Week 9 Lecture - skeletal health Flashcards
Bone structure, composition and remodelling:
- Trabecular/ Spongy bone: network of cross bridges filled with red bone marrow – found at ends of bone (lighter, more rapidly turnover)
- Cortical/ compact bone: dense, consisting of longitudinal cylindrical structures (osteons) – provide strength
- Outside = periosteal surface (periosteum)
- Inside = endosteal surface (endosteum)
Bone tissue composition:
Ground substance:
- 2/3rd of bone matrix
- Very hard but very brittle
- Minerals, predominantly crystals of hydroxyapatite Ca10(PO4 )6 (OH)2 with other calcium salts and ions
- One of its Function – store and release calcium
Protein:
- 1/3rd of bone matrix
- Most abundant protein type 1 collagen fibres – strong fibre that helps to reinforce the structure
Bone cells:
- Only 2% of bone mass
- Mesenchymal stem cells => => osteoblasts => osteocytes (mature bone cells)
Osteoclasts
Dissolve away old bone
Resorb bone
Osteoblasts
Secrete osteoid (protein) & mature into osteocytes.- form new bone.
Some of these osteoblasts will turn into osteocytes to maintain the bone.
Osteocytes
coordinate the remodelling of bone by signalling
Osteoid
Mineralised to form new bone
Measurement of bone mineral density:
- DXA – BMD: g/cm2 (most common) – provides a 2D image of the bone – tells us how much bone there is in a given area
- pQCT & Clinical QCT- BMD: g/cm3, bone shape – allows 3D assessment
Schematic of BMD according to age
BMD tends to increase to around 30 years old and then declines with age
Higher in men than women
Substantial decline in women after menopause as levels of oestrogen declines – increases bone reabsorption – release more calcium - an imbalance in bone remodelling, resulting in more bone being broken down than formed
BMD can decline by around 1/3rd with menopause
Osteoporosis
“Osteoporosis is a systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue (structural changes e.g., thinning of cortical bone), with a consequent increase in bone fragility and susceptibility to fracture” (WHO 1993)
- May also lose some trabeculae – make bone weaker and more likely to fracture
- Can affect respiratory function
- Result in loss of height
- Hip fractures are very common- they take a very long time to heal
Risk factors for osteoporosis
- Demographic: age, gender (female), family history
- Skeletal: low BMD, bone geometry (shape of the bones)
- Clinical: oestrogen deficient, cancer treatments, glucocorticoid use (supress immune responses), T2DM
- Extra-skeletal: falls risk, low BMI (less padding, less muscle), smoking
Bone shape and bone property:
- Smaller diameter of bone has a larger BMD
- However, larger diameter of bone has greater bending strength
- Wider bones haves a thinner cortical thickness
Cortical thickness in femoral neck fractures cases compared to controls
Cortical thickness is related to fracture risk
Superior part of femoral neck was significantly thinner in people who had a femoral neck fracture
- Increase risk with thinning of superior femoral neck
Mechanostat theory – proposed by HM Frost
Loading bone causing the bone to get fractionally smaller – applying forces to bones causes strains
- Applying greater stresses causes greater strains
Mechanoststat theory suggests this stress is detected by osteocytes and these cause the bones to adapt – signal for more bone to be added. Bone then becomes thicker as an adaptation to increases loading (stress)
- Continued stress (e.g., jumping) will eventually lead to in less strain as the bone is getting stronger
Strains in bones and the consequential bone change:
A lack of loading on the bone causes bone weakening
Increasing the force moderately acting on a bone – we will see an increase in bone mass – more osteons added to strengthen the bone
Extreme overload (adding much greater forces on the bone) can cause microdamage or even fractures
- We want to moderately overload the bone to increase strength. When adapted we moderately increase force again
- Gradual progressive moderate overload is what is required to increasing bone strength
Cellular responses to changed loading:
Osteocytes detect heighten strains to signal to osteoblasts
Modelling – changing the bone shape by forming new bone for strength
Targeting remodelling – when microdamage is present (e.g., from overloading), death of osteocytes may occur – this will signal for the damage parts of the bone to be removed by osteoclasts.
When inactive/ oestrogen deficiency – there can be a loss of osteocytes – and old bone will not be replaced with new bone – gradual loss of bone overtime – trabeculae may become thinner and weaker
With age bones tend to get wider – this greater width gives greater strength in bending to cope with the loss in bone density that can happen with age