1 Skeletal Organization Typically there are about 206 bones in the human skeleton For convenience the skeleton is divided into the: Axial skeleton Appendicular skeleton

2 Divisions of the Skeleton Axial Skeleton Skull Spinal column Ribs Sternum Hyoid bone 80 bones Hyoid Cranium Face Clavicle Scapula Sternum Ribs Humerus Ulna Hip bone Radius Femur Patella Tibia Fibula Tarsals Metatarsals Phalanges Skull Vertebral column Sacrum Coccyx Carpals Metacarpals (a)(b) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

3 Divisions of the Skeleton Appendicular Skeleton Upper limbs Lower limbs Shoulder girdle Pelvic girdle 126 bones Hyoid Cranium Face Clavicle Scapula Sternum Ribs Humerus Ulna Hip bone Radius Femur Patella Tibia Fibula Tarsals Metatarsals Phalanges Skull Vertebral column Sacrum Coccyx Carpals Metacarpals (a)(b) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Before week 8, the human embryonic skeleton is made of fibrous membranes and hyaline cartilage. After week 8, bone tissue begins to replace the fibrous membranes and hyaline cartilage. – The development of bone from a fibrous membrane is called intramembranous ossification. Why? – The replacement of hyaline cartilage with bone is known as endochondral ossification. Why? 7.3: Bone Development and Growth

5 Intramembranous Bones Intramembranous Ossification These bones originate within sheet-like layers of connective tissues (mesenchyme) They are the broad, flat bones Ex: Skull bones (except mandible), the facial bones, the clavicles, the pelvis and the scapulae

6 Endochondral Bones Endochondral Ossification Begins in the second month of development Requires breakdown of hyaline cartilage prior to ossification Bones begin as hyaline cartilage Form models for future bones These are most bones of the skeleton

7 Endochondral Ossification Hyaline cartilage model Primary ossification center Secondary ossification centers Epiphyseal plate Osteoblasts vs. osteoclasts (b)(c)(d)(e)(f)(a) Cartilaginous model Calcified cartilage Articular cartilage Developing periosteum Compact bone developing Primary ossification center Medullary cavity Medullary cavity Medullary cavity Secondary ossification center Secondary ossification center Blood vessel Epiphyseal plate Remnant of epiphyseal plate Remnants of epiphyseal plates Epiphyseal plates Compact bone Spongy bone Articular cartilage Spongy bone Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

8 Endochondral Ossification

Osteogenesis - 10 week fetus

Osteogenesis - 16 week fetus

Video

Video

Lab Skull Lab Exercise 13

Catalyst

Criteria for SUCCESS!!! I will be able to: 1.Identify and describe the functions of the four layers of cells involved in growth at the epiphyseal plate. 2.List the steps in the process of bone reabsorption. 3.List the steps in the process of bone deposition. 4.List the steps in the process of appositional growth. 5.Identify 3 nutritional needs to maintain bone growth/maintenance. 6.List the effects of 4 hormones on bone growth. 7.Describe the causes and effects of two types of homeostatic imbalance disorders in bone.

19 Growth at the Epiphyseal Plate First layer of cells Closest to the end of epiphysis Resting cells Anchors epiphyseal plate to epiphysis Second layer of cells Many rows of young cells Undergoing mitosis (a)(b) Bone tissue of epiphysis Zone of resting cartilage Zone of proliferating cartilage Zone of hypertrophic cartilage Zone of calcified cartilage Ossified bone of diaphysis Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. b: © The McGraw-Hill Companies, Inc./Al Telser, photographer

20 Growth at the Epiphyseal Plate Third layer of cells Older cells Left behind when new cells appear Cells enlarging and becoming calcified Fourth layer of cells Thin Dead cells Calcified extracellular matrix (a)(b) Bone tissue of epiphysis Zone of resting cartilage Zone of proliferating cartilage Zone of hypertrophic cartilage Zone of calcified cartilage Ossified bone of diaphysis Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. b: © The McGraw-Hill Companies, Inc./Al Telser, photographer

