Bone physiologynew /certified fixed orthodontic courses by Indian dental academy

Bone Physiology
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

Contents
• Introduction
• Functions of bone
• Structure of bone
• Gross bone histology
• Bone cells
• Bone development
• Nerve and blood supply of bone
• Bone modeling and remodeling
• Applied Clinical Aspect
• Conclusion
• References

INTRODUCTION:
Bone is a specialized mineralized connective tissue consisting
by weight of 33% organic matrix, 28% type I collagen, and
5%

noncollagenous

osteocalcin,

bone

proteins,including
morphogenetic

osteonectin,

proteins,

bone

proteoglycan, and bone sialoprotein.
This organic matrix is permeated by hydroxyapatite
(CalO(P04)6(OH), which makes up the remaining 67% of
bone.

Bone
67%
Inorganic
Hydroxyapatite

33%
Organic
28%

5%

Collagen

Osteocalcin
Sialoprotein
Phosphoprotein
Osteonectin
Bone specific protein


Bone is extremely important to the dental practitioner, insofar
as all his treatment procedures can be successful only if'
the bony support remains intact.
The success of orthodontic treatment is particularly
dependent on the degree of stability that the underlying
bone can maintain.
Furthermore, there is a direct relation between the force
required to move the teeth and the thickness of alveolar
bone

FUNCTIONS OF BONE :
1. Support. The skeleton serves as the structural framework
for the body by supporting soft tissues and providing
attachment points for the tendons of most skeletal muscles.
2. Protection. The skeleton protects many internal organs
from injury. For example, cranial bones protect the brain.
3. Assistance in movement. Because skeletal muscles attach
to bones, when muscles contract, they pull on bones.
Together, bones and muscles produce movement.
4. Mineral homeostasis. Bone tissue stores several minerals,
especially calcium and phosphorus. On demand, bone
releases minerals into the blood to maintain critical
mineral balances (homeostasis) and to distribute the
minerals to other parts of the body.

5. Blood cell production. Within certain bones, a connective
tissue called red bone marrow produces red blood cells,
white blood cells, and platelets, a process called
hemopoiesis. Red bone marrow consists of developing
blood cells, adipocytes, fibroblasts, and macrophages
within a network of reticular fibers.
6. Triglyceride storage. Triglycerides stored in the adipose
cells of yellow bone marrow are an important chemical
energy reserve. Yellow bone marrow consists mainly of
adipose cells, which store Triglycerides, and a few blood
cells. In the newborn, all bone marrow is red and is
involved in hemopoiesis. With increasing age, much of the
bone marrow changes from red to yellow.

STRUCTURE OF BONE:
The structure of a bone may be analyzed by considering the
parts of a long bone. A long bone is one that has greater
lenght than width. A typical long bone consists of the
following parts.
1.

The diaphysis (= growing between) is bone's shaft or
body-the long, cylindrical, main portion of bone.

2. The epiphyses (= growing over) are the distal and proximal
ends of the bone.


STRUCTURE OF A
LONG BONE


3. The metaphyses (sin is metaphysis) are the regions in a
mature bone where the diaphysis joins the epiphyses. In a
growing bone, each metaphysis includes an epiphyseal
plate a layer of hyaline cartilage that allows the diaphysis
of the bone to grow.
4. The articular cartilage is a thin layer of hyaline cartilage
covering the epiphysis where the bone forms an
articulating joint with another bone.
Articular cartilage reduces friction, absorbs shock at freely
movable joints. Because articular cartilage lacks a
perichondrium, repair of damage is limited.

5. The periosteum :(peri- = around) tough sheath of dense
irregular connective tissue that sum the bone surface
wherever it is not covered by articular cartilage. The
periosteum contains bone-forming cells that enable growth
in diameter or thickness, but not in length. It also assists in
fracture repair, helps nourish bone tissue, serves as an
attachment point for ligaments and tendons.
6. The medullary cavity (medulla- = marrow, pith) or marrow
cavity is the space within the diaphysis that contains fatty
yellow bone marrow in adults.
7. The endosteum (endo- = within) is a thin membrane that
lines the medullary cavity. It contains a single layer of
bone-forming cells and a small amount of connective
tissue.

