Anatomy & Physiology

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1 Anatomy & Physiology Unit 6 The Skeletal System Paul Anderson 2011

2 Skeletal System: Components Bones major organs of system, have all functions of system. Cartilages connect & protect bones at joints, form smooth articular surfaces of moveable bones. Ligaments connect bones at joints & stabilise joints. Joints (Articulations): regions where bones meet: form fulcrum of levers. costal (rib) cartilages cranium Clavicle scapula humerus pelvis Moveable fulcrum of lever Meniscus cartilage femur patella Elbow joint ligament Knee joint Patellar ligament Martini & Bartholomew fig 2 1-2b

3 Skeletal System: Major Functions: 1. Support of soft tissues. 2. Body shape. 3. Protection of vital organs (brain by cranium, heart & lungs by rib cage, spinal cord by spine. 4. Allows for adaptive (i.e. homeostatic) movements - forms attachment sites for muscles - has moveable joints - forms levers with muscles: movement occurs when muscles pull on bones 5. Production of blood cells (Hemopoiesis) - in adult red bone marrow forms all red blood cells, platelets & most white blood cells 6. Storage of minerals (Ca/P) in bone matrix & fat (in yellow marrow) - minerals harden bones for their normal functions - Bone deposition & resorption are controlled by hormones (e.g. PTH) - vit D required for absorption of Ca/P Diet Vit D Blood Ca +2 PO 4-3 Bone deposition Bone resorption Ca/P stored as Hydroxyapatite, Ca 5 (PO 4 ) 3 OH in bone matrix 3

4 Muscles, Bones & Joints form Levers Tendon of muscle pulls on bone Joint (allows movement) Bone Movement of bone 4

5 Skeletal System: Tissues Bones are organs consisting of several tissues. Bone (osseous tissue) Cartilage Fibrous connective tissue (in the surface layer or periosteum) Hemopoietic (blood forming) tissue in red marrow) - hemopoietic (myeloid) tissue occurs in vertebrae, sternum, ribs, skull, scapula, pelvis & proximal epiphyses of femur, and humerus Adipose tissue (in yellow marrow) - source of energy: can form red marrow in emergencies.

6 Cartilage vs Bone Tissue in the Skeletal System Cartilage and bone are distributed according to their properties. Cartilage Properties of resiliency & strength. Non calcified matrix -firm but not rigid. Mature cartilage cells chondrocytes. Non vascular so thin & slow to heal. Grows by appositional (surface) & interstitial (internal) growth. Forms most of embryonic skeleton. In adults found mainly at joints and in the upper respiratory tract. Bone Properties of rigidity, hardness & strength. Calcified matrix- hard and rigid. Mature bone cells osteocytes. Vascular (vessels run in canals). Grows by appositional growth only, due to its calcified matrix. In development bone gradually replaces cartilage to form the major tissue of all adult bones. Resiliency is due to the organic matrix ground substance. Strength is due to the organic matrix collagen fibers. Hardness & rigidity are due to calcified inorganic matrix.

7 Two Types of Growth Occur in Skeletal Tissues: Appositional Growth means growth at a skeletal surface. Appositional Growth occurs by cell division of osteogenic (or chondrogenic) cells in the periosteum or endosteum of bone or in the perichondrium of cartilage. Interstitial Growth means internal growth by cell division & production of new matrix internally, expanding the tissue from within. Interstitial growth occurs in cartilage but not in bone since its matrix is calcified (i.e. hardened). Growth in Skeletal Tissues Appositional (surface) Growth Interstitial (internal) Growth At surface of Bone & Cartilage Tissues In Cartilage Tissue only

8 Appositional Growth in Cartilage Perichondrium (surface membrane of cartilage) Fibrous layer: outer protective collagenous layer Cellular layer: inner chondrogenic layer with fibroblasts Collagen fibers fibroblasts form New matrix New chondrocytes Martini, Figure 4-13 new matrix new matrix old matrix Appositional Growth occurs in Bone & Cartilage

9 Interstitial Growth in Cartilage Interstitial growth means internal growth by cell division and production of new matrix internally, thus expanding the tissue from within. Interstitial growth occurs in cartilage but not in bone since its matrix is calcified (i.e. hardened). Non - calcified matrix old matrix Martini, Figure 4-13 Cartilage has a non -calcified matrix so can grow by Interstitial Growth. Bone has a calcified matrix so can only grow by Appositional Growth.

