bsi mod 3 Flashcards
compound vs simple gland
- compound gland: salivary. Simple is sebaceous with 1 duct
dense irregular connective tissue
- mesoderm but some neural crest
- structure, exchange, defense and fat storage
- MUCOSA
strat spinosum
- become spinous cells, larger than basal
- less nc ratio
- no prolif!
- integrin profile changes from a6b4 to a3b1. also keratin profile changes
- no organells, chromatin condense
cytokeratins
made by all epi cells
- int fila
- type 9-20 are type 1 and acidic
- KRT 1-8 are basic
- found in pairs
top layer in skin is called what in oral cavity, skin? characteristics
stratum superficiale is called superficial layer in mucosa and oral cavity, stratum corneum in skin
- this is no organelles, flat and varied width
- water resistant and barrier
hemidesmosome structure
cytokeratin molecules in cytoplasm are connected to integrin a6b4 via bullous pemphigoid 230 and 180 and plectin
- then integrin crosses plasma mem to bind laminin 5 (laminin 332)
desmosome structure
thick part: desmoplakin and plakogoblin
desmoglein and desmocollin are zipper in intercell space
where to find parakeratin
hard palate, dorsum of tongue and attached gingiva
- retained nuc
where to find orthokeratin
in skin!!
melanocytes
- neural crest derived
- live in basal skin and mucosa
- communicate to keratinocytes via dendrites
- melanin does uv rad protection
- cells take up this melanin (umbrella style)
- same number of melanocytes in everyone! pigment depends on number and size of MELANOSOMES, dispersion in skin
- sometimes even on attached gingiva
langerhans cells
- dendritic from bone marrow
- in strat spinosum
- found in all layers of epi and papillary derm
- granulated birbeck stuff thats black
- immune macrophages (1st cells)
merkel cells
- proprioception sensory cells
- from epi progenitor cells
- in basal layer
- from keratinocytes
- fingers, feet, hard palate, lips
- touch stuff. communicate with sensory nerves DIRECTLY
white sponge nevus
mutations in cytokeratin 4 or 13
- white tongue
pachyonychia congenita
mutations in cytokeratin 6,16, or 17
- happens in the accral skin (palms and soles)
- fingernails
- thickened keratin
epidermolysis bullosa (general)
mutations in cytokeratin 5 and 14
- the mitten hand one
- blisters, ulceration
- hereogneous
pemphigus vulgaris
desmoglein 3 is bad
desmosome
- red burning thing
- SUPRABASAL CLEAVAGE IN SPINOUS LAYER!!!
pemphigus foliaceus
desmoglein 1 bad
desmosome
mucous membrane pemphigoid
bp 230 and 180
- mucous problem ONLY
- blindness thing
- antibodies attach proteins that are sub-basilar (under basement mem)
- THIS IS HEMIDESMOSOMES
bullous pemphigoid
bp 230 and 180
- skin problem ONLY
lamina lucida
- made by basal epi
- unique to epi
- anchored by laminin 332 and collagen 17 (bp 180!)
lamina densa
- made by basal epi
- unique to epi
- collagen 4, nidogens nad perlecan
- anchored by collagen 7!!!!
- binds to 4 and laminin 332 above
- binds to collagen 1 and 3 below
“clothespin”
lamina reticularis
- made by fibroblasts
- NO part of basal lamina
- collagen 1 and 3, elastic fibers, fibronectin
epidermolysis bullosa simplex
cytokeratin 5 and 14 or plectin
- separation above basement mem
- all over the body
junctional epidermolysis bullosa
collagen 17, integrin a6b4 or laminin 332
- most severe
- can dev amelogenesis imperfecta, tooth loss and caries
- separation in lamina lucida layer of basement mem
dystrophic epidermolysis bullosa
collagen 7
- risk for skin and oral cancer!!
- separation under basement mem
fixed cells
fibroblasts (mesenchyme), myofibroblast (mesenchyme), adipocytes (mesenchyme), pericytes, mast (bone marroq) and macrophage (bone marrow)
transient cells
- from bone marrow!!!!
