DOC PREVIEW
UGA CBIO 2200 - Bone Growth
Type Lecture Note
Pages 5

This preview shows page 1-2 out of 5 pages.

Save
View full document
Premium Document
Do you want full access? Go Premium and unlock all 5 pages.
Access to all documents
Download any document
Ad free experience

Unformatted text preview:

CBIO 2200 1nd Edition Lecture 11 Outline of Last Lecture I Bone Tissue II Functions of the Skeleton III Bones and Osseous Tissue IV Long Bone V Flat Bone VI Bone Cells Outline of Current Lecture I The Matrix of Osseous Tissue II Bone Marrow III Bone Development IV The Fetal Skeleton at 12 Weeks V Bone Elongation VI Normal Orderly Remodeling vs Disorderly Bone Remodeling VII Mineral Resorption VIII Calcium Homeostasis Current Lecture I The Matrix of Osseous Tissue a Organic matter collagen proteoglycans etc 1 3 synthesized by osteoblasts i Collagen protein deficiency osteogenesis imperfect or brittle bone disease very fragile bone b Inorganic matter calcium phosphate etc or together as hydroxyapatite 2 3 These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute II III IV V i Mineral deficiency rickets soft bones bend easily Bone Marrow where you make blood cells a Red marrow myeloid tissue hemopoietic tissue in adult red marrow is mostly in axial skeleton b Yellow marrow can convert to red marrow if needed found in adults not children Bone Development a Ossification or osteogenesis the formation of bone b In the human fetus and infant bone develops by two methods i Intramembranous ossification bone forming within a membrane e g soft spots on baby s skull that produces bones 1 Makes flat bones 2 Mesenchyme means its undifferentiated 3 When mesenchyme condenses they form spicules 4 Blood vessels migrate to spicules 5 Forms compact bone on outsides with spongy bones in middle ii Endochondral ossification bone formation in collagen 1 Process that forms long bones 2 Start with cartilaginous model with primary ossification center in the middle first site of activity of osteoblasts 3 As bone matures in primary ossification center blood vessels invade osteoblasts and osteoclasts activity occurring 4 Secondary ossification center at ends of bones epiphyses 5 As cartilage is being replaced by bone you get the formation of the diaphysis 6 Cartilage that remains is the growth plate epiphyseal plate 7 After growth is over epiphyseal plate is replaced by bone also The fetal skeleton at 12 weeks a Bone has already formed but many of the joints are still cartilage b Primary ossifications have formed but the secondary ossification centers have not yet been replaced by bone Bone elongation a Epiphyseal plate b Growth zone transition zone cartilage is being replaced by bone is called metaphysis c Layers of the metaphysis i Zone of reserve cartilage Chondoblasts that are always producing cartilage ii Zone of cell proliferation Chondrocytes proliferate multiply iii Zone of cell hypertrophy cells grow in size iv Zone of calcification Minerals are added to the matrix calcified v Zone of bone deposition bone matrix is laid down d Bones grow in two directions i Length interstitial growth stops at some point in life VI ii Width appositional growth doesn t stop 1 Bones increase in width throughout life a Deposition of new bone at the surface doesn t get thicker because osteoclasts eat away on the inside b Wolff s law of bone architecture of bone is determined by the amount of stress put on bone c Blood vessel lines cylinder d Bone laid down over cylinder and you get layers creating osteons around blood vessels 2 Bone remodeling occurs throughout life 10 per year Normal Orderly remodeling vs disorderly bone remodeling a Balance between bone deposition and resorption break down b Disruptions in the balance can lead to bone deformities i Paget s disease osteitis deformans named for Sir James Paget weakens bones 1 Osteoblasts activity outweighs osteoclast activity a Bone is being laid down at such a fast rate that it is not properly mineralized 2 Excessive osteoclast activity a Bone is being eaten away faster than they are being laid down ii Osteogenesis imperfect brittle bones 1 Autosomal dominant disorder of type I collagen makes bones brittle iii Osteoporosis thinning of bone 1 Too much osteoclast activity 2 Kyphosis widow s hump regression of estrogen no bone deposition thinning of bone bones collapse and make older people appear shorter 3 Seen later in men than in women because men don t decrease in estrogen as early as in women 4 Can cause you to be confined to a bed c Dwarfism i Achondroplastic dwarfism 1 Normal torso but limbs are shorter than normal large head with prominent forehead 2 Long bones stop growing at normal rate 3 Spontaneous mutation defect in fibroblast growth factor receptor 3 FGFR3 ii Pituitary dwarfism 1 The pituitary secretes too little growth hormone 2 Everything is in proportion just overall stature is shorter d Mineral deposition mineralization VII VIII i Solubility product need critical concentration of minerals for bones to start mineralization ii Inhibitors keep other tissue from mineralization iii Osteoblasts neutralize these inhibitors iv First few crystals seed crystals v Abnormal calcification ectopic ossification when inhibitors don t work well and soft tissue undergoes mineralization calculus calcified mass that appears in soft tissue Mineral Resorption a Ruffled border on osteoclast which increases surface area b Hydrogen pumps on ruffled border pump hydrogen onto bone c Chloride ions followa d Hydrochloric Acid forms pH 4 dissolves bone minerals e Acid phosphatase dissolve protein portion of bone Calcium Homeostasis a About 1100 g of calcium in adult body b 9 2 to 10 4 mg dL c Slight changes can have serious consequences muscle contraction blood clotting etc d Hypocalcemia calcium deficiency can cause overly excitable nervous system muscle tremors can be caused by diarrhea vitamin D deficiency breast feeding sometimes when thyroid glands are removed etc e Hypercalcemia too much calcium very rare f Calcium homeostasis is regulated by three hormones i Calcitriol raise blood calcium levels 1 Vitamin D synthesis 2 Formation 7 dehydrocholesterol is found in the stratum basale and stratum spinosum in the presence of sunlight it is converted to cholecalciferol Vitamin D3 which goes to the liver and is converted to calcidiol and is converted to calcitriol in kidney active form of vitamin D why the skin plays an important role 3 Calcitriol behaves as a hormone that raises blood calium concentration in three ways a Increases kidney s reabsorption of calcium b Increases calcium reabsorption in small intestine c Increases calcium resorption from skeleton activates skeleton break down to


View Full Document
Download Bone Growth
Our administrator received your request to download this document. We will send you the file to your email shortly.
Loading Unlocking...
Login

Join to view Bone Growth and access 3M+ class-specific study document.

or
We will never post anything without your permission.
Don't have an account?
Sign Up

Join to view Bone Growth and access 3M+ class-specific study document.

or

By creating an account you agree to our Privacy Policy and Terms Of Use

Already a member?