Functions of bones

support protection movement storage o fat o minerals blood cell formation

2 basic types of osseus tissue

compact--dense, appears smooth spongy or cancellous--made up of tiny flakes of bone called trabeculae

Long Bone Structure:

The endosteum is a thin layer of connective tissue which lines the surface of the bony tissue that forms the medullary cavity of long bones.[1] The outer surface of a bone is lined by a thin layer of connective tissue that is very similar in morphology and function to endosteum. It is called "periosteum" and contain nutrient formen. Sharpey's fibers of collagen attach it to bone Metaphysis: Region where the diaphysis and epiphysis meet. Epiphysis line is the remnant of the epiphysis plate, a disc of hyaline cartilage that grows during childhood lengthen bone.

Four major cell types in bone tissue: Osteocytes Osteoclast ostoblast Osteogenic/osteogenitor cells mitotic stem cells found in the peristeum and endosteum. Some differenciate into osteoblast others stay as stem cells. COMPACT BONE Contain small passages that allow conduction of nerves, lymph and blood vessels. Structural unit is called osteon or haversian system. Lamella: A layer of the matrix tube in osteons, Osteon:Interconne cting cylindrical channels. In the core of each osteon Cenral canals contain blood vessels and nerve which supply the osteons cells. Volkmanns canals:Horizontal canals that connect blood and nerve supply of perosteum to those in the central canals and meduallary cavity.

SPONGY BONES: Trabecular bone align along lines of stress and help the bone resits stress. Contain irregularly arranged lamellae and osteocytes interconnection by canaculi. No osteons present. An osteoclast (from the Greek words for "bone" and "broken") is a type of bone cell that removes bone tissue by removing the bone's mineralized matrix. This process is known as bone resorption. Osteoclasts and osteoblasts are instrumental in controlling the amount of bone tissue. Osteoblasts form bone; osteoclasts resorb bone. Osteoclasts are formed by the fusion of cells of the monocyte-macrophage cell line.[

An osteocyte, a star-shaped cell, is the most abundant cell found in bone. Cells contain a nucleus and a thin ring of cytoplasm. Once osteoblasts become trapped in the matrix they secrete, they become osteocytes. Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi, which are used for exchange of nutrients and waste. The space that an osteocyte occupies is called a lacuna (Latin for a pit). Although osteocytes have reduced synthetic activity and, like osteoblasts are not capable of mitotic division, they are actively involved in the routine turnover of bony matrix, through various mechanosensory mechanisms. An osteoblast (from the Greek words for "bone" and "germ" or embryonic) is a mononucleate cell that is responsible for bone formation. Osteoblasts produce osteoid, which is composed mainly of Type I collagen. Osteoblasts are also responsible for mineralization of the osteoid matrix. Bone is a dynamic tissue that is constantly being reshaped by osteoblasts, which build bone, and osteoclasts, which resorb bone. Osteogenesis imperfecta (OI and sometimes known as Brittle Bone Disease) is a genetic bone disorder. People with OI are born without the proper protein (collagen), or the ability to make it, usually because of a deficiency of Type-I collagen.[1] People with OI either have less collagen than normal or the quality is poorer than normal. As collagen is an important protein in bone structure, this impairment causes those with the condition to have weak or fragile bones.[2] Osteopetrosis also known as marble bone disease and Albers-Schonberg disease is an extremely rare inherited disorder whereby the bones harden, becoming denser, in contrast to the more prevalent osteomalacia, in which the bones soften. Failure of oteoclast activity. BMU- BONE MULTICELLUAR UNIT, consisting of osteoclast and osteoblasts and form a bone remodelling unit. Occur at the surface of the periosteum and surface of endosteum. Remodelling is bone resorption and disposit at the surface of these places. Bonde deposits occur where ever bone is injuried and where added bine strenght is required. You need a healthy diest of vit c d and a and proteins and minerals including calcium phosphorus magnesium and manganese is essential for remodelling- obtimal bone deposit. Osteoclast move along bone surface digging groves as they break down the bone matrix. The part of the osteoclast that touched the bine is highly folded to form a ruffeled membranne that clings tightly to the bone. Sealing of the area of bone destruction. The ruffled border secreted: 1;lysosomal enzymes that digest the organic matrix. 2;HCl-that converts ca salt into soluble forms that pass easily into soulution. Osteoclast may also phagocytise the demineralies matrix and dead osteocytes. The digest matrixs end product, growth factors and dissolved mineral as then endocytosed, transported across the osteoclast by transcytosis and released at the opposite side where they first enter the interstitiual fluid and then the blood.

