oral med and pathology p262 (275) Flashcards
acquired diseases classification
VIITAMIIN
V ascular
I nfective
I nnflammatory
T rauma
A uto-immune
M etabolic
I diopathic
I atrogenic
N eoplastic
Vacular diseases of
circulatory origin
Infective diseases are
caused by the entrance into the body of organisms (bacteria, protozoans, fungi or viruses)
Inflammatory disorders
result in the immune system attacking the body’s own cells or tissues may cause abnormal inflammation, which results in chronic pain, redness, swelling, stiffness and damage to normal tissues
Trauma
physical injury, sometimes chronic and low stress or singular and dynamic
Auto-immune diseases are
caused by antibodies or lymphocytes produced against substances naturally present in the body
Metabolic diseases
disrupt the processes of energy conversion and utilisation on a cellular level
Idiopathic disease are
any diseases with an unknown cause or mechanism of apparently spntaneous origin
Iatrogenic disease
due to activity of a physician or medication effects
neoplastic diseases are
conditions that cause tumour growth - both benign and malignants
neoplasm
abnorma growth of cells (tumour)
congentital diseases
diseases, defects or deformities dating from birth but not necessarily hereditary
symptoms
something a pt feels or observes which they regard as abnormal e.g. pain, weakness of limb
discovered when taking hx
sign
functional abnormality demonstrated by a physical exam of pt
syndrome
combination of symptoms and/or signs which commonly occur together e.g. TMJD syndrome
how to present a case
name
age
occupation
residence
how long ago since presentation
presentation itself and duration of
macule
flat, non palpable lesions <10mm in diameter usally pigmented
papules
elevated, palpable lesions <10mm
plaques
either elevated/depressed compared to skin surface
>10mm diameter
may be flat topped or rounded
nodules
firm papules or lesions that extend into dermis or subcutanoues tissue
e.g. cysts, lipoma, fibromas
vesicles
small, clear, fluid filled blisters <10mm in diameter
vesicles are characteristic of herpes infections, acute allergic contact dermamtitis and some autoimmune blistering disorders
bullae
clear fluid-filled blisters >10mm in diameter
may be caused by burns, bites, irritant or allergic contact dermaitits and drug reactions
classic autoimmune bullous diseases inc pemphigus vulgaris and bullous pemphigoid
pustules
vesicles contain pus
common bacterial infections and folliculiltiis and can be seen in some inflammatory disorders
urticaries (wheals or hives)
characterized by elevated lesions caused by localized edema.
Wheals are pruritic and red.
are a common manifestation of hypersensitivity to drugs, stings or bites, autoimmunity, and, less commonly, physical stimuli including temperature, pressure, and sunlight.
typical wheal lasts < 24 h.
scale
heaped-up accumulations of horny epithelium that occur in disorders such as psoriasis, seborrheic dermatitis, and fungal
infections.
Pityriasis rosea and chronic dermatitis of any type may be scaly.
crusts/scabs
dried serum, blood, or pus. Crusting can occur in inflammatory or infectious skin diseases (eg, impetigo)
erosions
open areas of skin that result from loss of part or all of the epidermis.
can be traumatic or can occur with various inflammatory or infectious skin diseases.
An excoriation is a linear erosion caused by scratching, rubbing, or picking.
ulcers
result from loss of the epidermis and at least part of the dermis.
Causes include venous stasis dermatitis, physical trauma with
or without vascular compromise (eg, caused by decubitus ulcers or peripheral arterial disease), infections, and vasculitis
petechiae
nonblanchable punctate foci of hemorrhage.
Causes include platelet abnormalities (eg, thrombocytopenia, platelet dysfunction), vasculitis, and infections (eg, meningococcemia, Rocky Mountain spotted fever, other rickettsioses)
purpura
larger area of hemorrhage that may be palpable.
Palpable purpura is considered the hallmark of leukocytoclastic vasculitis.
