Chapter 6 Bone Physiology PDF

Chapter 6: Bone Tissues  Functions of the Skeletal System? Support Protect Movement Mineral Storage Blood Cell Production Fat Storage?? Cartilage Associated with Skeleton  Divisions of the Skeletal System Axial Vs Appendicular...

Chapter 6: Bone Tissues  Functions of the Skeletal System? Support Protect Movement Mineral Storage Blood Cell Production Fat Storage?? Cartilage Associated with Skeleton  Divisions of the Skeletal System Axial Vs Appendicular Figure 7.1 Bone shapes Sutural: inside sutures Figure 6.2 Classification of bones by shape.  Gross Anatomy: Long Bone vs Flat Bone (or short, round, irregular) Figures 6.3 and 6.4  Parts of a Long Bone Epiphysis – Articular Cartilage – Spongy Bone (cancellous) Metaphysis – Epiphyseal Line/Plate Diaphysis – Periosteum w/fibers – Compact Bone – Endosteum – Medullary Cavity Figure 6.3 Gross Anatomy: Flat/Short Bones Compact Spongy (Cancellous - dipolë) Compact Figure 6.4  Red Bone Marrow: Hematopoietic Tissue Stem cells produce all blood cells (both red AND white blood cells) Only spongy bone regions have RBM in adults Figure 6.4 Figure 6.5 The importance of bone matrices. Bone Connective Ground Bone Vs. Tissue Demineralized Bone Bone Matrix and Chemistry  Components of Bone Organic = 33-35% – Mostly collagen fibers – Proteoglycans, glycosaminoglycans, glycoproteins, and osteocalcin (bone protein) Inorganic = 65-67% – Hydroxyapatite crystals - Ca10(PO4)6(OH)2 (Calcium salts & Potassium) – Bicarbonate, magnesium, phosphate, sodium salts  Blood and Nerves to Bone Mainly found in the Periosteum – Especially for: short, flat, irregular and sesamoid bones With long bones – Diaphysis – 1-2 nutrient arteries enter the nutrient foramen – Epiphysis – mostly small blood vessels that enter small holes, also nutrient arteries – From Periosteum  Bone Cells Osteoclasts are These cell types are related: destroyers of Progenitor cells create osteoblasts bone Osteoblasts mature into osteocytes (produce bone) (maintain bone) Figure 6.6  Bone Production Osteoblasts – progenitor cells, deposit/produce new bone Osteocytes – mature cells, maintain bone matrix  Osteoclasts Responsible for bone resorption & remodeling – breakdown bone to release Calcium “Bone destroying cells” Compact Bone Histology – Long vs Flat Bones Figure 6.9 Spongy (Cancellous) Bone Histology Cancellous Bone is Not Random Figure 6.10  Bone Development: 2 Routes Intramembranous Endochondral Ossification: Ossification: Mesenchyme Mesenchyme Fibrous Mesenchyme Hyaline Cartilage Bone Bone = Flat Bones (skull, = Long Bones  Bone Development: 2 Routes Intramembranous ossification centers that produce the roofing bones of the skull Endochondral ossification centers that produce the structure of the long bones The process of intramembranous ossification. Figure 6.11 Intramembranous Ossification Cont. Gross Anatomy: Flat/Short Bones The final stage of intramembranous ossification: compact-spongy-compact Figure 6.4 Ossification Proceeds from Center Outward Fontanelles: Fontanelles: the remains of Fibrous Mesenchyme Later = continued ossification closes the fontanelles and suture lines Endochondral Ossification: Primary See Figure 6.12 Secondary Ossification See Figure 6.12  Primary Bone First bone to appear during development High number of osteocytes and random collagen fibers (woven) Low mineral content Replaced by secondary bone  Secondary Bone Composed of parallel or concentric bony lamellae (rings of matrix) Osteons are the are groups of “rings” that form around the haversian canal – Was called a Haversian System = central canal – Houses vascular and nervous tissues – Haversian canals of adjacent osteons are connected by Volkmann’s canals Interstitial lamellae are found between osteons or Haversian Systems Osteocytes are housed in lacunae with canaliculi connecting neighboring lacunae Figure 06.12a The process of endochondral ossification. Secondary Ossification Figure 6.12  Endochondral Ossification Requires a hyaline cartilage template Cartilage is eroded & replaced by osteoblasts producing osteoid Long bones are produced this way (and elongated) – Fetal hyaline cartilage template develops – Cartilage calcifies & periosteal bone collar forms around diaphysis – Primary ossification center forms in the diaphysis – Secondary ossification center forms in epiphysis – Bone replaces cartilage, except the articular cartilage and epiphyseal plates (hyaline) – Epiphyseal plates ossify & form epiphyseal lines (closures) Figure 06.13 Structure of the epiphyseal plate. Figure 06.14 Growth at the epiphyseal plate.  