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WEEK 24:

Bone 1:

QuestionAnswer
cartilage avascular, specialised connective smooth tissue
function of cartilage with bone and joints cartilage can act as a smooth surface for bone articulation within joints playing a role in bone formation and providing structural support
typical function of cartilage often functioning as shock absorbers of the body
cartilage can be tough or flexible depending on composition of matrix
cells in cartilage chondrocytes
bone organisation dense outer shell (compact bone) and inner spongy/ cancellous bone (arranged in interconnecting trabeculae with spaces for bone marrow)
periosteum fibrous connective tissue layer limiting bone (not present at joint ends of long bones)
endosteum lines interior of bones
matrix of cartilage composes of (3) type II collagen, proteoglycans, and other proteins
chondrocytes specialised cartilage cells that produce a matrix of collagen and other proteins (ECM)
collagen protein that helps give cartilage its shape and specific properties
type II collagen fibrillar collagen that is restricted to cartilages
proteoglycans special type of protein that provides biomechanical properties crucial for cartilages proper functioning and are key players in chondral diseases
non collagenous proteins help cartilage attract water and give it its shape and specific properties
perichondrium dense layer of fibrous connective tissue covering the surface of most of the cartilage in the body
layers in the perichondrium (2) outer fibrous layer and inner chondrogenic layer
outer layer of perichondrium fibrous
inner layer of perichondrium chondrogenic
inner chondrogenic layer of perichondrium contains chondroblasts
outer fibrous layer of perichondrium contains fibroblasts
cartilage ECM main components (2) fibres (collagen II) and ground substance (protein aggregates made of proteoglycans and GAGs)
proteoglycan aggregates proteoglycan monomers attached to a molecule of hyaluronin making it hydrophilic and provides compressive strength making it a flexible cushioned surface (proteoglycans + GAGs)
proteoglycans contain numbers glycosaminoglycans (GAGs) attached to a core protein (bottle brush structure with negatively charged chains)
the ground substance of cartilage ECM is woven with collagen to form an elastic and compressible structure
GAGs (3) chondroitin-4-sulphate, chondroitin-6- sulphate, and keratan sulphate.
cartilage cells are derived from embryonic mesenchyme
structure of cartilage cells clusters of chondroblasts (rounded) surrounded by a layer of perichondrium
growth of cartilage is via (2) interstitial and appositional growth
what happens to cells after matrix deposition they become less and active and become maintaining cells
interstitial growth of cartilage mainly happens during childhood and adolescence where chondroblasts in the cartilage divide and grow making the cartilage matrix expand from within
appositional growth of cartilage new chondroblasts from the perichondrium add new surface layers of matrix to the existing matrix, thus expanding the girth of the cartilage
how are chondrocytes arranged in hyaline cartilage in groups in a matrix containing type II collagen
perichondrium in hyaline cartilage usually present except at articular surfaces
where is hyaline cartilage found end of long bones, ventral rib cartilage, templates for endochondral bone formation, and tracheal rings
how are chondrocytes arranged in elastic cartilage compacted in matrix containing type II collagen and elastic fibres
perichondrium in elastic cartilage present
where is elastic cartilage found pinna of ear, auditory canal, laryngeal cartilages, and epiglottis
how are chondrocytes arranged in fibrocartilage in rows in a matrix with type I collagen bundles in rows
perichondrium in fibrocartilage absent
where is fibrocartilage found intervertebral discs, pubic symphysis, joint capsules, ligaments and tendons
hyaline cartilage type II collagen only - smooth glistening (glassy) articular surfaces
elastic cartilage type II collagen and elastin
fibrocartilage type II and type collagen - strong
what type of tissue is bone specialised connective tissue
what minerals does bone provide reservoir for calcium and phosphate
bone marrow in bone supports what process haematopoiesis (making new RBCs)
bone is composed of cells and ECM
requirements for bone ECM strong enough to support body yet light enough to be moved (max strength and low weight)
role of cells in the bone produce, mediate and maintain remodel matrix
bone structure and organisation dense outer shell (compact bone), inner spongy/ cancellous bone (arranged in interconnecting trabeculae with spaces for bone marrow)
dense outer shell of bone compact bone
inner spongy/ cancellous bone arranged in interconnecting trabeculae with spaces for bone marrow
periosteum fibrous connective tissue layer limiting bone and is not present at the joint ends of long bones
periosteum is not present where at the joint ends of long bones
endosteum lines the interior of bones
organic bone matrix produced by osteoblasts, containing type I collagen and non collagenous proteins (which mediate mineral deposition), providing tensile and compressive strength
inorganic bone matrix made of calcium phosphate (hydroxyapatite) and is deposited in the organic matrix making up 66% of the dry weight of bone (hardness)
bone cells are from mesenchymal stem cells
mesenchymal stem cells differentiate into osteoprogenitor cells
osteoprogenitor cells differentiate into osteoblasts
order of differentiation of bone cells mesenchymal stem cells -> osteoprogenitor cells -> osteoblasts
osteoblasts layer down organic bone matrix and mediates mineralisation of osteoid
when do osteoblasts become osteocytes when surrounded by mineralised bone
osteocyte maintains matrix
osteoclasts bone resorbing/eating cells
osteoblasts secrete collagen and matrix vesicles
matrix vesicles contain enzymes and proteins
