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Human Phys
Bone and joint disease
| Question | Answer |
|---|---|
| Intramembranous ossification (formation) | - flat bones formed within fibrous membrane - mesenchymal connective tissue remodelling - begins in utero and continues to adolescence - skull and clavicals not fully ossified at birth |
| Endochondral ossification | - long bones - forms from cartilage model replaced by bone |
| 1) Formation of ossification centre within membrane | Early in development MSC aggregate and differentiate into osteoblasts Forms ossification centre Osteoblasts begin to secrete osteoid- (unmineralized) |
| 2) Secretion of osteoid, which mineralises | Peripheral MSC still transforming into osteoblasts Osteoid secreted inward toward ossification centre Osteoblasts become trapped- (osteocytes) maintenance of the matrix |
| 3) Formation of woven bone & periosteum | Osteoid calcified and hardens -bone Blood vessels grow into the matrix Osteoid continue to be deposited in random manner-(woven) around the blood vessels forming inside MSC begins to condense and differentiate into periosteum |
| 4) Formation of compact bone & marrow | Lamellar (compact bone)- replaces woven bone at outer edge Spongy bone in centre- Red bone marrow, Osteoblasts remains- Surface to remodel the bone when needed |
| Endochondral ossification: Hyaline cartilage model formation | The hyaline cartilaginous precursor of the bones start to form in the 6-8 week embryo Mesenchymal cells condense and differentiate into chondroblasts that secrete extracellular matrix |
| Chondroblasts become encased in the cartilage matrix and become chondrocytes. Chondrocytes produce cartilage matrix- hyaline cartilage model. | |
| The perichondrium forms around the cartilage model The chondrocytes in the centre of the cartilage model hypertrophy (increase in size), and some burst releasing cell contents that trigger calcification | |
| Primary centre of ossification | The osteoblasts deposit bone material around the diaphysis bone collar Collar prevents nutrients diffusing into the hyaline cartilage and leads to chondrocyte death - cavities form Blood vessels penetrate bringing osteoblasts- deposit more bone |
| Secondary centre of ossification | The primary and secondary ossification centres have a thin cartilage layer between them, called the epiphyseal growth plate The chondrocytes in this plate continues to proliferate and form new cartilage which is replaced by bone until early adulthood |
| Epiphyseal line (Growth plate) | Chondrocytes divide rapidly forming columns and laying down cartilage matrix Calcification of the matrix causes chondrocytes begin to die as it restricts nutrient diffusion, leaves space |
| Osteoblasts and vessels penetrate the empty spaces and creating new bone Osteoclasts break down the calcified cartilaginous matrix | |
| Closure of the growth plate at adolescence | Only cartilage, on articulating surface Chondrocytes constrained from entering hypertrophy During osteoarthritis chondrocytes become hypertrophic |
| Fibrous cartilage | Pads within knee joint Between pelvic bones Intervertebral discs Support, tolerates distortion without damage Return to original shape |
| Elastic cartilage | Auricle of the external ear Auditory tube Epiglotis Support, tolerates distortion without damage Return to original shape |
| Hyaline cartilage | Covering surface of synovial joints Tips of ribs on bone of sternum Supporting trachea and larynx Nasal septum Still but flexible support Reduced friction between bony surfaces |
| Intervertebral disc cartilage | - fibrocartilaginous joint between the vertebral bodies - 23 discs in the spine; 6 cervical, 12 thoracic, and 5 in the lumbar region - movement of the vertebral column, and acts as a ligament - cushions the effect of shock and stress (reduced friction |
| Intervertebral disc cartilage | Outer ring of fibrous cartilage – Anulus fibrosus Collagen fibres at alternating angles, elastin fibres lie between the lamellae, (flexion or extension) |
| Gelatinous hydrated core- Nucleus pulposus: collagen fibres organised randomly, elastin organised radially Cartilaginous endplates, layer of hyaline cartilage connected to the vertebrae | |
| Chondrocytes | Rounded chondrocyte-like cells of the nucleus pulposus and inner annulus fibrosus regions- embryological derivative of notochordal cells |
