Full transcript
0:20hi everyone today we are going to
0:23continue with the rest of the chapter
0:27six which is the bone and skeletal
0:30tissues so let's talk about bone
0:34development the bottom development is
0:47starts with the ossification process so
0:50ossification the word osteogenesis is
0:54v3r refers to the bone formation the
0:58Earth's is referred to the bone the
1:01Genesis is approach to the beginning so
1:05ossification on osteogenesis is the
1:08process of bone tissue formation and the
1:12bone formation the skeleton begins in
1:15the month of the second month of the
1:18development and the postnatal bone
1:21growth occurs until the early adulthood
1:23and after that the bone remodeling and
1:27repair is happening like you know the
1:33formation of the bone skeleton starts
1:36before the 8th while you add the embryo
1:40and the fetus skeleton is made up from
1:43fibrous membranes and hyaline cartilage
1:47and the bone skeleton can be formed in
1:54two ways either endochondral
1:56ossification or the intramembranous
2:00ossification the bone forms by replacing
2:05hyaline cartilage in the endochondral
2:07ossification
2:09and the bones are called cartilage bones
2:12because they replaced this hyaline
2:14cartilage or we call them as
2:16endochondral bones and cartilage bones
2:21are found in most of the skeleton if the
2:27bones formed from the fibrous membrane
2:30then we call them as intramembranous
2:34ossification and these phones are called
2:38membranous bones let's look at these two
2:44ossification one at a time in the end of
2:51corner ossification it forms essentially
2:55in all things inferior to the base of
2:57the skull except the clavicle and this
3:01begins late in the second month of the
3:04development and it uses previously
3:08formed hyaline cartilage models and it
3:11requires breakdown of hyaline cartilage
3:15prior to the ossification in long bones
3:19critically begins at the primary
3:21ossification center which is you find in
3:26the shaft of those long bones what will
3:29happen is first the blood vessels they
3:33infiltrate the pericardium con dreams
3:35the outer surface of the cartilage and
3:38first it convert into the periosteum
3:42so the hyaline cartilage is covered by
3:45the perichondrium the blood vessels they
3:48come in invade it and then due to this
3:51invasion lots of nutritional changes
3:54happen
3:55so the perichondrium now converted into
3:58the periosteum and the underlying
4:02mesenchymal cells stem specialized into
4:07the osteoblasts bone forming cells with
4:13related to the endochondral ossification
4:16five main steps is happening
4:19the very first one will be the bone
4:21color formation and this is happening
4:25around the diabetes of the cartilage
4:28model and the next step would be the
4:32center cartilage in de-emphasis it
4:35starts to calcify the central portion of
4:39these statuses and that relieves to
4:42develop of development of some cavities
4:44into it
4:46next then a periosteal blood is invading
4:51these cavities and the periosteum band
4:53is composed of blood vessels nerves
4:58red marrow osteogenic cells and
5:03osteoclasts so if you remember the
5:06osteoblasts are formed by the
5:08mesenchymal cells and need the
5:11periosteum
5:12but the osteoclast they are now coming
5:15an arrest into the bone so the
5:19periosteal band is the one which carries
5:22that and the period invasion of the
5:24periosteal but leads to formation of the
5:27spongy bone later the dreyfuses it
5:33stands during long days as deposit
5:38unformed deposit calcium's and the
5:42medullary cavity starts to form so the
5:46secondary ossification centers then
5:49starts to appear in the epiphyses I hope
5:52you remember the diaphysis the epiphysis
5:55and the metal phases so the ends are we
5:59call them as the epiphyses the shaft
6:02area is called as the diaphysis so in
6:05the middle as the middle ear cavity
6:07forms then the dreyfuses starts real
6:11long gate and what will happen at the
6:14epiphyses you would find the secondary
6:17ossification centers and this is the
6:20secondary ossification centers
6:22appearance is happening closer to the
6:25birth then it starts to ossify the
6:30hyaline cartilage would only
6:32find then at the outer surface of the
6:35episode is where the articulation
6:38happening with the joint areas or at the
6:42area of the metathesis plate and your
6:48book describes nicely each and every
6:51figure over here you've seen so this is
