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Body Logistics > 7 - Bone > Flashcards

7 - Bone Flashcards

1
Q

definition: osteology

A

the study of bone

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2
Q

definition: osteogenesis

A

the formation of bone

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3
Q

definition: osteomyelitis

A

an infection within bone

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4
Q

definition: osteopathy

A

a disease within the bone

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5
Q

definition: osteoporosis

A

weak bone

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6
Q

definition: osteosarcoma

A

a cancer originating from bone forming cells

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7
Q

the skeleton, how many bones in categories etc

A
  • made of 206 named bones in 2 categories: axial and appendicular
  • axial consists of thoracic cage, vertebral column and skull 80 bones
  • appendicular consists of shoulder girdle and upper limbs, pelvic girdle and lower limbs 126 bones
  • there are sometimes 4 extra bones - these are round, small bones found in the back of the knee in tendons, which alleviate some tension in the tendons
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8
Q

what are the three main functions of bones

A

**mechanical **
- protect important and delicate tissues and organs
- provide a framework for the overall shape of the human body
- form the basis of levers involved with movement

synthetic
haemopoiesis (holds and protects red bone marrow)

metabolic
- mineral storage, eg calcium and phosphorous
- fat storage eg yellow bone marrow
- acid - base homeostatis (absorbs or releases alkaline salts to help regulate blood pH - calcium is alkaline)

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9
Q

cancellous vs compact bone

A

cancellous
- forms a network of fine bony columns or plates
- these are called trabeculae
- this combines strength with lightness
- the spaces in between trabeculae are filled with bone marrow
- ‘spongy bone’
- has spicules (spiky bits) → first bit of developing bone

compact bone
- forms the external surfaces of the named bones
- comprises mose of the body’s skeletal mass
- aka cortical bone
- many nerves, blood vessels and lymphatics run through cortical bone

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10
Q

what type of bone is found in medulla region of bone

A

only cortical/compact bone
→ hollow part of the bone that contains bone marrow

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11
Q

definition: ossification

A

bone formation

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12
Q

what are the two types of ossification

A

endochondral ossification
- inside cartialage
- the formation of long bones from a cartilage template
- continued lengtheneing is by ossification at epiphyseal plates
→ appositional growth (growth at edges)

intra-membranous ossification
- the formation of bone from clusters of mesenchymal stem cells in the centre of bone
→ interstitial growth (growth in the middle)

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13
Q

endochondral ossification

A

most bones form by this method, except the clavicles and the skull bones

  • mesnchymal cells first differentiate into chrondrocytes
  • these build a hyaline cartilage model
  • the centre of the hyaline cartilage model is the primary ossification centre
  • blood vessels enter primary ossification centre
  • these bring in nutrients, osteoblasts and osteoclasts
  • the osteoblasts replace the chondrocytes at the primary ossification centre, begin to replace cartilage with bone
  • osteoclasts then begin to collapse the bone in the middle, making it more porous, which is how bone marrow develops

long bones form first by this method - patella, wrist and ankle etc develop after birth

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14
Q

intramembranous ossification

A

flat bones develop by this method, including many in the skull
- mesenchymal cells differentiate directly into osteoblasts
- these create the primary ossification centre
- start building bone without any cartilage model
- blood vessels reach primary ossification centre
- the primary ossification centre already has osteoblasts, but the BVs bring in nutrients

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15
Q

cancellous bone conversion to cortical bone

A
  • mesenchymal stem cells convert into osteoblasts
  • these line recently formed trabeculae
  • lay down osteoid that becomes mineralised
  • osteoblasts become trapped → osteocyte
  • mesenchymal stem cells come back in and make more osteoblasts, and make another layer of bone tissue, repeat again etc
  • each layer of bone formed is called a lamella
  • forms a structure that leaves mesenchymal stem cells within it
  • those turn into blood vessels, nerves and lymphatic vessels
  • this structure is known as an osteon (aka haversian system) with a haversian canal running through it
  • volkmanns canals form between osteons in order to carry blood vessels
  • just made immature cortical bone
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16
Q

immature cortical bone → mature bone

A
  • immature bone has osteocytes in random arrangements and blood vessels that aren’t properly formed
  • need to form resorption canals (full of osteoclasts)
  • resorption canals job is to find weakenesses in that bone and rectify it, to make stronger bone
  • the canals usually run parallel to the existing osteons
  • the resorption canals move, and create new osteons
17
Q

structure of mature bone (cortical)