Purpura may indicate a coagulopathy. Large areas of purpura may be called ecchymoses or, colloquially, bruises
atrophy
thinning of the skin, which may appear dry and wrinkled, resembling cigarette paper.
may be caused by chronic sun exposure, aging, and some inflammatory and neoplastic skin diseases, including cutaneous T-cell lymphoma and lupus
erythematosus.
also may result from long-term use of potent topical corticosteroids.
scars
areas of fibrosis that replace normal skin after injury.
some scars become hypertrophic or thickened and raised.
Keloids are hypertrophic scars that extend beyond the original wound margin
telanglectases
foci of small, permanently dilated blood vessels that may occur in areas of sun damage, rosacea, systemic
diseases (especially systemic sclerosis), or inherited diseases (eg, ataxia-telangiectasia, hereditary hemorrhagic telangiectasia) or after long-term therapy with topical fluorinated corticosteroids.
erosion vs ulceration
Erosion - partial epithelial thickness loss, but can still clinically see epithelium
Ulceration - full loss of epithelium with possible yellow fibrin deposits
linear lesions
straight line and are suggestive of some forms of contact dermatitis, linear epidermal nevi, and lichen striatus. Traumatically induced lesions, including excoriations caused by the patient’s fingernails, are typically linear.
annular lesions
rings with central clearing.
Examples include granuloma annulare, some drug eruptions, some dermatophyte infections (eg, ringworm), and secondary syphilis
nummular lesions
circular or coin-shaped; an example is nummular eczema.
target lesions
bull’s eye/iris
appear as rings with central duskiness
are classic for erythema multiforme
serpigingous lesions
linear, branched, and curving elements. Examples include some fungal and parasitic infections (eg, cutaneous larva migrans).
reticulated lesions
lacy or networked pattern. Examples include cutis marmorata and livedo reticularis.
herpetiform lesions
grouped papules or vesicles arranged like those of a herpes simplex infection.
zosteriform lesions
lesions clustered in a dermatomal distribution similar to those of herpes zoster.
verrucous lesions
irregular, pebbly, or rough surface. Examples include warts and seborrheic keratoses.
lichenification
thickening of the skin with accentuation of normal skin markings; it results from repeated scratching or rubbing.
induration
deep thickening of the skin, can result from edema, inflammation, or infiltration, including by cancer.
Indurated skin has a hard, resistant feeling. Induration is characteristic of panniculitis, some skin infections, and cutaneous metastatic cancers
umbillicated lesions
have a central indentation and are usually viral. Examples include molluscum contagiosum and herpes simplex.
red lesion called
erythema
result from many different inflammatory or infectious diseases. Cutaneous tumors are often pink or red.
Superficial vascular lesions such as port-wine stains may appear red.
yellow skin due to
jaundice, xanthelasmas and xanthomas, and pseudoxanthoma elasticum.
violet skin due to
result from cutaneous hemorrhage or vasculitis. Vascular lesions or tumors, such as Kaposi sarcoma and hemangiomas, can appear purple. A lilac color of the eyelids or heliotrope eruption is characteristic of dermatomyositis.
shades of blue, silver or gray in oral tissues due to
result from deposition of drugs or metals in the skin, including minocycline, amiodarone, and silver (argyria). Ischemic skin appears purple to gray in color. Deep dermal nevi appear blue.
black skin lesions due to
melanocytic, including nevi and melanoma.
Black eschars are collections of dead skin that can arise from infarction, which may be caused by infection (eg, anthrax, angioinvasive fungi including Rhizopus,meningococcemia), calciphylaxis, arterial insufficiency, or vasculitis
Nikolsky sign
epidermal shearing that occurs with gentle lateral pressure on seemingly uninvolved skin in patients with toxic epidermal necrolysis and some autoimmune bullous diseases.
9 points for describing a mucosal swelling
Site
➡Trauma Area?
➡Gingiva?
Size
➡Static?
➡ Increasing/Decreasing
Surface
➡Normal Mucosa?
➡Granulation tissue?
➡Smooth?
➡Tessellated?
➡Ulceration?
Colour
Consistency
➡Soft/Friable?
➡Firm?
➡Hard/Bony?
Shape
Base
➡Pedunculated? (stalk)
➡Sessile? (immobile)
Bleeding
➡Spontaneous?
➡Trauma induced?
