PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 6 Bones and Skeletal Tissues: Part B

Copyright © 2010 Pearson Education, Inc. Moving on to chapter 11 after chapter 6 Begin on p. 389 Neurons. Thru p. 414 Stop at Neurotransmitters and their receptors This is online as 11b. We will cover other neurotransmitters and the rest of chapter 11 at a later date, time permitting. The study guide for chapter 5 is now available 6 will follow soon.

Copyright © 2010 Pearson Education, Inc. Bone Development Osteogenesis (ossification) — bone tissue formation Stages Bone formation—begins in the 2nd month of development Postnatal bone growth—until early adulthood Bone remodeling and repair—lifelong

Copyright © 2010 Pearson Education, Inc. Two Types of Ossification 1.Intramembranous ossification Membrane bone develops from fibrous membrane (mesenchyme) Forms flat bones, e.g. clavicles and cranial bones 2.Endochondral ossification Cartilage (endochondral) bone forms by replacing hyaline cartilage Forms most of the rest of the skeleton

Copyright © 2010 Pearson Education, Inc. Figure 6.8, (1 of 4) Mesenchymal cell Collagen fiber Ossification center Osteoid Osteoblast Ossification centers appear in the fibrous connective tissue membrane. Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center. 1

Copyright © 2010 Pearson Education, Inc. Figure 6.8, (2 of 4) Osteoid Osteocyte Newly calcified bone matrix Osteoblast Bone matrix (osteoid) is secreted within the fibrous membrane and calcifies. Osteoblasts begin to secrete osteoid, which is calcified within a few days. Trapped osteoblasts become osteocytes. 2

Copyright © 2010 Pearson Education, Inc. Figure 6.8, (3 of 4) Mesenchyme condensing to form the periosteum Blood vessel Trabeculae of woven bone Woven bone and periosteum form. Accumulating osteoid is laid down between embryonic blood vessels in a random manner. The result is a network (instead of lamellae) of trabeculae called woven bone. Vascularized mesenchyme condenses on the external face of the woven bone and becomes the periosteum. 3

Copyright © 2010 Pearson Education, Inc. Figure 6.8, (4 of 4) Fibrous periosteum Osteoblast Plate of compact bone Diploë (spongy bone) cavities contain red marrow Lamellar bone replaces woven bone, just deep to the periosteum. Red marrow appears. Trabeculae just deep to the periosteum thicken, and are later replaced with mature lamellar bone, forming compact bone plates. Spongy bone (diploë), consisting of distinct trabeculae, per- sists internally and its vascular tissue becomes red marrow. 4

Copyright © 2010 Pearson Education, Inc. Endochondral Ossification Uses hyaline cartilage models Requires breakdown of hyaline cartilage prior to ossification

Copyright © 2010 Pearson Education, Inc. Figure 6.9 Bone collar forms around hyaline cartilage model. Cartilage in the center of the diaphysis calcifies and then develops cavities. The periosteal bud inavades the internal cavities and spongy bone begins to form. The diaphysis elongates and a medullary cavity forms as ossification continues. Secondary ossification centers appear in the epiphyses in preparation for stage 5. The epiphyses ossify. When completed, hyaline cartilage remains only in the epiphyseal plates and articular cartilages. Hyaline cartilage Area of deteriorating cartilage matrix Epiphyseal blood vessel Spongy bone formation Epiphyseal plate cartilage Secondary ossification center Blood vessel of periosteal bud Medullary cavity Articular cartilage Childhood to adolescence Birth Week 9 Month 3 Spongy bone Bone collar Primary ossification center 12345

Copyright © 2010 Pearson Education, Inc. Postnatal Bone Growth Interstitial growth:  length of long bones Appositional growth:  thickness and remodeling of all bones by osteoblasts and osteoclasts on bone surfaces

Copyright © 2010 Pearson Education, Inc. Growth in Length of Long Bones Epiphyseal plate cartilage organizes into four important functional zones: Proliferation (growth) Hypertrophic Calcification Ossification (osteogenic)

Copyright © 2010 Pearson Education, Inc. Figure 6.10 Calcified cartilage spicule Osseous tissue (bone) covering cartilage spicules Resting zone Osteoblast depositing bone matrix Proliferation zone Cartilage cells undergo mitosis. Hypertrophic zone Older cartilage cells enlarge. Ossification zone New bone formation is occurring. Calcification zone Matrix becomes calcified; cartilage cells die; matrix begins deteriorating