10 Cartilage Tissues in the Skeletal System Two types of cartilage occur in the skeletal system. Hyaline Cartilage Fibrous Cartilage Marieb, 5th ed., Figure 7-1

11 Types of Cartilage : Hyaline Cartilage There are three types of cartilage. Only fibrous and hyaline cartilage occur in the skeletal system. articular cartilage Martini & Bartholomew, Figure 4-10(a) Hyaline Cartilage Matrix appears smooth but has many thin collagen fibers. Provides firmness, resiliency, strength and a smooth surface for joints. Found in articular surfaces of bones, embryonic skeleton, costal cartilages, upper respiratory tract. (surface membrane) 11

12 Fibrous Cartilage - Matrix has many thick parallel collagen fibers - Provides extreme strength - Fibrous cartilage is found in skeletal system pubic symphyses intervertebral disks menisci cartilages in knee joint Martini & Bartholomew, Figure 4-10(c) 12

13 Bone Tissue In Bone tissue the extracellular matrix secreted by bone cells consists of an organic component (osteoid) and a hardened inorganic component. The organic component (osteoid) consists of collagen fibers in a firm glycoprotein ground substance. Collagen provides strength to withstand tensile forces (due to stretching, bending and twisting) without breaking. The inorganic component consists mainly of hydroxyapatite, Ca 5 (PO 4 ) 3 OH, a hard mineral The inorganic component provides hardness and rigidity to withstand compression forces without bending. 13

14 Bone Tissue: Components & Properties Bone Tissue Extracellular Matrix Bone Cells (Osteocytes) Organic Matrix (Osteoid) Inorganic Matrix (hydroxyapatite) Ground Substance (glycoprotein) Collagen Fibers Strength Hardness & rigidity Properties of bone tissue 14

15 Bone Cells Mature bone cells (osteocytes) are connected to each other and to the nearest blood supply via many cytoplasmic processes which run through tiny canals (canaliculi) in the extracellular matrix. Unlike cartilage, bone matrix is impermeable so does not allow diffusion, except via canaliculi which are therefore lifelines for bone cells. Osteocytes non - dividing mature bone cells Extracellular calcified matrix Nucleus of osteocyte Lacuna: space surrounding osteocyte Cytoplasmic processes of osteocytes in canaliculi Canaliculi: allow diffusion between osteocytes & blood vessels CO 2 15 wastes O 2 nutrients

16 Compact Bone Tissue Two types of bone tissue occur, Compact Bone and Spongy Bone. Compact Bone has No marrow spaces Parallel osteons resist forces primarily in one direction Has no trabeculae Occurs externally on bones External membrane (periosteum) of bone organ Haversian System (osteon) Blood vessels in Central Canal Osteocyte in lacuna Concentric layers of bone tissue (lamellae) Fig. 6-3, Martini & Bartholomew; 16

17 Compact Bone Tissue: Haversian Systems Haversian Systems (osteons) consist of concentric layers (lamellae) of bone tissue surrounding a central (Haversian) canal containing blood vessels. Radiating canaliculi connect the osteocytes with the central canal. calcified Fig. 4-11, Martini & Bartholomew; 17

18 Spongy Bone Tissue Contains many spaces with marrow Spongy bone reduces the weight of bones and (where it contains red marrow) is a source of blood cells. Has lamellae but no osteons Consists of irregular bony bars or struts (trabeculae) aligned to withstand forces from many directions. Occurs internally in bones Opening of canaliculi Trabeculae Spaces containing marrow Internal surface (endosteum) Lamellae but no osteons Osteocyte in lacuna Fig. 6-4, Martini 18