Fnctional Limitation
ulceration key questions
8
where
size and shape
blister or ulcer
how long for - more than 2 weeks
recurrent - same or different sites
painful
margins - flat, raised, rolled
base - soft, firm, hard
parotid gland
secretion type
serous
submandibular gland
secretion type
mixed - mainly serous (90%)
sublingual gland
secretion type
mixed - mainly mucous
direct salivary gland problems
6
aplasia
duct atresia
sarcoidoisis
HIV
gland infiltration
cystic fibrosis
aplasia of salivary gland
congenital absence of one or more salivary glands
ectodermal dysplasia - abnormal development of anatomy of ectodermal origin e.g. skin, hair, teeth, sweat glands
duct atresia of salivary gland
failure of duct to canalise
can result in formation fo salivary retention cysts
sarcoidosis of salivary glands
presence of collection of glanulomas
can occur in any organ but often affect salivary glands causing large massess and facial palsy
HIV and salivary glands
partoid enlargement occurs in up to 10% of pts
2 types of salivary gland infiltration
amlyoidosis
haemachromatosis
amyloidosis of salivary gland
build up of protein fibrils
lymphoepithelial cysts
haemachromatosis of salivary glands
causes xerostomia
cystic fibrosis and salivary glands
causes plugging of acinar ducts with precipitated secretions
essentially microscoptic sialoliths
radiotherapy effect on saliva glands
salivary tissues are particularly sensitive to radiotherapy
* highly differentiated and specilised state
* reduction of quality and quantity of saliva
(not because of their high mitotic figures like other radiosensitive tissues)
radiotherapy effect on quality of saliva
usually reproduced 4-8weeeks after finishing tx
thick, viscous and bad tasting
fibrosis of salivary tissue can occur due to enderarteritis
Graft vs Host disease
and salivary glands
experienced mainly in haematopoetic stem cell pts
results in sjorgren’s syndrome
anti-neoplastic drugs and saliva glands
(chemo)
reduced secretion
early apoptosis of salivary glands cells
w
radioiodine effect on salivary glands
reduction in gland function
inc lymphocytic infiltrate
anti-muscarininc cholinergic drugs
e.g.
tricylic antidepressants - amitryptiline
antipsychotics - clozapine, risperidone
antihistamines - chlorphenenamine
atropine
diuretics - furosemide, bendroglumethiazide
cytotoxic - azathioprine, cyclosporin
drugs which can cause dry mouth
anti-muscarininc cholinergic drugs
indirect salivary problems
classess
chronic medical issues
acute medical problems
chronic medical issues which can cause dry mouth
6
dehydration
diabetes (mellitus and insipidus)
renal disease
stroke
addison’s disease
persistent vomitting
acute medical problems which can cause dry mouth
4
acute oral diseases
burns
vesiculobulous disease
haemorrhage
modified european criteria for sjorgren’s syndrome dx
dry eyes/mouth
need 4 or more for dx
* subjective or objective findings
* autoanitbody findings
* imaging findings
* radionucleotide findings
* histopahtology findnsg
eye symptoms for sjogrens
presistent troublesome dry eyes for >3months
recurrent sensation of sand/gravel in the eyes
tear subsitutes used >3times day
oral symptoms for sjogrens
daily feeling of a dry mouth for >3months
recurrent swelling of salivary glands as an adult
frequently drink liquid to aid swallowing fo dry foods
3 types of sjorgren’s
sicca syndrome
primary
secondary
sicca sjogrens syndrome
partial sjogren’s findings
primary sjogren’s syndrome
no connective disease but meets criteria otherwise
secondary sjogren’s syndrome
CT disease
SLE, rheumatoid arthritis, scleroderma
dry mouth management
prevent oral disease
caries
* fluoride
* OHI
* tx plan
candida/staphlyococci
* angular cheilits
* sore tongue
reduce symptoms
* salivary substitutes
* water/chewing gum
hypersalivation is
Constant stimulation of salivary centre of brain located in the superior salivary nucleus of the facial nerve
can have true (rare) or perceived (common)
true hypersalivation causes
stroke
