Bone/ dental implant courses

BONEBONE
 INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
Leader in continuing Dental EducationLeader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
 Introduction
 Classification of bone
 Functions of bone
 Division of skeletal system
 Structural anatomy of bones
 Composition of bone
 Osteogenesis
 Physiology of bone
 Disorders of bone
 Bone healing
 Correlation of bone structure & some of itsCorrelation of bone structure & some of its
propertiesproperties

IntroductionIntroduction
 BonesBones are rigidare rigid organsorgans that form part of thethat form part of the
endoskeletonendoskeleton ofof vertebratesvertebrates
 One of the types of tissues that makes up bone is theOne of the types of tissues that makes up bone is the
mineralizedmineralized osseous tissueosseous tissue, also called bone tissue,, also called bone tissue,
that gives it rigidity and honeycomb-like three-that gives it rigidity and honeycomb-like three-
dimensional internal structure.dimensional internal structure.

 Other types of tissueOther types of tissue
found in bones includefound in bones include
 marrowmarrow
 endosteumendosteum andand
 periosteumperiosteum,, nervesnerves,,
blood vesselsblood vessels andand
cartilagecartilage

 AA tendontendon (or(or sinewsinew) is a tough band of) is a tough band of
fibrous connective tissuefibrous connective tissue that connectsthat connects musclemuscle
toto bonebone and is capable of withstandingand is capable of withstanding tensiontension..
 Tendons are similar toTendons are similar to ligamentsligaments except thatexcept that
ligaments join one bone to another.ligaments join one bone to another.
 Tendons and muscles work together and canTendons and muscles work together and can
only exert a pulling forceonly exert a pulling force

 CartilageCartilage is a type of denseis a type of dense connective tissueconnective tissue..
 It is composed of specialized cells calledIt is composed of specialized cells called chondrocyteschondrocytes
that produce a large amount of extracellular matrixthat produce a large amount of extracellular matrix
composed ofcomposed of collagencollagen fibers, abundantfibers, abundant
ground substanceground substance rich inrich in proteoglycanproteoglycan, and, and elastinelastin
fibers.fibers.
 Cartilage is classified in three typesCartilage is classified in three types
 elastic cartilageelastic cartilage
 hyaline cartilagehyaline cartilage andand

DIVISIONS OF THE SKELETAL SYSTEM
REGIONS OF THE
SKELETON
NUMBER OF BONES
AXIAL SKELETON
SKULL
Cranium 8
Face 14
Hyoid 1
Auditery ossicles 6
VERTIBRAL COLUMN 26
THORAX
sternum
ribs
1
24
80www.indiandentalacademy.com

APPENDICULAR SKELETON
Pectoral (shoulder) girdles
Clavicle 2
Scapula 2
Upper extremities
Humerus 2
Ulna 2
Radius 2
Carpals 16
Metacarpals 10
Phalanges 28
Pelvic (hip) girdle
Coxal, Pelvic or hip bone 2
Lower extremities
Femur 2
Fibula 2
Tibia 2
Patella 2
Tarsals 14
Metatarsals 10
Phalanges 28
126 Total = 206www.indiandentalacademy.com

CRANIAL BONES
a. Frontal Bone 1
b. Parietal Bone 2
c. TemporalBone 2
d. Occipital Bone 1
e. Sphenoid Bone 1
f. Ethmoid Bone 1
abb
c
d
e
f

FACIAL BONES
Nasal Bone 2
Maxillae 2
Zygomatic Bones 2
Mandible 1
Lacrimal Bones 2
Palatine Bones 2
Inferior Nasal Conchae 2
Vomer 1

CLASSIFICATION OF BONES
 A. According to Position
 Axial : Bones forming the axis of the body,
e.g., skull, ribs, sternum and vertebrae.
 Appendicular : Bones forming the skeleton
of limbs (appendages of the body).

According to Size and Shape
 1. Long Bones : present
in upper and lower limbs.
 Possess three parts : (i)
upper end (ii) shaft (iii)
lower end.
 The two ends are usually
expanded for forming
articulations and giving
attachments to muscles and
ligaments. The shaft is
tubular with a central
medullary cavity.
 Examples : Humerus,
radius, ulna, femur, tibiawww.indiandentalacademy.com

 2. Short long bones :
Same as above but are
miniature in size.
Examples : Metacarpals,
metatarsals and
phalanges.

 3. Short Bones :
Small, polyhedral and
generally cuboidal in
shape. Examples :
Carpal and tarsal bones.

 4. Flat Bones : Expanded and plate like.
They protect vital structure and provide
extensive areas for muscular attachment.
Examples : Scapula, sternum, ribs, parietal and
frontal bones.

 5. Irregular bones : Irregular in general outline and
do not fit in any of the above categories. Examples :
Vertebrae, some skull bones.
 6. Pneumatic bones : Flat or irregular bones
possessing a hollow space within their body which
contains air. Presence of air filled spaces provide
economical methods of expansion of bones in size
and make them lighter. Examples : Ethmoid, maxilla

 7. Sesamoid bones : Sesamoid means “seed
like”. They are nodules of bone which develop
in certain tendons and do not possess
periosteum and Haversian systems. They ossify
after birth. Examples : Pisiform, patella (which
is the largest sesamoid bone and develops in
quadriceps femoris tendon).

C. According to Gross Structure
1. Compact (Lamellar)
Bone : the outer
cortical part of long
bones, which is hard
and has a
homogeneous
appearance.