- NEB, monocytes, macrophages, lymphocytes, plasma cells
fibroblasts
- make collagen, reticular (type 3), elastic
- trichrome, VVG and reticulin stain
collagen types
1 is found in skin and mucosa. most abundant
- type 2 in cartilage
- type 3 in blood vessels, support for hollow organs
- type 4 in basement mem (NON-FIBRILAR)
- type 5 needed for fibrillation of type 1 and 3
type 1 collagen
- found in almost all organs of the body including tendons, bones, ligaments
- found in dermis layer
- triple helix structure that decreases with age
3 proteins, 2 a1 chains and 1 a2 chain
- c terminal does triple helix in rough er, then procollagen in cyto, tropocollagen, fibril and fiber
type 3 collagen
- young skin tissue, blood vessels, lungs and internal organs
- papillary dermis
- 3 helix that is thin and shorter than type 1
scurvy
- gingiva and perio inflam
- loss of teeth
- bleeding
- impaired wound healing
ehlers danlos syndrome
- heterogenous
- bad collagen or NOT ENOUGH of 1,3,5
- if 3 then blood vessels integrity bad, bruising, hemorrage
- mess up the helix
elastic fiber
elastin and microfirbils (made of fibrilin)
- elastic in, fibrilin out
cutis laxa
sagging, non stretch skin
- wrinkeld
- elastin defect
marfan syndrome
- tall with long everything
- flexible joints
- high arched palate
- aortic rupture
- fibrilin defect
papillary lamina propria and reticular components + location
- papillary is loose tissue that is closer to basal mem, reticular is more collagenous and deeper
- contains; vasculature, fibroblast, collagen, elastin, nerves (PNS), meissner corpuscles ONLY FOUND IN PAP
submucosa
- under reticular lamina propria
- contains fibrocollagenous tissue, nerves, adipose, minor salivary glands, skeletal muscle
- varies by site!
- attached gingiva and hard palate don’t have submucosa (since bound directly to bone as MUCOPERIOSTEUM)
masticatory mucosa
- found on hard palate
- everywhere where skin touches food
- attached gingiva, tongue
- ## parakeratinezed
specialized mucosa
- dorsal tongue only
- parakeratin and non
- masticatory but also flexible and sensory
lining mucosa
- non keratin
- found everywehre else in mucosa
- thicker than masticatory and flex
tongue
- posterior 3 from branchail arches 3 and 4
- base of tongue contains lymphoid tissue
- entrance to oropharnyx!!!!
- anterior 2/3 from 1st arch
- has v shape terminal sulcus with foramen cecum at tip (remnant of thryoid gland!!)
filiform papillae
- cover anterior 2/3 tongue
- hair like
- point towards orophanyx (back)
- thick keratin
- non keratinized between papillae
- no taste buds!
fungiform papillae
- anterior 2/3
- scattered and mushroom like
- no keratin
- vascular
- taste buds!!
- the pink spots on tongue
foliate papillae
- at the lateral posterior surface
- 4-11 parallel ridges
- taste buds within the ridges
- no kerain
circumvallate papillae
- form the v shape at the terminal sulcus? converge at the foramen cecum
- keratin on top
- lateral walls are not keratin
- deep circular groove that opens to minor salivary glands
- SEROUS GLANDS OF VON EBNER!! only place
where to find taste buds
- fungiform, foliate, circumvallate, soft palate, pharynx
NOT IN FILIFORM
taste bud
- barrel shaped
- 30-80 spindle cells
- can taste in all cells
umami foods are rich in
l glutamate, inosine monophosphate and guanosine monophosphate
waldeyers ring
- ring of lymphoid tissue
- back is pharyngeal tonsil, then tubal tonsil, palatine tonsil, lingual tonsil, palatine tonsil, tubal tonsil
fordyce granules
- ectopic sebaceous glands in lamina propria
ORAL mucosa dev at 26 days
fusion of stomatodeum with foregut
ORAL mucosa dev at 5-6 weeks
stratification of epi
ORAL mucosa dec at 7 weeks
- tongue epi shows specialization
- circumvalate, foliate, and fungiform papillae
- taste buds form
ORAL mucosa dec at 8-12 weeks
- mouth begins to become defined, palatal shelves elevate and close
ORAL mucosa dec at 10-12 weeks
specific keratinization patterns become apparent, filiform papillae on anterior 2/3 tongue
ORAL mucosa dec at 13-20 weeks
- oral epithelia thicks, parakeratinization
internal lip contains
- labial mucosa, beginning of oral mucosa and minor salivary glands
attached gingiva
- pale pink, stipled (like an orange), keratin, no submucosa!!, collagen attaches to periosteum of bone
alveolar mucosa
- reddish, thicker epithelial layer, non keratin, submucosa, flexible
free gingiva
- keratinized on outside, non keratinized on segment facing tooth
- can be broken down by plaque!!
