Ossification of bone and disease Flashcards Preview

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Flashcards in Ossification of bone and disease Deck (41):

What is endochondral ossification?

-The replacement of hyaline cartilage template with bone


What is intramembranous ossification?

-The replacement of mesenchyme with bone


Where does intramembraneous ossification occur?

-In the formation of flat bones
-In the widening of long bones


Describe intramembraneous ossification

-Mesenchyme template of flat bones is invaded by osteoblasts from the periosteum
-Osteoid becomes mineralised and forms bone tissue spicules
-These bone tissue spicules develop to form trabeculae which radiate out from a central point which used to be the primary ossification centre


In endochondral ossification of long bones, does all the cartilage get replaced to bone immediately?

-No the epiphyseal growth plates remain to allow development of long bones


Describe endochondral ossification

-Initial cartilage model in embryo
-Collar of periosteal bone appears at the shaft
-Central cartilage calcifies, nutrient artery penetrates supplying osteogenic cells, primary ossification centre formed
-(postnatal) Medulla becomes cancellous, cartilage forms epiphyseal growth plates and epiphyses develop secondary ossification centres
-(pre-puberty) Epiphyses ossify and growth plates continue to move apart, lengthening bone
-(mature) Epiphyseal growth plate replaced by bone, articular cartilage remains


Describe how growth occurs at the epiphyseal growth plates (think zones)

-Zone of reserve cartilage
-Zone of proliferation-> Chondrocytes proliferate, enlarge and secrete matrix
-Zone of hypertrophy-> Chondrocytes become very large
-Zone of calcified cartilage -> Chondrocytes degrade and the matrix calcifies
-Zone of resorption-> Columns of calcified cartilage becomes mineralised forming bony spicules which develop into bone


Can you tell the difference histologically between intramembraneous and endochondral ossification?

-No they are both arranged in the same way with haversian systems


What inheritance pattern is osteogenesis imperfecta?

-Autosomal dominant


What is the cause of osteogenesis imperfecta?

-Mutation in the TI collagen gene


What morphological and mechanical abnormalities can bones show in osteogenesis imperfecta?

-Bones are often thin and bowed/curved with growth retardation
-Bones are highly susceptible to fracture due to the weakened structure of collagen fibres


How is osteogenesis imperfecta treated?

-Orthopaedic devices such as rods being insterted into the medulla


Why does ostogenesis imperfecta have medicolegal importance?

-The recurrent fractures can look like deliberate harm to the child


What is achondroplasia?

-Short-limbed dwarfism


What is the cause of achondroplasia?

-An autosomal dominant point mutation in the fibroblast growth factor receptor gene which results in a gain of function


How does the gain of function of the FGFR gene in achondroplasia result in short-limbed dwarfism?

Stops the action of the growth plates by:
-Decreased endochondral ossification
-Inhibited proliferation of cartilage in growth plates
-Decreased cellular hypertrophy
-Decreased cartilage matrix production


Can you be homozygous in achondroplasia?

-No it is fatal


What is the result of excessive growth hormone before puberty?



How does excessive GH cause gigantism?

-Promotion of epiphyseal growth plate activity


What is the result of excessive GH in an adult?

-Acromegaly (widening of bone through increased periosteal growth)


What is the result of decreased GH before puberty?

-Pituitary dwarfism


What is the most common cause of altered GH levels?

-Benign pituitary tumour (adenoma)


How do sex hormones influence growth?

-Influence the development of ossification centres
-Control pubertal growth spurt


What is the result of excessive sex hormones in puberty?

-Retards bone growth due to early closure of the epiphyseal growth plates


What is the result of deficient sex hormones in puberty?

-Prolonged bone growth and tall stature as epiphyseal growth plates persist till later in life


What is the cause of cretinism?

-Untreated thyroxine deficiency during development


Can thyroxine deficiency damage be reversed in neonates?

-Yes with prompt administration of thyroxine within a time-window


What is rickets?

-A childhood bone disease characterised by soft bones due to lack of vitamin D


What are the characteristics of rickets?

-Insufficient calcium deposition for rigidity
-Soft and malformed bones
-Distortion of the skull bone (bossing)
-Enlargement of the costochondral junctions in ribs


What is the cause of osteomalacia?

-Lack of calcium or vitamin D in adults


What are the common causes of osteomalacia? (what causes lack of vit D)

-Poor diet
-Lack of sunlight
-Intestinal malabsorption
-Liver/kidney damage


What are the common symptoms of osteomalacia?

-Bone pain
-Back pain
-Muscle weakness


What are the characteristics of the trabeculae like in osteomalacia?

-Trabeculae have large amounts of non-mineralised bone (osteoid) making them weaker


What sites are commonly effected in osteomalacia?

-Neck of femur


What is osteoporosis?

-A metabolic bone disease caused by a decrease in bone mass to the point where bone no longer provides adequate mechanical support


What is the cause of decreased bone mass in osteoporosis?

-Enhanced bone resorption relative to deposition


Why are bones susceptible to fracture in osteoporosis?

-Increased resorption causes thin traneculae, making them more prone to fracture


Why is osteoporosis associated with age?

-Outer surfaces of trabeculae are constantly remodelled, with ageing the resorption bays formed by osteoclasts are incompletely filled


What are the two types of postmenopausal causes of osteoporosis?

-T1-> Increased osteoclast activity due to oestrogen withdrawal
-T2-> generally occurs over 70 due to attenuated osteoblast function


How do genetic factors play a role in osteoporosis risk factors?

-Bone density is higher in black races


Why can lack of exercise be a risk factor for osteoporosis?

-If the bones are immobilised there is an acceleration of bone loss