1. classifications of bones by shape
(1) long bone
- long and thin
- arm and forearm, thigh (femur) and legs, palms, soles, fingers, toes
(2) flat bone
- thin with parallel surfaces
- skull, sternum, rib, scapulae
(3) sutural bone (Wormian bones)
- small, irregular bones
- between flat bones of the skull
(4) irregular bone
- complex shapes with short, flat, notched, or ridged surfaces
- spinal vertebrae, the bones of the pelvis, and several skull bones
(5) short bone
- small , thick and boxy
- tarsal (ankle), carpal (wrist)
(6) sesamoid bone
- small, flat, and shaped somewhat like a sesame seed
- develop inside the tendons; most commonly located near joints at the knees, …show more content…
the hands, and the feet
- everyone has sesamoid patellare/ kneecaps
2. bone markings p172 3.
(1) osteogenesis (“make new bone”)
- bone formation
(2) ossification
- the process of replacing other tissues with bone
- 2 main forms: intramembranous and endochondral
(3) calcification
- the process of depositing calcium salts
- occurs during bone ossification and in other tissues
4. long bone p173 (1) structure
Diaphysis
- the shaft
- heavy wall: compact bone/ dense bone
- central space: medullary(marrow) cavity
Epiphysis
- wide part at each end
- articulation with other bones
- mostly spongy bone/ cancellous/ trabecular bone
- covered with compact bone (cortex)
Metaphysis
- where the diaphysis and epiphysis meet (where the bone increase their length)
(2) compact bone p176
- osteon (Haversian system) is the basic unit
* osteocytes are arranged in concentric lamellae
* around a central canal (Haversian canal) generally run parallel to the surface of the bone contain blood vessels (normally a capillary and a venule)
- circumferential lamellae
* lamellae wrapped around the long bone (outer and inner), where they are covered by periosteum and endosteum ???
* bind osteons together
* produced during the growth of the bone
- interstitial lamellae
* fill in spaces between osteons in compact bone
* remnants of osteons whose matrix components have been almost recycled by osteoclasts
- canaliculi
* form pathways for blood vessels
* exchange nutrients and wastes
* radiate through the lamellae interconnect the lacunae of osteons with one another and with the central canal
- perforating canals (volkmann’s canal)
* perpendicular to the central canal
* carry blood vessels into bone and marrow blood vessels in canals supply blood to osteons deeper in the bone and to tissues of the medullary cavity
* allow for blood exchange between individual osteons and the cardiovascular system
- centric lamellae wrapped by collagen fibers which wind in “opposite” directions between adjacent lamellae
(3) spongy bone
- does not have osteons
- the matrix forms an open network of trabeculae
- trabeculae has no blood vessels nutrients reach osteocytes by diffusion along canaliculi that open onto the surface of canaliculi
- the space between trabecullae is filled with red bone marrow
* has blood vessels
* form red blood cells (spongy bones within epiphysis of long bone, e.g. femur, and the interior of the other large bones, e.g. sternum, ilium)
* supply nutrients to osteocytes and remove wastes
- yellow bone marrow
* in some bones
* yellow because it stores fat (energy reserve)
- * framework of trabeculae supports and protects cells of the bone marrow * located where bones not heavily stressed or where stress arrive from many directions * much lighter than compact bones; reduce weight of skeleton and make it easier for muscles to move bones
(4) ossification
- endochondral ossification
* ossify bones that originate as hyaline cartilage
* interstitial growth: expansion of cartilage matrix appositional growth: production of new cartilage at outer surface appositional growth
* 6 main steps
I.
i. chondrocytes near the center of the shaft increase in size ii. matrix reduced to a series of struts that soon begin to calcify iii. enlarged chondrocytes die and disintegrate, leaving the cavities within the cartilage
II.i. blood vessels grow around the edges of the cartilage ii. cells of the perichondrium convert to osteoblasts iii. the shaft of the cartilage then becomes unsheathed in a superficial layer of bone
III. i. blood vessels penetrate the cartilage and invade the central region ii. fibroblasts migrating with the blood vessels differentiate into …show more content…
osteoblasts iii. osteoblasts begin producing spongy bone at a primary ossification center iv. bone formation spreads along the shaft toward both ends
IV.
i. remodeling; create a medullary cavity ii. osseous tissue of the shaft becomes thicker iii. the cartilage near each epiphysis is replaced by shafts of bone iv. further growth involves increases in length and diameter
V. capillaries and osteoblasts migrate into epiphysis, creating the secondary ossification centers
- intramembranous ossification (dermal ossification)
* produce dermal bones, e.g. mandible, clavicle
* 3 main steps
I. i.mesenchymal cells aggregate, differentiate into osteoblasts ii. begin ossification iii. bone expands as a series of spicules that spread into surrounding tissues
II. as the spicules interconnect, they trap blood vessels within the bone
III. i. bone assumes the structure of spongy bone ii. areas of spongy bone may later be removed, creating medullary cavity iii. through remodeling, spongy bone formed can be converted to compact bone.