6:55formation of the bone color and forming
6:59the over here in the diaphysis
7:03the invasion of the periosteum blood the
7:07secondary ossification centers formation
7:10and the ossification is happening at the
7:13epiphyses and leaving the metaphase
7:16plate which is a cartilage plate and
7:18well as the articular cartilage area
7:21that would be at the ends of the
7:24epiphyses over here the other type of
7:30bone formation would be the
7:32intramembranous ossification they begins
7:36within the fibrous connective tissue
7:38membranes and they are formed by the
7:41mesenchymal cells cells so this
7:45intramembranous ossification can be seen
7:48in the cranial bones of the skull which
7:50is their frontal bone parietal bone
7:53occipital bone and the temporal bone and
7:55the clavicular bones four major steps
7:59involved in this ossification the first
8:03the ossification centers are formed when
8:05the missing kind of cells cluster and
8:08become osteoblast and they started to
8:11secrete the osteoid and eventually these
8:14osteon starts to calcify and the woven
8:19bone started to formed when these
8:21osteoid
8:22laid down around the blood vessels the
8:25woman boom is called as the network of
8:27traffic early and osteoid laid down
8:32around the blood vessels resulting
8:34trafficking deformation the outer layer
8:37of this bone then starts to form the
8:39periosteum and later the lamellar bone
8:43replaced the woman
8:45and then turn the red and you would see
8:49the red marrow of parents so here you
8:53would see some ossification centers this
8:56is a fibrous tissue some ossification
8:58centers appear in the fibrous connective
9:00tissue and they started to decrease the
9:03osteoid and then the cells which gets
9:06trapped in between those osteoid they
9:09start from osteocytes and then the
9:14trabecular is formed over here and at
9:18the end you would see find the marrow
9:21cavity and the lamellar bone replaces
9:24the woven bone and then it forms the
9:27periosteum towards the end and you would
9:31see the red marrow appears in the middle
9:33of this figure this is the inter
9:39membranous and in the condor
9:42ossification you would see until but
9:46while you're at the embroiling stage and
9:49the postnatal bones start to see the
9:55growth of the bones so postnatally the
9:59long bones they started to grow
10:01lengthwise my the interstitial growth
10:05and that will leaves to making the bones
10:07law and in the interstitial growth its
10:12originated in different centers within a
10:15structure or an area which is contra
10:17stuff a tissue formed of non rigid
10:19materials so that is white allowed to
10:23elongate the bone in addition bone can
10:29increase its thickness as well through
10:31the appositional growth that is forming
10:35new layers on the surface of the
10:37pre-existing layer so you have to
10:40remember the interstitial growth make
10:43the bones elongated make them long the
10:48appositional growth they make them bones
10:51increase in thickness
10:55in addition won't stop growing during
10:59the adolescence so however some bones in
11:03your body which is some facial bones the
11:05jaw bones awesome nose nasal bones they
11:08continue to grow slowly throughout the
11:11life growth in the length of the long
11:16bones is important for us to know as
11:21well so the interstitial growth requires
11:26the presence of FPC epiphyseal cartilage
11:29in the epiphyseal plate and this
11:32epiphysial plate it maintains some
11:35constant thickness throughout as it
11:40grows so the rate of how it happens is
11:44the rate of cartilage growth on one side
11:47balanced by the bone replacement on the
11:50other because remember the cartilage is
11:54the structure and then it's going to be
11:57awesome find
11:58and calcified and formed into like
12:01strong bones
12:03so the cartilage pay to their
12:05professional plate that you find during
12:08the growth it remains constant and how
12:12it remains constant would be the
12:14cartilage also is going to be formed as
12:17it's going to be the same pace as the
12:21bone it's turned into bones so we have
12:25to see the epiphyseal plate for a second
12:29the epiphyseal plate it consists of five
12:32zones the resting zone the plural
12:35formation zone the hypertrophic zone the
12:39calcification zone and the ossification
12:41zone so as you can see the resting zone
12:47is much more closer to the epiphysial
12:50area of site and as it moves down this
