Bones and Skeletal Tissues Skeletal Cartilages Contain no blood vessels or nerves Dense connective tissue girdle of perichondrium

contains blood vessels for nutrient delivery to cartilage Skeletal Cartilages Hyaline cartilages Provide support, flexibility, and resilience Most abundant type Elastic cartilages Similar to hyaline cartilages, but contain elastic fibers Fibrocartilages Collagen fibershave great tensile strength Growth of Cartilage Appositional Cells secrete matrix against the external face of existing cartilage Interstitial Chondrocytes divide and secrete new matrix, expanding cartilage from within Calcification of cartilage occurs during Normal bone growth Old age Bones of the Skeleton Two main groups, by location Axial skeleton (brown) Appendicular skeleton (yellow) Classification of Bones by Shape Long bones Longer than they are wide Short bones Cube-shaped bones (in wrist and ankle) Sesamoid bones (within tendons, e.g., patella) Flat bones Thin, flat, slightly curved Irregular bones Complicated shapes

Functions of Bones Support For the body and soft organs

Protection For brain, spinal cord, and vital organs Movement Levers for muscle action Storage Minerals (calcium and phosphorus) and growth factors Blood cell formation (hematopoiesis) in marrow cavities Triglyceride (energy) storage in bone cavities Bone Textures Compact bone Dense outer layer Spongy (cancellous) bone Honeycomb of trabeculae Structure of a Long Bone Diaphysis (shaft) Compact bone collar surrounds medullary (marrow) cavity Medullary cavity in adults contains fat (yellow marrow) Epiphyses Expanded ends Spongy bone interior Epiphyseal line (remnant of growth plate) Articular (hyaline) cartilage on joint surfaces Membranes of Bone Periosteum Outer fibrous layer Inner osteogenic layer Osteoblasts (bone-forming cells) Osteoclasts (bone-destroying cells) Osteogenic cells (stem cells) Nerve fibers, nutrient blood vessels, and lymphatic vessels enter the bone via nutrient foramina Secured to underlying bone by Sharpeys fibers Endosteum Delicate membrane on internal surfaces of bone Also contains osteoblasts and osteoclasts

Structure of Short, Irregular, and Flat Bones Periosteum-covered compact bone on the outside Endosteum-covered spongy bone within Spongy bone called diplo in flat bones Bone marrow between the trabeculae

Location of Hematopoietic Tissue (Red Marrow) Red marrow cavities of adults Trabecular cavities of the heads of the femur and humerus Trabecular cavities of the diplo of flat bones Red marrow of newborn infants Medullary cavities and all spaces in spongy bone Microscopic Anatomy of Bone Cells of bones Osteogenic (osteoprogenitor) cells Stem cells in periosteum and endosteum that give rise to osteoblasts Osteoblasts Bone-forming cells Cells of bone Osteocytes Mature bone cells Osteoclasts Cells that break down (resorb) bone matrix Microscopic Anatomy of Bone: Compact Bone Haversian system, or osteonstructural unit Lamellae Weight-bearing Column-like matrix tubes Central (Haversian) canal Contains blood vessels and nerves Perforating (Volkmanns) canals At right angles to the central canal Connects blood vessels and nerves of the periosteum and central canal Lacunaesmall cavities that contain osteocytes Canaliculihairlike canals that connect lacunae to each other and the central canal

Microscopic Anatomy of Bone: Spongy Bone Trabeculae Align along lines of stress No osteons Contain irregularly arranged lamellae, osteocytes, and canaliculi Capillaries in endosteum supply nutrients Chemical Composition of Bone: Organic Osteogenic cells, osteoblasts, osteocytes, osteoclasts Osteoidorganic bone matrix secreted by osteoblasts Ground substance (proteoglycans, glycoproteins)

Collagen fibers Provide tensile strength and flexibility Chemical Composition of Bone: Inorganic Hydroxyapatites (mineral salts) 65% of bone by mass Mainly calcium phosphate crystals Responsible for hardness and resistance to compression Bone Development Osteogenesis (ossification)bone tissue formation Stages Bone formationbegins in the 2nd month of development Postnatal bone growthuntil early adulthood Bone remodeling and repairlifelong Two Types of Ossification Intramembranous ossification Membrane bone develops from fibrous membrane Forms flat bones, e.g. clavicles and cranial bones Endochondral ossification Cartilage (endochondral) bone forms by replacing hyaline cartilage Forms most of the rest of the skeleton Endochondral Ossification Uses hyaline cartilage models Requires breakdown of hyaline cartilage prior to ossification