5. lengthening of long bones
- occurs at specialized regions: epiphyseal plates
- contain epiphyseal cartilage that actively osteogenesis that increases the length of the region
- occurs from birth will early 20s at puberty, the combination of rising levels of sex hormones, growth hormone and thyroid hormone stimulates bone growth
dramatically
- epiphyseal line
* epiphyseal cartilage disappears when long bone stops growing, after puberty
* is visible on X-rays as a epiphyseal line
- epiphyseal closure: completion of epiphyseal growth
6. nutrition, exercise and diet affect bone growth/formation
- exercise (exercise):
* heavily stressed bones become thicker and stronger
* bone degenerates quickly, bones which don’t see any activity quickly lose strength (1/3 of bone mass can be lost in a few weeks of inactivity)
- nutrition
* calcium and phosphate salts + small amounts of magnesium, fluoride, iron, and manganese
* Vitamin C: require for collagen synthesis, and stimulation of osteoblast differentiation scurvy: Vitamin C deficiency; one significant sign is a loss of bone mass and strength
* Vitamin A: stimulate osteoblast activity; particularly important for normal bone growth in children
* Vitamin K and B12: help synthesize bone proteins
7. parathyroid hormone, calcitonin, calcitriol
- calcium regulation (homeostasis) is regulated by 3 primary hormones:
* parathyroid hormone:
* calcitonin
* calcitriol
- 3 target sites and functions of calcitonin and parathyroid hormone
* bones: storage
* digestive tract: absorption
* kidneys: excretion
- Parathyroid Hormone (PTH)
* source: parathyroid glands in neck
* Increase plasma calcium ion level (< 8.5mg/dL) by
I. stimulate osteoclasts, and enhance the recycling of minerals by osteocytes (also stimulate osteoblasts, but less degree)
II. Increase intestinal absorption of calcium by enhancing the action of calcitriol (control on intestinal epithelium)
III. Decrease calcium excretion at kidneys
- Calcitonin
* source: C cells (parafollicular cells) in thyroid
* decrease plasma calcium ion level (> 11mg/dL) by
I. inhibiting osteoclast activity
II. increase calcium excretion at kidneys
(III. lower levels of PTH and calcitriol also reduce the intestinal absorption of calcium)
8. fractures
- types p190, 191
* colles fracture
* greenstick fracture
* epiphyseal fracture
* compression fracture
* pott fracture
* comminuted fracture
* transverse fracture
* spiral fracture
* displaced fracture
- fracture of repair (4 steps)
* Hematoma formation produces a clot (fracture hematoma) establish a fibrous network bone cells in the area die; disruption of circulation
* Soft callus formation
I .cells of the endosteum and periosteum (inactive in adults) divide and migrate into fracture zone
II. calluses form to stabilize the break external callus of cartilage and bone surrounds break internal callus develops in medullary cavity and between the broken ends of the shaft
(at the center, cells differentiate into chondroblasts and produce blocks of hyaline cartilage; at the edge, cells differentiate into osteoblasts and begin creating a bridge between bone fragments on either side of the fracture.)
* Bone formation
I. osteoblasts activity increases
II. replace central cartilage of internal callus with spongy bone
III. external callus replaced with compact bone
(external and internal calluses form an extensive and continuous brace at the fracture site
- struts of the spongy bone unite the broken ends
- surrounding area gradually reshaped as fragments of dead bone are removed and replaced
- ends of the fracture held firmly in space and can withstand normal stresses from muscle contractions
- cast can be removed at this stage.)
* Bone remodeling
I. osteocytes and osteoblasts remodel the fracture for up to a year (4 month - 1 year)
II. reducing bone calluses bone of calluses is gone, only living compact bone remains
---> under comparable stresses, a second failure will generally occur at a different site
9. osteopenia and osteoporosis
- osteopenia physiological causes:
* osteoblast activity begins to decline
* osteoclast activity continues at previous levels
physical consequences:
* begins between ages 30 and 40
* women lose 8% of bone mass per decade, men 3% not all parts of the skeleton are equally affected: epiphysis, vertebrae and jaws lose more mass than other sites
- osteoporosis physiological causes:
* Hormone and bone loss: sex hormones (estrogens and androgens) help maintain bone mass (inhibit osteoclast activity) bone loss in women accelerates after menopause (decline in circulating estrogens)
* Cancer and Bone Loss
Cancerous tissues release osteoclast-activating factor
I. stimulate osteoclasts (both number and activity)
II. produce severe osteoporosis (as secondary effect)
physical consequences:
* severe bone loss
* affect normal function
* over age 45, occurs in
I. 29% of women
II. 18% of men