I have described most of the things related to bone physiology so you can take the important things to stduy what you think from this seminar.

2. PRESENTED BY –
DR. PARAG S. DESHMUKH

3. CONTENTS
•
Introduction
•
Function
•
Classification of bone
•
Bone composition
•
Bone morphology
•
Bone ossification
•
•
•
Bone physiology
Conclusion
Refrence

4. INTRDUCTION

The Adult human skeleton has a total of 206 bones,
excluding the sesamoid bone.
AUDITORY 6
206
BONES
APPENDICULAR SKELETON
126

AXIAL 74
Each bone constantly undergoes modeling during
life to help it adapt to changing biomechanical
forces as well as remodeling to remove old,
microdamaged bone and replaced it with new,
mechanically stronger bone to help preserve bone
strength.

5. Functions of Bone
Supports & protects soft tissues
Store minerals (Ca & P) – mineral homeostasis
Blood cell production (hemopoiesis) in red bone marrow.
Energy storage -- yellow bone marrow
Buffering action – buffers blood by
absorbing or releasing alkaline salts
.
Detoxification – Bones can store heavy metals
and foreign elements, removing them from
blood and reducing there effects on other
organs.

6. Bones are Classified based on shape and structure

8. Based on location
AXIAL
SKELETON
APPENDICULAR
SKELETON
ACRAL
SKELETON
• Bones of skull, vertebral column, sternum
and ribs
• Bones of pectoral griddle, pelvis gridle
and limbs
• It‟s a part of appendicular skeleton and
includes bones of hands and feets.

9. Gross structure of long bones
Articular cartilage = covers joint surfaces,
reduces friction and absorbs shock
Epiphysis : End of long boes.
Metaphysis = area between epiphyses & diaphysis
includes epiphyseal plate in growing bones
Diaphysis = Shaft of long bones.
Medullary cavity = marrow cavity
Physis = epiphyseal growth plate

10. • Endosteum =
lining of marrow
cavity
• Periosteum = tough
membrane covering bone
 Fibrous layer: Fibrous and
madeup of dense irregular CT
 Osteogenic layer: contains
many osteoblasts & blood vessels
that nourishes bone

11. TYPES OF BONE TISSUE
 Based
on texture of cross
sections

Compact bone(dense bone or
cortical bone)

Spongy bone(trabecular bone,
cancellous bone)

12. Cortical bone
Represents 80% of skeletal mass
• Has slower turnover rate and high resistance to bending and torsion
Contains series of adjacent and overlapping bulls eye formations
known as, haversian system or osteon.
Between each osteons are interstitial lamellae(concentric layer of
mineralized bone)
Haversian canals communicate with medullary cavity through spaces in spongy
bone and with the surface of bone by oblique or transverse channels called as
VOLKMAN‟S CANAL.

14. Compact Bone

15. Haversian system / Osteon

16. SPONGY BONE
Located along the epiphyses of long bones
Site of Erythrocyte (RBC) formation
Collagen fibers are not arranged in concentric rings. But the lamellae form
rods called TRABACULAE. No Osteons or Haverian Systems are present.
Found in short, flat, irregular bones & epiphyses of long bones. Supports and
protect red bone marrow
It is less dense, more elastic and has a higher turnover rate
Trabeculae follows lines of stresses and can realign if the lines of stress
changes.

17. Trabeculae of Spongy Bone

18. BASED ON MATRIX
ARRANGEMENT

LAMELLAR BONE
(SECONDARY BONE TISSUE)
•
Matur bone with collagen fibers
that are arranged in lamellae
•
In spongy bone lamellae are
arranged parellel to each
other.
•
In compact bone lamellae are
concentrically organized
around vascular canal.

19. WOVEN BONE (PRIMARY
BONE TISSUE)
• It is immature bone, in which
collagen fibers are arranged in
regular random arrays and contain
smaller amounts of mineral
substance and higher proportion
of osteocytes than lamellar bone
• It is temporary bone.
• Eventually gets converted to
lamellar bone.

20. BASED ON MATURITY

IMMATURE BONE (Primary bone tissue)

It is woven bone.