19 Surrounds bone organs Bone Tissues - 1 Between osteons Surrounds osteons Perforating or Volkmann s canal Fig. 6-3, Martini & Bartholomew; Fig. 6-4, Martini 19

20 Bone Tissues - 2 alternate lines internal surfaces of bones strengthens osteon Concentric lamellae Fig. 6-3, Martini & Bartholomew; Fig. 6-4, Martini 20

21 Structure of a Long Bone Fig. 6-2, Martini & Bartholomew; Fig. 6-2, 6-11, Martini 21

22 Structure of a Long Bone - 2 Long bones consist of a diaphysis (or shaft) the walls of which are mostly of compact bone. The shaft of a long bone withstands forces mainly parallel to the bone. The diaphysis contains interstitial and circumferential lamellae as well as concentric lamellae. Perforating or Volkmann s canals connect the Haversian canals to the main blood supply. The diaphysis is hollow with a marrow cavity containing fatty yellow marrow. An expanded end at each end of the diaphysis called the epiphysis. This forms joints with other bones and contains spongy bone so is able to withstand forces from many directions. Yellow or red marrow occurs in the spaces between trabeculae. In adults red marrow occurs in the proximal epiphyses of the femur and humerus. The epiphysis is covered by a thin cortex of compact bone and, at the joint surfaces by an articular cartilage (hyaline cartilage). 22

23 Structure of a Long Bone -3 epiphysis metaphysis diaphysis Fig. 6-2, Martini & Bartholomew; Fig. 6-11, Martini Epiphyseal plate (immature bone) or epiphyseal line (mature ossified bone) The metaphysis is the junction between diaphysis and epiphysis. During growth years a layer of hyaline cartilage occurs on the epiphyseal side of the metaphysis called the epiphyseal plate. This is responsible for longitudinal growth (lengthening of long bones) until maturity by interstitial growth of cartilage and appositional growth of bone. At maturity the epiphyseal plate is completely ossified and is now called the epiphyseal line 23

24 Bone Tissues: Periosteum The external surfaces of bones (except at joint surfaces) are covered by the periosteum. This has two layers, an outer collagenous fibrous layer and an inner cellular layer. - The outer fibrous layer of the periosteum protects bones and binds tendons and ligaments to bones (via perforating or Sharpey s fibers). - The inner cellular layer of the periosteum is osteogenic, i.e. functions in appositional growth, remodeling and repair of bones Periosteum Fibrous layer Cellular layer Anchors bones to ligaments & tendons Protects bones Forms new bone by Appositional Growth Growth Remodeling Fracture repair 24

25 The Periosteum contains stem cells osteoblasts osteoclasts anchor periosteum to bone tissue Fig. 6-3, Martini & Bartholomew; Fig. 6-6, Martini 25

26 The Endosteum Internally the cavities of bones are lined with a thin cellular Endosteum which functions like the cellular layer of the periosteum. Fig. 6-8, Martini It therefore contains - stem cells (osteoprogenitor cells) - osteoblasts, the source of new bone tissue - osteoclasts which destroy bone tissue. 26

27 Fig. 6-3, Martini Compact bone Periosteum Endosteum Types of Bone Cells Osteocytes cannot normally divide forms Osteoblasts raise ph to form inorganic matrix forms Bone Deposition Bone Resorption Osteoclasts lower ph to dissolve inorganic matrix 27

28 Functions of Bone Cells mobile cells 28

29 Appositional Growth of Bone Tissue Osteogenic (bone forming) cells in the periosteum or endosteum are called osteoblasts. Osteoblasts exchange chemicals via cytoplasmic processes connecting the cells,, Osteoblasts secrete the organic matrix first and then create the alkaline environment causing precipitation of the inorganic matrix of hydroxyapatite around themselves. The osteoblasts are now mature non- dividing cells called osteocytes and are imprisoned within their lacunae in the calcified matrix and connected to their blood supply via canaliculi. secretes organic matrix calcified Raises ph to form 29

