WEEK 2 - Osseous Tissue Flashcards
important functions of bones
- support: for body and soft organs
- protection: protects the brain, spinal cord, and vital organs
- movement: levers for muscle action
- storage: calcium and phosphorus, and growth factors
- blood cell formation: hematopoiesis: occurs in red marrow cavities of certain bones
- hormone production: osteocalcin: is secreted by bones and helps regulate insulin secretion, glucose levels and metabolism
types of bone cells
1. osteoprogenitor
- a stem cell and lives in the periosteum (membrane that covers the bone) and endosteum (inside the bone, lines marrow cavity)
- osteoblast
- make the ECM and all of collagen, they can divide
gets trapped in matrix to form osteocyte
- osteocyte
- a mature bone cell that monitors and maintains the bone matrix
- osteoclast (like a macrophage)
- cell that breaks down tissue and releases Ca2+
multi-nucleated
inorganic component of bones
hydroxyapatite/mineral salts: calcium phosphate crystals sticks to collagen and makes bone hard and resists compression, lasts long after death due to mineral composition
bone development
ossification (osteogenesis) process of bone tissue formation, begins in month 2 of development, before that is all cartilage
intramembranous ossification
- skull, jaw and clavicle are not cartilage, grow from CT
endochondral ossification
everything else, start off as hyaline cartilage
endochondral ossification in a long bone (week 9)
bone collar formed around the diaphysis because osteoblasts secrete the matrix
chondrocytes in the middle of this bone collar die, it is called the primary ossification centre, hole is formed and tissue calcifies
cartilage calcifies in the centre, cavity develops
cont.
periosteal bud (hole) enters the cavity and spongy bone is formed in the middle
secondary ossification centres appear in the epiphysis (growth on ends), same events except the hole is not made
at birth
hyaline cartilage remains in two places: epiphyseal plate and articular cartilages
post natal bone growth
the epiphyseal plate does not change sizes because new cartilage forms on the epiphyseal side and then chondrocytes become bone or die on the diaphysis side
epiphyseal growth plate
resting zone:
- chondrocytes are resting
proliferation zone:
- cartilage cells undergo mitosis
- fresh chondrocytes, estrogen stimulates
hypertrophic zone:
- older cartilage cells enlarge
calcification zone:
- matrix becomes calcified, cartilage cells die, the matrix begins to deteriorate
ossification zone:
- blood vessels bring osteoclasts and degrade the calcified matrix and osteoblasts secrete new bone matrix, medullary cavity grows
when does it stop?
puberty: low levels of oestrogen activate growth spurt
near the end of adolescence: chondroblasts divide less often
epiphyseal plate thins
high levels of estrogen causes epiphyseal plate closure: epiphysis and diaphysis fuse
bone lengthening ceases
females: 18 yrs
males: 21 yrs
bone remodelling occurs
- bone resorption (breakdown) done by osteoclasts
- osteoclasts bind bone and seal edge, secrete H+ and lysosomal enzymes and the material is endocytose and absorbed by blood, then osteoclast dies
- bone deposition (production) done by osteoblasts
- osteoblasts secrete the ECM called osteoid (collagen)
- collagen binds calcium and phosphate ions and forms crystals thus more minerals/hydroxyapatites
- osteoblasts get trapped thus osteocytes form
bone disorders
- Imbalances between bone deposit and bone resorption underlie nearly every disease that affects the human skeleton.
Three major bone diseases:
- Osteomalacia and rickets
- Osteoporosis
- Paget’s disease
osteomalacia (called this in adults)
- Bones are poorly mineralised
- Osteoid is produced, but calcium salts are not adequately deposited
- Results in soft, weak bones
- Pain upon bearing weight
rickets (osteomalacia of children)
- Results in bowed legs and other bone deformities because bone ends are enlarged and abnormally long
- Cause: vitamin D deficiency or insufficient dietary calcium
osteoporosis
- is a group of diseases in which bone resorption exceeds deposition
- Matrix remains normal, but bone mass declines
- Bones become porous and light to due the absence of density
osteoporosis risk factors
- most often aged, postmenopausal women, affect 30% of women aged 60–70 years and 70% by age 80
- estrogen plays a role in bone density, so when levels drop at menopause, women run a higher risk
- men are less prone due to protection from the effects of testosterone
osteoporosis treatment
Traditional treatments include:
- Calcium
- Vitamin D supplements
- Weight-bearing exercise
- Hormone replacement therapy: slows bone loss but does not reverse it and is controversial because of the increased risk of heart attack, stroke, and breast cancer
