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Bone and Cartilage
Organisation of the Body
| Question | Answer |
|---|---|
| What are bone and cartilage | Connective tissues - cells embedded in an extracellular matrix In bone the matrix is rigid In cartilage the matrix is somewhat flexible but still strong Their functions are: resisting forces, ability to grow, ability to adapt, ability to repair |
| Types of cartilage | Hyaline cartilage-template of bony skeleton, articular surfaces of synovial joint, flexible skeleton parts of ribcage, trachea, bronchi and nose Fibrocartilage-very strong, intervertebral discs, intra articular discs in synovial joints Elastic cartilage |
| Types of bone | Compact bone - outer shell of all bones, cylindrical shaft in long bones Trabecular bone - internal supporting plates/struts (strong but lightweight) Lamellar (Haversian bone) - organised in osteons Woven bone - temporary bone during development/repair |
| Hyaline cartilage | Somewhat deformable Low friction due to smooth surface Covers articular surfaces - also present in growth plates Key molecules include collagen type II, proteoglycans with glycosaminoglycans. Often hyaluronic acid surrounded by others. Very hydrated |
| Structure of cartilage | Perichondrium - outer layer. Chondroblasts divide to form chondrocytes and secrete the ECM Chondrocytes remain in lacuna They receive nutrients etc by diffusion as there are no blood vessels present |
| Appositional growth of cartilage | New cartilage is added to the surface of the older cartilage by chondroblasts from the deep layer of the perichondrium, which take on more chondrocytic activity |
| Interstitial growth of cartilage | New cartilage is formed within older cartilage by chondrocytes that divide and produce a new matrix. The chondrocytes remain in lacuna, so many may sit in one lacuna |
| Cartilage in the epiphysial plate | Resting zone at top Proliferative zone where chondrocytes align and divide along the long axis Hypertrophic zone where chondrocytes stop dividing, increase in size and secrete ECM. Degeneration zone where matrix becomes calcified Ossification zone |
| Fibrocartilage | Present in intervertebral discs, knee menisci, entheses (bony attachments of tendons/ligaments) A layered structure with more type I collagen than hyaline. Thin at a bone surface but thick at periphery Can be squashed to maintain flexibility/compression |
| Elastic cartilage | Attached to vocal chords, ear, eustachian tube and epiglottis Matrix permeated with elastin fibres |
| Function of the skeleton | Support Protection- skull, rib cage Lever of motion Resistance to tensile and compressive forces Reservoir of calcium Repository of bone marrow |
| Development of bone - intramembranous ossification | Osteogenic progenitor cells differentiate in mesenchyme. These differentiate into osteoblasts,form the bone spicule. Osteoblasts secrete the ECM The spicules enlarge, osteocytes trapped in matrix (in lacuna) and blood vessels invade. These fuse |
| Bone formation -endochondral ossification | Bone laid down as cartilage. Compact bone laid down on cartilage at shaft. Periosteum contain bone forming cells. Blood vessel invade and bring more bone cells. Trabeculae laid down in centre of shaft. After birth the ends are ossified. |
| Adult bone architecture | Trabecular aligned with stress Osteocytes in lacunae between bony lamellae of osteon Middle of osteons is the haversian canal which contains blood vessels and nerves. Endosteum inside, periosteum outside |
| Osteons in compact bone | Osteocytes are linked to each other and surface osteoblasts by canaliculi and gap junctions Centre of an osteon is the Haversian canal Haversian canals linked by Volkmann's canal. Concentric circles of bones form lamellae |
| Arrangement of collagen fibres in bone | Type I collagen Helices at different angle in different lamellae. This allows for strength in multiple directions |
| Arrangement of calcium hydroxyapatite in bone | Crystals are attached to the collagen fibres Calcium salts e.g. phosphate, carbonate etc in platelets or rods 70% bone mass |
| Role of collagen and Hydroxyapatite crystals | Collagen gives tensile strength - when denatured by heading bone shatters Hydroxyapatite crystals give compressive strength - when demineralised by acid bone cannot hold structure under compression |
| Cells present in bone | Osteoblasts Osteoclasts Osteocytes These maintain the dynamic nature of bone and allow for remodelling |
