Oral Med Flashcards
Define xerostomia and hyposalivation
Xerostomia: dry mouth as result from
- absent/red. salivary flow
- change in saliva composition
- unknown reason
Hyposalivation: objective red. salivary secretion due to red. salivary gland function
Functions of saliva
Lubrication: swallowing, speech Defence, antimicrobial properties Taste Digestion: amylase (starch), lipase (fat) Lavage, buffering
Complications dry mouth
Dental: caries, depapillated tongue Oral soft tissue disease GIT dryness Dysphagia Dysphonia, hoarseness Psychological Nutritional, taste alteration
Aetiology of dry mouth
Dehydration/red. fluid intake Habits: mouth breathing Medications Salivary Gland Disease Systemic Disease Change in oral perception due to - nerve damage - Alzheimer’s - stroke Psychological Age Idiopathic
Salivary gland diseases possibly leading to dry mouth
Infection: viral (mumps), bacterial Obstruction - meal time syndrome - mucocele, ranula Damage: 2ry to cancer Tx Tumours Degernatiive: autoimmune destruction (Sjögren’s)
Systemic diseases possibly leading to dry mouth
Sjögren’s DM Liver disease Amyloidosis Sarcoidosis Thyroid disease HIV-related 🙀
Discuss sialadenosis
Sialosis Unspecific gland enlargement Non-painful Aetiology unknown - factors — eating disorder — medication — alcohol abuse — nutritional deficiency — DM — pregnancy
Discuss sialadentitis and sialolithiasis
Sialadentitis
- enlargement 1/+ glands due to infection/inflammation/obstruction
- parotid, submandibular
- conditions: mumps, Sjögren’s, sarcoidosis
Sialolithiasis
- stones/calculi in glands causing pain + swelling
- submandibular
Classification of salivary gland tumours
Benign
- nonepithelial
- epithelial
Malignant
- nonepithelial
- epithelial
Types of benign epithelial salivary gland tumours
Pleomorphic adenoma Warthin tumour Monomorphic adenoma Oncocytoma Intraductal papilloma Sebaceous neoplasms
Discuss pleomorphic adenoma and warthin tumour
Pleomorphic Adenoma
- most common tumour
- tail of parotid; minor glands H palate + U lip
- variable, diverse histological patterns of epithelium and connective tissue
- incomplete capsule: complete removal difficult = recurrence high
— radiotherapy common Tx following removal to kill cells
- slow growing + asymptomatic
Warthin tumour
- smooth, soft, parotid mass
- multicystic, well encapsulated
- recurrence low (5%); malignancy rare
Types of benign non-epithelial salivary glands tumours
Haemangioma Neural sheath tumour Angioma Lymphangioma (cystic hygroma) Lipoma
Discuss haemangioma
Benign non-epithelial salivary gland tumour
Vascular tumour
Usually parotid, sometimes submandibular
Solid mass cells + multiple anastomosing capillaries replace acinar structure
Rapid growth b/w 1-6/12, slowly red. until 12y
Dark red, lobulated, unilateral, compressible, asymptomatic mass
Types of malignant epithelial salivary gland tumours
Mucoepidermoid carcinoma Adenoid cystic carcinoma Carcinoma ex-pleomorphic adenoma Clear/basal cell carcinoma Squamous cell carcinoma Epithelial-myoepithlial carcinoma Salivary duct carcinoma Lymphoepithelial carcinoma Sialoblastoma
Discuss mucoepidermoid carcinoma
Malignant epithelial salivary duct tumour
Most common malignancy of parotid 8%
Mucous + epidermal cells
Grading: ratio epidermal cells inc. - low: non aggressive, good prognosis - int. - high: aggressive, high change metastasis regional lymph nodes — may resemble SSC
Discuss adenoid cystic carcinoma
Malignant epithelial salivary gland tumour
2nd most common malignancy tumour
Most common malignancy submandibular
Slow growing, painless mass Locally invasive Metastasis - regional lymph nodes uncommon - distant (lungs) common
Discuss carcinoma ex-pleomorphic adenoma
Malignant epithelial salivary gland tumour
Arises from incomplete removal of pleomorphic adenoma
2-4% all salivary gland malignancies
Sudden rapid growth otherwise stable/slow mass
Aggressive natural Hx + poor prognosis
Metastasis: regional + distant common
Types of tumour-like lesions of salivary glands
Necrotising sialometaplasia
Lymphoepithelial Hyperplasia/benign lymphoepithelial lesions
Cystic lymphoid hyperplasia (AIDS)
Salivary gland cysts
Discuss necrotising sialometaplasia + lymphoepithelial hyperplasia
Tumour-like lesions of salivary glands
Necrotising sialometaplasia
- benign, self-healing lesion minor glands
- mistaken for malignancy
— single, unilateral painless/slightly painful lesion H palate
- aetiology: unknown
— response to ischaemic necrosis of salivary tissue
Lymphoepithelial hyperplasia
- discreet mass/diffuse enlargement of part/whole parotid
- occasionally bilateral
- slow-growing, may be painful
Most common 2ry cause of xerostomia
Sjögren’s syndrome
What is Sjögren’s? Aetiology
Multisystem autoimmune disease
Aetiology: unknown
- virus triggering immune reaction
- genetic susceptibility
- gender predisposition: hormones (90% F >50y)
What is Sjögren’s syndrome characterised by?
Inflammation of exocrine glands w/ lymphocytic infiltration of lacrimal + salivary glands leading to xerostomia + xerophthalmia (sicca complex)
Compare 1ry and 2ry Sjögren’s
1ry (Sicca): dry eyes + mouth
2ry: connective tissue disease (rheumatoid arthritis) + dry eyes and mouth
General symptoms + signs of Sjögren’s
Dry mouth/eyes/skin/mucous membranes
Fatigue/fibromyalgia
Rheumatoid arthritis/connective tissue disease
Raynaud’s phenomenon
What is Raynaud’s phenomenon?
Condition in which spasm of capillaries causes extremities to change colour (white -> blue) and become painful
Usually response to cold
Oral signs + symptoms of Sjögren’s
No saliva pooling
Dry, atrophic mucosa
Sticky/glassy mucosa
Cracked lips
Oral burning sensation
Oral soreness
Sialadenitis: swelling, pain, fever
Oral candidiasis
Inc. DMF
Cervical + incisal decay pattern
Denture wearing difficulty
Dysohonia, dysphasia, dysgeusia
Halitosis
Discuss potential systemic complications/involvement of Sjögren’s
Haematological
- autoimmune haemolytic anaemia
- idiopathic thrombocytopenia purpura
- non-hodgkin’s lymphoma
Respiratory: interstitial fibrosis
Renal: renal tubular acidosis
Nervous: cranial/peripheral neuropathy
Classification criteria for Sjögren’s
1: ocular symptoms (subjective)
2: oral symptoms (subjective)
3: ocular signs (objective)
4: histopathology (objective)
5: salivary gland involvement (objective)
6: serum auto-Ab (objective)
What auto-Ab are involved in Sjögren’s?