 This tissue gives bones their smooth, white, and solidThis tissue gives bones their smooth, white, and solid
appearanceappearance
 It is thickest midway between the two ends of the boneIt is thickest midway between the two ends of the bone
& gradually tapers towards the ends& gradually tapers towards the ends
 Accounts for 80% of the total bone mass of an adultAccounts for 80% of the total bone mass of an adult
skeleton.skeleton.
 Compact bone may also be referred to as dense boneCompact bone may also be referred to as dense bone
or cortical boneor cortical bone
 Compact bone tissue provides protection and support
and helps the long bones resist the stress of weight
placed on them.

Provides numerous
routes so that nutrients
can reach the osteocytes
and wastes can be
removed.
Each central canal,
with its surrounding
lamellae, lacunae,
osteocytes and
canaliculi, is called an
osteon (Haversian
system). The areas
between osteons contain
interstitial lamellae.

Trabecular boneTrabecular bone
 Filling the interior of theFilling the interior of the
organ is theorgan is the
trabecular bonetrabecular bone tissue (antissue (an
open cellopen cell porousporous networknetwork
also called cancellous oralso called cancellous or
spongy bone)spongy bone)
 Accounts for the remainingAccounts for the remaining
20% of total bone mass,20% of total bone mass,
but has nearly ten times thebut has nearly ten times the
surface area of compactsurface area of compact
bone.bone.
 Examples :Flat, Short and
Irregular Bones and ends
of long bones www.indiandentalacademy.com

It consists of an irregular
latticework of thin plates of
bone called Trabeculae.
The spaces between the
trabeculae of some bones
are filled with red marrow.
The cells of red marrow are
responsible for producing
blood cells. Within the
trabeculae lie lacunae, which
contain osteocytes.

3.Diploic Bone : Consists of inner and outer
tables of compact bone with an intervening
porous layer which is occupied by a spongy
substance consisting of bone marrow and
diploic veins e.g., most of cranial bones

D. According to Development
 Embroyonic mesenchymatous tissue is the
precursor of a bone, further development
occurs by two methods.
1. Membranous (Ectochondral) bones : Which
develop in membrane.
2. Cartilaginous (Endochondral) bones : Which
develop in cartilage.

FunctionsFunctions
 Bones have eight main functions:Bones have eight main functions:
 Protection — Bones can serve to protect internalProtection — Bones can serve to protect internal
organs, such as theorgans, such as the skullskull protecting theprotecting the brainbrain or theor the
ribsribs protecting theprotecting the heartheart andand lungslungs..
 Shape — Bones provide a frame to keep the bodyShape — Bones provide a frame to keep the body
supported.supported.
 Blood production — TheBlood production — The marrowmarrow, located within the, located within the
medullary cavitymedullary cavity of long bones and interstices ofof long bones and interstices of
cancellous bone, produces blood cells in a processcancellous bone, produces blood cells in a process
calledcalled haematopoiesishaematopoiesis..www.indiandentalacademy.com

 Mineral storage — Bones act as reserves of mineralsMineral storage — Bones act as reserves of minerals
important for the body, most notablyimportant for the body, most notably calciumcalcium andand
phosphorusphosphorus..
 Movement — Bones,Movement — Bones, skeletal musclesskeletal muscles,, tendonstendons,,
ligamentsligaments andand jointsjoints function together to generate andfunction together to generate and
transfer forces so that individual body parts or thetransfer forces so that individual body parts or the
whole body can be manipulated in three-dimensionalwhole body can be manipulated in three-dimensional
space. The interaction between bone and muscle isspace. The interaction between bone and muscle is
studied instudied in biomechanicsbiomechanics..

 Acid-base balance — Bone buffers the blood againstAcid-base balance — Bone buffers the blood against
excessive pH changes by absorbing or releasingexcessive pH changes by absorbing or releasing
alkaline salts.alkaline salts.
 Detoxification — Bone tissues can also storeDetoxification — Bone tissues can also store
heavy metalsheavy metals and other foreign elements, removingand other foreign elements, removing
them from the blood and reducing their effects onthem from the blood and reducing their effects on
other tissues. These can later be gradually released forother tissues. These can later be gradually released for
excretion.excretion.
 Sound transduction — Bones are important in theSound transduction — Bones are important in the
mechanical aspect ofmechanical aspect of hearinghearingwww.indiandentalacademy.com

Structural Anatomy of
Bone


1. Diaphysis
( dia = through;
physis = growth).
 2. Epiphyses
(epi=above: physis
= growth,singular
is epiphysis).
 3. Metaphysis

 4. Articular
cartilage : A thin
layer of hyaline
cartilagecovering
the epiphysis where
the bone forms a
joint with
another bone.

 5. Periosteum : (peri= around;osteo= bone) A dense, white,
fibrous covering around the surface of the bone not covered
by articular cartilage. Two layers.

 Outer fibrous layer is
composed of
connective tissue
containing blood
vessels, lymphatic
vessels, and nerves that
pass into the bone.
 Inner osteogenic
layer contains elastic
fibers, blood vessels,
osteoprogenitor cells,
osteoclasts, and
osteoblasts.

