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145 Cards in this Set

  • Front
  • Back
tissue
an aggregation of similar cells or types of cells that are adapted to perform one or more functions
organ
composed of tissues and cells that are adapted to perform one or more functions
as part of a differentiated structure or system
integument functions
protection
sensation
thermoregulation
immunologic function
vitamin D production
integumentarysystem
integument (skin, cutis) and its derivatives integument = epidermis and dermis
derivatives of epidermis
hair, sebaceous glands, sweat (sudoriferous) glands, nails,
and mammary glands
hypodermis
subcutaneous fascia (superficial fascia)
hypodermis is not part of the integument
epidermis
keratinized stratified squamousepithelium
dermis
loose and dense connective tissue
dermatoglyphics
fingerprint identification-
integument grooves and ridges
each person genetically unique
thickest epidermis
located in the hairless palms of the hands and soles of the feet
stratum basale (stratum germinativum)
single cell layer
adjacent to basal lamina
cuboidalto low columnar cells
stem cells (mitoticallyactive)
extensive cell junctions
desmosomes
hemidesmosomes
stratum spinosum (prickle cell layer)
several cell layers thick
cuboidal to squamous cells
mitotically inactive
cytoplasmic processes (spines)
desmosomes (nodes of Bizzozero)
stratum granulosum
one to three cell layers thick
squamouscells
retain nuclei
keratohyalingranules
stratum corneum (with deep stratum lucidum in thick skin)
variable thickness of layer
squamouscells
anucleate
keratinized cells
papillary layer (dermis)
loose connective tissue
more cellular
thin collagen fibers (I, III)
finer elastic fibers
reticular layer (dermis)
dense connective tissue
less cellular
thick collagen fibers (I)
coarser elastic fibers
wound healing
stratum basaleramps up mitosis
migration of proliferating cells
exfoliation of dead keratinocytesfrees scab (blood clot)
Langer’s lines
collagen and elastic fibers oriented in parallel lines

surgical incisions parallel to Langer’s lines heal faster
keratinocytes
keratinizationis the process by which keratins
are assembled into keratin filaments or tonofilaments
(classified as intermediate filaments) which are then bundled into tonofibrils as keratinocytes differentiate and move outward

keratinization includes keratohyalin granules
releasing intermediate filament-associated
proteins like filaggrin to aggregate keratin filaments
into tonofibrils, thus converting granular cells into keratinized cells

water barrier formed by lamellar bodies
which contain pro-barrier lipids, lipid processing
enzymes, and proteases which are secreted
by exocytosisinto intercellular space between
stratum granulosum and stratum corneum

cell junctions undergo proteolyticdegradation
in a pH dependent manner
to exfoliate (desquamate) dead keratinocytes
nodes of Bizzozero
in keratinocytes' cell junctions

arrows indicate cytoplasmic processes that are
connected by desmosomes
melanocytes
neural crest derived and migrate to stratum basale
number similar across humans
produce and distribute melanin to keratinocytes
integument pigmentation determined by melanin content of keratinocytes

production of melanin granules
basal cell carcinoma
stratum basale
squamous cell carcinoma
stratum cornuem and stratum granulosum
malignant melanoma
melanocytes migrate through statrum spinosum
ABCD rule
asymmetrical shape of lesion
border of lesion is irregular
color variations
diameter greater than 6 mm
Langerhan’s cells
antigen-presenting cells
originate in bone marrow and migrate to stratum spinosum
indented nucleus
rod-shaped Birbeck granules
Merkel’s cells
located in stratum basale
most abundant in fingertips
contain dense-cored neurosecretory granules
synapse with pseudounipolar neurons function in tactile sensation
free nerve endings
pain
temperature
tactile
Pacinian corpuscle
deep pressure
vibration

found in reticular layer, deep connective tissue, below dermis
Meissner’s corpuscle
tactile, more superior

found in papillary layer
Merkel’s cell
tactile
Corpuscles
Connective tissue encapsulated
nerve endings
Ruffini’s corpuscle
tactile
list level of hair (epidermal derivatives)
M = medulla
Cx= cortex (contains cuboidal cells)
Cu = cuticle (squamous cells)
IRS = internal root sheath
ERS = external root sheath
GM = glassy membrane
CT = connective tissue
HP = hair papilla enclosed by hair bulb
sebaceous glands
holocrine secretion of sebum
sebum is lipid product plus cell debris after apoptosis
pilosebaceouscanal
sebum secretion into duct system
that begins with pilosebaceouscanal
correlation between sebum amount and acne
eccrine sweat glands
widely distributed in integument
coiled tubular gland
three cell types
merocrinesecretion
innervationis sympathetic cholinergic (ACh)
sweat and antibacterial glycoprotein granules
narrow lumen
apocrine sweat glands
primarily axilla, anus, and external genitalia
associated with hair follicles
coiled tubular gland
one cell type
merocrinesecretion
innervationis sympathetic adrenergic (NE)
protein-rich product can be stored in lumen
wide lumen
clear cells
columnar shape
produce sweat
increased mitochondria and glycogen
increased surface area of PM
adjacent to intercellular canaliculi