Auto-Ab to Ro/SSA and La/SSB auto-Ag
Act against auto-Ag in lacrimal and salivary glands
Classification criteria for 1ry and 2ry Sjögren’s
1ry
- symptomatic: any 4/6 +ve incl. histopathology and/or serum
- asymptomatic: any 3/4 objective measurements +ve
2ry
- systemic disease +
- 1/2 subjective measurement +
- 2/3 from ocular signs, histopathology, salivary gland involvement
Serious complications of Sjögren’s
Lymphoma
- 40x greater risk
- 10% SS pt develop non-Hodgkin’s lymphoma
Heart Block newborns
- maternal Ab cross placenta
Eye damage + Vision loss
- corneal ulcers due to unTx dry eyes + infection
Ix useful for Dx Sjögren’s
Salivary Assays (sialometry)
- whole unstim. salivary flow
- parotid/submandibular stim. flow
Bloods: specific auto-Ab (not all pt)
X-ray: sialograph
US
L lip minor gland biopsy (gold standard)
Tx/management of Sjögren’s/dry mouth
No cure
Regular appt; OHI, F- m/w
Tx/prevent candidiasis
Diet
- inc. H2O intake; esp. eating, speaking
- red. sugar
- avoid: caffeine, alcohol, fizzy drinks, tobacco
Stim. saliva: sugar free gum/sweets
Artificial saliva products: personal preference
Humidifier: esp. at night
Non/pharmacological management methods for Sjögren’s
Pharmacological
- parasympathetic nervous system agonist: pilocarpine
- only v severe cases
- many adverse effects: GIT, CVS, respiratory, GU (inc. urination)
Non-Pharmacological
- acupuncture
- electrostimulation: IO neural stim, (US approved)
Differentiate b/w ulcer and erosion
Erosion: partial loss skin/mucous membrane
Ulcer: total loss of epithelium
Define atrophy and plaque
Atrophy: loss of thickness
Plaque: raised uniformed thickening skin/mucous membrane w/ defined edge
Classification of oral ulcerative diseases by aetiology
Local - trauma: chemical, electrical, thermal, radiation - recurrent aphthous stomatitis Systemic Infective - bacterial: TB, ANUG, syphilis - viral: VZV, HSV, CAV, HIV, EBV - fungal: histoplasmosis, aspergillosis, candidiasis
Cutaneous systemic diseases causing oral ulcers
Erosive lichen planus Pemphigoid Pemphigus Erythema multiforme Dermatitis herpetiformis Epidermolysis bullosa Linear IgA disease Chronic ulcerative stomatitis
Blood diseases potentially causing oral ulcers
Anaemia
Leukaemia
Neutropenia
Myelodylastic syndrome
GI and CT diseases causing oral ulcers
GI
- coeliac
- Crohn’s
- ulcerative colitis
CT
- SLE/DLE
- Wegner’s granulomatosis
Drugs/Tx and malignancies potentially causing oral ulcers
Drugs/Tx
- cytotoxic drugs
- radiotherapy
- nicorandil (cardiac)
Malignancy
- SSC
- lymphoma
Classification of oral ulcers by recurrence
Recurrent - aphthae - erythema multiforme Persistent: 2ry to systemic disease Single episode - trauma - infective - drug Single persistent: neoplastic
Types of recurrent oral ulcers
Recurrent aphthous stomatitis - major - minor - herpetiform Smoking related aphthous stomatitis Associated w/ Behçet’s disease
Compare minor, major, herpetiform RAS
Age: 10-19; <10; 20-19
No.: 1-5; 1-10; 5-20
Size: <10mm; >10mm; 0.5-3mm
Shape: oval; irregular/oval; round, may coalesce
Colour: grey base, erythematous border; grey base, +/- indurated edge; yellow base, erythematous base
Site: non-keratinised (B mucosa); any (fauces); non-keratinised (V tongue, FoM)
Duration: 1-2/52; 2-12/52; 1-2/52
Scarring: N; Y; N
Discuss Behçet’s disease
Chronic autoimmune disease
- affects small blood vessels
Triad: oral ulcers, genital lesions, recurrent eye inflammation
- oral ulcers indistinguishable from RAS
Clinical
- ulcers: oral, genital (50%), skin
- skin: spots, sores, lesions, ulcers, red patches, lumps
- eye: uveitis (50%), retinal vasculitis
— floaters, haziness, loss of vision
— pain, inflammation
- joint inflammation: pain, swelling
Management of oral ulcers
Eliminate local aggravating factors Control infection Control pain Promote healing Prevent recurrence Assess response
General + local predisposing factors for candidiasis
General
- broad spectrum AB
- corticosteroids
- cytotoxics
- poorly controlled DM
- xerostomia
- nutritional deficiency
- immunosuppression
Local
- trauma: ill fitting denture
- smoking
- red. saliva flow
- carb rich diet
Discuss impact of drug therapy in candidal infections
Broad spectrum ABs, immunomodulators, xerogenic agents
ABs: alter commensal microflora
- Candida controlled by competition for dietary substrates + epithelial cell adhesion
Xerogenic: red. salivary flushing + antifungal components
Discuss impact of DM on candidal infections
Related to glycemic control
- poorly controlled = higher Candida carriage
Contributory - red. salivary flow - lower pH - inc. salivary glucose = inc. growth + colonisation
Discuss immunodeficiency + haematological factors related to candidal infections
Immunodeficiency
- candidiasis may be 1st presentation
- cell-mediated + humoral immunity in prevention + elimination of fungal infections
- candidiasis: >60% HIV, >80% AIDS
Haematological
- blood group H Ag acts as R for C. Albicans
- H Ag inc. blood type O
Discuss impact of diet on candidal infections
Protein energy malnutrition
Fe, folate, VitA/B12/C deficiency
Red. host defence + mucosal integrity
= hyphal invasion + infection
CHO rich: inc. candidal adhesion to epithelial
2 acute candidal infections
Pseudomembranous candidiasis
Erythematous candidiasis
Discuss pseudomembranous candidiasis
Detachable confluent creamy-white/yellowish patches on mucosa
- tongue rare; depapillated if occurs
Wiped off: erythematous, occasionally bleeding base
Plaques: desquamated epithelial cells, necrotic material, fibrin, fungal hyphae
Usually asymptomatic
Found in immunocompromised
- HIV: oesophageal candidiasis; dysphagia, odynophagia, chest pain
Freq. associated angular cheilitis
Management of pseudomembranous candidiasis
Improve OH
Tx systemic: immunosuppression, DM, anaemia, hypothyroidism
Live active yoghurt
Topical
- CHX m/w
- nystatin suspension
- miconazole gel; interactions, systemic absorption
Discuss erythematous candidiasis
Characterised by erythematous patches +/- pain
Common: D tongue + palate, occasionally B mucosa
Associated: chronic broad spectrum AB + corticosteroids, HIV
Discuss chronic hyperplastic candidiasis
Pre-malignant condition
- Candida prod. nitrosamines -> malignant transformation
- unTx: 5-10% dysplasia, may develop OSCCh
Chronic hyperkeratosis in which Candida identified
Common: middle age M smoker
Asymptomatic
Clinical findings of chronic hyperplastic candidiasis
B mucosa towards commissures w/ bilateral distribution
White to erythematous raised lesions
- don’t rub off
Nodular/speckled (inc. risk malignancy) or homogenous plaque-like
Possible angular cheilitis