why do matrix vesicles contain enzymes and proteins to control availability of calcium and phosphate so that mineral is precipitated
immature/ new bone woven bone which has haphazard fibre arrangement and is mechanically weak needing fracture repair
mature bone lamellar bone with regular parallel collagen, strong and found in all adult bone and is arranged as osteons (aligned with the direction of force)
osteogenesis imperfecta (OI)/ brittle bone disease congenital disease where defective collagen chain disrupts structure of triple helix leading to a fragile skeleton
type II OI fatal in utero or perinatal
type I OI increased childhood fractures
trabecular bone has lamellae with osteocytes in lacunae which is connected to one another via canaliculi
difference between trabecular bone and compact bone compact bone has central canals and perforating canals which contain blood and lymph vessels and nerves but trabecular bone does not have central canals or perforating canals and their vessels and nerves travel between spaces in the trabeculae
where do blood vessels, lymph vessels and nerves travel in compact bone in perforating and central canals
where do blood vessels, lymph vessels and nerves travel in trabecular bone between spaces in trabeculae
trabecular bone function reduces weight and provides space for marrow
struts/ trabeculae are arranged in trabecular bone to provide maximum resistance to stresses
where is trabecular bone found wrists, vertebrae and femoral neck
osteoporosis thinning of both cortical and trabecular bone but thinned trabecular are prone to fracture eg hip fractue and
compact bone is made of osteons which are functional units that act as weight bearing pillars
osteons are made up of concentric rings of lamellar bone around a central nutrient canal
central canal contains blood vessels, lymph vessels, and nerves
position of perforating canals to central canals perforating canals run at right angles to the central canals
what is normal bone maintenance and turnover continuous process where old bone tissue is broken down by cells (osteoclasts) and replaced with new bone formed by osteoblasts to allow bone to constantly remodel and repair to maintain its strength and structure (remodelling)
cortical bone (dense outer layer) turnover compared to trabecular bone (spongy inner bone) cortical bone has a slower turnover rate to trabecular bone
factors affecting turnover (2) hormones (oestrogen, parathyroid hormone PTH) and vitamin D
phases of bone remodelling (4) resting, resorption, reversal, and formation (RRRF)
osteoclasts bone resorbing cell which is a phagocytic cell from monocyte macrophage cell line. It is multinucleate and mobile which helps it attach to bone surface and resorb bone leaving a pit behind (Howships lacuna)
(Howships lacuna) pit left behind after osteoclast eats bone
resting phase prolonged resting period before new bone remodelling
when does resorption phase occur when osteoclasts are activated
resorption phase osteoclasts on the bone surface become activated and resorb bone matrix
reversal phase resorbed bone surface is prepared by mononuclear cells to allow maximum osteoblast adherence
formation phase osteoblast progenitors form osteoid matrix to complete the mineralisation of the bone
compare and explain bone remodelling in children and adults bone turnover and remodelling is slower in adults than children
how can bone remodelling increase (3) change in function (running, tennis, jumping), repair of fractures, and disease (eg Paget's disease)
how much compact bone is replaced annually 5%
how much cancellous bone is replaced annually 25%
PTH stimulates what bone resorption by osteoclasts
receptors for PTH are located where on osteoblasts
osteoclast precursors have RANK (receptor activator of nuclear factor Kappa B) receptors on their cell membranes
osteoblasts have ligand for RANK receptor on their cell membranes (RANKL)
PTH upregulates what RANKL
when PTH upregulate RANKL what happens RANKL bind to RANK and stimulates the differentiation of osteoclasts
osteoblasts also produce what by binding to RANKL osteoprotegrin- which prevents resorption
osteoprotegrin produced by osteoblasts and prevent resorption
what determines bone resorption ratio of RANKL: osteoprotegrin
relationship between osteoblasts and osteoclasts are via (3) PTH RANKL and osteoprotegrin process, direct cell to cell contact, and cytokine signalling
explain direct cell-cell contact osteoblasts and osteoclasts can directly interact through cell adhesion molecules eg E-cadherin, which facilitates signalling between them
explain cytokine signaling osteoblasts secrete various cytokines eg M-CSF (macrophage colony stimulating factor) that stimulate osteoclast proliferation and differentiation
factors which disrupt osteoblast and osteoclast balance (3) hormonal imbalance, mechanical stress, and aging
explain how hormonal imbalances disrupt osteoblast and osteoclast balance hormones like oestrogen and PTH imabalance/ dysregulation can lead to bone diseases like osteoporosis
explain how mechanical stress disrupt osteoblast and osteoclast balance changes in mechanical loading on bones can influence osteoblast and osteoclast activity impacting bone remodeling
explain how ageing disrupt osteoblast and osteoclast balance with age, balance between bone formation and resorption can shift towards increased resorption leading to bone loss
explain cause of osteoporosis loss of bone mass where mineralisation of bone is normal (increase porosity) but due to disuse (wheelchair, mobility problems), hormones (eg oestrogen levels decreased), and low peak bone mass
when is bone gradually lost after approximately 30 years old
why does menopause lead to osteoporosis oestrogen is osteoprotective but in menopause the levels are decreased
why does disuse like wheelchair or mobility problems lead to osteoporosis need mechanical stress (movement) for remodelling but wont occur if no move
Created by: kablooey
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