Bone Development. Two Types of OssificaDon 10/18/14. Osteogenesis ( ) bone Dssue formadon Stages. Bones and Skeletal Tissues: Part B

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1 Bone Development 6 Bones and Skeletal Tissues: Part B Osteogenesis ( ) bone Dssue formadon Stages Bone formadon begins in the 2nd month of development Postnatal bone growth undl early adulthood Bone remodeling and repair Two Types of OssificaDon 1. ossificadon Membrane bone develops from fibrous membrane Forms flat bones, e.g. clavicles and cranial bones 2. ossificadon CarDlage (endochondral) bone forms by replacing hyaline cardlage Forms most of the rest of the skeleton Mesenchymal cell Collagen fiber Ossification center Osteoid Osteoblast 1 Ossification centers appear in the fibrous connective tissue membrane. Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center. Figure 6.8, (1 of 4) 1

2 Osteoblast Osteoid Osteocyte Newly calcified bone matrix 2 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. Figure 6.8, (2 of 4) Mesenchyme condensing to form the periosteum Trabeculae of woven 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) Fibrous periosteum Osteoblast Plate of compact bone Diploë (spongy bone) cavities contain red marrow Endochondral OssificaDon Uses cardlage models Requires breakdown of hyaline cardlage prior to ossificadon 4 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, persists internally and its vascular tissue becomes red marrow. Figure 6.8, (4 of 4) 2

3 Week 9 Month 3 Hyaline cartilage Bone collar Primary ossification center Area of deteriorating cartilage matrix Spongy bone formation Blood vessel of periosteal bud Epiphyseal blood vessel Birth Secondary ossification center Medullary cavity Articular cartilage Spongy bone Epiphyseal plate cartilage Childhood to adolescence Postnatal Bone Growth growth: length of long bones growth: thickness and remodeling of all bones by osteoblasts and osteoclasts on bone surfaces 1 Bone collar forms around hyaline cartilage model. 2 Cartilage in the 3 The periosteal 4 The diaphysis elongates 5 The epiphyses center of the diaphysis calcifies and then develops cavities. bud inavades the internal cavities and spongy bone begins to form. and a medullary cavity forms as ossification continues. Secondary ossification centers appear in the epiphyses in preparation for stage 5. ossify. When completed, hyaline cartilage remains only in the epiphyseal plates and articular cartilages. Figure 6.9 Growth in Length of Long Bones Epiphyseal plate cardlage organizes into four important : ProliferaDon (growth) Hypertrophic CalcificaDon OssificaDon (osteogenic) Calcified cartilage spicule Osteoblast depositing bone matrix Osseous tissue (bone) covering cartilage spicules Resting zone 1 Proliferation zone Cartilage cells undergo mitosis. 2 Hypertrophic zone Older cartilage cells enlarge. 3 Calcification zone Matrix becomes calcified; cartilage cells die; matrix begins deteriorating. 4 Ossification zone New bone formation is occurring. Figure

4 Hormonal RegulaDon of Bone Growth Bone growth Bone remodeling Growth hormone sdmulates acdvity Thyroid hormone modulates acdvity of growth hormone Testosterone and estrogens (at ) Promote adolescent growth spurts End growth by inducing epiphyseal plate closure Cartilage grows here. Cartilage is replaced by bone here. Cartilage grows here. Cartilage is replaced by bone here. Articular cartilage Epiphyseal plate Bone is resorbed here. Bone is added by appositional growth here. Bone is resorbed here. Figure 6.11 Bone Deposit Occurs where bone is or added strength is needed Requires a diet rich in protein; vitamins C, D, and A; calcium; phosphorus; magnesium; and manganese Bone Deposit Sites of new matrix deposit are revealed by the Unmineralized band of matrix The abrupt transidon zone between the osteoid seam and the older mineralized bone 4

5 Bone ResorpDon secrete Lysosomal enzymes (digest organic matrix) Acids (convert calcium salts into soluble forms) Dissolved matrix is transcytosed across osteoclast, enters intersddal fluid and then Control of Remodeling What controls condnual of bone? Hormonal mechanisms that maintain calcium homeostasis in the blood Mechanical and forces Hormonal Control of Blood Ca 2+ is necessary for Transmission of nerve impulses contracdon coaguladon SecreDon by glands and Cell division Hormonal Control of Blood Ca 2+ Primarily controlled by parathyroid hormone (PTH) Blood Ca 2+ levels Parathyroid glands release PTH PTH sdmulates osteoclasts to degrade bone matrix and release Ca 2+ Blood Ca 2+ levels 5