21 Homeostasis of Bone Tissue Bone Resorption – action of osteoclasts via stimulation from parathyroid hormone (PTH) Bone Deposition – action of osteoblasts and via stimulation from calcitonin Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. © Biophoto Associates/Photo Researchers, Inc. Developing medullary cavity Osteoclast

22 Animation: Bone Growth in Width Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at

Check out the mechanism of remodeling on the right! Why might you suspect someone whose been a powerlifter for 15 years to have heavy, massive bones, especially at the point of muscle insertion? Astronauts tend to experience bone atrophy after they’re in space for an extended period of time. Why?

Long Bone Growth and Remodeling Figure 6.10

Normal bone growth/maintenance cannot occur without sufficient dietary intake of calcium and phosphate salts. Calcium and phosphate are not absorbed in the intestine unless the hormone calcitriol is present. Calcitriol synthesis is dependent on the availability of the steroid cholecalciferol (a.k.a. Vitamin D) which may be synthesized in the skin or obtained from the diet. Vitamins C, A, K, and B 12 are all necessary for bone growth as well. Nutritional Effects on Bone

Growth hormone, produced by the pituitary gland, and thyroxine, produced by the thyroid gland, stimulate bone growth.. Hormonal Effects on Bone

At puberty, the rising levels of sex hormones (estrogens in females and androgens in males) cause osteoblasts to produce bone faster than the epiphyseal cartilage can divide. This causes the characteristic growth spurt as well as the ultimate closure of the epiphyseal plate. Estrogens cause faster closure of the epiphyseal growth plate than do androgens. Estrogen also acts to stimulate osteoblast activity. Hormonal Effects on Bone

As a result osteoblasts begin producing bone faster than the rate of epiphyseal cartilage expansion. Thus the bone grows while the epiphyseal plate gets narrower and narrower and ultimately disappears. A remnant (epiphyseal line) is visible on X-rays (do you see them in the adjacent femur, tibia, and fibula?) At puberty, growth in bone length is increased dramatically by the combined activities of growth hormone, thyroid hormone, and the sex hormones.

Calcitonin Released by the C cells of the thyroid gland in response to high blood [Ca 2+ ]. Calcitonin acts to “tone down” blood calcium levels. Calcitonin causes decreased osteoclast activity which results in decreased break down of bone matrix and decreased calcium being released into the blood. Calcitonin also stimulates osteoblast activity which means calcium will be taken from the blood and deposited as bone matrix. Notice the thyroid follicles on the right. The arrow indicates a C cell

30 Factors Affecting Bone Development, Growth and Repair Deficiency of Vitamin A – retards bone development Deficiency of Vitamin C – results in fragile bones Deficiency of Vitamin D – rickets, osteomalacia Insufficient Growth Hormone – dwarfism Excessive Growth Hormone – gigantism, acromegaly Insufficient Thyroid Hormone – delays bone growth Physical Stress – stimulates bone growth

31 Animation: Bone Growth in Width Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at

Homeostatic Imbalances Rickets – Bones of children are inadequately mineralized causing softened, weakened bones – Bowed legs and deformities of the pelvis, skull, and rib cage are common – Caused by insufficient calcium in the diet, or by vitamin D deficiency Homeostatic Imbalances

Osteoporosis – Group of diseases in which bone reabsorption outpaces bone deposit – Spongy bone of the spine is most vulnerable – Occurs most often in postmenopausal women – Bones become so fragile that sneezing or stepping off a curb can cause fractures Homeostatic Imbalances

34 Animation: Osteoporosis Please note that due to differing operating systems, some animations will not appear until the presentation is viewed in Presentation Mode (Slide Show view). You may see blank slides in the “Normal” or “Slide Sorter” views. All animations will appear after viewing in Presentation Mode and playing each animation. Most animations will require the latest version of the Flash Player, which is available at