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C H A P T E R 6 Bonesand Skeletal Tissues: Part B Bones and Skeletal Tissues: Part B.

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Presentation on theme: "C H A P T E R 6 Bonesand Skeletal Tissues: Part B Bones and Skeletal Tissues: Part B."— Presentation transcript:

1 C H A P T E R 6 Bonesand Skeletal Tissues: Part B Bones and Skeletal Tissues: Part B

2 Bone Development Osteogenesis (ossification)  bone tissue formation 3 Stages Bone formation  begins in the 2nd month of development Postnatal bone growth  until early adulthood Bone remodeling and repair  lifelong

3 Two Types of Ossification 1.Intramembranous ossification At about 8 weeks of development, ossification begins on fibrous connective tissue. Forms clavicles and cranial bones (What bone shape are these?) 2.Endochondral ossification Beginning the 2 nd month of development, this process uses hyaline cartilage “bones” formed earlier as models for bone construction. Forms most of the rest of the skeleton below skull except clavicles

4 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 Intramembranous ossification

5 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

6 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

7 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

8 Endochondral Ossification Uses hyaline cartilage models Requires breakdown of hyaline cartilage prior to ossification

9 Figure 6.9, step 1 Bone collar forms around hyaline cartilage model. 1 Hyaline cartilage Week 9 Bone collar Primary ossification center

10 Figure 6.9, step 2 Cartilage in the center of the diaphysis calcifies and then develops cavities. 2 Area of deteriorating cartilage matrix

11 Figure 6.9, step 3 The periosteal bud inavades the internal cavities and spongy bone begins to form. 3 Spongy bone formation Blood vessel of periosteal bud Month 3

12 Figure 6.9, step 4 The diaphysis elongates and a medullary cavity forms as ossification continues. Secondary ossification centers appear in the epiphyses in preparation for stage 5. 4 Epiphyseal blood vessel Secondary ossification center Medullary cavity Birth

13 Figure 6.9, step 5 The epiphyses ossify. When completed, hyaline cartilage remains only in the epiphyseal plates and articular cartilages. 5 Epiphyseal plate cartilage Articular cartilage Childhood to adolescence Spongy bone

14 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

15 Postnatal Bone Growth Infancy  Adolescence bones grow by: Interstitial growth:  length of long bones Appositional growth:  thickness and remodeling of all bones by osteoblasts and osteoclasts on bone surfaces

16 Growth in Length of Long Bones Epiphyseal plate cartilage organizes into four important functional zones: Proliferation (growth) Hypertrophic Calcification Ossification (osteogenic)

17 Figure 6.10 Calcified cartilage spicule Osseous tissue (bone) covering cartilage spicules Resting zone Osteoblast depositing bone matrix Proliferation zone Cartilage cells undergo rapid Mitosis and push the epiphysis away from the diaphysis causing the bone to lengthen. Hypertrophic zone Older cartilage cells enlarge. Ossification zone New bone formation is occurring. Calcification zone Matrix becomes calcified; cartilage cells die; matrix begins deteriorating

18 Growth in Width (Thickness) Growing bones widen as they lengthen Bone thickening occurs through appositional growth Osteoblasts beneath the periosteum secrete bone matrix on the external surface of the bone Meanwhile, osteoclasts remove bone on the endosteal surface of the diaphysis to prevent the bone from becoming too heavy

19 Bones don’t begin as bones. What do they begin as? Answer: Cartilage Check Point!!!

20 What membrane lines the internal canals and covers the trabeculae of a bone? Answer: Endosteum Check Point!!!

21 Which component of bone – organic or inorganic – makes it hard? Answer: Inorganic Check Point!!!

22 What name is given to a cell that acts to break down bone matrix? Answer: Osteoclasts Check Point!!!

23 What name is given to a cell that acts to build up bone (secretes bone matrix)? Answer: Osteoblasts Check Point!!!

24 Hormonal Regulation of Bone Growth Growth hormone (pituitary gland) stimulates epiphyseal plate activity Thyroid hormone modulates activity of growth hormones ensures that the skeleton has proper proportions as it grows Excesses or deficits can cause abnormal skeletal growth such as gigantism or dwarfism Testosterone and estrogens (at puberty) Promote adolescent growth spurts End growth by inducing epiphyseal plate closure  ending longitudinal bone growth

25 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 Bone Remodeling & Repair

26 Bone Deposit Sites of new matrix deposits by osteoblasts are apparent due to the presence of the Osteoid seam Unmineralized band of gauzy looking bone matrix Calcification front The abrupt transition zone between the osteoid seam and the older mineralized bone

27 Bone Resorption Osteoclasts move along a bone surface, digging grooves as they break down bone matrix Osteoclasts secrete Lysosomal enzymes (digest organic matrix) Acids (convert calcium salts into soluble forms) Dissolved matrix enters interstitial fluid and then blood

28 Control of Remodeling What controls continual remodeling of bone? Hormonal mechanisms that maintain calcium homeostasis in the blood  Primarily involve parathyroid hormone (PTH) Mechanical and gravitational forces acting on the skeleton

29 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 Human body contains g of calcium more than 99% present in bone minerals

30 Hormonal Control of Blood Calcium Parathyroid Hormone (PTH) is released when blood levels of Calcium decline Increased levels of PTH trigger osteoclasts to resorb bone which releases calcium into the blood As blood concentrations of Calcium rise, the stimulus for PTH stops Remember homeostasis? What feedback mechanism is this?

31 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

32 Classification of Bone Fractures Bone fractures may be classified by four “either/or” classifications: 1.Position of bone ends after fracture: Nondisplaced—ends retain normal position Displaced—ends out of normal alignment 2.Completeness of the break Complete—broken all the way through Incomplete—not broken all the way through

33 Classification of Bone Fractures 3.Orientation of the break to the long axis of the bone: Linear—parallel to long axis of the bone Transverse—perpendicular to long axis of the bone 4.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

34 Common Types of Fractures All fractures can be described in terms of Location External appearance Nature of the break

35 Table 6.2

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38 Stages in the Healing of a Bone Fracture 1.Hematoma forms Torn blood vessels hemorrhage Clot (hematoma) forms Site becomes swollen, painful, and inflamed

39 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

40 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 (how long do you wear a cast for?)

41 Stages in the Healing of a Bone Fracture 4.Bone remodeling In response to mechanical stressors over several months Final structure resembles original

42 Figure 6.15

43 Homeostatic Imbalances Osteomalacia and rickets Osteomalacia includes a number of disorders where bones are inadequately mineralized Osteoid is produced but calcium salts are not deposited  bones soften and weaken Rickets (childhood disease) causes bowed legs and other bone deformities Because the ephyseal plates cannot be calcified, they continue to widen and the ends of long bones become enlarged and abnormally long Cause: vitamin D deficiency or insufficient dietary calcium

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45 Homeostatic Imbalances Osteoporosis Loss of bone mass—bone resorption outpaces deposit Bones become so fragile that something like a sneeze or stepping off a curb can cause them to break Spongy bone of spine and neck of femur become most susceptible to fracture Risk factors Lack of estrogen (smoking reduces estrogen levels), calcium or vitamin D; petite body form; immobility; low levels of TSH (thyroid); diabetes mellitus

46 Figure 6.16

47 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

48 Paget’s 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

49 Developmental Aspects of Bones Embryonic skeleton ossifies predictably so fetal age easily determined from X rays or sonograms At birth, most long bones are well ossified (except epiphyses)

50 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

51 Let’s Practice!!!

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