Mature bone(Secondary bone tissue)

It is charectiristically lamellar bone

Almost all bone in adults are lamellar bone

21. Histology of Bone Tissue
Bone: CT of widely-spaced cells separated by matrix
Matrix = 25% water, 25% collagen fibers, & 50%
crystallized mineral salts
4 types of cells in bone :
osteogenic cells
osteoblasts
osteocytes
osteoclasts

22. Matrix
Contains inorganic mineral salts & protein
- mostly hydroxyapatite( calcium phosphate )
- some calcium carbonate, K, Mg
- collagen fibers
Mineral salts deposited in a framework of collagen fibers
- calcification(=mineralization gives bone hardness
)
- collagen fibers give bone great tensile strength
–

23. BONE

Organic Framework
Osteoblasts, osteocytes, osteoclasts
 Collagen
 Other organic molecules


Inorganic Salts
calcium and phosphorus keep bone rigid
 Bone stores minerals and ions for body
functions


24. Non – collagenous organic
components
Osteonectin – Phosphorylated glycoprotein secreted by
osteoblasts, binds to collagen & hydroxyappatite, play a role
in hydroxy appatite crystallization.
Osteocalcin – Glycoprotein synthesized by osteoblasts, binds
hydroxyappatite & Ca, used as a marker of new bone
formation.
Bone proteoglycans biglycan & decorin may bind
transforming growth factor–β (TGF-β).
Bone sialoproteins, osteopontin & thrombospondin mediate
osteoclast adhesion to bone surfaces via binding to
osteoclast integrins.

25. Bone matrix also contains many growth factors,
proteases & protease inhibitors which are secreted by
osteoblasts, often in a latent form.
Transforming growth factor-β (TGF-β), secreted by
osteoclasts as well as osteoblasts, is activated in the
acid conditions of the ruffled border zone of the
osteoclast, & may be a coupling factor for new bone
formation at resorption site.

27. Osteoprogenitor or Osteogenic cells

Appearance

pale staining,

small, spindle shaped

Location



present on all nonresorbing surfaces in
lacunae within bone.
Extends protoplasmic
processes into small
canaliculiin intercellular
matrix.
periosteum and
endosteum
Function
give rise to osteoblasts in
vascularized regions
chondroblasts in avascular
regions

28. Osteoblasts

Appearance





large, nondividing
cells,
eccentric nucleus,
basophilic cytoplasm,
cytoplasmic
processes
Function


synthesize and
secrete organic
constituents of bone
matrix (osteoid)
aid in calcification

29. Osteocyte

Appearance



smaller and less basophilic
than osteoblast,
have interconnecting
processes
Function


keeps bone matrix in
good repair
release calcium ions
from bone matrix when
calcium demands
increase

30. Osteoclasts

Appearance




multinucleated,
non-dividing cells,
acidophilic.
Have a ruffled
border and a
clear zone on
front of
resorption side.

Origin


From blood
monocytes/
macrophages
Function



move around on
bone surfaces,
resorbs bone
matrix
Focal
decalcification and
extracellular
digestion by acid
hydrolases and
uptake of digested
material

32. Blood & Nerve Supply of Bone

33. BONE FORMATION
(OSSIFICATION)
•
. It is a process of formation of bone and it
includes proliferation of collagen and
ground substance with subsequent
deposition of calcium salts.

Two types
 Intramembranous
 Endochondral
ossification
ossification

35. INTRAMEMBRANOUS
OSSIFICATION

It is the direct laying down of bone into the
primitive connective tissue(Mesenchym).

It results in formation of cranial bones of the skull
and the clavicles

All bones formed this way are flat bones

It is also an important process during natural
healing of bone fractures

36. Stages of Intramembranous
Ossification

37. Stages of Intramembranous
Ossification

38. Stages of Intramembranous
Ossification

39. Stages of Intramembranous
Ossification

40. Endochondral Ossification

Results in the formation of all of the rest of
the bones

Begins in the second month of
development

Uses hyaline cartilage “bones” as models
for bone construction

Requires breakdown of hyaline cartilage
prior to ossification

41. 1. Development of
Cartilage Model

Mesenchyme forms
cartilage model of bone
during development
 There is an aggregation of
mesechymal cells
 Mesenchymal cells differentiate into
chodroblasts.
 These chondroblast secret hyaline
cartilage matrix

42. 2. Growth of Cartilage
Model
Cartilage grows by both :
 interstitial (mostly in length)
 Appositional(mostly in width)
 Sometimes during growth of cartilage model some of
Inner perichondral cells gives rise to osteoblast instead of
chondroblast (as a result fomer perichondrium is now
called the periosteum).
 Newly formed osteoblast secret osteoid forming bone
collar around cartilage model.