Management of chronic hyperplastic candidiasis
Biopsy: risk malignant transformation 15%
FBC: Fe, folate, B12, glucose, TFT
Remove predisposing: smoking
Topicals not effective
2-4/52 oral fluconazole
Discuss chronic erythematous candidiasis
Denture stomatitis
Chronic erythema of mucosa beneath fit surface acrylic denture
- excludes saliva from mucosa + allow candidal overgrowth
- 65% denture wearers
Associated: poor denture/OH + ill fitting denture
Usually asymptomatic; except angular cheilitis
Clinical findings + management of chronic erythematous candidiasis
Clinical
- marked erythema of P mucosa w/ sharply defined margin
- relief area present -> underlying spongy, granular change
- mistaken for acrylic hypersensitivity
Management
- OH
- eliminate trauma: tissue conditioner
- miconazole gel applies to fit surface
- no resolution = systemic or not compliant
Discuss angular cheilitis + aetiological factors
Symmetrical erythematous tissue @ angles of mouth/commissures
Elderly denture pt w/ denture stomatitis
Red. OVD + maceration of skin by saliva
C. Albicans, Staph. aureus, B-haemolytic Strep
Aetiology
- red. haematinics: B12/folate/Fe
- malabsorption: OFG, Crohn’s
- immunosuppression
- DM
- xerostomia
- ABs
Management of angular cheilitis
Remove predisposing Correct OVD Improve denture/OH Address fissuring Tx IO Candida Miconazole gel on corners of mouth Chronic: trimovate cream (AB, antifungal, steroid)
Discuss medium rhomboid glossitis + chronic mucocutaneous candidiasis
Median rhomboid
- chronic candidal infection w/ atrophy filiform papillae
- asymptomatic diamond shaped smooth area ant. circumvallate papillae
- associated smoking + corticosteroids
- may have kissing lesion on palate
Chronic mucocutaneous
- chronic candidal infections involving skin, nails, mucous membranes
- associated w/ rare congenital conditions
- aetiology: impaired cellular immunity
Discuss polyenes
Antifungal: fungicidal through interacting w/ ergosterol in membrane
Nystatin
- inhibit ergosterol synthesis
- no but absorption
- adverse: irritation, sensitisation, nausea
Amphotericin
- binds fungal membrane ergosterol; disrupt membrane
- no gut absorption
- IV: severe systemic infections
- adverse: mild GI disturbance
Discuss azoles
Antifungals; fungostatic (have to remove predisposing too)
Inhibit lanosterol demethylase = prevent ergosterol synthesis
Resistance rising
Types
- imidazoles
- triazoles
Discuss imidazoles
Antifungals
Miconazole
- topical gel; mucosa, denture (inc. compliance)
- AB activity
- gut absorption: interaction w/ warfarin, statins
Ketoconazoles
- rarely used
- hepatotoxic
- nonspecific: inhibit testosterone + cortisol synthesis
Discuss triazoles
Antifungals
Fluconazole
- better toxicity profile cf ketoconazole
- expensive
- contraindications: pregnant, breast feeding
- interactions: benzodiazepines, Ca channel blockers, warfarin, cyclosporin
Itraconazole
Vorticonazole
Define vesicle + bulla
Vesicle: small, fluid filled blister <5mm
Bulla: large, fluid filled blister >5mm
Clinical features of primary herpetic gingivostomatitis
HSV1
Prodromal: fever, malaise
Clinical - multiple herpetic oral ulcers — 2-3mm vesicles erupt keratinised tissues — rupture -> widespread painful ulcers; heal 7-10d - diffuse gingivitis - cervical lymphadenitis - fever, malaise - severe — lip erosions — lymphadenopathy — pharyngotonsilitis
Dx + management 1ry herpetic gingivostomatitis
Dx: clinical, possible viral culture
Management
- supportive
- antiviral if severe
- CHX m/w; prevent 2ry bacterial infection
- fluid intake
- analgesic, antipyretic
- prevent spread/limit contact
Discuss recurrent herpes labialis
Cold sores
40% pt experience recurrence
Prodrome: tingling/burning
Reactivation
- HSV1 dormant in DRG
- breakdown in local/systemic immunosurveillance
- trigger: UV, immunosuppression, trauma, post-op, infection, menstruation
Clinical
- vesicular eruption -> breakdown crusting lesion
- vesicles enlarge, coalesce, weep, rupture (2-3d), crust, heal (10d)
Prevention of recurrent herpes labialis
Suncream; red. freq.
Topical acyclovir/penciclovir
Severe/freq.: systemic prophylactic acyclovir
Discuss herpetic whitlow
HSV recurrence involving skin
Acquired from pt saliva
Highly infective
Intensely painful
Management
- analgesic
- elevation, splinting
- systemic antiviral
Discuss erythema multiforme
Mucocutaneous blistering condition
Mucosal erosions + lip blistering w/ skin lesions
T3 hypersensitivity
Aetiology
- drugs: NSAID, anti-epileptic, barbiturates, antifungals
- infection: HSV, Hep, HIV
- systemic: SLE, pregnancy, malignancy
- idiopathic 50%
Clinical features of erythema multiforme
Sites: extremities, mucous membranes
Oral - bullae on erythematous base — breakdown rapidly -> irregular ulcers, bleed, crust - lips freq.; swollen, bloody, crusted - gingiva rare
Skin
- erythematous macules + papules
- target/iris: central pale area surrounding by oedema + bands of erythema
Discuss chickenpox
VZV/HHV3
Condition of children (90%) Itchy maculopapular rash - back, chest, face, limbs - maculopapular -> vesicular -> pustular Initial site URT; droplet infection
Oral: erythematous ulcers of palate/fauces/uvula
Discuss shingles
Recurrence of VZV
Affect single dermatome, unilateral
Predilection for CN5/7
- oral/skin lesions if V2/3 affected
Occasionally underlying immunosuppression
- likely VZV lays in DRG or cranial nerve ganglion from childhood
- progressive + disseminated
Prodrome: pain, parathesia
Vesicles on erythematous base, scab, heal w/o scar
Discuss post-herpetic neuralgia and Ramsay-Hunt syndrome
Complications of VZV
Post-herpetic neuralgia
- severe shooting pain
- constant burning
Ramsay-Hunt
- VZV affect geniculate ganglion CN7
- ipsilateral LMNL; total paralysis
- vesicular rash EAM
- loss of taste ant. 2/3 tongue
Management of VZV
> 50y: antiviral (inc. risk PHN)
Commence within 72h rash
- dec.: duration, pain severity + duration
- red. neural damage; red. risk PHN
CNV1 assessment
Analgesics
Conditions caused by EBV
HHV4
Infectious mononucleosis Oral hairy leukoplakia Non-Hodgkin’s lymphoma Burkitt’s lymphoma Nasopharyngeal carcinoma
Discuss infectious mononucleosis
EBV
Kissing disease of teenager; salivary spread
Clinical
- fever, malaise, weight loss
- lassitude
- generalised tender lymphadenopathy
- pharyngitis
- faucial oedema
- cream tonsillar exudate
- oral petechia: H/S P junction
- gingival bleeding, ulcers
Dx + management of infectious mononucleosis
Dx: Paul Bunnell+; monospot+
Management
- symptomatic
- maintain fluid
- antiseptic m/w
- analgesic
Discuss oral hairy leukoplakia
Risk
- immunocompromised
- potent oral/inhaled corticosteroids