Classification of bone


1. Macroscopic

appearance of cut surfaces
Compact bone - the ivory surface layers of mature bone.
Trabecular bone---the interior of mature bones (also
termed cancellous or spongy bone).
2. Developmental origin
Intramembranous (mesenchymal or dermal bone)formed
by direct transformation of condensed mesenchyme.
Intracartilaginous (cartilage or Endochondral bone)replacing a;preformed cartilage model.
3. Regions of long bones
Diaphysis-intermediate region or shaft.
Metaphysis---developing,juxta.epiphyseal regions of
shaft.
Epiphysis-extremity with a separate center of ossification.

4. Organization of

collagen fibers
Woven bone (coarse-bundled bone), with an irregular
collagen network-includes embryonic bone, isolated patches
in adult bone, and repair tissue in fractures.
Parallel-fibred bone-includes all forms of lamellar bone
5. General microstructure
Non-lamellar bone-includes early woven bone and primary
osteons.
Lamellar bone-almost all mature bone.
6. Disposition of lamellae
Circurnferentia/lamellae (primary lamellae): parallel to
both periosteal and endosteal surfaces.


Osteonic lamellae (secondary lamellae)
concentric lamellae around vascular canals of mature bone.
Interstitial lamellae between osteons.
7. Types of osteon (Haversian system)
Primary osteons-first formed, lamellar or non-lamellar
osteons.
Secondary osteons- concentric lamellae around vascular
canals of mature bone.
8. General terms
Surface bone-usually circumferential lamellae but may
include woven and bundle (Sharpey or extrinsic fiber) bone.
Interstitial bone-between osteons; often lamellar remnants
of secondary osteons but may include woven or primary
osteon fragments.

GROSS HISTOLOGY OF BONE:
Bones have been classified as long or flat on the basis of their gross
appearance.
Long bones include the bones of the axial skeleton (e.g., tibia, femur,
radius, ulna, and humerus).
Flat bones include all the skull bones plus the sternum, scapula, and
pelvis.
Characteristic of all bones are a dense outer sheet of compact bone
and a central medullary cavity. In living bone the cavity is filled
with either red or yellow bone marrow.

Bone is not completely solid but has many small spaces
between its cells and matrix components.
Some spaces are channels for blood vessels that supply bone
cells with nutrients. Other spaces are storage areas for red
bone marrow.
Depending on the size and distribution of the spaces, the
regions of a bone may be categorized as compact or
spongy
Overall, about 80% of the skeleton is compact bone and 20%
is spongy bone.


COMPACT BONE TISSUE:
Compact bone tissue contains few spaces. It forms the
external layer of all bones and makes up the bulk of the
diaphysis of long bones. Compact bone tissue provides
protection and support and resists the stresses produced by
weight and movement.
Compact bone tissue is arranged in units called osteons or
Haversian systems
Blood vessels, lymphatic vessels , and nerves from the
periosteum penetrate the compact bone through transverse
perforating (Volkmann's) canals.
The vessels and nerves of the perforating canals connect with
those of the medullary cavity, periosteum, and central
(Haversian) canals.

The central canals run longitudinally through the bone.
Around the canals are concentric lamellae (rings of hard,
calcified matrix). Between the lamellae are small spaces
called lacunae (= little lakes;), which contain osteocytes.
Radiating in all directions from the lacunae are tiny
canaliculi (= small channels), which are filled with extra
cellular fluid. Inside the canaliculi are slender fingerlike
processes of osteocytes
Neighboring osteocytes communicate via gap junctions. The
canaliculi connect lacunae with one another and with the
central canals.

Osteons in compact bone tissue are aligned in the same
direction along lines of stress.
In the shaft, for example, they are parallel to the long axis of
the bone. As a result, the shaft of a long bone resists
bending or fracturing even when considerable force is
applied from either end.
Compact bone tissue tends to be thickest in those parts of a
bone where stresses are applied in relatively few
directions. The lines of stress in a bone are not static. They
change as a person learns to walk and in response to
repeated strenuous physical activity, such as occurs when a
person undertakes weight training. The lines of stress in a
bone also can change because of fractures or physical
deformity.