dentinogingival junction
- where oral mucosa meets tooth structure
- point of weakness, may be damaged by bac
- seal btw oral cavity and underlying tissues
dgj oral epi
this is the outer ridge part of the free and attached gingiva
- keratin
dgj sulcar epithelium
- these cells extend from edge of junctional epi to gingival margin
- no keratin
- depth of 0.5 to 3 mm (3- 3.5 is normal)
- sulcular epi contains fluid!
- thin sulcular epi
hair tongue and geographic tongue
- hairy is filifrom overgrowth (NOT NORMAL)
- geographic is changing atrophy of filiform
leukoedema
grey translucent mucosal coloration
- disappears when mucosa stretched
- marked intracell edema
juntional epi dgj
- no keratin, especially thin!!
- physically attached to enamel epi of tooth germ @ base of sulcus
- VERY REGENERATIVE
- derived from tooth germ!!!
pharyngeal arches
- 5 swellings
- ectoderm from neural crest
- numbered 1,2,3,4,6
- first arch has 2 prominences (max and mand)
- each arch has: cart from neural crest, specific skeletal muscles, CN, aortic arch artery
pharyngeal arch 1
incus malleas, sphenomand ligament
- max and mand bone
- first arch muscle moves the mand and max
- trigem innervation 5 of mand and max, plus two tensors (tympani and veli palatini - ear and soft palate)
pharyngeal arch 2
stapes, styoid process for muscles, stylohyoid ligament, upper hyoid (floor of mouth?)
- hyoid bone
- these muscle leave hyoid and go to face!!!
- facial nerve 7 also innervates stapedius (amp sound)
pharyngeal arch 3
lower half and greater horns of hyoid
- hyoid bone
- only 1 muscle stylopharyngeus but leaves hyoid for swallowing
- cn 9 glossopharyngeal
pharyngeal arch 4
thyroid and epiglottic cart of larynx
- larynx muscle
- cn 10 innervates all palate except veli palatini (arch 1) and all pharynx except for stylopharyngeus (arch 3)
4th aortic arch
gives rise to arch of aorta and r subclavian
6th aortic arch
pulmonary arteries and ductus arteriosus
3rd aortic arch
gives rise to common and internal carotid arteries
1st aortic arch
gives rise to max artery
pharyngeal arch 6
cricoid of larynx
- cn 10
- all larynx except for cricothyroid
- pumonary arteries and ductus arteriosu
preotic somitomeres
- cn 3,4,6 that innervate eyes
- not mixed!
- ONLY MOTOR FUNCTION off of arch 1
postotic somites
tongue, cn x
- skeletal by 11 and 12!! motor only
facial primordia formation
5 of them formed by neural crest, max and mand prominence dev in arch 1
- frontonasal process, 2 max process, 2 mand
- max prominence outgrowths fuse to form palatine shelves
- primary palate is the v at the front
- incisive foramen marks fusion pt of two palates
- cleft lip is bad fusion btw max prominences
pharyngeal pouch 1
- 4 from the pharynx!!!
