a+p skeletal physiology and maintenance

skeletal remodeling

• change to a bone’s shape

• occurs on periosteal (internal) and endosteal (external) surfaces

• deposition

• resorption

skeletal remodeling function

• reshape bone during growth

  • attachment sites will need to change

• reshape bone in response to use

  • add bone material in response to bone stress

• repair damage (fractures)

• release minerals into blood

skeletal remodeling deposition

osteoblasts responsible for deposition

• osteoblasts secrete osteoid

  • collagen fibers arranged in a spiral pattern along osteon

• mineralization

deposition: mineralization

calcium and phosphate crystalize on collagen fibers as hydroxyapatite (osteoid is going to be mineralized)

skeletal remodeling resorption

osteoclasts dissolve bone and return minerals to blood (cells that can dissolve and break down bone return the minerals)

• secrete H+ ions and enzymes

  • acidify tissue fluid - determined by concentration of H+ ions (pH) - break down mineral (inorganic) component of ECM

  • calcium + phosphate = inorganic

regulation of remodeling: calcium homeostasis

• needed for neuron signaling, muscle contraction, blood clotting

• balance between dietary intake, excretion, and exchanges (removing calcium from skeleton) between skeleton and blood

• regulated by calcitriol, calcitonin, and parathyroid hormone

calcitriol

• active form of Vitamin D that can have an impact on the body

  • UV light forms precursor to Vitamin D

• produced by actions of skin, liver, and kidneys

  • initiated by UV radiation

• raises blood calcium levels

• without enough Vitamin D, we don’t have enough calcium for mineralization in the skeleton

how does calcitriol raise blood calcium levels

• promotes calcium absorption in small intestine

  • increases skeletal resorption - reclaims calcium and returns it to the circulatory system

• increases calcium resorption from skeleton

• reduces calcium excretion in kidneys

  • helps maintain blood calcium levels

calcitonin

if blood Ca+ is too much

• secreted by thyroid in response to hypercalcemia

• inhibits osteoclasts

• stimulates osteoblasts

• suppresses bone resorption and support bone deposition

• suppresses calcium transport into blood

• hormones = effectors

• regulated by a negative feedback loop

parathyroid hormone (PTH)

in response to deficiency in calcium in the blood

• secreted by parathyroid glands in response to hypocalcemia

• stimulates osteoclast actvity

• inhibits osteoblast activity

• reduces calcium excretion in kidneys

• promotes calcitriol synthesis

• supports bone resorption, suppresses bone deposition - return calcium to circulatory system

regulation of remodeling: mechanical stress

bones reflect the stress they undergo

• stress = force/area

• more bone deposited in areas under high stress

  • monitored by osteocytes

    • one of their functions detect changes in stress and change remodeling in response

    • mediate skeletal remodeling and fix microdamage

• wolff’s law

wolff’s law

bones remodel in response to habitual demands

• stresses we are most often subjecting bones to

• compact bone thickest in diaphysis

• large projections occur where heavy active muscles attach - produce larger contractile forces

• exercise increases bone formation

  • increase in stretch during muscle action

orthodontic braces

• wires place tension on teeth

  • changing amount of tension on teeth, which causes a change in stress, causing bones in jaw to adjust to the change - allows teeth to change position

• alveolar bone is resorbed in response to increased pressure

  • allows tooth to move

• additional bone deposited to fill in space

fractures

inorganic component of bone makes it very strong, durable, and resistant to stress, but it can still fracture from extreme stress

• stress fracture

• pathological fracture

stress fracture

caused by abnormal trauma to a bone - strong force to relatively small bone will cause it to fracture more easily

pathological fracture

break in a bone weakened by disease - caused by an amount of stress that wouldn’t harm a healthy bone, but the weakened bone can’t handle it

healing of fractures

1. inflammatory response

2. soft callus formation

3. hard callus formation

4. remodeling

healing of fractures: inflammatory response

1st step

• blood clot formation - bone is highly vascular

• clot invaded by blood vessels, fibroblasts, macrophages, osteoclasts, osteoblasts, and chondrocytes

  • combination of all produces granulation tissue - needed for repair processes

healing of fractures: soft callus formation

step 2

• fibroblasts secrete collagen

  • provides structural support for further processes to occur

• chondrocytes produce fibrocartilage

  • contains lots of collagen fibers

  • durable and provides structural support - stabilize fracture site

healing of fractures: hard callus formation

step 3

• hard callus is formed by primary bone

• osteoblast produce bony collar around fracture site

• takes 4-6 weeks (ossification process)

• immobilization of healing bone is very important to not disrupt this healing process

  • casts help prevent movement

healing of fractures: remodeling

step 4

• osteoclasts remove bone fragments

• osteoblasts lay down cancellous bone

• continued ossification produces cortical bone

• hard callus remains for months while healing and secondary bone starts to replace primary bone

what impacts healing process?

age and extent of injury impact how long the healing process lasts

• the older we are, the longer fractures take to replace

effects of aging: children and adolescents

deposition > resorption

• balance of activity is shifted towards deposition to allow us to build the amount of bone we need

• greatest period of bone growth

• attainment of peak bone mass - most bone mass we will have for our lives

effects of aging: young adults

deposition = resorption

• deposition slows down - we are maintaining the bone we already have

effects of aging: older adults

deposition < resorption

• bone mass, mineralization, and healing ability decrease

• over time, loss of bone mass and capacity to heal - decreased deposition

osteoporosis

• excess resorption leads to severe loss of bone density

• related to decline in estrogen production

  • postmenopausal women have greatest risk

    • decline in estrogen produced in ovaries

  • occasionally in younger females with very low body fat

    • suppresses estrogen production, which leads to osteoporosis

  • males are at less risk because testosterone provides a thick protective layer on their bones

• trabeculae are narrower

bones most vulnerable to osteoporosis:

• cancellous bone of spine and femur are the most vulnerable

  • vertebral and hip fractures common - example of pathological fracture

  • regions of the body we are subjecting the most amounts of body weight

other risk factors for osteoporosis:

• race

• smoking

• diabetes

• nutritional deficit

  • deficit of calcium or vit. D

• activity level

  • if we’re not loading our bones, then they will not deposit as much

osteoporosis treatment

• estrogen replacement therapy (ex. after menopause)

  • increased risk of heart disease, stroke, and breast cancer

  • can help prevent an increase in bone resorption and support deposition

• medications

• weight-bearing exercise

  • walking, running, lifting weights, resistance training

• nutritional supplements

  • maintain dietary intake of calcium and vit. D

osteoporosis prevention

• calcium-rich diet

• weight-bearing exercise

• reduced consumption of alcohol and carbonated drinks

  • can acidify our bodily fluids

all these helps to increase our peak bone mass if we do these while we’re still growing