Postnatal Bone Growth Interstitial growth: length of long bones Appositional growth: thickness and remodeling of all bones by osteoblasts and osteoclasts on bone surfaces Growth in Length of Long Bones Epiphyseal plate cartilage organizes into four important functional zones: Proliferation (growth) Hypertrophic Calcification Ossification (osteogenic) Hormonal Regulation of Bone Growth

Growth hormone stimulates epiphyseal plate activity Thyroid hormone modulates activity of growth hormone Testosterone and estrogens (at puberty) Promote adolescent growth spurts End growth by inducing epiphyseal plate closure Bone Deposit Occurs where bone is injured or added strength is needed Requires a diet rich in protein; vitamins C, D, and A; calcium; phosphorus; magnesium; and manganese Sites of new matrix deposit are revealed by the Osteoid seam Unmineralized band of matrix Calcification front The abrupt transition zone between the osteoid seam and the older mineralized bone Bone Resorption Osteoclasts secrete Lysosomal enzymes (digest organic matrix) Acids (convert calcium salts into soluble forms) Dissolved matrix is transcytosed across osteoclast, enters interstitial fluid and then blood

Control of Remodeling What controls continual remodeling of bone? Hormonal mechanisms that maintain calcium homeostasis in the blood Mechanical and gravitational forces

Hormonal Control of Blood Ca2+ Calcium is necessary for Transmission of nerve impulses Muscle contraction Blood coagulation Secretion by glands and nerve cells Cell division Hormonal Control of Blood Ca2+ Primarily controlled by parathyroid hormone (PTH) Blood Ca2+ levels Parathyroid glands release PTH

 PTH stimulates osteoclasts to degrade bone matrix and release Ca2+ Blood Ca2+ levels Hormonal Control of Blood Ca2+ May be affected to a lesser extent by calcitonin Blood Ca2+ levels Parafollicular cells of thyroid release calcitonin Osteoblasts deposit calcium salts Blood Ca2+ levels Leptin has also been shown to influence bone density by inhibiting osteoblasts

Classification of Bone Fractures Bone fractures may be classified by four either/or classifications: Position of bone ends after fracture: Nondisplacedends retain normal position Displacedends out of normal alignment Completeness of the break Completebroken all the way through Incompletenot broken all the way through Orientation of the break to the long axis of the bone: Linearparallel to long axis of the bone Transverseperpendicular to long axis of the bone Whether or not the bone ends penetrate the skin: Compound (open)bone ends penetrate the skin Simple (closed)bone ends do not penetrate the skin Stages in the Healing of a Bone Fracture Hematoma forms Torn blood vessels hemorrhage Clot (hematoma) forms Site becomes swollen, painful, and inflamed Fibrocartilaginous callus forms

Phagocytic cells clear debris Osteoblasts begin forming spongy bone within 1 week Fibroblasts secrete collagen fibers to connect bone ends Mass of repair tissue now called fibrocartilaginous callus Bony callus formation New trabeculae form a bony (hard) callus Bony callus formation continues until firm union is formed in ~2 months Bone remodeling In response to mechanical stressors over several months Final structure resembles original Homeostatic Imbalances Osteomalacia and rickets Calcium salts not deposited Rickets (childhood disease) causes bowed legs and other bone deformities Cause: vitamin D deficiency or insufficient dietary calcium Osteoporosis Loss of bone massbone resorption outpaces deposit Spongy bone of spine and neck of femur become most susceptible to fracture Risk factors Lack of estrogen, calcium or vitamin D; petite body form; immobility; low levels of TSH; diabetes mellitus Osteoporosis: Treatment and Prevention Calcium, vitamin D, and fluoride supplements Weight-bearing exercise throughout life Hormone (estrogen) replacement therapy (HRT) slows bone loss Some drugs (Fosamax, SERMs, statins) increase bone mineral density

Pagets Disease Excessive and haphazard bone formation and breakdown, usually in spine, pelvis, femur, or skull Pagetic bone has very high ratio of spongy to compact bone and reduced mineralization Unknown cause (possibly viral) Treatment includes calcitonin and biphosphonates