1. BONE
PHYSIOLOGY,METABOLISM
AND BIOMECHANICS:
( part 1):
PRESENTED BY : KIRTI AGRAWAL
J.R.1
DATE: 24-10-2013

2. INDEX:
 Historical perspective
 Ca metabolism
 Ca Homeostasis
 Ca conservation
 Bone modeling and remodeling
 Biomechanics( mechanostat theory)
 specific assessment methodology
 A genetic aspect( role of RANK , RANKL and OPG
protien)
 Types of bones

3. HISTORICAL PERSPECTIVE:
IN 1947, the first modern text of bone anatomy was given by WIEMANN
and SICHER
REMODELING OF MINERALIZED
TISSUE ,PART 1 : THE FROST
LEGACY……….seminar in
orthodontics
IN 1960, MODERN PHYSIOLOGIC CONCEPT OF BONE WAS GIVEN BY HAROLD
FROST

4. INTRODUCTION:
 99%= bone+ teeth
 1% = outside of skeletal
 Dietary requirements:
Adult: 800 m.g/ day
Women during pregnancy: 1.5 g/ day
Children: .8 - 1.2 g/ day
Infant: 300- 500 mg/ day

5.  Sources: milk, bean , leafy vegetables,fish,
cabbage, egg yolk
 Absorption: duodenum

6. FACTORS PROMOTING Ca
ABSORPTION:
 VITAMIN D ( Ca binding protien)
 Parathyroid hormone
 Low( acidic)pH.
 Lactose
 Amino acid lysine and arginine

7. FACTORS INHIBITING THE Ca
ABSORPTION:
 Dietary phosphate( ideal Ca / po4 = 2: 1 )
 Free fatty acid( insoluble Ca soap)
 High Ph
 High content of dietary fibers

8. BIOCHEMICAL FUNCTION:
 MUSCLE CONTRACTION( activate ATPase ,
increases the interaction between actin and
myosin).
 BLOOD COAGULATION( factor IV)
 NERVE TRANSMISSION
 MEMBRANE PERMIABILITY
 ACTIVATION OF ENZYME( lypase, ATPase, )
 Ca as the intracellular messenger
 Facilitate the release of IN SULIN , PTH,
CALCITONIN)

9. Muscle contration:

10. Blood cougulation:

11. Neuro transmission:

12. PLASMA CALCIUM LEVEL:
 9- 11 mg/dl

13. CALCIUM HOMEOSTASIS:
 It is the process by which mineral equilibrium is
maintained
Instantaneous regulation
Short term control
Long term regulation

14. Instantaneous(rapid)regulation:
 Selective transfer of Ca ions into and out of
bony fluid in few seconds.
 Process:
Decrease in serum Ca level
Stimulation of PTH hormone
PTH enhances the transport of calcium ions
from bony fluid into osteocytes and bone
lining cells

15.  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)

17. 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
promonocyte precursors.
2) Increases the resorption rate of existing
osteoclast.
3) It suppress the rate at which osteoblast form
bone.

18. LONG TERM REGULATION:
 Biomechanical factors( exercise, posture,





habits)
Noncalcific hormones( sex steroid, growth
hormones)
Metabolic mechanism
Geometric distribution
Dictate mass.
Mean age of bone

19. Ca CONSERVATION:
 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.

20.  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
mozzarella cheese
swiss cheese
green leafy vegetables
Calcium carbonate is only 40% Ca( 500 mg of
tablet provides 300 mg of Ca)

21.  Factors inhibiting the Ca conservation:
kidney disease( renal osteodystrophy)
Vit D3 deficiency( Ca binding protien)
Liver disease

22. ENDOCRINOLOGY:
 BIND RECEPTOR at the CELL SURFACE:
peptide hormones( PTH, growth hormone,
insulin, calcitonin)
 BIND RECEPTOR at the NUCLEUS: steroid
hormones( vit D, androgen, estrogen) , it is
lipid soluble and passes through the plasma
membrane.

23. CALCITONIN:
 Secreted by PARAFOLLICULAR CELL of




thyroid gland.
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

24. PARATHYROID HORMONE:
 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
protien

25. ACTION ON BONE:
 It stimulates pyrophosphatase and
collagenase
 Demineralization of bone
 It increases the blood Ca level by resorption
of bone.