The areas between osteons contain interstitial lamellae, which
also have lacunae with osteocytes and canaliculi.
Interstitial lamellae are fragments of older osteons that have
been partially destroyed during bone rebuilding or growth.
Lamellae that encircle the bone just beneath the periosteum
are called outer circumferential lamellae;
those that encircle the medullary cavity are called inner
circumferential lamellae.


SPONGY BONE TISSUE:
In contrast to compact bone tissue, spongy bone tissue does not
contain osteons. it consists of trabeculae an irregular latticework
of thin columns of bone.
The macroscopic spaces between the trabeculae of some bones are
filled with red bone marrow. Within each trabecula are
osteocytes that lie in lacunae.
Radiating from the lacunae are canaliculi. Because osteocytes are
located on the superficial surfaces of trabeculae, they receive
nourishment directly from the blood circulating through the
medullary cavities.

Spongy bone tissue makes up most of the bone tissue of short,
flat, and irregularly shaped bones. It also forms most of the
epiphyses of long bones and a narrow rim around the
medullary cavity of the diaphysis of long bones.
At first glance, the structure of the osteons of compact bone
tissue may appear to be highly organized, whereas the
trabeculae of spongy bone tissue may appear to be far less
well organized.
However, the trabeculae in spongy bone tissue are precisely
oriented along lines of stress, a characteristic that helps bones
resist stresses and transfer force without breaking. Spongy
bone tissue tends to be located where bones are not heavily
stressed or where stresses are applied from many directions.

Spongy bone tissue is different from compact bone tissue in
two respects.
First, spongy bone tissue is light, which reduces the overall
weight of a bone so that it moves more readily when pulled
by a skeletal muscle.
Second, the trabeculae of spongy bone tissue support and
protect the red bone marrow. The spongy bone tissue in
the hip bones, ribs, breastbone, backbones, and the ends
of long bones is the only site of red bone marrow and,
thus, of hemopoiesis in adults.

BONE CELLS:
In bone, separate cells are primarily responsible for the
formation resorption,and maintenance of osteoarchitecture.
1.
Osteogenic cells:
Are un specialized stem cells derived from mesenchyme,
the tissue from which all connective tissues are formed.
They are the only bone cells to undergo cell division; the
resulting

daughter

cells

develop

into

osteoblasts.

Osteogenic cells are found along the inner portion of the
periosteum, in the endosteum, and in the canals within
bone that contain blood vessels.

Osteoblast:
Osteoblasts are uninucleated cells that synthesize both cartilaginous
and noncollagenous bone proteins (the organic matrix, osteoid).
They are responsible for mineralization and are derived from a
multipotent mesenchymal cell. The osteoblast is generally
considered to differentiate through a precursor cell, the
preosteoblast.
Preosteoblasts and, to a lesser extent, osteoblasts exhibit high
levels of alkaline phosphatase on the outer surface of their
plasma membranes. This enzyme, which is used experimentally
as a cytochemical marker, distinguishes the osteoblast from the
fibroblast.
Functionally it is believed to cleave organically bound phosphate.
The liberated phosphate likely contributes to the initiation and
progressive growth ofwww.indiandentalacademy.com
bone mineral crystals.

osteoblast


Osteoblasts secrete, in addition to type I and type V collagen and
small amounts of several noncollagenous proteins (some of
which [the phosphoproteins] are critical to bone
mineralization, a variety of cytokines). These autocrine or
paracrine factors, which include growth factors, help regulate
cell metabolism.
A key factor in the rate of bone cell development is the
elaboration by osteoblasts, their precursors, or both of a
number of growth factors. Osteoblasts secrete several
members of the bone morphogenetic protein (BMP) super
family, including BMP2, BMP7, and transforming growth
factor, in addition to the insulinlike growth factors (lGFI and
IGFII), plateletderived growth factor (pDGFAA), and
fibroblastic growth factor beta.

Under physiologic conditions that support resorption rather
than formation, osteoblasts can be stimulated by
lymphokines (e.g., interleukin 1, tumor necrosis factor
alpha) and by prostaglandins (E2) to produce interleukin 6.
Osteoblasts under the stimulation of interleukin 6 also
produce their own hydrolytic enzymes that aid in
destroying or modifying the unmineralized matrix or
pericellular coating, thus freeing the osteoblast from its
own secreted matrix. This dissociation may be critical
during the initial phases of bone turnover and repair, when
osteoblasts must be able to migrate and proliferate.