- pouch 1 forms auditory tube touching the ONLY reminant of pharyngeal groove 1 (xternal aud meatus). barrier is tympanic membrane
pharyngeal groove
- groove 1 remains (the only one that remains outside) as external auditory meatus
pharyngeal pouch 2
palatine tonsil
- oropharynx
pharyngeal pouch 3
parathyroid gland inferior and thymus
- migrate down following the thymus
pharyngeal pouch 4
parathyroid gland sup and parafollicular cells thing that migrates into thyroid gland
tympanic mem mucous and skin profile
mucosa is pharyngeal endo and skin is ectoderm
nasal cavity + oral cavity profile
ectoderm
- mostly branch 1 and 2 of V skin and mucosa innervation
tongue profile
front 2/3 is ecto, back is endo
- back is part of oropharynx: contains lingueal tonsil, palatine tonsil, pharyngeal tongue
- foramen cecum is site where thyroglossal duct descended
- sulcus terminalis is boundary btw oral and pharyngeal tongue- - cn 12 innervation since not in pharyngeal pouch
- MUCOSA innervation is diff: anterior 2/3 is cn 5 (not taste, pain, touch temp) and 7 (taste)
- posterior is cn 9 from arch 3
naso, oro, laryngo and esophagus profile
endoderm but not closed!
- rememnant of pouch 1, auditory tube is in naso
- palatine tonsil in tonsil fossa from pouch 2
- cn glossopharyngeal in oropharynx then cn 10 below
thyroid gland profile
- midline endoderm from 1/3 posterior tongue
- starts as diverticulum in part of tongue, then goes down midline to trachea via thyroglossal duct meaning its actually BELOW thryoid cart
- diverticulum forms from between 1 and 2 pharynngeal pouch
digeorge sequence
defect in pouch 3 and 4
- bad t cells, calcitonin leading to hypocalcemia, heart problems, ears
what innervates skin/mucosa of pharyngeal apparatus
- trigeminal only pretty much
- cn 7,9,10 do the pinna and external auditory meatus (ear)
vit d synth in skin
from 7 dehydrocholesterol to vit d3 using UV B!
skin development
WNT signal blocks fibroblast growth factor activity on neuroectoderm. these cells express k8 and 18 initially (multipotent)
- leads to expression of BMP that inhibits neural fate and diff to epidermis. now p63 active so induce k5 and 14 expression
- loss of p63 is lethal!!
dorsal dermis comes from
dermomyotome
ventral dermis comes from
lateral plate mesoderm
head dermis comes from
- neural crest
strat corneum epi
- cross linked proteins and lipids
- keratin
- ded
strat granulosum epi
- profilaggrin induces keratin aggregation in keratohyalin granules!
- cells are most flat
- contain keratin 1 and 10
- filagrrin and loricrin proteins
spinous layer epi
- committed to terminal diff
- k 1 and 10 (now all above cells have it too)
basal layer epi
dividing cells, k 5 and 14
palm skin layer
has thick corneum and granulosum, prominent rete ridges
eyelid skin
thin corneum and granulosum, not prominent rete ridges
hair development
found in dermis?
- starts with formation of placode (embryo thickening area)
- then regulated by wnt/ b catenin pathway
- first anagen (growth phase of hair) then catagen where hair detaches from nourishment supply then telogen (hair falls out)
- alopecia, hirsutism (some hair) and hypertrichosis (werewolf)
nails
- made of keratin
- eponychium is viable skin (bottom of nail)
- cuticle is layer of dead cells attached to nail plate
- lichen planus (scratchy nails = dystrophic)
- plummer vinson syndrome leads to koilonychia spoon nails
sebaceuous gland
- grease. located at top of hair follicle
- sebum lubricates and waterproofs hair. holocrine sec where cells die
eccrine sweat glands
- found eveywhere
- merocrine secretion (vesicles)
- most of glands are this
- put secretion right onto surface of skin
apocrine sweat glands
- only found with hair, apocrine secretion where it buds off to form blebs
- body odor
- influenced by bac!
