BIOL 252 1st Edition Lecture 10 Outline of Last Lecture I. Skeleton FunctionII. Histology of Osseous TissueIII. The MatrixIV. Long Bone StructureV. Structure of Flat BoneVI. Histology of Compact BoneVII. Histology of Spongy BoneVIII. Bone FormationOutline of Current LectureI. Poll EverywhereII. Bone Growth and RemodelingIII. Calcium HomeostasisIV. HypercalcemiaV. OsteoporosisVI. Muscles – basic structure of skeletal muscle Current LectureI. Poll Everywherea. In which of these locations would you NOT expect to find osteoblasts?i. Within trabeculaeii. Why? An osteoblast w/in matrix = osteocyteiii. Osteoblasts are on the surface (surrounding trabeculae) 1. On outer surface of compact bone and inner surface of compact bone (near medullary cavity)iv. Why can’t you build bone from inside the matrix?1. Can only build on the surface2. Osteocytes would be trapped in the matrix a. Matrix is solidv. Osteoclasts are on same surfaces as osteoblastsII. Bone Growth and Remodelinga. Bone Growthi. Interstitial growth of cartilage: bone elongation results from cartilage growthThese 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.1. Within2. Cartilage can do both interstitial and appositional ii. Appositional growth of cartilage and bone: deposition of new bone/cartilage on surface of existing cartilage/bone1. Grows on the outer position/surface 2. Make trabeculae fatter (like adding rings on a tree)b. Remodelingi. Repairs microfracturesii. Reshapes bonesiii. Releases minerals into blood1. Calcium and phosphate2. Phosphate is regulated the opposite of calcium3. Calcium is important for nervous system function and muscle function4. Osteoblasts deposit bone matrix – making calcium phosphate and collagen to build bonea. Where do they get calcium? From the bloodb. Mineralization: crystallization process in which calcium phosphate and other ions taken from blood plasma5. Osteoclasts: through secretion of acids, dissolve bone matrix into aqueous solution (picked up by the blood)a. Mineral resorption: process of dissolving bone and releasing minerals into blood 6. Calcium homeostasis a. Sources of calcium b. When blood Ca falls, body releases Ca from bones, increases Ca absorption from intestines, increases Ca retention in kidneys c. What do we need to absorb calcium?i. Vitamin D7. Job of kidney: filters blood (removes nitrogen compounds)a. Pulls back the good stuff after filtering everythingb. So lose calcium to the kidneys but then pull most of it backc. Can tweak the amount 8. Ex: hypocalcemiaa. Low calciumb. Release more (cell type responsible = osteoclasts)iv. Why would you want to change bone?1. Apply different stresses to bonev. Wolff’s law: architecture of bone determined by mechanical stresses placed on it and bones adapt to withstand those stresses vi. Osteoclasts – tear down bone matrix1. If add bone matrix to one side, in order to turn/move it – tear down the other side changing the orientation of boneIII. Calcium Homeostasisa. Regulators of blood-calcium levelsb. Calcitonin: released when Ca is high (thyroid gland)i. Lowers Cac. PTH: released when Ca is too low (parathyroid gland)i. Increase Cad. Calcitriol: released when Ca is lowi. Works together w/ PTHii. Comes from Vitamin DIV. Hypercalcemiaa. Which explains symptoms of depression, sluggishness, slow reflexesb. Prisoner in solitary confinement: hypocalcemia (no Vitamin D)c. Rickets as a child: hypocalcemia (vitamin D deficiency)d. Partial thyroidectomy: releases Calcitonin which lowers levels of calciume. Kidney removal: store calcitriol in kidneys, not enough calcitriol => cannot absorbVitamin D (hypocalcemia) V. Osteoporosisa. Normal spongy bone vs. osteoporotic spongy bone (has little pits due to activity of osteoclasts) i. Due to imbalanceii. Kyphosis – vertebrae curvatureiii. In females more common – bone matrix production stimulated by estrogen 1. Males testosterone => estrogen (amount of estrogen declines slowly)2. Females – less stimulus for bone matrix production because estrogen declines steeply3. Medication = calcium, Vitamin D, estrogenVI. Muscles – basic structure of skeletal muscle a. Striatedb. Voluntaryc. Multiple nuclei per celld. Each cell = fiber (has dozens of nuclei) e. Sarcolemma = muscle cell membranef. Sarcoplasm: has myoglobin – stores oxygen and glycogen – stored glucoseg. Mitochondria: produce ATP for muscle contractionh. Myofibrili. Not membrane-boundii. Do the contracting and generate forcei. Controlling when we contract – look superficially at cell membranej. Openings in membrane continue down into cell = transverse tubulesi. Passage way into muscle cellii. Extension of cell membrane iii. Bring cell membrane deeper into celliv. Where you have action potentials1. AP on cell membrane and on t-tubules to travel deep w/in cellv. Alongside each = two specializations of SR1. Triad = 2 terminal cisternae and transverse tubulek. Endoplasmic reticulumi. Same organelle = sarcoplasmic reticulum but specializedii. Stores calciumiii. In cytoplasm, low calcium levelsiv. Small storage of calcium in SR – constantly sucking up calcium ionsv. W/ AP- SR releases its calciumvi. Trigger for contraction = calciuml. Thick filamenti. Myosin heads generate movement by converting ATP energy to forceii. Each head has ATPase activity (using/breaking ATP apart into ADP and phosphate)iii. Tails join w/ other tails forming thick filamentm. Thin filamenti. F actinii. Tropomyosin - regulatoryiii. Troponin complex - regulatory iv. When calcium comes along (from SR) binds to troponin, changes shape, causes tropomyosin to roll out of the way n. Sarcomerei. Thin filament overlapping thick filament (alternating)ii. Slides past each other to generate