6 Hormonal Control of Blood Ca 2+ Calcium homeostasis of blood: 9 11 mg/100 ml BALANCE BALANCE Stimulus Falling blood Ca 2+ levels Osteoclasts degrade bone matrix and release Ca 2+ into blood. Thyroid gland Parathyroid glands PTH Parathyroid glands release parathyroid hormone (PTH). Figure 6.12 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 LepDn has also been shown to influence bone density by inhibidng Response to Mechanical Stress Load here (body weight) : A bone grows or remodels in response to forces or demands placed upon it ObservaDons suppordng Wolff s law: (right or lec 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 Large, bony projecdons occur where heavy, acdve aeach Tension here Point of no stress Head of femur Compression here Figure

7 ClassificaDon of Bone Fractures Bone may be classified by four either/or classificadons: 1. PosiDon of bone ends acer fracture: Nondisplaced ends retain normal posidon Displaced ends out of normal alignment 2. Completeness of the break broken all the way through not broken all the way through ClassificaDon of Bone Fractures 3. 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 the skin: (open) bone ends penetrate the skin (closed) bone ends do not penetrate the skin Common Types of Fractures All fractures can be described in terms of Table 6.2 7

8 Table 6.2 Table 6.2 Stages in the Healing of a Bone Fracture 1. forms Torn blood vessels hemorrhage Clot (hematoma) forms Site becomes swollen, painful, and Hematoma 1 A hematoma forms. Figure 6.15, step 1 8

9 Stages in the Healing of a Bone Fracture 2. callus forms PhagocyDc cells clear debris Osteoblasts begin forming spongy bone within 1 week Fibroblasts secrete to connect bone ends Mass of repair Dssue now called fibrocardlaginous callus Internal callus (fibrous tissue and cartilage) 2 Fibrocartilaginous callus forms. External callus New blood vessels Spongy bone trabecula Figure 6.15, step 2 Stages in the Healing of a Bone Fracture 3. formadon New trabeculae form a bony (hard) callus Bony callus formadon condnues undl firm union is formed in ~2 months Bony callus of spongy bone 3 Bony callus forms. Figure 6.15, step 3 9

10 Stages in the Healing of a Bone Fracture 4. Bone In response to mechanical stressors over several months Final structure resembles Healed fracture 4 Bone remodeling occurs. Figure 6.15, step 4 HomeostaDc Imbalances Hematoma Internal callus (fibrous tissue and cartilage) External callus New blood vessels Spongy bone trabecula Bony callus of spongy bone Healed fracture 1 A hematoma forms. 2 Fibrocartilaginous 3 Bony callus forms. 4 Bone callus forms. remodeling occurs. and rickets Calcium salts not deposited Rickets (childhood disease) causes bowed legs and other bone deformides Cause: deficiency or insufficient dietary calcium Figure

11 HomeostaDc Imbalances Loss of bone mass bone resorpdon outpaces deposit Spongy bone of spine and neck of femur become most suscepdble to fracture Lack of estrogen, calcium or vitamin D; pedte body form; immobility; low levels of TSH; diabetes mellitus Figure 6.16 Osteoporosis: Treatment and PrevenDon Calcium, vitamin D, and fluoride supplements Weight- bearing exercise throughout life Hormone ( ) replacement therapy (HRT) slows bone loss Some (Fosamax, SERMs, stadns) increase bone mineral density Paget s Disease Excessive and haphazard bone formadon and breakdown, usually in spine, pelvis, femur, or skull PageDc bone has very high rado of to bone and reduced mineralizadon Unknown cause (possibly ) includes calcitonin and biphosphonates 11

12 Developmental Aspects of Bones skeleton ossifies predictably so fetal age easily determined from X rays or sonograms At birth, most are well ossified (except ) Parietal bone Occipital bone Mandible Clavicle Scapula Ribs Vertebra Ilium Frontal bone of skull Radius Ulna Humerus Femur Tibia Figure 6.17 Developmental Aspects of Bones Nearly all bones completely by age 25 Bone mass decreases with age beginning in 4th decade Rate of loss determined by and environmental factors In old age, bone predominates 12