make up fluid part of sweat
dark cells
pyramidal shape
antibacterial glycoprotein granules
increased RER and Golgi
adjacent to lumen
myoepithelialcells
contraction assists secretion
nail matrix
epidermal germinativezone

keratinized cells of nail
contain hard keratin
and do not desquamate
eponychium
cuticle
hyponychium
thick epidermis
that secures free edge of nail
lines of Blaschko
named after investigator who first reported a common set of patterns in patients with dermatological disorders in 1901
Cartilage - general characteristics
Specialized CT: resist loading without permanent deformation

Dynamic tissue: responds to strain

Avascular(no blood/lymph), no innervation-reliance on diffusion to nourish tissue

Chondrocytesin lacunaesurrounded by ECM
Perichondrium
Layer of dense CT surrounding cartilage
-type I collagen, fibroblasts, vasculature
Inner layer has chondrogenic (stem) cells

Present in elastic& some hyaline cartilage
Perichondritis
inflammation of the perichondrium, often from trauma or infection from piercings. May result in fibrosis, causing deformed appearance (e.g., cauliflower ear)

auricular perichondritis and cauliflower ear
Which three cells would you see in growing cartilage?
chondrogenic cell
chondrocytes
chondroblast
Chondrogenic cells
Stem cells: give rise to cartilage cell lineage

Arise from multipotent mesenchymal cells that also give rise to bone cell progenitors

Small, flattened cells within the perichondrium
Chondroblasts (immature chondrocytes)
Growth: secrete ECM on cartilage surface

Derived from chondrogenic cells

Present in growingcartilage near perichondrium
Chondrocytes
Large; centrally-located in growing cartilage
Predominant cell type in adult cartilage
Growth & maintenance:
-secrete/digest ECM components
-mechanosensitive (regulate ECM synthesis)
-mitotic

rER (LM: basophilia)
Golgi (LM: pale regions)
Isogenous groups
clusters of recently
divided chondrocytes
Chondrogenesis
1. Mesenchymal (chondrogenic) cells migrate,
proliferate, and aggregate –avascular; Sox9
2. Differentiation into chondroblasts
3. Chondroblasts secrete ECM, tissue expands
4. Differentiation into chondrocytes, expansion
continues via mitosis & ECM secretion (forms isogeneous groups)
Appositional growth (cartilage)
growth on a surface
Chondroblasts arise from chondrogenic cells and synthesize ECM
Deposition on existing cartilage surface
Cells remain fairly stationary (tissue expands away from them)
Interstitial growth
growth from within

Chondrocytes divide and secrete ECM
-isogenous groups

Deposition within existing cartilage

Chondrocytes are “pushed” apart as tissue expands

Cartilage shape is achieved by differential interstitial and appositional growth (ex. shape of ear cartilage)
Why is cartilage thickness limited?
No vasculature = reliance on diffusionfrom neighboring tissues

Cartilage thickness is limited because tissue cannot grow beyond its ability to diffuse material across ECM
Chondrodysostosis
malformation of bone from a cartilage precursor

Madelung-type chondrodysostosis
Chondrodysplasia
faulty development of cartilage (e.g., achondroplasia)

achondroplasia dwarfism
Composition of (hyaline) cartilage
~5% Cells
~95% ECM
-water, collagen, ground substance
Composition changes with age:
-fewer PGs, less hydrated,
decreased thickness
Fibers
resist tension, type I, II, and II collagen
type II collagen fibrils
ALLtypes of cartilage

more resistant to compression
type I collagen fibers
fibrocartilage ONLY

more resistant to tension
Ground substance
resist compression, resilience, mechanosensory

PGs, PG aggregates
multiadhesive glycoproteins
PGs, PG aggregates
all types of cartilage

part of GS
multiadhesive glycoproteins
all types of cartilage

part of GS
Type II fibrils and PG aggregates (mostly aggrecan) in ECM -

State characteristics
are integrated-resists tension AND compression; regulates movement through tissue