Functions of periosteumFunctions of periosteum
 Provides a medium through which muscles,Provides a medium through which muscles,
tendons & ligaments are attached to bonetendons & ligaments are attached to bone
 Presence of blood vessels – nutritionPresence of blood vessels – nutrition
 Presence of osteoprogenitor cells in deeperPresence of osteoprogenitor cells in deeper
layers – forms bone when requiredlayers – forms bone when required
 Fibrous layer is sometimes calledFibrous layer is sometimes called limiting layerlimiting layer
prevents bone tissue from spilling out intoprevents bone tissue from spilling out into
neighboring tissues – exostoses, ridges, tubercleneighboring tissues – exostoses, ridges, tubercle

 6. Medullary or marrow
cavity.

 7. Endosteum. A layer
of osteoprogenitor cells
and osteoblasts that lines
and medullary cavity and
also contains scattered
osteoclasts

COMPOSITION OF BONE

Organic part – 33% - 35%
                    Collagen – 88% - 90% (Type – I)
                    Non collagen – 10% - 11%.
          Glycoproteins – 6% - 9%
          Proteoglycans – 0.8% (sulfated and Non sulfated)
          Sialoproteins – 0.35%
          Lipids – 0.4%
Inorganic Part – 65% - 67%
-   Calcium & Phosphates – 95%
     (Hydroxyapatite Crystals – Ca10
(Po4
)6
(OH)2
)
-   Magnesium
- Trace elements – Nickel, Iron, Fluoride, Cadmium,
Magnesium, Zinc and  Molybdenum.

Cellular structureCellular structure
 OsteoblastsOsteoblasts areare
mononucleate bone-formingmononucleate bone-forming
cells which descend fromcells which descend from
osteoprogenitorosteoprogenitor cells locatedcells located
in thein the periosteumperiosteum and theand the
bone marrowbone marrow

 When bone is no longer forming, the surface
osteoblasts become inactive and are termed
lining cells
 Osteoblasts exhibit high levels of alkaline
phosphate on the outer surface of their plasma
membranes, this distinguishes the osteoblast
from the fibroblast

 Osteoblasts secrete, in
addition to type I and
type V collagen and small
amounts of several
noncollagenous proteins,
a variety of cytokines.
 Osteoblasts under the
stimulation of interleukin
6 also produce their own
hydrolytic enzymes that
aid in destroying or
modifying the
unmineralized matrix.
Thus freeing the
osteoblast from its own
secreted matrix.

 Osteoid is primarily composed of Type IOsteoid is primarily composed of Type I collagencollagen &&
matrix glaprotein (MGP) or osteocalcin.matrix glaprotein (MGP) or osteocalcin.
 Other proteins are transforming growth factor (TGF),Other proteins are transforming growth factor (TGF),
insulin like growth factor (IGF) , fibroblast growthinsulin like growth factor (IGF) , fibroblast growth
factor (FGF) & platelet derived growth factorfactor (FGF) & platelet derived growth factor
(PDGF)(PDGF)
 They produceThey produce alkaline phosphatasealkaline phosphatase, an enzyme that, an enzyme that
has a role in the mineralisation of bone, as well ashas a role in the mineralisation of bone, as well as
manymany matrix proteinsmatrix proteins
 They cover all of the available bone surface andThey cover all of the available bone surface and
function as a barrier for certain ionsfunction as a barrier for certain ions

 OsteocytesOsteocytes originateoriginate
from osteoblasts whichfrom osteoblasts which
have migrated into andhave migrated into and
become trapped andbecome trapped and
surrounded by bonesurrounded by bone
matrix which theymatrix which they
themselves producethemselves produce

 Function –
 Maintain bone as living
tissue because of their
metabolic activity
 Maintain exchange of
calcium between bone &
ECF

 OsteoclastsOsteoclasts are the cellsare the cells
responsible forresponsible for
bone resorptionbone resorption
(remodeling of bone to(remodeling of bone to
reduce its volume).reduce its volume).

 Osteoclasts are large,Osteoclasts are large,
multinucleated cellsmultinucleated cells
located on bone surfaceslocated on bone surfaces
in what are calledin what are called
howships lacunae orhowships lacunae or
resorption pitsresorption pits

 These lacunae, or resorption pits, are left behindThese lacunae, or resorption pits, are left behind
after the breakdown of bone and often presentafter the breakdown of bone and often present
asas scallopedscalloped surfaces.surfaces.
 Osteoclasts mature and/or migrate to discreteOsteoclasts mature and/or migrate to discrete
bone surfaces. Upon arrival, active enzymes,bone surfaces. Upon arrival, active enzymes,
such assuch as tartrate resistant acid phosphatasetartrate resistant acid phosphatase, are, are
secreted against the mineral substrate.secreted against the mineral substrate.

OsteogenesisOsteogenesis

Area of mesenchyme prior to mesenchymal condensation.
Intramembranous bone formationIntramembranous bone formation

 At the site where
membrane bone is
to be formed, the
mesenchymal cells
become densely
packed.
 Region becomes
highly vascular

 Mineralisation involves osteoblasts secretingMineralisation involves osteoblasts secreting
vesiclesvesicles containing alkaline phosphatase.containing alkaline phosphatase.
 This cleaves the phosphate groups and acts asThis cleaves the phosphate groups and acts as
the foci for calcium and phosphate deposition.the foci for calcium and phosphate deposition.
 The vesicles then rupture and act as a centre forThe vesicles then rupture and act as a centre for
crystals to grow on.crystals to grow on.

