Bone Physiology

Bones are Classified by shape and structure limbs Carpals tarsals vertebrae Skull bones Ribs Sternum scapula

Epiphysis Epiphyseal Line Diaphysis Periosteum Articulating Cartilage Anatomy of Long Bone Epiphysis Epiphyseal Line Diaphysis Periosteum Articulating Cartilage

Compact Bone Canaliculi Haversian Canal Lamellae Osteon

Another picture of Compact Bone

Compact Bone

Spongy Bone Located along the epiphyses of long bones Site of Erythrocyte (RBC) formation (tra-BEK-ū-lē) Collagen fibers are not arranged in concentric rings. But the lamellae form rods called trabeculae. No Osteons or Haverian Systems are present.

Cells in Bones Osteocyte – mature bone cells; recycle Ca and PO4 Osteoclasts – dissolve bone by secreting enzymes and acids. Release Ca to be returned to blood stream Osteoblasts – cells that produce new bone cells referred to as osteogenesis Osteoclasts remove matrix, osteoblasts adds matris. When an osteoblast’s lacunae is calcified the cell becomes and osteocyte.

Endochondrial Ossification Bone tissue in a fetus begins as hyaline cartilage Inside is cartilage, cartilage becomes ossified. In 6 weeks cartilage is replaced to bone except at growth plates.

In 6 weeks cartilage is replaced to bone except at growth plates.

Longitudinal Growth at the Epiphyseal line

Two growth plates Composed of hyaline cartilage Longitudinal growth is completed when epiphyseal lines become completely ossified.

Chrondroblasts closest to epiphyses begin to undergo cell division Cells enlarge (hypertrophy) Cells die, bone eventually replaces cartilage (invasion zone)

Resting Zone Mitosis Zone Hypertrophy Zone Ossification Zone

Growth along Epiphyseal Line Resting Zone Mitosis Zone

Maturation/Hypertrophy Zone Ossification Zone

Longitudinal Growth Controlled by 3 hormones Growth Hormone Baby to prepuberty Sex Hormones (estrogen/testosterone) Causes growth spurt at puberty Shapes your skeleton to your sex Thyroid Hormones (PTH & Calcitonin) PTH = parathyroid hormone Controls whether bone growth occurs Affects Appositional Growth – bone growth in diameter

Bone Homeostasis Bone Remodeling Osteons are formed by osteoblasts In healthy adults: Bone deposit = bone resorption Osteoblasts = Osteoclasts Bone Remodeling refers to the regular mineral turnover that occurs in bone. In adults, 18 % of proteins and minerals turns over yearly. Not uniform. I.e. Head of femur is remodeled more. Why?

Bone Remodeling Controlled by Negative Feedback Loop Bone Deposit Occurs where bone is injured or added bone strength is required Deposits Ca+2 into bone Bone Resorption Osteoclasts break down bone Calcium is taken from bone and placed into blood stream Lysosomes assist in the process Ca and PO4 are released; eventually releasing the blood stream

Blood Calcium is the original stimulus Bone Remodeling is controlled by 2 hormones by a Negative Feedback Loop Blood Calcium is the original stimulus Normal Blood Ca is 9-11 mg CA/100 ml of blood When blood Ca decreases (< 9 mg) Parathyroid Hormone (PTH) is released into bloodstream. Bone resorption occurs causing Ca to leave bone and goto the blood stream Osteoclasts are working

High levels of blood Ca (>11mg) When blood Ca levels are high, Calcitonin is released. Causes bone deposit to occur Ca from the blood is stored into bone. (Osteoblasts and Osteocytes are working.) 99% of all Ca is found in bone.

PTH Calcitonin

Osteoclasts cause bone resorption Controlled by PTH Osteoblasts cause bone deposit Controlled by calcitonin

Factors that help with Bone Deposit Vitamin D – aids in the absorption of Calcium into the bone. Part of vitamin D is converted to the hormone calcitriol which allows Ca to pass through the S.I.(What food is Vitamin D fortified?) i.e. rickets results from Vitamin D deficiency Vitamin C – helps osteoblasts function i.e scurvy – caused from a reduction in osteoblast activity Calcium tablets - Diet -

Appositional Growth over time.

2nd Response to Regulating Bone Remodeling Wolff’s Law Bone grows or remodels in response to the forces or stresses placed on it. Appositional growth – growth in diameter is controlled by the amount of mechanical stress and gravity placed on the bone Heavy usage leads to heavy bones; nonuse leads to atrophy (bone loss)

Controlling Bone Remodeling Hormones PTH and Calcitonin determines whether and when bone remodeling occurs. Mechanical Stess determines where remodeling occurs. High stress areas grow appositionally.

Body’s Needs for Calcium Transmit nerve impulses Muscle contractions Blood coagulation Cell division If blood Ca levels are low for an extended time, bones continually lose Ca. Once bone density loss begins, women lose 8% of their bone mass every decade, men lose 3% every decade

Osteoporesis Osteoporesis Normal Bone Risk Factors Sex (females more affected than males; especially after menopasue) Insufficient exercise or too much exercise Poor diet (low in Ca and protein Smoking Race: Black > bone density

Change in Bone Density with Age

Bone Fracture and Repair Simple Fractures take 8-12 weeks to heal Healing time increases age due to poor circulation

Phases of Bone Repair Hematoma formation A mass of clotted blood appears Blood vessels hemorrhage, causing internal bleeding Blood pools and clots around fx area; which closes off injured blood vessels Hematoma formation

Fibrocartilage Callus Formation Macrophages invade and clean area Fibroblasts help form chondroblasts and collagen fibers Helps to form cartilage splint that will connect ends of broken bones

Osteoblasts replace the cartilage with spongy bone Bony Callus Osteoblasts replace the cartilage with spongy bone Bone cells replace cartilage from the outside fx toward the inside Cells are not organized in the bony callus

Bone Remodeling Continues 4 months to a year Removes excess material; a layer of compact bone is produced