skin microbiome
- bac, fungi, virus
- protection against invading path
- immune surveillance
- breakdown of natural products
aged vs young skin
- epi is thinner, dryer, impair wound healing and increased cancer
- dermis is thinner, less collagen and elastin
ectodermal displasia x linked hypohidroticc ED
- heterogenous
- EDA gene that is most common. no sweat
- there is no hair made (hypotrichosis), weird nails and hypohidrosis,
- hypodontia (less teeth) and oligodontia (like 2-5 teeth only)
- p63 leads to cleft palate phenotype
skin problems
- warts and herpes (cold sore stuff)
-basal cell carcinoma, squam cell carcinoma
melanin production
- sunlight stim
- a MSH activates melanocortin 1 receptor (MC1R)
- comes from acth pituitary then cleaved
- made of two pigments: eumelanin and pheomelanin
- l tyrosine to l dopa then l dopaquinone then melanin
- done using tyrosinase, in MELANOSOME
melanosomes
- melanin is packaged into melanosomes (granules)
- transported through dendrites to adjacent keratinocytes in basal and spinous layer
- keratinocytes engulft melanosomes and arrange pigment over nuclei
epidermal melanin unit
- epidermal melanin unit is function unit of 1 melanocyte to 36 keratinocytes
MC1R genetic variation
polymorphism is freckles. from point mutation no AA change
- sun darkens them
mutation: autosomal recessive is red hair, white skin
- decreased eumelanin synth and sensitive to uv light
oral melanotic macule
- not related to sun
- increased melanin NOT melanocytes
- mole on mucosa
nevus (mole)
- less than 5 mm in diameter
- prepubertal
- risk is sun exposure and geneticcs
- benign
melanoma
- 3rd most common skin cancer
- family history
- dysplastic nevi
- high number of nevi
- sunburns
ABCDE melanoma
- assymetry, border irregular, color, diameter over 6 mm, enlargement and elevation
melasma
- irregular symmetric sigmentation on sun area of face
- more common in women and dark skin ppl
- multifactoral causes
vitiligo
autoimmune loss of melanin
- white patch thing
albinism
- genetic inability to produce melanin
- tyrosinase
adrenocortical insufficiency (addison disease)
adrenal gland dysfunction
- so too much ACTH then overstim of pit, weird pigmentation
mast cells
bone marrow. inflam and sensitivity reactions, heparin histamine. first response to injury
- stain with toluidine blue
- NOT in CNS!
- CT proper are around blood vessels!!
macrophages
- bone marrow. enter as monocytes then mature in CT
- phagocytes and APC
- kupfer in liver, langerhans in skin
- microglia in brain
adipocytes
- full diff. white adipose is big droplet brown is many small in babies
myofibroblast
- contractile, derivative of fibroblast (mods), wound healing, can have many origins!
pericytes
endothelial cells of cap for contraction
specialized CT
reticular, bone, cart, ligament, fat, blood
langerhans cell histiocytosis
- abnormal clonal prolif of langerhans cells
- unifocal, multifocal unifocal(many lesions on 1 organ) and multifocal multisystem (many lesions)
- braf mutations result in RAS tyrosine kinase activation so cancer
merkel cell carcinoma
- highly aggressive skin cancer
- associated with polyomavirus
solar radiation bad stuff
- # 1 cause of skin cacner, lip, and precancerous lip and skin lesions, premature aging, catacts, immune suppression
uva
wavelength is 3125 to 400 nm
- 95% of radiation that hits earth BUT not absorbed by glass/clouds
- activates melanin, penetrates lamina propria dermis so skin becomes less elastic and wrinkly
- penetrates eye lens and increases INDIRECT cell ox damage
- NOT THE DIMER AND PHOTOPRODUCT MECH
uv b
wavelength is 290 to 315
- can be blocked but absorbs everywhere
- penetrates to epidermis
- causes sunburn not tan
- new melanin that is LONGER lasting than tan
- direct dna damage
- keratin cells stim to divide and prolif
- decreases langerhans cells
- absorbed by cornea
- cancer, sunscreen works
solar elastosis
- accumulation of abnormal elastin
- chronic sun damage
- pathoneumonic!!!!
