Bone Growth and Remodeling Interactions Animation

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Presentation transcript:

Bone Growth and Remodeling Interactions Animation Bone Remodeling You must be connected to the internet to run this animation

Bone Growth and Remodeling Normal bone metabolism depends on several factors: Minerals are an essential component. Large amounts of calcium and phosphorus and smaller amounts of magnesium, fluoride, and manganese are required for bone growth and remodeling.

Bone Growth and Remodeling Vitamins are also necessary for normal bone metabolism: Vitamin A stimulates activity of osteoblasts. Vitamin C is needed for synthesis of collagen. Vitamin D is essential to healthy bones because it promotes the absorption of calcium from foods in the gastrointestinal tract into the blood. Vitamins K and B12 are needed for synthesis of bone proteins.

Bone Growth and Remodeling Hormones are key contributors to normal bone metabolism. During childhood, the hormones most important to bone growth are human growth hormone (hGH) and growth factors called IGFs (produced by the liver). Both stimulate osteoblasts, promote cell division at the epiphyseal plate, and enhance protein synthesis. Thyroid hormones and insulin also promote bone growth by stimulating osteoblasts and protein synthesis.

Bone Growth and Remodeling Hormones continued… The sex hormones (estrogen and testosterone) cause a dramatic effect on bone growth, such as the sudden “growth spurt” that occurs during the teenage years. The sex hormones also promote widening of the pelvis in the female skeleton. They are also responsible for closing the epiphyseal plates at the end of puberty.

Bone Growth and Remodeling Hormones continued… Parathyroid hormone (PTH) and calcitonin are critical for balancing the levels of calcium and phosphorus between blood and bone. Maintaining a normal serum Ca2+ level takes precedence over mineralizing bone (usually both can be done) – can you suggest an explanation why this is true? Maintaining blood calcium levels is more “important” than bone mineralization because normal heart function depends on a normal ionized serum calcium level (between 8.5-10.2 mg/dl)

Calcium Homeostasis Day to day control of calcium regulation mainly involves: PTH stimulates osteoclastic activity and raises serum calcium level. Calcitonin (thyrocalcitonin), and to a lesser extent hGH and the sex hormones, stimulate osteoblastic activity and lower serum calcium level. Vitamin D is needed for absorption of the Ca2+ and PO4– ions from the small intestine, and reabsorption of those same ions in the kidneys. The role of regulating serum Ca2+ levels and mineralizing bone is under hormonal control, and is carefully balanced.

Calcium Homeostasis

Fracture and Repair The naming of fractures can be confusing because of the many different criteria that are used. Some schemes describe the anatomical appearance of the fracture: Partial, complete (fx is all the way through the bone), closed (simple), open (fx punctures the skin), “Green stick” (a small linear break in the bone cortex), impacted, comminuted, spiral, transverse, displaced

Fracture and Repair Anatomical appearance – like breaking a green twig Greenstick

Fracture and Repair Anatomical appearance – the distal part is shoved up into the proximal part. Impacted

Fracture and Repair Anatomical appearance – though not seen here, one or both bones are “open” to the outside. Open (compound)

Fracture and Repair Naming fractures, continued… Other fractures are classified by the disease or mechanism which produced the fracture. Pathological fracture (usually from a cancerous process or severe chronic disease), compression fracture (produced by extreme forces such as in trauma) Stress fracture (produced from repeated strenuous activities such as running) 

Fracture and Repair Naming fractures, continued… Still other fractures describe a common pattern of injury, often involving more than one bone, and usually denoted by an eponym (someone’s name): Colles’ fracture of the distal radius Pott’s fracture of the distal fibula

Fracture and Repair Eponyms – Colles’ is a fracture of the distal radius ± ulna. Colles’

Fracture and Repair Once a bone is fractured, repair proceeds in a predictable pattern: The first step, which occurs 6-8 hours after injury, is the formation of a fracture hematoma as a result of blood vessels breaking in the periosteum and in osteons.

Fracture and Repair The second and third steps involve the formation of a callus (takes a few weeks, to as many as six months). Phagocytes remove cellular debris and fibroblasts deposit collagen to form a fibro- cartilaginous callus...

Fracture and Repair ... which is followed by osteoblasts forming a bony callus of spongy bone.

Fracture and Repair The final step takes several months and is called remodeling : Spongy bone is replaced by compact bone. The fracture line disappears, but evidence of the break remains.

Exercise and Bone Tissue Under mechanical stress, bone tissue becomes stronger through deposition of mineral salts and production of collagen fibers by osteoblasts. Unstressed bones, on the other hand, become weaker. Astronauts in space suffer rapid loss of bone density. The main mechanical stresses on bone are those that result from the pull of skeletal muscles and the pull of gravity (weight-bearing activities).

Aging and Bone Tissue A decrease in bone mass occurs as the level of sex hormones diminishes during middle age (especially in women after menopause). Bone resorption by osteoclasts outpaces bone deposition by osteoblasts. Since female bones are generally smaller and less massive than males to begin with, old age has a greater adverse effect in females.

Aging and Bone Tissue There are two principal effects of aging on bone tissue: Loss of bone mass The loss of calcium from bones is one of the symptoms in osteoporosis. Brittleness Collagen fibers give bone its tensile strength, and protein synthesis decreases with age. The loss of tensile strength causes the bones to become very brittle and susceptible to fracture.

Aging and Bone Tissue Osteoporosis is a condition where bone resorption outpaces bone deposition. Often due to depletion of calcium from the body or inadequate intake

End of Chapter 6 Copyright 2012 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publisher assumes no responsibility for errors, omissions, or damages caused by the use of these programs or from the use of the information herein.

Bone Formation

Bone Formation

Bone Formation

Bone Formation Endochondral ossification is the method used in the formation of most bones, especially long bones. It involves replacement of cartilage by bone. There are one primary and two secondary centers of growth.

Bone Formation

Bone Formation

Bone Formation

Bone Formation

Bone Formation

Bone Formation

Bone Formation

Bone Formation Ossification contributing to bone length is usually complete by 18-21 years of age. Bones can still continue to thicken and are capable of repair even after the epiphyseal growth plates have closed.

Bone Formation Human growth hormone is one of the body’s many anabolic hormones. Among other things, its secretion will stimulate bone growth, muscle growth, loss of fat, and increased glucose output in the liver. The use of growth hormone has been increasing in popularity among athletes due to the numerous “benefits” associated with its use; side effects are often not thought of when young athletes use these drugs.

Bone Formation Interactions Animation You must be connected to the internet to run this animation

Bone Growth and Remodeling A balance must exist between the actions of osteoclasts and osteoblasts. If too much new tissue is formed, the bones become abnormally thick and heavy (acromegaly). Excessive loss of calcium weakens the bones, as occurs in osteoporosis. They may also become too “soft”, as seen in the bone diseases rickets and osteomalacia.