degenerative CNS condistions - CJD, MS, Alzheimers
drugs
perceieved hypersalivation causes
dysphagia
viral salivary gland infections
paramyxovirus
unilateral or second attacks possible
bacerial salivary gland infections
ALWAYS an underlying cause
dehydration and flow reduction
flow obstruction
diabetes
immune suppression
abnormal anatomy
salivary gland obstruction
3 possible
recurrent parotiditis
chronic obstructive saliadentitis
sialolithiasis
recurrent parotiditits
effect
HIV
bacterial infection
causes duct sclerosis
chronic obstructive sialadentitis
effect
usually caused by sialothiasis
can be post-op
sialothiasis
effect
usually submandibular
2x as much calcium in this gland Vs parotid
also alkaline and mucous
due to saliva flow at sight of food pain is often peri-prandial
possible link w gout
secretion retention can cause
2
mucocele
duct obstruction
mucocels can be
3
extravasation mucocele - trauma of excretory duct and escape of mucous into surrounding tissues
retention mucocele (mucous retention cyst) - intermittent duct obstruction in elderly pts
superficial mucocele
salivary gland hyperplasia can occur in
2
sialosis
sjorgrens
sialosis
chronic, bilateral, diffuse, non-inflammatory, non-neoplastic swelling of the major salivary glands that primarilyaffects the parotid glands, but occasionally involves the submandibular glands and rarely the minor salivary glands
This can be painless or in some instances tender.
most common salivary tumour
Pleomorphic adenoma - has dual origin in glandular and myoepithelial components
dental pain characterisitcs
short sharp pain
introduced by pressure, thermal and chemical inductions
gets worse with time
neuropathic pain characterisitcs
Constant burning/aching pain
Fixed location
Often a fixed intensity
Chronic Regional Pain Syndrome (CRPS)
* Autonomic nerve version of neuropathic pain
Usually a history of ‘injury’
possible ‘injuries’ that can cause neuropathic pain
trauma
extractions
routine tx without complications
herpes zoster (shingles) episode
destructive tx for pain
systemic meds for neuropathic pain
pregablin
gabapetin
tricyclic antidepressants (amitryptiline)
topical medication for neuropathic pain
capasaicin
EMLA
benzdamine
atypical odontalgia
Dental pain without detected pathology
Distinct pattern of pain
* Pain free or mild between episodes
* Intense unbearable pain
➡ 2-3 weeks duration
➡ Settles spontaneously
persistent idiopathic facial pain
pain which poorly fits into chronic pain syndromes
often high disability levels
often other systemic features - musculo-skeletal pain syndromes
often responds poorly to tx
trigeminal neuralgia
a trigeminal autonomic cephalgia (TACs)
acute spasms of sharp, shooting pain
trigger point may be identified
* brought on by: movement, eating, talking, worse with cold weather
remissions and relapses
trigemial neuralgia tx
carbamazepine (modified release)
oxcarbazepine
lamotrigine
MRI scan
surgical options for trigemial neuralgia
Peripheral neurectomies
trigeminal Nerve Balloon Compression
Microvascular decompression (MVD)
Radiosurgery – Gamma knife
after MRI scan
red flags for TN
Younger patient (>40yrs)
Sensory deficit in facial region - hearing loss – acoustic neuroma
Other Cranial nerve lesions
ALWAYS test cranial nerves (identify sensory deficit) systematic examination
ALL patients now get MRI
cluster headaches
‘Trigeminal Autonomic Cephalgias (TAC’s)’
Symptoms
Intense pain
➡generalised or localised headache
➡usually/evening night
vasomotor changes
➡lacrimation
➡nasal congestion
➡swelling over painful site
➡pupillary and conjunctival changes variable
dyseasethesia
Abnormal sensory PERCEPTION in ABSENCE OF ABNORMAL STIMULUS
ALL modes of oral sensation involved
* thermal
* taste
* touch
* moistness
burning mouth
TMD pain history
almost any chronic face/head/neck pain (inc wisdom teeth pai)
symptoms show periodicity
morning/evening exacerbation
parafunctional clenching
TMD exam
Focal muscle tenderness
➡ Masticatory muscles
➡ sternomastoid