| Osteoblasts | Bone lining cells important in appositional growth Derived from fibroblast like precursors that can also give rise to adipocytes, myocytes and chondrocytes Allow bone formation by laying down bone on existing bone Vitamins D and K are involved |
| Osteoblast derived matrix glycoproteins | Osteocalcin-local regulatory protein Osteonectin-binds calcium, hydroxyapatite and collagen Osteopontin-RGD sequences to bind osteoclasts Bone morphogenic protein-induce cartilage and bone formation Released in vesicle which break down away from bone |
| Molecular studies to identify bone inducer | Use fact that osteocalcin is specifically expressed in bone. Sequence the osteocalcin promoter and search database for similar sequences that bind TFs. Identified the protein coded Cbfa-1 rich in bone tissue Knock out mice have cartilage skeletons |
| Osteocytes | Control immediate area of bone tissue Formed when osteoblasts are embedded in matrix Gap junction linked processes form a network of force sensors in canaliculi through the bone connected to osteoblasts |
| Osteoclasts | Multinucleate cells formed from monocyte/macrophage lineage Attach via integrins to RGD sequences in matrix protein Osteopontin Form ruffled edge facing sealed (Howships lacuna) Secrete acid and proteases to break down bone |
| How to osteoclasts break down bone (part 1) | Integrins in osteoclast seal it onto bone-a ruffled border develops Osteoclast starts to produce and secrete H+ via a proton pump Carbonic anhydrase produces more protons via carbonic acid Chloride is exchanged for HCO3- be an exchanger |
| How to osteoclasts break down bone (part 2) | Chloride channel allows Cl to pass into lacuna and produce HCl Proteases are secreted to break down the collagen and other proteins in the bone Ca and signalling peptides released from degraded bone - peptides stimulate osteoblasts to fill in holes |
| Control of osteoclasts | Done by osteoblast products Osteoclast differentiation factor - RANK ligand, an activating receptor on osteoclasts OPG produced by osteoblasts inhibits the action of RANK by acting as a decoy receptor, inhibiting bone breakdown. |
| Bone remodelling | Stimulus to remodel - forces perceived by osteocytes, periosteal osteoblasts Osteoclasts remove unwanted bone then die Osteoblasts are recruited, form new bone, then become inactive in bone lining cells. This requires complex signalling between cells |
| Stages of bone remodelling | Differentiation of cells Fusion with bone Recruitment of other cells Chemotaxis Mechanical stimulus |
| Bones as an endocrine tissue | Releases signalling factors into circulation E.g. osteocalcin acts on the pancreas, brain, muscle, testes and fat as well as the bone |
| What controls long bone growth | Growth hormones IGF-1 and their receptors Rate of growth depends on rate of chondrocyte growth in the epiphyseal plate |
| Effects of growth hormone | Changes in growth hormone concentration determines size Mice without GH receptors are much smaller than normal mice |
| Achondroplasia | Very short 'long' bones A gain of function mutation. FGF receptor 3 promotes full chondrocyte differentiation. When over expressed dur to a mutation, chondrocytes differentiate too early. This terminates growth of the bone |
| Mice with mutated FGFR3 | Tend to have longer bones - a loss of function mutation, chondrocytes continue to grow without differentiating When the human gain of function mutation is introduced, a phenotype similar to human achondroplasia develops |
| Bone as a calcium reserve | Calcium levels must be precisely regulated in the body Hormones controlling calcium play a role in other area of the body Calcium can come from diet, reabsorption in the kidneys and from resorption of bone |
| Paget's disease | Osteoclasts increase in number and size, contain viral nuclear inclusions, antigens, transcripts. Increased osteoblastic bone formation leads to weaker woven bone May have a genetic component Leads to malformed bone due to constant remodelling |
| Osteogenesis imperfecta | In 90% of cases a dominant mutation in type I collagen gene leads to weakened bone which break easily leading to gross deformity. A recessive mutation in a protein CRTAP causes most other cases (abnormality in linking collage together) |
| Osteoporosis | Too much bone breakdown due to too much osteoclast activity or too little osteoblast activity. Trabecular bone is thinner and weaker. This level of bone resorption changes with age Highest risk in postmenopausal women - decreased bone mass |
| Rickets | Due to a lack of vitamin D Bones are deficient in calcium as they cannot absorb it. Bones remain intact but are flexible, so start to bend |
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