30 Appositional Growth of Long Bone Diaphysis Increased diameter of marrow cavity due to resorption by osteoclasts in endosteum. Increased bone circumference due to appositional growth by osteoblasts in periosteum. Fig. 6-6, Martini & Bartholomew; 30

31 Ossification Bone Formation occurs by Ossification and by Appositional Growth, processes that occur during the growth of the skeleton to maturity during remodelling of bone throughout life in the repair of bones. Ossification is the replacement of cartilage or fibrous connective tissues with bone tissue. Ossification occurs in development of the skeleton to maturity & in fracture repair. 31

32 Development of Skeleton In the embryo most bones are first formed as hyaline cartilage bone models which are gradually replaced by bone (osseous) tissue at maturity in a process called Endochondral Ossification. A few bones however, are formed instead as fibrous membrane models (most skull bones and the clavicle) in a different process called Intramembranous Ossification. Fig. 6-4, Martini & Bartholomew; Skeleton of 16 week old fetus 32

33 Intramembranous Ossification In both types of ossification, centers of bone forming tissue (called ossification centers) are formed within the model in a vascularised environment. Osteoblasts first secrete the organic matrix followed by calcification. Ossification then proceeds by appositional growth away from the ossification center. In Intramembranous Ossification embryonic mesenchyme cells differentiate to become osteoblasts (bone forming cells) within a fibrous membrane under the skin. Osteoblasts then form spongy bone to which is added compact bone, externally, beneath the newly formed periosteum. Fig. 6-2, Martini Periosteum 33

34 Endochondral Ossification: Summary For most bones embryonic mesenchyme cells first differentiate to become chondroblasts surrounded by a perichondrium. Hyaline cartilage is formed which grows by interstitial and appositional growth forming a cartilage bone model. In Endochondral Ossification calcification of the hyaline cartilage bone model occurs which causes death of most chondrocytes. The bone model is then invaded by vascularised tissue which form Ossification Centers within the model. Cartilage is replaced by spongy bone tissue as ossification spreads by appositional growth away from 34 the ossification centers.

35 Endochondral Ossification: Initial Steps Fig. 6-5, Martini & Bartholomew; 1. Death of chondrocytes in cartilage model Blood vessels (Bone collar) 2. Bone Collar Formation In the center of the diaphysis the cartilage model calcifies and chondrocytes die. Increased vascularisation of the perichondrium forms a periosteum which forms an external collar of compact bone around the diaphysis of the cartilage model. This collar spreads along the diaphysis. 35

36 Endochondral Ossification: Steps Periosteal bud Spongy bone 3. Formation of Primary Ossification Center in center of diaphysis 4. Ossification of diaphysis Spongy bone Fig. 6-5, Martini & Bartholomew; Vascularised bone - forming tissue from the periosteum (a periosteal bud) invades the center of the diaphysis forming a Primary Ossification Center. Osteoclasts digest away the calcified cartilage while osteoblasts form new spongy bone around the remnants of the cartilage within the diaphysis. Calcification of cartilage continues within the diaphysis and 36 ossification follows this, spreading along the diaphysis.

37 Endochondral Ossification: Steps 5. Formation of Secondary Ossification Centers in Epiphyses Secondary ossification center Marrow cavity Osteoclasts erode the newly formed spongy bone to create a marrow cavity in the center of the diaphysis which spreads along the diaphysis. Calcification of cartilage then occurs in each epiphysis at or after birth, followed by invasion by a periosteal bud, forming a Secondary Ossification Center in each epiphysis. Fig. 6-5, Martini & Bartholomew; 37

38 Endochondral Ossification: Final Steps Fig. 6-8, Martini 6. Ossification (closure) of Epiphyseal Plates by end of puberty Ossification forms spongy bone in each epiphysis between a layer of epiphyseal cartilage (the epiphyseal plate) and articular cartilage. Epiphyseal plate cartilage continue to grow by interstitial growth as fast as it replaced by bone tissue on the diaphyseal side of the plate. Therefore the long bone continues to grow in length until maturity when the epiphyseal plate is completely ossified ( closure of epiphyses ) forming an epiphyseal line. After this stage no further lengthening of bones can occur but bones continue to increase 38 in thickness.

