Bone Physiology Flashcards
What’re the constituents of connective tissue?
What’s the importance of ECM?
Made of cells and extracellular matrix
ECM made of fibrous proteins and ground substance
Ground substance = proteoglycans, glycoproteins and water
ECM composition determines the tissues physical properties
What are two features of bone and what substances form them?
Rigidity - mineralised ECM with hydroxyapatite
Resilience - type 1 collagen fibres
What are the functions of bone?
Movement Protection Site of haematopoiesis Mineral homeostasis Support
Where does the growth plate on a bone sit? How can you tell on imaging?
Between epiphysis and metaphysics
Children still have growth plates present so on imaging will see gaps in the ends of the bones (don’t confuse with a fracture)
What’s the difference between woven and lamellar bone?
Woven bone = immature/primary bone; first bone formed at any sites, collagen fibres arranged randomly
Lamellar bone = mature bone, collagen fibres are remodelled into an orderly arrangement to provide strength
Woven bone is the first type of bone to occur at fracture healing sites
Where do trabecular and cortical bone sit?
Trabecular provides the scaffolding in the centre of the bone
Cortical is the outside
Outline the microstructure of cortical (compact) bone
Lamellae = bony plates made of collagen fibres in parallel
There’s inner circumferential and outer circumferential lamellae
Interstitial lamellae is the result of bone remodelling and formation of new Haversian systems
Haversian systems are found within concentric lamellae (encircled by)
What are Haversian systems? (Osteons)
What do Haversian canals contain and how are they different to Volkmann’s canals?
Haversian systems are the functional unit of compact/cortical bone
Haversian canals contain blood vessels, lymphatic vessels and nerves
Volkmann’s canals run transversely, allowing communication between Haversian canals, the periosteum (outer bone layer) and the bone marrow cavity
Outline the microscopic structure of Trabecular bone (cancellous/spongy)
3D network of beams and struts of lamellar bone oriented along lines of stress
Large areas of intercommunicating spaces (marrow spaces) for haematopoiesis
What’s the blood supply along a bone? How does this relate to fractures?
Epiphyseal artery
Metaphyseal artery
Periosteal arteries
Nutrient artery
Bone fractures may cause bleeding and lead to compartment syndrome = pain as pressure rises from formation of haematoma around the bone
What’s the differentiation of bone cells from mesenchymal stem cells?
What are periosteal cells?
Mesenchymal stem cells -> osteoprogenitor cells -> osteoblasts -> osteocyte
Periosteal cells are bone lining cells that are just resting osteoblasts - they have an important role in fracture healing
What’s the role of osteocytes?
Mechanotransduction and matrix maintenance/calcium homeostasis
Outline the structure of osteocytes
They’re mature bone cells that don’t undergo cell division
Occupy lacunae surrounded by bone matrix; dendritic processes of osteocytes pass through canaliculus to radiate from lacunae and anastomose with those from other lacunae
Gap junctions between dendritic processes allow transfer of ions and nutrients
Outline the structure and role of osteoclasts
Haematopoitic origin
Large multinucleated cells with rugged border to resorb bone matrix by synthesising and secreting enzymes and acid
Involved in remodelling, growth and repair
Form Howship’s lacunae (resorption craters)
What do osteoblasts secrete?
Osteoid - the unmineralised organic component of bone
What’s the normal bone remodelling cycle?
Continual process throughout life in response to changing mechanical stress or micro fractures of bone
Relies on balance between bone resorption and formation by osteoclasts and osteoblasts
Formation (matrix synthesis) -> Quiescence (osteoclasts recruitment, differentiation and activation)-> Resorption (by osteoclasts) -> Reversal (osteoblast recruitment, differentiation and activation)
How is bone remodelling regulated?
By signalling molecules: ratio of OPG:RANKL determines degree of resorption (cytokines, hormones and drugs can alter the balance)
Osteoblasts secrete RANKL which binds to RANK on osteoclasts to active them for bone resorption
Osteoblasts also secrete OPG which prevents binding of RANKL to RANK
What drugs can affect RANKL and OPG activity - so alter bone remodelling?