➡ Trapezius
tenderness over TMJ itself
limitation of opening
locking (dispalcement with reduction)
Joint noise
➡ crepitus - degenerative OA changes
➡ click - related to disc dysfunction (dispalcement with reduction)
Deviation on opening
➡ common finding with muscle dysfunction
Dental occlusion upset
management of TMD
Physical therapy exercises
education - supportive yawning etc
stress management (CBT, mediatation)
Soft diet
analgesia
Bite splint (over all occlusal surfaces - soft or hard or hybrid)
Biochemical manipulation
➡ Tricyclic (not SSRI)
➡ other anxiolytic medication
non keratinised oral mucosa
lining mucosa
oral surface of lips, FOM, ventral tongue
keratinised oral mucosa
masticatory mucosa (hard and part of soft palate, gingiva)
orthokeratinised
nuclei free keratin layer
least common form of epithelium
hard palate and gingiva
parakeratinised
immature form of orthokeratinised
same layers but more indistict, not as many finger like projections as ortho
speciliased lingual papilla, partially nucleated
oral epithelium structure type
stratified squamous epithelium
characterisitcs of stratified squamous epithelium
has a cuboidal basal layer
flattened surface layer
ultimately they will shed as anucleate ‘squames’
cell division occurs in basal cell layers and suprabasal (ground up)
prickle cell layer formed from desmosomes joining
basement membrane in strat squam epith
basal lamina
➡lamina lucida (epithelium side)
➡lamina densa (lamina propria side)
reticular connective tissue (Type III collagen)
lamina propria characteristics
loose areolar connective tissue
Feeder vessels
elastic fibres
lymphatic vessels
submucosa
may or may not be present
contains adipose
salivary gland tissue
A variable number of Fordyce spots or granules are scattered throughout the nonkeratinized tissue. These are a normal variant, visible as small, yellowish bumps on the surface of the mucosa. They correspond to deposits of sebum from misplaced sebaceous glands in the submucosa that are usually associated with hair follicles
9 types of epithelium reactive lesions
keratosis
acanthosis
elongated rete ridges
atrophy
erosion
ulceration
oedema
blister
dysplasia
acanthosis
hyperplasia of stratum spinosum
elongated rete ridges
hyperplasia of basal cells
atrophy
reduction in number of viable layers
erosion
partial epithelial thickness loss but can still see epithelium
ulceration
full thickness loss with fibrin on surface (yello)
reactive oedema types
2
➡ Intracellular - also known as cloudy swelling, most common form of
cellular injury
➡ Intercellular (Spongiosis)
blister
Vesicle - circumscribed, elevated lesion < 5mm in diameter containing
clear serous fluid
Bulla - a vesicle with a diameter > 5mm
Contents
* Superficial epithelium (serous)
* Deep epithelium (blood filled) n.b feeder vessels
dysplasia
disordered maturation (growth) in a tissue
epithelial dysplaisa (cellular atypia) can only be dx histopathologically (not clinical)
predictors of malignancy
2
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia
cellular atypia
3 key features
pleomorphism
hyperchromatism
basal cell hyperplasia
WHO 2005 epithelial dysplasia grading
hyperplasia
dysplasia
➡ Mild
➡ Moderate
➡ Severe
carcinoma in situ
basal hyperplasia
WHO 2005
Increased cell numbers
Architecture
➡regular stratification
➡basal compartment is larger than normal
No cellular atypia
mild dysplasia
WHO 2005
Architecture - changes in lower 1/3
Cytology - mild atypia
➡ Pleomorphism
➡ Hyperchromatism
➡ Basal Cell hyperplasia
moderate dysplasia
WHO 2005
Architecture - change into the middle 1/3
Cytology moderate - atypia
severe dysplasia
WHO 2005
Architecture - changes in the upper 1/3
Cytology - severe atypia and numerous mitoses, abnormality high
carcinoma in situ
WHO 2005
theoretic concept of MALIGNANT CELLS IN THE LAMINA PROPRIA
malignant but not invasive
abnormal architecture
➡full thickness (or almost full) of viable cell layers
pronounced cytological atypia
➡mitotic abnormalities