43. 3. Development of Primary
Ossification Center
Chondrocytes differentiate and become hypertrophic.
Then it deposits mineralized matrix.
Cartilage calcification is initiated by matrix vesicles
Calcified matrix is partially resorbed by osteoclast.
After resorption osteoblast differentiate into this area
forming woven bone layer.
Blood vessels enter in this area.
And penetrate bone to allow seeding of bone marrow.

44. 4. Development of the
Medullary ( Marrow) Cavity
Osteoblasts deposit matrix
over calcified cartilage
form trabeculae of spongy
bone
Osteoclasts form medullary
cavity

45. 5) Development of Secondary
ossification centre

46. Formation of Articular Cartilage &
Epiphyseal Plate
6.
• Cartilage on epiphyses remains as
articular cartilage
• Epiphyseal (growth) plate also remains
as cartilage

47. -
source of interstitial growth

48. 4 Zones of Epiphyseal Plate:
Zone of resting cartilage
Zone of proliferating cartilage
Zone of hypertrophic cartilage
Zone of calcified cartilage

50. Zone of resting cartilage
anchors growth plate to bone
Zone of proliferating cartilage
rapid cell division (stacked coins)
Zone of hypertrophic cartilage
cells enlarge & remain in columns
Zone of calcified cartilage
thin zone of mostly dead cells
osteoclasts remove matrix
osteoblasts & capillaries build bone over
calcified cartilage

51. Factors Affecting Bone
Growth
Nutrition: need adequate levels of minerals
& vitamins

- Ca & P for bone growth

- vitamin C for collagen synthesis

- vitamins K & B12 for protein synthesis
Need adequate levels of specific hormones

- insulinlike growth factor ( IGF) needed during childhood

- promotes cell division at epiphyseal plate

- also need hGH, thyroid (T3 & T4) , & insulin

- sex hormones needed at puberty (estrogen &
testosterone):

- stimulate growth & male/female skeletal modifications

52. BONE PHYSIOLOGY
 Eugene
Roberts referred
orthodontists as craniofacial bone
specialist and hence torough
knowledge about bone
physiology will help us to treat
patients more effectively and
efficiently.

53. BONE REGULATORS
ENDOCRINE REGULATORS:
PTH harmone
Calcitonin
Vitamin D
Vitamin A
Estrogens
Androgens

54. Growth factors
Paracrine
regulators
Autocrine
regulators
Neurotransmitters
• Bone morphogenetic
protein(BMP)
• Insulin-like growth factors
• Transforming –growth factors
• Platelet derived growth factor
• Fibroblast growth factor
• RANKL (produced locally)
• OPG
Produced intracellularly.

55. WOLF‟S LAW
Wolff's law is a theory developed by the German anatomist
and surgeon Julius Wolff (1836–1902) in the 19th century
that states that
Bone reacts to mechanical functional stress through an
adaptive process resulting in a change of its external and
internal architecture to better withstand this stress.
If loading on a particular bone increases, the bone will
remodel itself over a period of time to become stronger to
withstand greatest strength with least amount of material

56. Mechanotransduction
The remodeling of bone in response to loading is
achieved via mechanotransduction, a process through
which forces or other mechanical signals are
converted to biochemical signals in cellular signaling.
The specific effects on bone structure depends on the
duration, magnitude and rate of loading, and it has
been found that only cyclic loading can induce bone
formation
When loaded, fluid flows away from areas of high
compressive loading in the bone matrix

57. Mechanotransduction
Osteocytes are the most abundant cells in bone and
are also the most sensitive to such fluid flow caused by
mechanical loading
Upon sensing a load, osteocytes regulate bone
remodeling by signaling to other cells with signaling
molecules or direct contact
Additionally, osteoprogenitor cells, which may
differentiate into osteoblasts or osteoclasts, are also
mechanosensors and may differentiate one way or
another depending on the loading condition.[

58. Example:

Weightlifters often display increases
in bone density in response to their training.