The osteoblast and the lining cell support resorption through
hydrolytic enzyme and interleukin6 production.
Osteoprogenitor cells, preosteoblasts, and osteoblasts can
undergo mitosis. Osteoblasts produce large amounts of
type I collagen and small amounts of proteoglycans and
glycoproteins.
The osteoblast modifies the adjacent matrix by removal or
modification of the proteoglycans or glycoproteins. The
osteoblast initiates the mineralization of the matrix by
secretion of several promoters or regulators of
mineralization (primarily phosphoproteins) and by
providing additional inorganic phosphate by the action of
membrane bound alkaline phosphatase.

Osteocyte
As osteoblasts secrete bone matrix, some of them become entrapped
in lacunae and are then called osteocytes.
The number of osteoblasts that become osteocytes varies
depending on the rapidity of bone formation: The more rapid the
formation, the more osteocytes are present per unit volume.
After their formation, osteocytes gradually loose most of their
matrixsynthesizing machinery and become reduced in size. The
space in the matrix occupied by an Osteocyte is called the
osteocytic lacuna. Narrow extensions of these lacunae form
enclosed channels, or canaliculi, that house radiating osteocytic
processes.

Thus osteocytes maintain contact with adjacent osteocytes and
with the osteoblasts or lining cells on the bone surfaces ,the
endosteum, periosteum, and Haversian canals.
Failure of any part of this interconnecting system results in
hypermineralization (sclerosis) and death of the bone. This
nonvital bone is resorbed and replaced during the process of
bone turnover
The functions attributed to osteocytes are that
(a) They probably maintain the integrity of the lacunae and
canaliculi, and thus keep open the channels for diffusion of
nutrition through bone
(b) They play a role in removal or deposition of matrix and of
calcium when required.

Osteoclast:
Osteoclasts are multinucleated nondividing
cells that move around on bone surfaces, resorbing bone
matrix from sites where it is either deteriorating or not
needed.
Compared to all other bone cells and their precursors,
the multinucleated osteoclast is a much larger cell.
Because of their size, osteoclasts can easily be identified
under the light microscope; they are generally seen in a
cluster rather than singly.
The osteoclast is characterized cytochemically by possessing
tartrateresistant acid phosphatase enzyme within its
cytoplasmic vesicles and vacuoles which distinguishes it
from other giant cells and macrophages.

osteoclast

Typically osteoclasts are found against the bone surface,
occupying shallow, hollowed-out depressions, called
Howship’s lacunae that they themselves have created.
At the sites of bone resorption the surface of an osteoclast shows
many folds, which are described as a ruffled membrane.
Removal of bone by osteoclasts involves demineralisation &
removal of matrix.
Bone removal can be stimulated by factors secreted by osteoblasts,
by macrophages, or by lymphocytes. It is also stimulated by the
parathyroid hormone. It is not certain whether osteoclasts are
formed by fusion of several monocytes or by repeated division
of the nucleus, without division of cytoplasm.

DEVELOPMENT OF BONE:
The process by which bone forms is called ossification or
osteogenesis. The "skeleton" of a human embryo is
composed of loose fibrous connective tissue membranes
and pieces of hyaline cartilage, which are shaped like
bones and are the sites where ossification occurs.
These embryonic tissues provide the template for subsequent
ossification, which begins during the sixth or seventh
week of embryonic development and follows one of two
patterns.
The two methods of bone formation involve
1.
Intramembranous ossification
2.
Endochondral ossification

Endochondral Bone Formation:
Endochondral bone formation takes place when
cartilage is replaced by bone. It occurs at the ends of all
long bones, vertebrae, and ribs and at the head of the
mandible and base of the skull. Early in embryonic
development, there is condensation of mesenchymal cells.
Cartilage cells differentiate from these mesenchymal cells,
and a perichondrium forms around the periphery. Rapid
growth of the cartilage anlage ensues-by interstitial growth
within the core of the engage and by appositional growth
through cell proliferation and matrix secretion within the
expanding perichondrium.