12:55is where the dreyfuses
12:56area so this is much more the
12:58ossification zone is much more closer to
13:01the die pieces the resting zone is much
13:05more closer to the epiphyses area
13:08and in here you would see the plur
13:10iteration so is where the cartilage
13:13cells undergo mitosis increases in
13:16number and then in hypertrophic zone
13:20this all the cartilage cells that starts
13:23to enlarge hypertrophy means enlargement
13:26making it size bigger so these cells
13:29cartilage cells going to be mitotic
13:34cartilage cells and then later in the
13:37calcification zones the main strip
13:40starts to calcify the cartilage cells
13:42die and then the matrix weak institute
13:46deteriorating and blood vessels invade
13:49and that ones cavities and here you will
13:52see in the ossification zone you see the
13:55newborns formation so near the end of
14:02the adolescence the chondroblasts says
14:05they divide less often and at that time
14:08the epiphyseal plate pins and it's
14:11replaced by a bone so epiphyseal plate
14:15coral sure happens when the epiphyses
14:18and type is fished together and there's
14:21no more cartilage in between those
14:23purposes and diathesis once the
14:26epiphyseal plate closed so because of
14:30that in bone lengthening ceases there's
14:33no longer lengthening happen and this is
14:36usually happen and the age of 18 in
14:39females but it's been said that it's
14:43around it will happen around like in
14:46males when they're turned into age 21
14:50lots of our regulations happening during
14:54the bone growth process the major ones
14:57would be the hormonal environment so the
15:00growth hormone played a most important
15:03hormone most important role during the
15:06infancy and the childhood stimulating
15:10the epiphyseal plate activity so that's
15:13why you would see the kids grow faster
15:15during that time and tyroid hormone it
15:19modulates the activity of this growth
15:22ensuring some proper proportion so if
15:26you would remember there's a growth
15:28spurt happening during the times of
15:30puberty time so Chi right hormone is
15:34active at that time we would see kind of
15:36kids suddenly becoming like tall so that
15:41is what is the influence with the
15:43thyroid hormone - it's a growth hormone
15:45on the other hand as sex hormones plays
15:49a role as well
15:51testosterone in males and estrogens in
15:54females and at the puberty not it
15:57promotes the Addyson growth spurt so in
16:00addition to tyroid puberty the sex
16:03hormones play a role - and the end of
16:06growth by inducing epiphysial plate
16:08closure happens excess of our deficits
16:13of any hormones can cause abnormal
16:15skeletal growth the next important topic
16:23would be the bone remodeling so bone
16:26remodeling it consists of both born
16:29deposited and bone resorption it occurs
16:33at the surface of the boat periosteum
16:35and the end ostium and we call them as
16:40remodeling units which we consider them
16:43as packets of adjacent osteoblast and
16:46osteoclast and they coordinate the
16:49remodeling process with related to the
16:54bone deposit the new bone matrix is
16:57deposited by osteoblasts and when you
17:02read the textbook you would find a word
17:04called osteoid sphere it which means
17:07like there are some bands of unrealized
17:10bone matrix which marks the area of new
17:14matrix and the calcification front would
17:17be between the abrupt transition area
17:20between the osteons seam and the older
17:25mineralized bone so you start with
17:27osteoid CM and you have the
17:30calcification front and
17:32you have the older mineralized bone in
17:36the resorption process it is a function
17:40of osteoclasts upon formation by blast
17:43bone resorption by osteoclast they dig
17:48depressions on all grooves as they break
17:50down the matrix and they secrete some
17:53lysosomal enzymes and protein iron
17:56proton ions and that will digest the
17:59matrix and it will convert the calcium
18:02salts into much more soluble forms which
18:06can get absorbed into the blood and also
18:10they perform some phagocytic functions
18:13which demon rise the phagocytic function
18:16in the demon rice matrix and the dead
18:19osteocytes how they do is they digest
18:22these products and trans itust across
18:25the cell and it released into the
18:27interstitial fluid or or and then into
18:31the blood and once this resorption is
18:34complete osteoclast they can undergo