Martial artists who strike objects with
increasing intensity (e.g., repeated elbow
strikes), display increases in bone density in
the striking area. This process is
termed cortical remodeling

59. Frost’s Mechanostat Concept
According to the Mechanostat, bone growth and
bone loss is stimulated by the local mechanical elastic
deformation of bone. The reason for the elastic
deformation of bone is the peak forces caused by
muscles
The Adaptation of bone according to the maximum
forces is considered to be a lifelong process. Hence
bone adapts its mechanical properties according to
the needed mechanical function – bone mass, bone
geometry and hence bone strength is adapted
according to the every-day usage / needs.

60. Frost’s Mechanostat Concept
Strain : Deformation per unit length.
It is a dimensionless parameter that is expressed as percent strain or
micro strain.
For instance, when a bone of 100 mm in length is elongated by 2 mm, the
associated strain is expressed as 2% strain, 0.02 strain, or 20,000 micro strain.
Normal=200-2500µ£=0.02%-0.25%
Atrophy=<200µ£=<0.02%
Hypertrophy =2500-4000µ£=0.25%-0.4%
Fatigue failure=>4000µ£=>0.4%
Spontaneous fracture=25000µ£=2.5%
Ultimate strength of bone=25000µ£=2.5%

61. Benninghoff’s Stress Trajectories

It states that lines of orientation of bony
trabeculae corresponds to the pathways of
maximal pressure and tension that bony
trabeculae are thicker in the region where the
stress is greater.

62. 
In Maxilla – frontonasal buttress, malar Zygomatic
buttress,pterygoid buttress

In Mandible - Condyle, Gonial angles, Coronoid process

63. Modeling & Remodeling

The modern physiologic concept of bone remodeling is
largely attributed to Harold Frost.

He differentiate Bone “modeling”(change in shape, size,
and position of bones)
FROM

Bone “remodeling”(coupled turnover sequence)

64. Modeling & Remodeling
Both trabecular & cortical bone grow, adapt & turn over
by means of these two fundamentally distinct
mechanisms
MODELING


Changes the shape,
size, or position of
bones in response to
mechanical loading
or wounding.
Independent site of
resorption & formation
change the form of a
bone.
REMODELING

Physiologic term for

It is a coupled
sequence of catabolic
and anabolic events to
support calcium
homeostasis and repair
/ renew aged or
damaged mineralized
tissue.
internal turnover of a
mineralized tissue,
without a change in its
overall form.

65. Modeling & Remodeling
Modeling
Remodeling
Independent
site of
resorption &
formation
change the
form of a bone
Specific coupled
sequence of
resorption &
formation occurs
to replace
previously
existing bone

66. An example of this process long
bone increases in length and
diameter.
Bone modeling occurs during
birth to adulthood and is
responsible for gain in skeletal
mass and changes in skeletal
form.
Dominant process of
facial growth &
adaptation to applied
loads such as
head gear, RPE,
functional appliance.
Changes can be seen on
the ceph tracings.
After peak bone mass has been
approached, remodeling
becomes the final common
pathway by which bone mass is
adjusted throughout adult life.
Take place at the
same time, but
apparent only at the
microscopic
level .
seen in bone scans and /or
histology.

67. Modeling & Remodeling
Where bone strains
exceed bone's modeling
threshold range,
modeling can switch on
to strengthen the bone.
whereas when bone strains stay
below a lower threshold range,
disuse-mode remodeling can turn on
to reduce whole bone strength by
removing some trabecular and
endocortical bone.