Endochondral bone formationEndochondral bone formation
 Endochondral bone formation occurs at the
ends of all long bones, vertebrae, ribs and at the
head of the mandible and base of the skull.
 Early in embryonic development, there is a
condensation of mesenchymal cells.
 Cartilage cells differentiate from these
mesenchymal cells, chondroblast.

 The early stages of hypertrophy the chondroblasts
secrete mainly type II collagen
 The combination of increased cell size and increased
cell secretion leads to an increase in the size of the
cartilaginous end of the bone.
 As the chondroblast reaches maximum size, it
secretes type X collagen, chondrocalcin, and bone
sialoprotein, which create a matrix environment with
the potential to mineralize matrix.

 Mineralization begins in the zone of mineralization

 Within the perichondrium in the diaphysis, there is
increased vascularization, perichondrium coverts to a
periosteum and bone begins to form
 The middle of the cartilage occurs, cells called
chondroclasts resorb most of the mineralized cartilage
matrix, making room for further vascular in growth.
 Mesenchymal (perivascular) cells accompany the
invading blood vessels, proliferating and migrating
onto the remains of the mineralized cartilage matrix

 The mesenchymal cells differentiate into obsteoblasts and
begin to deposit osteoid on the mineralized cartilage columns
and then to mineralize it.
 As the bone matrix is produced, the mineralized cartilage
matrix becomes an irregularly shaped central zone core for a
circular rim of new bone matrix.
 Some of the osteoblasts are surrounded by bone matrix and
become osteocytes. Collectively termed the primary
spongiosa
 Osteoclasts progressively remove both the core of mineralized
cartilage and the surrounding bone. This process occurs at
approximately the same rate as cartilage formation, so volume
of the primary spongiosa remains relatively constant.www.indiandentalacademy.com

Bone physiologyBone physiology
 Calcium Stores – Amount and Distribution
• Bone: major reservoir of calcium: 99% of calcium is in
skeleton; about 1-2 kg
• Less than 1% (about 10g) is in soft tissues and
body fluids
 Normal Plasma calcium level – 9.4 mg %Normal Plasma calcium level – 9.4 mg %
 Normal PTH level is 10-60 ng/L

Vitamin D PTH Calcitonin

Blood calcium Increased Drastically
increased
Decreased
Main action Absorption from
gut
Demineralisation Opposes
demineralization
Calcium
absorption from
gut
Increased Increased
(Indirect)

Bone resorption Decreased Increased Decreased

Deficiency
manifestation
Rickets Tetany
Effect of excess Hypercalcemia+ Hypercalcemia+ + Hypocalcemia

Comparison of action of three major factors affecting serum
calcium

Growth Hormone
• Stimulates overall growth, particularly epiphyseal
cartilage
• Produced in anterior lobe of pituitary gland
• Lack causes pituitary dwarfism
• Excess causes gigantism
• Epiphyseal plates are already closed in adults: bones can
not elongate; excess GH causes increases in width by
periosteal growth; cause acromegaly, in which bones
become very thickened

Thyroid Hormone
 Lack of thyroxine causes arresting of growth
 There is early closure of epiphysis
• Childhood deficiency is associated with
dwarfism and cretinism

Bone Nutrition
• Insufficient protein: decrease in collagen
synthesis by osteoblasts
Rickets
• Inadequate vitamin D in children
•Can lead to permanent deformities of skeleton
• Vitamin D required for calcium absorption
(vitamin D stimulates mineralization of bone)
• Collagen and mucopolysaccharides continue to
form but don’t calcifywww.indiandentalacademy.com

• Leads to uncalcified osteoid at growing ends
of bone
• Easily deformed by strains of body weight
and activity

Osteomalacia
• Calcium or vitamin D deficiency in adults (adult
rickets)
• Osteomalacia: osteon + Gr. malakia, softness
• Deficient calcification of recently formed bone and
partial decalcification of already calcified matrix
• Decrease in amount of calcium per unit of bone Matrix
Decrease in bone mass: due to decreased bone formation,
increased bone resorption, or both
• Increased fracture risk, especially of vertebrae, hip,
wrist/forearm
• Common in elderly

Scurvy
• Associated with vitamin C deficiency
• Vitamin C necessary for osteoblasts to form normal
amount of collagen
• Causes local changes in calcification sites
• Formation of osteoid tissue is reduced and bone cortex
thickness is decreased as a result
• Collagen formed is normal but deficient; still becomes
mineralized
• Collagen deficiency stunts skeletal growth in the young
• Collagen deficiency retards fracture healing

OsteoporosisOsteoporosis
 Osteoporosis is aOsteoporosis is a diseasedisease of bone - leading to anof bone - leading to an
increased risk ofincreased risk of fracturefracture..
 In osteoporosis, theIn osteoporosis, the bone mineral densitybone mineral density
(BMD) is reduced, bone microarchitecture is(BMD) is reduced, bone microarchitecture is
disrupted, and the amount and variety of non-disrupted, and the amount and variety of non-
collagenouscollagenous proteins in bone is altered.proteins in bone is altered.
 Osteoporosis is most common in women afterOsteoporosis is most common in women after
thethe menopausemenopause, when it is called, when it is called
postmenopausal osteoporosispostmenopausal osteoporosis

 But may develop in men and premenopausalBut may develop in men and premenopausal
women in the presence of particular hormonalwomen in the presence of particular hormonal
disorders and otherdisorders and other chronicchronic diseases or as adiseases or as a
result ofresult of smokingsmoking andand medicationsmedications, specifically, specifically
glucocorticoidsglucocorticoids
 steroid-steroid- oror glucocorticoid-inducedglucocorticoid-induced
osteoporosisosteoporosis (SIOP or GIOP).(SIOP or GIOP).