PGs highly sulfated and with hyaluronic acid (non sulfated)
How are PGs oriented and what is the relevance of their orientation?
Oriented in vertical line that branch out like a Y towards the lumen

Orientation of type II collagen fibrils resists shearing near surface

Orientation of PGs resists compression of the tissue
Multiadhesive glycoproteins (in cartilage ECM)
E.g., fibronectin, chondronectin
Integrin, actin cytoskeleton
Help bind cells to ECM
Mechanosensory role
-aid in regulation of ECM synthesis
in response to tissue strain
Capsular matrix
around chondrocytes
-verybasophilic (GAGs)
Territorial matrix:
-near chondrocytes, isog. groups
-basophilic
Interterritorial matrix
-away from chondrocytes
-light staining (more collagen)
Regional differences in ECM staining
-GAG (basic stain) & collagen concentrations (acidic)
Describe bone repair
Limited ability to repair damage: avascular, poor chondrocyte mobility
If repair occurs, it is initiated at the perichondrium
Typically, damage results in scar tissue deposition, bone formation, or degeneration(e.g., osteoarthritis)
Hyaline Cartilage
Found in:
Synovial joints
Costal cartilages
Nose
Larynx
Trachea, bronchi
Embryonic skeleton
Growth plate
Function:
Structural support
-resists compression

articular cartilage and growth plates lack periochondrium

only interstitial growth
Elastic Cartilage
Found in:
Pinna of external ear
External auditory meatus
Auditory tube
Larynx
Function:
Structural support
-elasticity, resist compression

Like hyaline cartilage, but with dense network of elastic fibers in the ECM that make it more elastic
Always has a perichondrium(w/ elastic fibers)

Exhibits appositional growth because of periochondrium
Fibrocartilage
Found in:
Articular discs & labra
Intervertebral discs
Pubic symphysis
Tendon/ligament insertions
Menisci
Function:
Structural support
-resist compression & tension

Type I collagen in ECM
No perichondrium

chondrocytes: rounder, often in isogenous groups
-basophilic matrix around cells (GAG’s)

Looks like dense CT
Bone characteristics
General Characteristics:Specialized CT (rigid; mineralized ECM)Dynamic tissue: responds to strainHighly vascular; innervated

Functions:-structural support-store minerals (e.g., 99% of Ca) -house hematopoietic tissue
Calcified bone looks like what in TEM
Surrounding cell is electron dense
Periosteum
Layer of dense CT surrounding bone except at articular surfaces; vascular
Inner layer has osteoprogenitor (stem) cells
Perforating fibers
in periosteum

Tendons & ligaments attach to bone via the periosteum
Perforating fibers (or Sharpey’s fibers):
-type I collagen fibers of the periosteum embedded firmlyin bone
Avulsion fractures
in perforating fibers

rip periosteum from bone so bone is also torn
Endosteum
Monolayer of cells covering the surfaceof the medullary cavity
Bone cell types (list and define role)
Osteoprogenitor cell (stem)
Osteoblast(synthesize)
Bone-lining cell (line)
Osteocyte(maintain)
Osteoclast(resorb)
Osteoprogenitor Cells
Stem cells that give rise to osteoblasts
-arise from multipotent mesenchymal cells that also give rise to
chondrogenic cells

Reside on bone surfaces
periosteum, endosteum, or lining central canals (neurovascular channels)
Osteoblasts
Synthesize& mineralizebone ECM: polarized; extensive rER, Golgi

Reside on bone surfaces
periosteum, endosteum, or lining central canals (neurovascular channels)

Arise from osteoprogenitor cells; give rise to bone-lining cells/osteocytes
Bone-Lining Cells/quiescent osteoblasts
flattened cell, condensed nucleus
Occupy bone surfaces where no formation/resorption is occurring

Reside on bone surfaces
periosteum, endosteum, or lining central canals (neurovascular channels)
Osteocytes
Former osteoblasts surrounded by bone ECM
Reside in lacunae: amitotic; no interstitial growth
Signal other bone cells to form/resorb bone (little rER, Golgi)
-mechanosensitive(adaptation to stress); calcium homeostasis
Which bone cells communicate via gap junctions?
Osteoprogenitor cells, osteoblasts, osteocytes, bone-lining cells (but not osteoclasts)
canaliculi
junctionsSmall, fluid-filled channels in bone called canaliculiconnect cytoplasmic processes of osteocytes to bone cells on bone surfaces
Osteoclasts
Large, multinucleated, polarized cells that resorb ECM
-lysosomes, rER, Golgi, transport vesicles