68. Growth factors that regulate bone
remodelling
1.
2.
3.
4.
Insulin – like growth factors (IGF) I & II
Transforming growth factor –b (TGF – b)
superfamily, including the bone
morphogenetic proteins (BMPs)
Fibroblast growth factors (FGF)
Selected cytokines of the interleukin (IL),
tumour necrosis factor (TNF), & colony –
stimulating factor (CSF) families

69. REMODELING:
 GOALS
:
•
It provides a way for the body to alter the
balance of essential minerals by increasing
or decreasing the concentration of these in
serum.
•
It provides a mechanism for the skeleton to
adapt to its mechanical environment
reducing risk to fracture

70. Basic multi-cellular unit
(bmu)
The process of bone resorption and formation are closely
linked within discrete temporary anatomic structures called
as „basic metabolizing units‟(by Frost)later called as basic
multicellular unit
They are readily present in cortical bone but there are
evidence for the same concept in cancellous bone.
The cellular components of a BMU maintains the same
spatial & temporal relationship to each other while moving
through or across the bone.

71. BASIC MULTICELLULAR UNIT

72. REMODELING IN CORTICAL
BONE

Axially oriented cutting & filing cones are the mechanism underlying
internal remodeling of dense compact bone.

The cutting/filling cone has a head of osteoclasts that cuts through
the bone & a tail of osteoblasts that forms a new secondary osteon.

10 osteoclasts dig a circular tunnel
osteoblasts that fill the tunnel .

It requires about 29 days to create resorption cavity (200-250µm in
diameter) and 134 days to refill it .

Remodeling rate 2%-10% per year.
followed by thousands of

73. REMODELING IN TRABECULAR
BONE

Due to much larger surface to volume ratio it is more actively
remodeled than cortical bone, with remodeling rate 10 times
higher .

In trabecular bone 151days ; remodeling here is surface event.

Here osteoclasts digging a trench rather than tunnel and
resulting structure that is formed is called a
hemi
cutting/filling cone .

Remodeling rate 20%-30% per year.

74. Hemi cutting/filling cone in showing the mechanism
for coupling bone resorption to formation

75. Summary of remodelling process
Micro cracks in bone causes
Release of inflammatory cytokines cells(prostaglandins,interleukin)
&exposure of mineralised collagen to extracellular fluid
T- cells produce RANKL which induces osteoclasts histogenesis
RANKL stimulates preosteoclasts from circulatory blood through RANKL receptors to form
osteoclasts
Bone resorption takes place
Growth factors are produced & they stimulate preosteoclasts to produce OPG
Mononuclear cells coat the irregular or scalloped resorbing surface with cementing surface
Perivascular cells migrate & differentiate to preosteoblast
Osteoblasts form new bone

76. Control of Remodeling


Two control loops regulate bone remodeling
Homeostasis in the blood (negative feedback)
Hormonal mechanism maintains calcium

Mechanical and gravitational forces acting on the
skeleton

77. Hormonal Mechanism




Rising blood Ca2+ levels trigger the thyroid to release
calcitonin
Calcitonin inhibits bone resorption and stimulates calcium
salt deposit in bone
Falling blood Ca2+ levels signal the parathyroid glands to
release parathyroid hormone (PTH)
PTH signals osteoclasts to degrade bone matrix and release
Ca2+ into the blood

87. Fracture & Repair of Bone
Healing is faster in bone (vascular) than in cartilage
(avascular)
Repair is still slow due to BV damage
Clinical treatment
- closed reduction: restore pieces to normal position by
manipulation
- open reduction: realignment during surgery

92. Aging & Bone Tissue

The loss of Ca+2 from bone
matrix (demineralization)

may result in osteoporosis

rapid in women age 40-45
( when estrogen levels decrease )

begins after age 60 in men
Decreased rate of protein
synthesis
less collagen production
less growth hormone

brittle bones more likely to
fracture

93. CONCLUSION

Bone physiologic concepts have important clinical
applications in orthodontics & dentofacial
orthopaedics

A detailed knowledge of the dynamic nature of bone
physiology is important for successful orthodontic
practice.

Mechanical adaptation of bone to forces used in
Orthodontics is the physiologic basis of Orthodontics
and dento-facial orthopedics.

94. REFRENCE:
•
Physiology- Robert M. Berne Fifth Edition
•
Physiology- sembulingam
• Anatomy- gray’s anatomy
• Craniofacial growth- Sridhar premkumar
• Wikipedia, the free encyclopedia

95. THANK YOU