 Normal is a T-score of -1.0 or higherNormal is a T-score of -1.0 or higher
 OsteopeniaOsteopenia is defined as less than -1.0 and greater thanis defined as less than -1.0 and greater than
-2.5-2.5
 OsteoporosisOsteoporosis is defined as -2.5 or lower,is defined as -2.5 or lower, Z-scoreZ-score
 The Z-score is the number of standard deviations aThe Z-score is the number of standard deviations a
patient's BMD differ from the average BMD of theirpatient's BMD differ from the average BMD of their
age, sex, and ethnicity.age, sex, and ethnicity.
 This value is used in premenopausal women, menThis value is used in premenopausal women, men
under the age of 50, and in children.under the age of 50, and in children.

Risk Factors
1. Female > 50
2. Postmenopausal
3. First degree female relative with osteoporosis
4. Thin build, small bone (genetic, anorexic, excessive athleticism
with estrogen suppression)
5.Caucasian or Asian
6. Prolonged use of cortisone or prednisone
,hyperparathyroidism, antiseizure therapy (e.g. Dilantin)
7. Decreased estrogen levels
8. Early or surgically-induced menopause
< age 45 www.indiandentalacademy.com

Modifiable Risk
Factors
1. Low lifetime calcium intake
2. Sedentary lifestyle
3. Smoker or ex-smoker
4. Excessive alcohol intake
5. Excessive caffeine intake
6. Amenorrhea
7. High meat consumption
8. High sodium intake
9. Immobilization

Pagets diseasePagets disease
 Paget’s disease is also called osteitis deformans.Paget’s disease is also called osteitis deformans.
It is named after Sir James Paget, an EnglishIt is named after Sir James Paget, an English
doctor who first described the disease in 1876.doctor who first described the disease in 1876.
 Paget’s disease causes a malfunction in thePaget’s disease causes a malfunction in the
normal process of bone remodelling.normal process of bone remodelling.

 When an area of bone is destroyed in a personWhen an area of bone is destroyed in a person
with Paget’s disease, the bone that replaces it iswith Paget’s disease, the bone that replaces it is
soft and porous.soft and porous.
 Soft bone can be weak and easily bend, leadingSoft bone can be weak and easily bend, leading
to shortening of the affected part of the body. to shortening of the affected part of the body.
 The bone replacement also takes place veryThe bone replacement also takes place very
quickly and excess bone may be formed. Thisquickly and excess bone may be formed. This
can cause the bone to get larger, be painful andcan cause the bone to get larger, be painful and
break easily.break easily.

 The bone affected by Paget’s disease also tends toThe bone affected by Paget’s disease also tends to
have more blood vessels than normal. This causes anhave more blood vessels than normal. This causes an
increase in the blood supply to the area, and as aincrease in the blood supply to the area, and as a
result the area may feel warmer than usual.result the area may feel warmer than usual.
 The disease can affect any bone but more commonlyThe disease can affect any bone but more commonly
affects the spine, pelvis, skull, femur and tibiaaffects the spine, pelvis, skull, femur and tibia
 Paget’s disease can lead to other medical conditionsPaget’s disease can lead to other medical conditions
including osteoarthritis, kidney stones and heartincluding osteoarthritis, kidney stones and heart
disease.disease.

 If Paget’s disease affects skull, head mayIf Paget’s disease affects skull, head may
increase in size from front to back. Hearing lossincrease in size from front to back. Hearing loss
may result if there is involvement of some of themay result if there is involvement of some of the
small bones in the middle ear or pressure issmall bones in the middle ear or pressure is
placed on the nerves related to hearing.placed on the nerves related to hearing.

Bone healingBone healing

 Immobilization and surgery may facilitate healingImmobilization and surgery may facilitate healing
 Fracture ultimately heals through physiologicalFracture ultimately heals through physiological
processes.processes.
 The healing process is mainly determined by theThe healing process is mainly determined by the
periosteumperiosteum
 The periosteum is the primary source of precursorThe periosteum is the primary source of precursor
cells which develop intocells which develop into chondroblastschondroblasts andand
osteoblastsosteoblasts that are essential to thethat are essential to the healinghealing of bone.of bone.
 TheThe bone marrowbone marrow ,, endosteumendosteum, small, small blood vesselsblood vessels,,
andand fibroblastsfibroblasts are secondary sources of precursorare secondary sources of precursor
cellscells

 Phases of fracture healingPhases of fracture healing
 1.1. Reactive PhaseReactive Phase
 i. Fracture and inflammatory phasei. Fracture and inflammatory phase
 ii. Granulation tissue formationii. Granulation tissue formation
 2.2. Reparative PhaseReparative Phase
 iii. Callus formationiii. Callus formation
 iv. Lamellar bone depositioniv. Lamellar bone deposition
 3.3. Remodeling PhaseRemodeling Phase
 v. Remodeling to original bone contourv. Remodeling to original bone contour