melanosis
- melanin produced
- chronic sun damage
hyperkeratosis
- thickened strat superficiale
- sun damage
acanthosis
- thickened stratum spinosum
- sun damage
dna damage from UV
- modifies nuc (thymine dniculeotide is fused to make a CYCLOBUTANE PYRIMIDINE dimer DIRECT and then 6-4 photoproduct that triggers indirect damage)
- ONLY FROM UVB
- first single strand breaks then second one. free radicals induce ox stress
dna damage response
- ionized rad is always 2 strand break
- activates chckpoint, dna repair, growth arrest (senescence) and apoptosis
- nucleotide excision repair (NER) is primary mechanism used by keratinocytes for repair of UV dna products
xeroderma pigmentosum
- extreme uv sensitivity, skin and lip cancer, eye problems
- heterogenous
- messes up NER
sun on lips
- no vermilion border, actinic chelitis, cancer, herpes cold sores
sun on skin
sunburn, solar lentigo (pigment spots), aging, actinic keratosis, cancer (basal, squam, melanoma)
oral mucosa layers
- below basement
- papillary lamina propria
- reticular lamina propria
- submucosa
skin layers
epidermis (come lets get sun burnt)
- then dermis (papillary and reticular) then fat
loose CT
contains: fixed cells, collagen, elastin, ground substance, fluid, nerves, blood vessels
- ground is filled with mucopolysac
minor salivary glands
- produce mostly mucous but circumvalate makes serous also. (papilla base)
- all over mouth even esophagus and oropharynx
- develop from ectoderm, except for von ebner (endo) at 8-12 wks
- NOT FOUND in gingiva, anterior hard palate, anterior dorsum tongue
- unencapsulated
- ducts open directly onto mucosal surface
- von ebner’s glands ARE SEROUS
- secrete igA
parotid
ectoderm, in 4-6 weeks
- largest gland, mostly serous
- long branching intercalated ducts
- many striated ducts
- mostly digestive enzymes
- stensen’s duct opens into mouth
- also has fat and lymph tissue!!
- cn 9, but cn 7 passes through
submandibular
6 weeks, endoderm
- second largest
- medium length intercalated ducts, many striated
- wharton’s duct opens into sublingual caruncle
- serous-mucous
- produces distinct MUCINS!!
- cn 7. has fat
sublingual
8-12 weeks, endodermal
- smallest
- short bad intercalated and striated ducts
- bartholins duct opens into SUBLINGUAL CARUNCLE
- ducts of rivinus open along SUBLINGUAL FOLD
- mucous serous
- cn 7. has fat.
salivary gland development
- epithelial cells proliferate in stomatodeum then form a tree thing that branches to form lumen in the middle.
- cytodiff: inner cells become secretory
- outer cells become myoepithelial
- maturation of glands continues till birth and increase in sice after
sublingual caruncle contains
- wharton’s duct from submand and bartholin duct from sublingual!!!
salivary gland structure
- acini (secretory endpiece) that are spherical/tubular buds at end. this is site of fluid and protein secretion
- ductal network is small ducts connected to acini, merge to form larger ducts then one main duct
- connective tissue surrounds glandular epi separated by septae (connective tissue) that divides into lobes called capsules
- has blood vessels and nerves
serous cells
- protein rich secretory granules
- pyramid that contains all protein to make saliva
mucous cells
mucin rich secretory granules
mixed acini
mucous cells in the center, then serous cells form cresent around the edge
- tubular shaped
- secrete into common lumen
Myoepi cells
- found in acini btw basal mem of secretory cells and basement mem
- also found along ducts
- functionally and structurally like smooth muscle that contract to force saliva out
intercalated ducts
- first duct from acini, small dia, cuboidal cells that are lined by myoepi cells
striated ducts
- main intralobular duct that is mostly in parotid, submand, unique to salivary glands
- simple columnar cells, larger dia then acini, larger luman then intercalated ducts, basal mem highly folded and filled with mito, small blood vessels surround ducts
excretory ducts
- large, interlobular ducts
- surrounded by ct, pseudostrat columnar epi, ducts merge to form single main duct
order of ducts
secretory portion, intercalated duct, interlobular duct (aka striated duct), then excretory duct
saliva components
- 600-1000 mL is normal
- major glands have levels based on circadian rhythm, but minor is continuous
- 99% water and organic is 1%
- ph is slighyly acidic 6.2-7.6
- binds bac, helps in taste, wound healing, tooth remin
pelicle formation
composed of saliva proteins, crevicular fluid( from sulcus) , oral mucosa and microbes
- on enamel surface (cervical tooth where it meets gingiva) for protection and remin
stim and unstim saliva
- unstim is basal secretion without exogenous stim (sleep, more mucous since its mostly submandibular gland)
- stim is in response to something and usually watery since mostly parotid!