As differentiation of cartilage cells proceeds toward the
metaphysis, the cells organize themselves roughly into
longitudinal columns. The longitudinal columns of cells
can be subdivided into three functionally different zones:
- the zone of proliferation,
- the zone of hypertrophy and maturation, and
- the zone of provisional mineralization.
- In the zone of proliferation, the cells (which are small
and somewhat flattened) primarily constitute a
source of new cells. The zone of hypertrophy and
maturation is the broadest zone


In the early stages of hypertrophy, the chondroblasts secrete
mainly type II collagen that forms the primary structural
component of the longitudinal matrix septa.
As hypertrophy proceeds, mostly proteoglycans are secreted.
As the chondroblast reaches maximum size, it secretes type
X collagen, chondrocalcin, and bone sialoprotein, which
together with partial proteoglycans breakdown; create a
matrix environment with the potential to mineralise.


Endochondral Ossification : The essential steps in the formation of bone by endochondral
ossification are:





At the site where the bone is to be formed, the
mesenchymal cells become closely packed to form a
mesenchymal condensation.
Some mesenchymal cells become chondroblasts and lay
down hyaline cartilage.
The intercellular substances between the enlarged
cartilage cells become calcified under the influence of
alkaline phosphatase, which is secreted by the cartilage
cells. The nutrition to the cells is thus cut off and they
die, leaving behind empty spaces called areolae.









Some blood vessels of the perichondrium now invade
the cartilaginous matrix. They are accompanied by
osteoprogenitor cells.
This mass of vessels and cells is called the periosteal
bud. It eats away much of the calcified matrix forming
the walls of the primary areolae, and thus creates large
cavities called secondary areolae, also called medullary
spaces.
The walls of secondary areolae are formed by thin layers
of calcified matrix that have not been dissolved. The
osteoprogenitor cells become osteoblasts and arrange
themselves along the surfaces of these bars, or plates, of
calcified matrix.
These osteoblasts now lay down a layer of ossein fibrils
embedded in a gelatinous ground substance, exactly as
in the intramembranous ossification. This osteoid is
calcified and a lamellus of bone is formed.



Osteoblasts now lay down another layer of the first
lamellus. This is also calcified. Thus two lamellae of the
bone are formed. Some osteoblasts that get caught
between the two lamellae become osteocytes .



As more lamellae are laid down bony trabeculae are
formed. It may be noted that the process of bone
formation in endochondral ossification is exactly the
same as in intramembranous ossification.



In this way formation of new cartilage keeps the pace
with the loss due to replacement by bone. The total
effect is that the ossifying cartilage progressively
increases in size.

Intramembranous Bone Formation:
Intramembranous bone formation occurs directly
within the mesenchyme. Bone develops directly within the
soft connective tissue rather than on a cartilaginous model.
As vascularity increases at these sites of condensed
mesenchyme, osteoblasts differentiate and begin to
produce bone matrix de novo. This occurs at multiple sites
within each bone of the cranial vault, maxilla, body of the
mandible and mid-shaft of long bones.
Once begun, intramembranous bone formation
proceeds at an extremely rapid rate. This first embryonic
bone is termed coarse-fibred woven bone and at first, the
woven bone takes the form of radiating spicules, but
progressively the spicules fuse into thin bony plates.

Intramembranous ossification:
The various stages in intramembranous ossification are
as follows.
 At the site where the membrane bone is to be formed,
the mesenchymal cells become densely packed (a
mesenchymal condensation is formed.)
 The region becomes highly vascular.
 Some of the mesenchymal cells lay down bundles of
collagen fibres in the mesenchymal condensation. In this
way a membrane is formed.
Some mesenchymal cells (possibly those that
had earlier laid down the collagen fibres) enlarge and
acquire a basophilic cytoplasm, and may now be called
osteoblasts.





Under the influence of osteoblasts, calcium salts are
deposited in osteoid. As soon as this happens the layer
of osteoid can be said to have become one lamellus of
bone.
Over this lamellus, another layer of osteoid is laid down
by osteoblasts. The osteoblasts move away from the
lamellus to line the new layer of osteoid. However, some
of them get caught between the lamellus and the osteoid.
The osteoid is now ossified to form another lamellus.
The cells trapped between the two lamellae become
osteocytes.


