Osteoporosis Flashcards by Kanxa Shah

What are osteoprogenitor cells

precursors for othe bone cells
undifferentiated cells
can divide to replace themselves
found in inner layer or periosteum and endosteum

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What are osteoblasts

builder cells
secrete collagen and other matrix components
from mesenchymal stem cells
secrete mand mineralise osteoid
some control over osteoclasts–> building and reabsorbing needs to be balanced

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What do mesenchymal cells differentiate into

osteoblasts, chondrocytes, myocytes, adipocytes

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What are osteocytes

mature bone cells located in lacunae (area surrounding an osteoblast bacomes calcified and results in osteoblast becoming encapsulated
Carry out daily maitenance of bone, nutrients and removal of wastes
Maintain mineral concentration of matrix
Direct the timing and location of remodelling

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What are osteoclasts

Reabsorb bone and release calcium into blood stream
Work at surfaces such as endosteum
From hematopoietic precursors (stem cells that are precursors for blood cells)

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When do you reach PBM/PBD

approx 30yrs

after 30yrs, reabsorption>formation

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What role does collagen protein play in bone strength

Collagen proteins provides tensile strength= able to twist and bend without breaking

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What role does mineralised osteoid play in bone strength

calcium gives compressive strength

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Cells with mesenchymal cells origin

Structural/muscle cells
Osteoblasts
chondrocytes
fibroblasts
adipocytes
muscle cells
due to same origin, they produce the same cytokines and colony stimulating factors as fibroblasts--> hence build bone/muscle

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Cells with hematopoietic cells origin

Blood cell line
Monocytes
macrophages
osteoclasts
due to same origin, they produce the same cytokines which are destructive--> stimulating osteoclastic activity

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What is the time frame within which osteoblasts and osteoclasts work

osteoblasts= take months to produce new bone

osteoclasts=take weeks to reabsorb

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What influences the difference in PBM b/w individuals

Activity
nutrition
Sunlight
Hormones

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What is osteoporosis

The failure to reach optimal PBM as a result of bone reabsorption > bone formation
Normal mineralisation occurs, but decreases bone mass and decreased bone quality–> predisposing it to #’s

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What type of disease is osteporosis

Progressive

common and systemic

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What is the epidemiology of OP

Elder white women most common
Majority of cases affect women
Risk increases with age
Asia>white>black

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What are the predisposing factors for OP

Genetics–> determines about *0% of PMB
decreased physical activity (sedentary lifestyle)
decreased vitamin D intake and calcium intake
Oestrogen and androgen deficiency (postmenopausal women at higher risk of OP, prevented with oestrogen supplement)
Increased parathyroid hormone level or function

How does parathyroid hormone affect calcium levels in blood

Parathyroid hormone promotes mobilisation of calcium from bone to blood, hence increased parathyroid hormone decreased calcium in bone, which results in softening of bone

What is primary juvenile OP

Occurs b/w 8-14yrs
normal gonadal function
abrupt bone pant and/or # following trauma
Condition usually goes away spontaneously, although early diagnosis is important to protect child’s spine

what is the cause of primary OP

idopathic hence no know cause–> occurs spontaneously

What is postmenopausal primary OP

Primary OP–> type I
Accelerate loss of bone post menopausal
Occurs as a result of oestrogen deficiency
Thin, white, sedentary smoker female at greatest risk
(sedentary affects PMB and wolffs law; smoking has toxins which cause inflammation)
Brest feeding-> lose calcium and hence reduced bone mass
females lose 30-40% cortical and 50% trabecular bone in their lifetime–> hence trabecula will contribute 50% less to weight
generally takes 10yrs post menopause for effects to start showing

What is senile OP

Primary OP–> type II
Age associated bone loss and calcium deficiency
Hence deterioration of bone structure
Decreased activity–> therefore decreased stress on bones (Wolffs law)

What is secondary OP

OP as a result of an underlying drug/deficiency or disease

What are genetic underlying causes of secondary OP

cystic fibrosis

Hypogonadal states

what are endocrine causes of OP

Acromegaly--> disorder where pituitary produces too much growth hormone
Oestrogen deficiency
Diabetes mellitus
Hyperparathyroidism
Hyperthyroidism

What are chronic inflammatory conditions of secondary OP

``` AS RA SLE--> systemic lupus erythematosus (autoimmune, affects skin, joints kidneys brain and other organs) Alcoholism Depression Emphysema Kidney disease--> reabsorbs calcium Pregnancy/lactation ```

What sort of deficiences contribute to OP

``` Malabsorption Malnutrition Calcium Magnesium Protein Vitamin D ```

How does celiac disease affect OP

``` An autoimmune disease immune response to eating gluten creates inflammation damages small intestine lining prevents absorption of some nutrients (e.g. Ca) associated with diabetic pts ```

How will OP present clinically

Asymptomatic Usually silent and not clinically apparent till well advanced or spontaneous # Small stress will cause # Pain in thoracic and lumbar--> usually as a result of vertebral #'s caused by loss of beams (trabeculae) Height loss and spine deformity--> kyphosis, lordosis, kyphoscoliosis

What are some common # risk sites

NOF wrist vertebrae WB exercises and diet help in prevention

How can OP be identified from x-rays

not apparent in x-rays till 30% bone mass gone thin cortices--> loss of cancellous bone vertebral bodies--> anterior wedging and #

Changes in vertebrae from OP

WB in vertebral body is longitudinal forces Greater loss of beams therefore less support for compressive forces--> only left with struts which break from longitudinal forces causing them to collapse and hence #

What is the oestrogen independent mechanism of OP

Parathyroid hormones regulates calcium physical stress on bone vitamin D intake/synthesis calcium intake

What are oestrogen dependent mechanisms of OP

Menopause--> decrease in oestrogen osteoblasts/clasts/cytes--> all have oestrogen receptors oestrogen moderates osteoclast production, activity and apoptosis (keeps osteoclasts under control) hence decreasedoestrogen = increased osteoclast production and activity (also prolonged survival of osteoclasts) oestrogen also affects bones indirectly through cytokines and local growth factors which have a 'turn-off' effect on osteoblasts and osteoclasts

Affect of exercise on OP

Works/benefits only when regular exercise | Spinal density is shown to increase by 4% in exercisers

What is the final common pathway of bone reabsorption

RANKL-RANK (OPG System)

What is RANKL

RANKL= recetor activator of nuclear factor-Kappa B Ligand--> a cytokine produced by osteoblasts and activated by T cell lymphocytes RankL is moderate by estrogen

What is RANK

Receptor Activator of Nuclear factor-kappa B--> on osteoclasts

What is OPG system

Osteoprotegerin system OPG secreted by stromal cells and osteoblasts a soluble decoy receptor Receptor inhibits RANK-RANKL by binding and sequestering RANKL Takes RANKL receptor spot for RANKL binding to RANK therefore blocking or decreasing bone reabsorption cycle, therefore more OPG promotes bone formation

Explain the RANK-RANKL pathway/process

RANKL binds to RANK expressed on osteoclasts and osteoclast precursors to promote osteoclast differentiation Increased RANKL results in recruitment of higher numbers of preosteoclasts as well as increased activity, vigor and lifespan of mature osteoclasts osteoporotic menopausal changes= increased bone turnover as a remodelling imbalance with increased bone reabsorbing osteoclast activity with pro-inflammatory cytokines and decrease bone forming osteoclast activity