A
  • many osteons (haversian systems) with haversian canals running through them
  • interstital lamellae between osteons
  • haversian canals have blood vessels, lymphatics and nerves
  • haversian canals are connected horizontally by the volkmanns canals
  • the volkmanns canals join up to the outside to the periosteum and endosteum
  • periosteum is dense connective tissue that surrounds bone where muscle etc attaches
  • endosteum is loose connective tissue on inside of bone where bone marrow is
18
Q

structure of mature bone - cancellous

A
  • made up of trabeculae
  • spaces between them filled with red bone marrow
  • no haversian or volkmanns canals
  • bone marrow surrounding is liquid
  • section of trabecula has layers of interstitial lamella, with ostocytes trapped in between layers. Osteoclast on one side of trabeculae and osteoblasts aligned along trabecula of new bone
  • teardrop shape due to gravity
  • note: no blood vessels etc because surrounded by liquid bone marrow, so transport is easy
19
Q

what are haversian and volkmann’s canals

A
  • found in cortical bone only
  • haversian canals have blood vessels, lymphatics and nerves
  • volkmanns canals only have blood vessels
  • haversian canals run through osteons (haversian system)
  • job is allowing bone to deliver oxygen and nutrients to the bone
  • volkmanns canals connect haversian canals horizontally
  • volkmanns canals join to periosteum and endosteum
  • used to communicate with osteocytes
20
Q

endosteum vs periosteum

A

cortical bone
- periosteum is dense connective tissue that surrounds bone where muscle etc attaches
- endosteum is loose connective tissue on inside of bone where bone marrow is

21
Q

where is the epiphysis, metaphysis and diaphysis of a long bone

A
  • epiphysis is top and and bottom areas of bone (ie the bits that form joints) - consists mainly of cancellous bone
  • diaphysis is shaft of long bone - predominantly hollow and filled with bone marrow. Consists of cortical bone around the sides
  • metaphysis is in between epiphysis and diaphysis
  • between metaphysis and epiphysis is epiphyseal growth plate (layer of cartilage) → allows bones to keep growing
22
Q

bone strength

A
  • bone (as a tissue) is very good at resisting force
  • it has great tensile + compressive strength
  • has a degree of flexibility
  • main force lines are through the cortical bone
  • lamellae of osteons can slip relative to each other
  • this can resist fracture
23
Q

how do osteons remodel themselves

A
  • bone becomes weak when there are not enough haversian systems (osteons) in the cortical bone
  • remodels by moving osteons around, using osteoblasts and osteoclasts
  • need to get material from somewhere to make the new osteons? this comes from inside the bone (endosteum) from the cancellous bone
  • osteoblasts then use that to make new osteons, and also put more tissue outside (periosteum)
  • this is known as appositional growth (taken from inside and put on outside)
  • bone is dynamic and is constantly remodelling itself

this happens in two stages (cutting + closing cone), details on future card

24
Q

why is exercise important for bone remodelling

A
  • bone is dynamic and is constantly remodelling itself
  • exercise is a key determinant of bone strength
  • inactivity increases bone resorption (1/3 mass lost when immobile)
  • bone density is optimum at 25 y/o
  • this is because bones widen when you exercise
  • this is due to osteoclasts taking bone off the endosteum, which gets resorbed on the periosteum (see prev card) to get thicker cortical bone
25
Q

bone remodelling steps

A

two main steps

1. osteoclasts make a wide tunnel in the bone)
- aka cutting cone
- osteoclasts (multiple nuclei) are at the front edge
- these break down the bone

2. osteoblasts make smaller tunnel of cortical bone
- aka closing cone
- osteoblasts start laying down osteoid behind the cutting cone
- osteoid becomes mineralised
- makes a smaller tunnel with more osteocytes in it
- osteoblasts fill up gaps and eventully produce new haversian system
- this allows it to control the breakdown of bone, making it stronger