ReactiveReactive
 The first change seen by light and electron microscopy is theThe first change seen by light and electron microscopy is the
presence of blood cells within the tissues which are adjacent topresence of blood cells within the tissues which are adjacent to
the injury site.the injury site.
 Soon after fracture, the blood vessels constrict, stopping anySoon after fracture, the blood vessels constrict, stopping any
further bleeding.further bleeding.
[1]Within a few hours after fracture, the extravascular blood[1]Within a few hours after fracture, the extravascular blood
cells, known as a "cells, known as a "hematomahematoma", form a blood clot. All of the", form a blood clot. All of the
cells within the blood clot degenerate and diecells within the blood clot degenerate and die
[2]Some of the cells outside of the blood clot, but adjacent to the[2]Some of the cells outside of the blood clot, but adjacent to the
injury site, also degenerate and die.injury site, also degenerate and die.
[3]Within this same area, the[3]Within this same area, the fibroblastsfibroblasts survive and replicate.survive and replicate.
They form a loose aggregate of cells, interspersed with smallThey form a loose aggregate of cells, interspersed with small
blood vessels, known asblood vessels, known as granulation tissuegranulation tissue

ReparativeReparative
 The cells of the periosteum replicate and transform.The cells of the periosteum replicate and transform.
 The periosteal cells proximal to the fracture gap develop intoThe periosteal cells proximal to the fracture gap develop into
chondroblastschondroblasts and form hyaline cartilage.and form hyaline cartilage.
 The periosteal cells distal to the fracture gap develop intoThe periosteal cells distal to the fracture gap develop into
osteoblasts and form woven bone.osteoblasts and form woven bone.
 The fibroblasts within the granulation tissue also develop intoThe fibroblasts within the granulation tissue also develop into
chondroblasts and form hyaline cartilage.chondroblasts and form hyaline cartilage.
 These two new tissues grow in size until they unite with theirThese two new tissues grow in size until they unite with their
counterparts from other pieces of the fracture.counterparts from other pieces of the fracture.
 This process forms theThis process forms the fracture callusfracture callus..
 Eventually, the fracture gap is bridged by the hyaline cartilageEventually, the fracture gap is bridged by the hyaline cartilage
and woven bone, restoring some of its original strengthand woven bone, restoring some of its original strengthwww.indiandentalacademy.com

RemodelingRemodeling
 The remodeling process substitutes the trabecularThe remodeling process substitutes the trabecular
bone with compact bonebone with compact bone
 The trabecular bone is first resorbed by osteoclasts,The trabecular bone is first resorbed by osteoclasts,
creating a shallow resorption pit known as acreating a shallow resorption pit known as a
"Howship's lacuna"."Howship's lacuna".
 Then osteoblasts deposit compact bone within theThen osteoblasts deposit compact bone within the
resorption pit.resorption pit.
 Eventually, the fracture callus is remodelled into aEventually, the fracture callus is remodelled into a
new shape which closely duplicates the bone's originalnew shape which closely duplicates the bone's original
shape and strength.shape and strength.www.indiandentalacademy.com

 Phase IPhase I
 1. Bleeding and fracture hematoma forms1. Bleeding and fracture hematoma forms
2. Inflammation2. Inflammation
3. Next 2-3 Days, granulation tissue formation3. Next 2-3 Days, granulation tissue formation
4. Osteogenic Cells invade tissue and lay down osteoid4. Osteogenic Cells invade tissue and lay down osteoid
 Phase IIPhase II
 5. At 3 weeks a soft callus forms consisting of osteoid5. At 3 weeks a soft callus forms consisting of osteoid
and cartilageand cartilage
6. Hard tissue callus forms in 6 - 12 weeks6. Hard tissue callus forms in 6 - 12 weeks
7. Clinical union of bone ends occurs in 12 - 16 weeks7. Clinical union of bone ends occurs in 12 - 16 weeks
 Phase IIIPhase III
 8. Remodeling of united fracture8. Remodeling of united fracture

Correlation of bone structure & someCorrelation of bone structure & some
of its propertiesof its properties
 Effect of function on bone was noted first inEffect of function on bone was noted first in
femurfemur
 Meyer an anatomist with the help ofMeyer an anatomist with the help of
mathematician Cullmann in 1867 propoundedmathematician Cullmann in 1867 propounded
what was later to be calledwhat was later to be called the trajectorialthe trajectorial
theory of bone formationtheory of bone formation

 The alignment of bonyThe alignment of bony
trabeculae in spongiosatrabeculae in spongiosa
followed a definitefollowed a definite
engineering principlesengineering principles
 If lines were drawnIf lines were drawn
following columns offollowing columns of
oriented bony elements-oriented bony elements-
trajectories similar totrajectories similar to
those seen in cranethose seen in crane

 Many of these trajectories crossed at right angles- anMany of these trajectories crossed at right angles- an
excellent arrangement to resist the manifold stressesexcellent arrangement to resist the manifold stresses
on the condyle of the femuron the condyle of the femur
 The design of the femur in its entirety was in harmonyThe design of the femur in its entirety was in harmony
with the best engineering principleswith the best engineering principles
 Femur is hollowed tube , using the same amount ofFemur is hollowed tube , using the same amount of
material it was best able to resist bending & shearingmaterial it was best able to resist bending & shearing
stressesstresses
 If the cross section of femur was solid with sameIf the cross section of femur was solid with same
cross sectional material the shaft would be smaller &cross sectional material the shaft would be smaller &
weakerweaker

 (John G. Skedros and Sidney L. Baucom)(John G. Skedros and Sidney L. Baucom) TheThe
trabecular tracts from the tension- and compression-trabecular tracts from the tension- and compression-
loaded sides of a bending environment will:loaded sides of a bending environment will:
(1) follow ‘lines’ (trajectories) of tension/compression(1) follow ‘lines’ (trajectories) of tension/compression
stress that resemble an arch with its apex on a neutralstress that resemble an arch with its apex on a neutral
axisaxis
(2) form orthogonal (90°) intersections. These predictions(2) form orthogonal (90°) intersections. These predictions
were analysed in proximal femora of chimpanzees andwere analysed in proximal femora of chimpanzees and
modern humans.modern humans.