39 Development of the Skeleton - 1 Intramembranous ossification forming dermal bone Hyaline cartilage bone models are sites for endochondral ossification Secondary ossification Centers in epiphyses 39

40 Development of the Skeleton - 2 Articular cartilage Epiphyseal plates shrinking 40

41 Development of the Skeleton - 3 Epiphyseal plate almost completely ossified. Eventually closes to become epiphyseal line. No more lengthening of bones can then occur. Articular cartilage remains throughout life 41

42 Bone Remodeling Bone remodeling refers to the changes in shape and thickness of bones throughout life due to two antagonistic processes, bone deposition and bone resorption at the periosteum and endosteum. Bone deposition and resorption occur in response to the need for a constant blood calcium level in response to mechanical stresses for repair of fractures and during bone growth to maturity. 42

43 Bone Deposition & Bone Resorption Bone deposition means appositional growth of new bone tissue by the activity of osteoblasts. Osteoblasts first secrete the organic matrix then the inorganic matrix. Formation of inorganic matrix is catalysed by locally increased concentrations of Ca +2 and PO 4-3 and by the creation of an alkaline environment for enzymes secreted by the osteoblasts. Bone resorption refers to the digestion of bone matrix by enzymes and acids secreted by osteoclasts which also phagocytose the cellular products. 43

44 Bone Tissue Responds to Mechanical Stress Bone is a living tissue and is constantly responding to the needs of the body to resist mechanical stress (Wolf s law). Wolff s law states that bones respond to the level of mechanical stress by structural changes (e.g. trabeculae of spongy bones form along lines which will resist the most stress). The fetal skeleton is relatively featureless. Athletes show increased bone mass. Astronauts & bedridden patients show decreased bone mass (Atrophy of Disuse). Bone remodeling occurs in response to the mechanical stresses placed upon bones. Bone: Use it or lose it! 44

45 Bone Tissue Responds to Body s Needs for Ca/P Bone is a living tissue and is constantly responding to the needs of the body for adequate blood levels of Ca +2 and PO 4-3. Two antagonistic hormones (Parathyryroid Hormone, PTH and Calcitonin) respond to the needs for adequate blood calcium and therefore affect bone remodeling. PTH raises blood calcium levels so is hypercalcemic Calcitonin lowers blood [calcium] so is hypocalcemic 45

46 How PTH & Calcitonin Control Blood Ca levels -ve feedback stimulus " Blood [Ca+2] Parathyroid gland Parathyroid Hormone (PTH) + osteoclasts Thyroid gland Calcitonin - osteoclasts -ve feedback + stimulus!blood [Ca+2]!Blood Ca! Bone Resorption! Bone deposition " Blood Ca 46

47 PTH Causes Bone Resorption & Increases Blood Ca PTH with calcitriol Ca +2 Ca +2 Ca +2 returned to blood PTH Ca +2 Intestine Ca +2 absorbed into to blood Stimulus for PTH " Blood [Ca] Ca +2 PTH Bone Ca +2 removed from bone Bone Resorption Kidney!Blood Ca PTH is released when blood calcium levels fall. 47 PTH stimulates osteoclasts so increasing Bone Resorption.

48 Calcitonin Causes Bone Deposition & Lowers Blood Ca Ca +2 excreted calcitonin Ca +2 Ca +2 Stimulus for Calcitonin!Blood [Ca] Ca +2 calcitonin Bone Ca +2 added to bone Bone Deposition Kidney Ca +2 lost in urine " Blood [Ca] Calcitonin is released when blood calcium levels rise. Calcitonin inhibits osteoclasts allowing osteoblasts to 48 increase Bone Deposition.

