bone 1 Flashcards
cartilage
Specialised connective tissue with a support function (often the shock absorbers of the body, can be tough or flexible depending on composition of matrix)
Cells: chondrocytes
Matrix: Type II collagen and proteoglycans + others depending on type of cartilage
cartilage cells
Derived from embryonic mesenchyme (spindle) – clusters of chondroblasts (rounded) surrounded by a layer of perichondrium (mesenchyme derived fibroblastic cells and collagen)
Growth of cartilage is by interstitial (limited division of chondroblasts in ECM) and appositional growth (new chondroblasts from perichondrium).
After matrix deposition cells become less active and become maintaining cells (chondrocytes) (lacuna is an artefact)
cartilage ECM: fibres and ground substance
Collagen II + ground substance.
Matrix is 70% water
proteoglycan aggregates- proteoglycan monomers attached to a molecule of hyaluronin. Hydrophilic. Provides compressive strength: flexible cushioned surface
Proteoglycans contain numerous glycosaminoglycans (GAGs) attached to a core protein (bottle-brush structure- negatively charged chains)
Woven with collagen to form an elastic and compressible structure.
GAGs: chondroitin-4-sulphate, chondroitin-6- sulphate, and keratan sulphate
cartilage types
Dependent on requirements of tissue:
Hyaline cartilage: Type II collagen only – smooth glistening (glassy) articular surfaces
Elastic cartilage: Type II collagen + elastin
Fibrocartilage: Type II and type I collagen-strong
Hyaline cartilage
Chondrocytes arranged in groups in a matrix containing Type II collagen.
perichondrium usually present except at articular surface.
locations: Articular ends of long bones, ventral rib cartilage, templates for endochondral bone formation, tracheal rings
elastic cartilage
Chondrocytes compacted in matrix containing Type II collagen and elastic fibers.
perichondrium present.
Locations: Pinna of ear, auditory canal, laryngeal cartilages, epiglottis
Fibro-cartilage
Chondrocytes arranged in rows in a matrix containing Type I collagen bundles in rows.
perichondrium absent.
Intervertebral discs, pubic symphysis, joint capsules, ligaments and tendons
hyaline cartilage at joints
Resists compression due to the elasticity and stiffness of proteoglycans
Tensile strength due to collagen and hydrogel ground substance
Most is avascular: limits repair and regeneration.
Nutrition is by diffusion: limits thickness
Articular surfaces of joint has no perichondrium-no source of new chondroblasts
Cartilage atrophy is reversible but it takes a long time
bone is a specialised connective tissue
Structurally strong-mechanical support and protection
Reservoir for calcium and phosphate in the body -role in calcium homeostasis
Supports haematopoiesis –bone marrow
Composed of cells and extracellular matrix
Matrix must be strong enough to support the body, yet light enough to be moved: max strength; low weight
Cells produce, mediate, maintain and remodel the matrix
bone organisation
Dense outer shell: compact bone
Inner spongy/cancellous bone arranged in interconnecting trabeculae with spaces for bone marrow.
Max strength, less weight
Periosteum: fibrous CT layer limiting bone. Carries blood supply and osteoprogenitor cells. Not present at the joint ends of long bones.
Endosteum lines the interior of bones
trabecular bone
Reduces weight
Provides space for marrow
Struts are arranged to provide maximum resistance to stresses
Found in e.g. wrists, vertebrae, femoral neck
osteoporosis
Thinning of both cortical and trabecular bone, but thinned trabeculae are prone to fracture
i.e. FOOSH, hip fracture, dowager hump
bone matrix
organic: Produced by osteoblasts Collagen type 1 Tensile and compressive strength Non collagenous proteins mediate mineral deposition
inorganic: Calcium phosphate (hydroxyapatite) Deposited in the organic matrix 66% of the dry weight of bone Hardness
brittle bone disease (osteogenesis imperfecta, OY)
Congenital disease
Defective collagen chain disrupts structure of triple helix
Fragile skeleton:
Many types with a range of clinical outcomes: type II fatal in utero or perinatal. Type I-increased childhood fractures (pre-puberty).
Extra-skeletal manifestations: where? (skin, joints, eyes: blue sclera)
bone cells
Derived from mesenchymal stem cells
Differentiate into osteoprogenitor cells or chondroblasts
Osteoprogenitor cells differentiate into osteoblasts
Osteoblast: lays down organic bone matrix
And mediates mineralisation of osteoid
Osteoblast becomes osteocyte when surrounded by mineralised bone
Osteocyte: maintains matrix
osteoid becomes mineralised
Osteoblasts secrete collagen and matrix vesicles
Matrix vesicles contain enzymes and proteins to control availability of calcium and phosphate so that mineral is precipitated.
Immature: Woven bone. haphazard fibre arrangement, mechanically weak – foetal development/fracture repair (rapid osteoid formation)
Mature: Lamellar bone: remodelled woven bone –regular parallel collagen, strong: all adult bone. arranged as osteons (aligned with the direction of force)
osteocytes
Mature osteoblasts – surrounded by mineralised matrix
Long cytoplasmic processes connecting to each other and osteoblasts (gap junctions)
Maintain matrix-no osteocytes: matrix is resorbed
In lacunae surrounded by extracellular bone fluid that allows nutrient diffusion through the bony channels (canaliculi)
Stress information: responsive to tiny currents generated when bone is deformed
Connected to both osteoblasts and osteoclasts
osteoclasts
Osteoclasts exist to destroy bone! Why??
Bone resorbing cell
Phagocytic cell from monocyte macrophage cell line
Multinucleate mobile cell which attaches to bone surface and resorbs bone leaving a pit behind (Howships lacuna)
Work with osteoblast to regulate bone turnover and remodelling
how do osteoclasts destroy bone?
Large multinucleate cells
Actin clear zone and integrins adheres it to the bone surface. Ruffled border increases surface area of the cell.
Mineral is dissolved by acids. Outside the cell due to low pH.
Lysosomal enzymes resorb organic matrix.
Number and function affected by PTH and calcitonin
Oestrogen also reduces activity-menopause
bone remodelling
Bone is constantly remodelled through the coordinated actions of osteoblasts, cytes and clasts, to adjust to stresses and strains. Affects density, orientation and responds to micro fractures and wear and tear
Keeps bone healthy!
The aim is to place bone struts the the location and direction of maximum stress while keeping the structure open to minimise weight.
In the adult 3-5% of skeleton continuously replaced - new Haversian system takes 3-4 weeks
5% compact bone replaced annually
25% cancellous bone replaced annually
osteoporosis
Rare group of inherited conditions
Reduced osteoclastic activity: defective bone remodelling
Osteoclasts can not excrete H+ ions to dissolve bone mineral (needs H+ for the acidic environment)
Dense ‘stone bone’ but brittle and easily fractured
Clinical effects: fractures, spinal nerve compression (excess bone) and recurrent infection (reduced bone marrow cavity). Hepatosplenomegaly due to haematopoiesis outside the bone
Bone marrow transplant to provide healthy osteoclast precursors can be effective
relationship between osteoblasts and osteoclasts
PTH stimulates bone resorption by osteoclasts
The receptors for PTH are located on osteoBLASTS
Osteoclast precursors have RANK (Receptor Activator of Nuclear factor Kappa B) receptors on their cell membranes
Osteoblasts have the ligand for this receptor on their cell membranes: RANKL
PTH upregulates RANKL which binds to RANK and stimulates the differentiation of osteoclasts
Osteoblasts also produce osteoprotegrin which prevents resorption by binding to RANKL
The ratio of RANKL:osteoprotegrin determines bone resorption