18:37their own cell death which we call as
18:40the apoptosis of the osteoclast is
18:45happening with the involvement of the
18:49parathyroid hormone and the immune
18:52t-cell protein so that is important
18:59remodeling has to be controlled and it
19:02occurs continuously but it is regulated
19:06with genetic factors and some two
19:08control loops the first one would be
19:11under hormonal control the second one
19:14would be in Adi in order to as a
19:17response to the mechanical stress so
19:20with related to the hormone control it's
19:22considered as a negative feedback loop
19:25which controls the blood calcium levels
19:28and of course everybody would know that
19:31calcium is important for many cellular
19:34functions and the body functions nerve
19:37transmission muscle contraction blood
19:40coagulation as well as cell division so
19:4399 percent of calcium you would
19:46find it in the bone and the rest would
19:48be in the blood and people would know
19:54that intestinal absorption calcium
19:56requires vitamin D with related to the
20:01hormonal control parathyroid hormone
20:03produces Parata which is produced by the
20:06parathyroid gland and it is produced in
20:12response to the low blood calcium levels
20:15so when it sends the low blood calcium
20:18levels the parathyroid hormone secretes
20:21by the parathyroid gland and it
20:24stimulates the osteoclast because they
20:27destruct the bone and releases calcium
20:30from the bone and the class get
20:34activated it Reece all of the bone and
20:36calcium is released into the blood and
20:39that will raise the calcium levels and
20:41once you have a particular level the PTH
20:46secretion stops with the homeostasis
20:48balance and the calcium levels falls
20:52back into the normal level the other
20:54hormone involved with the calcitonin
20:57which is produced by the para follicle
20:59cells of the thyroid gland and this is
21:02secreted in response to the high levels
21:05of blood calcium so it's been said that
21:09the effect is negligible in life in the
21:12physiological state of the human beings
21:15but it can be administered externally as
21:18a pharmacological effect when you have
21:21like high blood calcium levels in order
21:24to know where the calcium levels in the
21:26body so in this figure it shows what we
21:29have discussed with related to the
21:31parathyroid hormone when you have low
21:34calcium levels it will secrete this
21:36parathyroid glands there's four glands
21:40behind the thyroid gland and it's
21:43includes to increase PTH parathyroid
21:47hormone and that leads to stimulate
21:50osteoclast that will increase the
21:52calcium back into its normal levels
21:58the other hormonal controls involved
22:01some not popular but important hormones
22:06the leptin which is released by the
22:08adipose tissue and it's regulated this
22:12process by inhibiting the osteoblast and
22:16the serotonin is another important
22:20hormone which you know which is involved
22:24with the neurotransmitters which is a
22:26neurotransmitter which regulates moon
22:28and sleep but it's also interfere with
22:31the osteoblast activity which leads to
22:37in in the calcium level so certain
22:41knowing is meeting the gut and it's
22:43secreted into blood after a meal and it
22:47may inhibit one to know after me so bone
22:50calcium is locked in when new calcium is
22:52flooding into the bloodstream the other
22:58main control mechanism would be the
23:01response to the mechanical stress so
23:03bones reflex stresses and the encounter
23:07bones are stressed when weight fairs
23:09when they do their weight on them or due
23:15to the muscle pulls on them so according
23:19to the world's law what it says is that
23:22bones grow or remodel in response to the
23:25demands which is placed on them so
23:28stress is usually off-center and when
23:32you put weight on to the bone so born
23:35tends to bend and bending leads to
23:40compresses one side and stretch on the
23:43other side and it has been said that
23:46because of this mechanism the diathesis
23:49is going to be thickest where bending
23:52stresses and greatest the bone and also
23:57the bone can be hollow because the
24:00compression and tension they cancel each
24:03other out in the center of the bone so
24:06center of the bone is where you have the
24:09lots of hollow and
24:11okay to have a hollow in the center
24:14because that is not aware that the
