, diet, hypothyroid, medications (azathioprine for Crohn’s), alcohol/liver disease
Leukaemia
Bone marrow space obliterated with one type of malignant WBC = not enough space for the others.
- ALL, AML, CLL, CML
- Acute forms are more aggressive
- ALL in kids
Malignant cells take over marrow space and can go into other organs =
- Symptoms of anaemia
- Reduced healing and immunity
- Fewer platelets = bleeding and bruising
- Bone pain
- Lymphadenopathy, hepato/splenomegaly
- General cancer signs e.g. weight loss, sweating, tired
Multiple myeloma
Malignancy if plasma cells that obliterate bone marrow space = leukaemia symptoms
+ release lots of monoclonal antibodies which go all over body and aggregate in areas = bad
- Joints
- Osteoporosis
- Kidneys/nephrons damaged
Oral symptoms of anaemia
Palor Ulcers Depapillated tongue Altered taste Candida Dysphagia (webbing in the oesophagus can be pre-malignant) Burning mouth
General signs/symptoms of anaemia
Palor Tired Palpitations/fast heart rate Slow healing Mucosal atrophy Skin and nail changes Hair loss Headrush/dizzy