26. 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

27. ACTION ON INTESTINE:
 Indirect action
 It increases the intestinal absorption of Ca by
promoting the synthesis of vit D 3

29. CHOLECALCIFEROL:
 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
cell.
It increases the intestinal absorption of calcium and
phosphate
increases the blood calcium level
2) It also increase the Ca uptake by the bone and
promote the calcification and mineralization
.

32. SEX HORMONES:
 ANDROGEN:
1) Increase the musculoskeletal mass
2)Increases load generated by the enhanced
muscle mass.
 ESTROGEN:
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

33.  Estrogen replacement therapy is widely
recommended for Ca conservation and prevention
of osteoporosis in postmenopausal women.

34. BONE MODELING AND BONE REMODELING:
 In bone modeling , independent sites of resorption
and formation change the form ( size and shape)of a
bone.
 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.

35.  Modeling change can be seen in the
cephalometric tracing.
 But remodeling can not be imaged in the
clinical radiograph, it can be apparent only at
the microscopic level.

37. CONTROL FACTORS FOR BONE
MODELING:
MECHANICAL
•
•
•
•
Disuse atrophy<200
Bone maintenance 200to 2500
Physiologic hypertrophy2500to 4000
Pathologic overload>4000
ENDOCRINE
• Bone metabolic hormone: PTH,vit D , calcitonin
• Growth hormone: somatotropin,IGF I , IGF II
• Sex steroid: estrogen and testosterone
PARACRINE
AND
AUTOCRINE
• Variety of local agents

38. CONTROL FACTORS FOR BONE
REMODELING:
METABOLIC
MECHANICAL
• ESTROGEN:increase the
activation frequency
• PTH: decrease the activation
frequency
• <1000μє: more remodeling
• > 2000 μє: less remodeling

39. BIOMECHANICS:
OSTEOB LAST DIFFERENTIATION
Weightlessness
Mechanical loading
+
BONE FORMATION
 Mechanical loading is essential to skeletal
health.
 Remodeling and modeling process are
related to STRAIN HISTORY, which is defined
in MICROSTRAIN(μє)

40. MECHANOSTAT THEORY:
 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)
R>F
2)200μє <Physiologic loading<2500μє
steady-state activity
F=R
Maintenance phase

41. 3) Load exceeding the minimal effective
strain≈2500μє
Hypertrophic increase in modeling
Concomitant decrease in remodeling
R<F
4) Pathologic overload
Strain≥ 4000 μє
Structural integrity of bone is threatened
R>F

43. SPECIFIC ASSESSMENT
METHODOLOGY::
 Mineralized section:
 Polarized light
 Fluorescent label
 Microradiography
 Auto radioghaphy
 Nuclear volume morphometry
 Cell kinetics
 Finite element modeling(FEM)
 Microelectrodes

44. 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
R
F)
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.

49. INTRAVASCULAR AND PERIVASCULAR MECHANISM
OF COUPLING BONE RESORPTION AND
FORMATION:
 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

50.  R:
 Exposure of collagen to extracellular fluid and
Release of inflammatory cytokines(
prostaglandin, interlukin1 ) attracts the T cell
from the circulation to the site of
microdamage.
 T cell produce RANKL, which induce
osteoclast histogenesis.

51.  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
osteoclast.

52.  Mononuclear cells move in and coat the
scalloped resorbed surface with cementing
surface.
 Perivascular osteogenic cell migrate through
the low cell density zone and diffenciate to
the preosteoblast which divide in 2
osteoblast.
 Osteoblast form new bone , filling the
resorption cavity and completing the
turnover process

54. CLASSIFICATION OF BONE
TISSUE:
 WOVEN BONE: it is relatively weak,
disorgnized, and poorly mineralized.
 It is the first bone, forms in response to
orthodontic loading.
 It causes: rapid filling osseous defect
provide initial continuity for fracture
strengthening a bone ,weakened by surgery

56. LAMELLAR BONE:
 It is a strong, highly organized, well mineralized,
and make 99% of adult human skeleton.
 Strength of bone is directly related to mineral
content .
 Formation:
primary mineralization: a mineral component (
hydroxylapatite) is deposited by osteoblast.
Secondary mineralization: crystal growth occurs.

58. COMPOSITE BONE:
 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).

59. BUNDLE BONE( alveolar bone
proper/ lamina dura :
 Functional adaptation of lamellar structure to
allow attachment of tendon and ligament.
 Perpendicular striations is known as
SHARPEY’S FIBERS.
 EXAMPLE: distinct layers of bundle bone
usually are seen adjacent to PDL.