( part 1):
PRESENTED BY : KIRTI AGRAWAL
Bone modeling and remodeling
Biomechanics( mechanostat theory)
specific assessment methodology
A genetic aspect( role of RANK , RANKL and OPG
Types of bones
IN 1947, the first modern text of bone anatomy was given by WIEMANN
REMODELING OF MINERALIZED
TISSUE ,PART 1 : THE FROST
IN 1960, MODERN PHYSIOLOGIC CONCEPT OF BONE WAS GIVEN BY HAROLD
99%= bone+ teeth
1% = outside of skeletal
Adult: 800 m.g/ day
Women during pregnancy: 1.5 g/ day
Children: .8 - 1.2 g/ day
Infant: 300- 500 mg/ day
FACTORS PROMOTING Ca
VITAMIN D ( Ca binding protien)
Amino acid lysine and arginine
FACTORS INHIBITING THE Ca
Dietary phosphate( ideal Ca / po4 = 2: 1 )
Free fatty acid( insoluble Ca soap)
High content of dietary fibers
MUSCLE CONTRACTION( activate ATPase ,
increases the interaction between actin and
BLOOD COAGULATION( factor IV)
ACTIVATION OF ENZYME( lypase, ATPase, )
Ca as the intracellular messenger
Facilitate the release of IN SULIN , PTH,
It is the process by which mineral equilibrium is
Short term control
Long term regulation
Selective transfer of Ca ions into and out of
bony fluid in few seconds.
Decrease in serum Ca level
Stimulation of PTH hormone
PTH enhances the transport of calcium ions
from bony fluid into osteocytes and bone
Active metabolite of vit D ( 1,25 DHCC)
enhances the pumping of Ca ions from bone
lining cell into extracellular fluid .
( within the physiological limit , this
mechanism supports the Ca homeostasis
without resorbing bone)
SHORT –TERM CONTROL:
IT takes few minutes through 3 hormones:
PTH, 1,25 DHCC, and calcitonin.
Calcitonin controls the hypercalcimia by
suppressing the bone resorption.
PTH and DHCC :
1) Enhances the osteoclast recruitment from
2) Increases the resorption rate of existing
3) It suppress the rate at which osteoblast form
LONG TERM REGULATION:
Biomechanical factors( exercise, posture,
Noncalcific hormones( sex steroid, growth
Mean age of bone
Preservation of skeletal mass.
Kidney is the primary calcium conservation organ
in the body.
( it excretes the excess phosphate to minimize the
loss of Ca).
Zero calcium balance is ideal metabolic state for
maintaining the skeletal mass,
positive Ca balance occurs during growth period(
near about 10 years)
negative Ca balance occurs after early adult year,
progressively erode bone volume throughout life.
Recommended daily allowance(RDA) of Ca :
1000-1500 mg /day.
Growing adolescents , pregnant and lactating
women, post-menopausal women who are
not receiving the estrogen replacement
theraphy : 1500 mg / day.
Dietary products : milk
green leafy vegetables
Calcium carbonate is only 40% Ca( 500 mg of
tablet provides 300 mg of Ca)
Factors inhibiting the Ca conservation:
kidney disease( renal osteodystrophy)
Vit D3 deficiency( Ca binding protien)
BIND RECEPTOR at the CELL SURFACE:
peptide hormones( PTH, growth hormone,
BIND RECEPTOR at the NUCLEUS: steroid
hormones( vit D, androgen, estrogen) , it is
lipid soluble and passes through the plasma
Secreted by PARAFOLLICULAR CELL of
ACTION: antagonist to PTH
IT increases the calcification by increasing the
activity of osteoblast
It decreases the bone resorption and
increases the excretion of Ca into urine
Thus decreases the blood Ca level
Low Ca level promoted the secretion of PTH.
ACTION: it bind to the membrane receptor
protien on the target cells and activates
adenylate cyclase to liberate cAMP.
Thus increases the blood Ca level.
That promotes the phosphorylation of
ACTION ON BONE:
It stimulates pyrophosphatase and
Demineralization of bone
It increases the blood Ca level by resorption
ACTION ON KIDNEY:
IT promote( the hydroxylation of 25-
hydroxycholecaciferol ) the production of
vit D3 in the kidney
Increases the reabsorption of Ca by kidney
ACTION ON INTESTINE:
It increases the intestinal absorption of Ca by
promoting the synthesis of vit D 3
1, 25 – dihydroxy –cholecalciferol
Active form of vit D( it is not the vitamin at all; it
is a hormone)
ACTION: 1) it increases the synthesis of
CALCIUM BINDING PROTIEN in the intestinal
It increases the intestinal absorption of calcium and
increases the blood calcium level
2) It also increase the Ca uptake by the bone and
promote the calcification and mineralization
1) Increase the musculoskeletal mass
2)Increases load generated by the enhanced
It conserves the skeletal Ca by suppressing the
frequency of bone remodeling.