49 Homeostatic Control of Blood Ca by Calcitonin & PTH Thyroid gland secretes calcitonin Increased excretion of calcium in kidneys Calcium deposition in bone (inhibition of osteoclasts) Blood calcium levels decline HOMEOSTASIS DISTURBED Rising calcium levels in blood HOMEOSTASIS DISTURBED Falling calcium levels in blood Parathyroid glands secrete parathyroid hormone (PTH) HOMEOSTASIS RESTORED HOMEOSTASIS Normal calcium levels ( mg/dl) HOMEOSTASIS RESTORED Release of stored calcium from bone (stimulation of osteoclasts, inhibition of osteoblasts) Enhanced reabsorption of calcium in kidneys Stimulation of calcitriol production at kidneys; enhanced Ca 2+, PO 4 3- absorption by digestive tract Blood calcium levels increase Martini & Bartholomew Figure

50 Factors Affecting Growth of the Skeleton Growth of the skeleton requires Extrinsic Factors and Intrinsic Factors. Extrinsic Growth Factors include vitamin D (for Ca/P absorption & inorganic matrix formation) sunlight (for synthesis of vitamin D) vitamin C (for collagen synthesis) vitamin A (for osteoblast activity & normal bone growth in children) vitamins K & B12 (for protein synthesis) dietary protein (for synthesis of organic matrix) dietary calcium and phosphorus (for inorganic matrix formation) carbohydrate (for energy. Intrinsic Growth Factors include Genes, Growth Hormone (GH), Thyroid Hormones & Sex Hormones. 50

51 Factors Affecting Growth of the Skeleton - 2 EXTRINSIC GROWTH FACTORS VITAMINS SUNLIGHT MINERALS A Ca D P DIETARY PROTEIN DIETARY CARBOHYDRATE C K B12 Mg, Mn, F, I, Fe Amino acids energy I vit C collagen INTRINSIC GROWTH FACTORS HORMONES Calcitriol Thyroxine (from vit D) Growth Hormone Androgens Estrogens PTH Calcitonin GENES Vit C promotes formation of collagen & organic matrix. Vit D promotes Ca/P absorption & formation of inorganic matrix. 51

52 Formation & Functions of Vitamin D Vitamin D is synthesed from cholesterol in the skin in the presence of sunlight. Vitamin D promotes Ca and P absorption from the diet. Vit D is converted by the kidneys into the hormone calcitriol which targets the small intestine, increasing Ca/P absorption. Bones & teeth via blood Increased absorption of Ca/P Cholesterol in skin Small Intestine sunlight Calcitriol via blood diet Vit D precursor (vit D3) via blood Kidney activates vit D3 to hormone calcitriol (activated vit D) Integumentary System Martini & Bartholomew fig 1-2a via blood Liver stores vit D3

53 Rickets: a Childhood Bone Disorder due to Calcium or Vitamin D Deficiency Lack of vit D causes Rickets inadequate absorption of Ca Hypocalcemia Loss of inorganic bone matrix Softening of bones. Inadequate ossification of epiphyses which become enlarged. Softening of bones causes bowing of legs & other bone deformities 2 years later, with calcium & vit D supplements 53

54 Scurvy: a Connective Tissue Disorder From Deficiency of Vitamin C Deficiency of Vitamin C causes Scurvy Inadequate synthesis of collagen. With less collagen in organic matrix of bone, bones lose mass & strength. Bones become thin & fragile & break more easily. Inadequate collagen causes bruising & bleeding under the skin Inadequate collagen causes loose teeth & bleeding gums, 54

55 Effect of Growth Hormone on the Skeleton Growth hormone (GH) causes protein synthesis and cell division of osteogenic cells throughout the growing years. Growth Hormone causes the juvenile growth spurt and general growth of the skeleton to maturity. Pituitary Dwarf has short stature with normal skeletal proportions. Hypopituitary Dwarf "Height Normal proportions 55

56 Effect of Thyroid Hormone on the Skeleton Thyroid hormone (Thyroxine) causes energy release for bone growth and controls changes in skeletal proportions as bones grow. Thyroid hormone (thyroxine) works synergistically with GH to cause skeletal growth and controls changes in skeletal proportions. Hypothyroid Dwarf has short stature and infantile skeletal proportions. Hypothyroid Dwarf "Height Infantile proportions 56