26
Q

what is osteoid

A
  • it is the unmineralised, organic content of bone
  • it is mainly collagen I with ground substance
  • mineralised osteoid is bone tissue
27
Q

factors affecting bone stability

A

activity of osteocytes (osteoid recycling)
- can act like osteoblasts and lay down osteoid into their lacunae (inc by oestrogen and thyroid hormone)
- can act like osteoclasts and degrade bone a little, aka osteocyctic osteolysis (increased by PTH)

activity of osteoblasts (bone deposition)
stimulated by calcitonin, ostrogen, testosterone, growth hormone, thyroid hormones, vit A

activity of osteoclasts (bone resorption)
- increased by PTH (releases calcium ions into blood)
- calcitonin blocks the action of PTH at PTH receptor

28
Q

what are the main nutrients for bone

A

vit D3
- absorbed from gut or synthesised in skin
- produces calcitriol
- helps with calcium absorbtion from gut

vit C
synthesis of collagen I

vit K and B12
synthesis of bone proteins

29
Q

what are some diseases associated with bone

no details

A
  • osteogenesis imperfecta
  • rickets and osteomalacia
  • osteoporosis
  • achondroplasia

when you lose bone mass within cancellous bone leads to susceptibility to fracture

30
Q

osteogenesis imperfecta

A

brittle bone disease
- mutation in COL1A gene
- incorrect production of collagen 1 fibres
- mainly affects neonates and children

results in
- weak bones and increased fracture risk
- short stature (depends on type)
- presence of blue sclera
- hearing loss
- hypermobility, and flat or arched feet
- poor teeth development

31
Q

rickets

A
  • mainly affects children
  • due to vit D deficiency
  • poor calcium mobilisation
  • ineffective mineralisation
  • weakened bone development
  • soft bones
  • shortened height and stature
  • painful to walk
  • characteristic bowed legs
32
Q

osteomalacia

A

‘rickets’ in adults

vitamin D deficiency
- lower mineralisation (little or no hydroxyapatite deposits)
- increased osteoid

increased calcium resorption
- kidney disease (kidneys activate vit D)
- protection from sunlight (sunlight produces vit D)
- surgery (vit D is absorbed through stomach and intestine)
- drugs: phenytonin prevents vit D absorbtion

33
Q

osteoporosis

mechanism on next card

A

primary
type 1
- occurs in postmenopausal women
- due to increase in osteoclast number
- loss of oestrogen after menopause
- around age 50

type 2
- occurs in older men and women
- due to loss of osteoblast function (senile osteoporosis)
- loss of both oestrogen and androgen
- around age 70+

secondary
- result of drug therapy (ie corticosteroids)
- processes affect bone remodelling (malnutrition, prolonged immobilisation, weightlessness)
- metabolic bone diseases (eg hyperparathyroidism, metastatic cancers)

34
Q

mechansim of osteoporosis

A
  • quiescent phase we have osteoblasts on bone surface
  • the outer surface of the bony trabeculae of cancellous bone are regularly remodelled by osteoclast resorption and osteoblast deposition
  • resoptive phase osteoclasts start resorption of bone, forming a lacuna, in which some formation of bone needs to be created
  • reversal phase is when osteoclast stops as osteocyte has sent out signal
  • formative phase is where osteoblasts lay down osteoid, it becomes mineralised into bone tissue etc, and this continues

in normal individual, osteoblasts are able to lay down osteoid to normal level, repairing the bone.

in osteoporosis, unable to repair bone fully (incomplete refilling of osteoclast resorption bays). This makes the bones weak, and susceptible to further damage and compression fractures

35
Q

modifiable risk factors for osteoporosis

A

calcium intake
- recommended value for postmenopausal women is 700mg/day

exercise
- immobilisation of bone (eg cast or bed rest) leads to accellerated bone loss
- weightlessness experienced by astronauts can result in osteoporosis
- physical activity needed to maintain bone mass

cigarette smoking
- in women, smoking is correlated with increased incidence of osteoporosis

36
Q

achondroplasia

A
  • inherited mutation in FGF3 receptor gene
  • FGF promotes formation of collagen from cartilige
  • this means that endochrondral ossification is affected, but intramembranous ossification is unaffected
  • results in short stature, but normal sized head and torso
  • this is because long bones cannot lengthen properly
37
Q

what is the cement line

A

the point at which the osteid meets the existing bone

38
Q

what is the mineral that’s used to mineralise osteoid

A
  • hydroxyapatite
  • mineralises osteoid to form bone tissue
  • also found in teeth

Body Logistics (11 decks)

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