Copyright © 2010 Pearson Education, Inc. 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

Copyright © 2010 Pearson Education, Inc. Control of Remodeling What controls continual remodeling of bone? Hormonal mechanisms that maintain calcium homeostasis in the blood Mechanical and gravitational forces

Copyright © 2010 Pearson Education, Inc. Hormonal Control of Blood Ca 2+ Calcium is necessary for Transmission of nerve impulses Muscle contraction Blood coagulation Secretion by glands and nerve cells Cell division

Copyright © 2010 Pearson Education, Inc. Hormonal Control of Blood Ca 2+ Primarily controlled by parathyroid hormone (PTH)  Blood Ca 2+ levels  Parathyroid glands release PTH  PTH stimulates osteoclasts to resorb bone matrix and release Ca 2+   Blood Ca 2+ levels

Copyright © 2010 Pearson Education, Inc. Figure 6.12 Osteoclasts degrade bone matrix and release Ca 2+ into blood. Parathyroid glands Thyroid gland Parathyroid glands release parathyroid hormone (PTH). Stimulus Falling blood Ca 2+ levels PTH Calcium homeostasis of blood: 9–11 mg/100 ml BALANCE

Copyright © 2010 Pearson Education, Inc. Hormonal Control of Blood Ca 2+ May be affected to a lesser extent by calcitonin  Blood Ca 2+ levels  Parafollicular cells of thyroid release calcitonin  Osteoblasts deposit calcium salts   Blood Ca 2+ levels Leptin has also been shown to influence bone density by inhibiting osteoblasts

Copyright © 2010 Pearson Education, Inc. Response to Mechanical Stress Wolff’s law: A bone grows or remodels in response to forces or demands placed upon it Observations supporting Wolff’s law: Handedness (right or left handed) results in bone of one upper limb being thicker and stronger Curved bones are thickest where they are most likely to buckle Trabeculae form along lines of stress Large, bony projections occur where heavy, active muscles attach

Copyright © 2010 Pearson Education, Inc. Figure 6.13 Load here (body weight) Head of femur Compression here Point of no stress Tension here

Copyright © 2010 Pearson Education, Inc. Stages in the Healing of a Bone Fracture 1.Hematoma forms Torn blood vessels hemorrhage Clot (hematoma) forms Site becomes swollen, painful, and inflamed

Copyright © 2010 Pearson Education, Inc. Figure 6.15, step 1 A hematoma forms. 1 Hematoma

Copyright © 2010 Pearson Education, Inc. Stages in the Healing of a Bone Fracture 2.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

Copyright © 2010 Pearson Education, Inc. Figure 6.15, step 2 Fibrocartilaginous callus forms. 2 External callus New blood vessels Spongy bone trabecula Internal callus (fibrous tissue and cartilage)

Copyright © 2010 Pearson Education, Inc. Stages in the Healing of a Bone Fracture 3.Bony callus formation New trabeculae form a bony (hard) callus Bony callus formation continues until firm union is formed in ~2 months

Copyright © 2010 Pearson Education, Inc. Figure 6.15, step 3 Bony callus forms. 3 Bony callus of spongy bone

Copyright © 2010 Pearson Education, Inc. Stages in the Healing of a Bone Fracture 4.Bone remodeling In response to mechanical stressors over several months Final structure resembles original

Copyright © 2010 Pearson Education, Inc. Figure 6.15, step 4 Bone remodeling occurs. 4 Healed fracture

Copyright © 2010 Pearson Education, Inc. 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

Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Osteoporosis Loss of bone mass—bone 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

Copyright © 2010 Pearson Education, Inc. Figure 6.16

Copyright © 2010 Pearson Education, Inc. 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 increase bone mineral density: Fosamax (alendronate): decreases osteoclast activity number SERMs (selective estrogen receptor modulators): mimics estrogen beneficial bone sparing properties without affecting the uterus or breasts Statins: cholesterol lowering meds that have an unexpected benefit of increasing bone density

Copyright © 2010 Pearson Education, Inc. Developmental Aspects of Bones Nearly all bones completely ossified by age 25 Bone mass decreases with age beginning in 4th decade Rate of loss determined by genetics and environmental factors In old age, bone resorption predominates