Bone remodelling cycle: Resorptive phase: Activated multinucleated oestoclast derived from bone marrow monocytes resorbed a discrete area of mineralised bone matrix. Reversal phase: subsequently osteoprogenitor (osteoblast pregneitor) cell, can locally proliferate and difeerenciate into osteoblast migrating to the resorptive lucanae and disclose the former osteclastic activity. Formative phase: the osteoblast deposist new bone matrix which is initially unmineralised and called osteoid and in this way fill the resorption ;acunae. Resting phase: Once embedded in osteoid the osteblast mature into terminally difeferenciate osteocytes. The osteoblast lying on the surface of newly formed packet are quiescent lining cells until activated.

Osteoporosis is a disease of bone leading to an increased risk of fracture. In osteoporosis the bone mineral density (BMD) is reduced, bone microarchitecture is disrupted, and the amount and variety of non-collagenous proteins in bone is altered. Bone development bone matrix must be deposited on something i.e. 1. pre excisting bone 2. Membrane inramembraneous bone formation 3. Cartilage- endochondral bone formation Mechanicla force direct bone structure. Osteocytes mechanorecpetor, detect change in mechanical forces.

Cartilage

Major components: Collagen type 2, -water, proteoglycans AGGRECAN. FUNCTION: Schock absorber- hyaline cartilage. Facilitate longitudinal growth of long bones growth plate cartilage. Endochondrol ossification Long bone growth Formation of long bone typically begins in the centre of the hyaline cartilage shaft at a region called the primary ossification centres. First the perichondrium covering the hyaline cartilage is infiltrated by blood vessels converting it to a vascularised periosteum. As a result of this change in nutrition, the underline mesenchymel cells specialise into osteoblast. This sets the scene for ossification to begin. Step 1; A bone collar forms around the diaphysis of the hyaline cartilage model. Osteoblasts of the newly converted periosteum secrete osteoid again the hyaline cartilage dyphysis encasing it in a bone collar. Step 2; This is cartilage in the centre dyphysis calcifies and cavitates. As the bone collar formes chondrocytes within the shaft hyperthrophy and signal the surrounding cartilage matrix to calcify. Because calcified cartilage matrix is impremable to diffusing nutrirnet the chonrocyte die and the matrix begins to deteriorate. Although this detoriatiing opens up cavitie, the hyaline cartilage model is stabilised by the bone bone collar, elsewhere the cartilage remains healthy and contunites to grow briskly causing the cartilage model to enlongate. Step 3; This step is the periostial bud invades the internal cavities and spongy bones form. The forming cavities are invaded by the peristial bud which consists of nutrient artery and vein, lymphatics, nerve fibre,s red bone marrow element, osteoblast and osteoclast. The entering osteoclast partially erode the calcified cartilage matrix. And the osteoblast secrete osteoid around the remaining fragements of the hyaline cartilage forming bne covered \cartilage trabeculae. In this was the earlies version of spongy bone in the developing long bone formes. Step 2; The diaphysis elongates and medually cavity formes. As the primary ossification centres enlarges, osteclast break down the newly formed spongy bone, and open up a meduall cavity in centre of the diaphysis. Throught the fetal erpiod, the rapidly growing epiphysis consist only of cartilage and hyaline cartilage models continue to elangate by division of viable cartilage cells at the epiphysis. Because cartilage is calcifying, being errroded and then being replaced, the bony spicules on the epiphysial surface facing the meducally cavirty. Ossficiation chases the cartilage formation along the length of the shaft. Step 5; The epiphysis ossify. Shortly after/before birth, secondary ossification centre appear in one of both epiphysis and they gain bony tissue. The cartilage in the centre of epiphysis calcifies and detoriates opening up cavities that allow the periostial bud to enter. Then bone trabeculae appear. Secondary ossification reproduced almost the same event as the primary ossification except that the spngy bone in the interior is retained and no medullary cavity formes in the epiphysis. When 2dary ossifxation is complete

hyaline cartilage remain only at two places. 1 on the epiphysial surfaces as the articular cartilage 2; at the metaphysic where it forms the epiphysial plate. Anlage