Wolff's lawWolff's law by the Germanby the German
Anatomist/Surgeon Julius Wolff (1836-1902Anatomist/Surgeon Julius Wolff (1836-1902))
 States that bone in a healthy person or animalStates that bone in a healthy person or animal
will adapt to the loads it is placed under.will adapt to the loads it is placed under.
 He claimed that trabecular alignment wasHe claimed that trabecular alignment was
primarily due to functional forcesprimarily due to functional forces
 Roux & others introduced functional factors inRoux & others introduced functional factors in
the development of “ law of transformation ofthe development of “ law of transformation of
bone”bone”
 It stated that the stresses of tension or pressureIt stated that the stresses of tension or pressure
on bone stimulate bone formationon bone stimulate bone formation

 If loading on a particular bone increases, the bone willIf loading on a particular bone increases, the bone will
remodel itself over time to become stronger to resistremodel itself over time to become stronger to resist
that sort of loading.that sort of loading.
 The external cortical portion of the bone becomesThe external cortical portion of the bone becomes
thicker as a result.thicker as a result.
 The converse is true as well: As it is lessThe converse is true as well: As it is less
metabolically costly to maintain and there is nometabolically costly to maintain and there is no
stimulus for continued remodeling that is required tostimulus for continued remodeling that is required to
maintain bonemaintain bone

ExamplesExamples
 The racquet-holding arm bones of tennis playersThe racquet-holding arm bones of tennis players
become much stronger than those of the other arm.become much stronger than those of the other arm.
Their bodies have strengthened the bones in theirTheir bodies have strengthened the bones in their
racquet-holding arm since it is routinely placed underracquet-holding arm since it is routinely placed under
higher than normal stresses.higher than normal stresses.
 Astronauts who spend a long time in space will oftenAstronauts who spend a long time in space will often
return to Earth with weaker bones, since gravity hasn'treturn to Earth with weaker bones, since gravity hasn't
been exerting a load on their bones. Their bodies havebeen exerting a load on their bones. Their bodies have
reabsorbed much of the mineral that was previously inreabsorbed much of the mineral that was previously in
their bonestheir bones

 Weightlifters often display increases in boneWeightlifters often display increases in bone
density in response to their training.density in response to their training.
 Fighters who punch or kick objects withFighters who punch or kick objects with
increasing intensity (or of increasing hardness)increasing intensity (or of increasing hardness)
to develop striking power to damage opponents,to develop striking power to damage opponents,
often display increases in bone density in theoften display increases in bone density in the
striking area.striking area.

 Abnormal pressure on bone can change – patients withAbnormal pressure on bone can change – patients with
scoliosis who are treated with milwaukee bracescoliosis who are treated with milwaukee brace
 Constant pressure produces marked effect on verticalConstant pressure produces marked effect on vertical
dimension & teethdimension & teeth
 Stimulating influence of muscles causes bone toStimulating influence of muscles causes bone to
change-change-
 Adaptive changes occur in Muscles & soft tissue butAdaptive changes occur in Muscles & soft tissue but
once growth is complete muscles cannot lengthen toonce growth is complete muscles cannot lengthen to
accommodate an increase in bony bulkaccommodate an increase in bony bulk

 In pathologic situationIn pathologic situation
like acromegaly there islike acromegaly there is
morphologic change inmorphologic change in
the bone as it adapts tothe bone as it adapts to
length of mature muscleslength of mature muscles
which are not aswhich are not as
responsive to sameresponsive to same
endocrine stimulusendocrine stimulus

 In alveolar process surrounding teeth that have noIn alveolar process surrounding teeth that have no
opposing dental units the radiographs show looseopposing dental units the radiographs show loose
trabecular structure – generalised radiolucencytrabecular structure – generalised radiolucency
surrounding non functional teethsurrounding non functional teeth
 Restoration of these teeth by artificial replacementRestoration of these teeth by artificial replacement
brings an increase in bony trabeculaebrings an increase in bony trabeculae
 (Benninghoff ) study of architecture of cranial & facial(Benninghoff ) study of architecture of cranial & facial
skeleton & stress trajectories – involve both cortical &skeleton & stress trajectories – involve both cortical &
spongy bonespongy bone

 Purposefulness of design accounts for shape ofPurposefulness of design accounts for shape of
human headhuman head
 Maximum strength with minimum materialMaximum strength with minimum material
 Sinus cavities in headSinus cavities in head

 According to Benninghoff stress trajectoriesAccording to Benninghoff stress trajectories
obeyed no individual bone limits but demandsobeyed no individual bone limits but demands
of functional forcesof functional forces
 So head is composed of only 2 bones –So head is composed of only 2 bones –
craniofacial skeletal unit & mandible( the onlycraniofacial skeletal unit & mandible( the only
movable bone)movable bone)
 Stress trajectories emanating from above theStress trajectories emanating from above the
teeth in maxillary arch passing superiorly toteeth in maxillary arch passing superiorly to
zygomatic arch or jugal buttresszygomatic arch or jugal buttress