- stim can be taste, smell, thinking, chewing via cn 7,9,10
- inhibition is sleep, fear, dehydration
parasymp saliva secretion
- high volume, watery, rich in electrolytes and enzymes, parotid (cn 9) and submand (cn 7). inhibition leads to atrophy
symp saliva secretion
- low vol, viscous saliva, rich in mucus
- all fibers originate in superior cervical ganglion
- inhibition does not cause change
salivary secretion process
- begins as isotonic then cl and na added by acinar cells (Active) then water is pulled in through aqp5 and tight junctions (passive). na and cl reabsorbed by ductal cells then k and hco3- is added to saliva by ductal cells (BUT NO WATER FOLLOWS)
- adding and removing ions as it goes like cl, k out, h in
- BUT less hypotonic as flow rate increases!!
- ions stop at striated ducts
in the duct, transporters reabsorb na and cl to make it hypotonic
- ends up as hypotonic and acidic
sodium in saliva
higher in plasma, then gets higher when stim
potassium in saliva
- low in plasma, higher in basal then not much change with stim
calcium in saliva
stays the same
magnesium in saliva
higher in plasma, then same in basal and stim
chloride in saliva
higher in plasma, then higher in stim
bicarbonate in saliva
- higher in plasma, then gets higher with stim
what’s in saliva
salivary proteins, digestive enzymes, carbonic anhydrase, growth factors, proline rich proteins, glucocort, sex hormones, glucose!!!, AA, statherin and haptocorrin
saliva protein secretion
- exocytosis merocrine through acini cells. hormone stim
- DNA and rna is in there too!
salivary proteins
- mucins made by acini (esp 7 and 5b are imp!!!), secretory igA from plasma, histatins for digestion, lysozyme, lactogerrin
digestive enzymes in saliva
a amylase, lipase, peroxidase
- mostly from parotid
carbonic anhydrase saliva
for co2 exchange
growth factors in saliva
epidermal growth factor
slatherin in saliva
works in enamel min with hydroxyapetite
haptocorrin saliac
binds v b12
mucin functions
- bind bac and pelicle formation
- esp muc7 and 5b
- lubrication
- made by submand and sublingual glands!!!
von ebner glands
- von ebner’s glands ARE SEROUS
- secrete histacin and lingual lipase
- base of tongue in circumvallate papilla
(endo) at 8-12 wks
xerostomia treatment
sugarless gum, oral hygeine stuff like biotene, parasymp agonist drugs, fluoride or chlorhexidine rinses
primary shogen syndrome
- sicca syndrome
- xerostomia, xeropthalmia (dry eyes!)
- autoimmune
- 9:1 female ratio!! gland enlargement
- rampant caries
secondary shogen
sicca syndrome coupled with dry mouth, eyes and other maniffestations like arthritics and stuff
- 9:1 female ratio!! gland enlargement
- caries
sialorrhea
- xs salivation
- from lots of places like local anesthetic, new denture, rabies,
salivary gland agenesis, atresia or hypoplasia
- mandibulofacial dystosis (treacher collins syndrome)
- impacts rRNA production so basically no parotid and very dry mouth
mucocele
- rupture of salivary duct
- most common in lower lip. can also happen in ventral tongue, floor of mouth
- trauma!