It protects the female skeletal from bone loss
during childbearing years.
Clinical implication: symptomatic osteoporosis at
menopause( it enhances remodeling activation
slight negative calcium balance
Estrogen replacement therapy is widely
recommended for Ca conservation and prevention
of osteoporosis in postmenopausal women.
BONE MODELING AND BONE REMODELING:
In bone modeling , independent sites of resorption
and formation change the form ( size and shape)of a
Bone modeling is the dominant process of facial
growth and adaptation.
In bone remodeling, a specific, coupled,sequence of
resorption and formation occurs to replace the
previously existing bone.
It is turnover of existing bone.
Modeling change can be seen in the
But remodeling can not be imaged in the
clinical radiograph, it can be apparent only at
the microscopic level.
CONTROL FACTORS FOR BONE
Bone maintenance 200to 2500
Physiologic hypertrophy2500to 4000
• Bone metabolic hormone: PTH,vit D , calcitonin
• Growth hormone: somatotropin,IGF I , IGF II
• Sex steroid: estrogen and testosterone
• Variety of local agents
CONTROL FACTORS FOR BONE
• ESTROGEN:increase the
• PTH: decrease the activation
• <1000μє: more remodeling
• > 2000 μє: less remodeling
OSTEOB LAST DIFFERENTIATION
Mechanical loading is essential to skeletal
Remodeling and modeling process are
related to STRAIN HISTORY, which is defined
Proposed by: FROST
F and R are the modeling phenomenon that
change the shape and form of bone
Reviewed by: MARTIN and BURR
1) sub threshold loading < 200μє
disuse atrophy, decrease in modeling , and
increase in remodeling.( ATROPHY)
2)200μє <Physiologic loading<2500μє
3) Load exceeding the minimal effective
Hypertrophic increase in modeling
Concomitant decrease in remodeling
4) Pathologic overload
Strain≥ 4000 μє
Structural integrity of bone is threatened
A GENETIC ASPECT:
The genetic mechanism is the mean of
controlling the coupling of sequential resorption
and formation process of bone remodeling.
a bone remodeling cycle ( A
completes in 151 days.
Resorption cavity requires 29 days ,which is 200
to 250 μm in diameter and 134 days (≈ 4 months
)to refill it.
INTRAVASCULAR AND PERIVASCULAR MECHANISM
OF COUPLING BONE RESORPTION AND
A: ACTIVATION of inflammation causes the
the expression of nitrous oxide
synthatase, which triggers the localized
remodeling foci at the site of microdamage.
At the compression site, underlining
resorption starts, necrosis of PDL, loss of
cushion action of PDL, CORTICAL BONE
adjacent to it exposed to high peak load
Exposure of collagen to extracellular fluid and
Release of inflammatory cytokines(
prostaglandin, interlukin1 ) attracts the T cell
from the circulation to the site of
T cell produce RANKL, which induce
RANKL activates the RANK receptor of
preosteoclast from the circulating blood.
F: as the bone is resorbed, growth factor
stimulate the preosteoblast to produce OPG
protien which block the RANK receptor of
Mononuclear cells move in and coat the
scalloped resorbed surface with cementing
Perivascular osteogenic cell migrate through
the low cell density zone and diffenciate to
the preosteoblast which divide in 2
Osteoblast form new bone , filling the
resorption cavity and completing the
CLASSIFICATION OF BONE
WOVEN BONE: it is relatively weak,
disorgnized, and poorly mineralized.
It is the first bone, forms in response to
It causes: rapid filling osseous defect
provide initial continuity for fracture
strengthening a bone ,weakened by surgery
It is a strong, highly organized, well mineralized,
and make 99% of adult human skeleton.
Strength of bone is directly related to mineral
primary mineralization: a mineral component (
hydroxylapatite) is deposited by osteoblast.
Secondary mineralization: crystal growth occurs.
CANCELLOUS COMPACTION :It is an
osseous tissue formed by deposition of
lamellar bone within the woven bone
lattice.it is known as PRIMARY OSTEON.
It is intermediary type of bone in the
physiologic response to orthodontic loading.
It is the prominent osseous tissue for
stabilization during early process of
retention( postoperative healing).
BUNDLE BONE( alveolar bone
proper/ lamina dura :
Functional adaptation of lamellar structure to
allow attachment of tendon and ligament.
Perpendicular striations is known as
EXAMPLE: distinct layers of bundle bone
usually are seen adjacent to PDL.