Bones and Skeletal Tissues: Part B

1. Bonesand 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 • Intramembranous ossification • At about 8 weeks of development, ossification begins on fibrous connective tissue. • Forms clavicles and cranial bones (What bone shape are these?) • Endochondral ossification • Beginning the 2nd 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. Intramembranous ossification Mesenchymalcell Collagenfiber Ossificationcenter Osteoid Osteoblast 1 Ossification centers appear in the fibrousconnective tissue membrane. • Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center. Figure 6.8, (1 of 4)

5. Osteoblast Osteoid Osteocyte Newly calcifiedbone matrix 2 Bone matrix (osteoid) is secreted within thefibrous membrane and calcifies.• Osteoblasts begin to secrete osteoid, which is calcified within a few days. • Trapped osteoblasts become osteocytes. Figure 6.8, (2 of 4)

6. Mesenchymecondensingto form theperiosteum Trabeculae ofwoven bone Blood vessel 3 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. Figure 6.8, (3 of 4)

7. Fibrousperiosteum Osteoblast Plate ofcompact bone Diploë (spongybone) cavitiescontain redmarrow 4 Lamellar bone replaces woven bone, just deep tothe 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. Figure 6.8, (4 of 4)

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

9. Week 9 Hyaline cartilage Bone collar Primaryossificationcenter 1 Bone collar forms aroundhyaline cartilage model. Figure 6.9, step 1

10. Area of deterioratingcartilage matrix 2 Cartilage in the centerof the diaphysis calcifiesand then develops cavities. Figure 6.9, step 2

11. Month 3 Spongyboneformation Bloodvessel ofperiostealbud 3 The periosteal bud inavadesthe internal cavities andspongy bone begins to form. Figure 6.9, step 3

12. Birth Epiphysealblood vessel Secondaryossificationcenter Medullarycavity 4 The diaphysis elongates and a medullary cavity formsas ossification continues. Secondary ossification centersappear in the epiphyses in preparation for stage 5. Figure 6.9, step 4

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

14. Month 3 Birth Childhood toadolescence Week 9 Articularcartilage Secondaryossificationcenter Spongybone Epiphysealblood vessel Area ofdeterioratingcartilage matrix Epiphysealplatecartilage Hyalinecartilage Medullarycavity Spongyboneformation Bonecollar Bloodvessel ofperiostealbud Primaryossificationcenter 1 2 3 4 5 Bone collarforms aroundhyaline cartilagemodel. Cartilage in thecenter of thediaphysis calcifiesand then developscavities. The periostealbud inavades theinternal cavitiesand spongy bonebegins to form. The diaphysis elongatesand a medullary cavityforms as ossificationcontinues. Secondaryossification centers appearin the epiphyses inpreparation for stage 5. The epiphysesossify. Whencompleted, hyalinecartilage remains onlyin the epiphysealplates and articularcartilages. Figure 6.9

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. Resting zone Proliferation zone Cartilage cells undergo rapid Mitosis and push the epiphysis away from the diaphysis causing the bone to lengthen. 1 Hypertrophic zone Older cartilage cells enlarge. 2 Calcification zone Matrix becomes calcified; cartilage cells die; matrix begins deteriorating. 3 Calcified cartilage spicule Osteoblast depositing bone matrix Ossification zone New bone formation is occurring. 4 Osseous tissue (bone) covering cartilage spicules Figure 6.10

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

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

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

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

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

24. Bellringer!!! • What are the 3 stages of bone development? • What bones are created through intramembranous ossification? • What are the 4 important functional zones of the epiphyseal plates? • What does endochondral ossification develope from?

25. 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

26. Bone Deposit Bone Remodeling & Repair • 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

27. 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

28. 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

29. 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

30. 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 • Human body contains 1200-1400g of calcium more than 99% present in bone minerals

31. 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?

32. 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

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

34. Classification of Bone Fractures • 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 • 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

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

36. Table 6.2

37. Table 6.2

38. Table 6.2

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

40. Stages in the Healing of a Bone Fracture • Fibrocartilaginouscallus forms • Phagocytic cells clear debris • Osteoblasts begin forming spongy bone within 1 week • Fibroblastssecrete collagen fibers to connect bone ends • Mass of repair tissue now called fibrocartilaginous callus

41. Stages in the Healing of a Bone Fracture • 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?)

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

43. Figure 6.15

44. 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

46. 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

47. Figure 6.16

48. 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

49. 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

50. 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)