57 Effect of Sex Hormones on the Skeleton Sex Hormones (Androgens & Estrogens) cause Growth spurt of puberty. Ossification ("closure") of the epiphyseal plates at the end of puberty Secondary Sexual skeletal changes Bone Deposition throughout life (preventing osteoporosis). Normal spongy bone Bones porous & brittle Bone with Osteoporosis Martini fig

58 Summary of Effects of Hormones on Bones GH has indirect action on bones by acting as a trophic hormone for the liver liver hormone from liver T4 gonadotropin GH - Juvenile growth spurt T4 - Normal Skeletal proportions - energy for growth Sex hormones - adolescent growth spurt - closure of epiphyses 58

59 Changes in the Human Skeleton with Age Bone mass is not constant but increases and decreases during life due to two processes, bone deposition and bone resorption. Hormones help control these skeletal changes (along with diet and normal bone use). During growth years (0-20} the rate of deposition exceeds the rate of resorption and there is a net increase in bone mass. During adulthood (ages in females; in males) the rate of deposition equals the rate of resorption and bone mass is fairly constant. During later years (35+ in females; 60 +in males) the rate of deposition is less than the rate of absorption and there is a net decrease in bone mass. 59

60 Changes in the Human Skeleton with Age - 2 growth years (0-20yrs} deposition > resorption Middle years: deposition = resorption Closure of epiphyses Adolescent growth spurt Sex Hormones menopause "Sex hormones Bone mass -25% -30% Old age: deposition < resorption Juvenile growth spurt GH Thyroxine "Bone mass (osteopenia) osteoporosis // 70 Thyroxine Relative importance of hormones at various ages All continue to be secreted throughout life Growth hormone androgens estrogens 60

61 Specific Skeletal Changes with Age Changes in Body Proportions skull becomes proportionately smaller (rest of body grows faster) face becomes proportionately larger (compared to cranium) cranium becomes proportionately smaller (compared to face) legs become proportionately longer trunk becomes proportionately smaller female pelvis widens (during puberty) thorax changes shape (from round to elliptical) Marieb fig 7-34 Face 1 1 Skull

62 Specific Skeletal Changes with Age - 2 Ossification and Closure of Epiphyseal Plates (by 18 in females; 21 in males) due to sex hormones. Epiphyseal plates of growing long bones Martini fig 6-10 Epiphyseal lines of fully ossified long bones 62

63 Specific Skeletal Changes with Age - 3 Appearance of Secondary Spinal Curvatures. Cervical curvature by 3 months as infant lifts head up. Lumbar curvature by 1 year as child stands upright. cervical Secondary Spinal Curvatures Primary Spinal Curvatures lumbar Primary Spinal Curvatures 1-3 years Adult spine 63

64 Specific Skeletal Changes with Age - 4 Closure of Fontanels of Skull and formation of Sutures. - Fontanels are fibrous connections between cranial bones allowing cranial distortion during birth: fontanels disappear by age 4. Sutures start to form when brain stops growing at age 5. Sutures fuse in old age. Cranium of Cranium of newborn Infant adult Martini fig 7-15 Martini fig 7-3b 64

65 Repair of Bone Fractures - Early Stages 1. Breakage of blood vessels cause death of Bone Tissue & Formation of Fracture Hematoma (< 48h) 2. Formation of Internal & External Callus from Cells of Periosteum & Endosteum (48h to 3-4 weeks) Callus: a bridge of spongy bone & fibrocartilage between severed bone segments Fibro Martini & Bartholomew 65 fig 6-7

66 Repair of Bone Fractures - Later Stages 3. Fusion of Calluses & Ossification of Cartilage (3/4 weeks - 2/3 months): cast can be removed 4. Remodeling of Calluses by osteoclasts responding to stresses on bones (by 3 months upper extremity- 6 months lower extremity). New spongy bone in center of diaphysis resorbed by osteoclasts leaving marrow cavity - similar to ossification process during growth. 66

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