24:16weight is being transmitted too much on
24:19to it
24:19so here what it's been shown here is
24:21showing the weight bearing line and it's
24:24been created some tension which is going
24:28away from here and the center and then
24:31the compression also coming into the
24:34center so the tension away and the
24:37compression towards a to cancel out the
24:39tension over here so in these areas that
24:42you would find the hollow but wherever
24:45the tension is goes the vent the bone
24:48tends to be bent and those area is going
24:51to be much more hardened and stronger so
24:55the vault also explains the hardness
24:58handedness sorry handedness which is the
25:01right or left handedness is thought to
25:04be a result in the thicker and stronger
25:06bone of the corresponding upper limb and
25:09the more you use it the more you put on
25:13to the stress and that would be how we
25:16decide the handedness and the curved
25:19bones it's been according to the rules
25:22right says like then the thickest we're
25:24most likely to buckle the trabecular the
25:28wool also explains the trabecular
25:30formation because they form the trusses
25:34are stressed along the line of the
25:36stress and learning large bony
25:39projections occur we are heavy active
25:41muscles going to be attached and that's
25:44why like the weight lifters they have
25:46enormous thickening at the muscle
25:48attachment sites in most use muscles and
25:51the bones of the fetus are people their
25:56bones are very features because their
25:58bones are do not get much stress on the
26:01bones if they're bedridden or in the
26:04fetus you don't get much weight onto
26:06your big boss so how much let's in here
26:12we'll talk about how much mechanical
26:15forces communicate with the cells
26:16responsible for remodeling so it's been
26:20said that deforming a bone produces and
26:23electrical current in the book so since
26:26compressed and stressed regions they are
26:29oppositely be charged and this
26:31electrical signals directory modeling
26:35that would lead to the remodeling
26:38process and the compression or the
26:41tension they changes the fluid flows
26:43within the canonical I and it's thought
26:46that would also stimulate the remodeling
26:49process so all all in all the key
26:53feature that you need to remember is the
26:55homeowner controls they determined
26:57whether and when the remodeling has to
27:00happen and in response to the changing
27:04in the blood calcium levels but the
27:07mechanical stress is the one which
27:09determines where this remodeling needs
27:11to happen so after the remodeling
27:15process you would need to know about
27:18some detail about the bone repair so
27:22where you need to have a repair is when
27:25there is a fracture so fracture is
27:28called as breaks so the renewed most
27:31fractures can result from trauma
27:34because you're highly active and in old
27:37age it's most result from the weakness
27:39of the bone due to the bone thinning
27:41process so fractures we can classified
27:45either all in due to these reasons based
27:50on the position of the bone ends after
27:52the fracture the completeness of the
27:55break or whether the skin is penetrated
27:58if the bone ends retain in normal
28:02position we call them as non-displaced
28:05fractures if the bone ends out of the
28:10normal alignment we call them as
28:12displaced fractures also the bone is
28:18rock broken all the way through we call
28:21it as complete fractures if the bone is
28:25not broken all the way through we call
28:27them as incomplete fractures and if the
28:32skin is penetrated by the bone ends we
28:35call them as open
28:36compound fractures or if the skin is not
28:40penetrated by the bones and we call them
28:43as close or simple fractures so it can
28:47also these fractures can also be
28:49described by the location of the
28:51fracture its external appearance and the
28:54nature of the break so here it will show
28:57some fractures the spiral fractures the
29:01epiphysial fractures the compression
29:04fractures which is happening in the
29:06vertebral body as well as some community
29:10comminuted fractures comminuted so which
29:14means like a lot over here and the
29:19depressed fracture in skull and the
29:21greenstick fracture in the tibia with
29:30related to the fractures you need to
29:31know the fracture treatment and the
29:33repair process so the treatment in it
29:36was the reduction the realignment and