 There are 3 main vertical pillars of trajectories, allThere are 3 main vertical pillars of trajectories, all
arising from alveolar process & ending in base of skullarising from alveolar process & ending in base of skull
 The canine pillarThe canine pillar
 The zygomatic pillarThe zygomatic pillar
 The pterygoid pillarThe pterygoid pillar
 These trajectories curve around the sinuses & nasal &These trajectories curve around the sinuses & nasal &
orbital cavitiesorbital cavities
 Horizontal reinforcing members for vertical stressHorizontal reinforcing members for vertical stress
trajectory columns- supraorbital & infraorbital bonytrajectory columns- supraorbital & infraorbital bony
eminences & zygomatic buttresseseminences & zygomatic buttresses

 The canine pillarThe canine pillar
 The zygomatic pillarThe zygomatic pillar
 The pterygoid pillarThe pterygoid pillar

 Also included are hard palate, walls of orbit,Also included are hard palate, walls of orbit,
Lesser wings of sphenoid.Lesser wings of sphenoid.
 Sicher emphasizes the importance ofSicher emphasizes the importance of
supraorbital rim as a receptor of forcessupraorbital rim as a receptor of forces
transmitted to it by canine & zygomatic pillarstransmitted to it by canine & zygomatic pillars
 He believes that development of supraorbitalHe believes that development of supraorbital
ridge in lower primates & man is an adaptiveridge in lower primates & man is an adaptive
response to strong prognathism & heavyresponse to strong prognathism & heavy
masticatory pressuresmasticatory pressures

 Mandible- a unit byMandible- a unit by
itself & a movableitself & a movable
bonebone
 Trabecular columnsTrabecular columns
radiate from beneathradiate from beneath
the teeth in thethe teeth in the
alveolar process joinalveolar process join
together in a commontogether in a common
stress pillarstress pillar
terminating interminating in
mandibular condylemandibular condyle

 Mandibular canal & nerveMandibular canal & nerve
are protected at the sameare protected at the same
time by this concentrationtime by this concentration
of trabeculae – “ unloadedof trabeculae – “ unloaded
nerve concept”nerve concept”
 Thick cortical layer ofThick cortical layer of
compact bone along thecompact bone along the
lower border of mandiblelower border of mandible
offers the greatestoffers the greatest
resistance to bendingresistance to bending
forcesforces

 Other trajectories – sumphysis , gonial angle &Other trajectories – sumphysis , gonial angle &
leading downward from coronoid process intoleading downward from coronoid process into
the ramus & body of mandiblethe ramus & body of mandible
 Accessory trajectories are due to direct effect ofAccessory trajectories are due to direct effect of
attachments of muscles of masticationattachments of muscles of mastication

BibliographyBibliography
 Graber T.M :Orthodontics Principles And Practice, ThirdGraber T.M :Orthodontics Principles And Practice, Third
ed., Philadelphia 1996, W.B. Saunders Company,129-134ed., Philadelphia 1996, W.B. Saunders Company,129-134
 Enlow DH, Hans MG: Essentials of Facial Growth,
W.B. Saunders, ed. 3, 1996, Philadelphia
 John G. Skedrosand Sidney L. Baucom,MathematicalJohn G. Skedrosand Sidney L. Baucom,Mathematical
analysis of trabecular ‘trajectories’ in apparentanalysis of trabecular ‘trajectories’ in apparent
trajectorial structures: The unfortunate historicaltrajectorial structures: The unfortunate historical
emphasis on the human proximal femur , julyemphasis on the human proximal femur , july
2006,Elsevier,Edition 1.2006,Elsevier,Edition 1.
 Alexandrridis caputo Thanos,Alexandrridis caputo Thanos, J Oral Rehabil. 1985J Oral Rehabil. 1985
Nov;12(6):499-507Nov;12(6):499-507www.indiandentalacademy.com

 W.Eugene Robertsa , James K Hartsfield ,Bone
development and function: genetic and environmental
mechanisms
 Brighton, Carl T. and Robert M. Hunt (1986),Brighton, Carl T. and Robert M. Hunt (1986),
"Histochemical localization of calcium in the fracture"Histochemical localization of calcium in the fracture
callus with potassium pyroantimonate: possible role ofcallus with potassium pyroantimonate: possible role of
chondrocyte mitochondrial calcium in calluschondrocyte mitochondrial calcium in callus
calcification",calcification", Journal of Bone and Joint SurgeryJournal of Bone and Joint Surgery,, 68-A (5)68-A (5)::
703703
 Ten Cate AR: Oral Histology, ed.3, 1989, C.V Mosby,Ten Cate AR: Oral Histology, ed.3, 1989, C.V Mosby,
30-35.30-35.

 Text book of Medical Physiology – Guyton and
Hall – 9th Edition
 Principles of Anatomy and Physiology – Gerard J.
Tortora – 6th & 8th Editions
 Gray’s Anatomy – Peter L. Williams – 38th
Edition
 Oral Histology – Richard Tencate – 5th Edition
 Orban’s Oral Histology and Embryology – S.N.
Bhaskar – 10th Edition

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