Depressions formed via resorption = resorption bays

Arise frommonocyte precursor(mononuclear phagocyte system)
Organic (bone ECM)
resists tension
Primarily type I collagen with little ground substance
Inorganic (mineralized; bone ECM)
resists compression
Hydroxyapatitecrystals arranged along the collagen fibers
Osteoid
Organic matrix is not immediately mineralized
-observed as lighter-staining
Reasons why mineralization would slow down?
low vitamin D, low calcium, renal failure
osteocalcin and alkaline phosphatase
blood tests –what do they tell you about bone?
osteocalcin only tells you about organic matrix does not imply that bone is mineralized
Runx2
Osteoblast differentiation from osteoprogenitor or bone-lining cells
(Runx2-text calls it “Cbfa1”)
Osteocalcin
calcium binding proteins in organic matrix, secrete during osteoblast formation
alkaline phosphatase
Osteoblastsmineralizethe matrix
-secrete matrix vesicles containing alkaline phosphatasethat
catalyzes hydroxyapatite crystallization from extracellular minerals
RANKL
Osteoclast precursors travel in blood to exposed bone surface,
fuse & differentiate intoosteoclasts -induced by RANKL
clear zone
seal that contains lytic secretions
basolateral region
region where digested material is exocytosed
ruffled border
folds that increase surface area for resorption
mineral matrix is degraded during osteoclast formation by?
proton pumps
organic matrix is degraded during osteoclast formation by?
lysosomal enzymes
How does OPG affect osteoclast formation?
Osteocytes/blastssecrete RANKLthat promotes osteoclastogenesis and OPG that inhibits it

Bone diseases treated with OPG to inhibit RANKL
How does inflammation affect bone resorption?
Stromal cells in bone marrow promote osteoclastogenesis with cytokines and RANKL

T lymphocytes can promote osteoclasto-genesis with RANKL during inflammatory
response
Remodeling
coupled action of osteoblasts & osteoclasts to replace bone (resorption followed by formation)
Repairsdamage
Adaptsbone to stress
Hormonally and
mechanically regulated
What would signal a bone turnover disease? Give examples of diseases
Elevated osteocalcin and alkaline phosphatase serum levels indicative of bone turnover diseases

osteo-porosis, Paget’s disease, cancer, hyperparathyroidism
Osteopenia/osteoporosis
greater resorptionthan formation
-decreased bone mass
-increased bone weakness
Osteosclerosis/osteopetrosis
greater formation than resorption
-increased bone mass
-ultimately increases bone fragility
Calcitonin
Released from thyroid gland(C-cells) and targets osteoclasts
Decreases blood calcium levels by inhibiting bone resorption
Parathyroid hormone (PTH)
Released from parathyroid glandand targets osteoblasts, which secrete RANKL
Increases blood calcium levels by promoting bone resorption
Hyperparathyroidism:
bone loss and kidney stones
Estrogen
Released from gonadsand targets osteoblasts
Maintains bone mass(by inhibiting osteoblast apoptosis and promoting osteoclast precursor apoptosis)
Compact bone(
also: cortical, dense)
-forms outer bone cortex
Trabecular bone
also: cancellous, spongy)
-forms meshwork interior of bone

trabeculae oriented toward stress lines
Woven bone (immature bone)
Initial bone formed during development & early fracture repair
Laid down rapidly (irregular collagen bundles, highly mineralized) = weak
Replaced by lamellar bone

Found in many bone pathologies (e.g., Paget’s disease, bone tumors)
Lamellar bone (mature bone)
Always formed on existing calcified surface
Organized into lamellae (sheets of mineralized ECM); stronger
Adult bone is lamellar (exception: alveolar bone around teeth)
Osteons (Haversian Systems)
Osteon: concentric lamellae around a neurovascular canal
Formed during bone remodeling
Central Canals (Haversian Canals)
Central canal: centrally-located canal in osteons