- transplant pt
Clinical
- demarcated corrugated white lesion
- lat. border tongue
Management: control immunosuppression
Discuss measles
Paramyxovirus
Acute, contagious infection
Clinical
- fever, rhinitis, cough, conjunctivitis
- maculopapular rash
- Koplik’s spot; 1-2d pre-rash
— B/L mucosa, soft P
— irregular patchy erythema w/ tiny central white specks
Importance of Koplik’s spot
Pathognomonic of measles
Discuss mumps
Paramyxovirus
Painful swelling major salivary glands
— usually asymmetrical
Respiratory spread
Clinical
- headache, nausea, fatigue
- dry mouth, trismus
- joint pain
- pyrexia
- mild abdominal pain
General features of hand, foot + mouth disease
CAV16 mainly
1ry childhood, highly infectious
Prodrome: mild systemic upset
Triad: macular + vesicular eruptions hands, feet + oropharyngeal mucosa
Oral + dermatological clinical findings + management of hand, foot + mouth disease
Oral
- multiple shallow painless ulcers/vesicles
- pharynx, S palate, B mucosa, tongue
- rarely req. dental opinion
- no lymphadenopathy, gingiva spared
Skin
- erythematous macules + vesicles hands + feet
- may be deep + blister
- transient: 1-3d
Management
- supportive
- antiseptic m/w
- self resolving
Discuss herpangia
CAV2/4/5/6/8
Childhood
Clinical: mild - sudden onset pyrexia + pharyngitis - oral: 2d — multiple papules, vesicles, ulcers on S palate + fauces — salivary glands: swelling, pain
Management
- no active Tx
- self resolving: 10d
Clinical features of HPV
Human papillomavirus
HPV2/4: most commonly cause mucosal warts
Butcher’s warts: hands, fingers (HPV7)
Verruca vulgaris (HPV2/4)
- white warty lesions w/ granular surface (cauliflower appearance)
- auto-inoculation from fingers: L mucosa, palate, lingual frenum
Condyloma acuminatum (HPV6/11/60)
- soft pink papillary lesion
- venereal contact: labial + lingual mucosa
- multiple lesions
Management of HPV
Tx all sites simultaneously
May resolve spontaneously
Surgical excision
Cryotherapy
Laser Tx
Medical Tx: inc. immune system
Discuss Kaposi’s sarcoma
Cancer of endothelium (blood vessels)
Associated HHV8
Site: skin, eye, mouth, nose, mucosa
Clinical
- reddy-blue/purple macules/nodules
- may ulcerated
Pathognomonic of AIDS
Tx: ART
Discuss affect of haematinic deficiencies on oral mucosa
Clinically mild B12/folate/Fe deficiency -> generalised epithelial atrophy + depapillation D tongue
Altered epithelial metabolism -> abnormal structure + keratinisation
Filiform papillae sensitive -> soreness, red. taste, ulcer, candidiasis
Oral conditions associated w/ haematinic deficiencies
Glossitis - smooth, depapillated (Fe) - raw, beefy (B12, folate) Angular cheilitis, candidiasis Recurrent Oral Ulceration - B12/Fe/Folate in 20% - typically normal Hb +/- altered MCV Burning mouth Plummer-Vinson syndrome
Discuss Plummer-Vinson syndrome
F
Characterised by
- Fe anaemia
- post-cricoid web
- glossitis
Inc. incidence oropharyngeal carcinoma
Effects of malnutrition on mucosa
Protein Energy Malnutrition
- impairment of non/specific immunity
- ascorbate deficiency
- inc. blood + saliva free corticosteroids
Retinol/Zn
- diminished cell mediated immunity
- early breakdown oral mucosa integrity
Ascorbic Acid
- impaired phagocytosis
- altered Ab response to viral Ag
Oral signs of alcoholism
Sialosis (nonspecific gland enlargement)
Erosion (2ry reflux)
Liver cirrhosis signs: easy bruising, prolonged bleeding
Malnutrition
Discuss bulimia nervosa
Obsessive control of weight
- repeated bouts of over eating then purging
Typically young F, 20s
Clinical
- weight: normal range
- hypokalaemia: repeated vomiting
- sialosis
- erosion
- Russel’s sign: calluses D hand
- ulcers S palate
- angular cheilitis
Risk factors + clinical signs acute necrotising ulcerative gingivitis
Risk
- poor plaque control
- malnutrition
- smoking
- stress
- immunocompromised
Clinical
- punched out ulcers tip of interdental papilla; readily bleed
- necrotic slough covering interdental papilla
- lymphadenopathy
Aetiology + predisposing factors of necrotising stomatitis
Noma
Aetiology: bacterial
- porphyromonas gingivalis
- fusobacterium nucleatum
- prevotella intermedia
Predisposing
- poverty, proximity to livestock
- poor OH
- measles
- malaria
- PEM + vit(A,B)/Zn deficiency
- disease: AIDS, VZV, CMV
Clinical features of noma
Necrotising stomatitis
Putrid odour
Rapid devastating necrotising destruction of soft/hard tissues
Acute
- oedema
- cheek perforation
- 2ry infection -> rapid death
Chronic
- fibrous scar
- oral strictures
- trismus
- dental malposition (tooth movement)
- salivary incontinence
Discuss VitC deficiency
Essential collagen synthesis cofactor
Clinical
Initial: enlargement + keratosis follicles -> cork screw hairs
Later
- blood vessel proliferation around follicles + interdental papilla
- gingival hyperplasia w/ haemorrhage
- tooth mobility + exfoliation
- cutaneous bleeding + purpura
Causes of Zn deficiency
Moderate
- malabsorption
- deficient diet
- chronic renal disease
- sickle cell disease
Severe
- acrodermatitis enteropathica
- post-penicillamine Tx
Clinical signs of Zn deficiency
General
- diarrhoea, lost appetite
- lethargy, depression
- pustular bullous dermatitis
- alopecia
- retarded growth
- hypogonadism
- poor wound healing
Oral
- delayed wound healing
- hypogeusia
- angular cheilitis
- candidal superinfection
- perioral psoriasiform
- erythema migrans
What is coeliac disease?
Genetically determined chronic inflammatory small intestine disease due to gluten sensitivity
Clinical findings of coeliac disease
General
- malabsorption w/ chronic diarrhoea
- weight loss
- abdominal distension
- fatigue
- childhood anaemia
- LP exacerbation
Oral
- recurrent oral ulceration
- dental hypoplasia
- glossitis, burning mouth
- angular cheilitis
Occult manifestations of coeliac disease
Metabolic bone disease Fe/folate deficiency Infertility Autoimmune disease: Sjögren’s, DM Malignancy: SCC, NHL
Disease dental hypoplasia seen in coeliac disease
96%, children 83% adults Enamel defects; symmetrically + chronologically distributed Mild enamel defects - rough surface - horizontal grooves - shallow pits
What is Crohn’s disease? Aetiology
Chronic aggressive inflammatory bowel disease
Discontinuous (‘skip lesions’) pattern of transmural inflammation
Affect whole GIT w/ large ulcerations + occasional granulomata
Aetiology: unknown
- genetic: NOD2
- environmental: enteric microflora, nutrition
- host immune response
Oral features of Crohn’s
Gingival swelling + mucosal tags Cobblestone mucosa; ulcerated fissures Lip swelling: diffuse, soft, non-tender Angular cheilitis Persistent irregular ulcers, ROU
What is orofacial granulomatosis?