Blood and nerve supply of bone:
Bone is richly supplied with blood. Blood vessels, which are
especially abundant in portions of bone containing red
bone marrow, pass into bones from the periosteum.
Periosteal arteries accompanied by nerves enter the diaphysis
through many perforating (Volkmann's) canals and supply
the periosteum and outer part of the compact bone
Near the center of the diaphysis, a large nutrient artery passes
through a hole in the compact bone called the nutrient
foramen.
On entering the medullary cavity, the nutrient artery divides
into proximal and distal branches that supply both the
inner part of compact bone tissue of the diaphysis and the
spongy bone tissue and red marrow as far as the epiphyseal
plates (or lines).

Veins that carry blood away from long bones are evident in
three places:
(1)
One or two nutrient veins accompany the nutrient artery
in the diaphysis;
(2)
Numerous epiphyseal veins and metaphyseal veins exit
with their respective arteries in the epiphyses; and
(3)
Many small periosteal veins exit with their respective
arteries in the periosteum.
Nerves accompany the blood vessels that supply bones. The
periosteum is rich in sensory nerves, some of which
carry pain sensations. These nerves are especially
sensitive to tearing or tension, which explains the severe
pain resulting from a fracture or a bone tumor.


Modeling and remodeling
Both trabecular and cortical bones grow, adapt and turnover
by means two mechanisms
In bone modeling:-independent sites of resorption and
formation change the form of a bone
In remodeling:- a specific, coupled sequence of resorption
and formation occurs to replace previously existed bone
the biomechanical response to tooth movement
involves an integrated array of bone modeling and
remodeling.
Bone modeling is the dominant process of facial growth and
adaptation to applied loads such as head gear,RME and
functional appliances
Modeling changes can be seen on cephalometric tracing
but remodeling changes are only apparent at the
microscopic levels

Both modeling and remodeling are controlled by an
interaction of metabolic and mechanical signals


Bone modeling is directly under the integrated
biomechanical control of functional applied loads and
under harmonal influence particularly during periods of
growth and aging.



Remodeling response to metabolic mediators such as PTH
and estrogen is by varying the rate of bone turnover.



Bone scans with 99te biphosphate [bone marker] indicated
that the alveolar processes, but not the basilar mandible,
have a high remodeling rate.

Control factors for bone modeling


Mechanical:( peak load in micro strain)
disuse atrophy : less than 200 %deformation 10-4
bone maintenance: 200-2500
physiologic hypertrophy:2500-4000
pathologic overload:above 4000



Endocrine :bone metabolic harmones :PTH, Vit.D, calcitonin
growth harmones : somatotropin, IGF I & II
sex steroids : testosterone & estrogen


Control factors for bone remodeling


Mechanical :Less than 1000 % deformation 10-4 : more bone
remodeling
More than 2000 % deformation 10-4 : less bone
remodeling



Metabolic :PTH : increased activation frequency
estrogen : decreased activation frequency


Effect of hormones:

During childhood the most important hormone that stimulates
bone growth are the insulin like growth factor which is produced
by bone tissue it is inturn stimulated by human growth hormone.
At puberty the hormones known as sex steroids i.e estrogen and
androgens secreted by the adrenal glands. They are responsible
for the sudden growth spurt that occurs during the teenage years.


Parathyroid Hormone has a direct action on adult bone. It is
responsible for maintenance of blood calcium level (10 to
12 mg%).
It has four main sites of action
1.Kidney: Tubular reabsorption of calcium from the
glomerular filtrate and decrease in resorption of phosphate.
2.Bone: Stimulates osteoclastic activity and increases
resorption of bone leading to increased liberation of
calcium and phosphate.
3.Intestine: It increases absorption of calcium from diet.
4.Lactating Mammary Glands: It acts to decrease calcium
secretion.

The removal of osseous tissue during progressive tooth
movement is directly related to
1) bone porosity
2) remodeling rate
3) resorption rate
4) osteoclast recruitment
The osteoclast resorption rate is largely controlled by
metabolic factors mainly the PARATHYRIOD
HARMONE


Effect of Vitamins on bone:
Growth and maintenance of bone depends on adequate
dietary intake of minerals and vitamins.
Vitamin D:
Hypervitaminosis:
small overdose – Aberrant calcification in vessels in kidney
may take place.
Overdose in Excess – Generalized resorption changes may be
seen.
Hypovitaminosis:
In avitaminosis the ingestion of large quantities of calcium
will lead to formation of calcium phosphate in intestine.