sialolithiasis
- stone
- usually submand since complex thing
- radiopaque (white) mass
- block salivary flow, so lead to bac build up and need to remove stone
acute bacterial sialadenitis
- retrograde infx due to block of saliva
- pain, inflam, heat etc, swelling
- abscess in ducts and acini
- need antibiotics then drain
mumps
- paramyxovirus
- infect saliva, pee, breast, ovary, testes (long term = infertility)
- mainly bilateral parotid enlargement
- pain
pleomorphic adenoma
- benign salivary gland tumor most common
mucoepidermoid carcinoma
most common malignant salivary gland tumor
- parotid common or minor glands
order of diagnosis
cc, HPI (old carts), medical, social and family history, complete clinical examination (ROS), differential diagnosis, working diagnosis, tests, final diagnosis and treatment
clinical examination part
review of systems before examining sus stuff
- inspect, palpate, percuss and auscultate
- check both sides for symmetry
- refer patient for NOT oral stuff
signs and stuff of lesions
- size, color, consistency, mobility, tenderness, temp, function
- shape and outline
- arrangement of lesions
- distribution: diffuse is big lesion spread out or local
- multilocal is lesions on same part but diff area
macule
- discoloured flat spot not elevated
pustule
- visi8ble collection of pus beneath skin
- don’t picck this unless can see pus coming out
vescicle/bulla
vescicle is less than 5mm (fluid filled)
bulla is more than 5 mm
- ulcer after it pops
ulcer
- loss of surface epi
- for this, biopsy not only the ulcer but also the epi. usually disease is of the epi so want to see it all (since ulcer tissue won’t have it!)
papule/ plaque
- papule is small, solid elevation of skin less than 1 cm
- plaque is more rough and larger than 1 dm
nodule vs mass
- nodule is small bump
- mass is non specific description of mass (nodule = mass but not all mass = nodule)
- sessile is attached to a base, pedunculated is attached by stalk (can move it)
- exophytic is out, endo is in
- ALL peduncle is exophytic while sessile can be either
differential diagnosis process to final
- a list of things it could be
- then narrow it down to 3 when doing working diagnosis. #1 is working diagnosis
- determine tests and do them. This solidifies the working diagnosis
- final diagnosis = definitive usually done by pathologist.
- forms basis of development of treatment plan
what tests to order
- if u can see it, feel it then usually a biopsy!
mast cells mucosal
in Di and respiratory
- rich in chondrotin sulfate
alveolar ridges
mand and max divide teeth into oral cavity proper and oral vestibules (outer portion)
lip corner
commissure
frenum and frenulum
buccal and labial mucosa to alveolar mucosa
fold in inner lip
vestibule/mucobuccal fold
pad thing in corner of mouth
retromolar trigone
order of mucosa on teeth maxilla
Top is alveolar mucosa, then mucogingival junction then attached gingiva then free gingival groove then free gingiva (festooning)
enamel epi thing
oral epi is outside, then sulcular then junctional
inside the mouth palate parts
Rugae and incisive papilla
Raphe is line
pillar in back of mouth
soft palate then uvula
First fold is palatoglossal
Then gap is palatine tonsils
Then palatopharyngeal folds
Then oropharyngeal wall
bottom of mouth anatomy
lingual frenulum with sublingual caruncle on it
Under tongue tissue attached to frenulum is sublingual fold
which taste buds have keratin and which don’t
Filiform: keratin on top
Fungiform has no keratin but its vascular
Foliate is no keratin
Circumvallate is 100% keratin
migratory tongue
erythema migrans
what does foliate papillae look like
- non keratin so very thick at the top
- very branchy finger things
circumvallate papillae look like
thick top since keratin but thin sides
- deep grooves for the ebner glands
fungiform papillae look like
very round and budded
- thick all over since no keratin
parotid gland looks like
hella granules
submandibular gland looks like
lots of demilunes since white and pink mixed
sublingual looks like
very white since mucousy
melanocytes look like
little brown/red spots in basal mem layer (rugae)
langerhans cells look like
very dark brown all over the pegs
alveolar mucosa looks like
very thick top part since no keratin
gingiva looks like
very thin with a keratin layer