29:39realignment of the broken bone ends so
29:43the reduction would be either closed
29:45reduction where the physician can
29:47manipulate to correct position on the
29:50open reaction you need some surgical
29:53procedures it would keep in the secure
29:56in a positioned by pins or wires and it
30:00secures the ends and of course the
30:04immobilization is needed and it's been
30:07done either by cast or attraction and
30:09time needed to repair depends on the
30:12break the bone break broken drone or the
30:17age of the patient assembles the pastor
30:20some bones they do not hit fastest in
30:24young kids the bone healing is faster
30:27compared to the old age and the repair
30:30mechanism it involves four minute stages
30:33the hematoma formation
30:35fibrocartilaginous callus formation the
30:39bony callus formation and then the bone
30:42remodeling process when you have a
30:47fracture the arteries beta
30:49the blood supply to that area has been
30:52distorted and from the torn blood
30:54vessels the blood is seeping out it
30:57forms a hematoma and due to the influent
31:01release of the chemicals and the
31:03hematoma formation the site is now
31:06swollen and painful and inflamed next
31:11then the capillary starts to grow into
31:15the hematoma from the surrounding blood
31:17vessels the phagocytic cells comes into
31:21the area and they clear cell debris the
31:24fibroblast cells they start to secrete
31:26collagen fibers to spend break and
31:29connect the broken ends over here and
31:32then the fibroblasts cartilage and
31:35osteogenic cells begin the
31:37reconstruction of the bones of creating
31:40cartilage matrix of the repair tissue
31:43and in osteoblasts a chiffon spongy bone
31:47within the matrix so this mass of repair
31:51tissue is called fibrocartilaginous
31:54callus formation by Rustica fiber
31:58blasting water formation a cartilage is
32:01involved all these things
32:03fibrocartilaginous callus formation the
32:08bony callus starts to form within one
32:10week where the new traffic will appear
32:13in the file fibrocartilaginous callus
32:15the callus is then converted into borneo
32:18hard callus of the spongy bone and then
32:22the bony callus formation continues for
32:24about two months until it provides a
32:28firmer union between the broken end and
32:34the bone starts tree model begins during
32:37the bony callus formation and it
32:40continues for several months so excess
32:42material on the diathesis exterior and
32:45within the medullary cavity is going to
32:48be removed the compact bone is laid down
32:51to reconstruct the shaft wall you would
32:54see the compactable you would find at
32:57the periphery and the final structure
32:59resembles the original structure
33:01so responds to the same mechanical
33:05stresses this once again everything in
33:09one picture the next one would be the
33:20bone disorders so imbalance between the
33:22bone deposit and bone resorption
33:25underlying nearly every disease which
33:28affects to our human skeleton so there
33:30are three major bone diseases it's not
33:33the only list but let's talk about these
33:35ones in this lecture the osteomalacia
33:38and the rickets osteoporosis and the
33:42Paget's disease in osteomalacia the
33:47bones are poorly mineralized so osteoid
33:50is produced but the problem is that the
33:53calcium salts are not adequately
33:55depositing in the Ostia as a result they
34:00would get like soft weak bones and the
34:03main symptom of these patients would be
34:06paying occurring upon bearing weight
34:10rickets and austere Mellish just
34:13commonly seen in adults the rickets is
34:16the osteomalacia of children and this
34:19results in both legs and other bone
34:22deformities because the bones ends are
34:24enlarged and they're abnormally long the
34:28causes for rickets would be between D
34:31deficiency or insufficient dietary
34:35intake of calcium the other common bone
34:39disease would be the osteoporosis it's a
34:42group of diseases in which Moon
34:44resorption exceeds the deposit the
34:47matrix remain normal in osteoporosis but
34:51the problem is the bone mass is going to
34:54decline the spongy bone of the spine and
34:57the neck of the femur are the most
34:59susceptible one honorable places so what
35:03implement hip fractures are common with
35:06osteoporosis the risk factors would be
35:10aging postmenopausal women it
35:13thirty percent of women aged 60 to 70
35:17years and seventy percent by age 80 it's