Predominantly labial swelling associated w/ granulomatous inflammation
Continuum
- overt Crohn’s chronic granulomatous cheilitis Melkerson-Rosenthal syndrome
Clinical features of orofacial granulomatosis
Non-tender recurrent lip/lower face swelling
- eventually becomes persistent
Lymphadenopathy
Angular cheilitis Ulceration Vertical labial fissures Mucosal tags Tongue fissuring
Management of orofacial granulomatosis
Spontaneous remission unusual Diet: exclude benzoate, cinnamon Corticosteroids Topical tracolimus Thalidomide Adalimumab
Discuss Peutz-Jeghers syndrome
Rare, autosomal dominant
Multiple small perioral + vermillion freckles
Pigmented spots: IO, extremities, nasal + rectal mucosa
- no risk of melanoma
Hamartomatous intestinal polyps: abdominal pain + rectal bleeding
- risk internal malignancy: gut, breast, genital
Discuss black hairy tongue
Localised oral pigmentation
Aetiology
- elongation of filiform papillae
- extrinsic staining
- overgrowth pigment prod. bacteria/fungi
Associated
- smoking
- antiseptic m/w
- ABs
May alternate w/ white hairy tongue
Management
- reassure + info
- OH
- smoking cessation
- tongue brushing: avoid over brushing
- oxidising m/w
Discuss amalgam tattoo
Aetiology
- XLA amalgam filled tooth
- removal amalgam filling
Site
- mandibular gingiva
- alveolar mucosa
Slate grey, black/blue macules
No elevation
No size change; margins may blur
Histology
- lamina propria: fine granular black/brown pigment encases elastic fibres + basement membrane fo superficial capillaries
- within cytoplasm of histiocytes
Discuss graphite tattoo
2nd most common exogenous cause localised oral pigmentation
Ant. palate children
Biopsy: mandatory to rule out malignancy
- abundance granulation tissue
- destruction of labial cortical bone 1s
- residues of solid black granules
Histology
- mild chronic inflammatory cell infiltrate
- multinucleate giant cells
- solid granules consistent w/ pencil graphite
Management of amalgam/graphite tattoo
X-ray: amalgam in tissue Reassure: not health hazard Observation Excision: clinical doubt Q-switched ruby laser: shatters particles
Discuss metallic salt deposition
Metallic sulphide deposition along gingival margin
- bismuth, Pd, mercuric salts
Salts in crevicular fluid precipitate as sulphides by H2S from bacteria
Pd/Burton’s lines: linear grey/black lines along gingival margin
Discuss oral melanotic macule
F>M Benign, localised areas of pigmentation Focal inc. melanin prod. Uniformly flat black/brown macule Distinct borders, <5mm
Site
- any mucosal surface; OC rare
- lip lesion; reaction to sun damage
Management
- benign
- remove: Dx, avoid long term follow up
- lip: monitored if no suspicious feature
Discuss oral melanoma
Rare: 1-2% all melanomas
Site
- palate common
- any site
- lips, gingiva
Clinical
- darkish brown/black; 30% amelanotic
- irregular poorly defined borders
- irregular colour distribution
- thickening
Prognosis of oral melanoma
Poor: 5-20% 5yr survival
Late Dx Early metastasis; rich blood + lymphatics - lungs - liver - lymph node Aggressive histology Difficult local clearance
Discuss ecchymosis
Brushing
Red/blue
Hx: trauma
Spontaneous: underlying platelet/coagulation disorder
Discuss varices
Abnormal venous dilation
Site: lip, sublingual
Clinical - painless - blue, lobulated - blanch - thickened + hard — thrombosis w/ calcified phleboliths
Management
- observation
- excision
- sclerotherapy, laser ablation
Aetiology of Peutz-Jegher’s syndrome
Mutated LKB1 gene on chromosome 19
Codes serine-threonine kinase
Management Peutz-Jegher’s syndrome
No Tx req.
- no melanoma transformation
Counselling + monitoring
Risk internal malignancy: gut, breast, genital
Discuss racial pigmentation
POC; 5% Caucasian
Mostly gingiva (1s), any mucosa poss
Generalised
A/symmetrical
Discuss betel nut pigmentation
Areca nut pigmentation mucosa + teeth
Yellow/orange/brown
Risks
- TSL
- staining
- lichenoid reaction
- submucous fibrosis
- epithelial dysplasia
- OSCC
Discuss paan use
Combination: betel nut, leaf, slaked lime, spices, tobacco
All carcinogenic
Severe attrition
Management of betel nut/paan user
Info
Cessation advice
NRT
Biopsy if req.
Discuss post-inflammatory hyperpigmentation
Post-mucosal irritation + inflammation - inc. pigmentation during healing phase Usually generalised Common: chronic LP B mucosa Histology: melanin drop out
Discuss mediation related hyperpigmentation
Many medications + mechanisms
Mechanisms
- IO inflammatory reaction
- stim. melanin: arsenic combine w/ thiols groups
- react w/ melanin: phenothiazines + minocycline
S:
- palate
- B mucosa
- gingiva
Management: drug cessation
Examples of drugs causing hyperpigmentation
Blue-Grey
- chloroquine
- minocycline
- fluoxetine
- amiodarone
Brown
- bleomycin
- busulphan
- cyclophosphamide
- minocycline
- doxycycline
- aziodthymidine
- propranolol
Discuss Addison’s disease
1ry adrenal insufficiency - autoimmune - infection: HIV, TB, sarcoidosis Adrenal cortical atrophy + insufficiency - dec. cortisol + aldosterone
Hyperpigmentation: 2ry melanocyte stim. by inc. ACTH
Streaks/patches of blue/black pigmentation (water spaniel)
Management: steroid replacement therapy
Clinical features of Addison’s disease
Cutaneous bronzing sun exposed sites - hyperpigmentation scars + flexures Genital pigmentation Vitiligo Hypotension Hypoglycaemia Salt craving Weight loss, lethargy Nausea, vomiting
Discuss Cushing’s disease
Aetiology: inc. ACTH secretion from ant. pituitary gland Clinical - cataract - hypertension - hirsuitism - hyperglycaemia - skin thinning - ulcers - hyperpigmentation
What is Nelson’s syndrome?
Condition following removal both adrenal glands due to Cushing’s syndrome
Macro-adenomas develop which prod. ACTH
Discuss McCune-Albright syndrome and hyperthyroidism
Albright
- genetic disorder; mutation of GNAS gene
- affect: bone, skin, endocrine system
- clinical
— fibrous dysplasia
— cafe au lait macules
— hyper-functioning endocrine; Cushing’s, hyperthyroidism
Hyperthyroidism
- tachycardia
- heat intolerance
- palmar sweating
- weight loss, inc. hunger
- diarrhoea
Discuss lichen planus; epidemiology, aetiology, symptoms
Epidemiology
- 1-4% popn.