| Fibroblasts | Flattened fibroblasts-like cells of the outer annulus fibrosus- mesodermal in origin Passive diffusion of oxygen, nutrients, and metabolites occurs through the cartilaginous end plates |
| Ear cartilage | - Elastic fibre networks and collagen type II fibres - elastin protein allows movement |
| Synovial joint | - have the following: Articular cartilage Joint (synovial) cavity Articular capsule Synovial fluid Reinforcing ligaments Small synovial joint: the incudomalleolar joint Knee- largest most complex |
| Articulating knee joint | - flexion, load bearing - hyaline cartilage - no blood vessels, nutrients from diffusion from synovial fluid |
| Cartilage structure | - extracellular matrix: H20: 75% of the total weight Collagen (Type II): 15% Aggrecan: 10% - chondrocytes produce and maintain matrix |
| The extracellular matrix | - collagen type II: provides high tensile strength, abundant ECM - aggrecans: proteoglycan pulls water to ECM allowing resistance to compressive forces |
| The chondrocyte | Highly specialized, role in the development, maintenance, and repair of the ECM Respond to a variety of stimuli, including growth factors, mechanical loads, and hydrostatic pressures Limited healing due to low replication |
| Maintenance of cartilage homeostasis | Chondrocytes synthesize matrix components MMPs are a major group of enzymes that regulate the cell–matrix composition and are considered the major proteases involved in ECM degradation |
| Osteoarthritis | - prevalent degenerative joint disease - caused by imbalance of synthesis and degredation |
| Cartilage changes | Imbalance in signalling pathways (TGFb, WNT, FGF, NFKb) Hypertrophic chondrocytes/ Terminal differentiation Inflammatory cytokines Increased proteolytic enzymes Breakdown of proteoglycans/ collagen loss |
| Proteases involved in cartilage degradation | Local loss of proteoglycans and cleavage of type II collagen Increase in water content and loss of tensile strength in the cartilage matrix |
| Subchondral bone in OA | Bone marrow leisons Osteophytes- endochondral bone formation Changes to trabecular bone Bone density changes |
| Fracture repair 1) hematoma | Blood clot formation Inflammation triggers the growth of new cells |
| 2) Callus formation | Soft callus formation Blood vessels grow into the clot Macrophage clean up debris Fibroblasts produce collagen Chondroblasts derived from periosteum progenitors, produce cartilage |
| 3) Callus ossification | Cartilage is replaced by woven bone through endochondral ossification Osteoblasts enter internal callus produce bone |
| 4) Bone remodelling | Repair is complete when the woven bone and any dead bone is replaced with compact bone Internal callus is remodelled and becomes stronger External callus become smaller due to osteoclast activity |
| Osteoporosis | - progressive skeletal disease - Loss of bone matrix (mostly spongy bone), Low bone mass, microarchitecture deterioration Bones to become weak and brittle, deformed Prone to fractures (hip, wrist or spine) |
| Role of oestrogen in bone homeostasis and skeletal regrowth | - important role in the growth and maturation of bone as well as in the regulation of bone turnover in adult bone - at cellular level in bone oestrogen inhibits differentiation of osteoclasts |
| Treatment | Denosumab is a monoclonal antibody (Mimics the action of OPG)- binds to RANKL Prevents RANKL from activating its receptor RANK on the surface of osteoclasts precursors - increasing bone strength |
| Sclerosteosis | - rare autosomal recessive disorder that results from osteoblast hyperactivity - caused by loss-of-function mutations in the sclerostin gene, secreted glycoprotein - dense bone overgrowth, distortion of the face, and entrapment of cranial nerves |
| Wnt stimulate bone growth/ repair | - key role in embryonic bone formation and adult osteogenic differentiation of mesenchymal stem cells |
| Wnts bind a receptor complex consisting of LRP5 or LRP6 and Fz proteins Prevents phosphorylation of β-catenin by GSK3β and its subsequent degradation Stabilized β-catenin accumulates and translocates to the nucleus, | |
| Inhibition of Wnt binding | Sclerostin binds LRP Prevents Wnt binding b-catenin phosphorylated by GSK-3 b- catenin degraded in proteosome No expression of target genes Reduced osteoblast formation - decreased bone formation Mutations can't inhibit osteoblasts/excess bone |
Created by:
reub8n
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