Epiphyseal (Growth) Plate Hyaline cartilage being replaced with spongy bone Reproducing Chondrocytes Enlarging chondrocytes Calcifying/dying chondrocytes Spongy bone forming over dead cartilage Describe the process of endochondral ossification of a long bone. Primary & Secondary processes Primary Ossification: (shaft - diaphysis) -Hyaline Cartilage forms a “model” of the bone -chondrocytes enlarge, calcify, die…..degenerate -surface perichondrium becomes periosteum: osteoblasts form bone collar of compact bone -blood vessels from periosteum invade, fibroblasts become osteoblasts -osteoblasts build spongy bone over dead cartilage (bone collar continues to thicken on surface) -Later, osteoclasts invade and destroy spongy bone leaving medullary cavity -process begins in center and moves toward the epiphyses Secondary Ossification: (epiphyses) -Around birth, process begins in the epiphyses and follows same steps, produces spongy bone surrounded by compact bone, some cartilage remains as articular cartilage Unnumbered Figure 6.2_page 198 Figure 11-17  Appositional Growth: Osteoblasts working in Periosteum (and Endosteum) Osteoblasts working on either surface can thicken bone, most of the thickening occurs on the periosteum Appositional growth = increase in girth or diameter Figure 6.8  Periosteum & Endosteum External and internal surfaces of bone – covered by layers of bone-forming cells & vascular tissue Periosteum – outer surface of bone (external) – Outer layers consists of dense fibrous connective tissue – layers of collagen bundles and fibroblasts – Inner cellular layer contains mesenchymal stem cells – osteoprogenitor cells Endosteum – innermost layer (internal) – Line bone marrow cavities – Thin layers of CT, containing flattened osteoprogenitor cells and osteoblasts – Covers small spicules of trabeculae of bone  Bone Remodeling: Spongy being replaced with Compact Copyright © 2016 by Mosby, Inc., an affiliate of Elsevier Inc. All rights reserved. 42 Bone Remodeling Figure 11-21 NOTE: Proper remodeling requires stress 43  Bone Deposition vs. Resorption Note: both Osteoblasts and Osteoclasts work on either surface Unnumbered Figure, page 202 © 2019 Pearson Education, Inc.  Bone Remodeling Histology © 2019 Pearson Education, Inc. Mechanical Stress: Stimulates Osteoblasts No stress = no osteoblast activity Mod 6.3)  Hormonal Regulation of Bone Growth What Hormones Influence Bone Growth?  Hormonal Regulation of Bone Growth What Hormones Influence Bone Growth? GH: Growth Hormone TH: Thyroxine Testosterone Estrogen Progesterone Calcitonin Parathyroid Hormone-PTH  Metabolic Role of Bones Calcium is needed in the blood for many activities – Enzymes and proteins – Cell adhesions, cytoskeleton movement, exocytosis, membrane permeability – Muscle contraction, nerve function, etc. Hormone control the blood calcium levels – PTH – parathyroid hormone raises blood calcium levels Releasing form calcified lamellae of cancellous bone (younger) Osteoclast resorption is stimulated to liberate calcium – Calcitonin – Inhibits osteoclast activities Slows resorption, lowering blood calcium levels  Epiphyseal Plate -> Line Transition of hyaline cartilage to bone Puberty – estrogen, testosterone – 13-15 for females – 15-17 for males Epiphyseal plate closes and becomes the epiphyseal line  Hormonal Regulation of Blood Calcium PTH-Please Take it Higher Calcitonin- tone down calcium Figure 6.15  Hormonal Regulation of Blood Calcium PTH Calcitonin -Please Take it Higher -tone down calcium  Vitamins, Etc. for Bone Growth Calcium – intake from food = mineralize bone (inorganic matrix) Vitamin C – required for synthesis of collagen proteins (organic matrix) Vitamin D – to aids in calcium absorption in intestines and prevents loss through kidneys Vitamin K – aids in production of calcium ion- binding glycoproteins Protein – for synthesis of collagen and organic matrix Factors that influence bone remodeling. Figure 06.16. Osteoporosis Figure D.a Age vs Bone Mass Figure 6.23 osteopenia osteoporosis  Osteoporosis Risk Factors vs Causes Age dec activity? dec nutrition? dec GH? Gender lower mass, less testoserone dec estrogen (post-menopause) Race/Genetics Asian/Caucasian, runs in families? Body Mass thinner people = more likely Nutrition Calcium Vit. D. Protein? Soda? Exercise weight bearing vs cardio Drugs Certain drugs dec Ca; others interfere w/ osteoblasts/osteoclasts/estrogen  Other Bone Weakening Disorders Rickets and Osteomalacia (children) (adults) Paget’s Disease = Vit D deficiency = Low Ca+ disorganized bone = weakened bones = deformities Figure 11-26  Bone Fracture Types Incomplete vs Complete Non-displaced vs Displaced Closed vs Open (simple) (compound) Transverse, spiral, longitudinal, greenstick Comminuted, Compression Figure 13-12, p. 279  Bone Fracture Types Colles Fracture: Typical in falling injuries… Complete, Closed Complete, Open Comminuted Epiphyseal Fracture Damage to Epiphyseal Plate may lead to: Disrupted bone Growth Epiphyseal Fracture Damage to Epiphyseal Plate may lead to: Disrupted bone Growth Fracture Repair: 4 Steps Figure 6.21  Fracture Repair: 4 Steps Hematoma (Inflammation)  Fibrocartillage (Fibrosis)  Bony Callus (Regeneration) Figure 06.17 The process of fracture repair.  Remodeling Abnormal Growth Gigantism Figure B (Excess GH, tumor in pituitary gland) vs Pituitary Dwarfism (GH deficiency)  Acromegaly -Excess GH after growth plates have closed -Facial and hand bones continue to grow Achondroplasia Abnormal Growth of Cartilage: A (No) Chondro (Cartilage) Plasia (Growth) Marfan’s Syndrome: excess cartilage growth Genetic Disorder