35:20commonly seen in Caucasians thirty
35:23percent are is and women will fracture
35:27bone because of this osteoporosis and
35:30also estrogen prey rolling phone density
35:33so when the levels drop in the menopause
35:35then women's are tend to be in higher
35:38risk and mens of course they are less
35:41prone to do to protection by the effects
35:44of the testosterone because they do not
35:47go under like menopause kind of thing
35:51but if they get treatments for instance
35:55for androgen suppressing drugs then they
36:00are much more prone to osteoporosis as
36:02well in addition petite body
36:05insufficient exercise to stress bones
36:08died poor in calcium protein smoking
36:12hormone related conditions in mobility
36:15and as I mentioned before males with
36:18prostate cancer which takes engine
36:20surpressing dance leads to development
36:23of osteoporosis so the treatments would
36:26be traditional ones calcium vitamin D
36:29supplements weight-bearing exercises
36:32hormonal replacement therapy and HRT is
36:36slowing down the loss but it does not
36:39reverse it so you can slow down the
36:41process and HRT is associated with some
36:45risk with related to heart diseases the
36:50other drugs foster process would be
36:53divided phosphonate bisphosphonate it
36:55decreases the osteoclast activity and
36:58it's partially reversed osteoporosis in
37:02the spine and also selective estrogen
37:04receptor modulators and that will really
37:09prevent the targeting breasts and
37:12nutriskin sirs and the Dinos remap which
37:17is the monoclonal antibody show to
37:20reduce fractures in the men with
37:21prostate cancer and preventing would be
37:25the plenty of taking cast
37:27in early adulthood reduced consumption
37:31of carbonated beverages and alcohol
37:34plenty of weight bearing exercises the
37:38pageant's disease is seen like excessive
37:41and haphazard wound deposit and
37:43resorption and it's almost like
37:47sometimes detected accidentally when you
37:51go to take some x-rays and so on it's
37:55called the panting bone disease and the
37:59very high ratio are spongy to compact
38:01moon and what you would see is reduced
38:04mineralization of your bone and usually
38:07occurs in the spine pelvis female the
38:10skull this rarely occurs before the age
38:12of 40 so it's commonly seen in old age
38:15the cause for this Paget's disease is
38:18unknown but people would think that it's
38:20possibly due to viral the treatment
38:23includes the tell Tony and
38:25bisphosphonates with related to the bone
38:30development the embryonic skeleton
38:33ossifies predictable so fetal age is
38:37easily determined from x-rays or
38:39sonograms most wrong bones begin
38:42ossifying by eight weeks with their
38:45primary ossification centers and all of
38:48them have been developed by the week
38:51twelve then at birth most long bones
38:55ossified except the epiphyses the
38:58epiphysial plays they persist throughout
39:00the childhood and adolescence and endi
39:03age 25 all those they start up completes
39:06ossified and skeletal growth starts to
39:09cease and you would see here the fetal
39:14primary ossification centers at the 12
39:17we it's not like seeing properly the
39:20ossification centers but you would see
39:22most of the skeleton have been formed in
39:25this and with related to the age-related
39:29changes in the pole in children and
39:32adults
39:33$1 cents the bone formation exceeds the
39:36reabsorption so males also tend to have
39:40a greater mass
39:41business agenda play a role as well but
39:44in young adults both is going to be
39:47balanced for formation and the
39:49resorption
39:49is a balanced process and in young
39:54adults but in adults bone resorption is
39:57exceeding the formation so you have to
40:01be careful have to keep your diet
40:05including more calcium and so on the
40:08bone density they change over lifetime
40:11and largely determined by the genitive
40:14and chains for vitamin D cellular
40:17docking determines mass early in life
40:19and osteoporosis risk at the old age the
40:23bone man's mineralization and healing
40:25ability decreased with the age beginning
40:28in the for ticket so you don't find this
40:34decaying or demonization in the bones of
40:38the skull which is good so it's protects
40:40the brain area the bone loss is greater
40:43in the Caucasians and in females so this
40:48is the end of the chapter six and I will
40:54see you in the next neck