- 0.5-2% oral
- oral chronic: 4-25y
- skin: 18/12
Aetiology
- immunologically mediated
- cytotoxic T cell
- basal keratinocytes targeted; Ag unknown
- related: stress, spice, DM, liver disease
Symptoms
- asymptomatic
- pain/discomfort w/ spice/citrus
- aesthetics concerns
Discuss oral LP
Reticular: white lines, asymptomatic
Erythematous/Atrophic: superficial redding due to mucosal thinning
Erosive/Ulcerative: painful, chronic
Symmetrical: skin + oral
S: B mucosa, tongue, gingiva
- palate rare
What is Koebner phenomenon?
Feature of LP
Lesion in areas of inc. friction; flexures, O line
Discuss extra-oral forms of LP
Cutaneous - flexure surfaces wrists + shins - symmetrical, bilateral - koebner phenomenon - wickham’s striae: surface network fine white lines - purple pruritic polygonal papules + plaques — red -> violaceous — flat topped — few mm
Nails: 10%
- longitudinal pitting + grooving
- reversible
- possible onycholysis
Lichen planopilaris: scarring alopecia
Discuss vulvovaginal-gingival syndrome
Severe variant of LP Often unrecognised Usually ulcerative + symptomatic - desquamation of vulval, gingival + gingival mucosa Progressive vulval disease -> scarring Malignant transformations reported
Histological features of LP
Subepithelial band of inflammatory cells - lymphocytes Basal cell liquefaction/degeneration \+/- hyperkeratosis Saw tooth rete ridges in epidermis
Management of LP
No cure
- red. inflammation + pain
- prevent complications
Asymptomatic: reassure, GDP review
Symptomatic - remove provoking - red. irritation: spice, acid - OH — desquamative gingiva may prevent OH — alternative OH; alcohol free corsodyl
Medications for LP management
Corticosteroids: 1st line
- topical/systemic
- risk suppression HPA
Topical Calcineurin inhibitors - protein in synthesis IL2 — viral for T-cell activation - cyclosporine - tacrolimus - pimecrolimus
What is lichenoid reaction?
Condition clinically + histologically similar to LP w/ identifiable aetiology
No pathognomonic histology
Uni/bilateral
May be ulcerative
Dx: withdraw drug
Clinical features of lichenoid reaction
Clinical
- soreness similar to LP esp. erosive
- indistinguishable from LP
- asymmetric; if due to local cause
- more likely erosive + palate/tongue
Oral Contact Hypersensitivity Reaction
- sensitised to DM component
- Au, bisGMA, Am, Hg, Ni
- S: mucosa in direct contact
- patch test+
Histology of lichenoid reaction
Similar to LP
Infiltrate may be deeper + less defined Poss more plasma cells + eosinophils Perivascular infiltrate possible Colloid bodies + basal cell Ab in epithelium Consider bale basal cell liquefaction
Management of lichenoid reaction
Drug Hx + T relationship important
Patch test if local
Withdraw drug
As LP until resolution
Discuss discoid lupus erythematous
Chronic indolent disorder
Cutaneous + oral
Aetiology
- autoimmune
- may be precipitated by drug/environment/viral/hormonal
- auto-Ab + cell mediated immunity against cellular components
Cutaneous + oral features of DLE
Cutaneous - sun exposed sites - 1/+ oval plaques on face/scalp/hands - well demarcated red, atrophic scaly plaques — w/ keratin plugs in dilated follicles - generalised telangiectasia - scarring -> alopecia + pigmentation
Oral
- less well demarcated erythematous ares surrounded by fine white striae
- may ulcerate; active or in those progress to SLE
- bilateral on L/B/alveolar mucosa, vermillion border
- palate: SLE
DLE histology
Ortho/parakeratosis
Liquefaction of basal layer
Hyalinisation of subepithelial connective tissue
Chronic inflammatory infiltrate in subepithelial tissue
Irregular acanthosis
Civatte/colloid bodies
Keratotic plugging
Management of DLE
Oral: LP
Cutaneous
- chloroquine + potent topical steroids
- sunblock useful but not sufficient
- others: cytotoxics, dapsone, thalidomide, retinoids
Discuss graft v host disease
Common, serious complication follow allogeneic bone marrow transplantation
- within 6-24/12 post-BMT
Graft lymphocytes against recipient host cells
Risk
- poorly matched graft
- old donor/recipient
What is graft v leukaemia affect?
Ability of donor immune cells to eliminate/keep underlying disease in long term remission
Clinical features GvHD
May be asymptomatic Burning oral discomfort - lesions: reticular/ulcerative/erosive Salivary gland involvement -> oral dryness - superficial palatal + labial mucocele Red. opening following sclerotic GvHD
Management of GvHD
Topical analgesic: lidocaine, benzydamine
Corticosteroids: betamethasone m/w, fluocinonide/clobetasol gels
Tacrolimus ointment
Regular monitoring as OSCC inc. risk
What is pemphigus vulgaris?
Chronic organ specific autoimmune blistering disease
Aetiology: T2 hypersensitivity
- circulating + bound IgG auto-Ab against desmosome adhesins
— dissolution of cell-cell adhesion
- diet: garlic, onion, leaks, mustard
- medication: thiol containing drugs; penicillamine, captopril
Clinical features of pemphigus vulgaris
Nikolsky sign: blisters rapidly breakdown -> erosions
Desquamative gingivitis (60%)
Fragile blisters; slow healing
Dysphagia, odynophagia
Oral
- bullae fragile + short lived
- large shallow non-healing ulcers
- S: P, B mucosa, gingiva
Cutaneous
- large, non-healing erosions + ulcers
- 3-4/12 post-oral lesions
- frank blisters rare
Ix and histological features of pemphigus vulgaris
Ix
- biopsy of para-lesional and/or normal tissue
- routine histology
- blood for indirect immunofluorescence
Histology
- intraepithelial clefting + acantholysis
- intact bullae: clumps of acantholytic cells (Tzank cells)
- keratinocytes immunofluorescent+
— auto-IgG against desmoglein 3 in desmosomes in supra/basal keratinocytes
Management of pemphigus vulgaris
Systemic corticosteroids: prednisolone, deflazacort
Steroid sparing: azathioprine, cyclosporine, mycophenolate mofetil
Topical: potent corticosteroids
IV Ig
Plasmaphoresis
What is mucous membranes pemphigoid?
Chronic rare autoimmune blistering disease
Aetiology: unknown
Affects middle age-elderly; F>M
Circulating + bound Ab against basement membrane zone
- BP180/230 Ag in hemidesmosomes
Clinical features of mucous membrane pemphigoid; oral, ocular
Predominately mucosa, skin rare
Full thickness epithelium lifts off connective tissue
Large, tense bullae (blood filled) -> chronic, painful erosion
Oral
- S: any, lip rare
- nikolsky+
- blister rupture rapidly -> irregular pseudomembrane-covered painful erosions
- desquamative gingivitis
- chronic soreness, bleeding, dysphagia
- scarring uncommon
Ocular - lead to blindness - chronic conjunctivitis - blurring, irritation, photophobia - excess tears - unilateral -> bilateral within 2y - repeated fibrosis leads to scarring — symblepharon, entropion, trichiasis, blindness
Other sites of mucous membrane pemphigoid
Skin: rare 30%
- scalp: scarring alopecia
- face, neck, L trunk
Genital: 30%; sexual + urinary dysfunction
Larynx + oesophagus: infreq.