Contains neurovasculatureand is lined by bone cells
Perforating (Volkmann’s) Canals
Perforating canals: connect central canals with periosteum & endosteum
Bone Blood Supply describe
Blood vessels in marrow & periosteum anastomose via blood vessels in the central and perforating canals –“inside-out” blood flow

diffusion with caniliculi
Cement Lines (Reversal Lines)
Cement line: site where resorption stopped and formation began
Abundant in pathologies involving bone remodeling (e.g., Paget’s disease)
Bones often fractures along cement lines
Parietal mesoderm (lateral plate)
pelvis, shoulder, limbs, sternum
Somites, somitomeres (paraxial mesoderm)
post. cranium, vertebrae, ribs
Neural crest
mandible, ant. cranium
Hypoxia affects bone osteogenesis in what manner?
Vascularity affects mesenchymal cells
-hypoxia→ Sox9 → chondrogenic cells
Presence of oxygen affects bone osteogenesis in what manner?
Vascularity affects mesenchymal cells

-no hypoxia→ Runx2 → osteoprogenitor cells
Intramembraneous ossification center
1. Mesenchymal (osteoprogenitor) cells
migrate, proliferate, and aggregate at
ossification centers(vascular; Runx2)
2. Osteoprogenitor cells differentiate into
osteoblastsand form bone trabeculae
3. Trabeculaeenlarge & merge via
appositional growth

Forms: flat bones of cranium, mandible, medial clavicle

will see trabeculae (spicules) in cranium and in between cranial bone spots called fontanelles
Endochondral ossification center
1.
Mesenchymal (chondrogenic) cells migrate,proliferate, and aggregate after vasculature regresses -Sox9
2.
Differentiate into chondroblasts/cytesthat form a hyaline cartilagetemplate
3.
A bone collar is formed around the template (near perichondrial vasculature)by intramembranous ossification
4.
Osteoclastsperforate the bone collar to allow vasculatureinto the cartilageto form the primary ossification center
5.
Secondary ossification centers appear at other sites of vascularization(e.g., epiphyses, some attachment sites)
6.
Growth continues at the growth plate, which eventually ossifies (timing differs by bone)
Nutrient foramen
associated with endochondral

Nutrient foramen remains where primary vasculature invaded the cartilage; explains the “inside-out” blood flow of bone
JC 8.14
Bone diameter increases by appositional growth of boneat the periosteum
Bone length increases by interstitial growthof cartilageat the growth plate
Growth plate: (endochondrial ossif.)
remnant of hyaline cartilage template responsible for longitudinal bone growth
Bone is added to the diaphysis
(not epiphysis)
Vasculature is in the diaphysis
Divided into 5 zones
5 zones of growth plate
1. Zone of reserve cartilage
-standard hyaline cartilage
-supplies/directs proliferation
2. Zone of proliferation
-chondrocyte mitosis: isogenous groups
-columns parallel to growth
-secretetype II collagen, PGs
3. Zone of hypertrophy (maturation)
-chondrocytes enlarge (Runx2)
-secreteVEGF(for vascular invasion)
4. Zone of calcification
-chondrocytes calcifyECM (Runx2)
-chondrocyte apoptosis
5. Zone of ossification
-ossification occurs
-vasculature invades, brings osteoprogenitor cells-OP cells → osteoblasts: woven bone formed on calcified cartilage-woven bone remodeledinto lamellar bone; medullary cavity formed
zone of ossification (5th layer)
ossification occurs

-vasculature invades, brings osteoprogenitor cells-OP cells → osteoblasts: woven bone formed on calcified cartilage-woven bone remodeledinto lamellar bone; medullary cavity formed
Zone of calcification (4th layer)
chondrocytes calcifyECM (Runx2)
-chondrocyte apoptosis
zone of hypertrophy (3rd layer)
maturation - increase oxygen levels

-chondrocytes enlarge (Runx2)
-secreteVEGF(for vascular invasion)
Zone of proliferation (2nd layer)
chondrocyte mitosis: isogenous groups
-columns parallel to growth
-secretetype II collagen, PGs
Zone of reserve cartilage (1st layer)
-standard hyaline cartilage
-supplies/directs proliferation
What direction is growth plate?
Cells stay fairly stationary
-ECM expansion drives growth “upwards
Most common bone fracture type and describe?
Type II - growth plate is displaced and one side of metaphyses is fractured
Type V fracture would exhibit what pathology
Growth plate is crushed so there is stunted growth
Describe inflammatory stage of bone fracture
-clot forms seal & framework for inflammatory cells & fibroblasts
-granulation tissue, type III collagen → type I collagen
-fibrocartilage-like tissue forms soft callus –no vasculature
Describe reparative stage of bone fracture
-hard callus of woven bone isformed by both intramembranous &
endochondral ossification –vasculature developed
Describe remodeling stage of bone fracture
-woven bone replaced by lamellar bone
(bone is typically completely reconstituted)