Bisphosphonates reduce osteoclast activity to inhibit bone resorption and therefore increase bone mass in cortical and trabecular bone
How does bone develop by intramembranous ossification? What bones does this happen in?
Mesenchymal -> bone (direct replacement by bone tissue, without a cartilage precursor)
Ossification centre (lots of osteoblasts + osteoid) -> secretion of osteoid to form newly calcified bone matrix -> formation of woven bone and periosteum (blood vessels invade, mesenchymal condenses to form periosteum) -> formation of bone collar and appearance of red marrow (plate of compact bone with marrow cavities + osteoblasts and fibrous periosteum)
Occurs in flat bones of skull, clavicle and mandible
Outline bone development by endochondral ossification?
What type of bones does it typically occur in?
Mesenchymal -> Cartilage -> Bone
Miniature hyaline cartilage model is formed, which continues to grow providing a scaffold for bone development and is eventually resorted and replaced by bone
Primary ossification centre (osteoblasts secrete bone matrix onto calcified cartilage) -> secondary ossification centre (OPG invade cartilage and differentiate into osteoblasts, laying down bone on cartilage scaffold)
Occurs in weight bearing bones eg long bones, vertebrae, pelvis
What’s the difference between primary and secondary ossification centres?
Primary ossification in diaphysis, develops in foetal life
Secondary ossification centres in epiphysis and develops after birth
Outline the two types of bone growth?
Longitudinal growth: at the epiphyseal growth plate of weight bearing long bones: proliferation of cartilage cells followed by endochondral ossification
Apposition growth: growth in width, new bone formed under periosteum
What are the different zones are the epiphyseal growth plate?
After bone growth what happens to the zones?
Resting/quiescent zone (EPIPHYSIS) Growth/proliferation zone Hypertrophic zone Calcification zone Ossification zone (DIAPHYSIS)
Eventually ossification zone takes over the rest zones and the epiphyseal growth plate closes
What’s the clinical significance of the epiphyseal growth plate?
Relative weak point to shearing forces
Fractures involving growth plate (Salter-Harris fractures) = deformities in developing bone (shortened/angulation)
Disorders affecting bone mineralisation (Rickets) can affect size and shape of growth plate
What is a fracture?
What are the different types of fracture?
= a breach in the integrity of part, or whole of a bone Transverse fracture Oblique fracture Spiral fracture Grossly comminuted fracture Greenstick fracture Crush fracture (in vertebrae)
Compound/open fracture = direct communication between broken bone and skin surface
Simple/closed fracture = clean break with intact overlying tissues
What are the 6 stages of fracture healing?
Haematoma Granulation tissue Callus Woven bone Lamellar bone Remodelling
Outline the haematoma and granulation tissue stages of fracture healing
Haematoma: rupture of vessels in region of fracture form haematoma = necrosis of bone fragments = inflammatory reaction so phagocytes migrate to area to remove necrotic tissue
Granulation tissue forms: blood clot invaded by small capillaries and fibroblasts -> cytokines and growth factors induce cellular proliferation
Outline callus and woven bone formation stages in fracture healing
Callus: forms from fibrous tissue + inflammatory cells + cartilage, forming a bridge between bone ends
Woven bone: OPG cells proliferate and differentiate into osteoblasts to form woven bone -> strengthens callus and rigidity -> no more movement means fracture site is clinically united
Outline lamellar bone formation and remodelling stages of fracture healing
Lamellar bone gradually replaces woven bone (around reformed marrow cavity)
Remodelling: osteoclasts and osteoblasts remodel lamellar bone in response to stresses -> excessive callus is reabsorbed and medulla cavity reestablished
What factors affect fracture healing? (Aid and delay it)
Aid healing: stability of the fracture, apposition of bone ends, adequate blood supply
Delay healing: excessive movement of bone ends, poor blood supply, infection, foreign bodies
Define malunion, delayed union and non-union
Malunion = healing in unsatisfactory positions
Delayed union = takes longer than expected to unite
Non-union = leads to fibrous union or pseudoarthritis