Mucous membrane pemphigoid Dx + Tx
Dx
- exam, histology, biopsy + immunofluorescence
— sub-basilar split
- DIF
— homogenous linear IgG/C3 deposits in BMZ along dermo-epidermal junction
Tx
- often resistant
- topical corticosteroid: betamethasone, clobestasol
- systemic corticosteroid
- dapsone
- anti-inflammatory AB: doxycycline, minocycline
- immunosuppressants: azathioprine, cyclophosphamide
Discuss bullous pemphigoid
Auto-Ab against hemidesmosomes
Elderly
Clinical
- skin, mouth rare
- erythema + blisters; last long T
- large, tense blisters
- preceded by itchiness
- erosions, scarring not prominent
Management
- topical/systemic steroids
- anti-inflammatory AB, dapsone
- ocular exam req.
Clinical features dermatitis herpetiformis
Rare
Chronic pruritic papulovesicular rash
Younger age group
Associated: coeliac disease
Clinical
- smaller bullae + vesicles (herpetiform appearance)
- small blisters on urticated base
- S: bum, elbows, knees
- oral: superficial transient blisters -> nonspecific tender ulcers
Ix + Tx of dermatitis herpetiformis
Histology: localised splitting at BMZ
Speckled/granular IgA immunofluorescence involving BM of dermal papillae
Tx: diet restriction + dapsone
Discuss linear IgA disease
Chronic autoimmune blistering disease
Mucocutaneous
Oral + ocular common
DIF: linear IgA deposits are epithelium CT junction w/ separation at BMZ
Tx: dapsone, steroids
Discuss angina bullosa haemorrhagica
Aetiology: unclear, old
- genetic: loose adhesion b/w epithelium + corum of mucosa
- inhaled steroid: mucosal atrophy -> dec. epithelium elastic fibres
- DM: vascular fragility
Large, IO blood filled blisters
Feels like choking
Clinical features of angina bullosa haemorrhagica
Solitary, large (2-3cm) blood filled blister Develop suddenly S: H+S palate junction Burst spontaneously within 24h Superficial ulcerative area
Resolve: 7-10d
Recur 5-10 episodes over few yr
Management of angina bullosa haemorrhagica
FBC/coagulation screen
Symptomatic: benzydamine, CHX m/w
Large, intact blisters: incised to avoid respiratory arrest
Discuss epidermolysis bullosa
Genetic collagen defect disease Many forms - lethalis: incompatible w/ life - dystrophica: recessive, skin/mucosa fragility - simplex: least severe
Oral feature of epidermolysis bullosa
Mucosal fragility Minor trauma = mucosa separate from CT Scarring -> severe deformity Severe forms - OH, dental care, eating problematic
Discuss epidermolysis bullosa simplex
Most common: 92%
Blisters @ sites of friction
- hands, feet common
Multiple types
Dominant: keratin KRT5/14 affected
- keratinisation failure -> red. integrity + ability resist mechanical stress
Management
- no cure
- symptomatic + protection
- topical/systemic corticosteroid
Discuss epidermolysis bullosa acquisita
30-40y, F>M Autoimmune: associated - Crohn’s - SLE - amyloidosis - multiple myeloma
Trauma -> widespread blistering w/ scarring
Subepidermal blisters
DIF: linear IgG deposits
Tx
- corticosteroids
- immunosuppressants
- dapsone
Define pain
Unpleasant sensory + emotional experience associated w/ actual/potential tissue damage or described in such terms
What is orofacial pain?
Pain in area
- above neck
- ant. to ears
- below orbitomeatal line
Incl. OC
What chronic pain?
Pain persisted >3/12, outlived usefulness
Disease of neuromatrix
Cure unlikely; disability caused can be red.
Difference b/w chronic + persistent
Chronic: any never go
Persistent: not intractable
What are TMDs?
Temporomandibular joint disorders
Musculoskeletal disorder involv. MoM and/or TMJ
Incl.
- myosfacial pain disorder
- TMJ disc interference; displacement w/ or w/o reduction
- TMJ degenerative joint disease
Risk factors for TMJD
F 18-44 Depression, psychological distress Exogenous hormones Facial trauma Sleep problems Bruxism Multiple pain disorders
Hx of TMJD
S: uni/bilateral, TMJ area C: dull, aching, throbbing R: pre/post-auricular, MoM A: stress, clicking, tenderness T: intermittent/constant E: opening, chewing, yawning A: sleep, analgesic S: mild-mod.
Indicators of TMJ degenerative change
Clicking Crepitus Limited movement, locking Momentary hesitation Sudden inability to fully close
Pt self management methods for TMD
Empowerment Warm joints Attention to parafunctional habits Jaw exercise Relaxation Massage Simple analgesic
Pharmacological TMD management
Analgesics - opioids - NSAIDs - paracetamol Corticosteroids - iontophoresis - intracapsular injection
Antidepressants
Sedatives
Anxiolytics
Muscle relaxants
Adjunctive therapies for TMD
Splint Acupuncture CBT Physiotherapy Botox
What is persistent idiopathic facial pain?
Poorly localised pain w/ widespread radiation
Associated w/ repeated unsuccessful dental Tx (XLA) due to belief that is chronic dental pain
Initiation + persistence
- dental Tx
- prolonged dental pain
- severe dental infection
- stress
Associated features and risk factors for PIFP
Associated
- IBS
- head, neck/backache
- dysmenorrhea
- pruritus
- fatigue
- sleep disturbance
Risk: F
- genetic
- widespread pain
- passive coping traits
Hx of PIFP
S: uni/bilateral; no anatomical area, poorly localised
C: dull, nagging, throbbing, aching, sharp
R: H+N, down arms
A: pain, personality change, life events
T: constant/intermittent
E: chewing, dental/stress, cold weather
A: rest, relaxation
S: mod-severe
What is atypical odontalgia?
Pain associated w/ tooth/edentulous ridge w/o clinical or radiographic finding
Hx of atypical odontalgia
S: tooth/edentulous ridge; UP/M most common O: dental Tx (>80%) R: well localised, may move tooth T: persistent S: mod
Management of atypical odontalgia
Key: convince pt no current dental cause
Stop ongoing dental interventions/XLAs
TCA: amitriptyline, nortryptiline
Gabapentin/pregabalin
What is burning mouth syndrome?
Idiopathic burning pain/discomfort in pt w/ clinically normal mucosa and in which medical/dental cause excluded
Hx of burning mouth syndrome
S: lips, tongue, palate (whole mouth)
C: burning, tiring, smarting, annoying, tender
A: dryness, dysgeusia, depression, anxiety, F>50
T: constant/intermittent, worse pm
E: eating, tension
A: eating, rest, distraction
S: mild-mod
Pathophysiology of burning mouth syndrome
Hormonal
- menopause: red. gonadal + neuroactive steroids
- chronic anxiety + stress impair HPA a is = red. adrenal steroids
- neuroprotective effect lost
- oral nerve terminal neurodegenerative change
Dysguesia
- neuropathic changes affect gustatory nervous system (esp. chorda tympani)
- lose inhibitory control of small fibre afferents (responsible for burning)
- inhibition of glossopharyngeal nerve lost -> taste phantoms + altered pain/touch
Management of burning mouth syndrome
Reassurance: physiological cause Symptomatic - saliva substitute - benzydamine m/w TCA, SSRI CBT Allhalipoic acid, gabapentin, clonazepam
Hx glossopharyngeal neuralgia
S: unilateral, RHS more common C: stabbing R: ear, base of tongue, tonsillar fossa, beneath angle of jaw A: syncope, arrhythmias T: transient, remission may occur E: swallowing, chewing, speaking, coughing A: pulling on ear S: severe
Difference b/w 1/2ry glossopharyngeal neuralgia + aetiology
2ry has persistent background aching + exacerbations
Aetiology
- 1ry: nerve compression
2ry: congenital vascular abnormality/tumour/aneurysm
What is Eagle syndrome?