Tuomo Kantomaa and Brian K. Hall in 1991 studied the
importance of cAMP and Ca++ in mandibular condylar
growth and adaptation and concluded that calcium is
necessary for maturation of cell . Both calcium and cAMP
play a major role in bone formation .


Vitamin A:
Hypervitaminosis:
Acute violent headaches, vomiting, irritability, and,
occasionally, peeling of the
skin.
Chronic loss of appetite, itching, and painful swellings over
the limbs, hyper-ostosis of the shafts of long bones.
Hypovitaminosis:
Affects: primarily the epithelial structures. In general, it is believed
that over-all bone growth is retarded and that in the later stages of
the disease, endochondral bone growth ceases entirely.
Vitamin C:
Hypovitaminosis:
The pathologic findings in bone can be traced to the failure
of collagen production. A decreased activity of fibro-blasts,
osteoblasts, and odontoblasts, which ultimately affects collagen
production

Methods used to study bones
1.
Mineralized sections.
2.
Polarized light
3.
Fluorescent light
4.
Micro-radiography
5.
Auto radiography
6.
Nuclear volume morphometry
7.
Cell kinetics
8.
Finite element modeling
9.
microelectrodes


Clinical correlation :


1) Intermittent vs. continues mechanics
tooth movement is directly proportional to no.
of hours the force is applied. Even when motivation and
co-operation are optimal,the effectiveness of therapy is in
consistent.
2) Differential anchorage
the density of alveolar bone and the cross
sectional area of the roots in the plane perpendicular to the
direction of tooth movement are primary consideration for
assessing anchorage potential
anchorage value: the volume of osseous tissue that must
be resorbed for a tooth to move a given distance is its
anchorage value

Mandibular molars are difficult to move when compared
to maxillary molars because


Thin cortices and trabecular bone of maxilla offer less
resistance to resorption than the thick cortices and more
coarse trabeculae.



The leading root of mandibular molars being translated
mesially forms bone that is far more dense than the bone
formed by translating maxillary molars


There is change in trabecular pattern of bone in maxilla and
mandible because
 maxilla transforms most of its force to the cranium
 the mandible is subjected to substantial torsion and
flexure caused by muscle pull and masticatory function
 Maxilla is loaded predominantly in compression and there is no
major muscle attachment.
3) Rate of Tooth movement
the rate of tooth movement is inversely proportional to bone
density and the volume of bone resorbed.
maximal rate of translation of mid-root area trough
dense cortical bone is about 0.5 mm per month for the first few
months; the rate then declines to 0.3mm per month until 1st molar
site is closed

The 3 principle variables that determine rate of tooth
movement are
1)Growth
2)bone density
3)type of tooth movement
During growth period there is increase in tooth
movement.
Increase in density slow is the tooth movement
and vicevesra.
Bodily movement is difficult to produce when
compared to tipping movement.


Conclusion:
It is important to understand the details of the physiology of
bone. It is especially necessary to remember that such
factors as hormones, vitamins, age and probably heredity
may influence the resorption of bone.
The success of orthodontic treatment is dependent on


Amount of force applied



Reaction of bone to orthodontic forces



Ultimate stability of bone

So it is necessary to apply optimal forces to particular type of
bone to produce desired results and check for the stability
of the bone once the treatment is complete.

References
1.Oral Histology: Development, structure and function: Ten
Kate; 10th Ed
2.Fundamentals of anatomy and physiology: Tortora; 10th Ed
3. Orthodontics –principles and practice graber vanarsdall 3 rd
edition
4. Principles and practice of Orthodontics by T.M.Graber-3rd
edition
5. Contemporary Orthodontics by Proffit
6. Human physiology- Tortora
7. Guyton and Hall--Human physiology


Thank you
For more details please visit


Bone physiologynew /certified fixed orthodontic courses by Indian dental academy

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (6)

Similar to Bone physiologynew /certified fixed orthodontic courses by Indian dental academy

Similar to Bone physiologynew /certified fixed orthodontic courses by Indian dental academy (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Bone physiologynew /certified fixed orthodontic courses by Indian dental academy