Glossopharyngeal neuralgia differential
Due to elongation of stylohyoid process (age, trauma) compression CN5/9/1
Clinical
- shooting pain of throat, ear, jaw
- pain of tongue base
- worse on swallowing, turning head
- tinnitus, hypersalivation, feeling of something stuck in throat
Tx: styloidectomy
What is trigeminal neuralgia?
Sudden, unilateral, severe, brief, recurrent stabbing pain in 1/+ branches of CN5
Rare: 50-60y
- M: 108/mil
- F: 200/mil
Hx of trigeminal neuralgia
S: CN5; unilateral (97%), RHS (60%)
C: flashing, shooting, sharp, unbearable, terrifying
A: trigger zones, weight loss
T: seconds, remission wks/mnths
E: light touch, eating, talking, spontaneous
A: avoid touch, anticonvulsants, sleep
S: mod-severe
Aetiology of trigeminal neuralgia
Idiopathic
Aberrant cerebellar artery compressing nerve root @ root entry zone
Discuss multiple sclerosis + post. fossa tumours in relation to trigeminal neuralgia
MS: demyelination of nerve fibres
- 1-5% have TN
- present younger cf TH (20-40)
- likely bilateral
- therapy response poor
Post. Fossa Tumours
- meningiomas, neuromas
- 2% have TN
- facial numbness
- MoM weakness
- may be constant
Pharmacological management options for trigeminal neuralgia
Carbamazepine (gold)
Oxcarbazepine
Lamotrigine
Baclofen
Discuss carbamazepine use for trigeminal neuralgia
70% pt have pain red.
Failure usually due to inc. severity
Inc. dose slowly
- 300-800mg QTD
Adverse
- drowsiness
- dizziness
- nausea, constipation
- diplopia, blurred vision
- ataxia
What is giant cell arteritis?
Granulomatous arteritis affect M/L arteries esp. extracranial branches of carotid
- temporal most freq.
Clinical features of giant cell arteritis
Elderly pt new on sent/type of headache Carotidynia Superficial temporal arteries - thickened - tender - nodular - erythematous Ophthalmic - diplopia - blurring - amaurosis fugax (temp. loss of vision) - obscuration
Associated features giant cell arteritis
Tongue/jaw claudication whilst chewing Rare - necrosis tongue/scalp - toothache - trismus General - pyrexia - fatigue - weight loss Polymyalgia (50%) Ischaemic limb pain, angina, thoracic + abdominal aneurysm
Giant cell arteritis histology
Inflammatory cell infiltrate
Giant cells
Thrombus
Arterial wall hyperplasia
Management of giant cell arteritis
Corticosteroids
Ca + VitD supplements
Visual loss improves in only few pts
Causative species + transmission of syphilis
Causative: treponema palladium Transmission - venereal: close contact w/ lesion (main) - blood: IVDU - vertical: mother-child
Discuss 1ry and 2ry syphilis
1ry: 3-4/52 post-infection
- chancres: 1st symptom
— infectious, firm, painless nodule @ inoculation site
— breakdown -> painless sore/ulcer
— resolves spontaneously 2-6/52
— S: genital, oral
- lymphadenopathy: neck, groin, armpits
2ry: 2-6/12
- non-itchy maculopapular rash
- sore throat, several weeks
- condylomata lata
- general
— tiredness, headache
— fever
— weight loss
— patches of hair loss
— joint pain
- followed by latent period; last several years
3ry syphilis
3-15 post-infection
Gummatous: eyes, heart, liver (any organ)
- gummas: necrotic centre surrounded by inflammation
— painless
— OC: palate
Neurosyphilis: brain, nerves
CV syphilis: blood vessels
Complications
- blindness, deafness
- dementia
- stroke, heart disease
- paralysis
Potentially life threatening
Dx + management of syphilis
Dx
- Hx + exam
- serology: syphilis Ab
- swab: sores/ulcers
Management - referral to GUM - partners informed - ABs — early syphilis: penicillin, doxycycline — late: IV penicillin
HIV virus + transmission route
Lentivirus, retrovirus
Transmission
- general
- blood: IVDU
- vertical: perinatal
Pathogenesis of HIV
Attach to CD4 R on T helper lymphocytes; gain entry into cell
RNA -> DNA (reverse transcriptase) = viral replication + assembly
Cell lysis -> infect other cells
- cells destroyed or stop functioning
Immune system cells HIV particles and infected cells, lost T cells replace
Discuss stage 1 and 2 of HIV infection
1: 1ry infection
- lasts few wks
- short, flu-like illness
- 20%: serious enough to consult Dr; Dx missed
- large amount HIV in peripheral blood
- seroconversion: immune system prod. HIV Ab + cytotoxic lymphocytes
— test before seroconversion = false -ve
2: Clinically Asymptomatic
- 10yrs, no major symptoms (lymphadenopathy)
- peripheral blood HIV drops
— remain infectious, Ab detectable in blood
- not dormant: v active in lymph nodes
- many T cells infected + die, lots HIV prod.
- viral load test: measure HIV escapes lymph nodes (accurate to 50copies/mL)
Stage 3 and 4 of HIV
3: Symptomatic
- immune system loses struggle
— lymph nodes + tissues damaged
— HIV mutates: more pathogenic + stronger -> more T cell destruction
— failure to adequately replace T cells
- symptoms develop as immune system fails
4: AIDS
- immune system more damaged + illness more severe
- Dx: HIV+ pt develops 1/+ opportunistic infection/cancer
- CDCP: CD4 <200/microL
What opportunistic infections are diagnostic for HIV?
Pneumocystis carinii - most freq. - pneumocystis carinii pneumonia; rarely disseminates CMV HSV Toxoplasmosis Fungal Mycobacterium
Importance of oral manifestations of HIV
Can indicate HIV Predict progression HIV->AIDS Entry/endpoint in therapy/vaccine trials Determinant of anti-opportunistic infection + anti+HIV therapy Staging/classification
Group 1 oral manifestations of HIV
Strongly associated w/ HIV
Candidiasis: erythematous (denture), pseudomembranous (wipe off)
Hairy leukoplakia: corrugated tongue (EBV)
Kaposi sarcoma: HHV8, cancer endothelial cells
PD
- linear gingival erythema
- ANUG (interdental papilla tip), NUP (inc. destruction)
Non-Hodgkin’s lymphoma: singular firm nodule
Management of HIV
Antiretroviral therapy
- zidovudine
- Retrovir
- tenofovir
Effect of ART
Inc. CD4, dec. viral load
Oral: red. prevalence of manifestations
Commencing can cause deterioration/reestablishment of opportunistic infections as immune system strengthens and fights again
